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 ).




FIGURE 26-1


Two physiological concepts explaining the detrimental effects of excessive volume loading.

( A ) Normal ventricle: at end-systole (ES), the right ventricular (RV) free wall moves toward the septum compared with end-diastole (ED). ( B ) Pericardial restraining effects ( top , before volume loading; bottom , after excessive volume loading); RV dilation, as a result of excessive volume loading, can lead to the elevation of intrapericardial pressure, an increase in pericardial constraint ( red arrow ), and change geometry because of interventricular septum shift. These changes contribute to the low-output state by decreasing left ventricular (LV) distensibility, preload, and ventricular elastance. ( C and D ) Role of the interventricular septum ( C , pure RV infarction; D , RV infarction with septal ischemia). ( C ) At ES, the RV free wall moves toward the septum. At ED, the RV dilates during diastole, and the septum reverse curves toward the volume-reduced LV. At ES, the septum thickens, but moves paradoxically into the RV, displacing the RV volume despite RV free wall dyskinesis. ( D ) Septal ischemia depresses septal contraction and global LV function, resulting in LV dilation. The septum stops thickening, and there is increased systolic septal displacement into the RV. Pansystolic septal thinning and more extensive paradoxical displacement are associated with further depression of RV performance.

(From Inohara T, et al: The challenges in the management of right ventricular infarction. Eur Heart J: Acute Cardiovasc Care 2:231, 2013.)


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 ).




FIGURE 26-2


Summary of electrocardiography features of right ventricular myocardial infarction (MI) complicating inferior MI.

Coronary angiography confirmed proximal occlusion of the right coronary artery with minor left anterior descending artery disease.

(From Kakouros N, Cokkinos D: Right ventricular myocardial infarction: pathophysiology, diagnosis, and management. Postgrad Med J 86:722, 2010.)


Hemodynamics in Right Ventricular Infarction


The use of invasive hemodynamics at the time of revascularization or during the initial management of an inferior MI can provide insight into the degree of right heart dysfunction ( Figure 26-e1 ). If right atrial function is not compromised, the a-wave and x descent of the right atrial pressure are enhanced, but the y descent may be blunted because of pandiastolic RV dysfunction. In patients with associated right atrial dysfunction, the right atrial pressures are often higher, but the a-wave will be depressed, and the x and y descents will form an “M or W” pattern. A rapid y descent in RV infarction should also prompt consideration of concomitant tricuspid regurgitation (TR). If the TR is severe, the right atrial waveform will approximate the RV waveform. A “square root” sign may be present in the RV tracing, and it reflects poorly compliant RV filling exclusively in early diastole before the filling is suddenly truncated. Criteria for hemodynamically significant RV infarction include: (1) elevated right atrial pressure (RAP) more than 10 mm Hg; (2) an elevated RAP to pulmonary capillary wedge pressure (PCWP) ratio of more than 0.86; (3) a narrow pulmonary artery pulse pressure; (4) an increased ratio of RVEDP to LVEDP; and (5) a decreased pulmonary artery pulsatility index of less than 1 (PAPi = PA pulse pressure/RAP).


Echocardiography of Right Ventricular Infarction


Echocardiography is a widely available and inexpensive tool for the comprehensive evaluation of the structure, function, and hemodynamics of the RV (see also Chapter 31 ). Echocardiography of the RV has many technical challenges, including the complex shape of the RV, incomplete visualization in any single echocardiographic view, and the afterload dependence of the RV, which can lead to inaccurate interpretation of RV performance. Several traditional and novel parameters have been used to assess the degree of RV dysfunction in the setting of inferior MI ( Table 26-1 and Figure 26-3 ). It is important to note that echocardiographic findings of RV dysfunction may be temporary and can resolve within a few hours. Cardiac magnetic resonance (CMR) imaging (see Chapter 33 ) has become the gold standard for noninvasive assessment of RV function, and it is the most accurate method for determining the extent of infarction and RV mass, volume, and ejection fraction ( Figure 26-e2 ).



TABLE 26-1

Echocardiographic Parameters Used to Evaluate Right Ventricular Dysfunction in the Setting of Myocardial Infarction







Parameter



  • Increased ratio of RV to LV end-diastolic dimension



  • RV free wall motion abnormalities



  • Paradoxical interventricular septal motion



  • Fractional area change



  • Tricuspid annular plane systolic excursion



  • Doppler tissue imaging of the peak systolic tricuspid lateral annulus velocity (S′)



  • RV myocardial performance index or Tei index



  • RV peak systolic longitudinal strain



  • RV ejection fraction as assessed by 3D echocardiography


3D , Three-dimensional; LV , left ventricular; RV , right ventricular.



