+++
Fibrinolytic-Treated Patients
++
It should be noted that most patients with STEMI at hospitals without PCI capabilities may receive fibrinolysis if primary PCI is not immediately possible (within 60 minutes). These patients in general should be referred for elective angiogram within 3 to 24 hours if logistically possible.
+++
Additional Pharmacotherapy
+++
Inhibition of the Renin-Angiotensin-Aldosterone System
+++
Angiotensin-Converting Enzyme Inhibitors
++
Nine trials, with cumulative enrollment of more than 100,000 patients, have documented the effects of angiotensin-converting enzyme (ACE) inhibitors on mortality in a prospective randomized fashion. These trials can be conveniently divided into those in which all patients were given the drug and those in which drug administration was limited to only patients who were at higher risk. The four nonselective trials include the CONSENSUS-2 (Cooperative New Scandinavian Enalapril Survival Study-2),139 the GISSI-3 (Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto Miocardico-3),140 the ISIS-4 (Fourth International Study of Infarct Survival),50 and the CCS-1 (Chinese Cardiac Study).141 In CONSENSUS-2, intravenous enalaprilat was administered within 24 hours of presentation followed by oral enalapril.139 In the remaining studies, patients did not receive an initial intravenous load, and in three of these four trials, the drug was initiated within 24 hours of presentation. In CONSENSUS-2, mortality was nonsignificantly increased in the treatment group, but in the remaining three trials, a statistically significant reduction in mortality was observed in the treatment group with approximately 5 lives saved per 1000 patients receiving ACE inhibitor therapy.
++
Five trials studied the selective use of ACE inhibitors after AMI. These included the SAVE (Survival and Ventricular Enlargement) study,142 the TRACE (Trandolapril Cardiac Evaluation) study,143 the AIRE (Acute Infarction Ramipril Efficacy) study,144 the SMILE (Survival of Myocardial Infarction Long-Term Evaluation) study,145 and the CATS (Captopril and Thrombolysis Study).146 In SAVE and TRACE, patients were selected by laboratory evidence of an LV ejection fraction of less than 40% or wall motion abnormality. In AIRE, transient HF was the entrance criterion. Clinically and statistically significant mortality reduction of 40 to 70 lives saved per 1000 patients treated was documented in four of these five trials.
++
Given the results of these trials, it is reasonable to initiate therapy with ACE inhibitors within the first 24 hours as long as no contraindications exist and the patient is hemodynamically stable. Patients with an ejection fraction greater than 45% and no clinical evidence of HF, significant mitral regurgitation, or hypertension can have therapy discontinued after determination of risk status while still hospitalized. Because captopril has the shortest half-life, overdosing and inadvertent hypotension may be most easily correctable with the use of this agent. In addition, the short half-life allows for more rapid titration. Intravenous administration is unnecessary unless the patient is unable to take oral medication. Duration of treatment is uncertain; however, many patients will be treated indefinitely.
+++
Angiotensin Receptor Blockers
++
Additional blockade of the renin-angiotensin system with the angiotensin receptor blocker valsartan was investigated in VALIANT (Valsartan in Acute Myocardial Infarction Trial).147 This was a prospective, randomized, double-blinded trial involving 14,808 AMI patients complicated by impaired LV function (ejection fraction ≤ 0.35 on echocardiography or contrast angiography and ≤ 0.40 on radionuclide ventriculography) who were randomized to one of three groups: captopril only, valsartan only, or both captopril and valsartan. After a median follow-up of 25 months, the primary end point of cardiovascular death was 16.9% in the captopril group, 16.8% in the valsartan group, and 16.9% in the combination group (P = not significant). The combination group, however, experienced a statistically significant greater amount of hypotension and renal dysfunction. The results of VALIANT suggest that valsartan is as effective as captopril in the management of AMI patients with LV dysfunction, but the combination of an ACE inhibitor and an angiotensin receptor blocker should be avoided.
++
In OPTIMAAL (Optimal Trial in Myocardial Infarction With the Angiotensin II Antagonist Losartan), 5477 AMI patients were randomized to therapy with losartan or captopril.148 The 3-year primary end point of all-cause mortality occurred in 18% of patients in the losartan group and in 16% of those in the captopril group (P = .07). These studies suggest that ACE inhibitors should be used as primary therapy and that angiotensin receptor blockers should be used in those who cannot tolerate ACE inhibitors.
