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Biomedical subjects

J Delaye

Publications and source records attributed to J Delaye.

At least 55 records · Page 3Linked to original sources
PubMed1991

U74006F, a novel 21-aminosteroid, inhibits in vivo lipid peroxidation but fails to limit infarct size in a canine model of myocardial ischemia reperfusion.

Peroxidation of membrane lipids has been suggested to play a role in the pathogenesis of myocardial ischemia/reperfusion injury. We therefore assessed the efficacy of U74006F, a potent in vitro vitamin E-like inhibitor of lipid peroxidation, in limiting infarct size in a canine model of transient coronary artery occlusion. Twenty dogs underwent 2 hours of occlusion of the left anterior descending coronary artery and 6 hours of reperfusion. U74006F or saline solution was administered continuously from 1 hour of occlusion to the end of the experiment. U74006F blunted any increase in production of conjugated dienes (an index of lipid peroxidation) at both 30 minutes (1.73 +/- 0.16 mol/L x 10(-4) vs 2.62 +/- 0.22 in control dogs, p less than 0.05) and 6 hours (1.39 +/- 0.22 vs 2.06 +/- 0.18 in control dogs, p less than 0.05) after reperfusion. Furthermore, 6 hours after reflow vitamin E levels tended to be lower than baseline values in control dogs and higher than baseline values in dogs treated with U74006F. However, analysis of infarct size indicated no statistically significant difference between the two groups when expressed either as a percentage of the left ventricle (10.4 +/- 1.8% in U74006F vs 15.2 +/- 2.4% in control dogs) or as a percentage of the area at risk (33.0 +/- 5.5% in U74006F vs 37.8 +/- 4.5% in control dogs). Although U74006F appeared to be a potent in vivo inhibitor of lipid peroxidation, it failed to limit infarct size after 2 hours of occlusion and 6 hours of reperfusion in this canine model.

Animals↗
PubMed1991

Influence of associated valvular lesions on long-term prognosis of mitral stenosis. A 20-year follow-up of 202 patients.

Other valvular lesions associated with pure MS were studied in 202 consecutive patients whose mean age was 43.4 +/- 12.7 years; 76.7% were females. MS was isolated in 63.4%, associated with aortic regurgitation (AR) in 27.7%, aortic stenosis in 1.0%, tricuspid stenosis (+aortic valve lesion) in 1.0%. In isolated MS, 42.4% were NYHA class III or IV, compared with 49.0% in MS + aortic valve lesion. One hundred and sixty-nine (85.4%) patients were operated on; 23.1% had mitral valve replacement, 76.9% had closed (31.4%) or open (45.6%) mitral commissurotomy; 7.1% had associated aortic valve replacement. There were perioperative complications in 20.4%, and the perioperative death rate was 4.1%. Two patients were reoperated in the postoperative course, and 28 patients after this period. The follow-up was 13.3 +/- 4.5 years. The survival rate was 77.7 +/- 4.6% (SE) for isolated MS, and 71.1 +/- 6.3% for MS associated with an aortic valve lesion (NS). The prognosis of MS is very good: the survival rate at 20 years follow-up is 75%. The association of aortic stenosis or tricuspid stenosis does not appear to alter this survival, but numbers are small. Important aortic regurgitation is a significant predictor of higher mortality in patients with MS.

Adolescent↗
PubMed1991

Quantitation of reperfused myocardial infarction by Gd-DOTA-enhanced magnetic resonance imaging. An experimental study.

Because there is evidence that myocardial infarct size is modified by coronary artery reperfusion, an ex vivo experimental model of myocardial infarction was developed to determine the influence of the timing of gadolinium-tetraazacyclododecane tetraacetic acid (Gd-DOTA)-enhanced magnetic resonance imaging (MRI) on the accuracy of infarct size quantitation. Eighteen dogs underwent a 2-hour coronary occlusion followed by 1 (n = 6), 6 (n = 6), or 48 (n = 6) hours of reperfusion. Gd-DOTA was injected 10 minutes before the dogs were killed. T1 (SE 250/26) and T2 (SE 1500/78) weighted images were performed on excised hearts. Gd-DOTA concentration was measured in myocardium by atomic emission spectrometry, and correlated with myocardial blood flow evaluated by radioactive microspheres. All dogs presented with myocardial infarction (mean size 20.4% +/- 3.1% of the left ventricle), and a corresponding area of increased signal intensity on T1-weighted MR images. In none of the three groups did the area of high signal intensity correlate with the ischemic area. By contrast, after 6 and 48 hours of reperfusion, the high signal intensity area (17.9% +/- 2.4%) closely matched the area of nonreversible jeopardized tissue (16.4% +/- 2.5%), as determined on tetrazolium-stained heart slices. Although a noreflow phenomenon was observed in the jeopardized tissue, Gd-DOTA concentration was higher in the subendocardial central ischemic zone than in normally perfused myocardium. Gd-DOTA imaging enhancement seems to be the consequence of a delayed clearance of the agent from the injured tissue. Gd-DOTA-enhanced MRI accurately quantitates the size of reperfused myocardial infarction on the ex vivo heart for more than 6 hours after the beginning of reperfusion. It remains to be determined whether the in vitro results obtained here can be applied to assess the myocardial infarct size in vivo.

