Abnormalities of diastolic function as a potential cause of exercise intolerance in chronic heart failure.
Most research in the field of chronic heart failure during the last 20 years has been directed toward defining and understanding the abnormalities of systolic function seen in this disorder, but systolic performance is not a determinant of effort tolerance. Several lines of evidence, however, suggest a strong relation between exercise capacity and abnormalities of diastolic function in chronic heart failure. Of all the commonly measured hemodynamic variables, effort tolerance (whether limited by dyspnea or fatigue) varies more closely with the level of left ventricular filling pressure than the left ventricular ejection fraction. Consequently, drugs that lower ventricular filling pressures are more likely to enhance exercise capacity than drugs that primarily increase cardiac output and left ventricular ejection phase indexes. Vasodilator drugs do not reduce left ventricular filling pressure, however, by simply redistributing central blood volume to the peripheral capacitance circuits because these agents do not predictably decrease left ventricular volumes. Instead, clinically effective drugs seem to reduce left ventricular filling pressure primarily by producing a favorable shift in the left ventricular diastolic pressure-volume relation. Conversely, agents that adversely affect the diastolic pressure-volume relation frequently cause clinical deterioration. These findings suggest that abnormalities of diastolic rather than systolic performance may be the most important determinants of the clinical status and exercise intolerance of patients with chronic heart failure.
Packer
M
M
Department of Medicine, Mount Sinai School of Medicine, City University of New York, NY 10029.
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D004232:Diuretics / Q000627:therapeutic use; D015444:Exercise / Q000502:physiology*; D006333:Heart Failure / Q000188:drug therapy / Q000503:physiopathology*; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology*; D010726:Phosphodiesterase Inhibitors / Q000627:therapeutic use; D005082:Physical Exertion / Q000502:physiology; D011669:Pulmonary Wedge Pressure / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology; D014665:Vasodilator Agents / Q000627:therapeutic use
D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D002121:Calcium Channel Blockers; D004232:Diuretics; D010726:Phosphodiesterase Inhibitors; D014665:Vasodilator Agents