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Biomedical subjects

A Cohen-Solal

Publications and source records attributed to A Cohen-Solal.

At least 109 records · Page 6Linked to original sources
PubMed1991

[Properties of arteries, cardiac function and structure in chronic hypertension].

Hypertension is a condition which demonstrates the relationship between the properties of the left ventricle and arterial system. The spectrum of aortic impedence expresses the principal factors which oppose LV ejection into the initial aorta: 1) capacitive forces related to the viscoelastic properties of the arterial wall, directly proportional to its rigidity, 2) forces of inertia which increase with the acceleration of the blood and which are inversely proportional to the aortic cross sectional area, 3) reflection. With respect to a stroke volume which is usually normal, hypertension is characterised by: 1) an increase in mean aortic pressure (MAP), 2) with respect to the increase in MAP, an increase in systolic, late systolic and differential pressures. These changes in the level and morphology of aortic pressure are due to: a) the increase in systemic arterial resistances, a continuous expression of the spectrum of the module, b) an increase in the elastic forces (increased rigidity of the aorta related to increased pressure and structural wall changes) usually insufficiently compensated by a decrease in the inertial forces (aortic dilatation), c) an earlier return of the reflected pulse wave, well before the end of the anterograde wave. Overall, there is a relationship between the mass, the geometry (concentric hypertrophy) and pump function of the left ventricle and the properties of the arterial system expressed in terms of pulse wave velocity, characteristic impedence or the late systolic pressure/stroke volume ratio. The relationship is much closer than that of the properties of the LV and aortic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1990

[Disorders of diastolic function in chronic left ventricular insufficiency].

Abnormalities in the diastolic function of the left ventricular pump are the common determinant and, above all, the earliest manifestation of all forms of chronic left ventricular failure, whether or not the left ventricular systolic function is abnormal. Congestive signs, in particular, are directly related to abnormalities of ventricular filling. Primary diastolic dysfunction is the cause of left ventricular failure in about 40 p. 100 of the cases, but it may also be observed in almost all cardiopathies. In myocardial ischaemia the pressure-volume relation is displaced upwards owing to a slowed down, inhomogeneous and incomplete relaxation. Left ventricular hypertrophy, whether it is due to excessive pressure (arterial hypertension, aortic stenosis) or reflects a primary hypertrophic cardiomyopathy, is associated with a slowing down of ventricular relaxation and a reduction of left ventricular diastolic distensibility, even though the ventricular pump systolic function remains normal for a long time. Outside alterations in the distensibility of the ventricular muscle, ventricular dilatation alters ventricular filling by forcing the ventricle to function on the vertical part of its diastolic pressure-volume relation. Nowadays, the aged hearts is the most frequent cause of heart failure with normal systolic function. In all cases dysrhythmias and atrioventricular desynchronization act as aggravating factors. Treatment is often difficult since positively inotropic drugs or arterial vasodilators frequently have a modest or even deleterious effect.

Aged↗
PubMed1990

[Converting enzyme inhibitors and cardiac insufficiency: current findings and perspectives].

Angiotensin-converting enzyme inhibitors are mixed vasodilators with a prolonged sustained effect in chronic heart failure. They also act on the reactivity of peripheral circulation, on ventricular remodelling after myocardial infarction, on myocardial hypertrophy in arterial hypertension and on ventricular hyperexcitability. They alleviate the symptoms of symptomatic heart failure, and they constitute the only treatment that has been able to improve the survival of patients with the most severe heart failure. Several studies are in progress to determine whether these drugs should be used as first-line therapy.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

[Determination of the ventilatory threshold during the exercise test in patients with cardiac insufficiency. Relation of the lactate threshold].

The non-invasive assessment of the lactate threshold during exercise test is possible in normal subjects by the study of respiratory gas exchange: a ventilatory threshold may be determined using Wasserman's criteria. This determination is more unreliable in cardiac failure. Forty-four patients with cardiac failure underwent exercise tests with measurement of lactate concentrations and respiratory gas exchanges during the exercise. Despite a regular increase in the lactate concentration from the onset of exercise, it was possible to determine a lactate threshold in the majority of patients. A ventilatory threshold could be determined in 27 to 38 patients depending on the method used. The correlation between these two thresholds was excellent (r = 0.87). The determination of the ventilatory threshold during exercise is therefore possible in cardiac failure. The main limitation of the method is that no result can be obtained in a large number of patients (15 to 20%) which restricts its value as a principal method of therapeutic evaluation.

