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Biomedical subjects

C van Eyll

Publications and source records attributed to C van Eyll.

At least 19 recordsLinked to original sources
PubMed2001

Cardiac and hemodynamic effects of intravenous dofetilide in patients with heart failure.

This study assesses the effects of dofetilide, a new selective Ikr blocker with class III properties, on left ventricular function and hemodynamics of heart failure and compares these effects with those of placebo and amiodarone. Because available antiarrhythmic drugs may depress myocardial performance, an invasive hemodynamic study was performed to assess the safety of this agent. Hemodynamic and angiographic data were obtained at baseline and after 30 minutes of double-blind infusion of dofetilide (8 microg/kg; n = 12), placebo (n = 12), or amiodarone (5 mg/kg; n = 6) in heart failure patients (New York Heart Association class II or III, ejection fraction <35%). Intravenous dofetilide preserved the inotropic indexes and the end-systolic volume index despite a slight but significant decrease in heart rate, whereas intravenous amiodarone increased end-diastolic and end-systolic volume indexes. Amiodarone induced a negative inotropic effect illustrated by a rightward shift of the pressure-volume loop and a reduction in pressure-derived indexes of contractility. Intravenous dofetilide acutely prolonged QT interval more than intravenous amiodarone; however, dofetilide did not slow the overall relaxation rate and reduced QT dispersion. In an acute setting, compared with intravenous amiodarone, intravenous dofetilide preserves cardiac function offering a hemodynamic advantage to treat arrhythmias in patients with impaired left ventricular function.

Adult↗
PubMed1997

Dose-related hemodynamic and electrocardiographic effects of the calcium promoter BAY y 5959 in the presence or absence of congestive heart failure.

OBJECTIVES: The aim of this study was to assess the cardiovascular effects of BAY y 5959, a calcium promoter modulating myocardial calcium channels, in the presence or absence of congestive heart failure. BACKGROUND: There is still a clinical need for short-term administration of intravenous positive inotropes. BAY y 5959 was developed as a new approach to increase myocardial performance by selectively enhancing calcium influx in the myocytes. METHODS: Forty-one patients (21 without and 20 with congestive heart failure) were studied in an open label, dose-ranging study. Hemodynamic variables (including left ventricular [LV] angiography) and plasma samples were obtained at baseline and after 20 min of intravenous infusion of BAY y 5959 at doses ranging from 0.25 to 4.5 microg/kg body weight per min. RESULTS: In both study groups, BAY y 5959 produced dose-dependent increases in the indexes of inotropic state, without affecting isovolumetric relaxation rate. The magnitude of the response was comparable in patients with or without heart failure (average 38% increase in maximal first derivative of LV pressure [dP/dt max] at plasma levels of 100 microg/liter). BAY y 5959 also induced mild but statistically significant bradycardia and significantly decreased end-systolic volume while producing a leftward shift of the pressure-volume loop. Mean aortic pressure was unaffected at doses up to 3.0 microg/kg per min, and cardiac index improved in patients with heart failure at doses of 2.0 microg/kg per min (+23%, p < 0.05). However, at a dose of 4.5 microg/kg per min, mean aortic pressure and LV systolic wall stress increased, suggesting systemic vasoconstriction. The QT interval was also prolonged significantly at most doses. CONCLUSIONS: BAY y 5959 exhibits positive inotropic effects in patients with and without heart failure. The optimal response--combining bradycardia, reduced preload and improved cardiac output--appeared to be achieved at a dose of approximately 2.0 microg/kg per min. The impact of QT prolongation with regard to potential antiarrhythmic or proarrhythmic effects is unclear at this time.

Calcium Channel Agonists↗
PubMed1996

Hemodynamic and cardiac effects of the selective T-type and L-type calcium channel blocking agent mibefradil in patients with varying degrees of left ventricular systolic dysfunction.

