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Biomedical subjects

A Castaigne

Publications and source records attributed to A Castaigne.

At least 73 records · Page 4Linked to original sources
PubMed1994

Additive haemodynamic effects of piroximone and prostacyclin in severe chronic heart failure.

This study was undertaken to assess the haemodynamic effects of the combined infusion of prostacyclin and piroximone, a phosphodiesterase inhibitor, in 18 patients with severe congestive heart failure. Right heart catheterization was performed with a Swan-Ganz thermodilution catheter and arterial blood pressure was monitored using a radial line. After baseline haemodynamic measurements, prostacyclin was administered in all patients at the incremental infusion rate of 2, 4, 6 and 8 and 10 ng.kg-1.min-1 during 15 min each. After recovery of baseline haemodynamics, patients were randomly assigned to the piroximone infusion rate of 5 or 10 micrograms.kg-1.min-1 or placebo. After 24 h piroximone or placebo infusion, the same prostacyclin protocol was applied. Prostacyclin infusion added to piroximone resulted in a significant improvement in haemodynamics, as compared to the group receiving prostacyclin added to placebo. As compared to the curve observed with the placebo infusion, 10 ng.kg-1.min-1 prostacyclin infusion resulted in a further increase in cardiac index, by 41 and 38% (P < 0.01) at the piroximone-infusion rates of 5 and 10 micrograms.kg-1.min-1, respectively, whereas systemic vascular resistance decreased by 25 and 21%, respectively (P < 0.01). Additionally, a further decrease in pulmonary capillary wedge pressure by 13 and 11% (P < 0.05) and in pulmonary vascular resistance by 21 and 19% (P < 0.05) was observed at the piroximone-infusion rates of 5 and 10 micrograms.kg-1.min-1, respectively. Consequently, stroke work index increased significantly, as compared to the group receiving prostacyclin added to placebo. This haemodynamic improvement occurred without significant changes in heart rate and mean arterial pressure. Thus, this study shows that in patients with severe congestive heart failure, short-term infusion of prostacyclin is safe and has additive haemodynamic effects on phosphodiesterase inhibitors.

Adult↗
PubMed1994

Hemodynamic effects of a new calcium antagonist, SR 33557, in patients with coronary artery disease and normal left ventricular function.

SR 33557 is a new calcium antagonist which in vitro demonstrated selectivity for smooth muscle over cardiac muscle. To assess the hemodynamic effects of SR 33557 in humans, SR 33557 was administered intravenously (i.v.) in 9 patients with normal systolic left ventricular function [LV ejection fraction (EF) = 63.7 +/- 8%] undergoing right and left catheterization. Baseline measurements were recorded before and during right atrial pacing (100 beats/min), after which 5 mg SR 33557 was infused in 10 min and hemodynamic parameters were continuously recorded until 30 min after discontinuation of the infusion. Effects of SR 33557 were evident from discontinuation of the infusion, maximal between the tenth and twentieth min after discontinuation of the infusion. Without atrial pacing, the main effect of SR 33557 infusion was to decrease heart rate (HR) from 77.7 +/- 10.7 to 61.9 +/- 9.3 beats/min (p < 0.001). Cardiac index (CI) did not change; stroke volume index (SVI) increased from 44.2 +/- 13 to 50.4 +/- 15 ml.m-2, (p < 0.05). Mean arterial pressure (MAP) decreased from 104.7 +/- 29.6 to 94.3 +/- 22.9 mm Hg (p < 0.05) with no change in filling pressures or systemic vascular resistance (SVR). Consequently, rate-pressure product (RPP) decreased from 8,211 +/- 3,092 to 5,906 +/- 2,025 mm Hg.beat-1 (p < 0.01). Peak positive LVdP/dt decreased from 1,711 +/- 257 to 1,533 +/- 194 (p < 0.01). During the pacing phase, none of the hemodynamic parameters differed from baseline; especially peak positive LVdP/dt remained unchanged. SR 33557 has negative chronotropic action but shows no direct negative inotropic effect in patients with normal systolic LV function.

Aged↗
PubMed1994

[Reading of articles concerning treatment of acute phase of myocardial infarction].

