Manual of Cardiovascular Medicine

I.INTRODUCTION. In-hospital mortality after acute myocardial infarction (MI) is primarily caused by circulatory failure from severe left ventricular (LV) dysfunction and/or other acute complications of MI. These complications can be broadly classified as mechanical, arrhythmic, embolic, and inflammatory (e.g., pericarditis).

II.MECHANICAL COMPLICATIONS. Mechanical complications of acute MI include ventricular septal rupture (VSR), acute mitral regurgitation (MR), ventricular free wall rupture, ventricular pseudoaneurysm, and ventricular aneurysm.

A.Ventricular septal rupture

1.Clinical presentation. VSR occurred in 1% to 2% of patients after acute MI in the prethrombolytic era and accounted for 5% of the peri-infarction mortality. The incidence has dramatically decreased in the postthrombolytic era. In the substudy of the Assessment of Pexelizumab in Acute Myocardial Infarction of 5,745 patients with ST-elevation MI from 2004 to 2006, VSR occurred 0.17% of the time. VSR is more likely to occur in patients who are older, are female, had prior stroke, have chronic kidney disease, and have congestive heart failure. It commonly occurs in the setting of a first MI, in the background of delayed or absent reperfusion therapy. Early revascularization has been associated with lower risk of VSR and may account for the decreasing incidence.

a.Signs and symptoms. Patients with post-MI VSR may appear relatively stable early in the disease course. Recurrence of angina, pulmonary edema, hypotension, and shock may develop abruptly later in the course. Alternatively, precipitous onset of hemodynamic compromise characterized by hypotension, biventricular failure, and a new murmur may be the initial manifestation.

b.Physical findings. The diagnosis should be suspected when a new harsh pansystolic murmur develops, especially in the setting of worsening hemodynamic profile and biventricular failure. For this reason, it is important that all patients with MI have a well-documented cardiac examination at presentation and frequent evaluations thereafter.

(1)The murmur is usually best heard at the lower left sternal border; it is accompanied by a thrill in 50% of the cases. In patients with a large VSR and severe heart failure or cardiogenic shock, the murmur may be of low intensity or inaudible, but the absence of a murmur does not rule out VSR.

(2)Several features differentiate the murmur of VSR from that of acute MR (Table 3.1). The murmur may radiate to the base and the apex of the heart. A third heart sound (S₃), loud P₂, and signs of tricuspid regurgitation may be present.

TABLE 3.1 Differential Diagnosis of a New Systolic Murmur after Acute Myocardial Infarction
Differentiating Features	Ventricular Septal Rupture	Acute Mitral Regurgitation
Location of MI	Anterior = nonanterior	Inferoposterior > anterior
Location of murmur	Lower left sternal border	Cardiac apex
Intensity	Loud	Variable; may be faint
Thrill	50% of patients	Rare
RV failure	More likely	Less likely
Pulmonary edema	Less likely	More likely
V-waves in PCWP	Present or absent	Almost always present
V-waves in PA tracing	Absent	Present
O₂ step-up in PA	Almost always present	Absent

MI, myocardial infarction; PA, pulmonary artery; PCWP, pulmonary capillary wedge pressure; RV, right ventricular.

2.Histopathology. The defect usually occurs at the myocardial infarct border zone, located in the apical septum with anterior MI and in the basal posterior septum with inferior/lateral MI, and with similar frequency. A VSR almost always occurs in the setting of a transmural MI. The defect can be one single large defect or a meshwork of serpiginous channels. Multiple fenestrations are especially common with inferior MIs.

3.Diagnostic testing

a.An electrocardiogram (ECG) may show atrioventricular (AV) node or infranodal conduction abnormalities in approximately 40% of patients.

b.Echocardiography

(1)Transthoracic echocardiography is the test of choice for the diagnosis of VSR. It is important for the clinician to interrogate the area of interest with color Doppler ultrasound. Lowering the Nyquist limit will enable definition and help define the size of the defect. The echocardiogram will also provide insight into the choice of management.

Basal VSR is best visualized in the parasternal long axis with medial angulation, the apical long axis, and the subcostal long axis. Apical VSR is best visualized in the apical four-chamber view.

(2)In some cases, transesophageal echocardiography may help in determining the extent of the defect and assessing suitability for potential percutaneous closure.

(3)Echocardiography may help determine the size of the defect and the magnitude of the left-to-right shunt by comparing flow across the pulmonary valve with flow across the aortic valve.

(4)An assessment of right ventricular (RV) and LV function is key to prognostication and management as they remain important determinants of mortality.

c.Right heart catheterization. Pulmonary artery (PA) catheterization with oximetry measurement can help diagnose the presence and size of a left-to-right shunt. Diagnosis involves fluoroscopically guided measurement of the oxygen saturation in the superior vena cava (SVC) and inferior vena cava (IVC); high, mid, and low right atrium (RA); base, mid, and apical levels of the RV; and the PA.

