[Therapeutics of congestive myocardial failure: their immediate and remote evaluation].
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Adrenergic beta-Antagonists↗
Biomedical subjects
P Besse
Publications and source records attributed to P Besse.
[Metabolic aspects of hemodynamic behavior in left ventricular hypertrophy by 13C NMR].
During myocardial hypertrophy, histological modifications induce a partial ischemic state and hemodynamic perturbations are responsible for an increased myocardial oxygen demand. The purpose of this study is to better characterize the alterations of intermediary metabolism linked to hemodynamic perturbations by carbon 13 NMR using enriched substrates. Left ventricular hypertrophy was consecutive to a renal hypertension (Goldblatt 2K-1C, 9 weeks). Myocardial compliance and contractility (left ventricular end diastolic pressure (LVEDP), +dP/dt max, +dP/dt max normalized to developed pressure (+dP/dt max/DEVP)) were estimated on Langendorff isolated perfused hearts at a constant perfusion pressure (normo and hypertensive rats (RHR)). Using (2-13C) acetate enriched (10 nm) substrate, 13C NMR spectra were obtained from tissue perchloric extracts. Mathematical model proposed by Malloy was used to analyze these 13C NMR spectra terms of metabolic fluxes: Fc2 = The fraction of (2-13C) acetyl-CoA entering the tricarboxylic acid cycle; y = The ratio between the activity of anaplerotic reactions to that of citrate synthetase. The results showed after hypoxia: an increase of LVEDP more pronounced in RHR (RHR: 48 +/- 15 mmHg VS SHAM: 22 +/- 6 mmHg, p < 0.01); a significant impairment of coronary blood flow more important in RHR; a significant increase of the ratio y in hypertrophied hearts (RHR: 0.062 +/- 0.09 VS SHAM: 0.15 +/- 0.02, p < 0.05). In conclusion, this study allowed a new approach to correlate diastolic dysfunction with metabolic data consecutive to an increased sensitiveness hypertrophy to hypoxic damages.
Animals↗
Origin and evaluation of depressed inotropism in hypertensive cardiomyopathy.
Left ventricular pressure overload results in the development of left ventricular hypertrophy (LVH) which is considered an adaptive mechanism of the heart to normalize systolic wall-stress. Impairment of both contractility and relaxation occurs, implying that the hypertrophied myocardium is very sensitive to ischaemia, alterations in coronary haemodynamics and to mechanisms incompletely understood. Experimental data from papillary muscles and isolated coronary perfused hearts (renovascular hypertensive rats) demonstrated respectively: a decrease in velocity of shortening, an increase in isometric timing parameters, and an increase in developed pressure. In contrast, the first derivative of left ventricular pressure, normalized to developed pressure, was decreased for large balloon volumes, suggesting an impairment of systolic function at major loading in LVH. In humans, left ventricular systolic dysfunction occurs later (congestive heart failure) when ejection fraction is impaired. Increases in total minimal vascular coronary resistances observed both in humans and in animals could be related to structural and functional alterations in coronary microvessels. Studies of LVH regression under treatment with angiotensin-converting enzyme inhibitors, calcium-channel blockers and beta-receptor blockers have confirmed that only drugs that block the renin-angiotensin system or the sympathetic nervous system are effective in maximizing the reversal of LVH.
Animals↗
Platelet activation in thrombotic disorders.
Recent advances have resulted in the elucidation of the principal molecular pathways of platelet function. Parallel studies have led to the identification of glycoprotein antigens whose presence at the platelet surface indicates an activated state. Such markers include GMP-140 and other glycoproteins of intracellular membranes whose translocation requires secretion and fusion of granule membranes with those joined to the surface. Other markers include activation-dependent epitopes on the GP IIb-IIIa complex and adhesive proteins bound to the activated GP IIb-IIIa receptor. Such epitopes can be detected by specific monoclonal antibodies. Quantification of their binding by flow cytometry allows an estimation of epitope expression within the whole platelet population. Our studies are designed to answer the question of whether measuring these epitopes is useful for predicting thrombosis in patients with acute cardiovascular disease. For this, we have examined three states where platelet function may be modified and where the risk of thrombosis and/or bleeding is increased. These include (i) patients with severe burns, (ii) patients who have undergone coronary angioplasty, and (iii) patients receiving fibrinolytic therapy following myocardial infarction. Our results show that activated platelets can be detected in the circulation and that their level reflects the degree of the lesion. Nonetheless, we have as yet failed to show a direct correlation between their presence and a future pathological event.
Amino Acid Sequence↗
Thrombotic thrombocytopenic purpura associated with ticlopidine.
