Atrial Septal Defect (ASD, Ostium Secundum Defect)

Atrial septal defect (ASD) is a congenital heart defect. In foetal circulation there is normally an opening between the two atria (the upper chambers of the heart) to allow blood to bypass the lungs. This opening usually closes about the time the baby is born. If the opening is persistent it is called an ASD, and thus blood continues to bypass the lungs. This is called a shunt.

There are generally three types of ASD:

Ostium primum atrial septal defect: Occurs when there is interference with the development of the septum primum at its lower margin, associated with abnormal development of the endocardial cushions - there is no inferior rim of atrial septal tissue. This defect is associated with abnormalities of the mitral and tricuspid valves as well as abnormalities of the upper portion of the interventricular septum.Ostium secundum defect: Located in the central portion of the atrial septum, related to the foramen ovale. It results from the inadequate closure of the central hole in the septum primum by the septum secundum - this also produces the fossa ovalis defect. This is the most common form of ASD.Sinus venosus defect: In the superior portion of the atrial septum which generally extends into the superior vena cava.

About 1 in 2,000 live births. Females outnumber males 3:1 in incidence.

The aetiology of congenital heart defects is not understood but several factors are known to be associated:

Maternal drug abuse, alcohol abuse and radiation exposure;Maternal infection, particularly rubella;Genetic abnormalities;Chromosomal abnormalities (septal defects are associated with Trisomy 21- Down's syndrome).

ASDs may occur in isolation or may be associated with other malformations:

Spontaneous closure of ASDs is rare after the first 2 years of life;ASDs allow shunting of blood from one side of the circulation to the other. There are no great pressure differentials across the two atria and shunting is usually from left to right due to the greater compliance of the right heart chambers. Flow rates across the defect are usually not high;Increased flow to the pulmonary circulation eventually leads to pulmonary hypertension, usually by the 4th decade. Atrial arrhythmias, particularly AF are common due to the physical distention of the atria;In severe cases the shunt can eventually reverse so that blood bypasses the lungs - this is termed Eisenmenger's syndrome and is a poor prognostic factor.Most are asymptomatic until later in life; Susceptibility to chest infections is common; Subtle failure to thrive may occur in some children; Exertional dyspnoea (shortness of breath) and weakness are sometimes reported; Later in life, palpatations associated with AF and congestive heart failure are common with exertional dyspnoea and orthopnoea.

Chest x-ray: Prominent pulmonary vasculature may be seen. Right ventricular hypertrophy may be seen.

ECG: May show some right bundle branch block and right axis deviation.

Most commonly symptoms dont develop until the twenties when evidence of pulmonary vascular disease becomes apparent. With increasing age, risk of developing cardiac rhythm disturbances increases. By the age of 40 most patients are severely symptomatic. Cardiac failure is the most common cause of death. Others include emboli and infections.

Large ASDs (where pulmonary blood flow is greater than 150% normal) should be repaired surgically as early as possible, preferably before 10 years. The outlook is good if pulmonary hypertension (high blood pressure in the lungs) has not developed. Otherwise, medical management of heart failure and other complications such as arrhythmias should be instigated.

Anderson RH. Paediatric Cardiology. New York, NY: Churchill Livingstone; 1987. [Book]Behrman RE, Kliegman R, Jenson HB, et al. Nelson Textbook of Pediatrics (17th edition). Philadelphia: Saunders; 2004. [Book]Schlant RC, Alexander RW, Fuster V (eds). Hurst's The Heart (8th edition). New York, NY: McGraw-Hill; 1994. [Book]Kumar P, Clark M (eds). Clinical Medicine (4th edition). Edinburgh: WB Saunders Company; 1998. [Book]Rudolph CD, Rudolph AM, Hostetter MK, et al. Rudolph's Pediatrics (21st edition). New York, NY: McGraw-Hill; 2003. [Book]

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Atrial Fibrillation (AF)

Atrial fibrillation (AF) is a disorder of the rhythm of the heart. It results from disorganised electrical activity in the atria of the heart, which causes rapid stimulation of the ventricles, leading to an irregular pulse rate.  

Atrial fibrillation is the most common sustained rhythm disorder of the heart. It is more common in older people, and occurs in more than 5% of the population over 65 years in Western countries. In Australia, AF affects around 2% of the general population.

Many diseases of the heart can predispose to AF. This is particularly so for conditions that cause enlargement of the atria. In addition, there are also many non-cardiac disorders that predispose towards AF.

Common risk factors for atrial fibrillation include:

In 50% of patients with paroxysmal AF and 20% of patients with persistent or permanent AF, no underlying heart disease can be found. This is known as 'lone' AF.

In AF, the atria are continuously activated by rogue electrical currents at a rate of 350-600 beats a minute. The ventricles are unable to respond to such a high rate of stimulation, and therefore only a proportion of the impulses are translated into contractions of the heart.

AF can be classified into three groups:

Paroxysmal AF: The patient gets repeated, short episodes of chest palpitations that resolve spontaneously. In between these episodes, the heart is normal;Persistent AF: AF that does not resolve spontaneously, but resolves after treatment;Permanent AF: AF that persists or recurs despite treatment. It usually occurs in patients who already have diseased hearts.

If left untreated, AF can lead to various short- and long-term problems. In patients who have pre-existing heart failure, the rapid heart rate seen in AF can lead to low blood pressure, lung congestion, angina, or worsening of the heart failure. Untreated AF also increases the risk of stroke. This is because in AF the atria become dilated and contract ineffectively, which leads to blood clots developing in the atria. These clots can subsequently dislodge and travel to the brain and other organs, causing strokes and other organ damage.

The main risk factors for developing a stroke in patients with AF are:

Often, AF causes no symptoms and is discovered incidentally during routine examination or ECG. On the other hand, some patients can experience palpitations, light-headedness, fainting, fatigue, or shortness of breath. In patients with pre-existing heart failure, an episode of AF can cause worsening of their heart failure. A rapid heart rate can also cause angina in patients with pre-existing coronary artery disease.

As part of the assessment, the doctor may do an examination to look for signs of AF. This may involve feeling for the pulse and listening to the heart sounds. In addition, the doctor may also do a blood pressure measurement, check for signs of overactive thyroid (neck swelling, eye abnormalities, tremor), listen to the lungs, and check for leg swelling.

If the history and examination is suggestive of AF, an electrocardiogram (ECG) may be done to confirm the diagnosis. This is a simple test that records the electrical activity of the heart, and will show specific abnormalities if the patient is experiencing AF at that time. The image contains an example of the ECG in AF. Note that the distances/intervals between successive QRS waves (the tall spikes) are irregular in AF, in comparison with the regular QRS intervals in the normal ECG.

If the episodes of AF tend to come and go spontaneously and frequently, ambulatory ECG monitoring may be required. This involves wearing a device (Holter monitor) that records the ECG continuously over 24 hours so that any episodes of AF that occur during that period of time will be detected. For patients who experience less frequent but symptomatic episodes, a patient-activated event recorder may be used, whereby the patient activates the ECG recorder only when he/she experiences the symptoms of AF.

Sometimes a blood test may be needed to check for thyroid and electrolyte problems, both of which can cause AF. Lastly, some patients may need to have an echocardiogram, which uses ultrasound to look at the structure, size and functional capacity of the heart.

Although the symptoms of AF can be distressing and worrying, AF is a common condition with a good outlook if treated appropriately. With treatment, most patients can control their heart rate and rhythm to an acceptable level. 

The main aims of treatment of AF are:

Restore the normal heart rhythm;Reduce the risk of stroke.

If the episode of AF is precipitated by an illness such as pneumonia, pulmonary embolism or thyrotoxicosis, effective treatment of the primary illness will usually lead to spontaneous resolution of the AF.  

When to seek medical help

Anyone who experiences persistent palpitations should see their doctor for medical advice. If there are symptoms of a heart attack (chest pain lasting for more than 10 minutes that may radiate to the neck, jaw, back, shoulders or arms; shortness of breath; nausea; and sweatiness) or stroke (sudden weakness or numbness on one side of the face, arm or leg; slurred speech; balance difficulties; or loss of vision), it is an emergency and an ambulance should be called immediately.

Pharmacological treatment and cardioversion

Paroxysmal AF

People who experience occasional attacks without symptoms do not usually require treatment for their condition. However, those who experience troublesome symptoms may benefit from medication to control the attacks. Two classes of drugs, the ß-adrenoceptor antagonists and the class Ic antiarrhythmics (e.g. flecainide and propafenone), are drugs of first choice in this situation.

Persistent AF

A persistent episode of AF can be converted back to normal rhythm using electrical or pharmacological cardioversion. In electrical cardioversion, an electric 'shock' is given to the heart while the patient is anaesthetized, to restore the normal heart rhythm. In pharmacological cardioversion, medications are given as tablets or as an injection to revert the abnormal heart rhythm back to normal. 

It is important to restore normal rhythm early because the chance of success decreases and the chance of recurrence increases with longer durations of AF. In some situations, the patient may need to take an anticoagulant medication for 3 weeks before the procedure to reduce the risk of forming blood clots. After successful cardioversion, anticoagulant medication has to be continued for at least 4 weeks because the atria may take time to recover.

Cardioversion is sucessful in around 65-90% of patients, but relapse of AF is common. Some patients may need to take long term medications to maintain the normal heart rhythm and reduce the risk of relapse.

Permanent AF

In permanent AF where normal rhythm cannot be restored, treatment is then directed towards controlling the heart rate and reducing the risk of stroke. Various medications, including digoxin, ß-adrenoceptor antagonists and calcium antagonists (e.g. verapamil or diltiazem), are commonly used in these situations.

To minimize the risk of stroke, patients with AF may require long term medication (e.g. warfarin) to 'thin the blood' and stop it from forming blood clots. However, this is associated with an increased risk of bleeding complications. Aspirin has a lower risk of complications but is also less effective than warfarin. Therefore, the decision for 'blood-thinning' treatment has to be balanced between a patient's risk factors for stroke and the risk of bleeding complications.

Surgical treatment

Surgical treatment of AF is rarely necessary because medications achieve satisfactory control in most cases. Occasionally, permanent atrial pacing (an artificial pacemaker is implanted) or radiofrequency catheter ablation may be used to treat paroxysmal AF. Radiofrequency catheter ablation is a procedure that is done to remove or inactivate areas of the heart that are thought to be responsible for generating the abnormal electrical signals in AF.

In patients with troublesome, permanent AF, a surgical procedure may be done as a last resort to stop the conduction of all impulses from the atria to the ventricles (complete heart block), together with the implantation of a permanent pacemaker.

Lifestyle management

AF is often associated with other forms of cardiovascular disease. Therefore, it is important to manage the other general cardiovascular risk factors such as blood pressure, diabetes, weight loss, exercise, smoking cessation, and healthy eating.1 

For more information about exercise in patients with heart disease, go to the Virtual Medical Centre's page on Advising Patients About Aerobic Exercise. Patients who are on warfarin should avoid contact sports where there is a significant chance of injury, due to the risk of excessive bleeding.

