Search PubMed⌕ Search

Biomedical subjects

J M Lablanche

Publications and source records attributed to J M Lablanche.

At least 181 records · Page 10Linked to original sources
PubMed1983

[Hemodynamic and coronary effects of methylergometrin].

The methylergometrine test (ME) was performed during coronary angiography in 43 patients either by a single injection of 0,4 mg (34 cases) or by fractioned doses every 5 minutes of 0,1 mg, 0,2 mg, 0,3 mg, 0,4 mg (total 1 mg) (9 cases). Opacification of the coronary arteries was performed 1, 3 and 5 minutes after each injection; left ventricular pressures were recorded with a Millar catheter-tip transducer. The heart rate and first derivative of left ventricular pressure did not vary significantly after the 0,4 mg single dose ME. Left ventricular end systolic pressure rose by 11 p. 100 (p less than 0,001) and left ventricular end diastolic pressure from 18,3 to 23,1 mmHg (p less than 0,001). Myocardial oxygen consumption assessed by the TTI rose from 2873 +/- 896 to 3083 +/- 788 mmHg.s-1 .min (p less than 0,01), but myocardial contractility as assessed by the V max fell from 1,68 +/- 0,40 to 1,58 +/- 0,35 s-1 (p less than 0,001). The reduction in the calibre of the coronary lumen was identical after the single 0,4 mg dose and the 1 mg fractioned doses. In the later case, 50 p. 100 of the maximal response was observed after the first injection of 0,1 mg. After the single dose of 0,4 g ME the reduction in coronary lumen was very rapid over the first 3 minutes. Prolonged observation up to the 10th minute (7 patients) showed slight aggravation of the vasoconstriction between the 5th and 10th minutes, justifying an injection of a nitrate derivative before discontinuing surveillance. The vasoconstriction induced by ME seems to be within the physiological limits of vasoconstriction. The maximal overall decrease of the coronary diameter was 12,3 +/- 7,8 p. 100 and never exceeded 20 p. 100. There was a significant difference in the response of atheromatous patients in whom the vasoconstriction was greater in the presence of resting angina than in the absence of resting angina (16,4 +/- 8,7 p. 100 compared to 9,7 +/- 6,4 p. 100, p less than 0,01).

Angina Pectoris↗
PubMed1983

[Right ventricular dysplasia: Uhl's disease. Echocardiography and tomodensitometry study. Apropos of a case in an adult].

The author discusses Uhl's disease in a 60 year old patient as indicated by right ventricular insuficiency without troubles of the ventricular rhythm. Echocardiography revealed the distinctive symptoms of this illness (dilation of the right cavities, diastolic opening of the pulmonary valve, delayed closing of the tricuspid valve) emphasizing its diagnostic value. The contribution of tomodensitometry is considered.

Echocardiography↗
PubMed1983

Contribution of dynamic vascular wall thickening to luminal narrowing during coronary arterial vasomotion.

The hypothesis has been developed that increased coronary artery vasomotor tone superimposed on a preexisting obstruction is a possible mechanism responsible for resting and exertional angina. In 18 patients (22 stenotic lesions), the maximal changes in coronary artery diameter (mm) induced by an ergometrine test followed by an injection of isosorbide dinitrate were assessed by a quantitative computer-based angiographic system. If we assume that there is no change in the length of the artery as the result of changes in its diameter, then at any point of the artery the area of the arterial wall on a transverse cross section of the vessel will be constant regardless of its state of its contraction or dilatation. As vasoconstriction occurs, the luminal diameter decreases proportionally more than the outer diameter of the vessel and the wall thickness increases. Using elementary geometric principles, we calculated and reconstructed the changes that might occur at the stenotic sites as the result of vasomotion acting on the entire coronary segment. From the reference diameter in the control state (Ri:3.7 +/- 1.1 mm) and after vasoconstriction (Ric: 3.3 +/- 1.0 mm) and the obstruction diameter in the control state (ri: 2.2 +/- 0.9 mm), the minimal obstruction diameter after vasoconstriction (ric: 1.0 +/- 0.8 mm) was derived using the following equation: ric2 = ri2 - Ri2 + Ric2. In four of 22 lesions, the decrease in diameter of the lumen of the normal vessel was fully translated to the stenotic point and the decrease in diameter at the stenosis was correctly predicted.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗
PubMed1982

[Coronary artery dilatation induced by isosorbide dinitrate injection (author's transl)].

Twenty-six patients were given 3 mg isosorbide dinitrate either by direct intra-coronary injection (17 patients) or by intravenous injection ( patients), 5 minutes after an injection of 0.4 mg methylergometrine. In all 26 patients isosorbide dinitrate dilated the coronary arteries to a diameter that was 26% greater than the smallest diameter observed with methylergometrine and 14.8% greater than the basal diameter. The response was highly significant at 30 seconds, maximal at 2 minutes and lasted more than 10 minutes. At the dosage level used in this study, there was no significant difference between the two groups of patients. However, a rapid fall in systemic arterial pressure was noted after peripheral intravenous injection.

Coronary Vessels↗
PubMed1982

[Echocardiographic findings in children with chronic renal failure ].