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Aged↗
[Evaluation of trials on regression of atheromatous lesions with hypolipemic drugs].
Experimental studies have demonstrated regression of atheromatous lesions with diet and lipid lowering drugs. In order to confirm these results clinically, reliable angiographic methods of analysis must be developed along two lines: quantitative by consensus between independent "blinded" experts, qualitative by digitalizing radiological images. Given the reproducibility of these methods, a variation of 17 to 20% in the size of the atheromatous plaques should be required to affirm a change. Five studies have been performed in patients with atherosclerosis associated with variable degrees of hyperlipidaemia and compared with a control group. NHLBI type II: 59 out of 146 patients with type II hyperlipoproteinaemia were treated with cholestyramine for 5 years with reduction of the progression of > 50% stenosis but no evidence of regression (6%). CLAS: 80 out of 160 coronary patients were treated with cholestipol and nicotinic acid for 2 years and a reduction of progression and a regression of lesions were observed in 16% of cases. Nikkila: 28 coronary patients with hyperlipidaemia were given clofibrate or nicotinic acid for a 7 year period, stabilising the evolution but with no signs of regression. FATS: 74 of 120 coronary patients with apolipoprotein B concentrations of over 1.25 g/l were given lovastatine-cholestipol or nicotinic acid-cholestipol for 2.5 years: regression of coronary lesions was observed in 32 to 39% of cases depending on the treatment administered. Olsson: reported the same results for femoral atheroma with treatments associating fenofibrate and nicotinic acid: 20% regression and reduction of progression.(ABSTRACT TRUNCATED AT 250 WORDS)
Arteriosclerosis↗
Mechanical cardiac valve thrombosis. Is fibrinolysis justified?
BACKGROUND: Thrombosis is a serious complication of heart valve replacement, and management is often difficult. In recent years, thrombolytic therapy has been used as the primary technique by some investigators. METHODS AND RESULTS: Sixty-four consecutive patients presenting with 75 instances of prosthetic heart valve thrombosis (41 mitral, 33 aortic, one tricuspid) were treated with fibrinolytic agents. Obstructed prosthetic valves comprised 39 tilting disc and 36 bileaflet valves. The time interval between valve replacement and obstruction ranged from 15 days to 192 months (mean, 38 months). Fibrinolytic agents used were streptokinase (42 patients), urokinase (27 patients), or recombinant tissue-type plasminogen activator (six patients). Immediate results of fibrinolytic treatment were 1) full success after one or several consecutive fibrinolytic regimens in 55 cases (73%), 2) incomplete improvement in two cases, and 3) failure in 18 cases, leading to an emergency surgery in nine cases. Nine patients died (four strokes, four cardiac arrests, one hemorrhage). Only one severe hemorrhagic complication was observed, but 11 cases of embolism occurred during fibrinolytic treatment (14.6%) (four major cerebral embolisms with death). The immediate efficacy was better for thrombosed aortic prosthesis than with the mitral prosthesis (85% versus 63%). CONCLUSIONS: Fibrinolytic treatment appears to be an attractive nonsurgical alternative for prosthetic heart valve thrombosis, but because of the risk of cerebral embolism, its use should be reserved for tricuspid valve thrombosis or critically ill patients with mitral or aortic valve thrombosis. The use of a fibrinolytic agent in cases of small, nonobstructive paravalvular thrombosis demonstrated with transesophageal echocardiography needs further studies.
Aortic Valve↗
Digital-imaging microscopy analysis of calcium release from sarcoplasmic reticulum in single rat cardiac myocytes.
Digital imaging microscopy of fura-2 fluorescence has allowed us to assess the dynamic patterns of local Ca increase in newly isolated rat myocardial cells. Of the myocytes bathed in a saline solution (1.8 mM Ca2+, 37 degrees C, pH 7.4), 10%-20% exhibited local spontaneous contractions. The resting intracellular free calcium concentration ([Ca2+]i) of these cells was 106 +/- 4 nM versus 77 +/- 3 nM for non-contracting cells. The spontaneous contractile activity appeared to be closely related to internal spontaneous Ca waves that spread across the myoplasm (velocity approximately 50 microns/s, maximal Ca amplitude = 195 +/- 11 nM) along the major axis of the cells. Precise topographical examination of Ca wave propagation indicated a refractory period for internal Ca release. The occurrence of both the generation and propagation of spontaneous Ca increases appeared to be closely dependent on the extent of Ca loading of the cells. Most of our observations were in accordance with the assumption that local Ca overload of the sarcoplasmic reticulum (SR) is the main parameter involved in the spontaneous Ca-release phenomena. Using the same approach, the increase in internal Ca evoked by KCl (50 mM) addition was investigated, and compared with that seen during spontaneous activity. Total [Ca2+]i increase induced by K+ depolarization involved three consecutive local Ca-release patterns: (a) a peripheral Ca enhancement that remained during the total [Ca2+]i increase, (b) subsequent transversal local Ca increases occurring in Z-line regions, (c) longitudinal local Ca increases. In addition, a weak heterogeneous Ca distribution was detected in both peripheral and central parts of resting cardiac cells. Thus, the total Ca increase seemed to result consecutively from a peripheral Ca pool, from junctional SR and from longitudinal structures (possibly longitudinal SR).
