Biomedical subjects
Publications and source records attributed to A Cohen Solal.
Anaemia is common in severe cardiac failure due to systolic dysfunction. The mechanisms are varied. Anaemia is a negative prognostic factor. Treatment with erythropoietin seems to improve the quality of life, functional status, effort tolerance and systolic function of these patients. Large scale clinical trials are on-going.
Medical treatment of acute decompensated heart failure has little changed in the last years, except with the advent of non-invasive ventilation. Doppler-echocardiography and BNP dosing have simplified the diagnostic approach and limited the need for invasion evaluation. Vasodilators remain probably underused whereas some doubts have emergency regarding the safety of positive inotropes. Analysis of the hemodynamic profile is mandatory for an optimal management of these patients. The next decade will be that of morbimortality trials in this common form of heart failure with severe prognosis.
Despite recommendations from various learned establishments, there are strong reservations regarding betablockers, which have been contra-indicated in chronic cardiac failure for a long time. Several published enquiries have found a low prescription rate for betablockers. We performed an enquiry into the apparent modes of betablocker prescription in chronic cardiac failure. Questionnaires were sent to all the cardiologists in France, and 1622 were analysed. The dosage used, reasons for non-prescription, modes of repeat prescription, and the influence of the response to treatment were analysed. This enquiry shows that although the advantage of betablockers is acknowledged, there is still a block to their use.
BACKGROUND: Systolic dysfunction of the left ventricle is not the only mechanism of heart failure. An increasing number of patients are found to have heart failure with an ejection fraction > or = 40%. The proportion of heart failure patients with "diastolic" (or more appropriately preserved systolic function) heart failure increases with age. This clinical entity currently accounts for 30 to 40% of all hospitalizations for heart failure and in patients over 80 is found in more patients than is systolic dysfunction. PATHOPHYSIOLOGY: Diastolic heart failure generally associates prolonged ventricular relaxation with reduced left ventricular capacity for distention. The main causes are ischemic, hypertensive and age-related heart disease. Concentric remodeling of the left ventricle, with or without hypertrophy, always leads to diastolic functional disorders. A triggering factor is almost always found for episodes of acute congestion. CONCLUSION: The incidence of "diastolic" heart failure increases with age. Physicians should be aware of the complex underlying pathophysiological mechanisms.
A WELL-RECOGNIZED ENTITY: Diastolic heart failure is an increasingly common diagnosis. Signs may be misleading and positive etiological diagnosis remains difficult. CLINICAL SIGNS AND COMPLEMENTARY INVESTIGATIONS: Fatigue, and most importantly dyspnea, are the cardinal signs of diastolic heart failure. Cor pulmonale is often the inaugural sign. The physical examination contributes little to diagnosis. The chest x-ray shows a small heart. Electrocardiographic anomalies are almost always found. A hemodynamic exploration of the right heart, the key diagnostic tool not always performed in routine work-ups, evidences increased filling pressure of the left ventricle. Doppler-echocardiography is used widely. It demonstrates preservation of the left ventricle function (normal ejection fraction) and visualizes the anatomic subtratum of the diastolic dysfunction, quantifying filling and relaxation disorders and allowing an indirect estimation of pulmonary pressures. In the future, it will be possible to assay atrial natriuretic peptide which will provide a most useful tool for the positive diagnosis of this type of heart failure. CONCLUSION: The diagnosis of diastolic heart failure is complex, warranting rigorous, and critical, evaluation of left ventricular filling using noninvasive methods, particularly Doppler-echocardiography.
THERAPEUTIC OPTIONS: Many therapeutic options are proposed for the treatment of diastolic heart failure although no consensus has been established. In experimental trials, several drugs have demonstrated a potentially beneficial effect on ventricular diastolic dysfunction and could be used for diastolic heart failure: nitrate derivatives, converting enzyme inhibitors, angiotensin II antagonists, spirolactones and bradycardia agents. CLINICAL PRACTICE: In everyday clinical practice, low-dose diuretics and treatments aimed at reducing the triggering factor leading to episodes of heart failure are used alone or in combination with treatments aimed at the underlying cause of the diastolic dysfunction: betablockers, calcium inhibitors or nitrate derivatives for ischemic heart disease, drug therapy for hypertension, anti-diabetes agents, anti-arrhythmic agents for atrial fibrillation. Digitalics are not indicated. In experimental trials, converting enzyme inhibitors and angiotensin II antagonists have demonstrated interesting properties for the left ventricle but to date are not warranted for diastolic heart failure. TREATMENT OF THE CAUSE: Due to the lack of consensus on the optimal treatment for diastolic heart failure, most clinicians rely on treating the underlying heart disease and triggering factors.
Electrocardiographic changes are seen in 5-17% of acute ischemic stroke, but there is scarpe clinical evidence to correlate stroke location with cardiac abnormalities. A 17-year old man had infarct in the territory of the anterior choroidal artery with major but reversible electrocardiographic changes. Infarction involved the substantia innominata containing the ventral amygdalofugal pathway. Electrocardiographic changes could result from a small hemispheric lesion of structures involved in autonomic control. Correlation studies of stroke location with electrophysiologic changes should help to determine patients at risk for cardiac arrhythmia and prevent sudden death.
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The increase in left ventricular myocardial mass is a mechanism of adjustment of the ventricular pump to a normal process, such as growth or sports, or a pathological process (mechanical overload or cardiomyopathy). The associated geometrical changes tend to normalize systolic performance and/or strain--one of the main determinants of myocardial metabolic requirements. When left ventricular hypertrophy is inadequate quantitatively, geometrically and functionally, and when contractility and preload reserves are exhausted, the systolic performance of the ventricular pump becomes narrowly dependent upon the increased systolic strain. some types of "pathological" hypertrophy may ultimately result in alteration of myocardial intrinsic properties during contraction, relaxation and/or extension, and this in turn may induce or aggravate ventricular failure. The causes of left ventricular hypertrophy are imperfectly known, the views most commonly held being metabolic imbalance of the myocardium due to increased demands, and reduction of coronary reserve and exchange capacities.
Left ventricular failure is defined as an inability to maintain, under resting conditions, a cardiac output sufficient for the oxygen requirement. It is accompanied by a rise in trans-mural ventricular filling pressure and/or a reduction in systolic volume. It may be linked to an alteration in the systolic performance and/or an alteration in the characteristics of the left ventricle. The compensatory mechanisms are represented by the noradrenergic stimulation; a rise in the muscular mass of the left ventricle and the associated changes in its geometry the heterometric regulation of Frank Starling. Some peripheral adaptive mechanisms such as salt and water retention, arteriolar vaso-constriction and a rise in the peripheral extraction of oxygen contribute to compensating for the lower systemic cardiac output.
The medical treatment of left ventricular failure classically relies upon the use of diuretics with or without digitalis. The recent arrival of vasodilators allows for both an improvement in the quality of life as well as a prolongation of survival for people in heart failure. The "new" positive inotropic agents which can be used orally in the longterm have not yet given the results which were anticipated. The prognosis of left ventricular failure remains poor, underlining the importance of preventive treatment and in the last resort the possibility of cardiac transplantation.
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