+++
Aldosterone Antagonists
++
The use of an aldosterone antagonist in patients with AMI complicated by LV dysfunction was studied in the EPHESUS (Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study) trial.149 The 6642 patients with AMI and a resulting ejection fraction < 0.40 were randomized to the aldosterone antagonist eplerenone or placebo 3 to 14 days after admission. After a median follow-up of 16 months, the primary end point of death from any cause occurred in 14.4% of patients in the eplerenone group and 16.7% of patients in the placebo group (P = .008). As expected, eplerenone use was associated with a greater amount of hyperkalemia and less hypokalemia. Based on the results of the EPHESUS trial, it is reasonable to use an aldosterone antagonist in conjunction with β-blockade and ACE inhibition in patients with AMI and subsequent LV dysfunction (ejection fraction < 0.40). Diligent monitoring of the serum potassium must occur with patients who are treated with an aldosterone antagonist.
++
Initiation of β-blockade therapy in the coronary care unit is essential in the management of STEMI patients. β-Blockers have both acute and long-term benefits in STEMI patients treated with either lysis or primary PCI. A meta-analysis of 24,000 AMI patients demonstrated a significant 14% reduction in acute mortality and a 23% reduction in long-term mortality. Short-acting β-blockade with metoprolol should be initiated as early as possible and rapidly titrated to the maximally tolerated dose. In patients who present with shock or HF, the initiation of β-blockers should be delayed until patients become hemodynamically stable.
++
The clinical practice guidelines recommend the following29:
+
Class I
Patients receiving β-blockers within the first 24 hours of STEMI without adverse effects should continue to receive them during the early convalescent phase of STEMI. (Level of Evidence: A)
Patients without contraindications to β-blockers who did not receive them within the first 24 hours after STEMI should have them started in the early convalescent phase. (Level of Evidence: A)
Patients with early contraindications within the first 24 hours of STEMI should be reevaluated for candidacy for β-blocker therapy. (Level of Evidence: C)
++
Numerous trials have demonstrated that statins should be used in the secondary prevention of patients with coronary artery disease.150 In addition to lowering low-density lipoprotein (LDL) cholesterol, statins also improve endothelial function, have antiplatelet effects, and reduce inflammation.151 The benefits of initiating statin therapy during the acute setting in STEMI patients was investigated in the PROVE-IT (Pravastatin or Atorvastatin Evaluation and Infection Therapy) TIMI 22 trial.152 In this study, 4162 ACS patients (33% with STEMI) were randomized to standard therapy with 40 mg of pravastatin or to intense lipid-lowering therapy with atorvastatin 80 mg daily within the first 10 days of hospitalization for ACS. The combined primary end point of death from any cause, myocardial infarction, documented unstable angina requiring rehospitalization, revascularization (performed at least 30 days after randomization), and stroke occurred in 26.3% of the patients in the pravastatin group and 22.4% of patients in the atorvastatin group (P = .005). The final LDL was 95 mg/dL in the pravastatin group and 62 mg/dL in the atorvastatin group (P < .001).
++
It is therefore reasonable to initiate statin therapy during the acute setting of STEMI. Although the data are not clear regarding the benefits of early statin use, STEMI patients are more likely to be on statin therapy in the post–myocardial infarction period if treatment is initiated during the index hospitalization. An LDL goal of less than 70 mg/dL should be achieved.
++
Several studies have investigated the long-term benefits of statin therapy as secondary prevention in patients with coronary artery disease.
+++
Hemodynamic Complications
++
The most common major mechanical complications of acute STEMI include cardiogenic shock, RV infarction, acute mitral regurgitation, ventricular septum rupture, and free wall rupture.
++
Cardiogenic shock as a result of severe LV dysfunction occurs in approximately 7% of patients with myocardial infarction and has a historic mortality of approximately 80%.153 A population-based study analyzed temporal trends in cardiogenic shock complicating AMI in 9076 patients between the years 1975 and 1997.154 The frequency of cardiogenic shock remained relatively stable at 7.1%, and the mortality was approximately 72%. There was a trend toward increased in-hospital survival in the mid to late 1990s, which correlated with the increased application of reperfusion technologies.155 The SHOCK II (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock II) trial showed that the cardiogenic shock mortality remains elevated at near 40%.34
++
The goals for treatment are two-fold: first, hemodynamic stabilization to ensure adequate oxygenation, acid-base balance, and tissue perfusion; and second, rapid investigation of any potentially reversible causes for the patient’s condition. Hypovolemia, which is more common in older patients, those receiving chronic diuretic therapy, and those receiving narcotics or preload-reducing agents, must be corrected. Hemodynamic monitoring by using a balloon-tipped pulmonary artery catheter allows immediate access to valuable hemodynamic information. Forrester and others156,157 described the treatment of patients on the basis of hemodynamic subsets related to pulmonary artery wedge pressure and cardiac output (Table 40–8). The basic goals of this approach include adjustment of the intravascular volume status to bring the pulmonary artery capillary wedge pressure to 18 to 20 mm Hg and optimization of cardiac output with inotropic and/or vasodilating agents. Severely hypotensive patients can be temporarily aided by intra-aortic balloon pumping or possibly by a ventricular assist device. However, the benefits from these mechanical treatments are often temporary, and there may be a significant risk of complications.
