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Biomedical subjects

K I Lie

Publications and source records attributed to K I Lie.

At least 181 records · Page 10Linked to original sources
PubMed1994

Value of ambulatory electrocardiographic monitoring to identify increased risk of sudden death in patients with left ventricular dysfunction and heart failure.

To examine the predictive value of ventricular arrhythmias on ambulatory electrocardiographic (ECG) monitoring, 211 patients with left ventricular dysfunction and congestive heart failure (76% men, age 63 +/- 4 years, left ventricular ejection fraction 0.26 +/- 0.10) were studied. During a follow-up of 21 +/- 11 months, there were 45 cardiac deaths: 22 were due to progressive pump failure and 23 were sudden. Patients with a low left ventricular ejection fraction (< or = 0.27) and ventricular tachycardia on 24 h ECG were at higher risk of dying suddenly and from progressive pump failure (both P < 0.0001). Patients who died suddenly were found to have significantly longer (P = 0.003) and faster (P = 0.029) ventricular tachycardias on their baseline ambulatory ECG, than survivors. This association was not observed in patients who died of progressive pump failure. Therefore, low left ventricular ejection fraction and ventricular tachycardia on 24 h ECG recording predict an increased risk of cardiac mortality. Our results also suggest that longer and faster ventricular tachycardia recorded by 24 h ECG may identify patients at risk of sudden death, a finding which has not been described before.

Cohort Studies↗
PubMed1994

Effect of metoprolol on atrial fibrillatory rate, atrioventricular nodal concealed conduction, and ventricular response during atrial fibrillation in pigs.

We wished to elucidate the effect of beta-blockade on fibrillatory rate and atrioventricular (AV) nodal concealed conduction during atrial fibrillation (AF). Subsequent to determination of the effect on atrial functional refractoriness with the extrastimulus technique (basic cycle length 400 ms), the effect of metoprolol (0.3 mg/kg) on atrial fibrillatory rate was determined in 8 open-chest pigs with metacholine-facilitated AF. Once stable AF was established, fibrillatory rate was recorded with a bipolar epicardial electrode, together with the ventricular response during 500 ventricular intervals. For each episode of AF, three indexes were calculated to determine the degree of concealed conduction: the ratio of the longest to the shortest ventricular interval, the ratio of the median ventricular interval to the median atrial interval, and the coefficient of variation of the ventricular intervals. Metoprolol decreased fibrillatory rate (571-432 beats/min, p < 0.01), suggesting a proportionate increase (+32%) in atrial functional refractoriness during AF that far exceeded the increase (+7%) during sinus rhythm (217-233 ms, p < 0.05). None of the indexes of concealed conduction was affected by metoprolol. Metoprolol decreases fibrillatory rate in AF, possibly due in part to its class I effect, causing rate-dependent prolongation of atrial refractoriness. Despite reducing fibrillatory rate, metoprolol does not affect AV nodal concealed conduction measurably. Our results support the assumption that the reducing effect of beta-blockers on ventricular rate during AF is due to direct prolongation of AV nodal refractoriness.

Animals↗
PubMed1994

Effect of isradipine and nifedipine on diastolic function in patients with left ventricular dysfunction due to coronary artery disease: a randomized, double-blind, nuclear, stethoscope study.

To elucidate the effect of isradipine and nifedipine on left ventricular (LV) systolic and diastolic function, each drug was given intravenously (i.v.) in equihypotensive doses to 10 patients accepted for coronary arteriography for stable angina pectoris. All 20 patients had LV ejection fraction (LVEF) of < 40% owing to previous myocardial infarction (MI). Systolic and diastolic function was assessed by standard hemodynamic parameters and pressure-volume relations measured by nuclear stethoscope. All measurements were taken at rest and during ischemia caused by right atrial pacing. Both systolic and diastolic parameters improved equally with isradipine and nifedipine. LVEF and cardiac output (CO) increased owing to peripheral vasodilatation. A decrease in P/Vmax, indicating a negative inotropic effect, was noted in patients at rest with both medications, but not during pacing-induced ischemia. With either medication, the time constant of relaxation and the end-diastolic elasticity constant decreased during pacing, indicating improvement in diastolic function, probably owing to relief of myocardial ischemia.

Adult↗
PubMed1994

Effect of ibopamine on ventricular remodeling after experimental myocardial infarction: a comparison with captopril.

