Contraction frequency dependence of twitch and diastolic tension in human dilated cardiomyopathy (Tension-frequency relation in cardiomyopathy)

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Abstract
We studied isometric twitch tension and diastolic tension at 37 °C as a function of stimulation frequency (12–240 min−1) in very thin (.07– 5mm2), parallel fibered strips of left-ventricular myocardium. Non-failing control tissue (C) was obtained from epicardial biopsies taken during myocardial revascularization surgery on patients with normal ventricular function. End-stage failing tissue was obtained from endocardial and epicardial biopsies from explanted hearts with idiopathic dilated cardiomyopathy (DCM). The methods and apparatus for biopsy and dissection of myocardium are described. Maximal peak twitch tension at optimal stimulation frequency of 163 ± 5 mm−1 was 41.8 ± 10mN/mm2 in non-failing myocardium and it was reduced by 70% (p <.02) to 12.9 ± 1.6mN/mm2 at an optimal frequency of 72 ± 17 min−1 in DCM. The peaks of the tension-frequency curves occurred at frequencies between 12 and 60 min−1 in most DCM strips (5/9), while in C most of the peaks (8/9) fell between 156 and 180 min−1. The peaks from four DCM hearts fell in an intermediate range of frequencies (96–144 min−1) which also included one non-failing peak at 132 min−1. Diastolic tension declined in both groups as stimulation frequency increased above 12 min−1 and it began increasing when stimulation frequency rose above optimal frequency by 19 ± 5% and 110 ± 50% in C and DCM, respectively. Total duration of the isometric twitch diminished with tachycardia remaining shorter than stimulation intervals up to 140 ± 16 min−1 (3.1 ± 1 times optimal frequency) in DCM and up to 161 ± 14 min−1 (not different than optimal frequency) in C. Decline in peak twitch tension above optimal stimulation frequency was 4 to 6 times larger than the accompanying rise in diastolic tension in both groups. The premature decline in tension at lower than normal degrees of tachycardia in DCM does not arise from incomplete relaxation of the twitch response. The 70% deficit in tension generating ability of DCM may be a major contributor to heart failure. Moderate shift in the peak of the tension-frequency curves to lower frequencies (130 min−1) in C does not appear to predispose end-stage failure, but it may make the ventricle more susceptible to dilation.

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