++
++
Many observational studies suggest that reperfusion therapy, especially with primary PCI, can reduce the incidence of cardiogenic shock. In one of the largest observational series, 1321 patients with shock in the GUSTO-1 trial were analyzed with respect to revascularization within 30 days versus no revascularization therapy. After multivariable logistic regression analysis, revascularization was independently associated with reduced 1-year mortality (odds ratio [OR], 0.6; 95% CI, 0.4-0.9; P = .007). In-hospital mortality, however, remained high at 56%.158
++
The SHOCK trial evaluated the effect of early revascularization in AMI complicated by cardiogenic shock.159,160 The 302 patients with shock caused by LV dysfunction complicating myocardial infarction were randomly assigned to either emergency revascularization (n = 152) or initial medical stabilization (n = 150). Eighty-six percent of patients in both groups had intra-aortic balloon counterpulsation placement, and revascularization was accomplished by either coronary artery bypass grafting or angioplasty. The median time from symptom onset to revascularization was approximately 12 hours. The revascularization group had lower all-cause mortality at 30 days (46.7% vs 56%; P = .11), 6 months (50.3% vs 63.1%; P = .027), and 1 year (53.3% vs 64.4%; P < .03). There was an interaction between the effect of therapy and age in that only patients younger than age 75 years benefited from revascularization. Although the 20% relative mortality reduction was more modest than expected on the basis of observational studies, only eight patients would have to receive early revascularization to prevent one death at 6 months. This result compares very favorably with benefits achieved by fibrinolytic therapy or primary PCI in patients without shock.
++
Although vasoconstriction has traditionally been associated with cardiogenic shock, vasodilatation can also be present. The mechanism of vasodilatation occurs from an increase in inducible nitric oxide synthase and subsequent increased production of nitric oxide. Use of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine had been proposed as a potential therapy for these patients with vasodialtion,161 but definitive randomized clinical trials demonstrated no benefit of this therapy over placebo.162
++
The SHOCK II trial randomized patients to planned intra-aortic balloon pump (IABP) with PCI versus PCI alone. The trial found that there was not a significant reduction in mortality with IABP use. This has led to a change in guideline recommendations for routine IABP use with shock to Class IIA.
++
The clinical practice guidelines recommend the following29:
+
Treatment of Cardiogenic Shock: Recommendations
Class I
Emergency revascularization with either PCI or CABG [coronary artery bypass graft] is recommended in suitable patients with cardiogenic shock due to pump failure after STEMI irrespective of the time delay from MI onset. (Level of Evidence: B)
In the absence of contraindications, fibrinolytic therapy should be administered to patients with STEMI and cardiogenic shock who are unsuitable candidates for either PCI or CABG. (Level of Evidence: B)
Class IIa
The use of intra-aortic balloon pump (IABP) counterpulsation can be useful for patients with cardiogenic shock after STEMI who do not quickly stabilize with pharmacological therapy. (Level of Evidence: B)
Class IIb
Alternative LV assist devices for circulatory support may be considered in patients with refractory cardiogenic shock. (Level of Evidence: C)
+++
Cardiogenic Shock in Patients With ST-Segment Elevation Myocardial Infarction May Be Caused by Right Ventricular Infarction
++
Involvement of the right ventricle is a common sequela of acute inferior myocardial infarction,163 especially after proximal right coronary artery occlusion.164 However, hemodynamically significant dominant RV dysfunction is much less common, particularly in the reperfusion era, occurring in relatively few patients with RV infarction (RVI).
++
The diagnosis of hemodynamically significant RVI rests on the clinical triad of hypotension, increased jugular venous pressure, and clear lung fields in a patient with acute inferior myocardial infarction. Additional diagnostic techniques that can document RV involvement include ST-segment elevation in right-sided chest leads (V3R or V4R), visualization of RV wall motion abnormalities, and RV dilatation on radionuclide angiography or echocardiography.
