Biomedical subjects

M Schlepper

Publications and source records attributed to M Schlepper.

At least 19 recordsLinked to original sources

PubMed1992

Proof for piroximone's inotropic influence; can it safely be used in coronary artery disease? Analysis of end-systolic pressure-volume relations (conductance technique).

Improved contractility after applying piroximone (PIR) a new phosphodiesterase III inhibitor drug, is difficult to prove clinically. However, augmented contractility could increase the risk of myocardial ischemia when used in coronary artery disease (CAD). Analysis of the end-systolic pressure-volume relationship (ESPVR) as a load-independent parameter of the contractile left ventricular (LV) function allows for differentiation of PIR's effects: contractility vs. unloading. We therefore analyzed ESPVR and LV function in 16 CAD patients before and after PIR, 0.75 mg/kg intravenously. Emax increased by 39% (9/16 patients) and loops of the ESPVR (16 patients) moved leftward, indicating improved contractility. The difference in percent change PIR versus control (16 patients) demonstrated augmentation of LV function via unloading: LV volumes decreased (ESV by 37%, EDV by 19%), LV-filling pressure by 34%, and systemic vascular resistance by 19%; dP/dtmax increased by 28%, LV efficiency by 24%, cardiac index by 21%, and ejection fraction by 13%. Pacing-induced anginal threshold increased by 47% after PIR while the ischemic postpacing LV-filling pressure and ST-segment changes tended to normalize under the drug's influence. Thus, PIR improved LV function both by unloading and by positive inotropy. Lack of PIR-induced angina and an increased anginal threshold indicate that the drug can be used safely in CAD patients as well. The analysis of ESPVR proved to be safe and reliable in identifying contractility during the diagnostic cardiac catheterization routine.

Aged↗

PubMed1992

[Decreased fibrinolytic capacity in coronary patients by increased plasminogen activator inhibitor activity].

The fibrinolytic capacity of the blood mainly depends on the amount of tissue-plasminogen activator (t-PA) antigen and plasminogen activator inhibitor (PAI). In this study the fibrinolytic response to a venous occlusion test (VOT) was measured in 109 patients with angiographically documented coronary artery disease (CAD) and in 20 healthy volunteers at comparable age (controls). CAD-patients had higher plasma plasminogen activator inhibitor capacity before (24.4 +/- 11.0 vs. 15.4 +/- 5.2 arbitrary units [AU/ml]; p less than 0.0002) and after VOT (19.6 +/- 13.2 vs. 10.9 +/- 5.3 AU/ml; p less than 0.0001) compared with controls. Furthermore they showed significant lower plasma t-PA activity after VOT (3.0 +/- 6.8 vs. 6.6 +/- 10.6 AU/ml; p less than 0.0001). However there were no difference between both groups in plasma t-PA antigen levels after VOT (17.3 +/- 12.1 vs. 18.7 +/- 14.4 ng/ml). In 10% of patients the decrease in fibrinolytic activity resulted from a lower t-PA release ("lower" was defined as mean minus one standard deviation of the control group). 40% showed elevated plasma PAI capacity before VOT ("elevated" was defined as mean plus two standard deviations of the control group). Both caused significantly reduced post occlusion plasma t-PA activity and prolonged Euglobulin clot lysis time (p less than 0.003). A positive correlation was found between PAI capacity and serum triglyceride levels. Reduced fibrinolytic activity in 109 patients with coronary heart disease based either on a decrease in t-PA antigen release or a increased in PAI capacity in comparison with healthy controls. The mechanism of these findings is not yet well-known.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1991

[Nifedipine-clonidine combination in essential hypertension. Hemodynamic and neurohumoral findings of the combination in comparison with the effect of the individual substances].

In 10 patients with moderate essential hypertension, the neurohumoral and hemodynamic effects of 4 days' treatment with 2 x 75 micrograms clonidine (C), 2 x 20 mg nifedipine retard (N), and a combination of the two (C/N) were studied and compared with baseline values. The heart rate decreased significantly from a mean of 79 to 67 bpm (p less than 0.05) under C, increased again to 73 bpm (p greater than 0.05) under N, and decreased once more to 68 bpm (p less than 0.05) under C/N. The systolic blood pressure decreased from a mean of 184 to 171 under C, 168 after N, and 161 (p less than 0.01) under C/N; significant decreases of diastolic blood pressure were also observed (from 113 to 104 under C, 107 under N, 100 mmHg under C/N (p less than 0.05). Norepinephrine decreased from 440 to 281 under C (p less than 0.01), increased to 391 (p greater than 0.05) after N, and measured 404 pg/ml (p less than 0.05) under C/N. PRA decreased significantly under C, increased under N, and remained unchanged under C/N. These findings demonstrate that combined treatment with lowdose nifedipine and clonidine leads to an additive reduction of blood pressure. The disadvantage of neurohumoral counterregulation of nifedipine are neutralized by clonidine.