(1)Normal oxygen saturations for these chambers are 64% to 66% in the SVC, 69% to 71% in the IVC, 64% to 67% in the RA, 64% to 67% in the RV, and 64% to 67% in the PA.

(2)An oxygen step-up at the level of the RV is characteristically seen with VSR. A left-to-right shunt across the ventricular septum typically results in a 5% or greater increase in oxygen saturation between the RA and the RV or PA.

Shunt fraction is calculated as follows:

Q_p/Q_s = (Sao₂ – MVo₂)/(PVo₂ – Pao₂)

In this equation, Q_p is pulmonary flow; Q_s is systemic flow; Sao₂ is peripheral arterial oxygen saturation; MVo₂ is mixed venous oxygen saturation; PVo₂ is pulmonary venous oxygen saturation; and Pao₂ is pulmonary arterial oxygen saturation. MVo₂ is calculated by multiplying the SVC oxygen saturation by three, adding the IVC oxygen saturation, and then dividing the sum by four. PVo₂ is generally assumed to be equal to the peripheral oxygen saturation. Q_p/Q_s ≥ 2 suggests the presence of a considerable shunt.

(3)For a patient with an intracardiac shunt, cardiac output measured by means of the thermodilution technique is inaccurate; the Fick method should be used. The key to measurement of accurate systemic flow in the presence of a shunt is that the oxygen content measured in the PA will be abnormally elevated and must be measured in the chamber immediately proximal to the shunt (i.e., the RA or the SVC and IVC in the case of VSR). The Fick equation is normally calculated as follows:

Cardiac output = O₂ consumption/([Sao₂ − Pao₂] × hemoglobin [Hgb] × 1.34 × 10)

d.Left heart catheterization. Ventriculography performed after angiography or percutaneous coronary intervention (PCI) may reveal VSR if the suspicion is high. Visualization is best in the left anterior oblique projection with cranial angulation.

e.Cardiac magnetic resonance imaging (MRI) and computed tomography (CT) are additional imaging modalities that can be utilized. However, the studies are more difficult to perform in hemodynamically unstable patients and do not play a significant role in this setting.

4.Therapy

a.Priority of therapy. Surgical closure is the treatment of choice (American Heart Association [AHA]/American College of Cardiology [ACC] class I recommendation), although the timing of surgical repair is controversial. Data from the Society of Thoracic Surgeons (STS) database suggests lower mortality in those undergoing delayed repair allowing for evolution of the infarct and stability of the friable myocardium; however, this may simply be a result of survival bias. The mortality rate for patients with VSR treated medically is extremely poor and many do not survive to a delayed surgery. Ultimately the timing of closure must take into account the patient’s stability, the risk of clinical deterioration, surgical comorbidities, and the VSR anatomy.

b.Vasodilators can decrease left-to-right shunt and increase systemic flow by means of reducing systemic vascular resistance (SVR); however, a greater decrease in pulmonary vascular resistance may actually increase shunting. The vasodilator of choice is intravenous nitroprusside, which is titrated to a mean arterial pressure (MAP) of 70 to 80 mm Hg.

c.Mechanical support as a bridge to recovery and closure in patients with VSR is currently given a IIa (level of evidence C) recommendation by the European Society of Cardiology (ESC).

(1)An intra-aortic balloon pump (IABP) may be inserted as a bridge to a surgical procedure, unless there is marked aortic regurgitation. IABP counterpulsation decreases SVR, decreases shunt fraction, increases coronary perfusion, and maintains blood pressure. After insertion of an IABP, vasodilators can be tailored with hemodynamic monitoring.

(2)Case reports/series document other mechanical support devices as a bridge to surgery. These agents should be considered in the setting of cardiogenic shock and include both venoarterial extracorporeal membrane oxygenation (ECMO) and percutaneous ventricular assist devices (pVAD), specifically Tandemheart. Impella use has been reported but there is concern for harm in this setting.

d.Surgical therapy

(1)Cardiogenic shock and multisystem failure are associated with high surgical mortality, further supporting earlier operations on these patients before complications develop. Mortality in patients with cardiogenic shock and VSR was 81% in the SHould we emergently revascularize Occluded coronaries for Cardiogenic shocK? (SHOCK) trial registry. When surgical repair is considered unlikely or futile, appropriate patients may be considered for surgical mechanical support including Total Artificial Heart with a goal to cardiac transplantation.

(2)Surgical mortality is high among patients with basal septal rupture associated with inferior MI (70% compared with 30% in patients with anterior infarcts) because of the greater technical difficulty and the need for concomitant mitral valve repair in these patients, who often have coexisting MR. RV dysfunction because of infarction and/or pressure and volume overload further increases the risk profile of these subjects.

e.Percutaneous therapy. Although surgical closure remains the treatment of choice for VSR, emerging data suggest that percutaneous closure may be a viable treatment for high-risk surgical patients and patients in whom surgical closure has failed. In a 2013 series of 30 patients treated with percutaneous VSR closure (12 as primary closure and 18 for residual VSR after surgery), mortality at 30 days was 42% and 11% in the respective groups. In our institution, a percutaneous approach is utilized for temporary palliation and as a bridge to surgical repair only in patients considered too high risk to undergo surgery.

