The lecture below can be accessed on the Disease Management section of the Cleveland Clinic, under Allergy and Immunology (to go to this link and see others in the series, please click here)
Acute Myocardial Infarction
Adam W. Grasso
Sorin J. Brener
Published: July 2014
Complications of acute myocardial infarction (MI) include ischemic, mechanical, arrhythmic, embolic, and inflammatory disturbances (Table 1). Nevertheless, circulatory failure from severe left ventricular (LV) dysfunction or one of the mechanical complications of MI account for most fatalities.
Table 1: Complications of Acute Myocardial Infarction
|Ischemic||Angina, reinfarction, infarct extension|
|Mechanical||Heart failure, cardiogenic shock, mitral valve dysfunction, aneurysms, cardiac rupture|
|Arrhythmic||Atrial or ventricular arrhythmias, sinus or atrioventricular node dysfunction|
|Embolic||Central nervous system or peripheral embolization|
Ischemic complications can include infarct extension, recurrent infarction, and postinfarction angina.
Infarct extension is a progressive increase in the amount of myocardial necrosis within the infarct zone of the original MI. This can manifest as an infarction that extends and involves the adjacent myocardium, or as a subendocardial infarction that becomes transmural.
Following fibrinolytic therapy, reocclusion of the infarct-related artery (IRA) occurs in approximately 5% to 10% of patients by the time of discharge, and in 25% to 30% of patients at 1 year.1 These patients also tend to have a poorer outcome.2,3 Reinfarction is more common in patients with diabetes mellitus or prior MI. With the advent of primary percutaneous coronary intervention (PCI) and stent placement, risk of reinfarction has dropped substantially, to approximately 3% during the first 90 days after MI.4
Recurrent infarction in a separate territory may be difficult to diagnose within the first 24 to 48 hours after the initial event. Multivessel coronary artery disease is common in patients with acute MI. In fact, angiographic evidence of complex or ulcerated plaques in noninfarct-related arteries is present in up to 40% of patients with acute MI.
Angina that occurs from a few hours to 30 days after acute MI is defined as postinfarction angina. The incidence of postinfarction angina is highest in patients with non–ST-elevation MI (approximately 25%), and in those treated with fibrinolytics rather than with PCI.
Reinfarction occurs more often when the IRA reoccludes than when it remains patent; however, reocclusion of the IRA does not always cause reinfarction because of abundant collateral circulation. After fibrinolytic therapy, reocclusion is found on angiograms of 5% to 10% of patients and is associated with a worse outcome. When primary PCI is used for reperfusion, the incidence of IRA reocclusion is much lower. Of particular concern is the development of acute stent thrombosis, usually within the first few hours after primary PCI in ~1% of patients.5
The pathophysiologic mechanism of postinfarction angina is similar to that of unstable angina—plaque rupture—and should be managed in a similar manner. Patients with postinfarction angina have a worse prognosis with regard to sudden death, reinfarction, and acute cardiac events, compared with those without such symptoms.
Signs and Symptoms
Patients with infarct extension or postinfarction angina usually have continuous or intermittent chest pain, with protracted elevation in the creatine kinase (CK) level and occasionally, new electrocardiographic changes.
The diagnosis of infarct expansion, reinfarction, or postinfarction ischemia can be made with echocardiography or nuclear imaging. New wall motion abnormalities, larger infarct size, new area of infarction, or persistent reversible ischemic changes help substantiate the diagnosis. CK-MB is a more useful marker for tracking ongoing infarction than troponin, given its shorter half-life. Re-elevation and subsequent decline in CK-MB levels suggest infarct expansion or recurrent infarction. Elevations in the CK-MB level of more than 50% over a previous nadir are diagnostic for reinfarction.
Medical therapy with aspirin, heparin, nitroglycerin, beta blocker, and statin is indicated in patients who have had a MI and are experiencing ongoing ischemic symptoms.6 Depending upon the clinical situation, additional anti-platelet therapy (clopidogrel, prasugrel, ticagrelor) and a glycoprotein IIb/IIIa inhibitor (eptifibatide) may also be given. An intra-aortic balloon pump (IABP) should be inserted promptly in patients with hemodynamic instability or severe LV systolic dysfunction. However, it must be borne in mind that severe peripheral vascular disease of the aortoiliac and femoral arteries is a contraindication to IABP placement, due to increased risk of lower extremity ischemia. IABP use is also contraindicated in patients with severe aortic valve insufficiency (AI), because their AI will be worsened by the balloon pump. Coronary angiography should be performed in patients who are stabilized with medical therapy, but emergency angiography also may be undertaken in unstable patients, since restoration of coronary arterial blood flow, either by percutaneous or surgical means, is associated with an improved prognosis.
Mechanical complications of acute MI include ventricular septal defect (VSD), papillary muscle rupture or dysfunction, cardiac free wall rupture (FWR), ventricular aneurysm, LV failure with cardiogenic shock, dynamic LV outflow tract (LVOT) obstruction, and right ventricular (RV) failure.