The number of articles concerning the treatment of acute myocardial infarction is large, and systematic analysis can improve the comprehension of their results. The object of this paper is to propose a method of classifying these articles with respect to their qualities and defects in order to orient workers towards the use of the most satisfactory articles for bibliographic purposes. The questions that have to be addressed are: what is the object of the study; is the instrument of measurement adapted to the objective of the study; which patients were studied; was the study performed with a double-blind protocol; what was the number of cases and does this number allow a valid response to the question; what was the plan of the study; what were the judgement criteria and what significance can be accorded to these criteria, and finally, what was the type of analysis, were there analyses of sub-groups, and if so, are the analyses pertinent. Based on examples in the literature, the authors justify why these questions should be asked and how the responses to these questions influence the judgement of a given article. In conclusion, the quality of therapeutic trials in acute myocardial infarction is very variable: systematic analysis allows them to be classified in a subjective scale of quality.

Clinical Trials as Topic↗
PubMed1993

Coronary vasodilating action of dobutamine in patients with idiopathic dilated cardiomyopathy.

To assess the coronary hemodynamic effects of dobutamine in patients with idiopathic dilated cardiomyopathy, dobutamine was infused at the incremental infusion rates of 25, 50, 100, and 200 micrograms/min into the left main coronary artery of nine patients undergoing cardiac catheterization. In response to dobutamine infusion, systemic hemodynamic effects were dose related. At the highest infusion rate cardiac index and left ventricular peak positive rate of rise in ventricular pressure increased from 2.33 +/- 0.54 to 2.97 +/- 0.65 L/min/m (p = 0.001) and from 690 +/- 177 to 1157 +/- 275 mm Hg/sec (p = 0.001), respectively. Left ventricular end-diastolic pressure decreased from 17 +/- 8 to 8 +/- 7 mm Hg (p = 0.001) and a trend toward decrease in left ventricular wall stress was observed (from 166 +/- 75 to 148 +/- 66 gm/cm2, not significant). Heart rate and mean arterial pressure remained unchanged. The coronary hemodynamic response to dobutamine infusion was also dose related. At the highest infusion rate coronary sinus blood flow increased from 133 +/- 35 to 179 +/- 47 ml/min (p < 0.01) and was associated with an increase in coronary oxygen blood content from 4.5 +/- 0.6 to 7.8 +/- 1.7 ml per 100 ml (p < 0.01) whereas myocardial oxygen consumption remained unchanged. During dobutamine infusion norepinephrine decreased in the femoral artery and in the coronary sinus from 1.03 +/- 0.34 to 0.641 +/- 0.179 ng/ml (p < 0.05) and from 1.76 +/- 0.98 to 1.38 +/- 0.65 ng/ml (p < 0.05), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Intracoronary linsidomine abolishes acetylcholine-induced vasoconstriction of epicardial coronary arteries.

If the vasodilation of the epicardial coronary arteries caused by linsidomine (SIN-1), the active metabolite of molsidomine, is well established, few data are available concerning the effects of SIN-1 on the acetylcholine (ACh)-induced vasoconstriction of epicardial coronary arteries. Fourteen patients with mild lesions of the left anterior descending artery (LAD) were studied. Intracoronary blood flow velocity was measured by a Doppler probe placed in the proximal segment of the LAD, and cross-sectional arterial area was assessed by quantitative angiography. After initial hemodynamic parameters were measured, 12 mg papaverine was injected into the left main coronary artery. When hemodynamic parameters returned to baseline values, three increasing concentrations of ACh (5 x 10(-7), 10(-6), and 5 x 10(-6) M) were selectively administered into the LAD in a 3 min period for each concentration. While the infusion of ACh 5 x 10(-6) M was continued, 1 mg SIN-1 was injected as a bolus in the ostium of the left coronary artery. After the injection of papaverine, blood flow increased by 197 +/- 8%, with a trend toward vasoconstriction of the proximal and distal segments of the LAD (p = NS). The ACh injection induced a dose-dependent vasoconstriction, reaching 51 +/- 20% on the distal segment of the LAD at the maximum concentration (p < 0.001). After an initial increase in coronary blood flow of 47 +/- 10 and 28 +/- 11% during the first two concentrations of ACh, respectively, the values decreased after the last injection to the level of baseline values. The infusion of SIN-1 antagonized the ACh-induced vasoconstriction, leading to vasodilation of 7.5 +/- 3% (p < 0.005) and 16 +/- 7% (p < 0.001) of the proximal and distal segments of the LAD, respectively; this was associated with an increase in intracoronary blood flow by 42 +/- 8%. We conclude that intracoronary administration of SIN-1 can antagonize the ACh-induced vasoconstriction of epicardial coronary arteries.

