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Biomedical subjects

J P Mérillon

Publications and source records attributed to J P Mérillon.

At least 19 recordsLinked to original sources
PubMed1992

[Functional coupling of the left ventriculo-arterial system and aging in man].

In a haemodynamic and angiographic study at rest conducted in 25 men aged from 22 to 68 years who had no more than another risk factor for arterial disease and showed no evidence of cardiac or arterial disease several parameters were measured or calculated. Firstly, a global index of arterial system function (Ea) and its various factors: Ea = ESP/SV [ESP: left ventricular end-systolic pressure; SV: systolic volume]; Ea = (HR x TSR)+Ea' [HR: heart rate/min; TSR: total systemic resistance] where Ea' = (ESP - AoP/SV) [AoP: mean aortic pressure]. Secondly, the parameters concerning the left ventricle were the mass (m) and the m/EDV ratio [EDV: end-diastolic volume] and indices of the left ventricular systolic and diastolic functions, such as ELV = ESP/ESV [ESV: end-systolic volume], kp: the volumic distensibility module of the left ventricular chamber; relations EF - o ES [EF: ejection fraction; o ES: end-systolic constraint], and kp - m/EDV as indice of left ventricular muscle distensibility. In parallel with the subjects' age, Ea increased by joint augmentation of TSR and Ea' while m, m/EDV, ELV and kp also significantly increased. The inotropic quality of the left ventricular muscle and its intrinsic distensibility were found to be decreased in a few subjects aged over 45. Ea/ELV (reverse of ejection fraction -1) tended to increase (ELV relatively less than Ea), but this increase was not significant (P = 0.10). These results show that in the ageing man the improvement observed in the ejection fraction of the left ventricular pump corresponds roughly to the degradation of the arterial system transfer function, and the arterial system-left ventricle coupling, evaluated by the Ea/ELV ratio, is maintained (better in fact than in arterial hypertension and heart failure). This improvement is achieved by increases of m and, chiefly, m/EDV which compensate for both the increase of Ea and the relative decline of left ventricular muscle contractile quality. There is a disorder of the left ventricular pump diastolic function which is due to geometric changes in the chamber and to changes in the intrinsic distensibility of the left ventricular muscle.

Adult↗
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↗
PubMed1987

[Non-obstructive hypertrophic cardiomyopathy and systolic compression of 3 coronary arteries. Long-term improvement with verapamil].

Systolic compression of the three main coronary vessels was observed during the investigation of a 23 year old African with hypertrophic cardiomyopathy. The patient was admitted in 1982 for evaluation of retrosternal chest pain and one syncopal attack during exercise. The ECG showed left ventricular hypertrophy with important ST-T wave changes which became more severe on exercise. Diffuse myocardial hypertrophy without obstruction was confirmed by echocardiography and cardiac catheterisation. Coronary angiography showed systolic compression of the three main coronary arteries. There was no coronary vasodilatory response to rapid atrial pacing; increased left ventricular end diastolic pressure confirmed the poor tolerance of exercise. The therapeutic failure of betablockers suggested a possible coronary spasm. Long-term (4 years) clinical improvement was obtained with calcium antagonists (Verapamil 360 mg/day) without significant regression of the hypertrophy. Coronary vasodilation under Verapamil led to improved tolerance of rapid atrial pacing. Control angiography showed only mild systolic compression of the three main coronary vessels. The improvement of this functional coronary insufficiency with Verapamil was attributed to its negative inotropic effects associated with improved myocardial relaxation and ventricular filling.

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↗
PubMed1984

[Effects of molsidomine during the cold test in stable coronary insufficiency under beta-blocker treatment].

The heart rate, cardiac output, coronary sinus blood flow, systolic and end diastolic left ventricular pressures, femoral arterial pressure and coronary oxygen arterio-venous difference were measured in 12 patients with stable coronary artery disease without cardiac failure on long-term betablocker therapy, before and 45 minutes after 2 or 3 mg sublingual molsidomine. The measurements were repeated in 8 patients during a cold pressor test. Under basal conditions, molsidomine decreased the systolic and end diastolic left ventricular pressures, mean femoral arterial pressure, cardiac output and double product. The coronary oxygen arterio-venous difference was unchanged. Coronary sinus flow and myocardial oxygen consumption decreased. In the 2 patients who were given 3 mg molsidomine, a progressive reduction in systolic left ventricular pressure to 70% or less than its initial value, necessitated immediate treatment with volume expanders. During the cold pressor test before molsidomine the systolic and end diastolic left ventricular pressures, mean femoral arterial pressure and the double product increased. Coronary sinus flow was unchanged overall: it decreased in 6 patients, increased in 2 patients and remained the same in 1 patient. Coronary resistance increased in 6 patients and decreased in only one patient. During the cold pressor test after molsidomine there was a significant reduction in the increase of systolic left ventricular pressure, mean femoral artery pressure and double product. Coronary sinus blood flow increased in 5 patients and decreased in only one case. Coronary resistance decreased in half the cases.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1983

[Changes in passive left ventricular pressure-volume relations in acute volume expansion].