Ventricular Septal Defect
Independent predictors of VSD are shown in Box 1.
|Box 1: Independent Predictors of Ventricular Septal Defect|
|Worse Killip class on admission|
|Increased heart rate on admission|
VSD formerly occurred in 1% to 2% of patients after acute MI in the prethrombolytic era (Figures 1 and 2). The incidence has decreased dramatically with reperfusion therapy. For example, the GUSTO-I (Global Utilization of Streptokinase and Tissue plasminogen activator for Occluded coronary arteries) trial demonstrated an incidence of VSD of approximately 0.2%.7 Similar rates of VSD occurrence post-MI have been obtained from studies utilizing primary PCI.8 VSD was commonly seen 3 to 7 days after MI in the prefibrinolytic era, but now is generally diagnosed within the first 24 hours after MI.7,8
The defect usually occurs at the junction of preserved and infarcted myocardium in the apical septum with anterior MI, and in the basal posterior septum with inferior MI. VSD almost always occurs in the setting of a transmural MI and is more often seen in anterolateral MIs. The defect might not always be a single large defect; in 30% to 40% of patients, a meshwork of serpiginous channels can be identified.
Signs and Symptoms
Early in the disease process, patients with VSD may appear relatively comfortable, with no clinically significant cardiopulmonary symptoms. Rapid recurrence of angina, together with hypotension, pulmonary edema, and frank cardiogenic shock can develop later in the course.
Rupture of the ventricular septum is often accompanied by a new harsh holosystolic murmur best heard at the left lower sternal border. The murmur is accompanied by a thrill in 50% of cases. This sign is generally accompanied by a worsening hemodynamic profile and biventricular failure. Therefore, it is important that all patients with MI undergo a careful, well-documented cardiac examination at presentation and daily thereafter.
An electrocardiogram (ECG) may show atrioventricular (AV) nodal or infranodal conduction delay abnormalities in approximately 40% of patients. Echocardiography with color flow Doppler imaging is the best method for diagnosing VSD. There are two types of VSD, which can be visualized best in different echocardiographic planes. A posterobasal VSD is best visualized in the parasternal long axis with medial angulation, apical long axis, and subcostal long axis. An apical-septal VSD is best visualized in the apical four-chamber view. Echocardiography can define LV and RV dysfunction—important determinants of mortality—as well as the size of the defect and degree of left-to-right shunt by assessing flow through the pulmonary and aortic valves. In some cases, it may be necessary to use transesophageal echocardiography to assess the VSD.
VSD can also be diagnosed by demonstrating an increase or “step-up” in oxygen saturation in the right ventricle and pulmonary artery (PA) on right-heart catheterization. The location of the step-up is significant, because there have been case reports of increased peripheral PA oxygen saturation due to acute mitral regurgitation (MR). Diagnosis involves fluoroscopically-guided measurement of oxygen saturation in the superior and inferior vena cava, right atrium, right ventricle, and PA. With a left-to-right shunt across the ventricular septum, one will generally detect an increase in oxygen saturation of more than 8% when going from the right atrium to the right ventricle and PA. A shunt fraction can be calculated as follows:
where is the pulmonary flow, is the systemic flow, SaO2 is the arterial oxygen saturation, MvO2 is the mixed venous oxygen saturation, PvO2 is the pulmonary venous oxygen saturation, and PaO2 is the pulmonary arterial oxygen saturation. A calculated >2 suggests a large shunt, which is not likely to be well-tolerated by the patient.
Early surgical closure is the treatment of choice, even if the patient’s condition is stable. Initial reports suggested that delaying surgery could reduce surgical mortality.9However, these perceived benefits were probably the result of selection bias,10 because the mortality rate in patients with VSD treated medically is 24% at 72 hours and 75% at 3 weeks. Therefore, in order to reduce mortality, patients with postinfarction VSD should be strongly considered for early urgent surgical repair.
Cardiogenic shock and multisystem failure are associated with a high surgical mortality. This further supports earlier operative management before complications develop.11 Mortality is highest in patients with basal septal rupture associated with inferior MI (70%, compared with 30% in patients with rupture due to anterior infarction). The mortality rate with basal septal rupture is higher because of increased technical difficulty and the frequent need for mitral valve repair or replacement in the patients with MR.12 Regardless of the VSD location and the patient’s hemodynamic condition, surgery should always be considered, because it is associated with a lower mortality rate than conservative management.6
Intensive medical management should be started to support the patient before surgery. Unless there is significant aortic regurgitation, an IABP should be inserted urgently as a bridge to a surgical procedure. The IABP will decrease the systemic vascular resistance (SVR) and shunt fraction while increasing coronary perfusion and maintaining blood pressure. After the IABP is inserted, vasodilators can be used, with close hemodynamic monitoring. Vasodilators can also reduce left-to-right shunting and increase systemic flow by reducing SVR. Caution should be exercised to avoid a greater decrease in pulmonary vascular resistance than in SVR and a consequent increase in shunting. The vasodilator of choice is intravenous sodium nitroprusside (SNP), which is started at 0.5 to 1.0 µg/kg/min and titrated to a mean arterial pressure (MAP) of 60 to 75 mm Hg.
MR after acute MI portends a poor prognosis, as demonstrated in multiple trials.13–16 MR of mild-to-moderate severity is found in 13% to 45% of patients following acute MI. Whereas most MR is transient in duration and asymptomatic, MR caused by papillary muscle rupture (Figure 3) is a life-threatening complication of acute MI. Fibrinolytic agents decrease the incidence of rupture; however, when present, rupture can occur earlier in the post-MI period than in the absence of reperfusion. Although papillary muscle rupture was reported to occur between days 2 and 7 in the prefibrinolytic era, the SHOCK (SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK?) Trial Registry demonstrated a median time to papillary muscle rupture of 13 hours.17 Papillary muscle rupture is found in 7% of patients in cardiogenic shock and contributes 5% of the mortality after acute MI.18,19
MR can occur as a result of a number of mechanisms, including mitral valve annular dilatation secondary to LV dilatation, papillary muscle dysfunction with associated ischemic regional wall motion abnormality in close proximity to the insertion of the posterior papillary muscle, and partial or complete rupture of the chordae tendineae or papillary muscle.18
Papillary muscle rupture is most common with an inferior MI. The posteromedial papillary muscle is most often involved because of its single blood supply through the posterior descending coronary artery.20 The anterolateral papillary muscle has a dual blood supply, being perfused by the left anterior descending (LAD) and left circumflex coronary arteries. In 50% of patients with papillary muscle rupture, the infarct is relatively small.