B.Acute severe MR. Severe MR caused by papillary muscle rupture is a life-threatening complication of acute MI occurring in 0.25% of patients following an MI with a median time to presentation of 13 hours. Acute severe MR accounted for 7% of the cases of cardiogenic shock and 5% of the mortality observed after cardiogenic shock complicating acute MI in the SHOCK registry.

1.Clinical presentation

a.Signs and symptoms. These are variable and depend on the anatomy of the papillary muscle involved and its impact on the integrity of the mitral valve. Patients with partial or complete rupture of one or more heads of the papillary muscle lose significant leaflet support. The resultant torrential MR can result in pulmonary edema and severe respiratory distress along with cardiogenic shock. In the setting of rupture of a minor papillary head or a chordae tendinae, MR may occasionally be better tolerated.

b.Physical findings. A new pansystolic murmur that is audible at the cardiac apex with radiation to the axilla or the base of the heart suggests acute MR. In posterior papillary muscle rupture, the murmur radiates to the left sternal border and may be confused with the murmur of VSR or aortic stenosis. The intensity of the murmur does not predict the severity of the MR. The murmur may often be quiet, soft, or absent in patients with poor cardiac output or in persons with elevated left atrial pressure because of the rapid equilibration of pressures. Resting tachycardia and mechanical ventilation can also make murmur recognition challenging.

2.Pathophysiology. Papillary muscle rupture is more common with an inferior MI because the posteromedial papillary muscle receives blood supply from the posterior descending artery, whereas the anterolateral papillary muscle has dual blood supply from the left anterior descending and circumflex arteries. Papillary muscle rupture is more likely to occur in patients with a first MI, and in many patients the infarct size may be relatively small. The discordance between the degree of hemodynamic instability and the extent of myocardium in jeopardy is often a clue to this diagnosis.

3.Diagnostic testing

a.An ECG usually shows evidence of recent inferior or posterior MI.

b.A chest radiograph may demonstrate pulmonary edema. In some patients, focal pulmonary edema may be seen in the right upper lobe because of flow directed at the right pulmonary veins.

c.Transthoracic echocardiography with Doppler and color flow imaging is the diagnostic modality of choice.

(1)The mitral valve leaflet is usually flail with severe MR.

(2)Color Doppler imaging is useful in differentiating papillary muscle rupture with severe MR from VSR after MI.

d.Transesophageal echocardiography. Transthoracic echo may underestimate the degree of acute MR. Rapid equalization of pressure, resting tachycardia, and poor acoustic windows may contribute to this finding. An eccentric jet in this setting should lead to the performance of transesophageal echocardiography to quantify the severity and elucidate the mechanism of MR.

e.PA catheterization. Hemodynamic monitoring with a PA catheter may reveal large V-waves in the pulmonary capillary wedge pressure (PCWP) tracing. However, patients with VSR may also have large V-waves because of increased pulmonary venous return in a normal-sized and normally compliant left atrium. Among patients with severe MR and reflected V-waves in the PA tracing, oxygen saturation in the PA may be higher than that in the RA, complicating differentiation from VSR. There are two methods for differentiating MR from VSR with a right heart catheter:

(1)Prominent V-waves in the PA tracing before the incisura are almost always associated with acute severe MR (Fig. 3.1).

FIGURE 3.1 Giant V-waves on the pulmonary capillary wedge (PCW) tracing can be transmitted to the pulmonary artery (PA) pressure, producing a notch (asterisk) on the PA downslope. (Adapted from Kern M. The Cardiac Catheterization Handbook. 2nd ed. St. Louis, MO: Mosby-Year Book; 1991. Copyright © 1991 Elsevier. With permission.)

(2)Blood for oximetry is obtained with fluoroscopy to ensure sampling from the main PA rather than distal branches.

4.Therapy

a.Priority of therapy. Papillary muscle rupture should be identified early. Patients should receive aggressive medical therapy and consideration for emergent surgical repair.

b.Vasodilator therapy is beneficial in the treatment of patients with acute MR. Intravenous nitroprusside decreases SVR, reduces regurgitant fraction, and increases stroke volume and cardiac output. Nitroprusside can be titrated to a MAP of 70 to 80 mm Hg.

c.Mechanical support

(1)Intra-aortic balloon pump. Vasodilator therapy is contraindicated in patients with significant hypotension and an IABP should be inserted promptly. An IABP decreases LV afterload, improves coronary perfusion, and increases forward cardiac output. Patients with hypotension can often be given vasodilators after insertion of an IABP to improve hemodynamic values.