Davidson S, Haslett C. Davidson's Principles and Practice of Medicine (19th edition). Edinburgh: Churchill Livingstone; 2002. [Book] Feinberg WM, Blackshear JL, Laupacis A, et al. Prevalence, age distribution, and gender of patients with atrial fibrillation: Analysis and implications. Arch Intern Med. 1995;155(5):469-73. [Abstract]Hankey G. Atrial fibrillation [online]. Canberra, ACT: Heart Foundation; 2004 [cited 1 July 2008]. Available from: URL linkBraunwald E, Fauci AS, Kasper DL, et al. Harrison's Principles of Internal Medicine (16th edition). New York: McGraw-Hill Publishing; 2005. [Book]Peters NS, Schilling RJ, Kanagaratnam P, Markides V. Atrial fibrillation: Strategies to control, combat, and cure. Lancet. 2002;359(9306):593-603. [Abstract]Longmore M, Wilkinson I, Rajagopalan SR. Oxford Handbook of Clinical Medicine (6th edition). Oxford: Oxford University Press; 2004. [Book]

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Atrial Myxoma

Atrial myxomas are heart tumours that are usually found in the left atrium.

It is very rare; the incidence is less than 0.14% (< 5 in 10,000). However, atrial myxoma is the most common of all primary cardiac tumours.

Peak incidence is in the 30-60 year age group with higher rates seen in females than in males. Some familial patterns of atrial myxoma have been seen.

The tumour grows slowly and eventually may close the mitral valve and thus may cause pulmonary hypertension and right heart failure from back pressure. The tumour may also become infected or become a source of thrombi (clots) which then embolise, potentially causing a stroke or heart attack.

Atrial myxomas are usually associated with constitutional symptoms of dyspnoea, syncope, fever and weight loss.

Depending on the location and size of the tumour, acute heart failure symptoms may be seen, such as dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, cough, palpitations and chest pain.

Symptoms of embolic disease such as myocardial infarction or a stroke may dominate the presentation of the tumour.

Blood tests will frequently show mild anaemia and a raised ESR. A chest x-ray may show pulmonary congestion and possibly hypertrophy/dilatation of the left atrium.

Although atrial myxomas have the potential to embolise and to grow elsewhere, they are not believed to be able to spread to other sites. Surgical resection is usually curative and the main mortality and morbidity carried by these tumours is associated with complications such as embolisation - strokes or heart attacks.

Surgical excision is the treatement of choice and is usually curative.

Schlant RC, Alexander RW, Fuster V (eds). Hurst's The Heart (8th edition). New York, NY: McGraw-Hill; 1994. [Book]Kumar P, Clark M (eds). Clinical Medicine (4th edition). Edinburgh: WB Saunders Company; 1998. [Book]

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Ventricular Arrythmias (VT, Ventricular fibrillation VF)

Ventricular Arrythmia (VA) is a severely abnormal heart rhythm (arrhythmia) that, unless treated immediately, causes death. VF is responsible for 75% to 85% of sudden deaths in persons with heart problems.

To pump blood out to the body, all areas of the heart normally squeeze (contract) in a synchronised manner. The heart's upper chambers (the atria) contract first, and then the heart's bottom two chambers (the ventricles) contract. During VA, however, the ventricles contract independently of the atria, and some areas of the ventricles contract while others are relaxing, in a disorganized manner.

Ventricular arrhythmias are usually acute events with their incidence is related that of its causative pathology.

Most ventricular arrhythmias are caused by coronary heart disease, hypertension or cardiomyopathy.

Ventricular tachycardia

The heart rate is rapid, frequently 120 bpm and above. At this rate the ventricles do not have time to fill properly and cardiac output is reduced leading to hypotension. Fast VT is a peri-arrest rhythm and cardiac arrest may occur at anytime. Due to reduced cardiac output complications such as myocardial infarction can occur.

Cardiac failure can be precipitated by VT. VT sometimes reverts spontaneously or can be corrected with medical therapy.

Ventricular fibrillation

The heart rate is very rapid and irregular and no mechanical contraction fo the heart can occur. The patient is pulseless and rapidly loses consciousness and stops breathing. These rhythms do not revert spontaneously. This condition causes cardiac arrest.

Chest x-ray: may show evidence of congestive heart failure. Also, evidence of the underlying cardiac pathology may be seen such as ventricular enlargement.

Blood tests should exclude electrolyte imbalances.

Cardiac enzymes should be tested to establish whether an acute heart attack has occurred.

The prognosis of these arrhythmias is generally poor. Ultimately the prognosis depends on the nature of the underlying cause. The outlook for VT is slightly better than VF and some ventricular tachyarrhythmias (fast abnormal heart rates) are surprisingly well tolerated.

Cardioversion either with drugs (class one agents such as lignocaine) or DC shock. The patient should be resuscitated. Once the arrhythmia has been cardioverted, prophylaxis should be instigated to prevent recurrence (using agents such as beta-blockers). Patients whould also be placed on continuous cardiac monitoring and arrangements made for assessment by a cardiologist.

Hurst's The Heart 8th Edition, McGRAW-HILL 1994. Kumar and Clark Clinical Medicine 4th Edition, W.B SAUNDERS 1998. MEDLINE Plus.

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Metabolic Syndrome

Metabolic syndrome is diagnosed when a number of metabolic abnormalities (including insulin resistance and obesity) occur at the same time in an individual. Individuals who have the syndrome are more likely to develop cardiovascular disease and type 2 diabetes mellitus than those who do not. Metabolic syndrome is defined by the International Diabetes Federation as:

Metabolic syndrome is an alarmingly common health condition, occurring in some 20–25% of the world's population. In Australia, it is estimated that one in three people over the age of 25 years have the metabolic syndrome.

Individuals who have a higher risk of developing metabolic syndrome include:

Obese individuals, particularly those with obesity around their abdomen;Individuals consuming large amount of saturated fats;Individuals who consume more than one (in women) or two (in men) standard drinks of alcohol per day, or more than four (in women) or six (in men) standard drinks in a single session (commonly known as binge drinking) at least once a week;Individuals with schizophrenia are 2–4 times more likely to develop metabolic syndrome than non-schizophrenic individuals;Insulin resistant individuals;Individuals with a family history of insulin resistance and/or type 2 diabetes.

Unhealthy eating habits and lack of physical activity are the key lifestyle factors leading to metabolic syndrome. Extended periods of unhealthy eating and limited physical activity result in obesity and insulin resistance, which in turn affect the body's metabolism and increase the risk of metabolic syndrome. Once metabolic syndrome is diagnosed, the syndrome is likely to worsen. If left untreated, individuals may go on to develop additional metabolic abnormalities. In addition, once metabolic syndrome is diagnosed, other metabolic abnormalities (e.g. abnormal blood pressure response to changes in dietary salt) also tend to worsen.

Individuals diagnosed with metabolic syndrome are up to three times more likely to develop cardiovascular health problems, and up to five times more likely to develop type 2 diabetes, than individuals who do not have metabolic syndrome.

If a doctor suspects a patient to have metabolic syndrome, they will likely measure the patient's waist to assess central obesity (alternatively, a body mass index > 30 also indicates obesity).  If central obesity is diagnosed, further investigations may be undertaken to assess blood pressure and glucose, triglyceride and cholesterol levels.

This information will be collected for educational purposes, however it will remain anonymous.

Patients are diagnosed with metabolic syndrome if their waist circumference measure shows that they are centrally obese and their test results show at least two metabolic abnormalities.

While many individuals with metabolic syndrome go on to develop type 2 diabetes and CVD, the condition can be resolved through diet and lifestyle changes. Early intervention increases the chances of successful treatment. Individuals with metabolic syndrome may also develop conditions associated with diabetes, even if they do not receive a diabetes diagnosis. For example individuals with metabolic syndrome may develop diabetic retinopathy.

The treatment of metabolic syndrome generally focuses on diet and exercise therapy. To reverse the metabolic abnormalities of metabolic syndrome, regular physical activity and a diet with a restricted calorie intake, that is high in whole grains, monounsaturated fats and plant foods (such as the Mediterranean diet), are recommended.

Click here to watch a video on diet and the metabolic syndrome.

If diet and exercise interventions fail to regulate metabolic abnormalities, doctors may provide medications to reduce blood pressure or cholesterol levels.  A comprehensive approach to the management of metabolic syndrome, including diet, exercise and medication for metabolic abnormalities, is known as the ABCDE approach. This stands for:

A: Assessment of cardiovascular risk and aspirin therapyB: Blood pressure controlC: Cholesterol managementD: Diabetes prevention and diet therapyE: Exercise therapy

Overview of medical treatment of metabolic syndrome

There are currently no medications available that treat all the metabolic abnormalities of metabolic syndrome together. If a doctor prescribes medications to treat metabolic syndrome, they will prescribe specific medications to treat each abnormality separately.

Aspirin therapy is the most common treatment to reduce the risk of cardiovascular diseases, while angiotension-converting enzyme (ACE) inhibitors and angiotension receptor blockers (ARBs) are likely to be prescribed for patients requiring blood pressure control. Fibrates and statins are recommended for cholesterol control.

Assessment of cardiovascular risk and aspirin therapy

The doctor will assess the risk of cardiovascular disease, by using the Framingham risk score. When the Framingham risk score indicates a risk of cardiovascular disease greater than 5%, the doctor will probably recommend daily doses of aspirin to correct the problem. While aspirin does not require a prescription and is commonly used for dealing with fevers and headaches, individuals should always consult a doctor before taking aspirin on a daily basis. This is because daily consumption of aspirin can result in dangerous bleeding in some individuals.

Blood pressure control

Medications for blood pressure control may be prescribed for patients with metabolic syndrome and a blood pressure higher than 130/80 mmHg.  The most commonly prescribed medications are ACE inhibitors and ARBs.

Cholesterol management

There are two types of cholesterol in the body: low density lipoprotein cholesterol (LDL-C or bad cholesterol); and high density lipoprotein cholesterol (HDL-C or good cholesterol).  The goal of cholesterol management is to reduce levels of LDL-C and increase levels of HDL-C.

Diabetes prevention and diet therapy

Losing weight by eating less high fat foods is very important for individuals who have metabolic syndrome. It can reduce the risk of developing type 2 diabetes and may also reduce the risk of coronary heart disease.

For individuals with metabolic syndrome, reducing total calorie intake is important. However, eating the correct combination of foods is also very important.

Dietary modifications

Diets low in saturated fats (e.g. fat derived from animals), red meat and sugar, but high in monounsaturated fats (e.g. olive oil), fresh fruits, vegetables and whole grains, provide the greatest health benefit for individuals with metabolic syndrome (and individuals who wish to prevent metabolic syndrome). This nutritional combination is typical of a Mediterannean diet.

Exercise therapy

Increased physical activity increases weight loss and decreases the risk of diabetes and coronary heart disease. Exercise is therefore a very important component of any treatment for metabolic syndrome treatment.

At least 30 minutes of moderate intensity exercise per day is recommended for general health. Walking is a particularly good form of exercise and individuals with metabolic syndrome should try to walk more (e.g. to work or the shops, with friends or children).

