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Biomedical subjects

R Gourgon

Publications and source records attributed to R Gourgon.

At least 109 records · Page 6Linked to original sources
PubMed1986

[Hemodynamic evaluation of the Carpentier-Edwards porcine bioprosthesis and the Hancock pericardial bioprosthesis in aortic position].

Forty-four asymptomatic patients were catheterised at Boucicaut Hospital 9.5 months after aortic valve replacement to assess the haemodynamic performances of 21 Hancock pericardial (HP) and 23 porcine Carpentier-Edwards (CE) (standard model) bioprostheses, implanted in the aortic position. Left heart catheterisation was performed from a femoral approach; the simultaneous gradient was measured by planimetry and the functional valve surface area calculated at rest and after exercise. The resting calculated surface area of the HP was greater than that of the CE bioprostheses (equation: see text). The transvalvular pressure gradient was lower in the HP than in the CE group (7.8 +/- 4 vs 15.3 cf243 6 mmHg; p less than 0.005). After exercise (15 patients) the calculated surface area increased with the increased transvalvular blood flow in both groups but at each flow rate the calculated valve surface area was greater in the HP group. The haemodynamic performance of the CE bioprosthesis is inferior to that of the HP bioprosthesis, especially in the smaller models. However, the CE bioprosthesis would seem to be mechanically more reliable in the long term than the HP bioprosthesis has since been withdrawn from the market.

Adult↗
PubMed1985

[Coronary and renal circulation in patients with cardiac failure after converting enzyme inhibitors].

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.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1985

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)

Adult↗
PubMed1985

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)

Adult↗
PubMed1985

Assessment and follow-up of patients with aortic regurgitation by an updated Doppler echocardiographic measurement of the regurgitant fraction in the aortic arch.

The purpose of this study was to determine the value and limitations of an updated Doppler echocardiographic measurement of the aortic regurgitant fraction derived from the comparison of forward and reverse flows in the aortic arch. The method was based on the improvements in sampling and displaying Doppler frequencies and blood velocities provided by pulsed-emission, two-dimensional location, and spectral analysis and on an account for variations of aortic diameter through an M mode record of the aortic arch. Relevant statistical comparisons were performed between simultaneous noninvasive and invasive determinations of the regurgitant fraction in a group of 30 patients with aortic regurgitation (group I) and between simultaneous noninvasive and invasive measurements of variations of the regurgitant fraction induced by atrial pacing or vasodilator administration in 12 patients of this group. The two basal determinations were closely correlated (r = .90). The invasive regurgitant fraction ranged from 0% to 80%. The standard error of the Doppler estimate was 8.8% in group I as a whole and was only 6% in a subgroup of 20 patients with a high systolic aortic flow pattern, defined as both peak velocity above 0.8 m/sec and duration of systolic flow above 0.24 sec. This pattern was present in almost all (19/22) patients in whom the aortic regurgitation was more than moderate by invasive criterion (regurgitant fraction above 40%). The standard error of the Doppler estimate of variations of the regurgitant fraction was only 6.6%. Among 100 additional patients with aortic regurgitation (group II), only 12 had no pandiastolic reverse flow in the arch, and their regurgitation was always mild at aortographic examination.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

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.

Adult↗
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↗
PubMed1984

[Mitral insufficiency in an adult, due to an abnormal left coronary artery arising from the pulmonary trunk: echocardiographic aspects. Apropos of a case].

The case of a 20 year old woman followed up since adolescence for a progressive congestive cardiomyopathy with mitral regurgitation is reported. She was reinvestigated after hospital admission for cardiac decompensation and supraventricular arrhythmias; 2D echocardiography showed signs of severe mitral regurgitation with thickened mitral leaflets prolapsing into a dilated left atrium and, above all, abnormal diastolic wall motion related to restriction of left ventricular filling with no apparent systolic dysfunction : pulsed Doppler studies confirmed the diagnosis of mitral regurgitation but also showed retrograde diastolic flow in the aortic arch (without aortic regurgitation) and in the main pulmonary artery. Angiography showed these disturbances to be due to an abnormal origin of the left coronary artery in the main pulmonary artery. Reimplantation of the left coronary in the aorta and mitral annuloplasty were justified by the poor spontaneous prognosis of this congenital abnormality which has rarely been described in adults.

Adult↗
PubMed1983

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.

Adult↗
PubMed1983

Myocardial map derived from two-dimensional echocardiography: reproducible and standardized description of infarction topographies.

The aim of this study was to improve the reproducibility and the standardization of the topographical assessment of myocardial infarctions in routine two-dimensional echocardiography. A myocardial map of the left ventricle was derived from a necropsy study of normal human hearts; interventricular grooves and papillary muscles were used as anatomical landmarks defining 16 segments with similar planimetered surfaces. A reporting sheet was prepared, with diagrams of standardized echo sections and with a map showing the position of the corresponding outlines. The echocardiographic method consisted in identifying on each section the regions without systolic thickening, and displaying the results on the map, until a coherent picture of the abnormal areas was obtained. Interobserver reproducibility was studied in 50 consecutive patients with prior myocardial infarction; segments were classified as fully abnormal, partly abnormal, non-visualized, and normal. Among the 800 segments there were 1% severe and 12% moderate discrepancies; discrepancies were significantly lower for segments with confrontation in two different sections intersecting on the map. A classification of infarction topographies was obtained in 100 consecutive patients; it was compared with the data of two reanalysable pathologic series from the literature; a similar presentation of the results showed similar typical patterns of myocardial involvement, for which a nomenclature was proposed. A myocardial map may be used to provide a simple and reproducible description of infarction topographies; the results obtained lead us to recommend an echocardiographic standardization of ventricular segmentation and of nomenclature of infarction topographies, similar to that of pathological studies.

Echocardiography↗
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↗