Acetylcholine↗
PubMed1993

Positron emission tomography with 11C CGP-12177 to assess beta-adrenergic receptor concentration in idiopathic dilated cardiomyopathy.

BACKGROUND: Positron emission tomography (PET) with 11C-labeled CGP-12177 (CGP) has been shown to have the potential to noninvasively measure beta-adrenergic receptor concentration in dog heart. The present study was undertaken to evaluate the clinical value of this technique. METHODS AND RESULTS: Eight normal subjects and 10 patients with heart failure related to an idiopathic cardiomyopathy were studied. Estimation of beta-receptor concentration was based on a graphic method applied on myocardial PET time-concentration curves obtained after an intravenous injection of 11C-CGP followed 30 minutes later by a coinjection of labeled and unlabeled CGP. The clinical tolerance of these injections was good. Left ventricular concentration of beta-receptors was decreased in patients compared with controls (3.12 +/- 0.51 versus 6.60 +/- 1.18 pmol/mL, respectively; p < 0.001). This 53% decrease agrees with previous in vitro data. In eight of the 10 patients, the beta-receptor concentration obtained from PET was compared with the beta-receptor density determined on left ventricular endomyocardial biopsy samples by in vitro binding technique using 3H-CGP-12177. Results obtained with both techniques were correlated (r = 0.79, p = 0.019). Moreover, decreased beta-receptor concentration correlated with the beta-contractile responsiveness to intracoronary dobutamine infusion (r = 0.83, p = 0.003), indicating a direct link between changes in the receptor number and its biological function. CONCLUSIONS: PET appears to be a safe and reliable method of assessing in vivo changes in the number of left ventricular beta-adrenergic receptor sites of patients with idiopathic cardiomyopathy.

Adrenergic beta-Antagonists↗
PubMed1993

[Doppler echocardiographic evaluation of mitral flow velocity and prognosis of cardiac insufficiency].

The aim of this study was to determine the role of Doppler echocardiography in establishing the prognosis of Stages to 4 cardiac failure. The echocardiographic indices of left ventricular filling were correlated with catheter data and the 2 year out come of patients. The study population included 54 patients examined prospectively in the context of an evaluation of their cardiac failure. Two years after the initial examination, 19 patients were dead or transplanted. Of the remaining 35 patients, 18 were reevaluated at 6 months. Of the echocardiographic parameters, "hyper normal" mitral flow with a high E/A ration indicated poor prognosis; when E/A > 2, the one year survival was 50% and the 2 year survival 42%. There was overlap between the groups of dead or transplanted and surviving patients only when the E/A ratio was between 2 and 3. The patients with E/A < 2 were all alive without any major events at 2 years. All patients with E/A > 3 had a poor prognosis. The E/A ratio was closely correlated with pulmonary capillary pressure levels (p < 0.001, r = 0.55) and lees closely with cardiac index (p < 0.05, r = 0.4) and radionuclide ejection fraction (p < 0.05, r = 0.28). After 6 months' vasodilator treatment with an angiotensin converting enzyme inhibitor (captopril) the E/A ratio decreased significantly from 1.85 +/- 0.78 to 1.0 0.55 (p < 0.02). A "hyper-normal" mitral flow is related to many factors, including high left ventricular filling pressures, mitral regurgitation and reduced left ventricular compliance. This appearance of mitral flow is a poor prognosis factor in severe cardiac failure.

Actuarial Analysis↗
PubMed1993

[Regression of coronary atherosclerosis evaluated by angiography. A review of principal trials and critical study].