Animals↗
Surgery of post-infarction ventricular septal defect: risk factors for hospital death and long-term results.
From December 1971 to December 1989, 62 patients (pts) 42 males, 20 females, mean age 66 years (yr) 6 months (mth) (range 52-80) were operated upon for post-infarction ventricular septal defect (VSD), (anterior 34, inferior 28). Eight pts (13%), group (G) 1 presented with cardiogenic shock, 19 pts (30.5%), G2 with severe congestive heart failure (CHF); 31 pts (50%), G3 were stable with mild CHF and 4 pts (6.5%), G4 without CHF. Preoperative intra-aortic balloon pumping (IABP) was used in 49 pts (79%). One transplanted pt was excluded from this study. The VSD was closed from 1 day (d) to 5 mth (mean 13 d) after its occurrence. Hospital death (HD) occurred in 23 pts (37.7% +/- 6%). Of 44 incremental risk factors (RF) for HD studied, the preoperative status (PS) was the most significant (P less than 0.01). G1: 87% +/- 12%, G2: 42% +/- 12%, G3: 25.8% +/- 8%, G4: 0%. [table: see text] Non-survivors had a shorter mean delay between VSD occurrence and surgery than survivors: 5.6 +/- 3.7 d vs 18.2 +/- 30 d (P less than 0.05), but this delay was correlated to PS. The follow-up of the 38 early survivors ranges from 2 mth to 14 yr (mean 3 yr, 11 mth); 11 pts died between 45 d and 14 yr. No RF was identified for premature late death. HD included, the actuarial survival rate at 1, 5, 10 yr is: 57% (+/- 7%), 44% (+/- 8%), 30% (+/- 10%), respectively.
Aged↗
Effects of perindopril on left ventricular hypertrophy, coronary blood flow, and mechanical properties of cardiac muscle in renovascular hypertensive rats.
We studied the effects of perindopril on left ventricular hypertrophy, systemic and coronary hemodynamics, and mechanical cardiac performance in renovascular hypertensive rats (Goldblatt, two-kidneys, one-clip). Systemic and coronary hemodynamics, before and after carbochrome infusion, were assessed by radioactive microspheres injection via an atrial catheter in conscious rats. Mechanical performance was measured on isolated papillary muscle from the same animal. Twelve treated hypertensive rats were compared with 10 nontreated hypertensive rats and nine sham-operated normotensive rats of the same age. Perindopril treatment induced a complete control of blood pressure (mean blood pressure from 156 +/- 22 mm Hg in the untreated group to 100 +/- 24 mm Hg in the treated group (P less than .01), compared to 106 +/- 18 mm Hg in the sham group). This was associated with a nearly complete regression of left ventricular hypertrophy (left ventricular mass/body weight 2.26 +/- 0.38 mg/g in the treated group v 3.1 +/- 0.6 in the untreated group [P less than .01], compared to 2 +/- 0.25 mg/g in the sham group [p = NS]). Minimal left ventricular coronary resistances after carbochrome were slightly higher in the hypertensive group compared both to sham and treated group. A reversal of impaired myocardial mechanical parameters towards control values was observed, except for some parameters of relaxation. We conclude that perindopril allows in this model a complete control of blood pressure, and a regression of left ventricular hypertrophy with normalization of coronary hemodynamics and contractile function.
Angiotensin-Converting Enzyme Inhibitors↗
Nicardipine and cardiac hypertrophy: effects on left ventricular mass. Haemodynamics and mechanical performance in renovascular hypertensive rats.