OBJECTIVES: This study sought to assess the hemodynamic and cardiac effects of two dose levels of mibefradil in patients with varying degrees of ischemic left ventricular dysfunction. BACKGROUND: Mibefradil is a new, selective T-type and L-type calcium channel blocking agent. Because L-type channel blockade may depress myocardial performance, an invasive hemodynamic study was performed to assess the safety of this agent. METHODS: We performed an open label study, examining the effects of two intravenous doses of mibefradil, selected to produce plasma levels comparable to those measured after oral administration of 50 mg (dose 1: 400 ng/ml) or 100 mg (dose 2: 800 ng/ml) of the drug. Variables studied included the indexes of left ventricular function and neurohormone levels. Patients were stratified according to ejection fraction (EF) (> or = 40%, n = 26; < 40%, n = 24) and the presence (n = 15) or absence (n = 35) of heart failure. RESULTS: In patients with preserved systolic function, dose 1 had no clinically significant hemodynamic effects, but dose 2 decreased mean aortic pressure and systemic vascular resistance (-8.5 mm Hg, -12%, both p < 0.01) and also reduced end-systolic stress and volume, thus improving EF (52% to 58%, p < 0.01). Heart rate tended to decrease. In patients with depressed EF, heart rate decreased significantly with both doses. The effects of dose 1 mimicked those observed after dose 2 in patients with preserved EF. Dose 2 (plasma levels 1,052 +/- 284 ng/ml) still decreased left ventricular systolic wall stress and improved EF (24.0% to 28.5%, p < 0.05) but also significantly depressed the maximal first derivative of left ventricular pressure. Examination of individual pressure-volume loops in two patients with heart failure showed a clear rightward shift of the loop despite a decrease in systolic pressure, suggesting negative inotropy. Neurohormone levels were unchanged at both dose levels and in all subgroups. CONCLUSIONS: Intravenous mibefradil was well tolerated and produced an overall favorable cardiovascular response. However, high plasma concentrations might produce myocardial depression in patients with heart failure, and caution should be exerted in this setting.

Adult↗
PubMed1995

Contractile state is the major determinant of functional outcome in patients with left ventricular dysfunction treated with enalapril.

Large-scale drug trials have focused primarily on mortality and morbidity and less on the functional state of the myocardium. A model was developed to assess myocardial contractile state in patients with left ventricular (LV) dysfunction and to address the questions of differences in function between patients with and without overt heart failure, effects of enalapril, and best predictors of functional outcome. Pressure-angiographic data were obtained from 16 patients with overt heart failure and 47 without heart failure. Repeat studies were conducted in 41 patients following 1 year's treatment with enalapril or placebo. Left ventricular silhouettes were divided into 18 segments to estimate regional ejection fraction, wall stress and myocardial damage (% myocardial damage). Contractile state was assessed and ranked by ejection rate-preload-afterload relationships and by a score method based on 10 myocardial and ventricular function parameters. End-diastolic and end-systolic volumes (EDV, ESV) were significantly greater (P < 0.001), ejection fraction (EF) lower (P < 0.009), % myocardial damage greater (P < 0.008) and contractile state more depressed in patients with overt heart failure. Changes in EDV and ESV (delta placebo vs delta enalapril) were significant (delta EDV, P < 0.003; delta ESV, P < 0.014). Directional shifts in the diastolic pressure-volume relationships with enalapril or placebo depended primarily on the basal contractile state and diastolic volume range. The best single predictors of post-treatment EF were the score index (a surrogate parameter for the contractile state) and ESV. Added benefits of enalapril include the prevention of further dilatation in patients with less depressed contractile state and delay in the onset of heart failure. Asymptomatic patients with LV dysfunction should also be considered for angiotensin converting enzyme (ACE) inhibitor therapy.

Blood Pressure↗
PubMed1994

Effects of ranolazine on left ventricular regional diastolic function in patients with ischemic heart disease.

To assess the effects of ranolazine, a new antiischemic drug, on regional myocardium of the left ventricle, left ventricular (LV) hemodynamic and angiographic data were obtained in 15 patients with previous transmural myocardial infarction before and after intravenous infusion of ranolazine (200 or 500 micrograms/kg body weight). LV angiogram was analyzed by the area method and was divided into six segments. Regional LV segments were classified as normal (perfused by intact coronary vessels, n = 20), ischemic (perfused by stenotic vessels but without ECG evidence suggesting myocardial necrosis, n = 25), or infarcted (total coronary occlusion and with the ECG evidence for necrosis, n = 45). Regional area fractional shortening, peak filling rate, and segmental wall motion during isovolumic relaxation period were analyzed. After ranolazine, regional area fractional shortening was unchanged in all segments. However, regional peak filling rate was decreased in the normal segments (1499 +/- 315 to 1368 +/- 303 mm2/sec, p < 0.05). In the ischemic segments, by contrast, the administration of ranolazine significantly increased the regional peak filling rate (1050 +/- 410 to 1133 +/- 439 mm/sec, p < 0.05) and regional wall lengthening during the isovolumic relaxation period (0.9 +/- 4.1% to 2.8 +/- 5.7% of end-diastolic segmental area, p < 0.05), which indicates an improvement of regional diastolic function. Infarct segments were little affected by ranolazine. Thus, ranolazine improves diastolic function of the noninfarcted myocardium under chronic ischemic conditions and also may exert a mild negative lusitropic effect on the normal myocardium, although the former beneficial effect appears to be more clinically important.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetanilides↗
PubMed1993

Effects of D-nebivolol and L-nebivolol on left ventricular systolic and diastolic function: comparison with D-L-nebivolol and atenolol.