(2)ECMO, left ventricular assist device, and pVAD are also potential mechanical support devices that can be used as a bridge to surgical intervention.

d.Percutaneous therapy. Improvement in hemodynamic values and reduction in MR has been reported after PCI in patients with severe MR caused by papillary muscle dysfunction from ischemia but is unlikely to affect severity when mechanical integrity of the valve is compromised. PCI of the infarct-related artery has no role in this setting.

(1)Surgical therapy with concomitant revascularization should be considered immediately for patients with papillary muscle rupture.

(2)The prognosis is very poor among patients treated medically. Even though perioperative mortality (20% to 25%) is higher than that for elective surgical treatment, surgical therapy should be considered for every patient. Long-term survival in those with successful surgical correction is similar to those with an uncomplicated MI.

e.Coronary angiography should be performed before surgical correction, because concomitant revascularization is associated with improved short- and long-term mortality.

C.Ventricular free wall rupture

1.Clinical presentation. The incidence of ventricular free wall rupture after MI in the reperfusion era is <1%. However, ventricular free wall rupture accounts for approximately 10% of mortality after MI. In the SHOCK registry, in-hospital mortality associated with ventricular rupture was >60%. Rupture occurs in the first 5 days in 50% of patients and within 2 weeks in 90% of patients. Ventricular free wall rupture occurs in the setting of a transmural MI. Risk factors include advanced age, female sex, first MI, and poor coronary collateral vessels. The incidence of ventricular free wall rupture is lower in patients treated with primary PCI compared with thrombolytics.

a.Signs and symptoms

(1)Acute course. With acute rupture, patients develop tamponade, electromechanical dissociation, and sudden death. Sudden onset of chest pain with straining or coughing may suggest the onset of myocardial rupture.

(2)Subacute course. Some patients may have a contained rupture and present subacutely with pain suggestive of pericarditis, nausea, and hypotension. In a large retrospective analysis of post-MI patients, 2.6% of patients were found to have sustained subacute ventricular free wall rupture. Bedside echocardiography may reveal localized pericardial effusion or pseudoaneurysm.

b.Physical findings. Jugular venous distention, pulsus paradoxus, diminished heart sounds, and a pericardial rub suggest subacute rupture. New to-and-fro murmurs may be heard in patients with subacute rupture or pseudoaneurysm.

2.Pathophysiology

a.Rupture most commonly occurs at the anterior or lateral wall, although any wall may be involved.

b.There are three distinct types of ventricular free wall rupture (Fig. 3.2):

FIGURE 3.2 Morphologic classification of ventricular free wall rupture. (Reprinted from Becker AE, van Mantgem JP. Cardiac tamponade. A study of 50 hearts. Eur J Cardiol. 1975;3:349–358. Copyright © 1975 Elsevier. With permission.)

(1)Type I generally occurs within the first 24 hours and is a slit-like full-thickness rupture characterized by abrupt onset of symptoms (this rupture type increases with thrombolytics).

(2)Type II occurs as a result of erosion of the myocardium at the site of infarction. The rupture progresses more slowly and symptoms may be subacute.

(3)Type III occurs late and is characterized by expansion of the infarct zone with marked wall thinning and then rupture through the subsequent aneurysmal segment.

3.Diagnostic testing. There may not be time for diagnostic testing in the treatment of patients with acute ventricular free wall rupture.

a.In addition to evidence for new MI, an ECG may show junctional or idioventricular rhythm, low-voltage complexes, and tall precordial T-waves. A large proportion of patients have transient bradycardia immediately preceding rupture.

b.Transthoracic echocardiography reveals findings of cardiac tamponade in patients with a subacute course. Visualization of ventricular free wall rupture may be improved with echocardiographic contrast agents.

c.Cardiac catheterization. Hemodynamic evaluation with a PA catheter may reveal equalization of the RA pressure, RV diastolic pressure, PA diastolic pressure, and PCWP consistent with tamponade. During left heart catheterization, analysis of the arterial waveform may reveal significant respiratory variations in the systolic blood pressure (pulsus paradoxus). Ventriculography performed in the right anterior or left anterior oblique orientation may allow visualization of the rupture.

d.Cardiac MRI and CT can be utilized in hemodynamically stable patients but are usually not available for critical decision making.

4.Therapy. Reperfusion therapy has reduced the overall incidence of cardiac rupture.

a.Priority of therapy. The goal is to rapidly identify the problem and perform emergency surgical treatment.

b.Medical therapy has little role in the treatment of these patients, except for aggressive supportive care in anticipation of surgical correction.

c.Percutaneous therapy

(1)In the setting of hemodynamic extremis, immediate pericardiocentesis should be performed in patients with tamponade as soon as the diagnosis is made and while arrangements are being made for transport to the operating room.

