Biomedical subjects

M F Rousseau

Publications and source records attributed to M F Rousseau.

At least 55 records · Page 3Linked to original sources

PubMed1990

Relationship between positive inotropic responses and plasma concentrations of xamoterol in middle-aged and elderly patients.

1. We examined the relationship between the contractile state of the left ventricle and the plasma concentration of xamoterol in patients with ischaemic heart failure. 2. Identical studies were conducted in 14 middle-aged (all male; mean age 51.3 years, range 42-61) and 10 elderly patients (six male, four female; mean age 67.7 years, range 64-72). 3. Patients received seven cumulative doses (0.0005-0.2 mg kg-1) of xamoterol. After each dose the rate of change of pressure in the left ventricle at a developed pressure of 40 mm Hg and normalised for this pressure, (dP/dt)/DP40, and plasma concentrations of xamoterol were measured. 4. There were dose-related increases in (dP/dt)/DP40. Curves relating changes in (dP/dt)/DP40, expressed as a percent of the maximum observed response, to changes in xamoterol plasma concentrations were constructed for the middle-aged and elderly patients. From these curves the mean effective concentration (EC) value to produce a particular response could be calculated. In the sample sizes studied, the difference between the EC values over a range of responses for the middle-aged and elderly patients did not reach statistical significance, indicating that cardiac responsiveness to xamoterol was similar in the two groups of patients. 5. Plasma concentrations of xamoterol over the range of 39 to 150 ng ml-1 produced positive inotropic responses which varied between 70% and 90% of the maximum observed effect of xamoterol.

Adult↗

PubMed1990

Effects of the beta 1-adrenergic receptor partial agonist xamoterol on left ventricular diastolic function. An evaluation after 1-6 years of oral therapy.

Acute intravenous administration of the new beta 1-adrenergic receptor partial agonist xamoterol lowers left ventricular end-diastolic pressure and improves the isovolumic indexes of inotropic state and relaxation. To determine if these hemodynamic changes were maintained after prolonged administration, the dose-response relation to cumulative doses of xamoterol was determined in a group of 14 patients with mild (n = 6)-to-serve (n = 8) ischemic left ventricular dysfunction. These patients had been treated with xamoterol (200 mg, b.i.d.) for a mean of 51 +/- 17 months, and the drug had been stopped for 72 hours before testing the responsiveness to xamoterol. In these patients, xamoterol administration still induced dose-dependent decreases in left ventricular end-diastolic pressure from 21.4 +/- 8.2 to 15.8 +/- 7.7 mm Hg (p less than 0.01, vs. baseline and vs. the control data 51 +/- 17 months before). Peak positive dP/dt and dP/dt normalized to a developed pressure of 40 mm Hg [( dP/dt]/DP40) increased by 14% and 23%, respectively (p less than 0.01), whereas the rate of isovolumic pressure decrease improved by 12% (p less than 0.01). It is concluded that the myocardial response to xamoterol is maintained after years of continuous therapy, and that in patients with heart failure, this response was expressed mainly as a reduction in left ventricular end-diastolic pressure.

Administration, Oral↗

PubMed1990

Relation of diastolic function and exercise capacity in ischemic left ventricular dysfunction. Role of beta-agonists and beta-antagonists.

The relation between global left ventricular function at rest (evaluated during cardiac catheterization) and exercise capacity was examined in a group of 33 untreated patients with a previous anterior myocardial infarction. The resting ejection fraction (range, 24-68%) correlated poorly with exercise duration (r = 0.47) and did not separate patients with a depressed exercise capacity (exercise duration less than 500 seconds: group A, n = 18) from patients with preserved exercise tolerance (group B, n = 15). The resting left ventricular end-diastolic and end-systolic volume indexes were comparable in groups A and B, but the diastolic pressure-volume relation was shifted upward, and the mean left ventricular pressure during diastolic filling was higher in group A than in group B (19 +/- 8 versus 14 +/- 4 mm Hg; p less than 0.02). The heart rate at maximal exercise was similar in both groups (160 +/- 16 versus 160 +/- 17 beats/min; NS), but heart rate was higher at any given level of exercise in group A than in group B. When 12 patients of group A were treated with xamoterol, a beta 1-adrenoceptor partial agonist, their exercise duration increased by 20 +/- 14% (p less than 0.001), and their maximal exercise heart rate decreased from 158 +/- 16 to 143 +/- 11 beats/min (p less than 0.001). This improved exercise capacity was accompanied by a downward shift of the resting diastolic left ventricular pressure-volume relation and by a decrease in mean left ventricular pressure during diastolic filling.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗

PubMed1990

Effects of benazeprilat on left ventricular systolic and diastolic function and neurohumoral status in patients with ischemic heart disease.

