Skip to Main Content

INTRODUCTION

An acute coronary syndrome (ACS) encompasses a clinical spectrum of myocardial ischemia ranging from unstable angina (UA) and non–ST-segment elevation myocardial infarction (NSTEMI) to ST-segment elevation myocardial infarction (STEMI), and represents an acute phase of coronary atherosclerosis.1-3 Early recognition, diagnosis, and prompt revascularization of the culprit lesion with percutaneous coronary intervention (PCI) is the contemporary management strategy for patients presenting with STEMI or high-risk NSTEMI.1,2,4,5 Acute plaque rupture and subsequent atherothrombosis with consequent myocardial injury is the most common etiology for ACS; however, myocardial necrosis in the absence of unstable plaque may ensue in critically ill patients who are admitted for non–cardiac-related conditions, such as pulmonary embolism and septic shock. These patients pose a unique diagnostic and management challenge, as concomitant multiorgan failure, electrolyte derangements, and coagulopathy further complicate the clinical picture.6-8 In this chapter, we will review the universal definition of myocardial infarction (MI) and the related patient presentations, risk stratification models, complications, and management strategies.

PATHOPHYSIOLOGY

Acute myocardial infarction is characterized by myocardial necrosis and is diagnosed in the setting of a rise or fall in cardiac biomarkers in conjunction with clinical symptoms of ischemia, new ischemic electrocardiography (ECG) changes, new regional wall motion abnormalities on imaging, or findings on coronary angiography.9-11 Myocardial ischemia ensues when the supply of myocardial oxygen is insufficient relative to myocardial oxygen demand. The pathophysiology of ACS is similar in STEMI, NSTEMI, and UA, and involves a milieu of factors, including endothelial dysfunction, vulnerable plaque, plaque disruption, and atherothrombosis, as summarized in Figure 6-1. It is typically precipitated by rupture or erosion of atherosclerotic plaque within a coronary artery, causing thrombosis and leading to an acute and commonly critical reduction in coronary blood flow.1,12,13 This results in myocardial hypoperfusion, ischemia, diastolic dysfunction, systolic dysfunction, electrocardiographic changes, angina, and ultimately, necrosis.12,14 ST-segment elevation myocardial infarctions usually represent complete occlusion of the coronary artery, while in NSTE-ACS (NSTEMI and UA), there is a critical reduction in flow.

FIGURE 6-1

Summary of pathophysiology of myocardial ischemia: atherothrombosis secondary to spontaneous plaque rupture and demand ischemia (supply–demand mismatch). Pathophysiology of ACS is similar in STEMI, NSTEMI, and UA, and involves a milieu of factors, including endothelial dysfunction, atherothrombosis, vulnerable plaque, plaque disruption, and thrombosis secondary to rupture or erosion of atherosclerotic plaque. However, as commonly seen in critically ill patients, myocardial injury may ensue in the absence of plaque rupture in the setting of increased demand, such as tachyarrhythmias and anemia. ACS = acute coronary syndrome; MI = myocardial infarction; NSTEMI = non–ST-segment elevation myocardial infarction; STEMI = ST-segment elevation myocardial infarction; UA = unstable angina.

The universal classification of myocardial infarction is summarized in Table 6-1. Patients with acute plaque rupture ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.