Signs and Symptoms
Complete transection of both papillary muscles is rare and usually results in immediate pulmonary edema, cardiogenic shock, and death. Physical examination of the patient with anterolateral papillary muscle rupture usually demonstrates a new pansystolic murmur, which is audible at the cardiac apex and radiates to the axilla or the base of the heart. If there is a posteromedial papillary muscle rupture, the murmur radiates to the left sternal border and may be confused with the murmur of VSD or aortic stenosis (intensity of the murmur does not always predict the severity of MR). It is important to remember that in patients with severe heart failure, poor cardiac output, or elevated left atrial pressures, the murmur of severe MR may be soft or absent.
The ECG usually shows evidence of a recent inferior or posterior MI. The chest radiograph generally shows pulmonary edema. Focal pulmonary edema can occur in the right upper lobe when flow is directed at the right pulmonary veins.
The diagnostic test of choice is two-dimensional echocardiography with color flow Doppler imaging. In severe MR, the mitral valve leaflet is usually flail. Color flow imaging can be useful in distinguishing papillary muscle rupture with severe MR from VSD. Transthoracic echocardiography may not fully reveal the amount of MR in some patients with posteriorly-directed jets. In these individuals, transesophageal echocardiography can be particularly useful.
Hemodynamic monitoring with a PA catheter can reveal large (>50 mm Hg), early v waves in the pulmonary capillary wedge pressure (PCWP). Patients with VSD can also have large v waves as a result of augmented pulmonary venous return in a left atrium of normal size and decreased compliance, but they appear later in the cardiac cycle. Further complicating the diagnostic picture, patients with severe MR and reflected v waves in the PA tracing may have an increase in oxygen saturation in the PA.21 With Swan-Ganz catheterization, MR can be distinguished from VSD by two characteristics: First, prominent v waves in the PCWP tracing preceding the incisura on the PA tracing are almost always secondary to severe MR. Second, in order to identify a significant increase in oxygen content associated with VSD, blood for oximetry should be obtained with fluoroscopic control from the central PA rather than from its more distal branches.
Patients with papillary muscle rupture should be rapidly identified and receive aggressive medical treatment while being considered for surgery. Medical therapy includes vasodilator therapy. SNP is useful in the treatment of patients with acute MR. SNP directly decreases SVR, thereby reducing the regurgitant fraction and increasing the forward stroke volume and cardiac output. SNP can be started at 0.5 to 1.0 µg/kg/min and titrated to a MAP of 60 to 75 mm Hg. An IABP should be inserted to decrease LV afterload, improve coronary perfusion, and increase forward cardiac output. Patients with hypotension may tolerate vasodilators after an IABP is inserted, but certainly not before.
Patients with papillary muscle rupture should be considered for emergency surgery, because the prognosis is dismal in medically treated patients. Coronary angiography should be performed before surgical repair, since revascularization during mitral valve repair or replacement is associated with improved short-term and long-term mortality.19,22 Additional surgical candidates include patients with moderate MR who do not clinically improve with afterload reduction.
Left Ventricular Free Wall Rupture
While LV FWR was more common before the era of reperfusion, it now affects only 0.5% of MI patients. However, FWR carries with it a substantial mortality rate of 20%.8,23 The timing of cardiac rupture is within 5 days of infarction in 50% of patients and within 2 weeks in 90% of patients. FWR occurs only among patients with transmural MI (Figure 4). Risk factors include advanced age, female gender, hypertension, first MI, and poor coronary collateralization.
Compared with individuals who did not receive fibrinolytic agents, MI patients administered such drugs were found to experience FWR earlier in their clinical course. However, their overall risk of FWR was not increased.23–25 Although any wall can be involved, cardiac rupture most commonly occurs at the lateral wall.
FWR occurs at three distinct intervals, with three distinct pathologic subsets. Type I increases with the use of fibrinolytics, occurs early (within the first 24 hours) and is a full-thickness rupture. Type II rupture occurs 1 to 3 days after MI and is a result of erosion of the myocardium at the site of infarction. Type III rupture occurs late and is located at the border zone between infarcted and normal myocardium.
The reduction in Type III ruptures as a result of the advent of fibrinolytics has resulted in no change in the overall FWR rate. It has been postulated that Type III ruptures may occur as a result of dynamic LVOT obstruction and the resultant increased wall stress.26
Signs and Symptoms
Sudden onset of chest pain with straining or coughing can suggest the onset of myocardial rupture. Acutely ruptured patients often have pulseless electrical activity (electromechanical dissociation) and sudden cardiac death. Other patients may have a more subacute course as a result of a contained rupture, or pseudoaneurysm. They may complain of nausea, pain suggestive of pericarditis, and are usually hypotensive. In an older study evaluating 1,457 patients with acute MI, 6.2% had FWR. Approximately one third of these patients presented with a subacute course.27
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. A junctional or idioventricular rhythm, low-voltage complexes, and tall precordial T waves may be evident on the ECG. Additionally, a large number of patients have transient bradycardia just before rupture, as well as other signs or symptoms of increased vagal tone.