Clonidine↗

PubMed1991

Left ventricular muscle mass and diastolic function in patients with essential hypertension under long-term clonidine monotherapy.

To determine whether alterations of left ventricular (LV) structure are associated with improved LV function under chronic clonidine monotherapy (300-450 g/day) of essential hypertension, 11 male patients (age range 47-61 years) were followed for 5.4 +/- 0.9 months using echocardiography and Doppler echocardiography. Blood pressure decreased from a mean of 168/105 to 150/96 mmHg (p less than 0.01), heart rate remained unchanged (73 +/- 10 vs. 71 +/- 10 beats/min). LV muscle mass decreased from 350 +/- 73 to 297 +/- 56 g (p less than 0.02), LV volume/muscle mass ratio increased from 0.58 +/- 0.13 to 0.69 +/- 0.12 ml/g (p less than 0.005). Ejection time increased from 276 +/- 17 to 296 +/- 17 ms (p less than 0.01), whereas no significant change was found for pre-ejection period, ejection fraction, cardiac index and LV dimensions. Doppler analysis revealed improved isovolumic relaxation time (116 +/- 17 vs. 84 +/- 28 ms; p less than 0.05), but no change in isovolumic contraction duration, maximal inflow velocities, time-velocity integrals and their duration, rate of acceleration and deceleration of early and atrial filling, and of their ratios. It is concluded that no reliable improvement in diastolic or systolic LV function is observed in chronic clonidine monotherapy of essential hypertension despite a normalization of blood pressure and a regression of LV hypertrophy.

Blood Flow Velocity↗

PubMed1991

Hemodynamic, anti-ischemic, and neurohumoral effects of slow-release isosorbide-5-mononitrate in patients with coronary artery disease after short- and long-term therapy.

In 20 patients with established coronary artery disease, stable angina pectoris and reproducible ST-segment depression, the pharmacokinetics and pharmacodynamic effects of 60 mg slow-release isosorbide-5-mononitrate (IS-5-MN) (10 patients) after a 7-day therapy were compared with those of a placebo group (10 patients) using a randomized double-blind, placebo-controlled study design. Ten patients could be controlled after long-term therapy over a mean of 399 +/- 111 days. There was no significant change under IS-5-MN of either blood pressure, heart rate, rate-pressure product, or myocardial oxygen consumption. Treatment over one week significantly reduced ST-segment depression 4 and 8 h after drug intake (38-48% of the placebo value, p less than 0.01). Maximum reduction in ST-segment depression was found 4 and 8 h after IS-5-MN intake both after one-week and long-term therapy at the time of peak plasma drug concentration (341 +/- 95 and 405 +/- 125 ng/ml, respectively). At a residual plasma concentration below 100 ng/ml, ST depression was not significantly improved 24 h after drug intake compared with placebo. Technetium-99m ventriculography showed an insignificant increase in ejection fraction and a slight reduction of ventricular volumes after both short- and long-term therapy with IS-5-MN (p greater than 0.05). The drug's plasma levels were higher under chronic than under short-term therapy which may be due to enzyme saturation. Maximum IS-5-MN plasma concentrations at a mean of 445 +/- 116 ng/ml were reached after 5.8 +/- 2.9 h. Beta-phase half-life of elimination was 9 +/- 3 h. IS-5-MN administered as a single 60 mg dose of a slow-release preparation/day proved to have a favorable pharmacokinetic profile as well as an efficient antiischemic activity after both short- and long-term therapy. Problems of tolerance or activation of hormonal counter-regulation due to vasodilation were not observed.

Adult↗

PubMed1991

Interactions of clonidine and nifedipine in moderately severe hypertensive patients.