Remodeling after myocardial infarction (MI) is influenced not only by hemodynamic but possibly by neurohumoral factors as well. Ibopamine is an orally active dopamine agonist (DA) with both hemodynamic and neurohumoral properties in humans. The latter property prevails in rats. To study the dose-dependent effect of ibopamine on myocardial remodeling and compare it with the effect of captopril, we randomized rats with (n = 27) or without (n = 27) experimental MI to captopril (25 mg/kg/day), low-dose ibopamine (10 mg/kg/day), high-dose ibopamine (30 mg/kg/day), or no treatment. After 8-week treatment, hearts were isolated and left ventricular (LV) function, LV cavity volume, and infarct size (IS) were evaluated. Both ibopamine and captopril significantly reduced plasma norepinephrine (NE) levels in rats with MI. In untreated but not in treated infarcted rats, LV function was significantly reduced as compared with that of controls. IS was reduced in all three active treatment groups as compared with untreated rats. LV cavity volume was significantly increased in untreated rats with MI as compared with controls. This dilatation was attenuated by both ibopamine and captopril. Ibopamine, comparable to captopril, administered early after coronary ligation reduced IS and subsequent ventricular dilatation, resulting in preservation of cardiac function in this rat model. This observation suggests a major role for neurohumoral activation in the process of remodeling.

Animals↗
PubMed1994

Acute intravenous versus chronic oral drug effects of verapamil on left ventricular diastolic function in patients with hypertrophic cardiomyopathy.

The effects of acute intravenous (i.v.) versus long-term oral (p.o.) verapamil administration on diastolic function were studied in 20 patients with hypertrophic cardiomyopathy (HCM). We used a tip manometer catheter to record left ventricular pressure (LVP) tracings and a nuclear probe to measure LV volume changes. Infusion of verapamil resulted in an increase in time constant of relaxation (+15%, p < 0.001); LV peak filling rate, heart rate (HR), and stiffness constant of the diastolic pressure-volume relation were unchanged. During 18-week p.o. verapamil treatment, HR decreased (-16%, p < 0.0005) and the atrial contribution to LV filling decreased (-27%, p < 0.05); other parameters differed significantly from baseline values. Results demonstrate that acute i.v. versus long-term p.o. verapamil administration have different effects on diastolic function in HCM.

Administration, Oral↗
PubMed1994

Hemoperfusion during coronary angioplasty: first European experience with a new hemoperfusion pump.

Hemolysis tests with fresh human blood were performed in vitro with a new 5 ml, piston-type hemoperfusion pump, designed to prevent myocardial ischemia during coronary angioplasty. Despite driving pressures greater than 3 atmospheres, shear stress greater than 200 Pa, turbulent pump flow, and the presence of occlusive valves, hemolysis proved to be minimal. This effect is explained by the short amount of time that blood is subjected to mechanical forces that cause hemolysis in the system and by the small volumes of blood involved. During clinical application of the system, angina pectoris, electrocardiographic changes, and systemic blood pressure were used as parameters for myocardial ischemia. There was an effective reduction of ischemia during prolonged (10 min) balloon inflation, demonstrated by the absence of angina, minimal electrocardiographic changes, and normal blood pressure. In addition, the system proved to be safe and effective during high-risk angioplasty.

Adult↗
PubMed1994

Stimulation characteristics, complications, and efficacy of spinal cord stimulation systems in patients with refractory angina: a prospective feasibility study.

