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Clinical and therapeutic implications of chronic left ventricular dysfunction in coronary artery disease
1Centro di Fisiopatologia Cardiocircolatoria, Istituto di Clinica Medica, Universita' di Verona, Italy.
Insights
Chronic left ventricular dysfunction, often from myocardial stunning or hibernation, impacts heart disease patients. Nisoldipine improves heart function in these patients by enhancing systolic and diastolic performance.
Area of Science:
- Cardiology
- Cardiovascular Physiology
Background:
- Left ventricular dysfunction (LV) in myocardial ischemia stems from cell death, myocardial stunning, or hibernation.
- Chronic LV dysfunction typically involves hibernating myocardium, but chronic stunning can also occur.
- Recognizing stunning and hibernation is crucial as chronic LV dysfunction affects mortality and morbidity in coronary artery disease.
Purpose of the Study:
- To investigate the acute hemodynamic effects of nisoldipine in patients with chronic LV dysfunction.
- To assess nisoldipine's impact on both systolic and diastolic left ventricular function.
- To explore potential mechanisms behind nisoldipine's effects on hibernating myocardium.
Main Methods:
- The study involved patients with chronic LV dysfunction, likely due to hibernating myocardium.
- Acute hemodynamic effects of the dihydropyridine calcium antagonist nisoldipine were evaluated.
- Left ventricular systolic and diastolic functions were assessed before and after nisoldipine administration.
Main Results:
- Nisoldipine improved both left ventricular systolic and diastolic function.
- The drug did not activate the adrenergic system.
- Systolic improvement may result from coronary blood flow redistribution and afterload reduction.
- Diastolic improvement might be due to intrinsic mechanisms like reduced intracellular calcium overload.
Conclusions:
- Nisoldipine demonstrates beneficial effects on left ventricular systolic and diastolic function in patients with chronic LV dysfunction.
- These improvements suggest a potential therapeutic role for nisoldipine in managing hibernating myocardium.
- Nisoldipine's ability to improve function without adrenergic activation is clinically significant.
Abstract:
In patients with myocardial ischemia, left ventricular dysfunction (LV) may arise from irreversible damage (cell death), myocardial stunning (postischemic dysfunction), or myocardial hibernation (persistent myocardial dysfunction at rest due to underperfusion). Chronic LV dysfunction usually refers to hibernating myocardium. However, stunning might also become chronic, producing persistent myocardial dysfunction. Clinical studies have demonstrated that many patients with coronary artery disease have subsequent recurring ischemic (symptomatic or silent) episodes at short intervals in the same area and that each episode may be followed by myocardial stunning. In these patients the myocardium may not recover fully between episodes and function may remain reversibly depressed for long periods or may even be clinically depressed. The recognition of both stunning and hibernation is very important clinically and therapeutically, since chronic LV dysfunction may have a negative effect on mortality and morbidity in patients with coronary artery disease. Moreover, both clinical states are potentially correctable. Pharmacologic intervention with beta blockers, angiotensin-converting enzyme inhibitors, or calcium antagonists might improve or protect hibernating myocardium. The acute hemodynamic effects of the dihydropyridine calcium antagonist nisoldipine have been investigated in patients with chronic LV dysfunction probably arising from hibernating myocardium. Nisoldipine was found to improve both left ventricular systolic and diastolic function without activating the adrenergic system. The improvement in systolic function may be due to a redistribution of coronary blood flow and to a slight reduction in afterload induced by nisoldipine. On the other hand, nisoldipine may improve diastolic function in these patients by an intrinsic mechanism, Reducing intracellular calcium overload or balancing intracellular calcium homeostasis in the ischemic areas.(ABSTRACT TRUNCATED AT 250 WORDS)