++
Hemodynamic measurements in patients with significant RVI demonstrate elevation of the right atrial pressure, usually more than 10 mm Hg, and often show a right atrial pressure/pulmonary artery wedge pressure ratio of 0.8 or more. However, in cases with significant LV dysfunction and increased wedge pressure, this ratio may be lower and does not exclude the presence of significant RV involvement. Rarely, substantial arterial desaturation may be observed because of opening of a patent foramen ovale as a result of increased right atrial pressure and right-to-left atrial shunting. The incidence of bradyarrhythmias is increased in patients with RVI and can be detrimental because an increased heart rate may be necessary to compensate for the decrease in RV (and as a result LV) stroke volume caused by the RVI. Similarly, high-grade atrioventricular block may lead to loss of the atrioventricular synchrony with RV underfilling and further decrease in the RV and LV stroke volume.165
++
Treatment of RVI initially involves volume loading with normal saline to achieve a pulmonary artery wedge pressure of 18 to 20 mm Hg. In some patients, this alone is sufficient to improve cardiac output and systemic pressure. However, some patients will not respond to fluid-loading alone. This may be a result of marked RV enlargement within a relatively noncompliant pericardium, which may result in functional LV compression because of ventricular interaction. In addition to volume loading, use of dobutamine improves cardiac index.166 Patients requiring temporary pacing for heart block may also benefit from arteriovenous sequential pacing rather than lone ventricular pacing. Reperfusion by thrombolysis,167 and especially with primary PCI,168 improves both RV function and clinical outcomes.
++
The natural history of dominant RVI may be favorable because the right ventricle is very resistant to ischemia and usually recovers.163 Most patients, even those with substantial RV dysfunction, spontaneously improve in 48 to 72 hours after the acute event. Patients in shock may benefit from angioplasty of the occluded right coronary artery or from temporary use of an RV assist device; however, many of these patients have associated significant LV dysfunction, which complicates the picture.169 The overall balance between the extent of RV and LV dysfunction is a major determinant of long-term outcome, and the majority of patients with RVI and significant hemodynamic compromise usually have evidence of extensive biventricular infarction and cardiogenic shock.
++
The clinical practice guidelines recommend the following29:
+
Class I
Patients with inferior STEMI and hemodynamic compromise should be assessed with a right precordial V4RR lead to detect ST-segment elevation and an echocardiogram to screen for RV infarction. (See the ACC/AHA/ASE [American Society of Echocardiography] 2003 Guideline Update for the Clinical Application of Echocardiography.) (Level of Evidence: B)
The following principles apply to therapy for patients with STEMI and RV infarction and ischemic dysfunction:
Early reperfusion should be achieved if possible. (Level of Evidence: C)
Atrioventricular synchrony should be achieved, and bradycardia should be corrected. (Level of Evidence: C)
RV preload should be optimized, which usually requires initial volume challenge in patients with hemodynamic instability provided the jugular venous pressure is normal or low. (Level of Evidence: C)
RV afterload should be optimized, which usually requires therapy for concomitant LV dysfunction. (Level of Evidence: C)
Inotropic support should be used for hemodynamic instability not responsive to volume challenge. (Level of Evidence: C)
Class IIa
After infarction that leads to clinically significant RV dysfunction, it is reasonable to delay coronary artery bypass graft surgery for 4 weeks to allow recovery of contractile performance. (Level of Evidence: C)
+++
Acute Mitral Regurgitation
++
Severe mitral regurgitation caused by papillary muscle rupture is responsible for approximately 5% of deaths in AMI patients. Rupture may be complete or partial, and it usually involves the posteromedial papillary muscle because its blood supply is derived only from the posterior descending artery, whereas the anterolateral papillary muscle has a dual blood supply from both the left anterior descending and the circumflex coronary arteries. Most patients have relatively small areas of infarction with poor collaterals, and up to half of the patients may have single-vessel disease.
++
The clinical presentation of papillary muscle rupture is the acute onset of pulmonary edema, usually within 2 to 7 days after inferior myocardial infarction. The characteristics of the murmur vary; as a result of a rapid increase of pressure in the left atrium, no murmur may be audible. Thus a high degree of suspicion, especially in patients with inferior wall infarction, is necessary for diagnosis. Two-dimensional echocardiographic examination demonstrates the partially or completely severed papillary muscle head and a flail segment of the mitral valve. LV function is hyperdynamic as a result of the severe regurgitation into the low-impedance left atrium; this finding alone, in a patient with severe congestive HF, should suggest the diagnosis.