Although there is generally insufficient time for thorough diagnostic testing in the management of patients with acute rupture, transthoracic echocardiography is the emergent test of choice. Echocardiography typically demonstrates a pericardial effusion with findings of cardiac tamponade. These findings include right atrial (RA) and RV diastolic collapse, dilated inferior vena cava, and marked respiratory variations in mitral and tricuspid inflow. Additionally, a Swan-Ganz PA catheter may reveal hemodynamic signs of tamponade, with equalization of the RA, RV diastolic, and PCWPs.
The goal of therapy is to diagnose the problem early, and perform emergency open heart surgery to correct the rupture. Emergency pericardiocentesis may be performed immediately on patients with tamponade and severe hemodynamic compromise while arrangements are being made for transport to the operating room. The procedure carries with it considerable risk because as the intrapericardial pressure is relieved, communication is re-established between the intra- and extraventricular spaces, often leading to further bleeding into the pericardium. Medical management has no role in the treatment of these patients, except for the use of vasopressors to maintain blood pressure temporarily as the patient is rushed to the operating room.
Pseudoaneurysm is caused by contained rupture of the LV free wall. The aneurysm may remain small or undergo progressive enlargement. The outer wall is formed by the pericardium and mural thrombus. The pseudoaneurysm communicates with the body of the left ventricle through a narrow neck whose diameter is by definition less than 50% of the diameter of the fundus.
Signs and Symptoms
Some pseudoaneurysms remain clinically silent and are discovered during routine investigations. However, some patients have recurrent tachyarrhythmia, systemic embolization, and heart failure. Some patients have systolic, diastolic, or to-and-fro murmurs related to the flow of blood across the neck of the pseudoaneurysm during LV systole and diastole. A chest radiograph may show cardiomegaly, with an abnormal bulge on the cardiac border. There may by persistent ST-segment elevation on the ECG. The diagnosis may be confirmed by echocardiography, magnetic resonance imaging, or computed tomography.
Spontaneous rupture occurs without warning in approximately one third of patients with a pseudoaneurysm. Therefore, surgical intervention is recommended for all patients, regardless of symptoms or the size of the aneurysm, to prevent sudden death.
Left Ventricular Failure and Cardiogenic Shock
LV dysfunction is to be expected after an acute MI. The degree of dysfunction correlates with the extent and location of myocardial injury. Non-infarcted myocardium can also become temporarily hypokinetic or akinetic due to ischemic “stunning.” Patients with small, more distal infarctions may have discrete regional wall motion abnormalities with preserved overall LV function because of compensatory hyperkinesis of the unaffected segments.28 Prior MI, older age, female gender, diabetes, and anterior infarction are risk factors for development of cardiogenic shock.29,30
In the late 1960’s, Killip and Kimball31 developed a classification scheme to categorize patients’ prognosis based on their physical exam findings (Table 2). Individuals were classified into four subsets, from “no evidence of congestive heart failure” (Class I) to “cardiogenic shock” (Class IV). The authors reported a 67% mortality rate for Class IV patients.
Table 2: Incidence of Heart Failure in Acute Myocardial Infarction
|Killip Class||Characteristics||Patients (%)||30-Day Mortality (%)|
|I||No evidence of congestive heart failure||32||6|
|II||Rales, ↑ jugular venous distention, or S3||38||17|
Forrester and colleagues32,33 classified patients by their hemodynamic profile using a PA catheter to define PCWP and cardiac index. They reported a 50% mortality rate in the most compromised subset (PCWP >18 mm Hg; cardiac index <2.2 L/min/m2). Results of the GUSTO-I trial have indicated that 7% to 8% of acute MI patients develop cardiogenic shock. Fibrinolysis did not materially affect mortality, which remained high at 58%.34,35 In contrast, in the SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK (SHOCK) trial, urgent percutaneous or surgical revascularization markedly reduced early and late mortality, when compared with continued medical therapy, including IABP.36 Finally, when the study population of GUSTO-I was restricted to those with non-ST-elevation MI, the 30-day risk of mortality for pooled Killip Class III and IV patients was considerably lower, at 14%.37
Patients can develop cardiogenic shock in association with an acute MI due to multiple causes, including large LV infarction, severe RV infarction, VSD, FWR, acute MR, or pharmacologic depression of LV function (beta blockers in MI from a proximal LAD lesion). Patients who have cardiogenic shock as a result of acute MI typically have severe multivessel disease, with significant involvement of the LAD.38,39 Generally, at least 40% of the LV mass is affected in patients who present in cardiogenic shock as a result of a first MI.40,41 In patients with prior MI and baseline depressed LV function, a smaller acute insult can result in cardiogenic shock (Figure 5).
Signs and Symptoms
Patients who present in Killip Class III often have respiratory distress, diaphoresis, and cool, clammy extremities in addition to the typical signs and symptoms of acute MI. Patients in Killip Class IV (cardiogenic shock) can have severe orthopnea, dyspnea, and oliguria and may have altered mental status, as well as multisystem organ failure from hypoperfusion. It may be possible to palpate an area of dyskinesia on the precordium. An S3 gallop, pulmonary rales, and elevated jugular venous pressure are common findings on physical examination.
