The most common causes of aortic regurgitation are degenerative or congenital cause.

True. Severe aortic regurgitation is nowadays usually due to congenital (e.g. bicuspid aortic valve) or degenerative cause (e.g. annulaortic ectasia). Chronic rheumatic heart disease as a cause of severe aortic regurgitation is becoming less common.

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Poor exercise tolerance due to severe aortic regurgitation is a very useful clinical indicator for poor prognosis.

True. Patients in class III or IV by New York Heart Association classification (NYHA) are at high risk, with an annual mortality of 25%. Marked increase in left ventricular dimension or a decrease in left ventricular function by echocardiography also indicate poor prognosis. As a rule of thumb, a left ventricular end-systolic dimension >5.5 cm and a left ventricular ejection <55% are associated with poorer prognosis. In women, correction of left ventricular dimension with body surface area is important; otherwise the left ventricular enlargement may be underestimated. Asymptomatic patients without left ventricular dysfunction do not have an excess risk of death, but they will have higher rates of cardiovascular event (i.e., death from cardiac causes, heart failure, or new symptoms) at ~6% per year. Therefore, both clinical follow-up for symptoms progression and surveillance by regular echocardiography are very important tools in following up patients with significant aortic regurgitation.

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Surgery is indicated for most symptomatic patients.

True. Compared with medical therapy, surgery (usually aortic valve replacement) improves prognosis for patients in NYHA class III and IV. In fact benefits are also seen in patients with mild symptoms and severe aortic regurgitation. For asymptomatic patients, surgery is beneficial if there is significant left ventricular enlargement of dysfunction as described above. Combined correction of aortic regurgitation and aortic aneurysm should also be considered in asymptomatic patients with aneurysms of the ascending aorta that are more than 5.5 to 6 cm in diameter due to the increased risk of aortic rupture or dissection. The average mortality rate for aortic valve replacement is about 4%, depending on the experience of the center and the co-morbidities of the patient. The operative mortality is ~8% for those with an ejection fraction <35% and 2% for those >50%.

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Nifedipine is useful for patients with moderate aortic regurgitation.

True. For asymptomatic patients with moderate to severe aortic regurgitation without left ventricular dysfunction, vasodilators including nifedipine and ACEI reduce left ventricular wall stress and volumes. Antibiotic prophylaxis for endocarditis is recommended for all patients with significant aortic regurgitation.

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References:

Enriquez-Sarano et al. Aortic Regurgitation. NEJM volume 351 :1539-46.

What is the clinical diagnosis?

The clinical diagnosis is androgenetic alopecia (AGA). AGA is the most common cause of hair loss worldwide and affects both sex but is less severe in female. By the age of 50, half of the male population may be suffered from this condition. Affected male may present as early as in their twenties. There is gradual miniaturization of genetically marked hair follicles which are replaced by progressively finer and shorter hair. Emotional and physical stress can aggravate the hair loss. Clinically there is bi-temporal recession of hair line in male patients and hair thinning over vertex in both sex. In late stage, there is preservation of only the "horseshoe-shaped" hair at sides and back of scalp in male patients.

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What are the differential diagnoses?

Differential diagnoses include other conditions causing diffuse non-scarring alopecia such as telogen effluvium, anagen effluvium, diffuse alopecia areata, drug-induced alopecia and systemic diseases including iron deficiency, thyroid diseases, systemic lupus erythematosus, and secondary syphilis.

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What is the underlying cause of this condition?

As the name implies, AGA involves both androgen and genetic factors. The underlying mechanisms include increased 5-alpha reduction of testosterone to dihydrotestosterone in affected hair follicles and increased sensitivity of hair follicles in bald area to effect of androgen.

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Are there any investigations you want to order?

AGA can usually be diagnosed on a clinical ground. In otherwise healthy patients, laboratory tests including sex hormones are usually within normal range. However, other conditions may superimpose and worsen the alopecia. Appropriate blood test such as haemoglobin, thyroid function, and iron level may be checked. In female patients, laboratory analysis of dehydroepiandrosterone sulfate and testosterone level should be done if there are signs and symptoms of virilization.

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What are the treatments?

Topical minoxidil and systemic finasteride are the two drugs approved by the Food and Drug Administration, USA for treating male AGA. The mechanism of action of minoxidil is unknown, but may be due to lengthening the duration of anagen (growing) phase and increased blood supply to hair follicle. Finasteride is a 5-alpha reductase type 2 inhibitor, which decreases the production of dihydrotestosterone from testosterone. Minoxidil and finasteride may be used alone or in combination. Minoxidil but not finasteride is used in female patients. Long-term use is required to preserve improvement above baseline. Other treatment options include hair transplantation and hair-piece.

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