Coronary plaque rupture in patients with myocardial infarction after noncardiac surgery: Frequent and dangerous

Abstract

Purpose

The pathophysiology of acute coronary syndromes (ACS) after noncardiac surgery is not established yet. Thrombosis over a vulnerable plaque or decreased oxygen supply secondary to anemia or hypotension may be involved. The purpose of this study was to investigate the pathophysiology of ACS complicating noncardiac surgery.

Methods

Clinical and angiographic data were prospectively recorded into a database for 120 consecutive patients that had an ACS after noncardiac surgery (PACS), for 120 patients with spontaneous ACS (SACS), and 240 patients with stable coronary artery disease (CAD). Coronary lesions with obstructions greater than 50% were classified based on two criteria: Ambrose's classification and complex morphology. The presence of Ambrose's type II or complex lesions were compared between the three groups.

Results

We analyzed 1470 lesions in 480 patients. In PACS group, 45% of patients had Ambrose's type II lesions vs. 56.7% in SACS group and 16.4% in stable CAD group (P < 0.001). Both PACS and SACS patients had more complex lesions than patients in stable CAD group (56.7% vs. 79.2% vs. 31.8%, respectively; P < 0.001). Overall, the independent predictors of plaque rupture were being in the group PACS (P < 0.001, OR 2.86; CI, 1.82–4.52 for complex lesions and P < 0.001, OR 3.43; CI, 2.1–5.6 for Ambrose's type II lesions) or SACS (P < 0.001, OR 8.71; CI, 5.15–14.73 for complex lesions and P < 0.001, OR 5.99; CI, 3.66–9.81 for Ambrose's type II lesions).

Conclusions

Nearly 50% of patients with perioperative ACS have evidence of coronary plaque rupture, characterizing a type 1 myocardial infarction.

Introduction

Annually, more than 230 million noncardiac surgeries are performed worldwide [1]. Despite improvements in surgical and anesthetic techniques, mortality and cost related to these procedures are raising [2]. Cardiac complications are a major cause of morbidity and mortality after noncardiac surgeries, and patients experiencing a perioperative myocardial infarction (MI) have a high mortality and prolonged hospital stay [3].

The etiology and pathophysiology of myocardial ischemia and infarction after noncardiac surgery is still subject of controversies [1], [3], [4], [5], [6], [7]. In this setting, it may involve thrombosis over a vulnerable plaque or decreased oxygen supply secondary to anemia or hypotension, designated type 1 and type 2 by the universal definition of MI [8], [9]. Depending on the predominant mechanism, prognosis and treatment may be different. Although two retrospective pathology studies reported that nearly 50% of patients with fatal perioperative MI have plaque disruption [10], [11], it has been suggested that, in patients who survive a perioperative MI, the incidence of type 2 MI would be much higher than type 1 [1]. However, there are no studies designed to establish the pathophysiology in patients that survived a perioperative acute coronary syndrome (ACS).

The presence of coronary plaques with complex morphologic features in coronary angiography is the angiographic hallmark of unstable coronary syndromes and correlates with pathologic plaque rupture and thrombus, characterizing a type 1 MI [12], [13], [14], [15], [16], [17], [18], [19]. Ambrose's type II eccentric lesions are strongly associated to disrupted plaques and their finding have 92% specificity [17], [18], [19], [20].

In order to determine the pathophysiology of ACS complicating noncardiac surgery we compared the presence of plaque rupture as a marker of type 1 MI in patients with ACS after noncardiac surgery (PACS), patients in the emergency room with spontaneous ACS (SACS), and patients with stable coronary artery disease (CAD). The present study was performed at the biggest University Hospital in Brazil where, roughly, 40,000 non-cardiac surgeries are performed annually.