Animals↗
PubMed1991

[Mitral valve replacement in severe pulmonary hypertension. Long-term results].

Between 1972 and 1987, 43 patients underwent isolated mitral valve replacement with mean pulmonary arterial pressures greater than 50 mmHg. The valve disease was stenosis in 13 cases, regurgitation in 15 cases and mixed mitral valve disease in 15 cases. Forty-one patients (95 %) had invalidating cardiac failure (Stages III and IV of the NYHA Classification). The hospital mortality was 2.3%. Thirteen patients died during follow-up, 8 of cardiac failure, 3 of sudden death and 2 died of non-cardiac causes. The 8 year actuarial survival was 82 +/- 7% with an average postoperative follow-up of 96 +/- 41 months. No patients were lost to follow-up. Eighty six per cent of survivors (25/29) are asymptomatic or paucisymptomatic. Doppler studies were performed in 22 patients, showing normal prosthetic function in 18 cases and an obstructive prosthesis in 4 cases. Seventeen patients had tricuspid regurgitation showing normal pulmonary artery systolic pressures in 9 cases and less than 55 mmHg in 5 cases. On average, systolic pulmonary artery pressure fell from 88 +/- 11 mmHg before to 33 +/- 9 mmHg after surgery (p = 0.01). These results show that severe pulmonary hypertension is not prohibitive for mitral valve replacement. The long-term results are good with functional improvement and reduction of pulmonary hypertension.

Actuarial Analysis↗
PubMed1991

[Late results of isolated aortic valve replacement by Björk-Shiley prosthesis. Apropos of 596 cases].

Between 1970 and 1985, 596 patients underwent isolated aortic valve replacement with a Björk-Shiley prosthesis: 448 men and 148 women, average age 52 +/- 13 years (range 10-78 years). The valve lesion was aortic stenosis in 158 cases, aortic regurgitation in 218 cases and mixed valve disease in 220 cases. Fifty-four per cent of patients had invalidating cardiac failure (Stage III of the NYHA Classification). Thirteen per cent of patients had an associated non valvular surgical procedure. The hospital mortality was 5.7% and 77% of the early deaths were of cardiac origin. Results were analysed after an average follow-up period of 90 +/- 15 months, a total of 3817 patient-years. The late mortality was 94 (16.7%). Actuarial survival was 87 +/- 1% at 5 years and 79 +/- 2% at 10 years. A prognostic score was established from a multifactorial analysis: Cox = 0.44 (NYHA Stage 1, 2, 3, 4) + 5.29 C/T (absolute value) + 1.15 associated procedure (0.1) + 0.65 (RBBB) (0.1). In the long-term, 84.8% of survivors were asymptomatic (NYHA Stages I and II). The incidence of thrombo-embolism was 0.5/100 patient-years. At 10 years, 95% of patients had no thromboembolic complication. The incidence of ineffective endocarditis was 0.3/100 patient-years and that of complications of anticoagulant therapy was 0.4/100 patient-years. The incidence of valve dehiscence was 0.1/100 patient-years and the reoperation rate was 0.4/100 patient-years but there were no cases of valve dysfunction. The global complication rate in this series was 1.35/100 patient-years. These results confirm the good results of aortic valve replacement with a mechanical prosthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1991

[Long-term results and prognostic factors after mitral valve replacement using the Starr-Edwards 6120 prosthesis].