Patients with cardiogenic shock caused by acute MI generally have extensive electrocardiographic changes demonstrating a large infarct, diffuse ischemia, or prior infarcts. If these changes are absent, another cause of shock such as sepsis should be considered. Chest radiography usually reveals pulmonary edema. Laboratory tests may demonstrate lactic acidemia, renal failure, and arterial hypoxemia.
The patient in cardiogenic shock should be monitored with a PA catheter and an arterial line. These can help distinguish between primary LV failure and other mechanical causes of cardiogenic shock, as discussed above.
Transthoracic echocardiography helps determine the extent of dysfunctional myocardium. It also helps identify other mechanical complications of MI that may be contributing to cardiogenic shock, such as papillary muscle rupture.
A patient in cardiogenic shock should have a LV assist device (IABP, Impella™, TandemHeart™) placed urgently to reduce afterload, improve cardiac output, and enhance coronary perfusion. Medical therapy with vasodilators (e.g., nitroglycerin and SNP), angiotensin-converting enzyme (ACE) inhibitors and loop diuretics should be used as tolerated. Intravenous nitroglycerin is the first-line drug of choice among vasodilators because it is less likely to produce coronary steal than SNP and helps protect against ischemia. The starting dose is 10 to 20 µg/min and it may be increased by 10 µg/min every 2 to 3 minutes to a goal MAP of 70 mm Hg. Intravenous SNP can be added if further reduction in afterload is necessary. SNP is started at 0.5 to 1.0 µg/kg/min and is also titrated to a MAP of approximately 70 mm Hg. Patients who are hypotensive on presentation (MAP <70 mm Hg) may not tolerate vasodilators or other blood pressure-lowering agents prior to placement of an assist device.
ACE inhibitors improve LV performance and decrease myocardial oxygen consumption by reducing the cardiac afterload of patients with heart failure and acute MI. ACE inhibitors can reduce infarct expansion if started in the first 12 hours of an MI if the patient is not already in cardiogenic shock. It is recommended that captopril be started early, at 3.125 to 6.25 mg every 8 hours, with each dose subsequently doubled as tolerated to a maximum dose of 50 mg every 8 hours. Patients with mild pulmonary edema can be treated with diuretics such as intravenous (IV) furosemide, adjusted for serum creatinine and history of diuretic use.
Beta-adrenergic agonists such as dobutamine or dopamine may be needed for patients with severe heart failure and cardiogenic shock. This therapy should generally be reserved for those who have failed mechanical LV support and maximal vasodilator therapy, or for those with a RV infarct. Phosphodiesterase inhibitors such as milrinone may be beneficial for some patients, but can increase ventricular ectopy. The bolus may be omitted in patients with marginal blood pressures. Some patients may need norepinephrine to maintain arterial pressure. Norepinephrine is started at 2 µg/min and titrated to maintain the MAP at approximately 70 mm Hg.
PCI and emergency coronary bypass surgery have been associated with improved prognosis for patients in cardiogenic shock, reducing the mortality rate from 80% to 50%. Emergency PCI or surgical revascularization is indicated for patients with severe multivessel disease.6 Substantial left main coronary artery stenosis is also an indication for coronary bypass, as ongoing studies evaluate the efficacy of left main stenting in this situation. Other surgical modalities that may be considered include implantation of LV or biventricular assist devices or extracorporeal membrane oxygenation as a bridge to heart transplantation. Some patients may be gradually weaned from ventricular assist devices after the stunned portion of myocardium recovers, without the need for cardiac transplantation.
Right Ventricular Failure
Mild RV dysfunction is common after MI of the inferior or inferoposterior wall, with an incidence of approximately 40%. Hemodynamically significant RV impairment occurs in only 10% of patients with these types of MI, however (Figure 6).
The degree of RV dysfunction depends on the location of the right coronary artery occlusion. Only proximal occlusions of the right coronary artery (proximal to the acute marginal branch) result in marked dysfunction.42 The degree of RV involvement also depends on the amount of collateral flow from the LAD and the degree of blood flow through the thebesian veins. Because the right ventricle is thin-walled and has lower oxygen demand, there is coronary perfusion during the entire cardiac cycle; therefore, widespread irreversible infarction is rare.
Signs and Symptoms
The triad of hypotension, jugular venous distention with clear lungs, and absence of dyspnea has high specificity but low sensitivity for RV infarction.43 Severe RV failure can manifest with signs and symptoms of a low cardiac output state, including diaphoresis, cool clammy extremities, and altered mental status. Patients often have oliguria and hypotension. Other causes of severe hypotension in the setting of an inferior MI include bradyarrhythmia, acute severe MR, and VSD.
Patients with isolated RV failure have elevated jugular venous pressure and right-ventricular S3 heart sound in the setting of a normal lung examination. The presence of jugular venous pressure greater than 8 cm H2O and Kussmaul’s sign is highly sensitive and specific for severe RV failure. A rare but clinically important complication of RV infarction is right-to-left shunting secondary to increased pressures in the RA and RV and opening of the foramen ovale. This should be considered in patients with RV infarction and persistent hypoxemia.
Electrocardiographically, patients present with inferior ST elevation in conjunction with ST elevation in the V4R lead. These findings have a positive predictive value of 80% for RV infarction.44 The chest radiograph usually does not show pulmonary venous hypertension.