(D-L) Nebivolol is a new beta 1-selective adrenoceptor blocker which in normal individuals preserves rest and exercise hemodynamics. We assessed the effects of the enantiomers (L- and D-nebivolol) on left ventricular (LV) systolic and diastolic function and compared their effects with those of the racemic mixture. LV angiography (+Millar) was performed before and after intravenous (i.v.) infusion of either D- or L-nebivolol (1.25-2.5 mg, n = 22) in patients with ischemic heart disease and previous myocardial infarction. Neither L- nor D-nebivolol produced significant changes in heart rate (HR), peak (+) dP/dt, (dP/dt) DP40, cardiac index (CI) or ejection fraction (EF). Diastolic distensibility, evaluated from the shift of the pressure-volume data at the time of mitral valve opening, did not improve after D- or L-enantiomers administration. In contrast, both D-L-nebivolol 2.5 mg (n = 9) and atenolol 15 mg (n = 9) significantly reduced HR and peak (+) dP/dt, but in comparison to atenolol D-L nebivolol improved EF (+4% after D-L nebivolol vs. -4% after atenolol; p < 0.05 D-L nebivolol vs. atenolol) and maintained cardiac output CO, (+2% vs. -21%; p < 0.05 between groups). Moreover, unlike any of the other drugs in the study, the racemate shifted the diastolic pressure-volume data downward, suggesting improved LV distensibility. The beneficial effects of nebivolol on LV systolic and diastolic function appears to require the presence of both D- and L-enantiomers.

Adrenergic beta-Antagonists↗
PubMed1993

Effects of long-term enalapril therapy on left ventricular diastolic properties in patients with depressed ejection fraction. SOLVD Investigators.

BACKGROUND: The aim of the present study was to analyze the changes in left ventricular diastolic function that occur in patients with chronic severe left ventricular systolic dysfunction in the absence or presence of prolonged therapy with an angiotensin converting enzyme inhibitor. METHODS AND RESULTS: Left ventricular function data (cineangiography plus Millar, frame-by-frame analysis) and right ventricular volumes (radionuclide angiography) were obtained at baseline and after an average follow-up of 12.4 months in 42 patients with a left ventricular ejection fraction of 35% or less. After baseline measurements, the patients were randomized to placebo (n = 16) or enalapril (10 mg BID, n = 26). In the placebo group, the changes in left ventricular function were characterized by increases in end-diastolic (159 +/- 43 to 170 +/- 44 mL/m2) and end-systolic (119 +/- 38 to 128 +/- 49 mL/m2) volumes accompanied by a downward and rightward shift of the diastolic pressure-volume relation. In contrast, decreases in end-diastolic (166 +/- 43 to 156 +/- 47 mL/m2) and end-systolic (125 +/- 43 to 111 +/- 42 mL/m2) volumes accompanied by a slight upward and leftward shift of the diastolic pressure-volume relation were noted in the enalapril group. These changes in left ventricular volumes were significantly different between groups (both P < .005) but were not attended by changes in left ventricular end-diastolic pressure, in time constant of isovolumic pressure decrease, or in right ventricular volumes. However, the chamber stiffness constant beta decreased from 0.044 +/- 0.027 to 0.032 +/- 0.019 mL-1/m2 in the placebo group, whereas it increased insignificantly in the enalapril group (0.040 +/- 0.028 to 0.041 +/- 0.028 mL-1/m2). These changes in chamber stiffness constant beta between baseline and follow-up were significantly different between placebo and enalapril groups (P < .05). Another index of chamber compliance, delta V/delta P, also confirmed the presence of opposite changes in left ventricular chamber compliance in the placebo group and in the enalapril group. The mean diastolic wall stress increased with placebo but not with enalapril (+51 versus -13 kdyn/cm2; P < .04) whereas left ventricular mass and the indexes of left ventricular sphericity tended to improve in the enalapril group. The changes in plasma levels of norepinephrine, atrial natriuretic peptide, and arginine vasopressin were, however, comparable in both groups. CONCLUSIONS: The data indicate that in patients with severe systolic left ventricular dysfunction, the progressive left ventricular dilatation was accompanied by a decrease in left ventricular chamber stiffness; enalapril therapy was able to prevent or partially reverse these changes and tended to reduce left ventricular mass and ventricular sphericity. Those changes were suggestive of partial reversal of left ventricular remodeling by enalapril administration.