(2)An indwelling catheter should be clamped and left in the pericardial cavity and connected to a drainage bag during transfer to the operating room so that continued decompression of the pericardial cavity with recurrent hemodynamic compromise can be achieved.

d.Surgical therapy. Emergency thoracotomy with surgical repair is the definitive therapy and is the only chance for survival among patients with acute ventricular free wall rupture.

D.Ventricular pseudoaneurysm (i.e., contained rupture)

1.Clinical presentation. Ventricular pseudoaneurysm is more likely to occur with inferior MI than with anterior MI.

a.Signs and symptoms. Pseudoaneurysms may remain clinically silent and be discovered during routine investigation; however, patients may present with chest pain, dyspnea, recurrent tachyarrhythmia, and sudden cardiac death.

b.Physical findings. Systolic, diastolic, or to-and-fro murmurs related to flow of blood across the narrow neck of the pseudoaneurysm during systole and diastole may be appreciated.

2.Pathophysiology. Ventricular pseudoaneurysm is caused by contained rupture of the LV free wall.

a.The outer walls of a true ventricular aneurysm are formed by infarcted myocardium and scar, whereas the outer walls of a pseudoaneurysm are formed by the pericardium and mural thrombus. A pseudoaneurysm may remain small or undergo progressive enlargement.

b.Ventricular pseudoaneurysms communicate with the body of the ventricle through a narrow neck, the diameter of which is typically <50% of the diameter of the fundus.

3.Diagnostic testing

a.A chest radiograph may show cardiomegaly with an abnormal bulge on the cardiac border.

b.An ECG may demonstrate persistent ST-segment elevation, as with true aneurysms.

c.Ventriculography is a reliable method of diagnosis.

d.Echocardiography, cardiac MRI, and cardiac CT may be utilized in evaluation as well. Echocardiographic contrast agents may increase the diagnostic accuracy.

4.Therapy. Spontaneous rupture may occur without warning in approximately one-third of patients with a pseudoaneurysm. Surgical resection is recommended for patients with or without symptoms, regardless of the size of the pseudoaneurysm, to minimize the risk of death.

E.Ventricular aneurysm

1.Clinical presentation. The incidence of ventricular aneurysm after MI in the reperfusion era is approximately <5% and occurs more commonly with anterior MI than with inferior or posterior MI.

a.Signs and symptoms

(1)Acute aneurysm. Acute development of a large ventricular aneurysm can result in severe LV dysfunction and cardiogenic shock. Patients with an acute MI that involves the apex of the LV, particularly those with transmural anteroapical infarcts, are at greatest risk. Acute aneurysms expand during systole. This expansion wastes contractile energy generated by normal myocardium and puts the entire ventricle at a mechanical disadvantage.

(2)Chronic aneurysms persist >6 weeks after MI, are less compliant than acute aneurysms, and rarely expand during systole. Patients with chronic aneurysms may experience heart failure, ventricular arrhythmias, mural thrombus, and systemic embolism, but frequently are asymptomatic.

b.Physical findings. A dyskinetic segment of the ventricle may be apparent during inspection or may be felt during palpation. The apical impulse may be displaced to the left of the mid-clavicular line because of cardiac enlargement. An S₃ or S₄ gallop may be appreciated due to LV dilation and stiffening. A systolic murmur of MR may occur due to changes in LV geometry.

2.Pathophysiology. Infarct expansion and progressive LV dilation are consequences of absent or ineffective coronary reperfusion. The aneurysmal segment initially consists of necrotic tissue and is later replaced by fibrous scar tissue.

3.Diagnostic testing

a.ECG

(1)Acute aneurysm. The ECG reveals evidence of ST-segment elevation MI, which may persist despite evidence of reperfusion.

(2)Chronic aneurysm. ST-segment elevation that persists >6 weeks occurs in patients with chronic ventricular aneurysms.

b.Chest radiography may reveal a localized bulge in the cardiac silhouette.

c.Transthoracic echocardiography is the diagnostic test of choice and accurately depicts the aneurysmal segment. It may also reveal the presence of a mural thrombus. Echocardiography is useful in differentiating a true aneurysm from a pseudoaneurysm. Typically, true aneurysms have a wide neck, whereas pseudoaneurysms have a narrow neck in relation to the diameter of the aneurysm.

d.Cardiac MRI and CT may also be utilized to characterize ventricular aneurysm and better detect thrombus.

4.Therapy

a.Medical therapy

(1)Acute aneurysm. LV failure caused by acute aneurysm is managed with intravenous vasodilators and IABP therapy. Angiotensin-converting enzyme (ACE) inhibitors have been shown to reduce infarct expansion and progressive LV remodeling. Because infarct expansion starts early, ACE inhibitors should be initiated within the first 24 hours of the onset of acute MI if blood pressure allows.

(2)Chronic aneurysm. Heart failure associated with chronic aneurysm formation is managed with afterload reduction, namely with ACE inhibitors.