In ten patients (age: 47-59 yr) with moderately severe essential hypertension, the humoral and hemodynamic effects of a 4-day therapy with 2 x 75 micrograms clonidine, 2 x 20 mg nifedipine (slow-release), and their combination were investigated and compared with baseline values. The following measurements were observed under clonidine (C), nifedipine (N), and on combination (C/N), respectively: heart rate fell significantly under C from a mean of 79 to 67/min (P less than .05), increased to 73/min after N (P greater than .05) and fell again to 68/min under combination (P less than .05). Systolic blood pressure (Riva-Rocci method) decreased from a mean of 184 to 171 (C), 168 (N) and 161 mm Hg (C/N), respectively (P less than .01). Diastolic blood pressure was also significantly altered (113 vs. 104 (C), 107 (N), and 100 mm Hg (C/N); P less than .05). Stroke volume (ECHO) was not altered significantly (77 vs. 71 (C), 79 (N), and 80 mL (C/N), respectively), whereas cardiac output dropped from 5.9 to 4.9 L/min (C; P less than .05), increased to 5.7 (N; P greater than .05), and dropped again to 5.3 L/min (C/N; P greater than .05). Peripheral vascular resistance increased from a mean of 2091 to 2297 (C), fell to 1933 (N), and increased again to 2138 dyn/sec/cm-5 (C/N). Plasma norepinephrine levels fell from 440 to 281 (C; P less than .01), increased to 391 (N; P greater than .05), and fell again to 404 pg/mL (C/N; P greater than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗

PubMed1991

Hemodynamic and neurohumoral effects of moxonidine in patients with essential hypertension.

The hemodynamic and neurohumoral effects of a single oral dose (0.4 mg) of the novel centrally acting antihypertensive agent moxonidine were investigated over 4 hours in ten patients with essential hypertension (WHO I-II). Pulmonary pressure indices and cardiac output were determined both at rest and during ergometric exercise by means of Swan-Ganz catheterization. Blood pressure was measured by sphygmomanometry and in the brachial artery. Moxonidine induced a significant fall in blood pressure over the 4-hour observation period from 176/105 mmHg to 158/95 mmHg (p less than 0.01), accompanied by a decrease in systemic vascular resistance from 1695 to 1427 dyn.sec/cm5 (p less than 0.01). Cardiac output remained unchanged, while heart rate increased slightly from 69 to 75 beats/min (p less than 0.01). No significant changes were recorded for either pulmonary artery pressure or pulmonary vascular resistance. Plasma levels of noradrenaline (337 vs. 224 pg/ml) and renin (2.6 vs 2.0 ng/ml/hr) activity fell significantly after moxonidine (p less than 0.05), both at rest and during exercise. Although aldosterone plasma levels fell slightly, level of angiotensin II and ANF remained unchanged. Moxonidine has favorable effects on hemodynamics and the neurohumoral system in patients with essential hypertension and is well tolerated at the dose administered.

Adult↗

PubMed1991

Antiischemic and hemodynamic effects of an oral single dose of 150 mg of the phosphodiesterase inhibitor enoximone in patients with coronary artery disease--relation to plasma concentration.

The hemodynamic and antiischemic effects of a 150-mg single oral dose of the PDE inhibitor enoximone were correlated with the plasma levels of enoximone and its sulfoxide metabolite. Twenty-one patients with angiographically documented coronary artery disease were investigated by exercise testing 1 and 2 hours after drug administration. The control group consisted of 15 patients with proven coronary artery disease and stable reproducible angina pectoris on exercise. The enoximone group included 14 responders with therapeutic plasma concentrations 2 hours after drug intake and significantly reduced mean pulmonary artery pressures on exercise (from 42.4 +/- 8.6 to 30.9 +/- 11.2 mmHg, p less than 0.05). Compared to basal exercise values, responders showed a reduced ST-segment depression by 1 hour after drug intake (2.1 +/- 1.2 vs. 1.3 +/- 3 mm, p less than 0.05) and minimal values after 2 hours (0.9 +/- 1.0 mm, p less than 0.01) at comparable workloads. There were no significant changes in heart rate, blood pressure, cardiac output, and systemic vascular resistance. No significant improvement in the hemodynamic parameters and ST-segment depression was found in nonresponders with plasma concentrations below 100 ng/ml and 500 mg/ml for enoximone and its metabolite, respectively. In summary, oral administration of enoximone in patients with coronary artery disease led to favorable acute hemodynamic and antiischemic effects at sufficiently high plasma levels of enoximone and its sulfoxide metabolite.

Administration, Oral↗

PubMed1991

The use of intravenous milrinone in chronic symptomatic ischemic heart disease.