Between 1970 and 1984, 386 mitral valve replacements with the SE 6120 prosthesis were performed with a mean post-operative follow-up of 75 +/- 44 months or a total follow-up of 2520 patient years (PY). Rapid post-operative mortality was 6.7 percent and the delayed mortality 26.5 percent, the 5-year actuarial survival rate was 80 +/- 2% and that at 10 years 67 +/- 2% (including early mortality). There was no significant difference for survival between single-valve replacements (n = 183) and multiple-valve replacements (n = 203). Multifactorial prognosis analysis (Cox) gave two post-operative prognosis: X (n = 386) = 0.0391 (age) + 0.2421 (NYHA stage); Y (n = 147) = 0.8561 (X) + 0.6299 (VG type). The incidence of complications related to the prosthesis is 4.16 per 100 PY, including sudden deaths. The current actuarial analysis shows that at 5 years 91 +/- 1% at 10 years 78 +/- 2% of the operated subjects are devoid of any such complication and of thrombosis of the valve. Statistically, it was found that permanent atrial fibrillation (p = 0.03), the size of the right atrium (p = 0.02) played a promoting role. With a post-operative follow-up in excess of 8 years. 79% of the survivors are symptom-free or present few symptoms and the myocardial response is poor in 52 patients (NYHA stage III or IV).

Adult↗
PubMed1990

Inhibition of coronary artery thrombosis by SIN-1, a donor of nitric oxide.

Molsidomine and its metabolite, SIN-1, a donor of nitric oxide, are potent coronary vasodilator and anti-ischemic agents. Recently, SIN-1 and nitric oxide have also been shown to inhibit platelet adhesion and aggregation in vitro. The present study in dogs was designed to evaluate the in vivo antithrombotic properties of SIN-1. Coronary intimal damage and stenosis are known to induce coronary cyclic flow variations that reflect platelet thrombus formation followed by disaggregation and embolization (Folts preparation). This model of coronary artery thrombosis appears to simulate the combination of some of the factors contributing to unstable angina and myocardial infarction in human. SIN-1 infusion (10 micrograms/kg/min) significantly reduced the frequency of cyclic flow variations: 4.9 +/- 6.2/h vs. 14 +/- 4.6/h (before treatment, p less than 0.03, n = 6). Results were similar to those obtained with aspirin (5 mg/kg, bolus i.v.: 1.5 +/- 0.6/h vs. 11.7 +/- 3/h, p less than 0.03, n = 5) whereas saline had no effect (17.8 +/- 2.2/h vs. 19.3 +/- 2.4/h, n = 5). As expected, blood pressure was decreased only in the SIN-1 group: 56.2 +/- 7.8 vs. 87.3 +/- 9.3 mm Hg (p less than 0.02) (mean arterial blood pressure). The present results suggest that the well-documented anti-ischemic properties of SIN-1 could be partly due to its antithrombotic activity, clearly demonstrated with the model of coronary thrombosis used here in the dog.

Animals↗
PubMed1990

[An attempt to quantify myocardial ischemia by selective coronary arteriography: determination of a new score. An initial study].

An original model for estimating myocardial ischaemia from coronary arteriography is proposed. Four parameters are taken into consideration: anatomical variations, the myocardial mass perfused, the degree of reduction of basal flow across the stenosis, the eventual summation of several successive stenotic lesions. This scoring system was tested by simulation on a computer and evaluated in 100 anginal patients. Analysis of our preliminary results shows statistically significant differences in the score between the following groups of patients: patients with normal and those with abnormal LV wall motion; patients with and those without previous myocardial infarction; patients with Class II stable angina and those with other forms (III, IV and unstable angina).

Adult↗
PubMed1990

[The natural history of coronary disease. The role of cholesterol].

The natural history of the complications of coronary heart disease has been defined by anatomicopathological and epidemiological studies, particularly the Framingham study. At the same time, research is being carried out on risk factors which play a role in the progressive development of atheromatous plaque (atherogenic factors: hypertension: hypercholesterolaemia) and those factors which lead to complications in the atheromatous plaque (aggravating or precipitating factors: smoking, thrombosis, etc.). This schematic perspective may lead to the redefinition of the strategy to adopt in fighting atherosclerotic arterial disease; a better aim will thus the taken in the fight against hypercholesterolaemia.

Cholesterol↗
PubMed1989

[Angiographic morphology of the coronary arteries after a recent myocardial infarction treated by intravenous thrombolysis].