The effects of the intravenous administration of the angiotensin converting enzyme inhibitor benazeprilat on left ventricular function were examined in 18 patients with ischemic heart disease. Twenty minutes after drug infusion (0.3-10 mg), heart rate (78 +/- 17 to 71 +/- 16 beats/min, p less than 0.0003), left ventricular systolic pressure (-9 mm Hg, p less than 0.0004), and plasma norepinephrine concentration all decreased significantly. The isovolumic indexes of inotropic state also decreased slightly (-10% in dP/dtmax, p less than 0.001), whereas the ejection fraction (39 +/- 16% to 41 +/- 16%, p less than 0.08) and the end-systolic volume (-6%, p less than 0.04) tended to improve, probably because of the afterload reduction (-13% in mean systolic wall stress, p less than 0.05). After benazeprilat administration, the left ventricular end-diastolic pressure was unchanged at the group level, but there was a consistent downward shift of the diastolic pressure-volume relation during rapid filling, and the mean diastolic wall stress decreased from 99 +/- 73 to 69 +/- 42 kdyne/cm2 (p less than 0.007). These data indicate that the acute administration of benazeprilat has a dual action on left ventricular pump function, which is that the negative inotropic effect of bradycardia and reduced sympathetic drive are compensated by afterload reduction. The drug also improved left ventricular diastolic distensibility and significantly reduced wall stress during diastole. The beneficial effects on diastolic function were noted both in patients with mild left ventricular dysfunction and in patients with heart failure.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1990

Effects of nicardipine on regional diastolic left ventricular function in patients with angina pectoris.

The effects of the slow calcium channel blocker nicardipine on the synchrony of left ventricular filling were examined in eight patients with angina pectoris. Left ventriculography was performed at baseline (after pretreatment with propranolol to minimize reflex changes) and was repeated after the intravenous administration of 2.5 mg nicardipine. Regional peak filling rate and time to peak filling rate were determined in eight ventricular segments before and after nicardipine. At baseline, the time from the R wave to the regional peak filling rate was 380-680 msec, and there were a large number of segments with depressed peak filling rate (p less than 0.001, vs. distribution of regional peak filling rate in normal subjects using a Kolmogorov-Smirnov test), indicating both asynchrony of filling (p less than 0.001, vs. distribution of time to peak filling rate in normal subjects) and nonhomogeneity of diastolic distensibility. Nicardipine administration significantly reduced the distribution of the time to peak filling rate (p less than 0.001) and increased regional peak filling rate (p less than 0.001) in a large subset of segments. Segments with normal values of peak filling rate at baseline, however, frequently did not improve or even decreased their peak filling rate. The changes in global left ventricular filling rate after drug administration also correlated with the number of segments improved after nicardipine. It is concluded that intravenous nicardipine improves the synchrony of diastolic filling in patients with angina pectoris.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗

PubMed1989

Effects of long-term xamoterol therapy on the left ventricular mechanical efficiency in patients with ischemic heart disease.

Myocardial oxygen uptake and an index of mechanical left ventricular efficiency were determined in basal conditions or during prolonged therapy with the new beta 1-adrenoceptor partial agonist xamoterol in 16 patients with mild to moderate ischemic heart failure. During xamoterol therapy, left ventricular end-diastolic pressure decreased from 24.4 +/- 6.5 to 17.8 +/- 8.6 mm Hg (P less than 0.01) and the isovolumic index of inotropic state (dP/dt)/DP40 increased by 14% (P less than 0.01). The heart rate increased slightly and the mean systolic and peak systolic wall stress also tended to increase (+ 7%; NS) but myocardial oxygen uptake (14.1 vs 14.7 ml/min; NS) and the index of efficiency (8.77 +/- 3.44 to 8.82 +/- 4.27; NS) were not significantly modified. In conclusion, prolonged therapy with xamoterol was not accompanied by a deterioration in the mechanical efficiency of the ventricle, even in patients with ischemic heart disease.

