[Functional coupling of the left ventriculo-arterial system and aging in man]. / Couplage "fonctionnel" ventricule gauche-système artériel et vieillissement chez l'homme.

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.

[Properties of arteries, cardiac function and structure in chronic hypertension]. / Propriétés du système artériel, fonction et structure cardiaques dans l'hypertension artérielle permanente.

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)

[Non-obstructive hypertrophic cardiomyopathy and systolic compression of 3 coronary arteries. Long-term improvement with verapamil]. / Cardiomyopathie hypertrophique non obstructive et compression systolique des trois artères coronaires. Amélioration à long terme avec le vérapamil.

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.

[Left ventricular hypertrophy. Advantages and drawbacks]. / Hypertrophie ventriculaire gauche. Avantages et inconvénients.

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.

[Coronary and renal circulation in patients with cardiac failure after converting enzyme inhibitors]. / Circulations coronaire et rénale chez des malades en insuffisance cardiaque après inhibiteurs de l'enzyme de conversion.

The cardiac output and its peripheral distribution must fulfill the metabolic and/or functional requirements of the different organs. The various techniques used to measure blood flow rates in the coronary and renal arteries provide much information on this point, but they do not tell us all we would like to know about the distribution and "utilization" of these flows in tissues. In normal subjects the myocardial oxygen consumption is not markedly different from the renal oxygen consumption, but the mechanisms that regulate the coronary and renal circulations are not the same. The flow rate in the coronary vessels is about 10% of the cardiac output, the arteriovenous oxygen gradient is superior to 10 vol % and regulation is metabolic. In the renal vessels, which are primarily "functional", the flow rate is about 25% of the cardiac output and the arteriovenous oxygen gradient is inferior to 2 vol %. In heart failure patients, despite reduced cardiac output the blood pressure is kept normal for a long time by vasoconstriction of the arterioles, a process which involves, at least partly, the renin-angiotensin system. The vasoconstriction predominates in some circuits (the renal flow rate is less than 15% of the cardiac output) and spares the "privileged" circuits (the coronary flow rate is more than 15% of the cardiac output). Under the influence of angiotensin converting enzyme inhibitors, the cardiac output increases and its distribution is modified. The coronary flow rate remains stable or is reduced in proportion to the decrease in myocardial oxygen consumption, the metabolic regulation is preserved and there is no "coronary steal". The percent increase in renal flow rate is usually superior to that of the cardiac output. This peripheral redistribution of coronary and renal blood flow rates in heart failure patients after treatment with converting enzyme inhibitors seems to correspond to the physiological purposes of the two regional blood flows.

Hemodynamic and coronary effects of molsidomine at basal state, during atrial pacing, and during cold pressor test in patients with stable angina pectoris.

Heart rate (HR), cardiac output (CO), coronary sinus blood flow (CSF), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), mean arterial (MAP), and coronary arteriovenous difference for oxygen (AVDcO2) were measured in patients with stable angina pectoris without cardiac failure before and 40 to 60 minutes after administration of 2 or 3 mg of molsidomine. In 20 patients these measurements were made in basal state during spontaneous rhythm. In eight of these patients (including three receiving beta blockers) the measurements were made during atrial pacing. In eight other patients, all receiving long-term beta-blocker therapy, the measurements were made during cold pressor test. At the basal state in spontaneous rhythm, a gradual reduction in the LVSP to 70% or less of its initial value was observed in four patients receiving 3 mg of molsidomine (two of whom received beta-blocker treatment). The LVSP was immediately restored by vascular filling. In the 16 other patients molsidomine decreased LVSP, LVEDP, MAP, CO, and double product (DP = LVSP X HR). The AVDcO2 was unchanged. CSF and myocardial oxygen uptake index (MVO2 = CSF X AVDcO2) were decreased. During atrial pacing, hemodynamic and coronary effects were similar to those seen in the basal state. During the cold pressor test, the increases in LVSP, MAP, and LVEDP were significantly reduced by molsidomine. The variations in CSF and coronary resistance (MAP/CSF) were also significantly different after administration of molsidomine, with better metabolic regulation of the coronary circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in left ventricular performance during chronic pressure or volume overload: importance of physical properties of the arterial system.

The present study was aimed at evaluation of changes in systolic and diastolic left ventricular function during chronic pressure of volume overload, in comparison with normal subjects. Sixty-two patients were included: group 1 was composed of 25 normal subjects, group 2 was composed of 20 subjects with essential hypertension, and group 3 was composed of 17 subjects with aortic regurgitation without congestive heart failure. Cardiac output, aortic and left ventricular pressures (micromanometers), ventricular volume and ascending aortic radius (cineangiography), ejection fraction (EF), mean velocity of fiber shortening (VCF), ventricular mass (m), and the ratio m/EDV (EDV, end diastolic volume) were determined. Also measured were maxima for end systolic pressure (ESP), end systolic stress (ESS), and end systolic volume (ESV) and radius (ESR), as well as the modulus of left ventricular chamber and muscle stiffness (method of Gaash et al.) (1) and characteristic impedance of the ascending aorta (Zc). In hypertensive patients, m and m/EDV were increased, as was the ESP/ESV ratio, whereas EF and VCF were not modified and the ESS/ESR was normal or sometimes decreased. The systolic "pump" function thus appeared to be increased, whereas the muscle function appeared normal or decreased. The moduli of left ventricular chamber stiffness and muscle stiffness were increased. Zc was increased because of a greater pulse wave velocity, although aortic radius was larger. A close relationship was found between Zc and the ratio m/EDV. In patients with aortic regurgitation, the increased left ventricular mass was closely related to the regurgitant fraction (RF). The m/EDV ratio was normal. EF was unmodified and VCF and the ESP/ESV ratio were decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

[Effects of molsidomine during the cold test in stable coronary insufficiency under beta-blocker treatment]. / Effets de la molsidomine lors d'un test au froid chez l'insuffisant coronaire stable sous traitement bêtabloquant.

