In a recent issue of Diabetes Care, Schurgin et al. (1) demonstrated a twofold increased prevalence of coronary artery calcification in diabetic patients versus age- and risk-matched nondiabetic patients. This finding suggests two important questions that relate to whether such a finding fully correlates with potential coronary artery stenosis in diabetic patients: 1) does electron beam–computed tomography distinguish between intimal (i.e., plaque) calcification and medial calcification? and 2) if such a distinction is possible, then what fraction of the observed densities in diabetic patients was found to be intimal versus medial?
It has long been known (2) that medial calcification (Moenckeberg’s Atherosclerosis [MA]) is ubiquitous among diabetic patients and is possibly unique to diabetes. Primarily, it has been studied in the lower extremities, where it is inevitably associated with neuropathy. I have found no reports that speculate on or demonstrate the cause of this condition, but I myself have deliberated on its etiology for quite some time. For the past 18 years, I have tested 100% of my new diabetic patients (n = ∼2,000) for both postural hypotension and peripheral circulation. For the latter, I have used oscillometry, which not only elucidates distal arterial stenosis by diminished readings and vanishing exercise pulse, but also demonstrates MA by quantitatively bounding pulses far beyond that which is found in nondiabetic patients. I estimate that ∼20% of my diabetic patients who have a known duration of diabetes of ≥10 years have also postural hypotension, suggesting distal-sympathetic neuropathy of large arteries, and virtually all have MA. I propose that MA, which on roentgenography displays segmental (not continuous) calcification, stems from total or partial loss of sympathetic innervation of segments of the muscular tunica media of larger pulsatile arteries. Frequently, the end stage of muscle denervation is muscle atrophy, muscle death, and calcification.
There are only two clinical consequences of MA. First, because the rigid tunica media must be compressed by high-cuff pressure, blood pressure measurement in the lower extremities (as with ultrasonic studies) can be artifactually elevated (2). Second, vascular surgery becomes much more difficult when one must sew through stone (calcified tunica media). MA cannot possibly compromise circulation, as seen in coronary artery stenosis. Therefore, it is important that studies that attempt to use arterial calcification as an estimate of stenosis also isolate MA as a separate and irrelevant entity.
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After the above comments had been typeset, I came upon a review (3) suggesting a potent role for arterial smooth muscle cells in preventing rupture or vulnerable intimal plaques. Myocardial infarction is not caused by the slow narrowing of coronary arteries but rather by the sudden occlusion of a vessel by ruptured plaque. Apparently the invasion of such friable plaques by proliferating smooth muscle cells is a major factor in transforming vulnerable plaque to stable plaque.
Because MA involves the death of smooth muscle cells, it may well be a significant risk factor—not for stenosis but for occlusion. Thus, MA may not be benign when it is present in coronary arteries.
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Address correspondence to Richard K. Bernstein, MD, New York Diabetes Center, 1160 Greacen Point Rd., Mamaroneck, NY 10543.
