Abstract
Myocardial failure in dilated cardiomyopathy may result from subcellular alterations in contractile protein function, excitation-contraction coupling processes, or recovery metabolism. We used isometric force and heat measurements to quantitatively investigate these subcellular systems in intact left ventricular muscle strips from nonfailing human hearts (n=14) and from hearts with end-stage failing dilated cardiomyopathy (n=13). In the failing myocardium, peak isometric twitch tension, maximum rate of tension rise, and maximum rate of relaxation were reduced by 46% (p=0.013), 51% (p=0.003), and 46% (p=0.018), respectively (37°C, 60 beats per minute). Tension-dependent heat, reflecting the number of crossbridge interactions during the isometric twitch, was reduced by 61% in the failing myocardium (p=0.006). In terms of the individual crossbridge cycle, the average crossbridge force-time integral was increased by 33% (p=0.04) in the failing myocardium. In the nonfailing myocardium, the crossbridge force-time integral was positively correlated with the patient's age (r=0.86, p
Original language | English (US) |
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Pages (from-to) | 1225-1232 |
Number of pages | 8 |
Journal | Circulation Research |
Volume | 70 |
Issue number | 6 |
State | Published - 1992 |
Externally published | Yes |
Keywords
- calcium cycling
- crossbridges
- dilated cardiomyopathy myocardial failure
- human myocardium
ASJC Scopus subject areas
- Physiology
- Cardiology and Cardiovascular Medicine