++
The cornerstones of successful therapy are prompt diagnosis and emergency surgery. Emergent placement of an IABP and blood pressure control may be beneficial. The current approach of emergency surgery accrues an overall operative mortality of 0% to 21%, but this appears to be decreasing, and the late results of this approach can be excellent.170,171
++
The clinical practice guidelines recommend the following29:
+
Class I
Patients with acute papillary muscle rupture should be considered for urgent cardiac surgical repair unless further support is considered futile because of the patient’s wishes or contraindications/unsuitability for further invasive care. (Level of Evidence: B)
Coronary artery bypass graft surgery should be undertaken at the same time as mitral valve surgery. (Level of Evidence: B)
+++
Ventricular Septal Rupture
++
Before the reperfusion era, rupture of the ventricular septum occurred in 1% to 3% of acute infarctions and caused approximately 5% of peri-infarction deaths. Data from GUSTO-1, however, indicate that ventricular septal rupture (VSR) was confirmed in only 0.2% of more than 41,000 patients who received lytic therapy for ACS.172 These data indicate that mechanical complications of myocardial infarction appear to be substantially reduced since the advent of reperfusion therapies. When VSR occurs, however, the substrate is quite similar to that of free wall rupture in terms of number of vessels diseased and infarct size. Typically, VSRs associated with anterior infarction are located in the apical septum, and those associated with inferior infarction are located in the basal inferior septum. The prevalence of anterior and inferior infarctions is approximately equal, unlike papillary muscle rupture.173
++
The diagnosis should be suspected clinically when a new pansystolic murmur is present. As with other cardiac ruptures, surgical management is advocated, although the outcome is not as gratifying as in acute mitral regurgitation, because the extent of myocardial necrosis is generally larger.172,174 Percutaneous closure using occluding devices has been done in nonsurgical candidates with variable results: three of seven patients survived to hospital discharge in one report.175
++
The outcome of 91 patients seen in a single institution with VSR after AMI was reviewed by Lemery et al.174 Advanced age, cardiogenic shock, and long delay between septal rupture and surgery correlated with adverse outcome. In patients with cardiogenic shock and ventricular septal defect, only those operated on within 48 hours survived; thus the proportion surviving in this group was only 38%. For patients not in shock, mortality was similar for surgery either within 2 to 14 days or after 14 days; however, the clinical course was unpredictable, with rapid deterioration and death in approximately 50% of these patients.
++
The incidence and outcome of peri-infarction ventricular septal defect in the fibrinolytic era were reported in a study from the GUSTO-1 database.172 In 84 patients (0.2%), ventricular septal defect developed after fibrinolysis, and the median time from symptom onset to the diagnosis of ventricular septal defect was 1 day. Mortality at 30 days in this group was 73.8%, and in patients selected for surgical repair versus those managed medically, 30-day mortality was 47% versus 94%, respectively. All patients presenting in Killip class III or IV died regardless of therapy; however, 1-year survival was excellent in patients surviving the initial 30 days after infarction.
++
The clinical practice guidelines recommend the following29:
+
Class I
Patients with STEMI complicated by the development of a VSR should be considered for urgent cardiac surgical repair unless further support is considered futile because of the patient’s wishes or contraindications/unsuitability for further invasive care. (Level of Evidence: B)
Coronary artery bypass grafting should be undertaken at the same time as repair of the VSR. (Level of Evidence: B)
++
Rupture of the free wall of the left ventricle occurs in 1% to 4.5% of AMI patients and accounts for 10% to 15% of early AMI deaths.176,177,178,179,180,181 Rupture is more common in women, the elderly, and persons with delayed admission to hospital.176,178,181 Although any wall may be involved, rupture of the lateral wall is probably most common. Rupture occurs within the first 5 days of infarction in 50% of cases and within 14 days in 87% of cases. The area of rupture always occurs within the area of infarction but usually is eccentrically located near the junction with normal myocardium. The incidence of rupture has decreased in the fibrinolytic era, but the timing is earlier (24-48 hours).178 Further decrease in the rate of rupture can be achieved by primary PCI.177,181 Survival to discharge in patients with cardiogenic shock included in the SHOCK trial133 was 39.3%, similar to the survival of the other patients.182
++
The clinical presentation is usually sudden electromechanical dissociation. Most patients die even when rapid resuscitative measures, including pericardiocentesis, IABP insertion, and emergent cardiac surgery, are attempted.183 Surgical correction of acute free wall rupture is the treatment of choice, even though surgical mortality can be high.184 Surgical correction can be challenging because of the friability of the tissue that surrounds the rupture. A sutureless patch technique has shown encouraging initial results.185 Early diagnosis is critical and can be achieved by a high degree of suspicion in any patient with sudden hemodynamic deterioration, particularly in the absence of evidence for recurrent ischemia or infarct extension.
