A Surgeon’s View on the Pathogenesis of Atherosclerosis
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August 19, 2016, my coronary artery bypass grafting procedure #3431. A 67-year-old woman presents with calcified triple-vessel coronary artery disease, hypercholesterolemia, 42 pack-years of smoking, and arterial hypertension. Her left carotid artery is totally occluded, there is stenosis of the right subclavian artery, and she has had previous femoral artery reconstruction. Hours after completion of triple-bypass surgery, I am reflecting about the fact that atherosclerosis does not uniformly involve all large- and medium-sized human arteries, an observation I have made hundreds of times before. We had started the procedure by harvesting the left radial artery, which showed no evidence of atherosclerosis, but increased wall thickness with no visible vasa vasorum (VV) on its adventitial surface. After sternotomy, the left internal mammary artery was dissected, with no atherosclerosis, a thin wall, and again, no visible VV. Both grafts appeared unscathed from atherosclerosis despite the risk factors mentioned. Against the background of her coronary disease and the status of her supra-aortic and femoral vessels, it is remarkable that certain segments of the arterial tree remained free from disease.
Later, her ascending aorta appeared heavily calcified, as did the proximal segments of all epicardial coronary arteries. Distally, the left anterior descending and right coronary arteries exhibited localized calcified plaques, and highly vascularized areas with an inflamed adventitial layer, as well. Suitable sites for bypass insertion could be identified. The only branch of the circumflex artery large enough for a bypass anastomosis, however, displayed maximum sclerosis in its peripheral segments. One short …