The concepts of acceleration of atherosclerosis with fat rich diets and the regression or at least stabilisation of atherosclerosis by suppressing the cholesterol, introducing exercise programmes or administering calcium antagonists or aspirin, have been validated in the animal model. In the clinical situation, repeat coronary angiography has demonstrated that hyperlipidemia and the interval between two investigations are the main factors influencing the progression of atherosclerosis. However, the factors underlying the appearance and progression of atheromatous plaques remain unknown. Interventional trials based on the principle of introducing treatment after reference angiography have been undertaken. The results were assessed after variable time intervals. The general conclusion is that there is a direct relationship between the lowering of plasma cholesterol, the intensity of exercise and the slowing of progression of atherosclerosis as far as can be evaluated by repeat angiography. The data concerning the effect of calcium antagonists is confusing. The main criticism of these trials is the instrument of measurement and the practical significance or even the reality of the observed changes. In the present state of our knowledge, trials of the regression of atherosclerosis can not replace longitudinal studies of the long-term effects of drugs on cardiovascular and general morbidity and mortality.

Animals↗
PubMed1993

Assessment of coronary reserve in man: comparison between positron emission tomography with oxygen-15-labeled water and intracoronary Doppler technique.

This study compared positron emission tomography (PET) using oxygen-15-labeled water for measurement of coronary reserve with intracoronary Doppler in patients with left anterior descending artery stenosis and patients with no coronary lesion and a coronary reserve 3 as assessed by the invasive technique. To determine whether PET measurement of coronary reserve is altered by partial volume effect, patients with left ventricular dysfunction due to idiopathic cardiomyopathy were studied with both techniques. Direct ultrasonic measurement of coronary reserve was performed the day prior to the PET study: a Doppler catheter was placed in the proximal left anterior descending artery; mean velocity was recorded at baseline and after dipyridamole administration. Using a time-of-flight PET system, patients underwent: (1) an intravenous bolus of oxygen-15-labeled water at baseline and 4 to 6 min after intravenous infusion of dipyridamole using the same protocol as for Doppler study and (2) a 18F-fluorodeoxyglucose (FDG) myocardial imaging. Oxygen-15 time-activity curves were recorded in myocardial regions of interest (ROIs) drawn on a static FDG image. Using the left ventricular time-activity curve as an input function, a standard model with a single-tissue compartment was fitted to the PET data; myocardial blood flow was estimated as the blood-to-tissue transfer rate constant. Coronary reserve measured by PET was well correlated with the measured by intracoronary Doppler (r = 0.98, p < 0.001 for global population). This PET method is an accurate and reliable tool to noninvasively measure coronary reserve in patients, even in those with left ventricular dysfunction.

Blood Flow Velocity↗
PubMed1993

[Incidental finding of an isolated thrombus in the left atrium in a young woman with sinus rhythm 5 years after cerebral ischemic accident].

The authors report the case of a 40 year old woman who had an ischemic stroke. The initial investigation including a complete blood clotting analysis, failed to demonstrate the cause. Five years later, the investigations were completed systematically by transesophageal echocardiography which demonstrated an isolated thrombus localised in the left atrial appendage though the localisation heart was in sinus rhythm and morphologically normal. This case illustrates in the diagnostic yield of transesophageal echocardiography in the investigation of systemic embolism in young patients who have had a cerebral ischemic event of unknown cause, even in the absence of predisposing cardiac cause.

Adult↗
PubMed1993

[Effects of intracoronary injection of SIN-1 on vasoconstriction of epicardial arteries induced by acetylcholine].

Linsidomine or SIN-1, a vasodilator of epicardial arteries, is the active metabolite of Molsidomine which is regularly used for intracoronary injection. Although its vasodilatory action has been demonstrated on the large coronary vessels, it is not known whether this molecule can vasodilate epicardial coronary arteries which have been vasoconstricted with acetylcholine. Twelve patients with left anterior descending artery (LAD) disease were studied. Intracoronary flow velocity was measured with a Doppler catheter (Millar) placed in the proximal segment of the LAD and the diameter of the artery was evaluated by quantitative angiography. After recording the basal haemodynamic parameters, 12 mg of papaverine were injected into the left main coronary artery. After regaining the basal state, three incremental doses of acetylcholine (5 x 10(-7), 1(-6) and 5 x 10(-6) M) were selectively injected into the LAD over a 3 minute period for each injection. Then, during continuous infusion of 5 x 10(-6) of acetylcholine, 1 mg of SIN-1 was injected in a bolus into the left coronary ostium. After the papaverine, the coronary flow velocity increased by 199 +/- 8% associated with a vasoconstrictive tendency in the proximal and distal segments of the LAD (NS). In response to acetylcholine a dose-dependent vasoconstriction vas observed attaining 50 +/- 21% at the last injection in the distal segment of the LAD (p < 0.001). After an initial increase in coronary flow velocity of 46 +/- 11% (p = 0.004) and of 26 +/- 11% (p < 0.05) after the first two doses of acetylcholine, it decreased after the final injection to close to basal values (NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1993

[Endothelial dysfunction and coronary vasomotricity. Contribution of endocoronary echography].