Echocardiographic examinations were carried out in 2 groups of children with chronic renal failure. Group 1 consisted of 9 children who were not treated with hemodialysis. Group 2 consisted of 9 children undergoing chronic hemodialysis. Results in both groups were compared with a control group of 35 normal children. No difference was found between normal children and group 1 children. Group 2 children presented with a moderate myocardial hypertrophy and dilatation of the left atrium. Indices of contractility were also decreased. Comparison before and after hemodialysis showed no change in cardiac function.

Adolescent↗
PubMed1982

[Early detection of myocardial alterations in mitral insufficiency with the angiotensin test].

Left ventricular function was assessed at rest and after increasing systemic arterial resistance by angiotensin in 40 patients with isolated mitral insufficiency. Angiotensin was administered intravenously at a dose of 0,4 micrograms/mn until the systolic blood pressure rose by at least 30 mm Hg. Left ventricular and aortic pressures, cardiac index and left ventriculography in the 30 degree right anterior oblique projection (50 frames per second) were recorded before and during angiotensin infusion. The mean rise in systolic left ventricular pressure was 40 +/- 2,8 mm Hg; the heart rate increased slightly but significantly; left ventricular and diastolic pressure rose from 12,0 +/- 1,0 to 24,0 +/- 1,2 mmHg. The systolic index (Fick's method) was significantly decreased (37 +/- 1,6 ml/m2 to 26 +/- 1,6 ml/m2) though the angiographic systolic index remained unchanged. This is explained by an increase in the regurgitant fraction (51 +/- 2,5% ao 65 +/- 3%). The end diastolic volume index was unchanged; the ejection fraction was significantly decreased. The resting hemodynamic status was only slightly disturbed in 29 patients (mean capillary pressure less than 15 mm Hg, 8,8 +/- 0,52 mmHg). The left ventricular function curves with angiotensin distinguished two groups of patients: Group A (20 patients) with left ventricular dysfunction induced by angiotensin, Group B (9 patients) who maintained the systolic index despite the increase in left ventricular end diastolic pressure. These results suggest that the angiotensin test may be useful for detecting early left ventricular dysfunction in patients with isolated mitral insufficiency and virtually normal resting hemodynamic parameters.

Angiotensin II↗
PubMed1982

[Hemodynamic and coronary effects of isosorbide dinitrate: comparison of intravenous and intracoronary injection].

The hemodynamic and coronary effects of a single dose of 3 mg of isosorbide dinitrate (ISD) were studied in 26 patients after intra-coronary (17 cases) and intravenous injection (9 cases). The study was carried out after opacification of the coronary arteries and a 0,4 mg ergometrine test. The radiological contrast and ergometrine increased left ventricular end diastolic (10,4 +/- 0,89 mm Hg to 22,5 +/- 1,88 mm Hg) and systolic pressures (131,4 +/- 4,8 mm Hg to 158,7 +/- 5,8 mm Hg) without changing V max. After ergometrine, the diameter of the coronary vessels decreased by 8,8%. After ISD, these pressures fell significantly from the 10th second; the lowest pressure after ISD was related to the initial pressure at the end of the ergometrine test (systolic pressure Y = 0,68 X + 6,39, R = 0,89, p less than 0,001) ( end diastolic pressure : Y = 0,36 X + 0,17, R = 0,68 , p less than 0,01). Moderate transient tachycardia was probably a reflex reaction. The increase in V max, maximal after 1 to 2 minutes, seemed to have a different mechanism. The global effect is to decrease myocardial oxygen consumption as reflected by the fall in the tension - time - index (3083 +/- 2,13 to 2330 +/- 184 mm Hg . sec-1 . min . The diameter of the coronary vessels rose by 26% with respect to the smallest diameter observed after ergometrine. The intracoronary and intrafemoral venous injection gave identical hemodynamic and coronary changes from the first minute. The effects were maximal between 2 and 4 minutes and continued after 10 minutes. The only difference was a more rapid decrease in systolic pressure after intrafemoral administration. Dilatation occurred before the hemodynamic effects after intracoronary injection, which is an argument for using intracoronary ISD in the treatment of spasm induced by ergometrine.

Coronary Circulation↗
PubMed1982

[Surgical treatment of Prinzmetal's angina pectoris by plexectomy associated with aortocoronary bypass. Apropos of 56 cases].