The passive left ventricular pressure-volume relationship characterises left ventricular distensibility. However, it has recently been shown that acute pharmacological intervention can significantly change the position of the diastolic pressure-volume curve. We studied the effects of acute volumic expansion on the passive left ventricular pressure-volume relationship. In fact, the interpretation of left ventricular function curves during acute volumic expansion assumes that the left ventricular pressure-volume relationship remains unchanged. We measured the heart rate, cardiac output, left and right ventricular pressures with micromanometers, ventricular volumes by cineangiography 50 frames/sec (n = 6) or ventricular diameters by M mode echocardiography (n = 6) in 12 patients without valvular or coronary heart disease during rapid volumic expansion, and calculated stroke volumes and indices of left ventricular performance; the passive left ventricular pressure-volume or pressure-diameter relationship was adjusted to an exponential function P = a.ekp.V or P = a'.ek'p.De. After volumic expansion the cardiac output rose due to an increase in heart rate and stroke volume. The increase in stroke volume was related to that of end diastolic volume, the end systolic volume remaining unchanged: there was little difference in the indices of left ventricular performance. The pressure-volume and pressure-diameter curves were considerably shifted upwards and to the left during acute volumic expansion: this seemed to be due mainly to an increased intrapericardial pressure secondary to the increase in intrapericardial content. The relationship obtained by subtracting the simultaneous right ventricular from the instantaneous left ventricular pressure after volumic expansion was identical to the basal left ventricular pressure-volume curve. These observations demonstrate the importance of external factors of left ventricular compression in the changes in the passive left ventricular diastolic relationship during acute volumic expansion and invalidate the use of function curves obtained under these conditions for the assessment of left ventricular systolic function. The end diastolic pressure cannot be considered to reflect end diastolic volume and the function curves, in fact, illustrate changes in diastolic distensibility.

Adult↗
PubMed1983

[Thrombosis of a valve prosthesis: fatal cerebral embolism during thrombolytic treatment].

The authors report the first case of lethal cerebral embolism complicating thrombolytic therapy administered for thrombosis of a mitral valve prosthesis. The incidence of systemic embolism during this form of therapy appears to be at least one in five cases. It may be underestimated and should lead to further discussion as to the indications of thrombolytic therapy and surgery for thrombosis of a left heart valve prosthesis.

Adult↗
PubMed1983

[Hemodynamic and coronary effects of molsidomine in patients with stable coronary insufficiency in the basal state, during an atrial stimulation test and a cold test].

The heart rate (HR), the cardiac output (Qc) and the coronary sinus flow rate (Qcs), the left ventricular systolic and end-diastolic pressures (LVSP, LVEDP), the femoral artery pressure (FAP) and the difference between the coronary arterial and coronary venous oxygen tension (DAVcO2) were measured in patients with stable coronary insufficiency without cardiac failure, before and 40 to 60 minutes after 2 or 3 mg of molsidomine (M). In 20 patients, these measurements were made in the basal state, in spontaneous rhythm (SP). In 8 of these patient, (including 3 receiving beta-blockers) the measurements were made during an atrial stimulation test (ST) and in 8 other patients, all receiving long-term beta-blocker therapy, the measurements were made during a cold test (CT). At the basal state in SR, a gradual reduction in the LVSP to 70% or less of its initial value was observed in the patients receiving 3 mg of M (2 of whom received beta-blocker treatment). The LVSP was immediately restored by vascular filling. In 16 patients, M decreased the LVSP, the LVEDP, the FAP, the Qc and the double product (DP = LVSP X HR). The DAVcO2 was unchanged. Qcs and MVO2 (MVO2 = Qcs X DAVcO2) were decreased. In the course of ST, the haemodynamic and coronary changes are similar to those seen in the basal state. During the Ct, the increase in the LVSP, FAP and DP was significantly reduced by M. The variations in Qcs and coronary resistance (FAP/Qcs) were also significantly different after M., with better metabolic regulation of the coronary circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

[Changes in the physical properties of the arterial system and left ventricular performance with age and in permanent arterial hypertension: their interrelation].

The purpose of this work was to study interactions between physical properties of the arterial system and left ventricular performance during aging in normal and in hypertensive patients. 50 patients were studied; 28 normal patients (age range 22 to 68 years) and 22 patients with essential hypertension (age range 23 to 63 years). In hypertensive patients, the end systolic pressure-volume ratio (ESP/ESV), modulus of chamber stiffness (kp), left ventricular wall thickness (h), mass (m), m/LVEDV ratio (LVEDV: left ventricular end diastolic volume), systemic arterial resistance (SAR), pulse wave velocity (C) and characteristic impedance of the ascending aorta (Zc) were increased compared to normal subjects of similar age. The ejection fraction (EF), the mean velocity of fiber shortening (VCF) and dp/dt max were unchanged. In normal patients: the ESP/ESV ratio, kp, h, m, m/LVEDV ratio, SAR, C and Zc increased with age; there were no age related changes in EF, VCF or dp/dt max. In both groups, there was a close relationship between the m/LVEDV ratio and Zc, the characteristic impedance of the ascending aorta. These results suggest that: 1. aging and arterial hypertension lead to similar changes in the physical properties of the arterial system and in left ventricular performance; 2. in both cases, the development of concentric cardiac hypertrophy is closely related to the physical properties of the arterial system.