FIGURE 26-3


( A ) A patient with acute proximal right coronary artery (RCA) occlusion, resulting in ( B ) right ventricular dilation and ( C ) depressed right ventricular performance as indicated by reduced tricuspid annular plane systolic excursion (TAPSE). The apical four-chamber view is focused on the right ventricle (RV) to optimize the imaging of the lateral wall and to measure basal (RVD1) and midcavity (RVD2) right ventricular diameters. LA , Left atrium; LV , left ventricle; RA , right atrium.

(From Rallidis L, Makavos G, Nihoyannopoulos P: From right ventricular involvement in coronary artery disease: role of echocardiography for diagnosis and prognosis. J Am Soc Echocardiogr 27:227, 2014.)



FIGURE 26-e1


Hemodynamic recordings from a patient with right atrial (RA) pressure W pattern, timed to ( A ) electrocardiography (ECG) and ( B and C ) right ventricular (RV) pressures. Peaks of W are formed by prominent A waves with an associated sharp X systolic descent, followed by a comparatively blunted Y descent. Peak RV systolic pressure (RVSP) is depressed, RV relaxation is prolonged, and a dip and rapid rise occur in RV end-diastolic pressure (RVEDP).

(From Goldstein JA, et al: Determinants of hemodynamic compromise with severe right ventricular infarction. Circulation 1990;82:359; Fig 4.)





FIGURE 26-e2


Contrast-enhanced cardiovascular magnetic resonance image of ( A ) right ventricular myocardial infarction and ( B ) cine angiogram before and ( C and D ) after percutaneous angioplasty in the corresponding case. Enlarged short-axis view with infarction of the right ventricular wall ( red arrows ) and the inferior left ventricle. The occluded proximal right coronary artery was recanalized with percutaneous angioplasty, and the major right ventricular branch ( white arrows ) was recognized.

(From Inohara T: The challenges in the management of right ventricular infarction. Eur Heart J Acute Cardiovasc Care 2:228, 2013; Fig 1.)




Prognosis with Right Ventricular Infarction


Although RV infarction may result in profound acute hemodynamic effects, arrhythmias, and higher in-hospital mortality, chronic right heart failure secondary to RV infarction is rare. Patients with inferior MI have a substantially increased risk of short-term death during hospitalization if RV involvement is present, but those who survive hospitalization have a relatively good long-term prognosis. This paradox is attributed to the favorable supply–demand characteristics of the RV. Other unique anatomic and physiologic characteristics of the RV also contribute to recovery from RV infarction. First, the pulmonary circulation poses a significantly lower afterload compared with the systemic circulation, thus a minimal perfusion gradient is sufficient to maintain pulmonary blood flow. Second, the thin RV free wall allows for coronary perfusion in both systole and diastole. Third, the RV has a rich collateral arterial supply from the LAD artery, which also provides most of the blood flow to the ventricular septum.


Treatment of Right Ventricular Infarction


A concise summary of the assessment and treatment of inferior MI complicated by RV dysfunction is provided in Figure 26-4 . The mainstay of management of RV infarction is immediate revascularization. Once coronary flow has been established, attention is then directed toward hemodynamic and electrical stabilization. In patients with RV infarction, the dilated noncompliant RV is preload dependent, which will exacerbate a stiff LV that may be preload-deprived. Any measure that further reduces LV preload will be detrimental; therefore, vasodilators and diuretics are contraindicated. Although most patients (75%) with RV infarction are clinically silent without significant hemodynamic compromise, RV infarction may be subsequently “unmasked” with standard treatment for LV infarction (e.g., β-blockade, morphine, and nitroglycerin) that exacerbates the preload sensitive state.




FIGURE 26-4


Treatment algorithm for patients with suspected right ventricular (RV) infarction.

ECMO , Extracorporeal membrane oxygenation; IABP , intra-aortic balloon pump; LVEDP , left ventricular end-diastolic pressure; PAPi , pulmonary artery pulsatility index; PCWP , pulmonary capillary wedge pressure; pRVAD , percutaneous right ventricular assist device; RAP , right atrial pressure; RVEDP , right ventricular end-diastolic pressure; S′, pulse-wave Doppler tissue imaging of the lateral tricuspid annulus; TAPSE , tricuspid annular plane systolic excursion.