Aged↗
PubMed1990

[Influence of medical treatments on the functional status in patients with chronic cardiac insufficiency].

The discordance frequently observed between the hemodynamic effects of treatment and change in functional status may be explained by the fact that symptoms are related more to the circulatory changes caused by the heart failure than the heart failure itself. This is why angiotensin converting enzyme inhibitors and controlled exercise training improve exercise capacity of patients with chronic cardiac failure more than inotropic agents and direct vasodilator therapy, partly because of their marked beneficial effect on regional blood flow.

Cardiovascular Agents↗
PubMed1989

[Abnormalities of the peripheral circulation and tolerance to exertion of patients with heart failure].

Chronic heart failure is attended by a number of abnormalities of peripheral circulation. To a great extent, these abnormalities determine the patients' functional symptoms, their tolerance to exercise and their response to treatment, at least in the short term. The response to exercise of heart failure patients depends on their maximal oxygen consumption which is determined by their maximal cardiac output and by various peripheral adjustments, such as distribution of regional blood flow and peripheral oxygen extraction. Abnormalities of peripheral arteriolar and capillary dilatation are determined by hyperstimulation of neurohormonal systems. An increase in maximal muscular blood flow, which determines the patients' capacity of exercise, can be obtained with drugs which increase the muscular perfusion pressure (inotropic drugs) or which decrease muscular resistances without lowering the perfusion pressure (venous or balanced vasodilators, diuretics). Physical rehabilitation may improve maximal oxygen consumption by improving the peripheral use of oxygen. Thus, a better understanding of the physiopathology of heart failure will in the future improve the functional symptoms of these patients and prolong their survival, which has not always been the case with conventional therapies.

Heart Failure↗
PubMed1989

[Effects of thrombolytic treatments on the mortality of myocardial infarction. Characteristics of large-scale trials, main results].

The characteristic features and principal results of the 5 large-scale randomised therapeutic trials (GISSI, ISIS 2, ASSET, AIMS, ISAM), each including over 1000 patients, designed to evaluate the effects of thrombolysis on mortality in myocardial infarction, are reviewed. The methodologies are very different, which prevents comparison of results. The thrombolytic therapy significantly reduced hospital mortality in all the trials except ISAM. Early institution of therapy gave better results but one trial (ISIS 2) showed persistence of a significant benefit in patients treated late up to the 24th hour and in the most elderly groups of patients (up to and over 70 years of age). The benefits obtained during the hospital phase were maintained at medium term. The tolerance was satisfactory, the frequency of complications being comparable in all the trials. The association of aspirin therapy significantly reduced mortality and occurrence of myocardial infarction in the ISIS 2 trial and would seem to be therefore a recommended association with streptokinase and probably with other thrombolytic drugs. Other trials are needed to compare the efficacy of the different thrombolytic agents in reducing patient mortality.

Aged↗
PubMed1988

[Neuroendocrine changes in chronic cardiac insufficiency].

Throughout the course of chronic congestive heart failure cardiac and peripheral compensatory mechanisms are at play, most of them under the influence of the neuroendocrine system. The reserves of heart rate and contractility are regulated essentially by the noradrenergic system (NAS), but this mechanism is partial and transient owing to the gradual decrease in the density and sensitivity of myocardial beta-adrenergic receptors induced by overstimulation. Adaptation of the heart to exercise may be reduced. This escape phenomenon is also observed with almost all cardiotonic drugs which interfere with cyclic adenosine monophosphate (cAMP), in contrast with the paradoxically favourable effects of beta-blockers in small doses or of drugs that are both agonists and antagonists of beta-adrenergic receptors. The mechanisms which contribute to the induction of left ventricular hypertrophy are imperfectly known. The noradrenergic system and the renin-angiotensin-aldosterone system (RAAS) are probably not the only ones involved. The setting in action of Frank-Sterling heterometric regulation, at first during exercise then permanently, requires an increase in filling pressure obtained by venous constriction (predominantly controlled by the NAS) and, mostly, by an increase in circulating blood volume. NAS and RAAS intervene in the kidneys to produce water-and-salt retention.(ABSTRACT TRUNCATED AT 250 WORDS)

Arginine Vasopressin↗
PubMed1988

[Measurement of oxygen consumption during exertion in patients with cardiac failure].

