Background-Asynchronous electrical activation, induced by ventricular pacing, causes regional differences in workload, which is lower in early-than in late-activated regions. Because the myocardium usually adapts its mass and structure to altered workload, we investigated whether ventricular pacing leads to inhomogeneous hypertrophy and whether such adaptation, if any, affects global left ventricular (LV) pump function. Methods and Results-Eight dogs were paced at physiological heart rate for 6 months (AV sequential, AV interval 25 ms, ventricular electrode at the base of the LV free wall). Five dogs were sham operated and served as controls. Ventricular pacing increased QRS duration from 47.2Ϯ10.6 to 113Ϯ16.5 ms acutely and to 133.8Ϯ25.2 ms after 6 months. Two-dimensional echocardiographic measurements showed that LV cavity and wall volume increased significantly by 27Ϯ15% and 15Ϯ17%, respectively. The early-activated LV free wall became significantly (17Ϯ17%) thinner, whereas the late-activated septum thickened significantly (23Ϯ12%). Calculated sector volume did not change in the LV free wall but increased significantly in the septum by 39Ϯ13%. In paced animals, cardiomyocyte diameter was significantly (18Ϯ7%) larger in septum than in LV free wall, whereas myocardial collagen fraction was unchanged in both areas. LV pressure-volume analysis showed that ventricular pacing reduced LV function to a similar extent after 15 minutes and 6 months of pacing. Conclusions-Asynchronous activation induces asymmetrical hypertrophy and LV dilatation. Cardiac pump function is not affected by the adaptational processes. These data indicate that local cardiac load regulates local cardiac mass of both myocytes and collagen. (Circulation. 1998;98:588-595.)

Hearts of 11 anesthetized open-chest dogs were paced from the right atrium (RA), right ventricular outflow tract (RVOT), and left ventricular apex (LVA). Maps of the sequence of electrical activation (192 electrodes), fiber strain (video technique), and blood flow (microsphere technique) in the epicardial layers were obtained from a 15- to 20-cm2 area of the anterior left ventricular wall. Electrical asynchrony in this area was 10 +/- 5 (RA), 52 +/- 12 (RVOT), and 30 +/- 16 ms (LVA, mean +/- SD, P less than 0.05 for RVOT and LVA compared with RA). Epicardial fiber strain during the ejection phase was uniformly distributed during RA pacing. However, during ventricular pacing it ranged from 13 +/- 33% (RVOT) and 23 +/- 29% (LVA) of the value during RA pacing in early-activated regions to 268 +/- 127% (RVOT) and 250 +/- 130% (LVA) of this value in late-activated regions. Epicardial blood flow ranged from 81 +/- 22% (RVOT) and 79 +/- 23% (LVA) in early-activated regions to 142 +/- 42% (RVOT) and 126 +/- 22% (LVA) in late activated regions. In all above values P less than 0.05 compared with RA. During RVOT pacing, gradients of epicardial electrical activation time, fiber strain, and blood flow pointed in the same direction. Compared with RVOT pacing, during LVA pacing all gradients were opposite in direction, and the gradients of electrical activation time and blood flow appeared to be smaller. These results indicate that timing of electrical activation is an important determinant for the distribution of fiber strain and blood flow in the left ventricular wall.

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The distribution of blood platelets flowing in arterioles (21-35 microns) of the mesentery of anesthetized rabbits was studied using intravital fluorescence microscopy. Sites were selected without upstream branch points within at least 10 vessel diameters. The distribution was determined by counting in flashed video frames the number of platelets present in each of six equal segments across the vessel. Only platelets were counted that could be localized objectively within a thin optical section around the median plane of the vessel. It could be shown that differences in counting volume between the six segments were negligible. Because of the use of flashed pictures (flash duration less than 0.1 ms; interval 180 ms), the method is independent of differences in velocity over the cross-sectional area of the vessel. In all measurements (15 sites in 13 vessels in 10 animals) the distribution was nonuniform, the wall segments containing the highest platelet numbers. The general distribution as calculated from all measurements (total platelet number 6,571) and expressed in percentages was found to be 23.0, 14.6, 12.5, 12.1, 13.6, and 24.2.