Adrenergic beta-Agonists↗

PubMed1989

Effects of alinidine on metabolic response to high-demand myocardial ischemia.

Alinidine is a new bradycardic agent that interferes with ion channels and the if pacemaker current. To determine if alinidine had antiischemic effects unrelated to its bradycardic action, myocardial metabolism was studied during a pacing-stress test in 20 patients with coronary artery disease and angina pectoris, before and after intravenous infusion of alinidine (10 mg, n = 10; 50 mg, n = 10). When compared to the control pacing-stress test, the low dose of alinidine had no significant effect on aortic pressure, coronary sinus flow (-3%, NS), myocardial oxygen extraction, or myocardial lactate uptake. After the high dose of alinidine, aortic pressure and coronary sinus flow remained unchanged but the arteriocoronary sinus difference in oxygen content increased (12.2 +/- 1.3 to 12.7 +/- 1.4 ml/100 ml; p less than 0.0002) above the values observed during the control pacing-stress test, while both the chemical lactate extraction fraction (-19 +/- 30 to 15 +/- 21%; p less than 0.025) and the L-[1-14C]lactate extraction fraction increased. Accordingly, the net myocardial lactate uptake (corrected for production) had increased from 14 +/- 32 during the control pacing-stress test to 29 +/- 24 mumol/min during the pacing repeated after the high dose of alinidine (p less than 0.05). After the high dose of alinidine, the free fatty acid uptake also rose slightly (+23%; NS) and the alanine production was reduced in 7 of 10 patients (-3.6 +/- 1.7 to -1.4 +/- 0.6 mumol/min; NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Focus on diastolic dysfunction: a new approach to heart failure therapy.

1. Although heart failure is commonly associated with depressed systolic function, there is increasing evidence that impaired diastolic performance is also universally present and might be a key determinant of symptoms, physical capacity and even survival in some subsets of patients. 2. Reduced diastolic distensibility increases cardiac filling pressure not only at rest, but even more during exercise when diastolic filling time is reduced. The increases in filling pressure and diastolic wall stress lead to pulmonary congestion and subendocardial ischaemia, it also triggers myocardial hypertrophy and a detrimental remodelling of the ventricular cavity. Perhaps even more importantly, impaired ventricular distensibility limits the use of the Frank-Starling mechanism, impairing systolic pump function and cardiac output adaptation during exercise. Therapies able to improve the distensibility of the ventricle are, therefore, desirable in heart failure. 3. Nitrates, angiotensin converting enzyme (ACE) inhibitors and diuretics may indirectly increase left ventricular chamber compliance by their effects on the right side of the heart. Cardiac glycosides do not improve myocardial relaxation and may even cause diastolic contracture at toxic doses. The new beta 1-adrenoceptor partial agonist, xamoterol, on the other hand, consistently lowers left ventricular filling pressure at rest and during exercise, and produces an increase in left ventricular dynamic compliance through the direct lusitropic effect of beta 1-adrenoceptor stimulation. These beneficial effects are maintained during prolonged therapy and also appear sufficient to slow the remodelling of the ventricular cavity. The improvement in symptoms and in exercise tolerance observed during xamoterol (Corwin, Carwin, Corwil, Xamtol, ICI 118,587) therapy might, therefore, be related to the improvement in left ventricular diastolic distensibility induced by this drug.

Adrenergic beta-Agonists↗

PubMed1989

The efficacy and safety of chronic oral administration of xamoterol to patients with severe heart failure treated with ACE inhibitors.

Xamoterol 200 mg twice daily was given for 2 months to nine patients with severe heart failure already being treated with angiotensin converting enzyme (ACE) inhibitors. Left ventricular end-diastolic pressure fell from 28 to 13 mmHg and end-systolic volume fell from 115 to 106 ml m-2; indices of contractility improved and ejection fraction rose from 33 to 38%. The time constant of ventricular relaxation, T1, improved from 62 to 44 ms. Exercise tolerance improved. Thus, in this group of patients with severe heart failure, xamoterol produced benefits in systolic and diastolic function. There were no adverse effects.