(3)Anticoagulation. Anticoagulation with warfarin should be prescribed (AHA/ACC class I indication) to patients found to have a LV mural thrombus or embolic phenomenon. See below for discussion.

b.Surgical therapy. Patients with refractory heart failure and/or refractory ventricular arrhythmias should be considered for aneurysmectomy. Surgical resection may be followed by conventional closure or newer techniques (e.g., inverted T-closure and endocardial patch) to maintain LV geometry.

F.LV failure and cardiogenic shock. Please refer to Chapter 4 addressing this condition.

G.RV failure. Mild RV dysfunction is common after MI of the inferior or inferoposterior wall; however, hemodynamically significant RV impairment occurs in only 10% of patients. The proximal right coronary artery (RCA) is commonly involved. Extensive, irreversible RV damage is unusual because the RV has lower oxygen requirements because of its smaller muscle mass, is perfused during systole and diastole, and often receives extensive left-to-right collateral blood flow. Restoring patency of the infarct-related artery usually results in restoration of RV function within 48 to 72 hours.

1.Clinical presentation

a.Signs and symptoms. The triad of hypotension, jugular venous distention, and clear lung fields is highly specific (but has poor sensitivity) for RV infarction. Patients with severe RV failure have symptoms of a low cardiac output state, including diaphoresis; cool, clammy extremities; and altered mental status. Patients often are hypotensive and oliguric. The use of nitrates or β-blockers during routine MI treatment may precipitate profound hypotension and provides the first clue of RV involvement. Table 3.2 lists causes of hypotension among patients with inferior wall MI.

TABLE 3.2 Causes of Hypotension in Patients Presenting with Inferior Myocardial Infarction

Right ventricular infarction

Left ventricular failure

Bradyarrhythmia

Acute severe mitral regurgitation

Ventricular septal rupture

Bezold–Jarisch reflex

b.Physical findings. Patients with RV failure without concomitant LV failure may have elevated jugular venous pressure (JVP) and an RV S₃ with clear lungs. The combination of JVP >8 cm H₂O and Kussmaul sign (i.e., failure of JVP to decrease with inspiration) is sensitive and specific for severe RV failure. Elevated right-sided pressures can occasionally result in right-to-left shunting through a patent foramen ovale and manifest as desaturation. This should be considered in patients with RV infarction and hypoxia. Table 3.3 lists the clinical findings associated with an RV infarction.

TABLE 3.3 Clinical Findings Associated with Right Ventricular Infarction

Hypotension

Elevated jugular venous pressure

Kussmaul sign

Abnormal jugular venous pressure pattern (y ≥ x descent)

Tricuspid regurgitation

Right-sided S₃ and S₄

Pulsus paradoxus

High-grade atrioventricular block

2.Pathophysiology. RV involvement depends on the location of the RCA occlusion. Marked dysfunction occurs only if occlusion is proximal to the acute marginal branch. The degree of RV involvement also depends on the presence of left-to-right collateralization and the extent of diastolic reverse perfusion through the Thebesian veins.

3.Diagnostic testing

a.An ECG usually shows inferior ST-segment elevation. ST-segment elevation in V₄R in the setting of suspected RV infarction has a positive predictive value of 80%. RV infarction is also suggested by ST-segment elevation that is greater in lead III than lead II. ST-segment elevation exceeding 1 mm may be seen in V₁ and occasionally in V₂ and V₃ (Fig. 3.3).

FIGURE 3.3 Electrocardiogram demonstrating acute inferior myocardial infarction with right ventricular involvement.

b.A chest radiograph is usually normal and there is no evidence of pulmonary congestion.

c.Transthoracic echocardiography is the diagnostic study of choice for RV infarction. It may demonstrate RV dilation and severe RV dysfunction and usually shows LV inferior wall dysfunction. It is also useful in differentiating RV infarction from other syndromes that can mimic it, such as cardiac tamponade.

d.PA catheterization. Hemodynamic monitoring with a PA catheter usually reveals high RA pressures with low PCWP. Acute RV failure results in underfilling of the LV and a low cardiac output state. The PCWP is usually low unless concomitant, severe LV dysfunction is present. In some patients, RV dilation can cause decreased LV performance resulting from ventricular interdependence. As the RV dilates, the septum flattens or bows into the LV and restricts ventricular filling. RA pressure >10 mm Hg with an RA pressure to PCWP ratio ≥0.8 strongly suggests RV infarction.

4.Therapy

a.Medical therapy

(1)Fluid administration. Management of RV infarction involves volume loading to increase preload and cardiac output. Fluid boluses up to a liter may be considered with monitoring of hemodynamic status. Overzealous fluid administration in a patient may result in marked RV dilation with a shift in the interventricular septum that can impede LV filling and further decrease LV preload. A central venous pressure of approximately 15 mm Hg may serve as a target.