Thirty patients (26 men, 4 women) aged from 32 to 73 years (mean 54 years) who developed anterior (14 cases) or posterior (16 cases) myocardial infarction received intravenous streptokinase in doses of 1,500,000 units 2 to 10 hours (mean 4 hours) after the onset of infarction. Coronary angiography, performed 18.6 days on average after thrombolysis, showed a distinct predominance of asymmetrical stenosis with irregular walls and a narrow neck (10 cases, 33 p. 100) or of complete occlusion (12 cases, 40 p. 100) in the artery responsible for the infarction. Complete occlusion probably was the ultimate stage of stenosis. In contrast, the various angiographic images observed in arteries unrelated to the infarction were evenly distributed. The radiological morphology of coronary arterial lesions after a recent infarction is suggestive of ruptured atheromatous plaque, sometimes complicated by thrombosis in situ. Identical images are seen in unstable angina. These findings indicate that one single therapeutic approach should be applied to the most severe types of coronary disease due to atherosclerosis.

Adult↗
PubMed1989

[Prognosis of chronic non-dystrophic and surgically treated aortic insufficiency].

Between January 1972 and March 1983, 123 patients with isolated non dystrophic aortic insufficiency underwent aortic valve replacement. During a mean follow-up period of 4.3 years per patient, 25.6 p. 100 of the patients died, including a 4.1 p. 100 hospital death rate. The actuarial survival rate was 74 p. 100 at 5 years and 62 p. 100 at 10 years. The main causes of mortality were heart failure, dysrhythmias and sudden death. A study of prognostic factors based on the preoperative data showed that clinical, radiological, electrocardiographic and haemodynamic signs were informative. In agreement with other authors, we found that preoperative cardiac dilatation and left ventricular dysfunction were predictive of a poor prognosis.

Adult↗
PubMed1988

[The tolerance phenomenon in the therapeutic management of angina pectoris].

Tachyphylaxis in the treatment of angina pectoris may be found in widely different situations, such as stable angina turned unstable owing to local coronary changes, interference with another pathology (intricate angina) or true "escape phenomenon". In clinical practice, angina from tachyphylaxis may be due to a variety of causes, including lack of compliance (often difficult to diagnose), untimely drug administrations, insufficient dosage or habituation. Habituation corresponds to adaptation of the cells to their chemical environment. In the case of angina, it is due to gradual depletion of sulfhydryl radicals in the vascular endothelial cells. This progressive insensitivity to nitrites accounts for some therapeutic failures. Molsidomine is thought to be of great interest in such cases.

Angina Pectoris↗
PubMed1988

Valvular aortic stenosis and coronary atherosclerosis: pathophysiology and clinical consequences.

New methods of investigation (ECG, echocardiography, angiography, histology) allow a better understanding of the pathophysiology of valvular aortic stenosis (VAS) associated with coronary atherosclerosis. The progressive decrease in valvular aortic area modifies the coronary blood flow and leads to myocardial ventricular hypertrophy. These two mechanisms worsen left ventricular function. A significant atherosclerotic stenosis on a large coronary artery creates a considerable reduction of the available coronary blood flow. This reduction is permanent: present at rest, it is obviously increased during exercise. The study of the relationship between the severity of the VAS and the myocardial hypertrophy (MH) is of great interest. It seems that in VAS with coronary artery disease, different situations exist: (i) when the hypertrophy is severe (left ventricular mass greater than 180 g m-2), the angina pectoris is more attributable to the VAS than to the coronary lesions. Thus the removal of the aortic outflow obstruction is the most essential therapy; (ii) when the hypertrophy is less severe (left ventricular mass less than 180 g m-2), surgical treatment of the valvular lesion and myocardial revascularization are justified.

Aortic Valve Stenosis↗
PubMed1988

Acute heart failure due to Q fever endocarditis.

We report a case of Q fever endocarditis in a patient who presented with a slight pyrexia and acute cardiac failure due to aortic incompetence. The diagnosis was made by detecting high titres of serum IgG and IgA antibody against Coxiella burnetii phase I antigens and confirmed by demonstrating C. burnetii on the excised aortic valve using immunofluorescence and electron microscopy. Aortic valve replacement was followed by initially successful antibiotic treatment for 15 months. Reappearance of IgA anti-phase I antibodies 5 months later suggested continued presence of bacteria, although the patient's condition remained satisfactory. In endemic areas, such as rural southern France, Q fever endocarditis should be considered when there is evidence of acute heart valve damage but are few other features of infection.

Acute Disease↗