Echocardiography is the diagnostic study of choice for RV infarction. It will demonstrate RV dilation and dysfunction and usually LV inferior wall dysfunction as well. It is also helpful in excluding cardiac tamponade, which can mimic RV infarction hemodynamically. The hemodynamic profile of acute RV infarction can also be due to an acute pulmonary embolism in the absence of a cardiac ischemic event.
Hemodynamic monitoring with a PA catheter typically reveals high RA pressures with a low PCWP, because RV failure results in underfilling of the left ventricle and a low cardiac output. A RA pressure of higher than 10 mm Hg and a RA pressure-to-PCWP ratio of 0.8 or greater strongly suggest RV infarction.45 If severe LV dysfunction is also present, the PCWP can be higher. In some patients, RV dilatation can impair LV performance by flattening or bowing of the septum into the left ventricle. This can restrict ventricular filling and elevate the PCWP.
Volume loading to increase LV preload and cardiac output is key to the management of RV infarction. Some patients require several liters in 1 hour to reach a target central venous pressure of 15 mm Hg and a target PCWP of 15 mm Hg. It is important to have hemodynamic monitoring with a PA catheter in these patients, because overzealous fluid administration can further decrease LV output. This occurs as a result of septal shift toward the left ventricle and an intrapericardial pressure shift. When volume loading is insufficient to improve cardiac output, inotropes are indicated. Administration of dobutamine can increase cardiac index and improve RV ejection fraction. Vasodilators such as nitroglycerin and SNP, while effective for afterload reduction in acute LV infarction, will almost universally cause hypotension and hemodynamic decompensation in acute RV infarction.43
Patients may benefit from reperfusion therapy, because those who undergo successful reperfusion of RV branches have enhanced RV function and a lower 30-day mortality rate.46,47 Patients with RV infarction and bradyarrhythmias or loss of sinus rhythm may have significant improvement with AV sequential pacing. Optimal pacer settings tend to utilize longer AV delays (approximately 200 msec) and a heart rate of 80 to 90 beats per minute.
Although an IABP acts primarily on the LV, there have been case reports of IABP improving the cardiac index when used in combination with dobutamine for acute RV infarction. Pericardiectomy may be considered for patients with refractory shock because it reverses the septal impingement on LV filling. Most patients with RV infarction improve after 48 to 72 hours. An RV assist device is indicated for patients who remain in cardiogenic shock in spite of these measures.
Patients who do not receive reperfusion therapy are at greatest risk for developing this complication (in 10%-30%). Among the various infarct locations, patients with apical transmural MIs are at the highest risk for aneurysm formation, followed by those with posterior-basal infarcts.
The early open artery hypothesis states that early reperfusion should result in improved myocardial salvage and prevention of infarct expansion. Even late reperfusion limits infarct expansion through a number of mechanisms, including immediate change in infarction characteristics, preservation of small amounts of residual myofibrils and interstitial collagen, accelerated healing, the scaffold effect of a blood-filled vasculature, and elimination of ischemia in viable but dysfunctional myocardium. Persistent occlusion of the IRA, on the other hand, can lead to infarct expansion and progressive LV dilation. The aneurysm consists of a stretched portion of the myocardium which contains all three tissue layers and is connected to the ventricle by a wide neck (greater than half the diameter of the fundus). The differences between a pseudoaneurysm (false aneurysm) and true aneurysm are highlighted in Table 3.
Table 3: Differences Between True Aneurysms and Pseudoaneurysms
|Wall||All three layers—scar||Pericardium and thrombus|
Signs and Symptoms
Acute decompensated heart failure and even cardiogenic shock can develop as a result of a large LV aneurysm. Because acute aneurysms expand during systole, contractile energy generated by a normal myocardium is wasted and puts the entire ventricle at a mechanical disadvantage. Chronic aneurysms persist for more than 6 weeks after the acute event, are less compliant than acute aneurysms, and are less likely to expand during systole. Patients with chronic aneurysms may have heart failure, ventricular arrhythmias, and systemic embolization, or they may be asymptomatic. Palpation of the precordium can reveal a dyskinetic segment of the ventricle. An S3 gallop may be heard in patients with poor ventricular function.
Typical electrocardiographic findings include Q waves and ST elevation, which can persist despite application of reperfusion therapy. When electrocardiographic changes (ST elevation) persist for more than 6 weeks, patients may have a chronic ventricular aneurysm. A chest radiograph may reveal a localized bulge in the cardiac silhouette. Echocardiography is the gold standard for accurate identification of the aneurysmal segment. It may also demonstrate the presence of a mural thrombus. Additionally, echocardiography is useful in differentiating true aneurysms from pseudoaneurysms. Magnetic resonance imaging may also be useful and diagnostic for delineating the aneurysmal section.
Acute decompensated heart failure with acute aneurysms is managed with IV vasodilators. ACE inhibitors have been shown to reduce infarct expansion and unfavorable LV remodeling. As tolerated by blood pressure, ACE inhibitors are best started within the first 12 to 24 hours of onset of acute MI because infarct expansion starts early. Corticosteroids and nonsteroidal anti-inflammatory drugs (NSAIDs) should be avoided in the acute setting because they have been shown to promote infarct expansion and aneurysm formation in experimental models. Chronic heart failure with chronic aneurysms can be managed with ACE inhibitors, beta-blockers, and diuretics.