Measurement of O2 (VO2) consumption makes it possible to refine non-invasive assessment of congestive heart failure (CHF). The peak of VO2 during exercise is determined by the maximum values of cardiac output and of the arteriovenous O2 difference. It thus provides semi-quantitative hemodynamic information. In addition, reproducibility of the VO2 peak is quite satisfactory in these patients; it allows them to be classified according to their VO2 peak and permits more objective assessment of therapeutic management. Finally, the anaerobic threshold, when it can be determined, provides the same type of information during sub-maximum exercise.

Dyspnea↗
PubMed1988

[Multiparameter correlative study of respiratory gas exchange during exercise].

Patients with chronic heart failure were evaluated simultaneously by conventional methods and by heart-lung exploration during exercise with the purpose of validating the latter method. Only 50 patients were evaluated on two occasions and therefore included in the correlative statistical study. In this study such data as NYHA classification, cardiothoracic ratio, ejection fraction, echocardiographic fibre shortening fraction and biochemical values (venous lactate, plasma noradrenaline levels) were compared with data obtained from evaluation during exercise, i.e. VO2 max, VO2 peak, anaerobic threshold, oxygen pulse, VCO2, O2 equivalent and respiratory quotient, alveolar ventilation per minute, duration and load of exercise. Very good correlation was found with the indices obtained from VO2 and in particular with the O2 pulse and the VO2 max percentage. Good correlation was also found with VCO2 and the O2 equivalent as well as with alveolar ventilation per minute. In contrast, the anaerobic threshold and respiratory quotient correlated poorly with the first set of data and therefore were disappointing. It appears from this study that the indices obtained from VO2 are highly representative of the heart-lung unit in patients with heart failure. It seems, however, that the muscular status of the patients plays a considerable role in their exercise capacity. We suggest that these indices should be used in clinical pharmacology studies.

Aged↗
PubMed1987

[Hydatid cyst of the right heart and post-embolic pulmonary hypertension].

A 22-year old man with hydatid cyst of the right ventricle presented, for about 10 years, with clinical signs of post-embolic pulmonary hypertension. Despite tumoral resection, the patient died post-operatively of his pulmonary hypertension. Post-mortem examination showed a hydatid cyst on the main pulmonary artery and fixed post-embolic pulmonary hypertension, but we were unable to determine whether we were dealing with old migrated cysts or blood clot emboli developed in contact with the cardiac tumour.

Adult↗
PubMed1987

[Evaluation of bidimensional echography in the etiological orientation of pericardial disease. Apropos of 39 anatomo-echographic comparisons].

Echocardiography provides a firm diagnosis of pericardial effusion and evaluates its repercussions on the cardiac cavities. The images obtained with two-dimensional echocardiography are of such quality that the anatomical lesions can be analyzed, but the predictive value of this examination for the aetiological diagnosis has not yet been established. To investigate this point we have compared the images recorded in 39 episodes of pericardial disease with the corresponding anatomical data provided by surgery (n = 38)) or necropsy (n = 1) less than 48 hours after the ultrasonic examination. In one case, the purely solid nature of the pericardial content, suspected on the presence of an echo-filled cavity with adherent membranes, was confirmed at surgery. Conversely, the totally or partly liquid nature of the effusion was ascertained whenever the two pericardial membranes were separated by an echo-free cavity in at least one portion of the region examined, and there was no false-positive result (n = 38). The images obtained could be compared with the anatomical lesions in 28 out of 38 cases of partly or totally liquid pericarditis. The pericardial cavity was entirely echo-free in 12 of these cases, and this was confirmed by the anatomical examination, except in one case where epicardial nodules were found at surgery. Abnormal intrapericardial images were detected in the other 16 echocardiographic examinations, viz.: round masses in 2 cases, linear echoes in 2 cases and mattress-like deposits in 12 cases. In 9 of these 16 cases corresponding intrapericardial formations were discovered at surgery.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1987

[Reduction of auricular fibrillation and tachycardia using intravenous flecainide].