The regulation of flow and diameter of the coronary arteries depends on many factors. In normal subjects, increased coronary flow is associated with an increase in diameter of the epicardial coronary vessels. The coupling of these two independent variables depends on the integrity of endothelial function. In isolated arteries suppression of the endothelium induces an abnormal vasomotor response to acetylcholine. The presence of atherosclerotic lesions on the coronary vessels also induces the opposite response to the administration of acetylcholine, even in apparently normal segments. Other physiological coronary vasodilator stimuli, especially those which increase the concentration of noradrenaline, become vasoconstrictor in diseased coronary vessels. Finally, increasing coronary blood flow is not associated with increases in coronary diameter in patients with coronary atherosclerosis. This loss of flow-dependent vasodilatation is an early and diffuse phenomenon in subjects with cardiovascular risk factors. The authors have shown that this inversion of vasomotor responses observed by angiographic techniques, may also be documented by endocoronary ultrasonography. Their results demonstrate that the vasodilatation induced by papaverine or by the cold pressor test in 6 normal subjects is lost in 20 patients with coronary atherosclerosis and that the administration of Sin 1 induces a comparable vasodilatation in normal and diseased vessels. This study confirms that endothelial function is globally altered in atherosclerotic coronary artery disease.

Acetylcholine↗
PubMed1993

[Implantation of an endoprosthesis for the repair of stenosis of valved tube between right ventricle and pulmonary artery].

The author report the case of a 35 year old man who had undergone a Rastelli procedure in 1976 for transposition of the great arteries and who required indertion of a stent for stenosis of the valved right ventricular-pulmonary artery conduit. The patient presented with florid signs of right ventricular failure due to degenerescence of the conduit which had a 60 mmHg pressure gradient between the right ventricle and the pulmonary artery. This palliative procedure was decided upon given the high risk of reoperation. The valved conduit was dilated with a balloon catheter before insertion of a Gianturco stent (30 mm diameter and 50 mm long) to cover both conduit and the valvular apparatus. The insertion of the stent was easy with immediate normal expansion and the procedure was well tolerated. After insertion of the stent, the right ventricular-pulmonary artery pressure gradient fell from 60 to 35 mmHg. Angiographic control one month later showed a sustained hemodynamic result with a perfectly patent stent. The patient was pauci-symptomatic when reviewed six months after the procedure.

Adult↗
PubMed1993

[A survey on the management of myocardial infarction in France.The Infarctus Top Chrono Survey].

An enquiry was carried out between December 1989 and January 1990 involving 749 cardiologists and 8,846 general practioners based throughout France to evaluate the number of myocardial infarctions diagnosed each year, to determine how the patients are transported to hospital and to assess the average delays of transportation. This enquiry showed that cardiologists diagnosed 15 cases of myocardial infarction per year: their first reflex is to visit the patient, sometimes accompanied by the emergency medical service if available at the time of the patient's call, or to advise the patient to call the emergency service straight away if it is not possible for them to visit the patient immediately. The delay of transportation is less than 30 minutes in 45% of cases and over 60 minutes in 10% of cases. Regional differences were observed and are analysed. General practitioners diagnose 4 cases of myocardial infarction per year: the principal attitude is the same as that of the cardiologists, except that the general practitioner is available to visit the patient more often and is called out more easily. The means of transport and the delays of transportation are very similar to those observed with the cardiologists. This analysis of the management of myocardial infarction in France in 1990 may help organise actions to shorten the time between the onset of chest pain and the institution of thrombolytic therapy.

Family Practice↗
PubMed1992

[Converting enzyme inhibitors and coronary failure].

