Mechanical Complications of Myocardial Infarction

Introduction

Myocardial infarction (MI) caused by coronary artery disease remains the leading cause of death in the United States (see Chapter 2 ). Although the advent of coronary care units and early reperfusion therapy has decreased in-hospital mortality rates for acute MI by one-third, acute MI remains an important cause of death. Along with cardiogenic shock (see Chapter 25 ), complications from severe myocardial injury are a major contributor to the in-hospital mortality of MI. Among these complications are right ventricular (RV) infarction, mechanical complications (left ventricular [LV] free-wall rupture, pseudoaneurysm, ventricular septal rupture, or acute mitral regurgitation), ventricular aneurysm, and LV thrombus with or without embolization. Rapid diagnosis of MI and rapid reperfusion therapy have decreased the incidence of these complications; however, when they do occur, survival remains dependent upon timely diagnosis and emergent or urgent treatment.

Right Ventricular Infarction

RV infarction rarely occurs in isolation. Fifty percent of patients with inferior MI and ≤10% of patients with anterior infarction have some degree of RV involvement. Significant RV infarction almost always results from a proximal occlusion of the right coronary artery, which compromises flow to major RV branches. Infarction of the ventricular septum from a proximal left anterior descending (LAD) artery occlusion can also affect RV performance because of the important impact of septal systolic function on RV ejection. The RV is more resistant to infarction than the LV because it has less myocardial oxygen consumption, which is caused by its smaller muscle mass and some oxygen delivery from the endocardium into the thin free wall. Because RV function often recovers after infarction, some investigators have preferred the concept of RV “stunning” rather than permanent infarction.

RV infarction may lead to decreased cardiac output as a result of acute RV distension, a reduction in RV contractility, and the inability to fill the LV through the pulmonary circulation. Acute RV diastolic dysfunction and enlargement produces an impediment to RV filling and leads to venous congestion. The decreased RV forward stroke volume from decreased RV contractility is further compromised by significant functional tricuspid regurgitation as a consequence of acute RV dilation. Moreover, RV systolic performance may be further impeded by passive pulmonary hypertension as a consequence of increased LV end-diastolic pressure (EDP) from concomitant LV infarction. The decrease in RV forward stroke volume ultimately leads to an inability to fill the LV.

Increased RV volume and RVEDP also displaces the interventricular septum toward the volume-compromised LV, further impairing LV filling and compliance. Ischemia of the interventricular septum, with loss of contribution to global RV systolic function, will further reduce RV stroke volume. Finally, RV dilation within the noncompliant pericardium results in elevated intrapericardial pressures, causing a further decrease in LV filling and equalization of diastolic pressures ( Figure 26-1 ).

Diagnosis of Right Ventricular Infarction

Physical Examination in Right Ventricular Infarction

The clinical triad of hypotension, clear lung fields, and an elevated jugular venous pressure has been traditionally considered a marker of RV infarction in patients with inferior MI. However, this triad has a low sensitivity (25%) and high specificity (96%). Kussmaul sign (distention of the jugular vein with inspiration), which is indicative of poor RV compliance, and pulsus paradoxus (a decrease in systolic blood pressure >10 mm Hg with inspiration), which is indicative of increased interventricular dependence when the RV suddenly distends in the fixed pericardial space, may also occur with RV infarction. The primary differential diagnostic consideration is cardiac tamponade from free-wall rupture, which is characterized by the presence of pulsus paradoxus but a lack of Kussmaul sign. Auscultation may reveal a right-sided S3 and S4 gallop and a tricuspid regurgitation murmur. An RV heave may be present from the acutely dilated RV. Occasionally, a harsh systolic murmur may signify the coexistence of an inferobasal ventricular septal defect complicating the concomitant inferoposterior MI. Cannon a-waves in the jugular pulse and bradycardia may suggest concomitant heart block as well. Hepatojugular reflux may also be present. Hypoxemia that does not correct using high-flow oxygen may be indicative of an in atrial shunt through a patent foramen ovale if right atrial pressure exceeds left atrial pressure. However, electrocardiography and noninvasive imaging are the cornerstones of the diagnosis of RV infarction because of their high specificity and the low sensitivity associated with physical examination.

Electrocardiography of Right Ventricular Infarction

RV infarction is frequently diagnosed with the electrocardiogram (ECG) and is best accomplished with the right precordial leads. Because of the association of RV infarction with inferior MI, ST-segment elevation in the inferior leads (II, III, avF) should always be accompanied by assessment of the right precordial leads. Suspicion for RV infarction is heightened further when there is disproportionate ST-segment elevation of lead III greater than lead II. On a right-sided ECG, ST-segment elevation of more than 1 mm in lead V ₄ R is considered significant, and it is also a strong independent predictor of major complications and in-hospital mortality. This ST-segment elevation is believed to represent an ischemic injury to the posterobasal septum. Several other ECG criteria have been proposed in the evaluation of patients with suspected RV infarction ( Figure 26-2 ).

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