Adrenergic beta-Agonists↗

PubMed1989

Contrasting effects of single doses of pindolol and xamoterol on left ventricular diastolic function.

Impaired left ventricular diastolic dysfunction is common in patients with ischaemic heart failure. The beta 1-adrenoceptor partial agonist xamoterol was compared with pindolol, a beta-adrenoceptor blocker with intrinsic sympathomimetic activity, in a haemodynamic study in 17 patients with ischaemic heart disease. Pindolol caused left ventricular end-diastolic pressure, wall stress and T1 to rise, whereas xamoterol produced improvements in all three parameters. These results suggest that xamoterol may be of greater benefit to patients in heart failure.

Adrenergic beta-Agonists↗

PubMed1989

Effects of pimobendan (UD-CG 115 BS) on left ventricular inotropic state in conscious dogs and in patients with heart failure.

The purpose of this study was to examine the time course of the changes in left ventricular inotropic state after intravenous pimobendan administration. In conscious dogs, cumulative doses of 1 and 2.5 mg of pimobendan significantly increased heart rate and the isovolumic indices of inotropic state and relaxation. The maximal effect, however, required 2 h to be present. The changes in cardiac index and capillary wedge pressure after the intravenous administration of 5 mg to patients with heart failure confirmed this slightly delayed action of pimobendan. Accordingly, the effects of pimobendan on left ventricular inotropic state in patients with moderate to severe heart failure were determined during cardiac catheterization 130-150 min after injection of 5 (n = 3) or 2.5 (n = 4) mg. After drug administration, heart rate increased slightly (+7 beats/min; NS) while left ventricular end-diastolic and systolic pressure both decreased significantly (from 22.7 to 9.2 mm Hg, p less than 0.007 and from 123 to 90 mm Hg, p less than 0.025, respectively). The isovolumic index of contractility (dP/dt)/DP40 increased by 19.6 +/- 14.7% (p less than 0.02) and the slope of the late systolic stress-volume relationship improved by 48% (p less than 0.05). It is concluded that pimobendan is a positive inotropic agent in the failing human heart as well as a powerful veno- and arteriodilator.

Animals↗

PubMed1988

Changes in coronary blood flow and myocardial metabolism during aortic balloon valvuloplasty.

The effects of balloon inflation on myocardial perfusion and metabolism were studied during aortic valvuloplasty in 17 patients with aortic stenosis, including 6 with associated coronary artery disease. Coronary sinus flow and blood samples were obtained before and during the first inflation, and 5 to 10 minutes after the last inflation. During inflation, coronary blood flow decreased (272 +/- 111 standard deviation to 166 +/- 92 ml/min; p less than 0.05), myocardial oxygen uptake fell and transcardiac lactate handling shifted from extraction to production (35 +/- 54 to -41 +/- 48 mumol/min; p less than 0.01). At the end of the procedure, aortic valve area had increased from 0.51 +/- 0.22 to 0.81 +/- 0.48 cm2 (p less than 0.002). Coronary sinus flow increased slightly above control values (+6%; difference not significant) and myocardial oxygen and lactate uptakes were back to control values. However, myocardial alanine production had increased from -3.6 to -6.6 mumol/min (p less than 0.05) and glutamine production was reduced or replaced by extraction (-3.3 +/- 2.1 to 3.5 +/- 3.8 mumol/min; p less than 0.05). Recovery of coronary flow, oxygen and lactate uptakes was not significantly different in patients with or without coronary artery disease, although the former patients tended to have less glutamine extraction and less improvement in their ejection fraction at the end of the procedure. Thus, aortic balloon valvuloplasty produces brief episodes of low-flow ischemia. Recovery of oxidative metabolism is almost immediate after deflation and no detrimental effect seems to persist at the end of the procedure.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1988

Effects of long-term combined dosing with nicardipine and propranolol on coronary hemodynamics, myocardial metabolism, and exercise tolerance in patients with angina pectoris: comparison with monotherapy.