OBJECTIVES: In a prospective study with a 1-year follow-up we evaluated: (1) the feasibility of a method for the adjustment of spinal cord stimulator (SCS) parameters, (2) complications of SCS, and (3) efficacy of SCS. METHODS: In patients receiving an SCS for severe angina unresponsive to standard therapies, SCS characteristics were evaluated within 1 week and at 4, 14, 26, and 52 weeks after SCS treatment. Step-by-step adjustment of pulse output parameters was performed at the electrode configuration at which paresthesias occurred ("sensory threshold"), covered the anginal area ("adjusted setting"), or provoked pain ("motor threshold"). In addition, the number of anginal attacks and intake of glyceryl trinitrate (GTN) tablets were recorded at regular intervals. RESULTS: Twenty-two patients with either a bipolar (14) or a unipolar (8) system were evaluated. In the 14 patients with bipolar systems, alteration in paresthesias required 26 reprogrammings of the configuration. In the eight patients with bipolar systems who completed the follow-up without lead dislocation, the mean "sensory threshold" was 3.3 V (1.7-5.6), the mean "adjusted stimulation" output was 4.5 V (2.8-7.6), and the mean "motor threshold" was 4.9 V (2.8-7.7) after 4 weeks SCS. The mean stimulation duration per 24 hours was 14.1% (5%-24%), and the mean standardized impedance was 821 omega (748-893) after 4 weeks SCS. The unipolar group demonstrated comparable results. After 1-year follow-up the parameters had not changed significantly. During the 1-year follow-up, 6 of 22 patients experienced lead dislocation that required surgery. In all patients, anginal attacks (P < 0.003) and GTN intake (P < 0.005) were reduced significantly with SCS. The effect lasted during the 1 year. CONCLUSIONS: During a 1-year follow-up, the stimulation parameters did not change significantly in the 16 patients without lead dislocations. Our standardized method appears to be feasible for follow-up of SCS. Moreover, SCS seems to be an effective adjuvant therapy for intractable angina, despite a relatively frequent dislocation of the electrode.

Aged↗
PubMed1994

Laser thrombolysis in acute myocardial infarction: results of a clinical feasibility study.

Laser thrombolysis is a new, experimental, catheter based intervention aimed at selectively removing intracoronary thrombus. This first clinical study was performed to assess the feasibility and safety of laser thrombolysis, as well as its potential therapeutic place in acute myocardial infarction. Eighteen patients with acute myocardial infarction, who were either noncandidates for, or failures on, intravenous fibrinolytic therapy were included for treatment with laser thrombolysis followed by balloon angioplasty. As a result of catheter and technical failures, the laser was actually fired in only 12 patients. Improvement in TIMI flow from grade 0-1 to grade 2-3 was observed in 10 of these 12 patients after laser application. The overall results of 18 patients were: increase in TIMI grade flow from 0.33 +/- 0.49 after wire passage to 1.28 +/- 1.23 (P = 0.0051) after attempted laser application, and to 2.67 +/- 0.97 after PTCA (P = 0.0004). Two patients with previous infarctions died from left ventricular failure despite successful laser thrombolysis. One patient died during emergency bypass surgery after a failed recanalization attempt. Perforation or laser related dissection did not occur. The concept of selective laser thrombus ablation seems to be safe and feasible, but substantial improvements of the laser delivery catheters are needed. Laser thrombolysis is not an effective stand-alone therapy in acute myocardial infarction, but other possible applications warrant further research and development efforts for this potentially useful interventional tool.

Angioplasty, Balloon, Coronary↗
PubMed1994

Effects of spinal cord stimulation on myocardial ischaemia during daily life in patients with severe coronary artery disease. A prospective ambulatory electrocardiographic study.

BACKGROUND: Spinal cord stimulation (SCS) may be a useful additional therapy for pain in patients with therapeutically refractory angina pectoris. But doubts remain about whether it also relieves ischaemia. METHODS: Indices of ischaemia were studied with and without SCS in 10 patients with otherwise intractable angina and evidence of myocardial ischaemia on 48 h ambulatory electrocardiographic (ECG) recording. Primary end points assessed by 48 h ECG recordings were total ischaemic burden, number of ischaemic episodes, and duration of ischaemic episodes. In addition, symptoms were assessed by a diary of glyceryl trinitrate intake and angina attacks. RESULTS: During SCS the total ischaemic burden of the entire group was significantly reduced from a median of 27.9 (1.9-278.2) before SCS to 0 (0-70.2) mm x min with SCS (p < 0.03). In six out of the 10 patients there was no myocardial ischaemia during 48 h ambulatory ECG monitoring with SCS. The number of ischaemic episodes was reduced from a median of 3 (1-15) before SCS to 0 (0-9) with SCS (p < 0.04). The duration of ischaemic episodes decreased from a median of 20.6 (1.7-155.4) min before SCS to 0 (0-48.3) min with SCS (p < 0.03). This was accompanied by a significant improvement in symptoms with a reduction in daily glyceryl trinitrate intake from a median of 3.0 (0-10) before SCS to 0.3 (0-10) tablets per 48 h (p < 0.02) and a decrease in the frequency of anginal attacks from a median of 5.5 (2-14) before SCS to 1.0 (0-10) per 48 h with SCS (p < 0.03). CONCLUSIONS: SCS not only reduced symptoms but also myocardial ischaemia. Therefore, SCS appears to be both a safe and an effective therapy for patients with refractory angina.