For more information on fitness and exercise, including stretches, types of exercise, exercise recovery and exercise with health conditions, as well as some useful videos, see Fitness. For more information on nutrition, including information on types and composition of food, nutrition and people, conditions related to nutrition, and diets and recipes, as well as some useful videos and tools, see Nutrition. For more information on obesity, health and social issues, and methods of weight loss, as well as some useful tools, see Weight Loss.International Diabetes Federation. The IDF consensus worldwide definition of the metabolic syndrome [online]. 4 September 2006 [cited 26 September 2008]. Available from: URL linkWorld Health Organization. Definition, diagnosis and classification of diabetes mellitus and its complications. Report of a WHO consultation, Part 1: Diagnosis and classification of diabetes mellitus, Geneva, 59p, WHO/NCD/NCS/99.2 [online]. 1999 [cited 26 September 2008]. Available from: URL linkExpert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the third report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. 2001;285(19):2486-97. [Abstract]Alberti KG, Zimmet P, Shaw J. The metabolic syndrome: A new worldwide definition. Lancet. 2005;366:1059-62. [Abstract]Dunstan W, Zimmet P, Welborn T, Cameron AJ, Shaw J, et al. The Australian Diabetes, Obesity and Lifestyle Study (AusDiab): Methods and response rates. Diab Res Clin Prac. 2002;57(2):119-29. [Abstract]Esposito K, Ceriello A. Giugliano D. Diet and the metabolic syndrome. Metab Syndr Relat Disord. 2007;5(4):291-6. [Abstract]Fan AZ, Russell M, Naimi T, Li Y, Liao Y, et al. Patterns of alcohol consumption and the metabolic syndrome. J Clin Endocrinol Metab. 2008;93(10):3833-8. [Abstract | Full text]Saari KM, Lindeman SM, Viilo KM, Isohanni MK, Järvelin MR, et al. A 4 fold risk of metabolic syndrome in patients with schizophrenia: The Northern Finland 1966 Birth Cohort Study. J Clin Psychiatry. 2005;66(5):559-63. [Abstract]Blaha M, Elasy TA. Clinical use of metabolic syndrome: Why the confusion? Clin Diab. 2006;24(3):125-31. [Abstract | Full text]Blaha MJ, Bansal S, Rouf R, Golden SH, Blumenthal RS, Defilippis AP. A practical "ABCDE" approach to the metabolic syndrome. Mayo Clin Proc. 2008;83(8):932-41. [Abstract | Full text]Correia ML. Metabolic syndrome and blood pressure: The salty connection. J Hum Hypertens. 2007;21(6):427-30. [Abstract]Heiskanen T, Niskanen L, Lyytikäinen R, Saarinen PI, Hintikka J. Metabolic syndrome in patients with schizophrenia. J Clin Psychiatry. 2003;64(5):575-9. [Abstract]Redline S, Storfer-Isser A, Rosen CL, Johnson NL, Kirchner HL, et al. Association between metabolic syndrome and sleep-disordered breathing in adolescents. Am J Respir Crit Care Med. 2007;176(4):401-8. [Abstract | Full text]Wu G, Management of proliferative diabetic retinopathy. Chap 9. Diabetic Retinopathy- The Essentials. 2010. pp122-137. [cited 2011, Mar 10] [Book]

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Sick Sinus Syndrome (SSS, Bradycardia-tachycardia syndrome)

Sick sinus syndrome is a group of abnormal heartbeats (arrhythmias) presumably caused by malfunction of the sinus node, the heart's "natural" pacemaker.

Sick sinus syndrome is more common in elderly adults, where the cause is often a non-specific, scar-like degeneration of the conduction system. Cardiac surgery, especially to the atria, is a common cause of sick sinus syndrome in children.

Ischaemia, infarction or generalised degeneration of the sinus node tissue. Other factors include negatively chronotropic drugs (drugs thats slow the heart rate), hypothyroidism and hypokalaemia.

In SSS, the sinus node fires at a reduced rate causing a pathological sinus bradycardia. The long interval between sinus depolarisations may allow supraventricular tachycardias to emerge heralding the development of the tachy-brady syndrome.The irregular slow heart rhythm can predispose to clot formation and emboli that can cause cerebrovascular accidents (stroke) and myocardial infarctions (heart attacks).The electrocardiogram image below exhibits the alternating patterns of bradycardia and tachycardia.

Blood tests should investigate electrolyte imbalance and thyroid hormone deficiency.

If the patient remains in a state of bradycradia, the risk of cardiac arrest is increased with the increased risk of developing spontaneous tachyarrhythmia. If the patient is symptomatic or has suffered an episode of tachyarrhythmia, they should be considered for cardiac pacing using an implanted pacemaker device. Mortality is increased because of complications such as myocardial infarction and thrombo-embolic disease.

The mainstay of treatment is ventricular pacing for bradyarrhythmias (slow pulse rate) for pauses of 2-3 seconds or more. Attempting to increase heart rate with drugs such as isoprenaline is usually ineffective, except as a short term emergency measure (eg while preparing for emergency pacing).Permanent pacing allows more aggressive treatment of tacharrhythmias because the ventricle is prevented from beating too slowly.

Hurst's The Heart 8th Edition, McGRAW-HILL 1994. Kumar and Clark, Clinical Medicine 4th Edition, W.B SAUNDERS 1998. MEDLINE Plus.

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Stroke (Cerebrovascular accident; CVA)

 

Stroke is a disease defined as a sudden neurological deficit (e.g. weakness, loss of sensation or other) due to a vascular cause. The deficit must last for longer than 24 hours and is of sudden onset. There are two main types: Ischaemic (85%): can be due to a thrombus (a clot forming in one of the blood vessels supplying the brain); or due to an embolus - a clot which travels from another site (usually the heart) to block off one of the arteries in the brain. Haemorrhagic (15%): this is due to rupture of one of the arteries in the brain - usually due to an aneurysm (an outpouching of an artery - causing a point of weakness). 

There are several other types - including dissection (splitting) of the wall of one of the blood vessels to the brain, or trauma, and others - but they make up a very small percentage. A TIA (or transient ischaemic attack) has the same symptoms as a stroke, but the neurological deficit lasts for less than 24 hours - i.e. the person recovers completely within that time. It is usually caused by a small embolus which is resorbed.

Stroke is the third most common cause of death in developed countries. It is uncommon before the age of 40 and is more common in males. Stroke affects around 1.2% of Australian patients at sometime in their lives, which corresponds to 217,500 Australians affected. With the growing incidence of obesity in Australia (which contirbutes to stroke through hypertension and atherosclerosis- fatty plaques in blood vessels) the incidence of strokes is expected to sky-rocket by 2050. However, the incidence in younger age groups - eg. 40-60 is dropping with better control of hypertension. Stroke is more common in certain races - eg. Afro-Caribbean.

Men

Men are at greater risk of stroke than women up until the age of 55 years, after which both sexes have similar risks. Stroke is a major cause of morbidity and mortality in the elderly.

Women

Whilst stroke is considered a disease more commonly affecting men, women are actually twice as likely to die from stroke than men. In addition, females have additional risk factors for stroke such as oral contraceptives, that are not present in men.

Children

Stroke is uncommon in children accounting for only a small percentage of stroke cases each year. Stroke in children is often secondary to congenital heart disease (embolic stroke), genetic disorders, abnormalities of intracranial vessels or blood disorders such as Thrombophilia. Half of strokes in children are haemorrhagic and these may be associated with long term disabilities.

 

The risk factors for ischaemic stroke are similar to the risk factors for coronary artery disease:  

Unavoidable risk factors

Age greater than 60 (risk of stroke doubles every decade), male sex, family history of stroke, racial origin.

Avoidable risk factors

Hypertension, Diabetes, Smoking, Excess Alcohol consumption, Obesity, Lack of exercise.

Women

Prolonged use of the Oral Contraceptive Pill.

The risk factors for haemorrhagic stroke are

Hypertension, anticoagulant drugs, bleeding disorders, cerebral aneurysm.

Prior to the onset of the stroke, the patient may have previous symptoms due to a TIA -for example transient episodes of weakness on one side or inability to speak, or more commonly - loss of vision in one eye, which usually develops as a "black veil which gradually goes down" - amaurosis fugax. The onset of the stroke is usually sudden, although it can evolve in a step-wise manner over several hours in thrombotic stroke. The deficit lasts for longer than 24 hours. After its development, the neurological deficit may improve gradually over the next few weeks to months, and sometimes it may completely improve, although most patients are left with a residual deficit - often severe. Haemorrhagic stroke also occurs suddenly, though it is usually accompanied by a severe headache. It is more likely to cause coma than ischaemic stroke, due the increase in pressure in the brain.

Early diagnosis of stroke is extremely important so all patients with symptoms suggesting stroke should be assessed in hospital. Stroke commonly presents with loss of sensory and/or motor function on one side of the body (85% of ischemic stroke patients have hemiparesis), change in vision, gait (walking), or ability to speak or understand or sudden, severe headache. Your doctor will ask specific questions about the onset of symptoms, description of the syptoms and possible risk factors such as hypertension and smoking.

The doctor will carefully examine your head and neck looking for signs of trauma or infection. They will also examine your cardiovascular system and neurological system. Due to possible loss of consciousness, important vital signs will be monitored and an airway established.

CT is very important in the early stages to distinguish haemorrhagic stroke (blood may be seen on the CT scan) and ischaemic stroke (there may be no signs acutely) because this will guide management.

In addition a host of blood tests will be taken including:

Full blood count - a high white cell count may indicate inflammation or infection; Blood glucose: a low blood glucose (eg in a diabetic) may show similar signs to stroke; Cholesterol studies - these are often performed to look for treatable high cholesterol.

Around 25% of people die in the first one month following an ischaemic stroke, and up to 75% after a haemorrhagic stroke. Furthermore, the patients that survive are at a high risk of further strokes - recurrent strokes occur are seen in 10% of survivors in the first year. In addition, patients that have suffered a stroke are also at a very high risk for a myocardial infarction (heart attack) due to concominant coronary artery disease. Patients that have surivived the initial period after a stroke are usually left with significant morbidity. Around 1/3 are independently mobile (move on their own), and 1/3 have a severe disability requiring on-going institutional care, and the rest are in between.There is usually some improvement in function after a stroke, although the patient may be left with a severe deficit. The improvement made in the first month can be used to indicate the likely improvement the patient will make in future. A TIA alone is also an important prognostic factor on its own. After a patient has one TIA - there is a 40% chance of them suffering a stroke in the next 5 years, and a 25% risk of death due to heart disease or stroke.

The treatment of a patient with stroke is divided into immediate and long-term management. Immediate treatment is different for ischaemic and haemorrhagic strokes but general principles of management for both are listed:

Blood glucose monitoring Blood pressure control Cardiac monitor- ECG for ischemic changes or atrial fibrillation Intravenous fluids Oxygen- If hypoxic Maintaining normal temperature.