Anticoagulation with warfarin is indicated for patients with a mural thrombus. Patients should be treated initially with IV heparin, with a target partial thromboplastin time of 50 to 70 seconds. Warfarin is started simultaneously. Patients should be treated with warfarin at a target international normalized ratio (INR) of 2 to 3 for a period of 3 to 6 months. It is controversial whether patients who have large aneurysms without thrombus should receive anticoagulants. Many clinicians prescribe anticoagulants for 6 to 12 weeks after the acute phase. Patients with LV aneurysms and a low global ejection fraction (<40%) have a higher stroke rate and should take anticoagulants for at least 3 months after the acute event. Subsequently, they will undergo regular surveillance with echocardiography (usually every year). Anticoagulation should be reinitiated if a new thrombus develops.
Refractory heart failure or ventricular arrhythmias in patients with aneurysms are indications for surgical resection, also referred to as LV reconstructive surgery. Resection of the aneurysm may be followed by conventional closure or newer techniques to maintain LV geometry. Revascularization is beneficial for patients with a large amount of viable myocardium around the aneurysmal segment.
Dynamic Left Ventricular Outflow Tract Obstruction
Dynamic LVOT obstruction is an uncommon complication of acute anterior MI and was first described in a case report by Bartunek and associates.48
This event is dependent on compensatory hyperkinesis of the basal and midsegments of the left ventricle in patients with distal LAD infarcts. Predictors of enhanced regional wall motion in noninfarct zones are the absence of multivessel disease, female gender, and higher flow in the infarct-related vessel. The increased contractile force of these regions decreases the cross-sectional area of the LVOT during systole. The resulting increased velocity of blood through the outflow tract can produce decreased pressure below the mitral valve and cause the leaflet to be displaced anteriorly toward the septum (Venturi effect). This results in further LVOT obstruction resulting from systolic anterior motion (SAM) of the anterior mitral valve leaflet, and in posteriorly-directed MR.
It has been postulated that dynamic LVOT obstruction can play a role in causing FWR. LVOT obstruction leads to increased end-systolic intraventricular pressure, which induces increased wall stress of the weakened, necrotic infarct zone. This frequently fatal complication occurs most often in women, in older patients (older than 70 years), and in those without prior MI.
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 LVOT obstruction may appear to be in cardiogenic shock with severe orthopnea, dyspnea, and oliguria, and may have altered mental status from cerebral hypoperfusion. Patients may present with a new systolic ejection murmur heard best at the left upper sternal border, with radiation to the neck. Additionally, a new holosystolic murmur can be heard at the apex, with radiation to the axilla as a result of SAM of the mitral leaflet. An S3 gallop, pulmonary rales, hypotension, and tachycardia can also be present.
Echocardiography is the diagnostic test of choice and can accurately characterize the hyperkinetic segment, LVOT obstruction, and mitral leaflet SAM.
Treatment centers on decreasing myocardial contractility and heart rate while expanding intravascular volume and increasing afterload (modestly). Beta blockers should be added slowly and with careful monitoring of heart rate, blood pressure, and SvO2. Patients can receive gentle IV hydration with several small (250 mL) boluses of 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 with a PA catheter. Vasodilators, inotropes, and balloon pumps should be avoided because they can increase LVOT obstruction. In contrast, the pure peripheral vasoconstrictor phenylephrine can be useful, since it will increase afterload and diminish the LVOT gradient.
Ventricular arrhythmia is a common complication of acute MI, occurring in almost all patients, even before monitoring is possible. It is related to the formation of re-entry circuits at the confluence of the necrotic and viable myocardium, as well as to irritable ischemic myocardium.
Premature ventricular contractions occur in approximately 90% of patients with acute MI. At the other end of the spectrum, the incidence of ventricular fibrillation (VF) is approximately 2% to 4%. Although lidocaine has been demonstrated to reduce somewhat the rate of primary VF in patients with MI, there is no survival benefit and there may be excess mortality. Therefore, it is not recommended that patients receive prophylactic lidocaine therapy.49 Amiodarone may be used in patients with MI with nonsustained ventricular tachycardia (VT), or after defibrillation for VF. The recommended dosing is a bolus of 150 mg and then administration of 1 mg/min for 6 hours, followed by 0.5 mg/min. When starting this medication for VF or pulseless VT, the bolus should be increased to 300 mg (the 150 mg bolus can be repeated in 10 minutes). Ventricular arrhythmias not responding to amiodarone may be treated with lidocaine (1 mg/kg bolus to a maximum of 100 mg, followed by a 1-4 mg/min drip),50or with procainamide. Polymorphic VT is a rare complication of acute MI, usually associated with recurrent ischemia. It can be treated with amiodarone, lidocaine, procainamide, or a combination of drugs, as described for the more commonly-observed monomorphic VT. Accelerated idioventricular rhythm, sometimes referred to as “slow VT,” often occurs during the reperfusion phase of PCI, is self-limited, and usually does not require treatment.
The importance of VF in the setting of MI has been re-evaluated in the context of the interaction between severe systolic dysfunction and the potential for sudden cardiac death. Implantable cardioverter-defibrillators have been shown to reduce mortality in post-MI patients with an ejection fraction less than or equal to 30%, regardless of whether or not ventricular dysrhythmia has been observed.51
Supraventricular arrhythmias occur in less than 10% of patients with acute MI, and are not directly ischemic in origin. Because patients who develop these arrhythmias tend to have more severe ventricular dysfunction than those who do not, they will generally experience a worse outcome. Although isolated RA infarction or small inferior infarcts leading to atrial arrhythmias are not associated with higher mortality rates, the appearance of atrial arrhythmias usually heralds the onset of heart failure in the setting of acute anterior MI.
