Cardiac alternans: mechanisms and pathophysiological significance.

Abstract

Time for primary review 31 days. Mechanical alternans (pulsus alternans) is a condition in which there is a beat-to-beat oscillation in the strength of cardiac muscle contraction at a constant heart rate. Since the first description of pulsus alternans by Traube in 1872 [1], there has been continuing interest in understanding the mechanisms and clinical manifestations of this phenomenon [2,3]. Initially observed in the hearts of laboratory animals, the phenomenon has been reported frequently in patients particularly those with severe heart failure and aortic valve disease. Although much is known about the cellular mechanisms of alternans in isolated cardiac muscle preparations, little is known about the mechanisms by which changes in preload or afterload evoke alternans in the intact heart. The purpose of this review article is to discuss the mechanisms of alternans at both the cellular level and in the intact heart. The relationship between mechanical and electrical alternans is reviewed. The role of sympathetic nervous system is discussed as a means of protecting the heart from alternans during accelerations of heart rate. Since pulsus alternans has been reported in patients with cardiac disease, the diagnostic and prognostic significance of mechanical and electrical alternans is also discussed. The ability to induce mechanical alternans by rapid driving frequencies appears to be a fundamental property of mammalian ventricular muscle. Experimental studies have shown that by varying the pacing cycle length over a wide range, it is possible to define a critical cycle length (threshold) for the induction of sustained mechanical alternans [4–7]. Driving the heart at cycle lengths shorter than the threshold cycle length may increase the amplitude of the beat-to-beat oscillations in contraction strength (Fig. 1). Driving the heart at cycle lengths just longer than the threshold may produce transient alternans [4,6]. Transient alternans may also … * Tel.: +1-612-315-2155; fax: +1-612-315-2199