Ischaemic strokes

The patient should be admitted into a dedicated stroke unit with multidisciplinary staff for rehabilitation. Aspirin (300mg) should be given. The patient's swallowing ability should be tested (by a speech therapist) and a naso-gastric tube should be given if required to prevent aspiration. Further management is then centred on rehabilitation (physiotherapists, OT's and speech therapists are important here) and prevention of complications and further strokes. Prevention of further strokes is important and the patient's risk factors should be addressed. Long term medical management focuses on reduction of cerebrovascular risk to reduce recurrent stroke. Low dose aspirin (+/-clopidogrel) is typically prescribed to prevent formation of further clots. Other management of stroke includes changing lifestyle factors (increased exercise, healthy diet and smoking cessation), reduced blood pressure, lipid control (with statins) and strict blood glucose control. Thus additional management will depend on individual patient factors and concurrent disease.

Haemorrhagic strokes

Haemorrhagic strokes are managed differently acutely. The patient is not given Aspirin for fear of further bleeding, and if there are signs of increasing ICP (intra-cranial pressure) urgent neurosurgical treatment is sought. Hypertension should be controlled. In addition, dexamethasone is often prescribed to reduce brain swelling, and nimodipine may be used to lower blood pressure acutely. Long term management is as per ischaemic strokes. Patients with TIA or strokes that have narrowing of the carotid arteries may benefit from surgery - carotid endarterectomy. This procedure involves stripping away the inside of the artery to allow for incresed blood flow. It may be complicated by a stroke, however, hence it is reserved for patients with >70% stenosis and symptoms.

AIHW- Stroke, Cardiovascular Health, 2005. Arnold J, Stroke, Ischaemic, eMedicine, Web MD, 2005. available [online] at URL: http://www.emedicine.com/emerg/topic558.htm. Bath P, Lees K, ABC of arterial and venous disease- Acute stroke, BMJ 2000;320:920-923. Braunwald, Fauci, Kasper, Hauser, Longo, Jameson. Harrison's Principles of Internal Medicine. 15th Edition. McGraw-Hill. 2001. Caplan L, Overview of the evaluation of stroke, UpToDate, 2005. Cotran, Kumar, Collins 6th edition. Robbins Pathologic Basis of Disease. WB Saunders Company. 1999. Jauch E, Kissela B, Acute stroke Management, eMedicine, Web MD, 2005. Available [online] at URL: http://www.emedicine.com/neuro/topic9.htm Kumar P, Clark M. Clinical medicine. WB Saunders, 2002. Longmore M, Wilkinson I, Torok E. Oxford Handbook of Clinical Medicine. Oxford Universtiy Press. 2001 Nassisi. Stroke, Hemorrhagic. eMedicine. Web MD, 2005. Available [online] at URL: http://www.emedicine.com/emerg/topic557.htm Smith et al. 'Principles for National and Regional Guidelines on Cardiovascular Disease Prevention- A Scientific Statement from the World Heart and Stroke Forum,' American Heart Association 2004. DOI: 10.1161/01.CIR.0000133427.35111.67.

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Tetralogy of Fallot

Tetralogy of Fallot is a type of heart defect present at birth (congenital) consisting of four different abnormalities. It usually results in insufficiently oxygenated blood being pumped to the body causing cyanosis (bluish discoloration of the skin). The classic form of Tetralogy includes 4 defects within the heart structures: Ventricular septal defect (hole between the right and left ventricles). Narrowing of the pulmonic outflow tract (tube that connects the heart with the lungs). An aorta (tube that carries oxygenated blood to the body) that arises from both ventricles, rather than exclusively from the left ventricle. A thickened muscular wall of the right ventricle (right ventricular hypertrophy).

Occurs in less than 1 in 2000 live births. Nonetheless, Tetralogy of Fallot is the most common cyanotic congenital heart defect.

The aetiology (origins) of congenital heart defects is not understood but several factors are known to be associated:(1) Maternal drug abuse, alcohol abuse and radiation exposure.(2) Maternal infection during pregnancy (particularly rubella.)(3) Genetic abnormalities.(4) Chromosomal abnormalities (septal defects are common with Trisomy 21- Down's syndrome.)

As the aorta overlies the VSD, it receives blood from the right ventricle and the left ventricle. This causes circulation of deoxygenated blood and central cyanosis (bluish discoloration). The high right ventricular pressure, caused by the outflow obstruction, facilitate this. Because less blood goes through the pulmonary circulation, cyanosis is independant of pulmonary hypertension (in contrast to Eisenmenger's syndrome).

Chest x-ray: a large right ventricle and small pulmonary arteries may be present. ECG: shows evidence of right ventricular hypertrophy (large right heart).Full Blood Picture: haemoglobin, haematocrit, and red blood cell count are usually elevated, depending on the degree of arterial oxygen desaturation.

With the advancement of surgical technology and increased medical management, the prognosis for Tetrlogy of Fallot is quite good. Over 95% of patients with simple Tetralogy of Fallot go on to live beyond 20 years of age.

Complete surgical correction of the Tetralogy is possible and is mandatory for long-term survival of these patients. Beta blocker medication can be used to help with hypoxic spells while the patient awaits definitive surgical intervention. To the right is an image of the afflicted area post operative:

[1] Anderson et al. Paediatric Cardiology. Churchill Livingstone 1987.[2] Behrman, Kliegman, Jenson. Nelson Textbook of Paediatrics 17th Ed. Saunders 2004.[3] Hurst's The Heart 8th Edition, McGRAW-HILL 1994.[4] Kumar and Clark, Clinical Medicine 4th Edition, W.B SAUNDERS 1998.[5] Robinson MJ., Roberton DM. Practical Paediatrics 4th Edition. Churchill Livingstone 1999.[6] Rudolph et al. Rudolphs's Paediatrics (21st edition). McGraw-Hill 2003.

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Tricuspid Valvular Disease

Tricuspid Valvular Disease is a disease of the heart, namely the tricuspid valve between the right ventricle and right atrium.

These valvular lesions are rare, particularly in isolation.

Tricuspid stenosis (TS) is usually due to rheumatic fever and is usually seen in association with left heart valve disease. TS is also sometimes associated with carcinoid syndrome. Tricuspid regurgitation (TR) is usually secondary to right ventricular dilatation as in pulmonary vascular disease. Primary TR is less common and usually caused by rheumatic heart disease or infective endocarditis (heart valve infection).

TS: Causes a reduction in cardiac output that is compensated for by right atrial hypertrophy. Eventually, the back pressure causes a syndrome of right heart failure. TR: causes a volume over load of the right heart with dilatation of the right atrium. Right heart failure ensues. Atrial arrhythmias, particularly atrial fibrillation are common due to the dilatation of the right atrium.

Chest x-ray may show an atrial bulge in either condition. An ECG may show evidence of right atrial hypertrophy with tall peaked p-waves.

The prognosis of tricuspid valve disorders is good. Right heart failure should be treated with standard measures. Surgical replacement of the valves may be necessary to improve symptoms and prevent irreversible cardiac changes that arise which long term cardiac dysfunction.

Medical treatment of complications such as right heart failure (diuretics, salt restrictions). Surgical options such as valve replacements are sometimes necessary for more severe disease.

Hurst's The Heart 8th Edition, McGRAW-HILL 1994. Kumar and Clark Clinical Medicine 4th Edition, W.B SAUNDERS 1998.

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Rheumatic Fever Rheumatic Heart Disease

Rheumatic fever is an inflammatory disease which may develop after an infection with streptococcus bacteria (such as strep throat or scarlet fever) and can involve the heart (especially the valves), joints, skin, and brain.

Rare in developed countries such as the UK, the US and Australia. Incidence has declined from 10% of children in the 1920's to 0.01% of children today. This drop in incidence reflects advances in infection control and treatment of streptococcal infections with antimicrobials. The disease is still common in developing nations such as the Middle and Far East and South America.

Rheumatic fever is preceded by a throat infection with group A streptococcus organsisms.

Following a group A streptococcus pharyngeal infection, usually in childhood (5-15yo) is followed by a systemic syndrome thought to be caused by an autoimmune response triggered by the infection. The systemic syndrome includes:1) Polyarthritis (multiple join pain and inflammation)2) Carditis (heart inflammation) 3) Skin manifestations 4) Nervous system manifestations5) Fever, joints pains etc.About 50% of patients who develop carditis during the initial phase of the illness will go on to develop long term rheumatic heart disease and associated valvular heart disease.

1) Blood tests: ESR and CRP (non-specific markers of inflammation), leukocytosis2) Chest x-ray: may show evidence of carditis, pericarditis, pericardial effusion.3) ECG: may show evidence of carditis (prolonged P-R interval) or of pericarditis (saddle shaped ST segment elevations).

Some parts of the acute clinical syndrome may recur after the intial episode. However the prognosis for the joint disease, skin disease and nervous system disease associated with rheumatic fever is excellent with no known long term sequelae. Rheumatic heart disease has traditionally been hailed the major causative factor in valvular heart disease and carries the associated morbidity and mortality.

Residual strep infection should be treated with a single intramuscular dose of 916mg of benzylpenicillin. Rest is important. The acute syndrome is treated with high dose aspirin therapy to the limit of tolerance as judged by the development of tinnitus. If carditis is present, steroid therapy may play a role in reducing progression to chronic rheumatic heart disease. Subsequent strep infections should be treated promptly.

[1] Hurst's The Heart 8th Edition, McGRAW-HILL 1994.[2] Kumar and Clark Clinical Medicine 4th Edition, W.B SAUNDERS 1998.[3] MEDLINE Plus.

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Deep Vein Thrombosis (DVT)

Deep Vein Thrombosis is the formation of a blood clot in one of the deep veins of the body. DVT clots usually occur in those deep veins within the leg, particularly within the calf muscles. The veins in the arm, eye or brain may also rarely be affected. Deep vein thrombosis is quite rare, affecting approximately one or two people in every thousand, mainly older people.

The true incidence of deep vein thrombosis is not entirely known as many studies have not been accurate nor conclusive to date. However, overall it is thought approximately 80 cases of deep vein thrombosis occur per 100,000 persons occur annually. The incidence of deep vein thrombosis in the hospitals is much higher, especially in surgical patients. This is thought to be related to long periods of immobilisation which encourage the blood the clot.

Unlike arterial emboli, DVTs often occur in structurally normal vessels. They frequently develop due to stasis of blood (for example cardiac failure) or hypercoaguable states.4 Previous history of venous thromboembolic disease is a key risk factor for DVT. Other important risk factors are listed below:

Increasing age. Family history. Drugs- Synthetic oestrogens in the oral contraceptive pill, Tamoxifen or hormone replacement therapy increase patient's risks of DVT. Pregnancy and the puerperium. Recent surgery or trauma- Pelvic and orthopaedic surgeries (e.g. hip) are particularly high risk.5 Clotting disorders- Thrombophilia, Protein C or S deficiency, Anti-thrombin deficiency and Antiphospholipid syndromes have all been associated with increased rates of DVT.4 Malignancy. Obesity. Smoking. Varicose veins. Periods of immobility- This includes long air travel.6 Reduced physical activity reduces the muscular mechanisms that aid venous return to the heart.

