A hairy fall: syncope resulting from topical application of minoxidil.

We describe the case of a young man who developed syncope after using a high strength formulation of topical minoxidil as a hair growth restorer. Other potential cardiovascular and endocrine causes were excluded, and his symptoms resolved on discontinuation of the product. While syncope is a recognised side effect of using this powerful systemic antihypertensive agent, few cases are documented in the literature, which we illustrate in our discussion.

Cardiac sarcoidosis: diagnosis and management.

Cardiac sarcoidosis is one of the most serious and unpredictable aspects of this disease state. Heart involvement frequently presents with arrhythmias or conduction disease, although myocardial infiltration resulting in congestive heart failure may also occur. The prognosis in cardiac sarcoidosis is highly variable, which relates to the heterogeneous nature of heart involvement and marked differences between racial groups. Electrocardiography and echocardiography often provide the first clue to the diagnosis, but advanced imaging studies using positron emission tomography and MRI, in combination with nuclear isotope perfusion scanning are now essential to the diagnosis and management of this condition. The identification of clinically occult cardiac sarcoidosis and the management of isolated and/or asymptomatic heart involvement remain both challenging and contentious. Corticosteroids remain the first treatment choice with the later substitution of immunosuppressive and steroid-sparing therapies. Heart transplantation is an unusual outcome, but when performed, the results are comparable or better than heart transplantation for other disease states. We review the epidemiology, developments in diagnostic techniques and the management of cardiac sarcoidosis.

A patient with a red eye and pulmonary oedema.

A middle-aged black male patient presented with symptoms and radiological features indicative of pulmonary oedema. Following several admissions for the same symptomology, and poor resolution of chest radiographic features, the patient developed a red eye. The latter was diagnosed as uveitis, which prompted consideration and proof of a diagnosis of cardiopulmonary sarcoidosis. The patient was subsequently treated with high dose steroids resulting in a partial recovery, complicated by issues of fluid retention.

A prospective observational study of stroke volume responsiveness to a passive leg raise manoeuvre in healthy non-starved volunteers as assessed by transthoracic echocardiography.

Current guidelines for intra-operative fluid management recommend the use of increments in stroke volume following intravenous fluid bolus administration as a guide to subsequent fluid therapy. To study the physiological premise of this paradigm, we tested the hypothesis that healthy, non-starved volunteers would develop an increment in their stroke volume following a passive leg raise manoeuvre. Subjects were positioned supine and stroke volume was measured by transthoracic echocardiography at baseline, 30 s, 1 min, 3 min and 5 min after passive leg raise manoeuvre to 45°. Stroke volume was measured at end-expiration during quiet breathing, as the mean of three sequential measurements. Seventeen healthy volunteers were recruited; one volunteer in whom it was not possible to obtain Doppler measurements and a further five for reasons of poor Doppler image quality were not included in the study. Mean (SD) percentage difference from baseline to the largest change in stroke volume was 5.7 (9.6)% (p = 0.16). Of the 11 volunteers evaluated, five (45%) had stroke volume increases of greater than 10%. Mean (SD) maximum percentage change in cardiac index was 14.8 (9.7)% (p = 0.004). A wide variation in baseline stroke volume and response to the passive leg raise manoeuvre was seen, suggesting greater heterogeneity in the normal population than current clinical guidelines recognise.

Heritable retinoblastoma and accelerated aortic valve disease.

Heritable retinoblastoma is associated with a germline mutation in the tumour suppressor gene RBI. The Rb protein (pRb) arises from the RB1 gene, which was the first demonstrated cancer susceptibility gene in humans. Second primary malignancies are recognised complications of retinoblastoma. Furthermore, pRb is implicated in valve remodelling in calcific aortic valve disease. We report a family with hereditary retinoblastoma and associated secondary primary malignancies. There are two interesting aspects to this family. The first is the concept of 'cancer susceptibility genes'; the RBI gene being the first reported in humans. A further feature of note is that two family members also have bicuspid aortic valves. We discuss a potential association between the gene defect responsible for retinoblastoma (with its associated propensity for further malignancies) and accelerated deterioration of the bicuspid aortic valve in the proband carrying this gene defect.

Leptospirosis and Weil's disease in the UK.

The recent high-profile death of a British Olympic rower from leptospirosis has raised awareness to this uncommon but potentially fatal disease. The re-emergence of the disease abroad is well documented in the literature, but less is known about cases in the UK. The increase in participation in water sports, foreign travel and often a combination of the two, has increased the exposure of tourists subsequently returning to the UK from areas of high prevalence. Leptospirosis is a zoonotic infection. The bacteria are shed in the urine of animals to the environment from where humans are infected by incidental hosts. There is a wide spectrum of severity of symptoms, from a self-limiting febrile illness to fatal pulmonary haemorrhage, renal or liver failure. It is thought that cases remain unrecognized every year in the UK, largely due to the mild nature of symptoms and the wide differential for febrile illness and partly due to lack of awareness among clinicians. This review examines the epidemiology of leptospirosis in the UK, over the period 2006-10, the clinical features, diagnostic techniques and treatment.

Amyloid diseases of the heart: current and future therapies.

Amyloid diseases in man are caused by as many as 23 different pre-cursor proteins already described. Cardiologists predominantly encounter three main types of amyloidosis that affect the heart: light chain (AL) amyloidosis, senile systemic amyloidosis (SSA) and hereditary amyloidosis, most commonly caused by a mutant form of transthyretin. In the third world, secondary amyloid (AA) is more prevalent, due to chronic infections and inadequately treated inflammatory conditions. Much less common, are the non-transthyretin variants, including mutations of fibrinogen, the apolipoproteins apoA1 and apoA2 and gelsolin. These rarer types do not usually cause significant cardiac compromise. Occurring worldwide, later in life and of less clinical significance, isolated atrial amyloid (IAA) also involves the heart. Heart involvement by amyloid often has devastating consequences. Clinical outcome depends on amyloid type, the extent of systemic involvement and the treatment options available. An exact determination of amyloid type is critical to appropriate therapy. In this review we describe the different approaches required to treat this spectrum of amyloid cardiomyopathies.