[The long-term treatment of angina pectoris with pindolol and isosorbide dinitrate in fixed combination. A multicenter trial (author's transl)].
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Biomedical subjects
Publications and source records attributed to J L Rivier.
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The role of the renin angiotensin system was evaluated in 18 normotensive patients with chronic congestive heart failure and in 5 controls. No correlation was observed between plasma renin activity and cardiac index. There was a significant inverse correlation between renin and pulmonary capillary wedge pressure (r = -0.61, P less than 0.01). Renin values of the patients appeared to be increased when compared with controls with similar left ventricular filling pressure. Specific angiotensin II inhibition by saralasin decreased arterial pressure in 8 out of 14 patients: their renin was significantly higher than that of the remaining 6 patients (P less than 0.01). The 2 patients with the lowest renin levels responded to saralasin with a blood pressure increase. Left ventricular filling pressure decreased in all but these latter 2 patients with either little change or an increase in stroke volume. Thus, renin levels appear to be increased in normotensive patients with congestive heart failure when related to left ventricular filling pressure. Renin via angiotensin II plays a role in the blood pressure control of many patients with congestive heart failure. In some patients angiotensin II blockade appears to improve cardiac function by unloading the left ventricle.
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Five of 11 normotensive patients with congestive heart failure responded to an infusion of the specific angiotensin II antagonist, saralasin, by reducing systemic vascular resistance from 2274 +/- 418 to 1690 +/- 351 dynes/sec/cm-5 (mean +/- standard error). This decrease was accompanied by a reduction in left ventricular filling pressure from 19.4 +/- 5.9 to 11.6 +/- 4.0 mm Hg, an increase in cardiac index from 2.2 +/- 0.4 to 2.7 +/- 0.4 l/min/m2 and a decrease in mean arterial pressure from 95 +/- 9.8 to 86 /+- 8.6 mm Hg. In the other 6 patients with congestive heart failure and in 4 controls, saralasin produced either no change or slight increases in systemic vascular resistance. Plasma renin activity did not differentiate responders from non-respnders. Specific inhibition of angiotensin may provide a means for reducing inappropriately high peripheral resistance in some patients with congestive heart failure.
In the patient suffering from angina, the protective effect of oxprenolol in the isoprenaline test is demonstrated by the reduction of disappearance of ischemic-type electrocardiographic alterations and of angina and rhythm disturbances. In our study, these results were obtained in spite of neutralization of the negative chronotropic effect of the beta-blocker through the use of an endo-auricular pacemaker. This points indirectly to the role played by the contractile state of the myocard in catecholamine-induced modifications of the oxygen intake of cardiac muscle.
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In 285 patients who underwent selective coronary arteriography and atrial pacing for electrocardiographic diagnosis of suspected coronary failure, the sensitivity of this test was found to be rather poor: 43% positive results for atrial pacing compared to 50% for the submaximal exercise test, 75% for the maximal exercise test and 63% for the isoprenaline infusion test. In our experience atrial pacing is of diagnostic value only where uncertainty persists after a negative isoprenaline infusion test and an exercise test likewise negative but for some reason submaximal.
This study was designed to obtain information under general practice conditions on the efficacy and tolerability of a fixed combination of the beta-blocking agent oxprenolol 80 mg (Trasicor 80) and hydrochlorothiazide + KCl (Esidrex-K) in the treatment of moderate essential hypertension. Patients with a diastolic pressure of 100 to 130 mm Hg were covered by the study. The dosage of Trasicor was kept relatively low and at a constant level, i.e. one tablet twice daily throughout. In the group of 370 patients whose record had been completed according to the treatment plan, the systolic and diastolic pressures fell on the average by 28 and 17 mm Hg respectively. After 10 weeks of therapy, the diastolic pressure was normalized (i.e. below 95 mm Hg) in 226 patients. The mean decreases in pressure were statistically significant after two weeks' treatment. The mean pulse rate fell from 79 to 73. Tolerance of the regimen was very good in 75% of patients; 57 patients were withdrawn from the study for various reasons.
53 patients aged from 65 to 76 years underwent surgery for valvulopathies (23 patients), atherosclerotic heart disease (24 patients) or both diseases combined (6 patients). All these cases were in NYHA fonctional classes III and IV except for one patient in class II. Hospital mortality after surgical treatment of these cardiopathies was 3.8% (2 deaths). The late mortality of 19% (10 deaths), though high, was of non-cardiac origin in 7 of these patients. The clinical and hemodynamic findings in the two patients who died in the postoperative period were compared with those in the others. These two patients were more severely ill and had a greater degree of cardiomegaly than the average patient in the surviving group. The satisfactory clinical improvement in these elderly cardiac patients suggests that surgery can be recommended at least up to 75 years of age if there are no obvious contraindications. Life expectancy of 13-16 years for patients aged 65 and 8-9 years for patients aged 75 is a further reason for advocating surgical intervention.
Previous investigations concerning isoproterenol infusion (PI) in the diagnosis of myocardial ischemia have shown that ischemic ECG changes are only significant if they persist or appear after discontinuing PI. In an effort to explain the mechanisms of this delayed response, hemodynamic parameters were measured in 10 patients with angiographically proven coronary disease before, during and after PI. It was found that the principal determinants of myocardial oxygen consumption (TTI and contractility) remain significantly elevated in the recuperation phase, but that aortic pressure and systemic arterial resistance, which diminish during PI, return to pre-infusion levels immediately after halting PI. The combined effects favor the late appearance of ischemic changes in the ECG. The coronary vasodilatation with resultant increased oxygen delivery to the myocardium seen during PI may be sufficient to meet the increased myocardial oxygen demand during PI but disappears immediately if PI is discontinued.
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Intravenous infusion of 10 to 30 gamma/min. of Isuprel for 3 to 7 minutes is accurate in diagnosing coronary disease in at least 80% of cases in our series of 100 patients with segmental coronary artery stenoses of 50% or more, demonstrated by coronary angiography. By comparing these 100 patients with a control group of 30 healthy subjects we can state that the late "ST" segment changes (persisting or appearing 3 minutes after stopping the infusion) are typical of coronary insufficiency. In patients without previous infarction, coronary insufficiency is expressed by a horizontal "ST" depression of 1 mm or more. In patients with previous infarction we observed either an "ST" depression or an "ST" elevation. The "ST" elevation, never observed in the control group, seems to have a different significance depending on whether or not a previous myocardial infarction has occurred. If there was no previous necrosis, severe coronary artery disease seems to be suggested and is a bad prognostic sign. This is not so if the patient has previously presented a myocardial infarction.
The authors report a further well-documented case of long-standing atrial palsy, which they feel should be called "persistant" rather than "permanent", as "specific" treatment seems to have been responsible for its regression after about two and a half months. The case was one of atrial palsy with leukaemic infiltration of the auricles (acute leukaemia with paramyeloblasts), an aetiology without precedent in the published literature. Treatment with corticosteroids and antimitotic drugs resulted simultaneously in remission of the leukaemia and conversion to atrial fibrillation. Remission of the dysrhythmia is probably attributable to the specific treatment of the underlying pathology, which makes this case so unusual.
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