Adult↗
PubMed1981

[Hemodynamic and coronary effects of intravenous verapamil in coronary insufficiency].

Verapamil inhibits calcium influx through the slow calcium canals. The coronary an haemodynamic effects of intravenous Verapamil were studied in 8 patients with chronic coronary insufficiency documented by coronary arteriography. The following measurements were made in spontaneous rhythm and during atrial pacing under basal conditions and 10 minutes after intravenous Verapamil (0.10 to 0.17 mg/kg) relayed with a continuous infusion of 5 x 10(-3) mg/Kg/mn: heart rate, cardiac output, left ventricularr pressure (Millar 5 F micromanometer), femoral artery pressure, coronary sinus flow by continuous thermodilution, oxygen and lactate concentrations in arterial and arterio-venous oxygen difference, and index of myocardial oxygen consumption and the coefficient of lactate extraction were then calculated. The coronary and haemodynamic effects of atrial pacing were similar before and after Verapamil at a given rate. Left ventricula end diastolic pressure decreased, cardiac output and total systemic resistance were unchanged, dP/dt max increased but to a lesser degree after Verapamil (P less than 0.05). Coronary arterio-venous oxygen difference decreased after Verapamil. The coronary and haemodynamic effects of Verapamil were similar in spontaneous rhythm and during atrial pacing. In spontaneous rhythm, the heart rate and left ventricular end diastolic pressure increased. In spontaneous and paced rhythm, femoral artery pressure, total systemic resistance and dP/dt max decreased. Cardiac output remained the same. Myocardial oxygen consumption decreased mainly because of a reduced coronary arterio-venous oxygen difference and because of unchanged coronary flow in spontaneous rhythm oxygen consumption seems to have a favourable effect on the myocardial energy equilibrium as shown by the increased coefficient of lactate extraction during atrial pacing after Verapamil. This study shows the negative inotropic and arterial vasodilator effects of Verapamil to be responsible for the reduced myocardial oxygen consumption. It also caused coronary artery vasodilation.

Adult↗
PubMed1980

[Aortic pressure and velocity signals processing: application to human aorta characterization (author's transl)].

The input to and characteristic impedances of the ascending aorta and the mean, pulsatile and maximum hydraulic powers generated by the left ventricle have been determined in 16 patients by simultaneous measurements of aortic pressure (by miniature transducer), velocity (by electromagnetic probe) and diameter (by cineangiography). Eight patients had normal blood pressure and eight were hypertensive. Harmonics of pressure and flow were calculated by processing the signals for 40 cycles, taking into account the frequency response of the velocity probe (Figs. 1 and 2). 1. The invariance of input impedance with heart frequency confirms the linearity of the arterial system under resting conditions (Fig. 3). 2. The characteristic impedances calculated by averaging the input impedance modulus above 2 Hz (Fig. 5) and from cineangiography are in good agreement for normotensive patients but discrepancies arise for hypertensive patients (Fig. 4). 3. Comparison of input impedance spectra (Fig. 6) reveals that in hypertensive patients the point of minimum modulus and zero phase is shifted towards higher frequencies while the characteristic impedance is higher. 4. The hydraulic power generated by the left ventricle is higher for hypertensive patients (Table I) and the increase in pulsatile power is almost entirely due to the increase in pressure harmonics (Figs. 7 and 8). These results suggest that the aorta plays an important role in left ventricular performance and that it may be characterized by its input impedance spectrum.

Adult↗
PubMed1979

[Hemodynamic changes during increasingly rapid atrial pacing].

The cardiac output (Qc), indices of left ventricular function in the isovolumic period (dp/dt/Pt), max, and during the ejection period (EF, VCF), the end diastolic and end systolic ventricular volumes, the speed of ventricular filing, the module of elasticity of the ventricular chamber (kp) and the end systolic pressure-volume relationships were measured in 20 patients (11 normal in group I and 9 with and apparently primary cardiomyopathy in group II) at rest and during progressively rapid atrial pacing. The Qc was lower and the indices of left ventricular function in the isovolumic and ejectional phases, the end systolic pressure-volume relationship and speeds of ventricular filling were decreased in group II: kp was the same in both groups of patients. At progressively higher heart rates the cardiac output slightly in both groups, the systolic volume decreased, (dp/dt/Pt) max increased, the ejection fraction and VCF were unaltered. The speeds of filling and kp were unchanged. The end systolic pressure-volume relationship increased. In group I the reduction in systolic volume seemed to be related to a greater reduction in the end diastolic volume than in the end systolic volume. In group II, the reduction of the systolic volume was related only to a reduction of the end diastolic volume.

Adult↗