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)

Aortic input impedance in heart failure: comparison with normal subjects and its changes during vasodilator therapy.

This study was aimed at the evaluation of aortic impedance in patients with congestive heart failure. Aortic impedance (simultaneous measurements of aortic pressure and blood flow), mean (Wm) and pulsatile (Wp) powers were compared in 11 normal subjects and in 12 patients with heart failure. Pulse wave velocity (C: modified Moëns-Korteweg equation, simultaneous measurements of aortic pressure and radius) was determined under control conditions in all normal subjects and in 7 patients with heart failure. Impedance curves in patients with heart failure were characterized by increased values of the impedance modulus at 0 Hz (peripheral resistance) and at low frequencies. The characteristic impedance, C, and phase were not different from normal subjects. In six patients with heart failure, impedance curves were studied during nitroprusside infusion. During the infusion of the vasodilator, the impedance modulus at 0 Hz and at low frequencies decreased. The characteristic impedance was unchanged. The zero intercept of the phase was shifted towards lower frequencies. These results show that the changes in impedance curves in patients with heart failure are due to greater peripheral resistance and wave reflection. During nitroprusside infusion the stroke volume increased and the aortic blood flow became more pulsatile (greater values of low frequency components). This modification accounts for the increased values of Wm and Wp, and is related to decreased peripheral resistance and wave reflection.

[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]. / Effets hémodynamiques et coronaires de la molsidomine chez des insuffisants coronaires stables à l'état basal, lors d'une épreuve de stimulation auriculaire et lors d'un test au froid.

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)

Forward and backward waves in the arterial system, their relationship to pressure waves form.

The purpose of this work was to analyze, in human subjects, the shape of the aortic pressure wave from its forward and backward components calculated by use of Westerhof's model. Twenty-nine patients were studied: 11 normal subjects, 11 hypertensive patients and 7 patients with congestive heart failure. The following measurements and calculations were performed both under control conditions and during either angiotensin infusion in 5 normal subjects or nitroprusside infusion in 6 hypertensive patients: cardiac output, aortic blood pressure (catheter tip micromanometer), blood flow velocity (electromagnetic catheter-tip velocity transducer) in the ascending aorta, aortic impedance and reflection coefficients allowing the calculation of the aortic forward and backward pressure waves. The results show that the shape of aortic pressure wave in hypertensive patients is related to increased arterial wall stiffness which determines greater values and overlap of the forward and backward waves. This result is corroborated by the changes observed during angiotensin infusion in normal subjects. The shape of pressure wave in heart failure patients is dicrotic. This shape is related to smaller values and overlap of forward and backward waves. This appears related to a reduced stroke volume. During peripheral vasodilation the shape of pressure wave in hypertensive patients becomes dicrotic. However, this was mainly related to later backward waves. These results confirm that the shape of pressure waves depends both on the arterial wall stiffness and on the left ventricular performance: mainly on the stroke volume. The calculation of forward and backward waves allows a quantitative analysis of pressure waves.

[Thrombosis of a valve prosthesis: fatal cerebral embolism during thrombolytic treatment]. / Thrombose de prothèse valvulaire: embolie cérébrale mortelle lors du traitement thrombolytique.

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.

[Changes in passive left ventricular pressure-volume relations in acute volume expansion]. / Modifications de la relation pression-volume passive ventriculaire gauche lors d'une expansion volumique aiguë.

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.

Aortic input impedance in normal man and arterial hypertension: its modification during changes in aortic pressure.

The purpose of this work was to study the factors determining aortic input impedance in hypertensive patients. Aortic input impedance (simultaneous measurements of aortic pressure and blood flow), mean (Wm) and pulsatile (Wp) powers and the Wp/Wm ratio were compared in normal subjects (n = 13) and hypertensive patients (n = 12) under basal conditions and during blood pressure manipulation--angiotensin infusion in five normal patients and nitroprusside infusion in six hypertensive patients. Pulse wave velocity (Möens-Korteweg equation; simultaneous measurement of aortic pressure and radius) was determined under basal conditions in normal subjects and in 11 hypertensive patients. The results show that: 1) the changes in impedance curves in hypertensive patients are related to increased peripheral resistance, pulse wave velocity, wave reflection and aortic radius; 2) in most hypertensive patients impedance curves are normalised when blood pressure is reduced, whereas the Wp/Wm ratio remains higher. This latter result demonstrates that pulsatile energy losses are greater in hypertensive patients and suggests either that the aortic wall remains stiffer, despite the reduction in aortic pressure, or that the flow wave becomes more pulsatile since impedance curves of hypertensive patients seen after lowering blood pressure are similar to those of normal subjects.