Aged↗
PubMed1994

Functional capacity before and after cardioversion of atrial fibrillation: a controlled study.

OBJECTIVE: To evaluate the effect of cardioversion on peak oxygen consumption (peak VO2) in patients with long-standing atrial fibrillation, to assess the importance of underlying heart disease with respect to the response to exercise, and to relate functional capacity to long-term arrhythmia outcome. DESIGN: Prospective controlled clinical trial. SETTING: Tertiary referral centre. PATIENTS: 63 consecutive patients with chronic atrial fibrillation accepted for treatment with electrical cardioversion. Before cardioversion all patients were treated with digoxin, verapamil, or a combination of both to attain a resting heart rate < or = 100 beats per minute. INTERVENTIONS: Electrical cardioversion. MAIN OUTCOME MEASURES: Peak VO2 measured before and 1 month after electrical cardioversion to compare patients who were in sinus rhythm and those in atrial fibrillation at these times. Maintenance of sinus rhythm for a mean follow up of 19 (7) months. RESULTS: Mean (1SD) peak VO2 in patients in sinus rhythm after 1 month (n = 37) increased from 21.4 (5.8) to 23.7 (6.4) ml/min/kg (+11%, P < 0.05), whereas in patients with a recurrence of atrial fibrillation 1 month after cardioversion (n = 26) peak VO2 was unchanged. In patients who were in sinus rhythm both those with and without underlying heart disease improved, and improvement was not related to functional capacity or left ventricular function before cardioversion. Baseline peak VO2 was not a predictive factor for long-term arrhythmia outcome. CONCLUSION: Restoration of sinus rhythm improved peak VO2 in patients with atrial fibrillation, irrespective of the presence of underlying heart disease. Peak VO2 was not a predictive factor for long-term arrhythmia outcome after cardioversion of atrial fibrillation. These findings suggest that cardioversion is the best method of improving functional capacity in patients with atrial fibrillation, whether or not they have underlying heart disease and whatever their functional state.

Atrial Fibrillation↗
PubMed1994

Heart rate variability in left ventricular dysfunction and heart failure: effects and implications of drug treatment.

OBJECTIVE: To review the importance of heart rate variability analysis in left ventricular dysfunction and heart failure and to assess the effects of drug treatment. In patients with left ventricular dysfunction or heart failure, a low heart rate variability is a strong predictor of a low probability of survival. Because drug treatment in these patients has rapidly changed over the past two decades, the effect of these drugs on heart rate variability needs special attention. DESIGN: A study of published reports to give an overview of heart rate variability in patients with left ventricular dysfunction or heart failure and how it is affected by drug treatment. RESULTS: Analysis of heart rate variability provides an easily obtained early marker for progression of disease. It seems to be more closely related to the degree of neurohumoral activation than to haemodynamic variables. Cardiovascular drugs may either stimulate or inhibit the degree of neurohumoral activation, and the effects of pharmacological intervention can be closely monitored with this method. CONCLUSIONS: The analysis of heart rate variability, including spectral analysis, is a novel non-invasive way to obtain potentially useful clinical information in patients with reduced left ventricular function. The effects of drug treatment on heart rate variability are in general consistent with their long-term effects in left ventricular dysfunction and heart failure.

Heart Failure↗
PubMed1994

Association between reduced heart rate variability and left ventricular dilatation in patients with a first anterior myocardial infarction. CATS Investigators. Captopril and Thrombolysis Study.