Adequate plasma volume expansion, ideally with the aid of invasive monitoring, is essential in the treatment of RV infarction when a low cardiac output and shock are present (see Chapter 25 ). Fluid replacement can be challenging in patients with severe RV dysfunction, but it is recommended to passively “drive” filling of the LV (e.g., a Fontan-like circulation). An overly aggressive approach to volume expansion can result in further clinical deterioration because of the detrimental effects of excess volume loading. Consequent excessive RV dilation can compromise LV output because of pericardial restraint and exaggeration of biventricular interdependence. By compromising LV filling, this situation will decrease LV stroke volume and precipitate a low-output state, particularly if concomitant bradycardia is present. The optimal RV filling pressure in RV infarction is not known; studies that used standard volume loading protocols have not demonstrated improvements in cardiac output, but may have been limited by the variable initial volume status of patients.


Interventricular septal contraction contributes to 30% to 50% of RV stroke work. Patients with intact LV septal contraction (manifest as paradoxical septal motion with preserved thickening on echocardiography) have a better prognosis. In RV infarction associated with significant septal dysfunction, hypotension and low cardiac output may be refractory to initial fluid optimization. Under these circumstances, the use of inotropic stimulation (commonly with dobutamine) will improve RV performance by enhancing global LV contraction and increasing septal displacement into the RV.


Electrical stabilization, including an adequate heart rate and atrioventricular (AV) synchrony, are essential in preserving cardiac output in RV infarction. High-grade AV block and bradycardia-related hypotension without AV block commonly complicate inferior MI. These arrhythmias are attributed to the effects of AV nodal ischemia and cardioinhibitory (Bezold-Jarisch) reflexes arising from stimulation of vagal afferents in the ischemic LV inferoposterior wall. The ischemic RV has a relatively fixed stroke volume as does the preload-deprived LV. Therefore, biventricular output is heart rate–dependent. In some hypotensive bradycardic patients, atropine may restore physiologic rhythm. If temporary pacing is required, right atrial rather than RV pacing is favored to maintain AV synchrony. Acute transvenous pacing can be technically difficult with placing and securing a transvenous lead in the right atrial appendage. In the case of emergency ventricular pacing, both sensing and pacing may be inadequate in an acutely infarcted RV, which is also prone to perforation and ventricular arrhythmias.


Mechanical circulatory support (see Chapter 27 ) may also be necessary for those with refractory hypotension unresponsive to volume resuscitation, inotropic therapy, and treatment of bradyarrhythmias. The use of an intra-aortic balloon pump may be beneficial in patients with RV infarction, although the exact mechanism of benefit is unclear. Balloon pump counterpulsation does not directly improve RV performance; however, the increase in coronary perfusion pressure and effects on LV systolic and diastolic function (e.g., improved contraction of the interventricular septum) may be critical. When RV failure is unresponsive to medical therapy and balloon pump support, an RV assist device may be appropriate. These devices are discussed in Chapter 27 .




Mechanical Complications of Myocardial Infarction


The most dramatic complication of acute MI involves tearing or rupture of acutely infarcted tissue. Such a diagnosis should be considered in MI whenever there is severe hemodynamic instability or a sudden change in clinical condition. The clinical presentation of myocardial rupture depends upon the extent and site of rupture, which includes the interventricular septum, papillary muscles, or the free wall of either ventricle ( Figure 26-5 ). Most ruptures occur in the first 2 to 5 days after MI, when the necrotic myocardium is most vulnerable to rupture from the systolic pressures arising within the LV. Before the reperfusion era, the reported incidence of rupture was up to 6%. In the current era, with advances in timely revascularization and adjunctive pharmacologic therapies, the reported incidence is less than 2% ( Figure 26-e3 ). Definitive management requires surgical intervention but is limited in practice by different thresholds for surgical risk by cardiac surgeons. Figure 26-6 provides an overview of the clinical findings, diagnosis, and treatment of these mechanical complications encountered after an MI.


Aug 10, 2019 | Posted by in CARDIOLOGY | Comments Off on Mechanical Complications of Myocardial Infarction
Premium Wordpress Themes by UFO Themes