Coronary angiography is not picture perfect for determining perioperative MI pathophysiology

Each year more than 200 million patients worldwide have major noncardiac surgical procedures. Many suffer a serious perioperative vascular complication, with myocardial infarction (MI) being the most common. In a study [1] of more than 8,000 patients participating in an international perioperative randomized controlled trial, 5% experienced a perioperative MI within 30 days of their procedure. Most (74%) occurred within 48 hr of surgery and few (35%) were symptomatic. Patients with perioperative MI—whether symptomatic or asymptomatic—were at increased risk for another cardiovascular event and death within 30 days; 11.6% died and most (58%) did so within 48 hr of the MI. Although numerous studies have identified patient and procedural variables associated with an increased risk for perioperative cardiovascular events, few have elucidated the precise pathophysiologic mechanism responsible for perioperative MI or the most effective therapy to prevent it. Two autopsy studies [2,3] with a total of 68 patients reported that approximately half had evidence of coronary plaque rupture, fissure, or hemorrhage that are typical of individuals with an acute coronary syndrome. Conversely, a study [4] of 21 patients who experienced perioperative MI or death after major nonthoracic vascular surgery and had a preoperative coronary angiogram performed within 6 months of the procedure showed that collateralized chronic total occlusions and ‘‘nonobstructive’’ lesions were often the cause of MI and death. Thus, the scant available data suggest that coronary thrombosis is a prominent feature of patients with fatal perioperative MI, but ‘‘demand’’ ischemia is more prevalent in survivors of perioperative MI. The study by Duvall et al. [5] in this issue of CCI attempted to identify the pathophysiology of perioperative MI by reviewing coronary angiograms of 66 individuals who were suspected to have a perioperative MI that led to coronary angiography as determined by a retrospective review of hospital records. Based on the coronary angiographic findings—the degree of stenosis, TIMI flow, ACC thrombus grade, calcification score, and lesion morphology—the etiology of the perioperative MIs were categorized as demand (55% of patients), thrombotic (26% of patients), or non-obstructive (19% of patients). Interestingly, though the study identified demand ischemia as the predominant etiology of perioperative MI, no difference between groups was noted with regard to the occurrence of prolonged hypotension or tachycardia or the preoperative use of antiplatelet agents, beta blockers, or statins. Compared to previously published studies [2–4], this one [5] has a larger number of patients, few of whom (2%) had a fatal MI. In addition, angiography was performed days after MI—rather than weeks or months before—which is more valuable for determining the cause of the event. The investigation by Duvall et al. [5] also has several limitations. First, the study is retrospective and involved a limited (n 5 66), select, subgroup of patients (i.e., those with symptomatic MI and referred for coronary angiography); not included were patients with silent MI, those considered too ‘‘sick’’ (or well) for angiography, and those with fatal MI. Since most (65%) perioperative MIs occur without symptoms [1] and most studies report perioperative mortality rates of 10–25% (5–10 times higher than in the current study), the relevance of the findings of the current study to the general population remains uncertain. Second, since several days elapsed from the MI to coronary angiography (average 3.5 days for all patients, 5.1 days in the demand group, and 1.2 days in the thrombotic group), thrombus formation and subsequent spontaneous lysis in the days prior to angiography may have occurred, which would lead to an overestimation of