The single most important risk factor for deep vein thrombosis is a prior history of DVT or pulmonary embolism (PE). However, if any of your first-degree relatives (parents or siblings) has had a clot, you are also at higher risk. The reason for this is that an inherited blood factor imbalance that causes increased susceptibility to clotting. Deep vein thrombosis post-surgery patients continue to be at risk for several months after surgery, as do women after delivery of their baby. One study also found that people with varicose veins and older people were at greater risk of deep vein thrombosis. The more risk factors you have, the greater your chances of clotting.

Additional risk factors:

Recent surgery. Smoking. A malignancy. Taking synthetic hormone replacement therapy or oral contraceptives. Being obese or pregnant.

Deep vein thrombi usually develop when there is a reduction in the amount of blood flow (called stasis) or there is an increased clotting tendency (either inherited or acquired). The thrombi can grow by clumping more red blood cells and fibrin together. Occasionally the thrombus can obstruct the vessel involved or parts can break off ans spread to the rest of the vasculature.

DVT often presents as a painful or aching calf. You may also notice some redness, swelling or warmth over the area. These deep vein thrombosis symptoms are serious so you should always obtain medical advice as dislodgement of a clot to elsewhere in the body can be life-threatening. Your doctor will ask you several questions about the pain and possible risk factors for DVT such as travel, surgery and drug use.

The principal clinical features of DVT include: Leg pain in one leg only- Felt as an ache or tightness in the calf. Leg tenderness in one leg only. Acute diffuse swelling (oedema) of only one leg. Changes in skin color of one leg, eg. redness. Increase in the warmth of one leg. Mild fever. Increased pain or resistance on dorsiflexion of the foot (Homan's sign)- This is not a reliable sign and generally should not be performed due to risks of dislodging the thrombus.5,6Your doctor will carefully examine your leg looking for: Tenderness or pain within the calf. Swelling of the limb. Redness. Warmth.They may check if bending your foot up is painful (a sign of DVT) but there are risks of dislodging the clot associated with this manoeuvre.

Investigations for deep vein thrombosis inculde: Blood tests- A particular test called a D-Dimer is performed which measures a breakdown product of clots. If this test is negative it can rule out DVT. However, a positive test result is not always reliable because other things like infection, pregnancy and cancers can also cause it to rise. Therefore if the test is positive more specific investigations are needed such as: Venography- This is probably the most reliable test for detecting clots in the veins. For this procedure a radiologist will inject contrast material into a vein on the top of the foot. This spreads through the veins and shows up on an x-ray. The clot area will be seen as a defect in the contrast. The venography is reasonably accurate, but it is also a costly and painful procedure. Moreover, the irritation of the vein by the contrast material may in itself contribute to the formation of new clots. Ultrasonography is a less invasive test that is also quite reliable detecting clots. Ultrasound works by emitting sound waves that can determine the flow of blood within the vessels. The clogged veins are easily distinguished on color pictures produced by this method. This method is painless, no foreign material is injected, and no radiation is required. The method is also cheaper than venography, but it is less accurate at detecting thrombi in smaller veins within the calf. Computed tomography or Magnetic Resonance Imaging may also occasionally be used.The doctor may do additional tests to determine if you have a clotting disorder. This involves a series of blood tests looking for abnormal levels of some proteins in the blood. This is particularly important for patients with recurrent deep vein thrombosis family history of DVT or cases where there is no obvious cause (such as recent surgery or immobilisation) for the clot forming.

The majority of deep vein thrombosis will disappear without any complications, however there is a significant risk for recurrence. Pulmonary embolus is uncommon when deep vein thrombosis are treated properly but they can occur and can be life threatening.

Complications:

If left untreated, deep vein thrombosis can cause a lot of pain and discomfort. DVT can also lead to varicose veins and certain other irreversible changes in the skin and the tissue. If the thrombus gets detached from the site it can lead to pulmonary embolism. Deep vein thrombosis can lead to non-healing venous ulcers.

Treatment of deep vein thrombosis largely aims to prevent the development of a pulmonary embolus (a clot in the lung) as this can be a life-threatening condition. To do this doctors will aim to reduce the size of the clot using anticoagulant (blood thinning) medications.

The first main deep vein thrombosis treatment is called heparin which can be given through a vein in the arm. This results in almost immediate anticoagulation and treatment of the clot. For this treatment you need to stay in hospital so your APTT can be measured in the blood. This basically is a measure for how well your blood clots which indicates if the drug is working or not.

Heparin is also available as an injection under the skin and this can be given on an out-patient basis. This type of heparin is called low-molecular- weight heparin (such as enoxaparin) and has the advantage of more predictable actions. A standard dose can be given based on your weight and monitoring is not needed.

Along with heparin an oral medication called warfarin is given. Because warfarin usually takes several days to reach effectiveness (until it reaches a therapeutic level), the heparin is continued until the warfarin is able to be effective. The effect of warfarin is also monitored using another blood test called the INR. When this reaches approximately 2.5 for two days in a row, the heparin can be stopped. Heparin needs to be given for at least five days. Warfarin is continued for around 3-6 months to prevent further clot formation. INR needs to be continually monitored because there is a risk of bleeding when the dose gets too high.

Other treatments for DVT included pressure stockings and early mobilisation. These help prevent pooling of blood within the legs. In some patients who have pulmonary emboli or that can't take anticoagulant medications, a filter may be need to be inserted into the inferior vena cava. This is the main vein returning blood from the lower part of the body to the heart and lungs. The filter traps blood clots before they can enter the lungs. All patients who are at risk for DVT (e.g. pregnant, elderly, clotting disorder) will require special preventative methods during hospital visits or surgery. This includes wearing the pressure stockings, physiotherapy, early ambulation and calf compressors during surgery. Around the time of surgery patients will also be given regular heparin to prevent clot formation.

Anderson DR. Wells PS. Stiell I. MacLeod B. Simms M. Gray L. Robinson KS. Bormanis J. Mitchell M. Lewandowski B. Flowerdew G. Management of patients with suspected deep vein thrombosis in the emergency department: combining use of a clinical diagnosis model with D-dimer testing. Journal of Emergency Medicine 2000; 19(3):225-30. Gallus A, Baker R, Chong B, Ockelford P, Street A. on behalf of the Australasian Society of Thrombosis and Haemostasis. Consensus guidelines for warfarin therapy. MJA 2000; 172: 600-605. Hirsh J. Warkentin TE. Shaughnessy SG. Anand SS. Halperin JL. Raschke R. Granger C. Ohman EM. Dalen JE. Heparin and low-molecular-weight heparin: mechanisms of action, pharmacokinetics, dosing, monitoring, efficacy, and safety. Chest 2001; 119: 64S-94S. Kumar, Clark. Clinical Medicine. 5th Edition. Saunders. 2002. Longmore, Wilkinson, Rajagopalan. Oxford Handbook of Clinical Medicine. 6th Edition. Oxford University Press. 2004. Murtagh J. General Practice. 3rd Edition. McGraw-Hill Australia. 2003. Tovey C, Wyatt S. Diagnosis, investigation, and management of deep vein thrombosis. BMJ 2003; 326: 1180-1184.

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Arrhythmia

Arrhythmia is a condition characterised by the heart's failure to contract or beat at the correct time. Some people are able to feel an arrhythmia when it happens, while others cannot. Arrhythmias can be divided into two main groups: tachyarrhythmias, where the heart beats faster than normal; and bradyarrhythmias, where the heart beats slower than normal.

Tachyarrhythmias include:

Bradyarrhythmias include:

The occurance of arrhythmia is common; as many as 2.2 million Americans are living with atrial fibrillation (one type of arrhythmia). A recent study has also suggested that 1 in 4 Adult Americans over the age of 40 could develop an irregular heartbeat.

Heart disease (coronary artery disease): The coronary arteries are blood vessels that surround the heart and carry oxygenated blood to the hard-working heart muscle that is performing the pump function for itself and the rest of the body. Blood is also necessary to maintain a biologically sound electrical conduction system within the heart. Cardiac valvular disease: Deposits in the cardiac valves can also involve the heart wall between the 2 large pumping chambers - the ventricles. Without the unrestricted use of the valves, regular heart rate becomes difficult at best. Heart failure: Heart failure results in the inability of the heart to efficiently and consistently pump, causing excess fluid to collect in the legs and lung. Conductive tissue disease: A number of diseases can cause excessive amounts of substances to circulate in the bloodstream, including proteins and calcium. These substances may be deposited in different locations including the kidneys, connective tissue, and the specialized conducting tissues in the heart. When these deposits do form, the conducting tissue may become abnormal in turn affecting heartbeat. Ingested substances: Caffeine, tobacco, alcohol, cocaine, amphetamines, certain over-the-counter medications such as some cold medications, and prescribed medications may contribute to arrhythmia. Most of these substances act as artificial stimulants. Physical or psychological demands placed upon the heart due to exercise, fatigue and stress. These demands generate a cariety of hormones and stimulants which are common in people with irregular heartbeats.

Symptoms include:

A sensation of feeling ones own heart beat (palpitations); Fainting; Light-headedness, dizziness; Chest pain; Shortness of breath; Paleness; Temporarily absence of ability to breath.Blood tests may be done in an attempt to idenitfy the cause of the arrhythmia;ECG;Chest x-ray;Ambulatory cardiac monitoring;Echocardiogram.

The outcome is dependent on several factors:

The form the arrhythmia takes;Whether it is an atrial arrhythmia (originating from the atrium) or a more dangerous arrhythmia such as ventricular tachycardia or ventricular fibrillation, which are potentially fatal;The overall pumping ability of the heart. In other words, the percentage of blood that the heart pumps from the ventricles to the body with each beat; andThe individual patient's health.

When an arrhythmia is serious, there may be insufficient bloodflow to the body's vital organs, such as the brain, kidneys and the coronary arteries of the heart. When these cases exist, treatment is urgent and may include electrical "shock" (defibrillation or cardioversion), the implantation of a temporary pacemaker to interrupt the arrhythmia by making the heart beat faster (overdrive supression), or the immediate administration of intravenous medications.

For long-term treatment of arrhythmias, daily medications become part of everyday life. These include antiarrhythmic medications, medications to increase or decrease heart rate and others. Over the past decade, life-threatening arrhythmias have been increasingly treated with an implantable cardioverter-defibrillator (ICD). As soon as an arrhythmia begins, the ICD can detect it and send an automatic electrical shock to terminate it, or it can activate a pacemaker function to overdrive the arrhythmia.

Arrhythmia [online]. Dallas, TX: American Heart Association; 1998 [cited 15 September 2004]. Available from: URL linkArrhythmia [online]. Washington DC: American College of Cardiology; 2004 [cited 15 September 2004]. Available from: URL linkArrhythmias [online]. Omaha ,NE: eMedicine; 2004 [cited 15 September 2004]. Available from: URL link

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Aortic Stenosis (AS)

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Aortic Regurgitation (AR)

Aortic regurgitation is reflux of blood from the aorta (the big vessel carrying blood out of the heart). The problem occurs when some of the blood pumped out falls back into the heart, because of an incompetent aortic valve which would normally stop this from happening.

The disease increases in incidence with increasing age and the vast majority of people over 80 years of age show evidence of regurgitation on testing with or without symptoms. The disease occurs more commonly in men, but the majority of patients with rheumatic AR are women.