SUBJECT OBJECTIVE: The aim was to determine the effects of nicardipine treatment (10-15 mg.kg-1.d-1 intraperitoneal) on left ventricular hypertrophy, coronary haemodynamics, and mechanical performance in renovascular hypertensive rats. DESIGN: Systemic and coronary haemodynamic variables were evaluated by using microspheres in conscious rats, while mechanical performance and elasticity were measured on isolated papillary muscles from the same animals. EXPERIMENTAL ANIMALS: Male Sprague-Dawley rats, weight 150-180 g, were used. Nine treated rats were compared with control groups, consisting of 9 sham operated, 12 untreated hypertensive, and 9 nephrectomised rats. MEASUREMENTS AND MAIN RESULTS: Eight weeks after clipping, removal of the ischaemic kidney allowed the normalisation of ventricular mass and the reversal of changes induced by hypertrophy except prolongation of timing parameters. Nicardipine administration led to an efficient but incomplete control of blood pressure, which fell from 208(SEM 5) mm Hg in untreated hypertensive rats to 155(4) mm Hg in treated rats, p less than 0.01. After eight weeks of treatment, the reduction in left ventricular mass, from 3.10(0.10) mg.g-1 in untreated rats to 2.72(0.018) mg.g-1 in treated rats was significant (p less than 0.01) but was less than the pressure decrease. In treated hypertensive rats, coronary blood flow was increased and redistributed at rest in favour of the subepicardial layers but was significantly reduced after maximum vasodilatation, to 1.618(0.077) litre.min-1.100 g, in nicardipine treated rats. A reversal of impaired myocardial mechanical indices towards control values was observed except for time to peak force and time to half relaxation. CONCLUSIONS: Nicardipine treatment allowed blood pressure control, reduction of left ventricular mass, and improvement in mechanical performance, but was unable to restore minimal coronary vascular resistance. The results suggest that, although blood pressure decrease is obviously important, it may not be the sole factor in the reversal of cardiac hypertrophy.
Animals↗
A case of the Budd Chiari syndrome attributed to a deficit in protein C.
We report a case of Budd Chiari syndrome associated with a deficit in protein C, in a young women admitted to hospital for investigation of thromboembolic disease and ascites. This coagulation defect was thought to be an aetiological factor in the suprahepatic vein thrombosis. The diagnosis and treatment of this rare form of the syndrome are discussed.
Budd-Chiari Syndrome↗
[Mass and geometry of the left ventricle. Methods of angiographic determination].
Hypertrophy is a myocardial adaptation to pathological conditions of overload and leads to a reduction of cardiac afterload. Angiocardiography (the so-called reference method) allows calculation of mass and volume after opacification of the left ventricle in two orthogonal planes, based on different mathematical models: the area-length method: the left ventricle is assumed to be ellipsoid. The short axis diameter and the volume are calculated from measurements of the area of the left ventricle in the long axis; Simpson's method: the ventricle is divided into sections along its long axis. The diameters of the sections are measured in each incidence. Left ventricular volume is calculated from the area of each section and the distance between two sections; myocardial mass: calculation of the myocardial mass requires measurement of the volumes of the left ventricle with the diameters increased by twice the wall thickness. The accuracy of these measurements depends on several factors: geometrical: true parallelism between the long axis of the ventricle and the planes of projection; influence of the contrast medium in the volume and contraction; this is negligible in the first three systoles; detection of the ventricular contours: this may be manual or automatic and requiring techniques of image digitalization. Therefore, the calculation of ventricular mass is directly related to volume determination, and hypertrophy can only really be quantified by mass/volume or wall thickness/diameter ratios.
Adolescent↗
[Acute aortic dissecting: contribution of transesophageal echography. Apropos of 10 cases].
The diagnostic value of combined transthoracic (TTE) and transesophageal echocardiography (TEE) was evaluated in 10 consecutive patients with acute dissecting aneurysm of the aorta and compared to aortography (10 cases) and computed tomography (7 cases). TEE seems to be highly superior to TTE because the intimal flap in always seen (versus 4 of the 10 TTEs) and the descending aorta and the entry site are better visualized. TEE is superior to X-ray computed tomography because it shows the direction of the flow in the false lumen (an advantage of a color Doppler), the entry site and aortic regurgitation. In spite of false-positives (1/10), TEE seems to be at least as good as aortography, the most reliable, but highly invasive, technique available. Thus, transesophageal echocardiography, performed at the patient's bedside, appears to be a promising non-invasive tool for diagnosing suspected dissecting aneurysms of the aorta.
Acute Disease↗
Clinical characteristics affecting success or failure of PTCA in patients with multiple vessel disease and poor candidates for surgery.