++
Alternatively, rupture may be subacute, with periodic small amounts of blood leaking into the pericardial space.183,186 ECG evidence of regional pericarditis may be a warning of impending rupture. Persistent and severe pericardial pain also may be a manifestation of this phenomenon, and the subsequent inflammatory process may serve to wall off the area of pericardial leakage from the remaining pericardial space, forming a false or pseudoaneurysm of the left ventricle. The entity is easily and reliably detected by two-dimensional echocardiography and, when acute, mandates early surgical intervention because of the risk of further expansion of the false aneurysm or rupture producing tamponade and death. It is critically important to have a heightened level of sensitivity for the possibility of subacute rupture in all patients with evidence of pericarditis and especially if a friction rub is present. Immediate performance of echocardiography is mandatory. Chronic LV false aneurysm has a relatively low risk of rupture. Survival is reduced from multiple causes. In one observational series of 21 patients followed for a mean of 3.6 years, mortality was 64%, although no patient died of rupture.187
++
The clinical practice guidelines recommend the following29:
+
Class I
Patients with free-wall rupture should be considered for urgent cardiac surgical repair, unless further support is considered futile because of the patient’s wishes or contraindications/unsuitability for further invasive care. (Level of Evidence: B)
Coronary artery bypass grafting should be undertaken at the same time as repair of free wall rupture. (Level of Evidence: C)
+++
Electrical Complications
++
The bradyarrhythmias are reviewed, but in the modern reperfusion era, the incidence and permanent pacemaker use have declined significantly.188
++
Bradyarrhythmias usually result from ischemic injury to the sinus node/conduction system or abnormal reflexes that are vagally mediated or both. The blood supply to the sinus node arises from the proximal right coronary artery in 55% of patients and from the proximal left circumflex in the remainder. The blood supply to the atrioventricular node arises from the distal branches of the right coronary artery in 90% of patients and from the distal portions of the left circumflex artery in the remaining 10% of patients. The right bundle branch is supplied primarily by the septal perforator vessels originating from the left anterior descending artery, as is the distal portion of the anterior left bundle branch. The main left bundle branch has a dual supply from both distal branches of the right coronary and proximal circumflex vessels, and the posterior division of the left bundle branch is supplied from branches of the circumflex coronary artery.
++
In general, conduction disturbances associated with inferoposterior infarction are related to enhanced vagal activity, tend to be more transient, are often responsive to atropine, and imply a somewhat more benign outcome than those involved in anterior infarction. Conversely, major conduction disturbances associated with anterior infarction usually imply extensive septal necrosis and more significant reduction in LV function.
++
Sinus bradycardia and sinus pauses are usually benign. First-degree atrioventricular block occurs in 4% to 13% of myocardial infarctions. Observation and avoidance of any medications that might prolong atrioventricular conduction are required.
+++
Second-Degree Atrioventricular Block
++
This usually develops within the first 24 hours of myocardial infarction in 3% to 10% of individuals. With type I second-degree atrioventricular block, progressive prolongation of the PR interval is observed. This is usually seen in inferoposterior infarction and may often respond to atropine. A narrow QRS complex is usually present, and temporary pacing is not needed unless the ventricular rate decreases to less than 45 bpm or symptoms of impaired perfusion develop. Type II second-degree atrioventricular block is identified by intermittent dropped beats in the absence of progressive PR prolongation and implies extensive infranodal conduction system injury. Often the QRS complex is wide, indicating associated bundle branch block, and progression to complete heart block occurs in approximately one-third of these patients. Most patients with anterior infarction and type II second-degree atrioventricular block need temporary transvenous pacing because of the unpredictable risk of complete heart block.
++
This occurs in 3% to 12% of AMIs.189,190 In general, patients with inferoposterior infarction progress to third-degree heart block after a period of second-degree heart block and again may demonstrate some responsiveness to atropine or aminophylline.191 A stable junctional escape rhythm is often present, and recovery tends to occur within 3 to 7 days. The occurrence of complete heart block in a patient with inferior infarction confers a 1.5- to 4-fold increase in risk of in-hospital mortality.189,190 Consequently, these patients should be carefully observed, often with standby temporary transcutaneous pacing patches in place. Complete heart block in the presence of anterior infarction usually indicates an extensive area of myocardial necrosis and has a poor prognosis. Most patients require temporary transvenous pacing, and some physicians advocate permanent transvenous pacing. Late mortality in these patients is usually the result of contractile failure or ventricular fibrillation rather than persistent, high-grade atrioventricular block.
++
The occurrence of any new bundle branch block with AMI also identifies patients with extensive infarction who are at higher risk for complications. Unifascicular block, especially left anterior hemiblock, occurs in approximately 5% of patients and has a relatively benign prognosis. Complete right or left bundle branch block occurs in 10% to 15% of patients and most commonly (two-thirds of cases) involves the right bundle branch. Both LBBB and right bundle branch block are associated with higher in-hospital and long-term mortality.192 In the past, the new occurrence of LBBB or right bundle branch block has been a generally accepted indication for temporary transvenous pacing.
