Coronary Artery Bypass Grafting (CABG): Reassessing Efficacy, Safety, and Cost

David K. Cundiff

In This Article

The Nonlinear Progression of CAD

Giroud and colleagues[12] reported a coronary angiogram study of stable angina patients who later had repeat coronary angiography shortly after AMI. They said, "the infarct-related artery was significantly stenosed (ie, greater than 50% blocked) on the first angiogram in only 20 of 92 (22%) patients."[12] In another serial angiogram study, Ambrose and colleagues[13] observed, "in two thirds of patients presenting with an acute ischemic syndrome, the culprit lesion seemed insignificant on a previous coronary angiogram." Overall, the published serial angiographic literature showed that only 13% of the culprit lesions had > 70% stenoses before myocardial infarction.[13,14,15,16,17,18]

Looking at CAD pathogenesis from another perspective, Ambrose and colleagues found numerous atherosclerosis patients with a completely occluded coronary artery but good cardiac function and no myocardial infarction because of the development of collaterals.[13] Betriu and colleagues[19] published the angiographic findings of patients with CAD 1 month after a confirmed AMI. Three percent of the patients had completely normal coronaries, and another 4% had nonobstructive lesions only (ie, arteries with < 50% stenosis).

Dr. Eugene Braunwald's textbook of cardiology summarized this body of recent research by asserting, "mild stenoses can rupture, thrombose and occlude causing a myocardial infarction or sudden death. In contrast arteries with severe preexisting stenoses may proceed to clinically silent complete occlusion, often without infarction, presumably due to the formation of collaterals."[20]

Serial angiograms have demonstrated that atherosclerosis progresses 3-6 times faster in grafted vessels than ungrafted.[21,22] On this issue, Braunwald's heart disease textbook commented, "these data suggest that grafting a vessel with minimal disease even if initially successful may ultimately be harmful to the patient who incurs both the risk of graft closure and accelerated obstruction of the native vessels."[20]

Summarizing the recent studies on pathogenesis of CAD, the high-grade coronary artery stenoses (ie, > 70% blockage) that surgeons typically bypass serve only as markers of the disease's extent. In people who have AMIs, including those who die, the rapid occlusion of mild to moderately stenotic blockages -- not the high-grade lesions -- is the usual cause. Therefore, the rationale of CABG to prolong lives by preventing closure of critically stenosed arteries does not withstand our newer understanding of the unpredictability of the progression of individual CAD lesions.

If the original theoretical basis of efficacy of CABG no longer explains its clinical benefit on angina and survival, what does account for its clinical effects? Analyzing the experimental evidence supporting the procedure may give clues.


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