Bradyarrhythmias, including AV block and sinus bradycardia, occur most commonly with inferior MI. Complete AV block occurs in approximately 20% of patients with acute RV infarction. Infranodal conduction disturbances with wide complex ventricular escape rhythms occur most often in large anterior infarctions and portend a very poor prognosis.
Temporary transvenous pacing is indicated for patients who present with Mobitz type 2 second-degree AV block, complete AV block, or asystole. Consideration for transvenous pacing should be given to patients with bifascicular block or “trifascicular block” (bifascicular block with concurrent first-degree AV block) in the setting of acute MI.52 Pacing is not indicated for the patient in sinus bradycardia or AV dissociation with a slow sinus rate and a more rapid ventricular escape rhythm as long as the patient is maintaining adequate hemodynamics. If mild symptoms exist, the initial treatment for these rhythm disturbances is IV atropine, 0.5 to 1.0 mg. This may be repeated every 5 minutes, to a maximum dose of 2 mg.
The incidence of clinically evident systemic embolism after MI is less than 2%. The incidence increases in patients with anterior wall MI. The overall incidence of mural thrombus after MI is approximately 20%. Large anterior MI may be associated with mural thrombus in as many as 60% of patients.53,54
Most emboli arise from the left ventricle as a result of wall motion abnormalities or aneurysms. Atrial fibrillation in the setting of ischemia can also contribute to systemic embolization.
Signs and Symptoms
The most common clinical manifestation of embolic complications is stroke, although patients may have limb ischemia, renal infarction, or mesenteric ischemia. Most episodes of systemic emboli occur within the first 10 days after acute MI. Physical findings vary with the site of the embolism. Focal neurologic deficits occur in patients with central nervous system emboli. Limb ischemia manifests with limb pain in a cold, pulseless extremity. Renal infarction manifests with flank pain, hematuria, and acute renal insufficiency. Mesenteric ischemia manifests with abdominal pain out of proportion to physical findings, anorexia and bloody diarrhea.
In the absence of active bleeding, IV heparin should be started immediately with a target partial thromboplastin time of 50 to 70 seconds and continued until warfarin treatment has brought the INR into the therapeutic range. Warfarin therapy should be started immediately, with a goal INR of 2 to 3, and continued for at least 3 to 6 months for patients with mural thrombi and for those with large akinetic areas detected by echocardiography.
The incidence of early pericarditis after acute MI is approximately 10%. This inflammatory condition usually develops between 24 and 96 hours after MI.55,56 Dressler’s syndrome, or late pericarditis, occurs with an incidence between 1% and 3%, typically 2 to 8 weeks after MI.
The pathogenesis of acute post-MI pericarditis is an inflammatory reaction in response to necrotic tissue. Acute pericarditis thus develops more often in patients with transmural MI. The pathogenesis of Dressler’s syndrome is unknown, but an autoimmune mechanism involving circulating myocardial antigens has been suggested.
Signs and Symptoms
Most patients with early pericarditis report no symptoms. Patients with symptoms from early or late pericarditis describe progressive, severe chest pain that lasts for hours. The symptoms are postural—worse in the supine position—and are alleviated by sitting up and leaning forward. The pain is pleuritic in nature and therefore tends to be exacerbated by deep inspiration, coughing, and swallowing. Radiation of pain to the trapezius ridge is almost pathognomonic for acute pericarditis. The pain also can radiate to the neck and, less commonly, to the arm or back.
A pericardial friction rub on examination is a very specific finding to support acute pericarditis; however, it can be ephemeral, and is not found in all patients with pericarditis (low sensitivity). Frequent cardiac physical examinations will increase the chance of hearing the rub. It is best heard at the left lower sternal edge with the diaphragm of the stethoscope. The rub has three components: atrial systole, ventricular systole, and ventricular diastole. In about 30% of patients with rubs it is biphasic, and in 10% it is uniphasic. A pericardial effusion can cause fluctuation in the intensity of the rub.
Evolving MI changes can mask the diagnosis of pericarditis. Pericarditis produces generalized ST-segment elevation, which is concave-upwards or saddle-shaped. As pericarditis evolves, T waves become inverted after the ST segment becomes isoelectric. Conversely, in acute MI, T waves can become inverted when the ST segment is still elevated. Four sequential phases of electrocardiographic abnormalities have been described in association with pericarditis (Table 4).57
Table 4: Electrocardiographic Changes of Pericarditis
|I||ST elevation, upright T waves|
|II||ST elevation resolves, upright to flat T waves|
|III||ST isoelectric, inverted T waves|
|IV||ST isoelectric, upright T waves|
A pericardial effusion on echocardiography strongly suggests pericarditis, but the lack of an effusion does not rule it out.
Aspirin is the therapy of choice for post-MI pericarditis, 650 mg every 4 to 6 hours, for at least 4 weeks. During this time, a proton-pump inhibitor or other anti-secretagogue should be co-administered for gastric protection. NSAIDs and corticosteroids should be avoided, as they can interfere with myocardial healing and contribute to expansion of the infarct. NSAIDs should also be avoided in patients with coronary artery disease, due to the increased risk of further cardiac events on such drugs. The anti-inflammatory agent colchicine can be used as initial therapy, and is also the preferred add-on drug in the treatment of chronic or recurrent post-MI pericarditis if aspirin monotherapy is ineffective.
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