Adult↗
PubMed1993

Cardiac mechanics during development of heart failure. SOLVD Investigators.

BACKGROUND: The changes in myocardial performance responsible for the progression from a stage of asymptomatic left ventricular dysfunction toward overt congestive heart failure are still poorly understood. Accordingly, using invasive methods, we examined the differences in baseline left ventricular function between a subgroup of patients enrolled in the treatment arm (presence of congestive heart failure) and in the prevention arm (asymptomatic patients) of the Studies of Left Ventricular Dysfunction. METHODS AND RESULTS: High-fidelity left ventricular pressures and frame-by-frame angiographic volumes were simultaneously obtained under baseline conditions in 65 patients with left ventricular ejection fraction < or = 35%. Sixteen patients had New York Heart Association congestive heart failure (class II or III), whereas the remaining 49 patients had no clinical signs of heart failure and did not receive therapy for this syndrome. A second set of data was obtained an average of 12.4 months later in 42 patients. The group with heart failure had significantly greater end-diastolic and end-systolic volumes than the asymptomatic group (both p < 0.001), but the stroke index at rest was similar in both groups. Accordingly, ejection fraction was significantly lower in the heart failure group (19.6 +/- 7.0% versus 26.3 +/- 7.2%; p < 0.02). Left ventricular end-diastolic pressure was greater and peak +dP/dt was lower in heart failure patients, but the difference did not reach statistical significance after Bonferroni correction for multiple comparisons. Moreover, the individual end-systolic stress/end-systolic volume data of the heart failure patients fell within the 95% confidence interval of the relation observed in the patients without heart failure both at baseline and after 1 year of follow-up irrespective of their changes in functional status. It was also noted that during follow-up, the changes in end-diastolic and end-systolic volumes correlated linearly, as if both dimensions always shifted in parallel, whereas alterations in contractility primarily influence end-systolic volume. CONCLUSIONS: These observations are compatible with the hypothesis that a depression in the mechanical performance of the viable myocardial areas is not the major determinant for the progression from asymptomatic to symptomatic left ventricular dysfunction. Abnormalities in left ventricular diastolic distensibility, on the other hand, might underlie the progressive ventricular dilation and create a vicious cycle through the afterload mismatch.

Adult↗
PubMed1992

Analysis of the mechanisms underlying the changes in left ventricular filling dynamics during oral nisoldipine therapy in patients with anterior myocardial infarction.

The aim of this study was to clarify the mechanisms responsible for the increase in early filling rate observed during oral nisoldipine therapy in patients with ischaemic left ventricular (LV) dysfunction. For that purpose, the global and regional LV function was analysed before and after 2 months of double-blind monotherapy with nisoldipine (10 mg twice daily) or a placebo, in 17 patients with a previous anterior myocardial infarction. The baseline LV ejection fraction ranged from 34-51% and no patient had heart failure. Compared to the placebo, nisoldipine significantly lowered LV systolic pressure and end-diastolic pressure (-3 mmHg vs +6 with the placebo; P less than 0.01) and the LV pressure at the time of mitral opening (-2.0 +/- 3.4 mmHg vs +3.5 +/- 3.0; P less than 0.01). Despite this reduction in driving pressure, the global LV early peak filling rate improved with nisoldipine only and this improvement was related to a selective increase in expansion rate of the anterior areas, from 1010 +/- 360 to 1339 +/- 496 mm2.s-1 (P less than 0.001). The time to regional peak filling rate (-8%; P less than 0.01), the asynchrony of diastolic wall motion and the regional ejection fraction (33 +/- 10 to 38 +/- 12%; P less than 0.001) also improved in the anterior areas with nisoldipine but not with the placebo. In contrast, in the inferior, control zones, the regional ejection fraction and filling rate remained unchanged, both when compared to baseline and to the placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Effects of intravenous epinine administration on left ventricular systolic performance, coronary hemodynamics, and circulating catecholamines in patients with heart failure.

