![]() ![]() 43 Extramural, epicardial segments in cholesterol-fed rabbits developed intimal atherosclerosis with accumulation of ApoB and proliferating cell nuclear antigens (PCNA) in smooth muscle cells of the intima. This is supported by studies on a cellular and ultrastructural level 43,44 : In contrast to proximal and distal segments, foam cells and modified smooth muscle cells were missing in patients’ tunneled segments. The segment proximal to the bridge frequently shows atherosclerotic plaque formation, although the tunneled segment is typically spared 5,8 ( Figures 3 and 4 ). Presence and Absence of Atherosclerosis in Relation to Myocardial BridgingĬoronary atherosclerosis in association with myocardial bridging has primarily been studied in the LAD. 14 However, myocardial loops and venous bridges appear to have no clinical relevance. Occasionally, a bridge may involve a coronary vein. 8 They are usually thinner compared with LAD bridges (0.1 to 0.3 mm) and have a width of 10 to 15 mm (range 2 to 30 mm). Myocardial loops derive from atrial myocardium, surround the vessel three quarters of the circumference, and return to atrial myocardium. Such “incomplete” bridges may appear during adulthood in concomitant disease, 2 in which a segment is compressed during systole although its surface is not fully covered by myocardial fibers, but by a thin layer of connective tissue, nerves, and fatty tissue. Arterial segments may also be located in a deep interventricular gorge. Copyright 2000 Springer-Verlag GmbH & Co.įerreira et al 12 distinguished between two types of bridging: (1) superficial bridges (75% of cases) crossing the artery perpendicularly or at an acute angle toward the apex, and (2) muscle bundles arising from the right ventricular apical trabeculae (25% of cases) that cross the LAD transversely, obliquely, or helically before terminating in the interventricular septum. Reprinted from Figure 3.8 of reference 36 with permission from Springer-Verlag GmbH & Co. (1) The tunneled segment runs in the interventricular sulcus, giving off a large septal branch, (2) dives into the septal myocardium approaching the right ventricular chamber, (3) passes along the right ventricular endocardium, and (4) returns to the interventricular sulcus. Myocardial bridge of the LAD in consecutive 1 cm thick left ventricular slices with the use of post mortem coronary angiography. 33 De novo, previously nonexistent myocardial bridging has been suggested for both transplanted hearts 34 and HOCM, 35 but conclusive proof is lacking. Myocardial bridging may be found at multiple sites in HOCM, 32 but also in patients without. 31 In the latter, more rigorous contraction may unmask otherwise undetectable bridges. ![]() 26,30Ī high prevalence has also been reported in heart transplant recipients 23 and in patients with hypertrophic obstructive cardiomyopathy (HOCM). In subjects with angiographically normal coronary arteries, the use of provocation tests may enhance systolic myocardial compression and thereby reveal myocardial bridges in ≤40% of cases. The rate of angiographic bridging is <5%, attributable to thin bridges causing little compression. Patients with normal coronaries, use of provocation tests LAD only (13 of 19 patients with an isolated bridge) Patients with otherwise normal angiograms Prevalence of Myocardial Bridging at Autopsy and Angiography Author (Reference No.)Īll patients, exclusion of associated disease Customer Service and Ordering Information.Stroke: Vascular and Interventional Neurology.Journal of the American Heart Association (JAHA). ![]() Circ: Cardiovascular Quality & Outcomes.Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB). ![]()
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