The results of coronary bypass surgery are generally not as good in Prinzmetal angina as in classical angina pectoris. The percentage of myocardial infarction, recurrent angina and death is much higher. One reason for these failures could be the persistence of coronary spasm. In order to prevent this, denervation of the pre-supra and retro aortic nerve plexuses was carried out in 56 patients (54 male, 2 female) with Prinzmetal angina and operable coronary arterial lesions. Forty patients had documented coronary spasm mainly of the left anterior descending (20 cases) or the right coronary artery (13 cases). Surgery consisted of cardiac denervation associated with direct myocardial revascularisation by implantation of I (37 cases), 2 (13 cases) or 3 (6 cases) aorto coronary bypass grafts. Two deaths were observed in the perioperative period (one low output syndrome and one severe arrhythmia) and one myocardial infarction in the postoperative period. Of the 54 survivors, 49 are asymptomatic and 2 have recurrent spontaneous angina. Exercise electrocardiography in 44 patients was negative in 40 cases. Continuous electrocardiographic recordings (Holter method) in 33 patients was negative for ischemia and of 25 bypass grafts controlled, 24 were patent. Seventy five methylergometrine provocation tests were performed: only 2 were positive, both in patients with recurrent attacks. Therefore, with respect to the total numbers of recurrent angina (2), post operative infarction (I), peri and post operative deaths (3), the percentage of poor results was only 10,7 p. 100, almost three times lower than in previously reported series. In conclusion, we can say that the association of cardiac denervation with coronary bypass surgery significantly improves the percentage of good results (89,3 p. 100 of patients presenting with Prinzmetal angina).

Adult↗
PubMed1982

[Treatment of a severe coronary artery spasm, refractory to complete denervation of the heart (autotransplantation)].

The case reported is that of a 49 year old man with very severe Prinzmetal angina due to spasm of the left circumflex artery. Despite intensive medical treatment he continued to suffer frequent attacks with atrioventricular block. As plexectomy was not possible in this case, complete cardiac denervation was performed. After surgery, he had no further attacks and continuous ECG monitoring showed no ischemic phenomena. Nevertheless, a stress test was still able to induce spasm of the same artery which was painless but associated with ECG changes. Eighteen months postoperatively, resting angina recurred with positive stress tests giving painful attacks. Four hypotheses are discussed: 1) the local factor was very important, with a zone of hyperactivity on the left circumflex artery, 2) one of the mechanisms of coronary artery spasm could be the nervous stimulation of this zone, 3) this zone was insensitive to nervous stimulation after autotransplantation but remained sensitive to methylergometrine, 4) the recurrence of resting angina and painful symptoms on stress testing suggests the possibility of reinnervation of the heart, as has been shown after cardiac transplantation, the autonomic nervous system does not play the role generally attributed to it in the genesis of spasm.

Aged↗
PubMed1981

Complete denervation of the heart (autotransplantation) for treatment of severe, refractory coronary spasm.

A 49 year old man had severe refractory Prinzmetal's variant angina and angiographically documented coronary arterial spasm of a dominant circumflex artery. The spasm was provoked by methergine (an ergot alkaloid) and seemed resistant to various forms of medical therapy including administration of nitrates, nifedipine, verapamil, diltiazem and amiodarone. The attacks of angina at rest persisted at the rate of 7 to 15/day and were frequently associated with atrioventricular (A-V) block. After unsuccessful plexectomy performed in another institution, the patient underwent complete cardiac denervation (produced by autotransplantation). The follow-up data have interesting implications in relation to treatment of refractory variant angina, as well as possible mechanisms of coronary arterial spasm.

Angina Pectoris↗
PubMed1981

Treatment of Prinzmetal's variant angina. Role of medical treatment with nifedipine and surgical coronary revascularization combined with plexectomy.

This study describes three forms of treatment of Prinzmetal's variant angina. Coronary spasm, frequently found at coronary arteriography in patients with Prinzmetal's variant angina, can be treated with intravenous or intracoronary injection of nitroglycerin as well as of nifedipine. Nifedipine (0.2 mg) was injected directly into the involved artery in 12 patients and suppressed spasm in 9; in 3 patients, nifedipine increased coronary sinus flow, which had been decreased by spasm in one of the branches of the left coronary artery. Patients with Prinzmetal's variant angina who have spasm superimposed on atherosclerotic lesions can benefit from coronary arterial bypass grafting combined with partial denervation of the heart. This combination yielded acceptable results (83.4 percent favorable outcome); recurrence of attacks occurred in only 6.7 percent of this group. In those forms of angina in which spasm occurs in angiographically normal coronary arteries, therapy is essentially medical. In 13 patients treated with oral nifedipine (30 to 40 mg/day), suppression of attacks was achieved in 11 instances. During the period of treatment, the methergine provocative test, which had been consistently positive before treatment, converted to negative in 12 patients. Transient withdrawal of nifedipine caused recurrence of pain in two patients.

Adult↗
PubMed1981

[Congestive cardiomyopathy associated with a stiff spinal column. "Rigid spine syndrome"].

The "rigid spine syndrome" is a rare form of myopathy characterised by rigidity of the dorso-lumbar spine, hyperextension of the neck and muscular retraction limiting mobility, especially of the upper limbs with elbows fixed in semi-flexion. This condition, which was first described relatively recently, has been little studied: only 8 cases have been published to this day. We report the case of a 20 year old man with this syndrome, associated with a severe diffuse non-obstructive hypertrophic cardiomyopathy. Electronic microscopy and histoenzymological studies were performed on the skeletal muscle. They confirmed myopathic changes, demonstrating a great variation in diameter of the fibres, but there was no evidence of a predominating histoenzymological form (type I muscular atrophy) as previously reported. Although there have been no other reports of cardiac involvement in the "rigid spine syndrome", a link between the two conditions would seem to be likely.

Adult↗