To evaluate the antiischemic effects of intravenous milrinone, 20 patients with angiographically proved coronary artery disease and stable angina were studied at rest and during exercise under control conditions and after an intravenous loading injection of milrinone (50 micrograms/kg/10 min) followed by an infusion with 0.5 micrograms/kg/min. Hemodynamic parameters, epinephrine, norepinephrine, and atrial natriuretic factor were assessed. Control ergometry revealed ischemia; however, during exercise with intravenous milrinone, ischemia was eliminated. Because of unloading effects, there was also a significant decrease in ST segment depression (p less than 0.001). Heart rate increased significantly (p less than 0.001) at rest but increased significantly less after exercise testing (p less than 0.001). The changes in mean arterial pressure, cardiac output, and myocardial oxygen consumption during exercise were not significantly different between the milrinone and control phase. Intravenous milrinone delayed the onset of angina (p less than 0.001) and significantly shortened the duration of anginal attacks (p less than 0.05); exercise duration in the milrinone phase was longer than in the control phase (p = 0.051). Because of vasodilatation, a mild secondary increase in norepinephrine was observed during the milrinone phase, and there was a significantly smaller increase in atrial natriuretic factor during exercise while receiving milrinone as a result of preload reduction (p less than 0.05). Intravenous milrinone produced beneficial hemodynamic and antiischemic effects in patients with coronary artery disease, stable angina, and reproducible ST segment depression probably by enhancing myocardial contractility and reducing preload and afterload.

Aged↗

PubMed1991

Catecholamines and thrombocyte alpha 2-adrenoceptors in patients with acute myocardial infarction.

In 28 patients with first myocardial infarction plasma catecholamines and thrombocyte alpha 2-adrenoceptors were studied. The first determination (by HPLC and radioligand binding, respectively) was performed immediately after hospital admission and 6 weeks later. In the acute phase of myocardial infarction plasma adrenaline and noradrenaline levels were high. No significant differences in thrombocyte alpha 2-adrenoceptors and plasma concentrations of adrenaline and noradrenaline were observed between diabetic and non-diabetic patients. In three non-surviving patients only the affinity of the alpha 2-adrenoceptor to the radioligand was decreased (P less than 0.05), the relatively high catecholamine levels failed to reach statistical significance. Six weeks after hospital admission, adrenaline plasma levels were significantly decreased in diabetic and non-diabetic patients, while noradrenaline was only lowered in non-diabetic patients (P less than 0.05). Only in this group did the receptor number (BMAX) show a significant elevation 6 weeks after hospital admission. We conclude that, in acute myocardial infarction, alpha 2-adrenoceptors mainly interact with noradrenaline. Accordingly, no adrenoceptor alteration occurred in diabetic patients, who showed only a decrease in adrenaline but not in noradrenaline plasma concentrations 6 weeks following myocardial infarction. The different patterns in diabetic and non-diabetic patients suggest an alteration of catecholamine metabolism in diabetes mellitus.

Blood Platelets↗

PubMed1991

[Continuous enoximone infusion in patients with severe heart failure in dilated cardiomyopathy, hemodynamic, neurohumoral, chemical laboratory and clinical results].

UNLABELLED: The hemodynamic, clinical, and neurohumeral effects of a prolonged (6-days) intravenous enoximone-infusion therapy were evaluated in 12 patients suffering from severe cardiac failure due to dilated cardiomyopathy. The loading dose of enoximone was 1.5 mg/kg. The maintenance dose during the two phases of constant intravenous infusion were 4 and 8 mcg/kg/min, respectively. The enoximone infusion therapy produced sustained salutary effects on cardiac hemodynamics and on clinical status in every patient. The enoximone infusion therapy caused a decrease in mean pulmonary artery pressure by 38%, an increase in cardiac index by 60%, the pulmonary and systemic vascular resistance decreased by 61% and 37%, respectively. Side effects and therapy-related cardiac arrhythmias were not observed. CONCLUSION: Enoximone infusion therapy provides sustained salutary hemodynamic and clinical effects in patients with severe cardiac failure.

Aldosterone↗

PubMed1991

[Effects of the phosphodiesterase III inhibitor in ischemic heart disease].