A special form of complex coronary angioplasty is represented by the extension of indications for percutaneous transluminal coronary angioplasty (PTCA) to patients with multivessel disease (MVD) for whom surgery is not indicated, and thus for whom surgical standby is not available. Over a two-year period, 254 consecutive coronary patients with multivessel disease underwent PTCA under such conditions. These patients could not benefit from surgery for various reasons. Of the 612 arteries involved, 155 were occluded, 47 had been previously bypassed. A distal nonbypassable lesion in one of the three major arteries was found in 244 patients, 61 had suffered from a previous infarct, 24 demonstrated an ejection fraction below 0.40, and in 19 a single patent vessel was found. Fifteen patients were in cardiogenic shock and 69 procedures were undertaken for unstable angina. Of this latter group, 25 emergency PTCA were attempted for refractory unstable angina, and 44 additional emergency procedures were directed to the treatment of acute infarct. A total of 40 intra-aortic counterpulsations were needed. As far as possible the procedure aimed at full revascularization. Immediate outcome is strongly affected by the clinical context, and despite a rather constant initial success rate (88-95%), the procedural mortality (directly related or not) can change dramatically with clinical factors.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
[Enoximone, vasodilator and/or inotropic agent in congestive cardiac insufficiency? Hemodynamic and ventriculographic study of 20 cases].
The aim of this study was to document the effects of enoximone in congestive cardiac failure. The haemodynamic data (aortic pressure, pulmonary pressures, left ventricular pressure, cardiac output, isovolumic contractility index: Vmax) and left ventricular kinetics of 20 patients with dilated cardiomyopathy (11 ischemic and 9 idiopathic in Stages III or IV of the NYHA Classification before recompensation) were recorded under basal conditions, after 30 minutes infusion of dobutamine (10 micrograms/kg/mn) and after 3 hours infusion of enoximone (total dose: 3.6 mg/kg). The two drugs had an equivalent inotropic effect: ejection fraction + 4 +/- 22% with dobutamine and + 16 +/- 39% with enoximone; Vmax increased from 1.53 +/- 0.5 c/sec to 2.49 +/- 0.8 c/sec with dobutamine and to 1.82 +/- 0.5 c/sec with enoximone. Enoximone induced a greater degree of vasodilation (systemic resistances - 14 +/- 21% with dobutamine and - 21 +/- 27% with enoximone) and a more pronounced fall in ventricular filling pressures (- 35 +/- 42% with dobutamine and - 58 +/- 24% with enoximone). Enoximone was less effective than dobutamine in increasing cardiac output (+ 46 +/- 42% with dobutamine and 16 +/- 33% with enoximone) and stroke volume (+ 23 +/- 47% with dobutamine and + 2 +/- 41% with enoximone). This difference in efficacy may be explained by the major reduction in ventricular preload which enoximone induced after that observed with dobutamine. "Responders" (12 patients) had basal cardiac outputs of less than 2.3 l/mn/m2; the peripheral vasodilatation caused by enoximone was greater. Finally, the reduction in left ventricular end diastolic pressure and the increase in Vmax were significantly less in the 11 patients with ischemic cardiomyopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Multicenter pilot study of the efficacy and safety of systemic rt-PA administration in the treatment of deep vein thrombosis of the lower extremities and/or pelvis.
Patients with symptoms of deep vein thrombosis for less than 10 days were treated with a standard dose of heparin. In the open label phase of the trial, 11 patients received 100 mg rt-PA on the first day and 50 mg on the subsequent day in an 8 hour infusion. In the double-blind phase, 8 patients were randomized to the same rt-PA regimen, 6 patients to an infusion of 50 mg rt-PA over 8 hours on days 1 and 2, and 7 patients to placebo infusions. The mean change in venographic score in all patients treated with rt-PA plus heparin is -3.8 units compared to -0.6 units in patients treated with heparin alone (p = 0.06). Bleeding complications classified as major were noted in 8/25 patients receiving the combined treatment.
Adolescent↗
[Mortality of dilated myocardiopathies as a function of continuation of alcohol drinking. Multivariate analysis concerning 236 patients].
A retrospective study was conducted in 236 consecutive patients with dilated cardiomyopathy to determine the characteristics of the disease in heavy alcohol drinkers (n = 110) and to study its outcome, using a Cox model, according to whether the patients were abstainers (n = 49) or continued to indulge drinking (n = 61). At the time of diagnosis, pulmonary pressures were higher in heavy drinkers than in abstainers. During a mean follow-up period of 39 +/- 27 months, 80 patients died of heart disease, viz.: 46 out of 127 non-alcoholic patients (36.2 per cent), 31 out of 61 heavy drinkers (50.8 per cent) and 3 out of 49 patients who had given up alcohol (6.12 per cent). Thus, independently of other parameters, abstinence is a highly significant (P less than 0.001) factor of favourable prognosis in dilated cardiomyopathy.
Adult↗