(2)Inotropes. When volume loading fails to increase cardiac output, the use of inotropes is indicated. Administration of dobutamine will augment RV contractility and increases cardiac output.

b.Percutaneous therapy

(1)Patients who undergo successful reperfusion of the infarct-related artery have improved RV function and decreased 30-day mortality rates. This is ideally achieved by performing immediate primary PCI.

(2)AV sequential pacing may markedly improve hemodynamics in a patient with RV infarction and bradyarrhythmia or loss of sinus rhythm. A longer AV delay of approximately 200 ms and a heart rate of 80 to 90 beats/min are usually optimal for these patients.

(3)In a patient with refractory shock, an IABP may be considered. When available, support with a temporary RV support device like an RP Impella or a Protek Duo should be considered.

H.Dynamic left ventricular outflow tract (LVOT) obstruction. Dynamic LVOT obstruction is an uncommon complication of acute anterior MI. Although this complication has been cited only in case reports, it may be an underappreciated and underreported complication.

1.Clinical presentation

a.Signs and symptoms. Patients may have respiratory distress, diaphoresis, and cool, clammy extremities in addition to the typical signs and symptoms of acute MI. Patients with severe obstruction may appear to be in cardiogenic shock, with severe orthopnea, dyspnea, and oliguria in addition to altered mental status from cerebral hypoperfusion.

b.Physical findings frequently include a new systolic ejection murmur heard best at the left upper sternal border with radiation to the neck. A new systolic murmur can be heard at the apex with radiation to the axilla, as a result of systolic anterior motion (SAM) of the mitral leaflet. An S₃ gallop, pulmonary rales, hypotension, and tachycardia may also occur.

2.Pathophysiology. The dynamic LVOT obstruction that may occur as a complication of acute anterior MI is related to compensatory hyperkinesis of the basal and mid segments of the LV. The increased contractile force of these regions decreases the cross-sectional area of the LVOT. The resultant increase in velocity of blood through the outflow tract can produce decreased pressure below the mitral valve and cause anterior mitral valve leaflet displacement toward the septum (i.e., Venturi effect). This results in further outflow tract obstruction and MR. It has been postulated that this complication can play a role in ventricular free wall rupture. LVOT obstruction leads to increased end-systolic intraventricular pressure, which leads to increased stress of the weakened, necrotic infarcted zone.

3.Diagnostic testing. Transthoracic echocardiography is the diagnostic test of choice and helps evaluate the hyperkinetic segments, the LVOT obstruction, and the presence of systolic SAM of the mitral leaflet.

4.Medical therapy is focused on decreasing myocardial contractility and heart rate while expanding intravascular volume and increasing afterload modestly.

a.β-blockers should be added judiciously and with careful monitoring of the heart rate, blood pressure, and cardiac output.

b.Intravenous hydration should be initiated with several small (250 mL) boluses of normal saline to increase preload and decrease LVOT obstruction and SAM. The patient’s hemodynamic and respiratory status should be monitored closely during this therapeutic intervention.

III.ARRHYTHMIC COMPLICATIONS. Arrhythmias are a common complication after acute MI and are associated with significant mortality. Please refer to the dedicated chapters for further discussion.

IV.EMBOLIC COMPLICATIONS. The contemporary incidence of LV mural thrombus after acute MI is approximately 1% to 2%. The incidence of mural thrombus in patients with a large anterior wall MI may increase to approximately 10%, especially in the absence of timely reperfusion. Other factors associated with LV mural thrombus include decreased LV ejection fraction, wall motion abnormalities, and LV aneurysm.

A.Clinical presentation

1.Signs and symptoms. The most common clinical presentation of an embolic complication is stroke, although patients may have limb ischemia, renal infarction, and intestinal ischemia. Most episodes of systemic embolization occur in the first 2 weeks after acute MI.

2.Physical findings. The physical findings depend on the site of embolism.

a.Patients with stroke present with neurologic deficits.

b.Embolism to the peripheral circulation results in limb ischemia and cold, pulseless, and painful extremities.

c.Renal infarctions may cause hematuria and flank pain.

d.Mesenteric ischemia causes abdominal pain and bloody diarrhea.

3.Diagnostic testing

a.Transthoracic echocardiography is the initial diagnostic test of choice to evaluate for LV mural thrombus. Echocardiographic contrast agents may increase the diagnostic accuracy.

b.Cardiac MRI has similar specificity but is more sensitive than echocardiography in the detection of an LV mural thrombus.

B.Therapy with anticoagulation is recommended in the early setting of a ventricular thrombus associated with an acute MI and is a class IIa recommendation by the ACC/AHA.

1.Vitamin K antagonists reduce the rate of embolization. Intravenous heparin or low molecular weight heparin can be used in the acute setting until therapeutic on warfarin. Goal international normalized ratio is 2 to 3. Anticoagulation does not necessarily resolve the thrombus and it may become calcified and laminated over time. Controversy exists on the duration of anticoagulation necessary if there is persistence of the thrombus beyond 3 to 6 months.

