Society of Cardiovascular Anesthesiologists

Drug and Innovation Review

New insights into diastolic dysfunction: Does it really exist?

Mark A. Chaney, MD
Associate Professor
University of Chicago

Congestive heart failure (CHF) remains a major medical problem(1). Approximately half of all patients with CHF demonstrate normal or near normal systolic function and thus are diagnosed with diastolic dysfunction via reasoning of exclusion. Traditionally, it has been thought that diastolic dysfunction is caused by a wide variety of pathophysiologic changes that include myocardial ischemia, hypertension and aging that lead to impaired relaxation and increased passive stiffness of the left ventricle. Because diastolic function can only be accurately assessed via cardiac catheterization using multiple laborious measurements, diastolic dysfunction has persisted as a clinical diagnosis of exclusion. Traditional treatment of diastolic dysfunction has involved volume reduction (diuretics, fluid and sodium restriction), prolongation of diastolic filling time (beta blockers, calcium channel blockers), and restoration of atrial contraction (if atrial fibrillation is present), among others. Such a view of diastolic dysfunction has been widely accepted and has formed the sole basis of both basic research and clinical trials of new treatments for the past three decades(1-3). However, despite this intense investigation, we are still without a single effective treatment for diastolic dysfunction in patients with CHF and normal systolic function. New research indicates that the reason for this failure to find effective therapy in this clinical scenario may be because diastolic function may in fact be normal in these patients(4). Diastole consists of active processes (ventricular relaxation) and passive processes (ventricular distensibility). Characterization of passive diastolic properties is a challenging task that requires simultaneous assessment of both pressure and volume across a wide range of values. A recent investigation by Kawaguchi and associates, the first to thoroughly assess diastolic function in patients with CHF and presumed normal systolic function, indicates that diastolic function is, in fact, normal and undermines the premise that increased diastolic stiffness impairs the ability of the heart to increase preload volume during exercise(5). These investigators revealed that CHF with presumed normal systolic function is not solely a diastolic disease but is also characterized by systolic-ventricular and arterial stiffening and, thus, adverse coupling between the systems. Furthermore, one should not imply in this clinical scenario that normal systolic function is present (even though ejection fraction is normal). Their findings are sufficient to raise the provocative hypothesis that there exists no consistent abnormality of intrinsic diastolic properties that can explain the occurrence of heart failure with a normal ejection fraction(4). The increase in left ventricular filling pressures seen in these patients may be the cause and not the result of abnormalities of diastolic filling that are observed in this disorder. Such a conclusion presents a direct challenge to the diastolic dysfunction hypothesis(4). Thus, in patients with CHF and normal ejection fraction (which does not imply normal systolic function), we should not automatically assume diastolic dysfunction is present. Hopefully, future investigation will better explain common clinical features of CHF with normal ejection fraction and help broaden its pathophysiological and therapeutic focus. Expanding the conceptual view to include abnormal cardiac-arterial coupling and testing the impact of reducing heart or arterial stiffening in these patients should further help in the search for beneficial therapies.

References

1. Angeja BG, Grossman W. Evaluation and management of diastolic heart failure (Clinician Update). Circulation. 107:659-663, 2003.

2. Buckberg GD. Congestive heart failure: treat the disease, not the symptom - return to normalcy (Editorial). J Thorac Cardiovasc Surg. 125:S41-S49, 2003.

3. Burkhoff D. New heart failure therapy: the shape of things to come? (Editorial). J Thorac Cardiovasc Surg. 125:S50-S52, 2003.

4. Burkhoff D, et al. Heart failure with a normal ejection fraction; is it really a disorder of diastolic function? (Editorial). Circulation. 107:656-658, 2003.

5. Kawaguchi M, et al. Combined ventricular systolic and arterial stiffening in patients with heart failure and preserved ejection fraction; implications for systolic and diastolic reserve limitations. Circulation. 107:714-720, 2003.

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