Barlow syndrome is mitral valve prolapse (also known as "click murmur syndrome"), the most common heart valve abnormality, affecting 5-10% of the world population. Most patients have no symptoms and require no treatment. However, the condition can be associated with fatigue and/or palpitations. The mitral valve prolapse can often be detected by a doctor during examination of the heart and can be confirmed with anechocardiogram. Patients are usually given antibiotics prior to any procedure which might introduce bacteria into the bloodstream, including dental work and minor surgery.
Causes: The underlying problem with the valve is a degeneration of the tissue causing the leaflets to become stretched and enlarged. This redundant tissue bulges into the atrium, preventing the valve from closing properly. The exact reason for this tissue change is not known, but it is associated with the tissue degenerative disorders. Functional MVP can occur with completely normal valve leaflets: this is found in conditions of abnormal papillary muscle function due to myocardial ischaemia, and in dilated cardiomyopathy. Patients with hypertrophic cardiomyopathy are also at risk.
Symptoms: Most patients do not experience symptoms. However, when they do the symptoms include: • Fatigue ï Migraine ï Dizziness ï Panic attacks ï Low blood pressure when lying down ï Shortness of breath ï Palpitations ï Chest pain that is not angina However, these non-specific symptoms are not reliable indicators of the condition. When the doctor listens to the heart, a murmur may be heard. This is caused by irregular blood flow through the valve. A click may also be heard, thought to be due to the snapping of the anchoring “ropes” – the chordea – as the valve billows and then is suddenly held taut. This is much like the snapping taut of the sails on a boat. These sounds are often transient or absent, and might only be detected by an experienced cardiologist. If there are problems with the function of the left ventricle, the patient may experience shortness of breath and troublesome irregularities of heart rhythm. Barlow’s syndrome may result in severe dysfunction of the mitral valve, leading to what is called mitral regurgitation (MR), a leaking, or incompetent valve. Mitral regurgitation means that blood flows back into the left atrium during contraction rather than moving forwards into the aorta as it should do. About 25% of people with Barlow's syndrome also suffer from lax joints, and a high arched palate in the mouth (these patients may also have a degree of Marfan's syndrome), and other abnormalities of their skeleton such as scoliosis, a funnel chest and a straight back.
Treatment: Individuals with mitral valve prolapse, particularly those without symptoms, often require no treatment. Those with mitral valve prolapse and symptoms of dysautonomia (palpitations, chest pain) may benefit from beta-blockers (e.g., propranolol). Patients with prior stroke and/or atrial fibrillation may require blood thinners, such as aspirin or warfarin. In rare instances when mitral valve prolapse is associated with severe mitral regurgitation, mitral valve repair or surgical replacement may be necessary. Mitral valve repair is generally considered preferable to replacement. Current ACC/AHA guidelines promote repair of mitral valve in patients before symptoms of heart failure develop. Symptomatic patients, those with evidence of diminished left ventricular function, or those with left ventricular dilatation need urgent attention.
Statistics: Chronic rheumatic heart disease is a common cause of mitral valve disorders in Aboriginal and Torres Strait Islander populations, with a prevalence of 16.6 per 1,000 population in the Top End of the Northern Territory and 12.5 per 1,000 in Central Australia, compared with respective figures of 1.7 per 1,000 and 0.6 per 1,000 amongst other Australians.  Although more commonly associated with mitral stenosis, rheumatic heart disease may result in a combined stenosis and insufficiency, or occasionally, an isolated rheumatic insufficiency. The findings of our study indicate that primary chordal rupture is almost invariably a complication of myxomatous valve disease. This was not the case in only 2 of our 31 patients. There are surprisingly few published studies of primary chordal rupture of the mitral valve and three of the four major series were published more than a decade ago. In 1967, Saunders et al. (21) reported that in 18 (46%) of 39 patients with chordal rupture found at autopsy or surgery there was no definite cause of the rupture, and in the same year Selzer et al. (9) described the clinical features of 14 patients with isolated chordal rupture, reporting that the leaflets, inspected at autopsy or surgery, were normal. Microscopic examination of leaflet tissue was not reported in either of these studies. It was also undertaken in only a minority of the series by Caves et al. (22), who found that 17 (8%) of 212 patients undergoing surgery for severe mitral regurgitation had idiopathic chordal rupture.