To determine whether the association of nicardipine with propranolol had additive effects on myocardial metabolism, 16 patients with angina pectoris were studied invasively before and after 1 month of therapy with a combination of nicardipine and propranolol and compared to a group of 42 patients treated with nicardipine (n = 17) or propranolol (n = 25) alone. When data were compared at a fixed heart rate (atrial pacing), mean blood pressure was reduced with combined treatment from 96 +/- 19 to 76 +/- 13 mm Hg (p less than 0.003). Myocardial oxygen uptake and coronary sinus flow decreased significantly from 20 +/- 9 to 14 +/- 6 ml/min (p less than 0.015) and from 152 to 111 ml/min (p less than 0.05), respectively. The arterio-coronary sinus difference in oxygen content also decreased (13.3 to 12.5 ml/dl; p less than 0.0025), suggesting an improved balance between oxygen supply and demand. Such changes in coronary blood flow and myocardial oxygen uptake were not observed in the group of patients assigned to monotherapy. Lactate uptake rose and the abnormal glutamine production, which worsened with propranolol monotherapy, improved with nicardipine and propranolol (-2.0 to -1.4 mumol/min; p less than 0.05 vs propranolol). The superiority of nicardipine and propranolol over propranolol monotherapy was maintained during a pacing stress test. Thus the combination of nicardipine with a beta blocker had greater oxygen-sparing effects and restored aerobic metabolism better than either drug alone, allowing optimal use of the coronary reserve.

Adult↗

PubMed1988

Effects of intracoronary infusion of nicardipine during silent ischaemia on myocardial metabolism and function.

The effects of an intracoronary infusion of nicardipine (0.2 mg over 10 min) on myocardial substrate uptake and function were studied in 16 patients with coronary artery disease and angina pectoris. Silent ischaemia, demonstrated by myocardial lactate production, was induced twice by pacing below anginal threshold. Nicardipine or saline was randomly infused during the first or second pacing. During pacing with nicardipine, no systemic effect was noted but coronary sinus flow increased (+ 18%; P less than 0.015) and myocardial oxygen uptake decreased by 12% (P less than 0.025). Transcardiac lactate production did not improve (-8 to -10 mumol min-1; NS) but net lactate uptake, estimated from radiolabelled lactate uptake, tended to rise and the glutamine uptake increased from 1.8 to 5.5 mumol min-1 (P less than 0.04). During recovery after pacing, lactate production decreased faster and LV peak (+) dP/dt and relaxation rate were significantly better after nicardipine infusion than after saline. Thus, during silent ischaemia induced by an increased oxygen demand, intracoronary nicardipine did not prevent lactate release but allowed a faster metabolic and functional recovery. These beneficial effects of nicardipine could be explained by an improved myocardial perfusion or by an effect on intracellular calcium homeostasis.

Adult↗

PubMed1988

Non-invasive data provide independent prognostic information in patients with chest pain without previous myocardial infarction: findings in male patients who have had cardiac catheterization.

From 1978 to 1985, 470 consecutive male patients with complaints of chest pain underwent a maximal exercise test with a thallium scan and coronary angiography (CA). Patients with a history of myocardial infarction (MI) were excluded. During the follow-up (from 12 to 96 months), 32 patients died and 30 had a non-fatal MI. Survival (SR) and event-free rates (EFR) were estimated by actuarial methods; the influence of non-invasive and invasive variables were examined in univariate and multivariate models using Cox analysis. The five-year SR was 89% and EFR was 81%. Among historical data, age (less than 0.001), type of complaints (less than 0.01) and pretest likelihood of CAD (less than 0.01) were univariate predictors of EFR; by multivariate analysis, age was the only significant predictor (less than 0.001). Most of the maximal-exercise (MEX) test data were good univariate predictors; by multivariate analysis, workload (less than 0.001) and the maximal-exercise test score (less than 0.001) were the significant predictors. From history and maximal-exercise test data, multivariate analysis indicated that the prognostic information was given by age (less than 0.05) and maximal-exercise test score (less than 0.001). Among the invasive data, the number of diseased vessels (less than 0.001) and ejection fraction were the predictors. The combination of invasive and non-invasive data indicated that age, MEX score, number of diseased vessels and ejection fraction contributed significantly and independently to the estimation of prognosis. Among 242 patients with two or three diseased vessels, the prognosis was determined by the maximal workload (less than 0.01); ejection fraction (less than 0.07) was no longer significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1988

Effects of asynchrony on myocardial relaxation at rest and during exercise in conscious dogs.

