Search

Silent or painless myocardial ischaemia is common: it can occur in totally asymptomatic patients, in stable or unstable angina sufferers, or after infarction. In most instances, it is detected electrocardiographically (or ambulatory recording by treadmill test). It is essential to establish a firm diagnosis because patients are high-risk subjects. Tomoscintigraphy or echocardiography, on exertion or after drug stimulation, are therefore to be used before it is decided to perform coronary angiography. In all cases treatment is required to suppress ischaemia. It should primarily be medical, the choice being governed by the results of exploration, and should bear upon anatomical lesions and their functional effects. Revascularization, generally by angioplasty, is thus increasingly indicated despite the fact that, in contrast to painful ischaemia, there are no comparative studies available on painless ischaemia to help guiding the treatment decision.

Single photon emission computed tomography (SPECT) is superior to conventional radionuclide scintigraphy. The most widely used marker is thallium-201, despite the fact that it is not exclusively flow-dependent. Thallium-201 SPECT can be performed in patients at rest, during exercise followed by a redistribution study, under dipyridamole or nitrate infusion, or combined with spasm provocation test. When performed at rest, it is helpful to diagnose and, above all, quantify a myocardial infarction. Under nitrate infusion, it delineates the viable muscle remaining around the infarct. During exercise or under dipyridamole infusion, it is more effective than any other non-invasive method in detecting myocardial ischaemia (sensitivity 95%, specificity 90%). Following surgical revascularization, a normal exercise SPECT indicates a functional aorto-coronary bypass in 80% of the cases. It is a good method to detect post-angioplasty restenosis (sensitivity 82%, specificity 86%, negative predictive value 93%). Like all paraclinical examinations, SPECT has its limitations: left bundle branch block, reverse redistribution, non-ischaemic (i.e. dilated or hypertrophic) cardiopathies.

Hypertrophic cardiomyopathy (HCM) is currently considered to be a condition characterised by abnormal diastolic function, sometimes associated with left ventricular outflow obstruction which appears to be a secondary phenomenon. It is important to avoid overlooking this diagnosis especially in young subjects, because of the risk of sudden death, but conversely, false positive diagnosis can result in a serious social and psychological handicap. Echocardiography has assumed a major role in the diagnosis and follow-up of HCM over the last decade. It allows analysis of the localisation, extension and severity of the septal hypertrophy and of the mechanism of systolic anterior motion of the mitral valve. Cardiac doppler completes the non-invasive assessment of this condition by demonstrating the presence or absence of outflow tract obstruction, evaluating diastolic dysfunction, and documenting mitral and occasionally aortic valve regurgitation. Only severely symptomatic patients who do not respond to high dose medical therapy and for whom surgery might be an option need cardiac catheterization. Strenuous physical activity and sport are not recommended in asymptomatic forms. It is vital to identify those patients at high risk of sudden death (family history of sudden death, 48 to 72 hour Holter monitoring). In the absence of silent arrhythmias, preventive therapy should be more general in patients under 30 years of age. Despite a better understanding of the disease, the indications of medical and surgical treatment remain controversial and poorly defined. Treatment is mainly medical with Propranolol as the drug of choice. The dosage has to be tailored for each individual patient.(ABSTRACT TRUNCATED AT 250 WORDS)

The failing heart is unable to provide some organs, notably the brain and the myocardium, with the amount of blood flow they require. To this myocardial inadequacy and resulting "circulatory insufficient" the body reacts by setting in action compensatory mechanisms which are "intracardiac" first (Starling's heterometric regulation, ventricular hypertrophy), then neurohormonal, with the activation of vasoconstrictor systems (noradrenergic system, renin-angiotensin-aldosterone system, arginine-vasopressin system) counterbalanced by the activation of vasodilator systems (vasodilator prostaglandins, atrial natriuretic factor and kinins). However, the vasoconstrictor systems outweigh the vasodilator systems. They create an excessive arterial and venous vasoconstriction, together with water-and-salt retention, which leads to an increase of left ventricular work during both systole and diastole and to a gradual worsening of the heart failure. The present-day treatment of heart failure aims at reducing the water-and-salt retention and at restoring the balance between the vasoconstrictor and vasodilator systems.