Perioperative Myocardial Infarction Pathophysiology

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Similar to myocardial infarction (MI) outside the context of surgery, perioperative MI can result either from atherosclerotic plaque rupture, with subsequent thrombotic occlusion of the involved coronary artery, or from a transient stress-induced mismatch of myo-cardial oxygen supply and demand, often in the setting of a fixed coronary artery stenosis. Among patients with fatal perioperative MI, autopsy series have demonstrated histologic characteristics of recent plaque rupture in approximately 50% of cases. Clini cal studies employing routine continuous electrocardiographic (ECG) monitoring during and after noncardiac surgery demonstrate that the most nonfatal perioperative MIs are preceded by ST-segment depression rather than elevation, supporting the concept that most surgically related MIs result from a myocardial oxygen supply-demand mismatch rather than acute thrombotic occlusion. Clinical studies also suggest that most perioperative MIs are nontransmural in nature. For example, in a study of 232 high-risk individuals who had routine myocar-dial enzyme determinations after noncardiac surgery, 10% of patients were ruled-in for postoperative MI, but only 1% ultimately developed new Q waves on their ECG.

In one large retrospective analysis that examined clinical and angiographic data from 1242 patients who underwent preoperative coronary angiography followed by vascular surgery at a single center from 1984 to 1991, the incidence of perioperative MI or death was 1.7%. In 57% of instances, MI could be attributed to a known occluded collateralized coronary artery, again invoking the development of a myocardial supply-demand mismatch as an important contributor to the development of MI.1 Within this same cohort, however, several patients did develop a postsurgical MI in a coronary territory without a corresponding obstructive lesion on the presurgical angiogram, corroborating the finding from autopsy series that plaque rupture with subsequent vessel thrombosis serves as a potential mechanism for perioperative MI. From a clinical standpoint, the potential for rupture of a previously nonobstruc-tive plaque highlights a mechanism by which perioperative MI can occur despite the absence of ischemia on presurgical stress testing or of significant coronary stenosis on coronary angiography.


In most instances, perioperative MI does not occur during the surgical procedure itself, but rather within the first 48 hours after surgery. Among MIs diagnosed in one cohort of 323 patients undergoing noncardiac surgery, 94% occurred by the second postoperative day, with approximately half occurring on the day of surgery. Indeed, the first few hours after surgery, when the patient is emerging from general anesthesia, is the period that poses the greatest risk for myo-cardial ischemia (Fig. 7-1). This period is associated with multiple hemodynamic stresses and hemato-logic alterations that can predispose to either plaque rupture or a myocardial oxygen supply-demand mismatch. Spikes in plasma catecholamine levels and increases in sympathetic nervous system tone are observed during withdrawal of general anesthesia. These changes typically result in increased heart rate, blood pressure, and myocardial contractility, leading to greater myocardial oxygen demand. Likewise, these neuroendocrine alterations can favor coronary vasospasm or changes in shear stress within the coronary arteries. In addition, tissue injury inherent in

Shear Stress Coronary Artery


Clinically silent in a 50% of cases

Figure 7-1. Pathophysiologic events contributing to the genesis of perioperative myocardial infarction (MI). BP, blood pressure; HR, heart rate; NSTEMI, non-ST-segment elevation myocardial infarction.


Clinically silent in a 50% of cases

Figure 7-1. Pathophysiologic events contributing to the genesis of perioperative myocardial infarction (MI). BP, blood pressure; HR, heart rate; NSTEMI, non-ST-segment elevation myocardial infarction.

surgical procedures tends to engender a procoagulant state, often associated with generalized platelet activation, reductions in endogenous tissue plasminogen activator levels, and increased plasminogen activator inhibitor levels, all changes that can favor coronary thrombosis. Other factors that may adversely influence the balance of myocardial oxygen delivery and demand in the early postoperative period include anemia resulting from surgical blood loss, tachycardia or hypertension induced by postoperative pain, and fluid shifts frequently seen after surgical procedures.


The incidence of myocardial ischemia and infarction in the period surrounding noncardiac surgery is a function of both the type of surgery and the risk profile of the population being studied. The type of surgery influences the likelihood of adverse perioperative cardiac events in two primary ways. First, the specific condition being addressed by the surgical procedure often can serve as an indicator of the patient's likelihood of harboring concomitant coronary artery disease. For example, because of the systemic nature of atherosclerosis, approximately two thirds of patients undergoing vascular surgery also possess significant coronary artery disease, and only 10% of such patients have angiographically normal coronary arteries (Fig. 7-2). Second, the type of surgery being performed can greatly influence the degree of intraoperative hemodynamic stress to which the patient will be exposed, and consequently has a bearing on the likelihood of cardiac complications. Surgical procedures associated with greater amounts of perioperative pain or blood loss, longer periods of recovery and immobility, or greater degrees of intraoperative alterations in blood pressure or heart rate (e.g., cross-clamping of the aorta during abdominal aortic aneurysm repair, manipulation of the carotid

Prevalence of PAD among patients undergoing cardiac catheterization

Atmer (1995) Ciccone (1993) Aronow (1993) Rigatelli (2006)

Sukhija (2003) Bhardwaj (2001)

Prevalence of angiographic CAD among patients with PAD

Figure 7-2. Frequency of concomitant coronary artery disease (CAD) and peripheral arterial disease (PAD) among patients referred for coronary angiography (top) and among patients undergoing coronary angiography in the setting of documented PAD (bottom). (Data from Aronow WS, Ahn C: Am J Cardiol 1994;74: 64-65; Atmer B, et al: International Angiol 1995;14:89-93; Bhardwaj R, et al: Indian Heart J 2001;53:189-191; Ciccone M, et al: International Angiol 1993;12:25-28; Rigatelli G, Rigatelli G: Int J Cardiol 2006;106:35-40; Sukhija R, et al: Am J Cardiol 2003;92: 304-305.)

baroreceptor during carotid endarterectomy) typically are associated with greater likelihoods of perioperative cardiac events.

The incidence of myocardial ischemia during vascular surgical procedures has ranged from 10% to 30% in various studies.2 In one study of 188 individuals who underwent continuous ECG monitoring during and after vascular surgery, ST abnormalities compatible with myocardial ischemia were noted in 20% of patients, 6.5% of whom were ultimately ruled-in for MI. Whereas the duration of ischemia was variable (range, 29 to 625 minutes), in all instances the ST depression was preceded by the onset of tachycardia and marked by eventual resolution of ECG changes without the development of new Q waves.3 The American College of Cardiology/American Heart Association (ACC/AHA) guidelines for perioperative assessment classify specific operations as high risk (>5% reported cardiac event rate), intermediate risk (1%-5%), or low risk (<1%) (Table 7-1).

Table 7-1. Cardiac Risk* for Noncardiac Surgical


Rights were not granted to include this table in electronic media. Please refer to the printed publication.

From Eagle KA, Berger PB, Calkins H, et al: ACC/AHA guideline update tor perioperative cardiovascular evaluation for noncardiac surgery: Executive summary. A report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines. Circulation 2002;105:1257-1267.

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