++
Permanent transvenous pacing is indicated in patients with persistent complete or high-grade atrioventricular block or persistent type II second-degree atrioventricular block after myocardial infarction and in patients with a new bundle branch block and transient but resolved complete heart block during the acute course of infarction. Occasionally, patients may require an electrophysiologic study to determine the site of atrioventricular block and to aid in the decision about whether permanent pacing is indicated. Permanent pacing also may be indicated in the rare patient with profound sinus node dysfunction. However, this complication is rarely related to myocardial infarction.
++
The clinical practice guidelines recommend the following29:
+
Class I
Permanent ventricular pacing is indicated for persistent second-degree atrioventricular block in the His-Purkinje system with bilateral bundle branch block or third-degree atrioventricular block within or below the His-Purkinje system after STEMI. (Level of Evidence: B)
Permanent ventricular pacing is indicated for transient advanced second- or third-degree infranodal atrioventricular block and associated bundle branch block. If the site of block is uncertain, an electrophysiology study may be necessary. (Level of Evidence: B)
Permanent ventricular pacing is indicated for persistent and symptomatic second- or third-degree atrioventricular block. (Level of Evidence: C)
Class IIb
Permanent ventricular pacing may be considered for persistent second- or third-degree atrioventricular block at the atrioventricular node level. (Level of Evidence: B)
Class III
Permanent ventricular pacing is not recommended for transient atrioventricular block in the absence of intraventricular conduction defects. (Level of Evidence: B)
Permanent ventricular pacing is not recommended for transient atrioventricular block in the presence of isolated left anterior fascicular block. (Level of Evidence: B)
Permanent ventricular pacing is not recommended for acquired left anterior fascicular block in the absence of atrioventricular block. (Level of Evidence: B)
Permanent ventricular pacing is not recommended for persistent first-degree atrioventricular block in the presence of bundle-branch block that is old or of indeterminate age. (Level of Evidence: B)
++
Multiple factors play a role in the genesis of tachyarrhythmias in patients with myocardial infarction. Decreased blood flow leads to anaerobic metabolism, and decreased venous outflow allows accumulation of by-products of this process, resulting in acidosis, increase in extracellular potassium concentration, and an increase in intracellular calcium concentration. In addition to these ionic changes, there may be alterations in sympathetic and vagal tone and increased concentrations of circulating catecholamines. The electrophysiologic correlates of these cellular abnormalities include slowing of conduction and prolongation of refractoriness, which, coupled with the inhomogeneous nature of the infarction process, produces an ideal situation for the occurrence of reentrant arrhythmias. The presence of injury currents may directly enhance phase IV depolarization of Purkinje cells, resulting in increased automaticity. Fiber stretch, resulting from increased atrial and ventricular end-diastolic pressures, is also arrhythmogenic. Finally, reperfusion, possibly caused by intracellular calcium overload or production of free oxygen radicals, may generate reperfusion arrhythmias that may be either automatic or reentrant.
+++
Supraventricular Arrhythmias
++
Sinus tachycardia may occur in up to 25% of patients with acute infarction and often results from pain, anxiety, and sometimes hypovolemia. Persistent sinus tachycardia may be a marker of severe LV dysfunction and is a poor prognostic sign. After relief of pain and assessment for the presence of pulmonary congestion, it is desirable to decrease the heart rate to less than 70 bpm by intravenous administration of β-adrenergic receptor blockers. A short-acting β-adrenergic receptor blocker, such as esmolol, may be appropriate for patients in whom the extent of LV dysfunction is of particular concern.