Positive inotropy requires a rise in myocardial oxygen consumption (MVO2); as far as PDE-III-inhibitors' beneficial hemodynamic effects, increases in contractility are controversial, in part probably because accurate proving is rather tedious. The clinician, however, requires a clear concept of whether or not enoximone (EN), for example, carries the risk of myocardial ischemia when used in patients with coronary artery disease. Using the analysis of pressure-volume relations, we recently established contractility-increasing as a partial effect of EN. There are indications suggesting that the inotropy-induced added increase in MVO2 of the PDE-III-inhibitor drugs could be compensated for by the simultaneous vasodilation and changes in compliance, so that as a net effect an unchanged MVO2 might result. Since, on the other hand, PDE-III-inhibitor drugs have been said to generate antiischemic properties, further clinical investigations with EN clearly seemed indicated and they are the subject of the present report: In five patient groups with stabile angina (AP) studied the following parameters and methods, respectively, were used for the evaluation of EN-induced changes of the anginal threshold: exercise, using pacing and ergometry; PA- and PC-pressure measurements; MVO2, indirectly assessed; hemodynamic profile and regional wall motion as assessed in the immediate post pacing phase; ST- T-segment evaluation; thalium-201 perfusion scintigraphy; myocardial perfusion, indirectly assessed. Lack of EN-induced AP (ischemia) and an increased AP threshold indicated that the drug can be used safety in patients with heart failure, including that due to coronary artery disease.

Cardiac Output↗

PubMed1991

[Alinidine in multi-vessel coronary disease: reduction of stress-induced ischemic reaction].

Ten patients suffering from an angiographically documented coronary two- or three-vessel disease were examined to evaluate the effects of the specific bradycardiac agent alinidine during a bicycle stress test. Hemodynamic and electrocardiographic parameters were compared before and after an intravenous application of 30 mg of the substance. The alinidine plasma levels 30 min after the injection were 160.6 +/- 22.5 ng/ml) (mean +/- SEM). Alinidine significantly (p less than 0.05) reduced the resting levels of heart rate (8.5%), double product (10.3%), myocardial oxygen consumption (9.1%), and cardiac output (9.0%). During exercise, significantly less ST-segment depression (p less than 0.001) in the EKG was observed after alinidine application in nine out of 10 patients, and the rise of pulmonary artery pressure was significantly reduced (34.7 vs 38.1 mm Hg, mean p less than 0.05). However, alinidine had no effect on the maximum heart rate at the end of exercise. We, therefore, assume that the substance has additional anti-ischemic properties.

Adult↗

PubMed1990

Improved diastolic LV filling after acute application of ajmaline in patients with coronary artery disease and normal systolic LV function.

To determine whether ajmaline (A) can be safely applied in coronary artery disease (CAD), changes of left ventricular (LV) function after acute ajmaline application were analyzed by pulsed Doppler echocardiography in 10 CAD patients. LV pressures in systole and end-diastole and LVEF remained normal and comparable. Doppler normalized peak filling rate (p less than 0.02), peak early/atrial filling velocity (E/A) ratio (p less than 0.01) and E-deceleration (p less than 0.05) increased. The increase in E/A and in E-deceleration relative to base values was directly correlated (p less than 0.001). PEP increased, LVET remained unchanged. LV diastolic filling is improved after acute application of ajmaline in patients with CAD and normal systolic function; its application may be advised not only for therapy of arrhythmia but also to improve left ventricular diastolic mechanics in these patients.

Aged↗

PubMed1990

Enoximone: true inotropic effects? Do they cause ischemia? Analysis of end-systolic pressure-volume relations using the conductance (volume) catheter technique.

True positive inotropy of enoximone is hard to prove clinically. It could increase the risk of myocardial ischemia when used in coronary artery disease (CAD). The analysis of the end-systolic pressure-volume relationship (ESPVR) as a load-independent parameter of the contractile left ventricular function (LVF) allows for differentiation of enoximone's unloading effects. Therefore, we analyzed ESPVR and LVF in 12 of 18 CAD patients before and after enoximone, 0.75 mg/kg intravenously. The slope k increased (seven patients) and loops of the ESPVR (12 patients) moved leftward with the enoximone an average of 32% and downward 19%, in the diastolic portion. The delta percent changes in enoximone versus control (18 patients) indicated an improved LVF via load changes: LV filling pressure fell by 50% and end-systolic volume by 28%, while dp/dt max rose by 25%, LV work by 10%, and ejection fraction by 11%. Lastly, the pacing-induced myocardial ischemia threshold increased from an average of 58 +/- 18 sec to 89 +/- 12 sec after eximone, while ischemic postpacing LV filling pressure and ST-segment changes normalized under the drug's influence. Thus, enoximone improved LVF, both by unloading and by true positive inotropy. Lack of enoximone-induced angina and an increased anginal threshold indicate that the drug can be used safely in CAD patients as well.

