The two main phases of the mammalian cardiac cycle are contraction and relaxation; however, whether these phases are linked in human myocardium is not well understood. Prior investigations have shown that the structural and biochemical myocardial remodeling secondary to exercise training and/or myocardial infarction does not disrupt contraction-relaxation (CR) coupling in the canine model system. In addition, in a wide variety of murine transgenic models targeting EC coupling, the coupling between contraction and relaxation was unaltered. Given the vast differences between inbred animal models and the human population, we investigated whether contraction and relaxation are also coupled in human myocardium, and if so, whether that coupling is affected by heart failure disease status. We retrospectively analyzed data from contractility measurements taken under conditions closely mimicking those in vivo and calculated the correlation between the maximal speed of contraction and the maximal speed of relaxation in human ventricular multicellular preparations. We categorized our data based on heart failure status as follows: non-heart failure, heart failure with ischemic cardiomyopathy, or heart failure with non-ischemic cardiomyopathy. In every case isolated right ventricular trabeculae and/or left ventricular trabeculae (n=53 subjects LV and RV analyzed, 38 subjects only LV, 27 subjects only RV) were isolated from freshly explanted human hearts. Multicellular preparations were then electrically paced at different muscle lengths, frequencies, and with increasing β-adrenoceptor stimulation. In all conditions, contraction and relaxation were very tightly linearly correlated regardless of disease category (typical R 2 of >0.98). While the mechanism governing this coupling is unknown, based on data form this study and past studies, we posit that CR-coupling is a fundamental myocardial property that resides in the structural arrangement of proteins at the level of the sarcomere at the basis of cross-bridge cycling.