BACKGROUND: Reduced heart rate variability has been identified as an important prognostic factor after myocardial infarction. This factor is thought to reflect an imbalance between sympathetic and parasympathetic activity, which may lead to unfavourable loading conditions and thus promote left ventricular dilatation. PATIENTS AND METHODS: 298 patients in a multicentre clinical trial were randomised to captopril or placebo after a first anterior myocardial infarction. All patients were treated with streptokinase before randomisation. In the present substudy full data including heart rate variability and echocardiographic measurements were available from 80 patients. Patients were divided into two groups: those with a reduced (< or = 25) heart rate variability index and those with normal heart rate variability index (> 25). Heart rate variability was evaluated by 24 h Holter monitoring before discharge. Left ventricular volumes were assessed by echocardiography before discharge and three and 12 months after myocardial infarction. Extent of myocardial injury, severity of coronary artery disease, functional class, haemodynamic variables, and medication were also considered as possible determinants of left ventricular dilatation. RESULTS: Before discharge end systolic and end diastolic volumes were not different in the two groups. After 12 months in patients with a reduced heart rate variability, end systolic volume (mean (SD)) had increased by 6 (14) ml/m2 (P = 0.043) and end diastolic volume had increased by 8 (17) ml/m2 (P = 0.024). Left ventricular volumes were unchanged in patients with a normal heart rate variability. Also, patients with left ventricular dilatation had a larger enzymatic infarct size and higher heart rates and rate-pressure products. A reduced heart rate variability index before discharge was an independent risk factor for left ventricular dilatation during follow up. Measurement of heart rate variability after three months had no predictive value for this event. CONCLUSION: Assessment of the heart rate variability index before discharge, but not at three months, gave important additional information for identifying patients at risk of left ventricular dilatation.

Captopril↗
PubMed1994

A comparison of internal mammary artery and saphenous vein grafts after coronary artery bypass surgery. No difference in 1-year occlusion rates and clinical outcome. CABADAS Research Group of the Interuniversity Cardiology Institute of The Netherlands.

BACKGROUND: Superior patency rates for internal mammary artery (IMA) grafts compared with vein coronary bypass grafts have been demonstrated by retrospective studies. This difference may have been affected by selection bias of patients and coronary arteries for IMA grafting. METHODS AND RESULTS: To estimate the difference between IMA and vein grafts, we analyzed graft patency data of 912 patients who entered a randomized clinical drug trial. In this trial, 494 patients received both IMA and vein grafts (group 1) and 418 only vein grafts (group 2). Occlusion rates of IMA grafts and IMA plus vein grafts in group 1 were compared with those of vein grafts in group 2. Multivariate analysis was used to compare occlusion rates of IMA and vein grafts while other variables related to graft patency were controlled for. In addition, 1-year clinical outcome was assessed by the incidence of myocardial infarction, thrombosis, major bleeding, and death. Occlusion rates of distal anastomoses in group 1 versus group 2 were 5.4% (IMA grafts) versus 12.7% (vein grafts) (P < .0001) and 10.4% (IMA plus vein grafts) versus 12.7% (vein grafts) (P = .14). There was no difference in adjusted risk of occlusion between IMA grafts and vein grafts (P = .089). Type and location of distal anastomosis and lumen diameter of the grafted coronary artery were shown to be predictors of occlusion. Clinical events occurred in 17.8% (group 1) and 16.0% (group 2) of patients (P = .53). CONCLUSIONS: The observed difference in 1-year occlusion rates between IMA and vein grafts can be explained by a maldistribution of graft characteristics by selection of coronary arteries for IMA grafting rather than being ascribed to graft material. One-year clinical outcome is not improved by IMA grafting.

Aged↗
PubMed1994

Effects of acetylsalicylic acid on peripheral hemodynamics in patients with chronic heart failure treated with angiotensin-converting enzyme inhibitors.

Cyclooxygenase inhibitors may affect the hemodynamic status of patients with heart failure adversely and may also block the vasodilatory effects of angiotensin-converting enzyme (ACE) inhibitors in such patients. Relatively low doses of the cyclooxygenase inhibitor acetylsalicylic acid (ASA) are now used routinely in ischemic heart disease, the most important cause of heart failure. Therefore, we investigated the hemodynamic interaction between ASA and captopril in heart failure. In a randomized, cross-over study, 13 patients with congestive heart failure (CHF) who were already receiving maintenance treatment with an ACE inhibitor received a single dose of 25 mg captopril combined with 236 mg ASA or placebo. Peripheral blood flow was studied noninvasively by venous occlusion plethysmography of the calves. Liver blood flow was estimated from indocyanine green (ICG) clearance. Administration of captopril alone significantly decreased blood pressure (BP), and ICG clearance. Calf blood flow remained unchanged. However, after arterial occlusion, hyperemic calf blood flow persisted for longer. Captopril alone did not significantly change the plasma levels of the vasodilating prostaglandins PGI2 and PGE2 or the vasoconstricting thromboxane A2 (TXA2). In contrast, captopril combined with ASA reduced the plasma levels of these vasoactive substances, with significant decreases in PGE2 and TXA2 as compared with captopril alone, yet the hemodynamic alterations after captopril plus ASA were similar to those observed after captopril alone. A single antithrombotic dose of ASA (236 mg) in 13 patients with CHF [New York Heart Association (NYHA) class II-IV] undergoing chronic treatment with ACE inhibitors had no discernible effect on hemodynamic status.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Hemodynamic effects of the new antiarrhythmic agent restacorin in patients with normal and decreased left ventricular function.

