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Troglitazone improves cardiac function in patients with congestive heart failure
Kazuhide Ogino1, Yoshiyuki Furuse, Kazuhiko Uchida
1Division of Cardiology, Department of Medicine, Faculty of Medicine, Tottori University, 36-1 Nishimachi, Yonago 683-8504, Japan. k-ogino@umin.ac.jp
Insights
Troglitazone improved heart function in diabetic patients with heart failure by increasing stroke volume and ejection fraction. This cardiac improvement occurred without altering blood pressure or activating the sympathetic nervous system.
Area of Science:
- Cardiology
- Pharmacology
- Endocrinology
Background:
- Troglitazone is known to improve cardiac output in diabetic patients with normal cardiac function.
- The cardiovascular effects of troglitazone in patients with heart failure (HF) remain largely unknown.
- Understanding these effects is crucial for managing diabetic patients with co-existing heart conditions.
Purpose of the Study:
- To evaluate the acute cardiovascular effects of a single oral dose of troglitazone in type II diabetic patients with congestive heart failure.
- To assess changes in hemodynamic parameters, cardiac function, and neurohormonal activity.
- To determine if troglitazone induces positive inotropy in this patient population.
Main Methods:
- A randomized, placebo-controlled study involving eight type II diabetic patients with congestive heart failure.
- Administration of a single 400 mg dose of troglitazone or placebo.
- Evaluation of blood pressure, echocardiographic findings, plasma catecholamines, and coefficient of variance of RR intervals (CVRR) at baseline and at 1, 2, 3, and 4 hours post-administration.
Main Results:
- Troglitazone significantly increased left ventricular (LV) end-systolic dimension, % fractional shortening, E/A ratio, stroke volume, and LV ejection fraction compared to placebo.
- No significant changes were observed in heart rate, blood pressure, or LV end-diastolic dimension.
- Plasma catecholamines significantly decreased, while CVRR remained unchanged, indicating no sympathetic nervous system activation.
Conclusions:
- A single oral dose of troglitazone induces positive inotropic effects in diabetic patients with congestive heart failure.
- These beneficial hemodynamic changes occur without sympathetic nervous system activation.
- Troglitazone may represent a potential therapeutic option for improving cardiac function in diabetic patients with heart failure.
Abstract:
Troglitazone increased cardiac output and stroke volume, as a result of decreased peripheral resistance, in diabetic patients with normal cardiac function. The cardiovascular effects of troglitazone in patients with heart failure are unknown. The aim of the study was to evaluate the cardiovascular effects of troglitazone in patients with heart failure. Blood pressure and echocardiographic findings were evaluated before and 1, 2, 3 and 4 hours after a single dose of troglitazone (400 mg) or placebo, in eight type II diabetic patients with congestive heart failure. The plasma catecholamines and coefficient of variance of RR intervals (CVRR) were also measured. Neither heart rate nor blood pressure changed after the administration of troglitazone. Left ventricular (LV) end-diastolic dimension did not change either, however, the LV end-systolic dimension significantly decreased compared with its baseline value and with that of the placebo group. On the other hand, the % fractional shortening and the E/A ratio increased significantly after troglitazone. The LV end-diastolic volume did not change, whereas the LV end-systolic volume significantly decreased. The stroke volume and the LV ejection fraction significantly increased compared with its baseline value and with that of the placebo group. The peripheral vascular resistance did not change after the administration of troglitazone, whereas plasma catecholamines significantly decreased, and CVRR remained unchanged in both groups. These hemodynamic changes suggest that a single oral dose of troglitazone induced inotropy without activation of the sympathetic nervous system.