2.Novel anticoagulants such as dabigatran, rivaroxaban, and apixaban have not been studied in this population and not currently approved for this indication.

3.For those requiring dual antiplatelet, care must be taken when initiating “triple therapy.” Bleeding risks must be considered in each individual patient. Newer strategies, such as early discontinuation of aspirin, are being studied in those requiring triple therapy.

V.INFLAMMATORY COMPLICATIONS

A.Early pericarditis. The incidence of pericarditis has decreased in the reperfusion era. Cardiac MRI studies, however, suggest that it is underdiagnosed as it may be asymptomatic, or masked by the ECG changes and symptoms that accompany acute MI.

1.Clinical presentation. Early pericarditis occurs in patients with transmural MI. A transient pericardial friction rub may be audible in some patients before symptoms become prominent.

a.Signs and symptoms

(1)Patients report progressive, severe chest pain that lasts for hours. The pain is postural: worse when the patient is supine and alleviated if the patient sits up and leans forward. The pain is usually pleuritic in nature and is worsened with deep inspiration, coughing, and swallowing.

(2)Radiation of pain to the trapezius ridge is nearly pathognomonic for acute pericarditis and does not occur in patients with ischemic pain. The pain may also radiate to the neck and less frequently to the arm or back.

b.Physical findings. The presence of a pericardial friction rub is pathognomonic for acute pericarditis; however, it can be evanescent.

(1)The rub is best heard at the left lower sternal edge with the diaphragm of the stethoscope.

(2)The rub has three components: one component each in atrial systole, ventricular systole, and ventricular diastole. In about 30% of patients, the rub is biphasic, and in 10% it is uniphasic.

(3)The development of pericardial effusion may cause fluctuations in the intensity of the rub, although the rub may still be heard despite substantial pericardial effusion.

2.Etiology and pathophysiology. Pericarditis typically results from an area of localized pericardial inflammation overlying the infarcted myocardium. The inflammation is fibrinous in nature. The development of an evanescent pericardial rub correlates with a larger infarct and hemodynamic derangements.

3.Diagnostic testing

a.An ECG is important in the diagnosis of pericarditis; however, evolving electrocardiographic changes may make the diagnosis difficult for patients who have had MI. Unlike ischemia, in which the changes are limited to a particular territory, pericarditis produces generalized electrocardiographic changes.

(1)The ST-segment elevation seen with pericarditis is a concave upward or saddle-shaped curve.

(2)In pericarditis, T-waves become inverted after the ST-segment becomes isoelectric, whereas in acute MI, T-waves may become inverted when the ST-segment is still elevated.

(3)Four phases of electrocardiographic abnormality have been described in association with pericarditis (Table 3.4).

TABLE 3.4 Electrocardiographic Changes of Pericarditis
Stage I	ST-elevation, upright T-waves
Stage II	ST-elevation resolves, upright to flat T-waves
Stage III	ST-isoelectric, inverted T-waves
Stage IV	ST-isoelectric, upright T-waves

b.Echocardiography may reveal pericardial effusion, which strongly suggests pericarditis, although the absence of effusion does not rule out the diagnosis. When suspected, an MRI may be confirmatory with enhancement of the involved pericardium noted on gadolinium imaging.

4.Therapy

a.Aspirin is used to manage post-MI pericarditis and doses as high as 650 mg every 4 to 6 hours may be needed (class I recommendation).

b.Nonsteroidal anti-inflammatory agents and corticosteroids should not be used to treat these patients (class III recommendation). These agents may interfere with myocardial healing and contribute to infarct expansion.

c.Colchicine may be beneficial in those when aspirin is not effective. Colchicine 0.6 mg every 12 hours plus conventional therapy with aspirin decreases symptom recurrence in patients with idiopathic pericarditis.

B.Late pericarditis (i.e., Dressler syndrome). This is rarely seen and occurs 1 to 8 weeks after MI. The pathogenesis is unknown, but an autoimmune mechanism has been suggested.

1.Clinical presentation. Patients may present with chest discomfort that suggests pericarditis, pleuritic pain, arthralgia, malaise, fever, pericardial friction rub, elevated leukocyte count, and an elevated sedimentation rate. Echocardiography may reveal a pericardial effusion.

2.Therapy is similar to that for early post-MI pericarditis: aspirin, colchicine, and avoidance of nonsteroidal anti-inflammatory drugs and corticosteroids. However, if >4 weeks have elapsed since the MI, nonsteroidal anti-inflammatory agents may be indicated for severe symptoms.

ACKNOWLEDGMENTS: The authors would like to thank Drs. Michael Bruner, David Tschopp, John Galla, and Debabrata Mukherjee for their contributions to earlier editions of this chapter.