The hemodynamic and pharmacokinetic effects of the novel class 1c antiarrhythmic drug restacorin were investigated in two groups of patients. Group I consisted of 5 patients with normal left ventricular (LV) function, and group II consisted of 10 patients with mild heart failure [New York Heart Association (NYHA) II; mean LV ejection fraction 33 +/- 6%]. The study had an open label, baseline-controlled, single-dose design. Restacorin was infused in a total dosage of 1.2 mg/kg. In group I, the only significant change as compared with baseline findings was a 25% increase in right atrial pressure. In group II; cardiac output (CO), dP/dt, and stroke work index (SWI) decreased significantly (-18, -11, and -24%, respectively). In addition, a significant 32% increase was noted in pulmonary artery wedge pressure (PAWP), and a 27% increase occurred in systemic vascular resistance (SVR). No changes were observed in heart rate (HR) or mean arterial blood pressure (MAP). CO and SVR at baseline correlated with the average plasma concentrations (r = -0.65 and p = 0.009 and r = 0.56 and p = 0.028 respectively). Creatinine clearance was inversely correlated to the restacorin plasma concentration (r = -0.51, p = 0.05). The half-life (t1/2) elimination time of restacorin was 2.60 h for group I, and 4.06 h for group II. Clearance was 51.4 and 32.2 L.h-1, respectively. Restacorin appears to be well tolerated in patients with normal LV function. The drug is not recommended for use in patients with reduced LV function because of its moderate negative inotropic effect.

Adolescent↗
PubMed1994

Oral anticoagulation in the prevention of one-year vein graft occlusion after aortocoronary bypass surgery: optimal therapeutic range and practical limitations. CABADAS Research Group of the Interuniversity Cardiology Institute of The Netherlands.

To assess the optimal level of oral anticoagulation to prevent occlusion of vein coronary bypass grafts, 318 patients from a graft patency trial were analysed retrospectively. Oral anticoagulant therapy was started one day before surgery and continued for one year, after which graft occlusion was assessed by angiography. The aimed level of anticoagulation was 2.8-4.8 International Normalized Ratio (INR). Clinical outcome was assessed by the incidence of myocardial infarction, thrombosis and major bleeding. The observed anticoagulation level was 2.8-4.8 INR for 54%, and 1.8-3.8 INR for 75% of time per patient. Occlusion rates in patients who spent < 35, 35-70, and > or = 70% of time within INR range 2.8-4.8 were 10.5%, 10.8% and 11.8%, respectively (differences not statistically significant). Patients who spent > or = 70% of time within INR range 1.8-3.8 versus 2.8-4.8 showed comparable occlusion rates. The risk of graft occlusion was not related to quality of anticoagulation early (0-3 months) or late (3-12 months) after surgery. Myocardial infarction, thrombosis and major bleeding occurred in 1.3%, 2.0% and 2.9% of patients. To maintain vein graft patency in the first postoperative year by oral anticoagulation, a level within INR range 1.8-3.8 for > or = 70% of time seems to be sufficient.

Administration, Oral↗
PubMed1994

Restacorin, a new antiarrhythmic drug: a review of its electrophysiologic and hemodynamic properties.

Restacorin is a recently developed effective antiarrhythmic agent with primarily class Ic properties. The present paper reviews the electrophysiologic and hemodynamic effects of this compound. The major electrophysiologic effects are a depression of Vmax and an increase in AH, HV and QRS duration. The administration of restacorin does not induce significant side effects. In subjects with a normal left ventricular function, restacorin does not show negative inotropic effects. However, in patients with a decreased left ventricular function, restocorin produces a moderate negative inotropic effect.

Animals↗