Twenty-six patients with mild to moderate heart failure were studied to determine the effects of epinine infusion (at a rate producing plasma levels similar to those measured after oral administration of 100 mg of the prodrug ibopamine) on left ventricular (LV) function (14 patients), and coronary flow and circulating catecholamines (12 patients). The only significant hemodynamic change at an infusion rate of 0.5 microgram/kg/min was a 9% (p less than 0.05) decrease in systemic vascular resistance (SVR). At an infusion rate of 1 microgram/kg/min (mean free epinine plasma levels 14.3 +/- 3.7 ng/ml), heart rate (HR), dP/dtmax (1,405 +/- 255 to 1,490 +/- 320 mm Hg, NS), (dP/dt)/DP40, and the relaxation rate remained unchanged, but the ejection fraction (EF) increased from 32 to 38% (p less than 0.001), cardiac output (CO) increased, and SVR decreased by 22% (p less than 0.05). In a separate group of 12 patients, epinine infusion at rates of 0.5-1 microgram/kg/min produced no significant changes in coronary blood flow or myocardial oxygen uptake. At these infusion rates, arterial norepinephrine (NE) and dopamine (DA) levels decreased slightly and arterial and coronary sinus epinephrine increased. In conclusion, epinine, at concentrations similar to those achieved during therapeutic use of ibopamine, had negligible effect on myocardial contractility and relaxation rate in heart failure patients. Cardiac pump function was improved by a decrease in SVR rather than by inotropic stimulation. The data also suggest that these low concentrations of epinine may modulate the sympathetic nervous system, but further studies are needed to determine whether this effect could have clinical significance.

Adult↗
PubMed1992

Effects of prolonged nisoldipine administration on the "hibernating" myocardium.

To assess the effects of nisoldipine on chronically underperfused myocardial areas ("hibernating myocardium"), the global and regional left ventricular (LV) function was analyzed before and after 2 months of double-blind monotherapy with nisoldipine (10 mg twice daily) or placebo in 17 patients with a previous anterior myocardial infarction. The baseline LV ejection fraction ranged from 34 to 51%, and no patient had heart failure. Compared to placebo, nisoldipine significantly lowered the LV systolic pressure and end-diastolic pressure (-3 vs. +6 mmHg with placebo; p < 0.01) and the LV pressure at the time of mitral valve opening (-2.0 +/- 3.4 vs. +3.5 +/- 3.0 mm Hg; p < 0.01). Despite this reduction in driving pressure, the global LV early peak filling rate improved only with nisoldipine and this improvement was related to a selective increase in the expansion rate of the anterior areas, from 1,010 +/- 360 to 1,339 +/- 496 mm2/s (p < 0.001). The time to regional peak filling rate (-8%; p < 0.01), the asynchrony of diastolic wall motion, and the regional ejection fraction (33 +/- 10 to 38 +/- 12%; p < 0.001) also improved in the anterior areas with nisoldipine but not with placebo. In contrast, in the inferior control zones, the regional ejection fraction and filling rate remained unchanged, both when compared to baseline and to placebo. In conclusion, prolonged nisoldipine therapy had no significant effect on the normal myocardium but improved systolic and diastolic function in hypokinetic areas.(ABSTRACT TRUNCATED AT 250 WORDS)

Double-Blind Method↗
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↗
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↗
PubMed1986

Impaired regional diastolic distensibility in coronary artery disease: relations with dynamic left ventricular compliance.

The regional left ventricular distensibility and its relations with the dynamic left ventricular chamber compliance were studied in 11 normal subjects and in 30 patients with coronary artery disease. The regional peak filling rates were calculated from angiographic data in eight ventricular segments and used as an index of regional distensibility. A depressed global peak filling rate was observed in only 30% of the patients with angina pectoris, but regional abnormalities in peak filling rate were detected in 75% of these patients. A relation between alterations in regional peak filling rate and left ventricular compliance was evident in these patients. Despite comparable end diastolic volume and pressure (10 +/- 2 mm Hg vs. 10 +/- 3 in normal subjects; not significant), the patients with angina pectoris, whose ventricle had at least three segments with a reduced peak filling rate, had indeed significant increases in mean left ventricular filling pressure (14 +/- 4 mm Hg vs. 8 +/- 3 in normal subjects; p less than 0.01) and upward shifts of their left ventricular pressure-volume relation during rapid filling. Conversely, an increase in regional peak filling rate produced by intravenous administration of the calcium antagonist nicardipine in a subgroup of patients with poor diastolic function was accompanied by a reduction in mean left ventricular filling pressure and by a downward shift of the early diastolic left ventricular pressure-volume relation. It is concluded that even in the absence of clinical signs of ischemia and of a previous myocardial infarction, large areas with impaired distensibility are frequently present in patients with angina pectoris.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