Aged↗

PubMed1990

Effects of the calcium antagonist, isradipine, and nifedipine on resting and exercise haemodynamics and the neurohumoral system in patients with stable chronic angina.

In a randomized double-blind study, the haemodynamic and anti-ischaemic effects of the new dihydropyridine calcium channel blocker isradipine (5 mg and 10 mg thrice daily (t.i.d.) were investigated over 1 week in nine patients with coronary artery disease and chronic effort angina and compared with nifedipine (20 mg t.i.d.) and placebo. In standardized exercise stress tests and exercise radionuclide ventriculography, haemodynamics improved under medication compared with placebo: resting end-diastolic and end-systolic volume index decreased on isradipine 5 mg, 10 mg and on nifedipine, and ejection fraction at rest increased with all medications. Resting mean arterial pressure was reduced compared with placebo accompanied by a decrease in systemic vascular resistance (P less than 0.05) and systolic wall tension (P less than 0.05). Cumulative ST-segment depression was significantly reduced by all three medications (-48%, -23%, -36%), while the increase in work capacity was insignificant. No significant change was found for either heart rate, double product, cardiac index, or stroke work index. Resting plasma levels of noradrenaline, adrenaline and renin activity increased with all three medications (except adrenaline at isradipine 5 mg). Isradipine has favourable effects comparable with those of nifedipine in patients with chronic stable angina and can be safely administered in these patients.

Angina Pectoris↗

PubMed1990

Do class 1 antiarrhythmic drugs impair myocardial contractility? The class 1A example of ajmaline (conductance catheter technique).

Antiarrhythmic drug effects may include cardiodepression. This risk is theoretically well recognized but clinically rather poorly defined. To evaluate the risks of ajmaline treatment, we monitored hemodynamic parameters and end-systolic pressure-volume relations (ES-PVR) to evaluate potential negative inotropic effects. Twelve patients (nonischemic CAD) underwent hemodynamic analysis with and without the influence of ajmaline, 1 mg/kg i.v., both (a) at rest (paced constant heart rate of 90 beats/min) and (b) during tachycardia of 160 beats/min. With ajmaline, LV pump function was found to have diminished moderately; ejection fraction by 23 and 10%, stroke volume by 10 and 0%, cardiac work by 5 and 16%, and dP/dtmax by 14 and 19%, respectively. While preload increased under the influence of ajmaline (LVEDP by 17 and 30%, respectively), the LV volumes increased (EDV by 18 and 12%, and ESV by 58 and 21%, respectively), and afterload remained unchanged. Ajmaline caused the loops of the ESPVR to move rightward and the slope k to decrease, thus indicating loss of inotropy under the influence of the antiarrhythmic agent. In essence, ajmaline's negative inotropic components were defined by the conductance technique, but they failed to induce clinically relevant cardiodepression in the above NYHA class II patients. This technique proved to be sensitive, useful, and safe in the assessment of inotropic effects by analyzing the ESPVR within the routine of the catheterization laboratory.

Aged↗

PubMed1990

[Effect of the class IA anti-arrhythmic agents ajmaline on end-systolic pressure-volume relations (conductance technique)].

To evaluate cardiodepressive risks of antiarrhythmic treatment with ajmaline, we monitored, in addition to conventional hemodynamic parameters, end systolic pressure-volume relations (ESPVR) to assess potential negative inotropic effects. Twelve patients (CAD without ischemia; EF = 60 +/- 3%) underwent hemodynamic analysis with and without the influence of ajmaline (1 mg/kg, i.v.) both 1) at rest (paced heart rate of 90 bpm) and 2) during tachycardia of 160 bpm. As a result, LV-pump function was found to have diminished moderately: EF by 23% vs 10%, respectively; stroke volume by 10% vs 0%; cardiac work by 5% vs 16%, and dP/dtmax by 14% vs 19%. While preload increased under the influence of ajmaline (LVEDP by 17% vs 30%), the LV-volumes increased (EDV by 18% vs 12%; ESV by 58% vs 21%), afterload remained unchanged. Ajmaline caused the loops of the ESPVR to move rightward and the slope k of the ESPVR to decrease, thus indicating loss of inotropy during the influence of the antiarrhythmic agent. Thus, ajmaline showed a tendency to generate cardiodepressive effects in patients with normal LV-function, and to depress contractility in single cases that clinically had no consequences. The conductance technique proved useful and safe in the assessment of inotropic drug effects by analyzing the ESPVR within the catheterization laboratory routine.

Aged↗