The major predisposing factors are:

Rheumatic heart disease, syphilis;Damage to the cusps of the valve secondary to infective endocarditis;Any primary cause of aortic stenosis (progressive narrowing of the aortic valve) can lead to AR when the valve cusps become fixed and can not close adequately any longer.

Rarer associations include:

The reguritation of blood back into the left ventricle of the heart leads to dilatation of the ventricle. This reflects and attempt to maintain heart output by increasing the volume of blood being pumped out. This dilatation leads eventually leads to cardiac failure.

Left ventricular dilatation also decreases the amount of blood entering the heart causing angina and can also cause atrial fibrillation, infective endocarditis and mitral regurgitation. However, there are frequently no clinical symptoms until the onset of ventricular failure.

Clinical suspicion should dictate:

Compensation usually prevents the disease from becoming symptomatic for many years. As many as 85-95% of patients with mild-moderate regurgitation will live another 10 years. However after the onset of symptoms of heart failure, there is a fairly rapid deterioration within a couple of years.

General

Treatment of underlying causes- such as syphilis and infective endocarditis. Antibiotic prophylaxis agains development of infective endocarditis should also be used.

Specific

Surgical replacement of the valve should be undertaken but timing of the operation is important. Because a significantly enlarged heart will not recover completely, the operation should take place before the development of severe disease. Any heart failure should be treated with drug regimes.

Schlant RC, Alexander RW, Fuster V (eds). Hurst's The Heart (8th edition). New York, NY: McGraw-Hill; 1994. [Book]Kumar P, Clark M (eds). Clinical Medicine (4th edition). Edinburgh: WB Saunders Company; 1998. [Book]

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Angina Pectoris and Unstable Angina

Angina pectoris and unstable angina is a condition of the coronary arteries - the arteries that supply blood to the heart muscle. When the heart is not receiving sufficient blood supply because of the narrowing of the coronary arteries - this causes pain referred to as "angina". The narrowing of the arteries is usually due to a process called "atherosclerosis" or "atheroma", where the walls of the arteries become coated with a fatty plaque over time.

About 2% of the overall population suffer from angina pectoris as a result of coronary artery disease. The condition is much more common in older patients with the risk factors mentioned below.

There are many risk factors for coronary artery disease:

Hypercholesterolaemia (elevated levels of cholesterol in the blood) plays a central role in the development of the plaques.Increased age and being of the male sex.Family history of coronary artery disease.Smoking: The risk is directly related to number of cigarettes smoked.Diabetes mellitus: Abnormal blood sugar levels promote vascular damage and the development of plaques.Hypertension: High blood pressure promotes artery damage which may initiate or exacerbate atherosclerosis causing plaque rupture. It should be noted that hypertension also worsens myocardial ischaemia (heart attack) through the adaptive changes it causes in the left ventricle. In hypertension the heart has to work harder to pump blood and as a consequence the left ventricle becomes hypertrophied (increased muscle bulk). This bulkier muscle then has higher blood requirements. This is theoretically independent of vessel narrowing.

Other, less important risk factors (soft factors) include:

Stress/anxious personality.Obesity. Alcohol consumption. It should be noted that a variant form of angina pectoris exists called Prinzmetal Angina which usually occurs at rest. This is not due to atherosclerosis but rather to spasmodic contraction of the coronary arteries. Prinzmetal angina is rare.

Early in the disease process angina pectoris (chest pain) is experienced when the demand for blood is increased, as in exercise. Angina may progress to become unstable angina. This is when the chest pain becomes more frequent, or begins to occur at rest. However a definitive diagnosis of MI cannot be made because no ECG or enzymatic patterns are seen. Left untreated, over 10% of cases will progress to frank MI (heart attack), consequently when it is discovered it is treated aggressively.

Angina can limit the amount of work one is able to perform and can result in hospitalisation.if untreated it can result in a heart attack and death.

The physical examination will involve the doctor taking the blood pressure,feeling the pulse and listening to the heart.

ECG (electrocardiogram): Resting ECG generally shows nothing in between attacks. During an attack, slight changes may be seen such as ST segment flatting or depression. Exercise ECG may be very useful in confirming a clinical diagnosis of angina by reproducing the symptoms.

Angina spontaneously remits in 1/3 of patients. It is associated with a mortality rate of up to 4% per year depending on the number of vessels affected. Unstable angina has a higher mortality of 15% within one year if untreated.

General treatment

This involves addressing the risk factors and counselling the patient to:

Cease cigarette smoking; Lose excess weight;Achieve good diabetes control.

Medical treatment

Includes preventative therapy, symptomatic therapy, and interventions.

Preventative therapy

Aspirin: reduces the risk of adverse events (myocardial infarction) by reducing the coagulability of the blood. Statins (eg. simvastatin): these drugs decrease the amount of cholesterol in the blood and increase the percentage of good fats (HDL- high density lipoproteins).

Symptomatic relief

Vasodilators (Nitrates, Beta Blockers and Calcium channel blockers) all help to prevent attacks of angina. The nitrates (eg. GTN-glyceryl trinitrate) are particularly effective at relieving the pain of an attack. Heparin: In the case of unstable angina: use either in intravenous form or as low molecular weight heparin (subcutaneous). Analgesia: In the case of unstable angina morphine and metoclopramide may be given. Newer drugs such as the Potassium channel agonist Nicorandel and the Nitric Oxide modulator Perhexiline are being used in cases of angina which are not sufficiently controlled with more traditional regimes. The use of spinal cord stimulation is currently being investigated for treatment of chest pain in patients with Angina.

Interventions

Coronary angioplasty: Percutaneous transluminal coronary angioplasty (PTCA) is a technique whereby a catheter is introduced into the coronary arteries by way of the femoral artery. When an area of stenosis (narrowing) is detected on angiography, it can then be stretched open by the introduction of a "balloon" which is inflated by the cardiologist. Once this has been achieved, a decision on whether to place a stent is made. A stent is a metallic mesh tube which then holds the stretched portion of the artery open, preventing re-stenosis. In general, patients with single discrete stenoses are good candidates for PTCA. In stable angina which is well controlled by medication, angioplasty may confer better symptomatic control but is of uncertain prognostic benefit.Coronary Artery Bypass Grafting (CABG): This is a surgical procedure where a donor blood vessel from another site in the body is used to bypass area of stenosis. CABG confers significant symptomatic and prognostic benefits in patients with severe triple vessel disease (areas of stenosis in all three coronary arteries). Wherever possible the LIMA (left internal mammary artery) is used to supply blood to the coronary circulation downstream from the stenosis. Grafts using the saphenous vein (from the leg) are still frequently used. Newer minimally invasive techniques using laparoscopic (keyhole) technology are currently being developed.
For more information on keeping your heart healthy, including information on how the heart works, the effect of cholesterol and eating for heart health, as well as some useful videos and tools, see Heart Health.  Kumar P, Clark M (eds). Clinical Medicine (5th edition). Edinburgh: WB Saunders Company; 2002. [Book]Longmore M, Wilkinson I, Torok E. Oxford Handbook of Clinical Medicine (5th edition). Oxford: Oxford University Press; 2001. [Book]Topol EJ (ed). Textbook of Cardiovascular Medicine (3rd edition). Philadelphia, PA: Lippincott Williams & Wilkins; 2007. [Book]Grundy SM. Primary prevention of coronary heart disease: Integrating risk assessment with intervention. Circulation. 1999;100(9):988-98. [Abstract | Full text]Grundy SM. Coronary calcium as a risk factor: Role in global risk assessment. J Am Coll Cardiol. 2001;37(6):1512-5. [Full text]27th Bethesda Conference. Matching the Intensity of Risk Factor Management with the Hazard for Coronary Disease Events. September 14-15, 1995. J Am Coll Cardiol. 1996;27(5):957-1047. [Abstract]Kelemen MD. Angina pectoris: Evaluation in the office. Med Clin North Am. 2006;90(3):391-416. [Abstract]Third report of the expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III) [online]. Bethesda, MD: National Heart, Lung and Blood Institute; 2004 [cited 7 January 2008]. Available from: URL linkBoden WE. High-density lipoprotein cholesterol as an independent risk factor in cardiovascular disease: Assessing the data from Framingham to the Veterans Affairs high-density lipoprotein intervention trial. Am J Cardiol. 2000;86(12A):19-22L. [Abstract]Beller G. Relative merits of cardiovascular diagnostic techniques. In: Braunwald E (ed). Heart Disease: A Textbook of Cardiovascular Medicine (6th edition). Philadelpha, PA: Saunders; 2001: pp 422-41. [Book]Abrams J. Clinical practice: Chronic stable angina. N Engl J Med. 2005;352(24):2524-33. [Abstract]  Hoffman SN, TenBrook JA, Wolf MP, et al. A meta-analysis of randomized controlled trials comparing coronary artery bypass graft with percutaneous transluminal coronary angioplasty: One- to eight-year outcomes. J Am Coll Cardiol. 2003;41(8):1293-304. [Abstract | Full text]Hannan EL, Racz MJ, Walford G,  et al. Long-term outcomes of coronary-artery bypass grafting versus stent implantation. N Engl J Med. 2005;352(21):2174-83. [Abstract | Full text]Al Suwaidi J, Holmes DR Jr, Salam AM, et al. Impact of coronary artery stents on mortality and nonfatal myocardial infarction: Meta-analysis of randomized trials comparing a strategy of routine stenting with that of balloon angioplasty. Am Heart J. 2004;147(5):815-22. [Abstract]

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Heart Diseases

Heart Diseases. Beside cancer, heart disease kills more than 2,000 Americans everyday. Approximately 60 million Americans have heart disease.

I. Causes of Heart Diseases 

There are many causes of heart diseases. Most of heart diseases are caused by high blood pressure contributes to hardening of the arteries. High levels of bad cholesterol (LDL) build up in the arteries as a result of uncontrolled diet with high levels of saturated fat and trans fat. All these add to the formation of atherosclerosis lesions and eventually arterial blockage or anything that serves to damage the inner lining of blood vessels and impedes the transportation of oxygen and nutrition to the heart can be defined as a risk of heart disease.

II Symptoms of Heart diseases

Here are some early indication of heart disease symptoms:

1. Leg cramps during walking
Leg cramps during exercise might be caused by dehydration. It is important to drink a lot of fluid during exercise. Leg cramps occur when the muscle suddenly and forcefully contracts. The most common muscles to contract in this manner are muscles that cross two joints. Leg cramps during walking might be an indication of heart disease caused by arteries in your leg being clogged up by cholesterol in result of not enough oxygen being delivered to the cells in your leg.

2. Chest pain
Chest pain is caused by blood vessels in the heart temporarily being blocked up. It is also caused by inadequate oxygen supply to the heart muscle or coronary . The persistence of chest pain would be an early indication of heart diseases.

3. Shortness of breath
Shortness of breath (dyspnea) is the major symptom of the left ventricular insufficiency. People with shortness of breath are four times more likely to die from a heart disease related cause than individuals without any symptoms.

4. Headaches
People see sparkling zigzag lines or loss of vision before a migraine attack may be at particular risk of future cardiovascular problems. Generally headaches do not cause heart diseases but a sudden, explosive onset of great pain might be.

