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.

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