The effect of left ventricular asynchrony induced by right ventricular pacing on relaxation indexes was studied at rest and during exercise in seven conscious dogs instrumented for chronic measurements of left ventricular pressure, coronary blood flow, and arterial pressure and with right atrial and ventricular pacing electrodes. Increasing heart rate with atrial pacing resulted in an increase in both left ventricular maximum and minimum rates of pressure development, LV dP/dtmax and LV dP/dtmin, respectively, as well as in a decrease in the relaxation constant T. In contrast, increasing heart rate with ventricular pacing resulted in a decrease in LV dP/dtmax, a small increase in LV dP/dtmin, and a significant decrease in T. During exercise with heart rate kept constant with atrial pacing, both LV dP/dtmax and LV dP/dtmin increased and T decreased to the same extent as during exercise in sinus rhythm. In contrast, exercising during right ventricular pacing resulted in a significant increase in T, expressing a slowing of relaxation. It is concluded that increasing heart rate alone in the presence of asynchrony of LV contraction induced by abnormal electrical activation results in a depressed contractile response, while the relaxation phase is not significantly affected. However, during sympathetic stimulation, a condition where synchronization should be improved, the relaxation phase is considerably lengthened.

Adaptation, Physiological↗

PubMed1988

Long-term effects of xamoterol on left ventricular diastolic function and late remodeling: a study in patients with anterior myocardial infarction and single-vessel disease.

The purpose of the study was to examine whether the prolonged administration of the beta 1-adrenoceptor partial agonist xamoterol could improve left ventricular diastolic function and affect the global remodeling process of the left ventricle after anterior myocardial infarction. In 22 patients with anterior myocardial infarction and single-vessel disease, left ventricular angiography (+ Millar) was performed under basal conditions 1 to 2 months after the acute myocardial infarction. Eight patients were then treated for 3 months with placebo and 14 were treated with xamoterol (200 mg bid) and a second left ventricular angiographic study was performed. Angiograms were digitized frame by frame to derive the diastolic pressure-volume relationship and to compute wall stress. An index of elastic myocardial stiffness was computed at a constant stress of 30 kdynes/cm2 before and after treatment. To evaluate changes in left ventricular shape, segmental areas in anterior and inferior segments were computed and compared at end-diastole and end-systole. After xamoterol, left ventricular end-diastolic pressure and mean diastolic wall stress decreased (from 24 +/- 5 to 15 +/- 5 mm Hg and from 57 +/- 32 to 38 +/- 22 kdynes/cm2, respectively; both p less than .01 vs baseline and vs placebo). These changes were accompanied by a downward shift in the diastolic pressure-volume relationship and by a decrease in the index of myocardial stiffness from 526 +/- 270 to 371 +/- 194 kdynes/cm2 (p less than .02).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗

PubMed1987

Myocardial protection by intracoronary nicardipine administration during percutaneous transluminal coronary angioplasty.

To determine if the calcium antagonist nicardipine protects the myocardium against ischemia, myocardial lactate, hypoxanthine and prostanoid function was studied in 12 patients during percutaneous transluminal coronary angioplasty (PTCA). Values were obtained before balloon inflation and during 4 minutes after deflation. Intracoronary injection of 0.2 mg of nicardipine distal to the stenosis was done randomly before the first or second inflation; the other inflation served as a control. One minute after deflation, coronary sinus flow levels were similar during the nicardipine and control procedure (161 +/- 61 vs 159 +/- 72 ml/min); lactate (-9 +/- 21% vs -17 +/- 21%, p less than 0.025) and hypoxanthine production (-107 +/- 85% vs -218 +/- 153%, p less than 0.05) were less severe after nicardipine pretreatment than after control. All patients reverted to lactate extraction 4 minutes after inflation plus nicardipine infusion, whereas lactate was still produced 4 minutes after control inflation. No significant changes in thromboxane B2 or prostacyclin levels were observed in the coronary sinus 1 minute after inflation, but higher arterial thromboxane B2 values were observed after control inflation than after inflation with nicardipine infusion (median values 169 vs 78 pg/ml, p less than 0.05). In conclusion, intracoronary infusion of nicardipine reduced signs of ischemia and alterations in prostanoid handling after coronary occlusion. The mechanisms of myocardial protection appeared unrelated to coronary sinus blood flow changes or to a systemic effect of nicardipine.

Angina Pectoris↗