5. Dizziness
Dizziness can have many causes including low blood count, low iron in the blood stream and other blood disorders, dehydration, and viral illnesses. Since there are many different conditions that can produce these symptoms, anybody experiencing episodes of severe headaches or dizziness ought to be checked by your doctor.

6. Palpitations
Palpitations is an extremely common symptom of heart disease. Palpitations are skips in the heart beats and irregular heart beats.

7. Loss of consciousness
It is a common symptom, most people pass out at least once in their lives. However, sometimes loss of consciousness indicates a dangerous or even life-threatening condition such as heart disease so when loss of consciousness occurs it is important to figure out the cause.

There are many more symptoms such as fatigue, memory defects, and changes in skin tone and temperature.

III. Types of Heart Diseases

The heart is a four chambered, hollow muscle and double acting pump that is located in the chest between the lungs. Heart diseases caused by high blood pressure contributes to hardening of the arteries. High levels of bad cholesterol (LDL) build up in the arteries as a result of uncontrolled diet with high levels of saturated fat and trans fat. All these add to the formation of atherosclerosis lesions and eventually arterial blockage.
There are some major types of heart diseases:

1. Type of heart disease affecting heart chambers

As we mention in the previous article, the heart is a four chambered hollow muscle and double acting pump that is located in the chest between the lungs. Heart diseases caused by high blood pressure contributes to hardening of the arteries. High levels of bad cholesterol (LDL) build up in the arteries as a result of uncontrolled diet with high levels of saturated fat and trans fat. All these add to the formation of atherosclerosis lesions and eventually arterial blockage.
In this article, we will discuss heart disease affecting the heart chambers.

Heart failure is caused by the heart not pumping as much blood as it should and so the body does not get as much blood and oxygen that it needs. The malfunctioning of the heart chambers are due to damage caused by narrowed or blocked arteries leading to the muscle of your heart.

Heart diseases affect the heart chambers include:

A. Congestive heart failure
Heart failure is caused by the heart not pumping as much blood as it should and so the body does not get as much blood and oxygen that it needs. The malfunctioning of the heart chambers are due to damage caused by narrowed or blocked arteries leading to the muscle of your heart.

a) Diastolic dysfunction:
The contraction function is normal but there's impaired relaxation of the heart, impairing its ability to fill with blood causing the blood returning to the heart to accumulate in the lungs or veins.

b) Systolic dysfunction:
The relaxing function is normal but there's impaired contraction of the heart causing the heart to not pump out as much blood that is returned to it as it normally does as a result of more blood remaining in the lower chambers of the heart.

B. Pulmonary heart disease
Pulmonary heart disease is caused by an enlarged right ventricle. It is known as heart disease resulting from a lung disorder where the blood flowing into the lungs is slowed or blocked causing increased lung pressure. The right side of the heart has to pump harder to push against the increased pressure and this can lead to enlargement of the right ventricle.

2. Heart Disease affecting heart muscles
In the case of heart diseases affecting heart muscles, the heart muscles are stiff, increasing the amount of pressure required to expand for blood to flow into the heart or the narrowing of the passage as a result of obstructing blood flow out of the heart.
Heart diseases affecting heart muscles include:

A. Cardiomyopathy
Heart muscle becomes inflamed and doesn't work as well as it should. There may be multiple causes such as high blood pressure, heart valve disease, artery diseases or congenital heart defects.

a) Dilated cardiomyopathy
The heart cavity is enlarged and stretched. Blood flows more slowly through an enlarged heart, causing formation of blood clots as a result of clots sticking to the inner lining of the heart, breaking off the right ventricle into the pulmonary circulation in the lung or being dislodged and carried into the body's circulation to form emboli .

b) Hypertrophic cardiomyopathy
The wall between the two ventricles becomes enlarged, obstructing the blood flow from the left ventricle. Sometimes the thickened wall distorts one leaflet of the mitral valve, causing it to leak. The symptoms of hypertrophic cardiomyopathy include shortness of breath, dizziness, fainting and angina pectoris.

c) Restrictive cardiomyopathy
The ventricles becomes excessively rigid, so it's harder for the ventricles to fill with blood between heartbeats. The symptoms of restrictive cardiomyopathy include shortness of breath, swollen hands and feet.

B. Myocarditis Myocarditis is an inflammation of the heart muscles or the weaken of the heart muscles. The symptoms of myocarditis include fever, chest pains, congestive heart failure and palpitation.

3. Heart disease affecting heart valves

Heart diseases affecting heart valves occur when the mitral valve in the heart narrows, causing the heart to work harder to pump blood from the left atrium into the ventricle.

Here are some types of heart disease affecting heart valves:
a. Mitral Stenosis
Mitral Stenosis is a heart valve disorder that involves a narrowing or blockage of the opening of the mitral valve causing the volume and pressure of blood in the left atrium increases.

b. Mitral valves regurgitation
Mitral regurgitation is the heart disease in which your heart's mitral valve doesn't close tightly causing the blood to be unable to move through the heart efficiently. Symptoms of mitral valve regurgitation are fatigue and shortness of breath.

c. Mitral valves prolapse
In mitral valve prolapse, one or both leaflets of the valve are too large resulting in uneven closure of the valve during each heartbeat. Symptoms of mitral valves prolapse are palpitation, shortness of breath, dizzy, fatigue and chest pains.

d. Aortic Stenosis
With aging, protein collagen of the valve leaflets are destroyed and calcium is deposited on the leaflets causing scarring, thickening, and stenosis of the valve therefore increasing the wear and tear on the valve leaflets resulting in the symptoms and heart problems of aortic stenosis.

e. Aortic regurgitation
Aortic regurgitation is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole, from the aorta into the left ventricle. Symptoms of aortic regurgitation include fatigue or weakness, shortness of breath, chest pain, palpitation and irregular heart beats.

f. Tricuspid stenosis
Tricuspid stenosis is the narrowing of the orifice of the tricuspid valve of the heart causing increased resistance to blood flow through the valve. Symptoms of tricuspid stenosis include fatigue, enlarged liver, abdominal swelling, neck discomfort and leg and ankle swelling.

g. Tricuspid regurgitation.
Tricuspid regurgitation is the failure of the right ventricular causing blood to leak back through the tricuspid valve from the right ventricle into the right atrium of the heart. Symptoms of tricuspid regurgitation include leg and ankle swelling and swelling in the abdomen.

4. Heart disease affecting coronary arteries and coronary veins

The malfunctioning of the heart may be due to damage caused by narrowed or blocked arteries leading to the muscle of your heart as well as blood backing up in the veins. Types of heart disease that affect the coronary arteries and veins include:

A. Angina pectoris
Angina pectoris occurs when the heart muscle doesn't get as much blood oxygen as it needs. Here are 3 types of angina pectoris:
a) Stable angina
Stable angina is chest pain or discomfort that typically occurs with activity or stress due to oxygen deficiency in the blood muscles and usually follows a predictable pattern. Symptom of stable angina include chest pain, tightness, pressure, indigestion feeling and pain in the upper neck and arm.

b) Unstable angina
Unstable angina is caused by blockage of the blood flow to the heart. Without blood and the oxygen, part of the heart starts to die. Symptoms of unstable angina include pain spread down the left shoulder and arm to the back, jaw, neck, or right arm, discomfort of chest and chest pressure.

c) Variant angina also known as coronary artery spasm
Caused by the narrowing of the coronary arteries. This is caused by the contraction of the smooth muscle tissue in the vessel walls. Symptoms of variant angina include increasing of heart rate, pressure and chest pain.

B. Heart attacks known as myocardial infarction or MI
Heart attacks caused by plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium. Symptoms of MI include a squeezing sensation of the chest, sweating, nausea and vomiting, upper back pain and arm pain.

C. Heart disease also known as coronary artery disease or coronary heart disease
Caused by arteries hardening and narrowing, cutting off blood flow to the heart muscle and resulting in heart attack. Symptoms of heart disease include shortness of breath, chest pains on exertion, palpitation, dizziness and fainting.

D. Atherosclerosis or hardening of arteries
Arteries are blood vessels that carry oxygen-rich blood to your heart and to other parts of your body. Atherosclerosis is caused by plaques that rupture in result of blood clots that block blood flow or break off and travel to another part of the body. Atherosclerosis has no symptom or warning sign.

E. Silent ischemia.
Ischemia is a condition in which the blood flow is restricted to a part of the body caused by narrowing of heart arteries. Silent ischemia means people have ischemia without pain. There is also no warning sign before heart attack.

5. Heart disease affecting heart lining
Rheumatic heart disease results from inflammation of the heart lining when too much fluid builds up in the lungs leading to pulmonary congestion. It is due to failure of the heart to remove fluid from the lung circulation resulting in shortness of breath, coughing up blood, pale skin and excessive sweating. Heart disease resulting from inflammation of either the endocardium or pericardium is called heart disease affecting heart lining.

Endocardium is the inner layer of the heart. It consists of epithelial tissue and connective tissue. Pericardium is the fluid filled sac that surrounds the heart and the proximal ends of the aorta, vena vava and the pulmonary artery.

a. Endocarditis
Endocarditis, which is an inflammation of the endocardium is caused by bacteria entering the bloodstream and settling on the inside of the heart, usually on the heart valves that consists of epithelial tissue and connective tissue. It is the most common heart disease in people who have a damaged, diseased, or artificial heart valve. Symptoms of endocarditis include fever, chilling, fatigue, aching joint muscles, night sweats, shortness of breath, change in temperature and a persistent cough.

b. Pericardium
Pericarditis is the inflammation of the pericardium. It is caused by infection of the pericardium which is the thin, tough bag-like membrane surrounding the heart. The pericardium also prevents the heart from over expanding when blood volume increases. Symptoms of pericarditis include chest pain, mild fever, weakness, fatigue, coughing, hiccups, and muscle aches.

6. Heart disease affecting electrical system
The electrical system within the heart is responsible for ensuring the heart beats correctly so that blood can be transported to the cells throughout our body. Any malfunction of the electrical system in the heart causes a fast, slow, or irregular heartbeat. The electrical system within the heart is responsible for ensuring that the heart beats correctly so that blood can be transported throughout our the body. Any malfunction of the electrical system in the heart malfunction can cause a fast, slow, or irregular heartbeat.