Nearly 15 years ago, it has been shown that myocardial infarction is accompanied by left ventricular dilatation. In the following years more details were obtained on morphological changes consecutive to myocardial infarction, now grouped together under the term left ventricular remodelling. These changes enable the patients to survive despite reduction of the contractile ventricular mass, but they expose the ventricles to constraints resulting in excessive work load. It has been shown that these changes can be reduced by early myocardial reperfusion and by administration of angiotensin-converting enzyme (ACE) inhibitors. These findings were established first in animals, then in man. Administering ACE inhibitors to patients with symptomatic heart failure consecutive to advanced ischaemic cardiopathy prolongs the patients' survival. When ACE inhibitors are given to patients with severe asymptomatic left ventricular dysfunction which started soon or long after a myocardial infarction, they reduce the frequency of ischaemic events, passage to symptomatic heart failure and, at least in one study, mortality. ACE inhibitors have also been shown to reduce the size of myocardial necrosis when administered in the acute phase of experimental myocardial infarction. Preliminary data have demonstrated that ACE inhibitors given in the acute phase of myocardial infarction reduce the left ventricular dilatation which follows infarction. However, a study of ACE inhibitors administered to a large number of patients in the acute phase of myocardial infarction had to be interrupted because of the over-mortality in the treated group. These facts are reviewed in this article, and attempts have been made at deducing from them the current indications of ACE inhibitors in patients with coronary heart disease.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

Effects of infusion of L-arginine into the left anterior descending coronary artery on acetylcholine-induced vasoconstriction of human atheromatous coronary arteries.

Hypercholesterolemia and atherosclerosis are conditions associated with impaired endothelium-dependent relaxation. In hypercholesterolemic animals, intravenous administration of L-arginine, the precursor of nitric oxide, normalizes endothelium-dependent vasodilator activity. In the present study, we questioned whether intracoronary administration of L-arginine in patients with coronary artery disease could improve coronary vascular reactivity to acetylcholine. Thirteen hypercholesterolemic patients with diffuse coronary atherosclerosis but nonstenotic lesions of the left anterior descending (LAD) coronary artery were investigated. Quantitative coronary angiography and subselective intracoronary Doppler flow velocity measurements were performed to determine LAD diameters and coronary blood flow. Intracoronary infusion of acetylcholine was performed during 3 consecutive 3-minute periods at incremental rates adjusted to achieve estimated final concentrations of 5 x 10(-7), 10(-6) and 5 x 10(-6) M. After evaluation of the response to acetylcholine, L-arginine was infused into the LAD at the rate of 25 mg/min (10(-3) M) and the same stepwise 3-minute infusions of acetylcholine were repeated during infusion of L-arginine. Infusion of acetylcholine induced a dose-dependent reduction of distal epicardial LAD diameter reaching -48.5 +/- 17% at 5 x 10(-6) M (p < 0.01 vs control values). L-arginine alone had no effect on the distal LAD diameter but attenuated acetylcholine-induced vasoconstriction to -21 +/- 9% at 5 x 10(-6) M acetylcholine (p < 0.01). Coronary blood flow showed a biphasic response to acetylcholine, increasing by 41 +/- 12% at 5 x 10(-7) M (p < 0.01) and decreasing by 21 +/- 13% at 5 x 10(-6) M (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1992

[Which medical treatment after myocardial infarction?].

Patients leaving the hospital after a myocardial infarction are given a prescription containing several drugs. The purpose of this paper is to determine which of these drugs have a proven value and for which types of patients. Antithrombotic agents (be it acetyl-salicylic acid or antivitamin K drugs) have been shown to be efficient after a myocardial infarction. Beta-blockers are certainly useful, notably in cases with severe necrosis. Conversely, the usefulness of calcium antagonists for secondary prevention has not been demonstrated and indeed, it seems probable that the drugs of this class might be harmful in patients who had severe infarction. There is little divergence concerning the necessity to control the risk factors for coronary atherosclerosis after a myocardial infarction. The evidence is strong concerning giving up smoking; it is intuitive as regards controlling arterial hypertension and more controversial as regards the need for lowering blood cholesterol levels. The systematic prescription of antiarrhythmic agents after myocardial is certainly noxious. Finally, prospects are now opened by the prevention of left ventricular remodelling under treatment with angiotensin-converting enzyme inhibitors.

Adrenergic beta-Antagonists↗