Fifty-one consecutive patients with atrial tachycardia [atrial fibrillation (FA) 37, atrial flutter (Fl) 10, tachycardia (TSA) 4] received a single 2 mg/kg dose of flecainide injected intravenously over 5 to 10 minutes. Patients over 75 years of age or presenting with heart failure or disorders of conduction were excluded from the study. Sinus rhythm was restored during the injection or within the following 5 minutes in 15 patients (FA 12, Fl 1, TSA 2). The most frequent side-effects were visual disorders (5 cases) and moderate prolongation of QRS (all cases). Five patients had more pronounced disorders of conduction, but none developed heart failure. Reduction was obtained in 12 of the 18 patients whose arrhythmia had lasted for less than 8 days, against only 3 of the patients whose arrhythmia was more than 8 days old. Drug-induced reduction always failed in patients with left atrial dilatation (greater than 45 mm at echocardiography). An increase in the ventricular rate of unreduced flutter was observed in only one patient. Plasma flecainide levels were high (1.5 and 5.5 mg/l) at the end of the injection, but they fell to the therapeutic range within less than 10 minutes. Flecainide therefore appears to be effective in reducing recent atrial fibrillation on a non-dilated atrium. In cases with disorders of conduction, altered ventricular function or flutter, the therapeutic risk is such that another method of conversion should be used.

Adult↗
PubMed1987

[Value of early vasodilator treatment with prazosin in chronic cardiac insufficiency].

The purpose of the present study was to find out whether the beneficial effect of prazosin in congestive heart failure persists after 2 and 6 months of treatment and whether the clinical and haemodynamic data obtained correlate with the response to treatment. Twenty-four patients of mean age 50.0 +/- 3.00 years presenting with congestive heart failure stage II (3 cases), stage III (18 cases) or stage IV (3 cases) in the NYHA functional classification were treated. All abstained from taking digitalis at least one week before treatment and were given prazosin 14.5 +/- 0.77 mg/day together with spironolactone 25 to 100 mg/day. The results of treatment were assessed by its effects on echocardiography, systolic time intervals, ejection fraction and cardiac index measured by the radioisotope method, and maximal duration of a 60-watt exercise on an ergometric bicycle. Treatment was discontinued before the 6th month in 9 out of 10 non-responders. The remaining 14 patients responded to treatment and their condition improved. Mean blood pressure rose in 6 months from 95.4 +/- 3.92 to 104 +/- 3.06 mmHg (p less than 0.05). The cardiothoracic ratio was reduced at 2 months (-0.05 +/- 0.01, p less than 0.01) and at 6 months (-0.08 +/- 0.02, p less than 0.01). Systolic time intervals were not significantly altered.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

[Left ventricular hypertrophy. Advantages and drawbacks].

The increase of the muscular mass of the left ventricle represents, for the ventricular pump, a mechanism of adaptation to a normal process (growth, sport, etc.) or a pathological process (mechanical overload or cardiomyopathy). The geometrical variations which are associated, tend to normalize the performances and/or the systolic constraints, determining elements of the metabolic needs of the myocardium. If left ventricular hypertrophy is not quantitatively, geometrically and functionally adequate and if the contractility and precharge reserves become exhausted, the systolic performance of the ventricular pump is altered and becomes extremely dependent upon the systolic constraints which are then increased. It may be difficult to take into consideration an insufficiency of the contractility of the ventricular muscle in front of clinical signs of cardiac insufficiency which is conditioned by abnormalities in the filling of the ventricular pump. In addition, some "pathological" hyperthophies may secondarily induce an alteration of the intrinsic properties of the muscle (during its contraction, relaxation an/or extension), susceptible to induce or aggravate a ventricular insufficiency. The causes remain uncertain, since a metabolic imbalance of the myocardium by increase of the needs as well as a decrease of the coronary reserve and the exchange capabilities are commonly accepted. What are the mediators of these mechanisms of quantitative, geometric adaptation and also--at least in some animals--structural adaptation (isoenzymes of myosin)? Why do they seem, at times, strangely absent or quickly out-of-date, or sometimes excessive, with all the drawbacks specific to hypertrophy? The answer to these questions would perhaps represent a new therapeutic approach to left ventricular insufficiency.

Adaptation, Physiological↗