Types of heart disease that affect the electrical system are known as arrhythmias. They can cause the heart to beat too fast, too slow, or irregularly. These types of heart disease include:

a. Sinus tachycardia
Sinus tachycardia occurs when the sinus rhythm is faster than 100 beats per minute therefore it increases myocardial oxygen demand and reduces coronary blood flow, thus precipitating an ischemia heart or valvular disease.

b. Sinus bradycardia
Sinus bradycardia occurs when a decrease of cardiac output results in regular but unusually slow heart beat less than 60 beats per minute. Symptoms of sinus bradycardia includes a feeling of weightlessness of the head, dizziness, low blood pressure, vertigo, and syncope.

c. Atrial fibrillation
Atrial fibrillation is an irregular heart rhythm that starts in the upper parts (atria) of the heart causing irregular beating between the atria and the lower parts (ventricles) of the heart. The lower parts may beat fast and without a regular rhythm. Symptoms of atrial fibrillation include dizziness, light-headedness, shortness of breath, chest pain and irregular heart beat.

d. Atrial flutter
Atrial flutter is an abnormal heart rhythm that occurs in the atria of the heart causing abnormalities and diseases of the heart. Symptoms of atrial flutter includes shortness of breath, chest pains, anxiety and palpitation.

e. Supraventricular tachycardia
Supraventricular tachycardia is described as rapid heart rate originating above the ventricles, or lower chambers of the heart causing a rapid pulse of 140-250 beats per minute. Symptoms of supraventricular tachycardia include palpitations, light-headedness, and chest pains.

f. Paroxysmal supraventricular tachycardia
Paroxysmal supraventricular tachycardia is described as an occasional rapid heart rate. Symptoms can come on suddenly and may go away without treatment. They can last a few minutes or 1-2 days.

g. Ventricular tachycardia
Ventricular tachycardia is described as a fast heart rhythm that originates in one of the ventricles of the heart . This is a potentially life-threatening arrhythmia because it may lead to ventricular fibrillation and/or sudden death. Symptoms of ventricular tachycardia include light headedness, dizziness, fainting, shortness of breath and chest pains.

h.Ventricular fibrillation
Ventricular fibrillation is a condition in which the heart's electrical activity becomes disordered causing the heart's lower chambers to contract in a rapid, unsynchronized way resulting in little heart pumps or no blood at all, resulting in death if left untreated after in 5 minutes.

There are many heart diseases affecting electrical system such as premature arterial contractions, wolf parkinson, etc.

7. Congenital heart disease
There are several heart diseases that people are born with. Congenital heart diseases are caused by a persistence in the fetal connection between arterial and venous circulation. Congenital heart diseases affect any part of the heart such as heart muscle, valves, and blood vessels. Congenital heart disease refers to a problem with the heart's structure and function due to abnormal heart development before birth.Every year over 30,000 babies are born with some type of congenital heart defect in US alone. Congenital heart disease is responsible for more deaths in the first year of life than any other birth defects. Some congenital heart diseases can be treated with medication alone, while others require one or more surgeries.

The causes of congenital heart diseases of newborns at birth may be in result from poorly controlled blood sugar levels in women having diabetes during pregnancy, some hereditary factors that play a role in congenital heart disease, excessive intake of alcohol and side affects of some drugs during pregnancy.

Congenital heart disease is often divided into two types: cyanotic which is caused by a lack of oxygen and non-cyanotic.

A. Cyanotic
Cyanosis is a blue coloration of the skin due to a lack of oxygen generated in blood vessels near the skin surface. It occurs when the oxygen level in the arterial blood falls below 85-90%.
The below lists are the most common of cyanotic congenital heart diseases:
a)Tetralogy of fallot
Tetralogy of fallot is a condition of several congenital defects that occur when the heart does not develop normally. It is the most common cynaotic heart defect and a common cause of blue baby syndrome.

b)Transportation of the great vessels
Transportation of the great vessels is the most common cyanotic congenital heart disease. Transposition of the great vessels is a congenital heart defect in which the 2 major vessels that carry blood away from the aorta and the pulmonary artery of the heart are switched. Symptoms of transportation of the great vessels include blueness of the skin, shortness of breath and poor feeding.

c)Tricuspid atresia
In tricuspid atresia there is no tricuspid valve so no blood can flow from the right atrium to the right ventricle. Symptoms of tricuspid atresia include blue tinge to the skin and lips, shortness of breath, slow growth and poor feeding.

d)Total anomalous pulmonary venous return
Total anomalous pulmonary venous return (TAPVR) is a rare congenital heart defect that causes cyanosis or blueness. Symptoms of total anomalous pulmonary venous return include poor feeding, poor growth, respiratory infections and blue skin.

e)Truncus arteriosus
Truncus arteriosus is characterized by a large ventricular septal defect over which a large, single great vessel arises. Symptoms of truncus arteriosus include blue coloring of the skin, poor feeding, poor growth and shortness of breath.

B. Non-cyanotic
Non-cyanotic heart defects are more common because of higher survival rates.
The below lists are the most common of non-cyanotic congenital heart diseases:
a)Ventricular septal defect
Ventricular septal defect is a hole in the wall between the right and left ventricles of the heart causing right and left ventricles to work harder, pumping a greater volume of blood than they normally would in result of failure of the left ventricle. Symptoms of ventricular septal defect include very fast heartbeats, sweating, poor feeding, poor weight gain and pallor.

b)Atrial septal defect
Atrial septal defect is a hole in the wall between the two upper chambers of your heart causing freshly oxygenated blood to flow from the left upper chamber of the heart into the right upper chamber of the heart. Symptoms of atrial septal defect include shortness of breath, fatigue and heart palpitations or skipped beats.

c)Coarctation of aorta
Coarctation of aorta is a narrowing of the aorta between the upper-body artery branches and the branches to the lower body causing your heart to pump harder to force blood through the narrow part of your aorta. Symptoms of coarctation of aorta include pale skin, shortness of breath and heavy sweating.

There are many more types of non-cyanotic such as pulmonic stenosis, patent ductus arteriorus, and atrioventricular cana. These problems may occur alone or together. Most congenital heart diseases occur as an isolated defect and is not associated with other diseases.

8. Other Types of Heart Diseases

In this article, we will discuss other types of heart diseases that can affect any part of the heart including the following:

*A cardiac tumor can be either malignant or benign

A) Benign tumors
a. Myxoma
Myxoma is a cardiac benign tumor. It is the most common tumor inside of cavities of the heart and most of them occur in the left atrium of the heart obstructing the normal flow of blood within the chambers of the heart. Symptoms of Myxoma include paroxysmal dyspnea, weight loss, feverhemoptysis, lightheadedness and sudden death.

b. Rhabdomyomas
Most of rhabdomyomas occur in children or infants and are associated with tuberous sclerosis. It develops in the myocardium or the endocardium and accounts for about one out of every five tumors that originate in the heart causing obstruction of blood flow, valvular insufficiency, and cardiac arrhythmias. Symptoms of rhabdomyomas include palpitations, chest pains, shortness of breath, and nausea.

c. Fibromas
Fibromas develop in the myocardium or the endocardium. These tumors are composed of fibrous or connective tissue and tend to occur on the valves of the heart and may be related to inflammation. Other than seeing or feeling the fibroma, there are no usual symptoms.

d. Teratomas of the pericardium
It is often attached to the base of the great vessels, usually occurring in infants. They are rarer than cysts or lipomas, usually causes no symptoms.

B) Malignant tumors
Malignant tumors that originated elsewhere in the body and spread to the heart are more common than ones that originate in the heart. Malignant heart tumors can originate from any heart tissue. They occur mostly in children.

a. Angiosarcomas
Angiosarcomas account for about a third of all malignant heart tumors and usually start on the right side of the heart. The cause of angiosarcomas is usually unknown and symptoms of angiosarcomas differ according to the location of the tumour. Often symptoms of the disease are not apparent until the tumour is well advanced.

b. Fibrosarcomas
Fibrosarcomas occur as a soft-tissue mass or as a primary or secondary bone tumor. The 2 main types of fibrosarcoma of bone are
i) Primary fibrosarcoma is a fibroblastic malignancy that produces variable amounts of collagen
ii) Secondary fibrosarcoma of bone arises from a preexisting lesion or after radiotherapy to an area of bone or soft tissue. Symptoms of fibrosarcomas include broken bone, pain, swelling, lump found under skin or bone, frequent urination and urinary obstruction.

c. Rhabdomyosarcomas
Rhabdomyosarcomas are a cancer made up of cells that normally develop into skeletal muscles of the body and are also more common in children. They usually have some type of chromosome abnormality in the cells of the tumor, which are responsible for the tumor formation. Symptoms of rhabdomyosarcomas include bleeding from the nose, vagina, rectum, throat and tingling, numbness, and pain.

d.) Liposarcomas
Liposarcoma normally appears as a slowly enlarging, painless, nonulcerated submucosal mass in a middle-aged person. Symptoms include palpation, weakness, limitation of motion weight loss, fatigue, and lassitude.

*Sudden cardiac death
The victim may or may not have diagnosis of heart diseases, and the death is totally unexpected. Sudden cardiac death is a result from abrupt loss of heart function. The cause of sudden cardiac dealth might be a result of coronary heart disease.

* Hypertensive heart disease
Hypertensive heart disease are caused by high blood pressure that increases the work load of the heart. Overtime the muscles of the heart become thick in result of an enlarged left ventricle and decreased blood pump from the heart. Symptoms of heart failure include shortness of breath, swelling in the feet, ankles, or abdomen, fatigue, irregular pulse, nausea and frequent urination at night.

IV. Heart Diseases- Prevention and Treatment

Anything that serves to damage the inner lining of blood vessels and impedes the transportation of oxygen and nutrition to the heart can be defined as a risk of heart disease.
Unhealthy diet is a major cause of heart diseases resulting in the buildup of cholesterol and fat in the inner wall of arteries that narrows the arteries, impedes the circulation and eventually causes heart attacks.

1. Prevention and Treatment of Heart Disease with Diet

To prevent heart diseases, your daily diet should contain:
a) Fiber
Fiber can be soluble or insoluble. As we mentioned in a previous article, soluble fiber can lower your LDL and raise your HDL cholesterol while insoluble fiber has no effect on cholesterol but promotes regular bowel movements. The intake of fatty foods causes the liver to release bile into the intestines to break down the fat.

b) Reduce intake of saturated fat and trans fat
We know that saturated and trans fat are toxins causing cholesterol to build up in the arteries damaging the arterial wall and narrows the arterial passage in result of poor circulation and oxygen transportation to our body in result of high blood pressure as the heart has to work harder than normal in order to provide enough nutrition to the body`s cells. Eventually, the heart will fail and result in heart diseases. It is recommended that you reduce the intake of animal fat and increase the intake of cold water fish which is the best sources of omega 3 and 6 fatty acids that can help your cholesterol levels as well as lowering your blood pressure.

c). Diet high in complex carbohydrates
Vegetables, fruits, some beans and grains contain high amounts of plant pigments known as flavonoids that provide healthy protection against heart diseases. Unfortunately study shows that diets high in complex carbohydrate may increase the release of too much insulin to respond to carbohydrates in the diet. The type and amount of carbohydrate foods may need individual monitoring.

d). Drink half of your body weight of water or juices in ounces
If you weigh 160 pounds then you are require to drink 80 ounces of water or juices to prevent the cells in our body to become dehydrated. Maintaining normal function of our body's cells is a healthy way to normalize high blood pressure.

2. Prevention and Treatment of Heart Disease with natural remedies

Beside foods and herbs, nutritional supplements also play an important role in preventing heart diseases and stroke. Here are some nutritional supplements which have proven record in treating heart diseases:

a. L-Arginine 

b. L- Carnitine 

c. Lecithin 

d. Niacin 

e. Selenium 

f. Taurine 

g. Calcium and potassium 

h. Magnesium 

i. Lutein 

j. Flax seeds 

k. Ginkgo biloba 

l. Cayenne