Diastolic heart function--pathophysiology, characterization, and therapeutic approaches.
In recent years diastolic cardiac function has attracted increasing attention since parameters of diastolic function were found to be altered earlier or more specifically than parameters of systolic function. Diastolic cardiac function is determined by both active (muscular relaxation, redistribution of calcium, synchronization, etc.) and passive (myocardial structure, fibrosis, etc.) factors. As a consequence, a comprehensive assessment of diastolic cardiac function cannot be based on one single parameter. For a complete analysis of diastolic function it is necessary to perform invasive diagnostic procedures involving the measurement of atrial and ventricular pressures, as well as the registration of volume changes with a high time resolution. In addition, it is necessary to measure wall thickness and ventricular configuration, so that apart from filling parameters the stress-strain relationship can be obtained. Noninvasive techniques (Doppler echocardiography, radionuclear ventriculography, apexcardiography) may suggest alterations in diastolic function as well. They ought to be complemented by additional diagnostic procedures (pulmonary pressure, stress testing, etc.). Therapy must consider potentially harmful effects on diastolic function parameters, particularly if changes in myocardial oxygen consumption may result (heart rate, parietal wall stress). Calcium antagonists (verapamil, diltiazem, nifedipine), phosphodiesterase inhibitors (milrinone), beta-adrenergic agonists and antagonists with vasodilating effects (e.g., celiprolol) all have beneficial effects on diastolic myocardial function. A range of diastolic function parameters is being reviewed in the following paper. Their role in the estimation of cardiac function and their responsiveness to therapy in hypertrophy, cardiomyopathy, and coronary heart disease is being discussed.
Modersohn
D
D
Humboldt University Berlin, Department of Cardiology, Germany.
Walde
T
T
Bruch
L
L
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D001696:Biomechanical Phenomena; D001794:Blood Pressure; D002306:Cardiac Volume; D006332:Cardiomegaly / Q000188:drug therapy / Q000503:physiopathology; D002312:Cardiomyopathy, Hypertrophic / Q000188:drug therapy / Q000503:physiopathology; D002316:Cardiotonic Agents / Q000627:therapeutic use; D003327:Coronary Disease / Q000188:drug therapy / Q000503:physiopathology; D003971:Diastole / Q000187:drug effects / Q000502:physiology*; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D006801:Humans; D009200:Myocardial Contraction; D013599:Systole; D014665:Vasodilator Agents / Q000627:therapeutic use
D000319:Adrenergic beta-Antagonists; D002316:Cardiotonic Agents; D014665:Vasodilator Agents