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1 Lab of Cardiac Energetics NHLBI, National Institutes of Health, Bethesda, Maryland, United States; Laboratory of Cardiac Energetics, National Heart, Lung and Blood Institute, Bethesda, Maryland, United States; 10B/B1D416, NIH, United States
2 Lab of Cardiac Energetics NHLBI, National Institutes of Health, Bethesda, Maryland, United States; 10B/B1D416, NIH, United States
3 Laboratory of Cardiac Energetics, NHLBI, Bethesda, Maryland, United States
4 Cardiothoracic Surgery Research Program, National Heart Lung and Blood Institute, Bethesda, Maryland, United States
5 Lab of Cardiac Energetics NHLBI, National Institutes of Health, Bethesda, Maryland, United States
* To whom correspondence should be addressed. E-mail: rsb{at}nih.gov.
Much attention has been focused on the passive mechanical properties of the myocardium which determines left ventricular (LV) diastolic mechanics, but the significance of the visceral pericardium (VP) has not been extensively studied. A unique en face 3-D volumetric view of the porcine VP was obtained using two-photon excitation fluorescence to detect elastin, and backscattered second harmonic generation to detect collagen, in addition to standard light microscopy with histological staining. Below a layer of mesothelial cells, collagen and elastin fibers, extending several millimeters, form several distinct layers. The configuration of the collagen and elastin layers as well as the location of the VP at the epicardium providing a geometric advantage led to the hypothesis that the VP mechanical properties play a role in the residual stress and passive stiffness of the heart. The removal of the VP by blunt dissection from porcine LV slices changed the opening angle from 53.3 ± 10.3°, to 27.3 ±5.7°(mean ±SD, p<0.05, n=4). In four porcine hearts where the VP was surgically disrupted a significant decrease in opening angle was found (35.5 ± 4.0°) as well as a rightward shift in the ex vivo pressure-volume relationship before and after disruption and a decrease in LV passive stiffness at lower LV volumes (P<0.05). These data demonstrate the significant and previously unreported role that VP plays in the residual stress and the passive stiffness of the heart. Alterations in this layer likely occur in various disease states that effect diastolic function.
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