++
Although its incidence in the era of reperfusion with lytics and PCI has declined, atrial fibrillation may occur in approximately 6% to 21% of patients with acute infarction.193,194,195 Risk factors for the development of atrial fibrillation in AMI include advanced age, HF symptoms, LV dysfunction, and tachycardia on admission.195 Its early presence signifies atrial ischemia; later, it may also represent atrial stretch caused by increased filling pressures, which is why it is associated with such an adverse prognosis. This adverse prognosis is not only limited to the primary hospitalization. Long-term mortality regardless of the treatment received for the presenting myocardial infarction is also affected. Immediate cardioversion is the best treatment for patients with symptomatic rapid atrial fibrillation or in whom the rapid ventricular response produces ischemia. If the ventricular response is only moderate and the patient is asymptomatic, diltiazem or esmolol (in patients with a normal ejection fraction) given intravenously is useful for control of heart rate, along with digoxin given orally; the latter may take 4 to 8 hours for full effect. Recurrent episodes of atrial fibrillation should be suppressed with an antiarrhythmic agent such as procainamide or intravenous amiodarone. The treatment of atrial flutter is similar to that of atrial fibrillation, except that drug treatment is less effective in controlling the ventricular response. Occasionally, atrial overdrive pacing may be used to terminate atrial flutter without resorting to cardioversion. Atrial fibrillation in the setting of AMI, especially if it occurs after admission, is associated with higher mortality and incidence of stroke.193,194
++
The clinical practice guidelines recommend the following29:
+
Class I
Sustained atrial fibrillation and atrial flutter in patients with hemodynamic compromise should be treated with one or more of the following:
Synchronized cardioversion with an initial monophasic shock of 200 J for atrial fibrillation and 50 J for flutter, preceded by brief general anesthesia or conscious sedation whenever possible. (Level of Evidence: C)
For episodes of atrial fibrillation that do not respond to electrical cardioversion or recur after a brief period of sinus rhythm, the use of antiarrhythmic therapy aimed at slowing the ventricular response is indicated. One or more of these pharmacologic agents may be used:
Intravenous amiodarone. (Level of Evidence: C)
Intravenous digoxin for rate control, principally for patients with severe LV dysfunction and heart failure. (Level of Evidence: C)
Sustained atrial fibrillation and atrial flutter in patients with ongoing ischemia but without hemodynamic compromise should be treated with one or more of the following:
β-Adrenergic blockade is preferred, unless contraindicated. (Level of Evidence: C)
Intravenous diltiazem or verapamil. (Level of Evidence: C)
Synchronized cardioversion with an initial monophasic shock of 200 J for atrial fibrillation and 50 J for flutter, preceded by brief general anesthesia or conscious sedation whenever possible. (Level of Evidence: C)
For episodes of sustained atrial fibrillation or flutter without hemodynamic compromise or ischemia, rate control is indicated. In addition, patients with sustained atrial fibrillation or flutter should be given therapy with anticoagulants. Consideration should be given to conversion of sinus rhythm in patients without a history of atrial fibrillation or flutter before STEMI. (Level of Evidence: C)
Reentrant paroxysmal supraventricular tachycardia, because of its rapid rate, should be treated with the following in the sequence shown:
Carotid sinus massage. (Level of Evidence: C)
Intravenous adenosine (6 mg IV [intravenously] over 1-2 seconds); if no response, 12 mg IV after 1-2 minutes may be given; repeat 12 mg dose if needed. (Level of Evidence: C)
Intravenous β-adrenergic blockade with metoprolol (2.5-5.0 mg every 2-5 minutes to a total of 15 mg over 10-15 minutes) or atenolol (2.5-5.0 mg over 2 minutes to a total of 10 mg in 10-15 minutes). (Level of Evidence: C)
Intravenous diltiazem (20 mg [0.25 mg/kg]) over 2 minutes followed by an infusion of 10 mg/h. (Level of Evidence: C)
Intravenous digoxin, recognizing that there may be a delay of at least 1 hour before pharmacologic effects appear (8-15 µg/kg [0.6-1.0 mg in a person weighing 70 kg]). (Level of Evidence: C)
Class III
Treatment of atrial premature beats is not indicated. (Level of Evidence: C)
+++
Ventricular Tachyarrhythmias
++
Accelerated idioventricular rhythm may occur in up to 40% of continuously monitored patients and may be a marker of reperfusion in some. This rhythm disturbance is generally considered benign and is usually untreated (see Chap. 85).
++
The clinical practice guidelines recommend the following29:
+
Class III
Antiarrhythmic therapy is not indicated for accelerated idioventricular rhythm. (Level of Evidence: C)
Antiarrhythmic therapy is not indicated for accelerated junctional rhythm. (Level of Evidence: C)
++
Ventricular tachycardia occurs in up to 15% of patients during AMI. The ventricular rate is usually between 140 and 200 bpm, and this rhythm disturbance may degenerate to ventricular fibrillation. The rhythm disturbance usually responds to lidocaine given intravenously. However, procainamide, bretylium, cardioversion, ventricular overdrive pacing, or amiodarone may all be required in the acute stages for resistant cases. The use of lidocaine prophylactically for prevention of ventricular tachycardia is not currently recommended. Pooled results of studies showed that the incidence of ventricular tachycardia was decreased, but fatal asystole was more common and no survival advantage was observed.
++
Ventricular fibrillation is seen in approximately 8% of patients surviving to hospitalization for acute infarction. It is more frequent in large ST-segment elevation infarcts and may occur with or without warning arrhythmias. The occurrence of ventricular fibrillation within the first 24 hours of hospitalization was previously thought not to confer any long-term risk to patients successfully resuscitated; however, some studies indicate a poorer outcome for patients with ventricular fibrillation at any time during their hospital course. Ventricular fibrillation or tachycardia occurring late in the hospital course may be the result of pump failure, severe electrolyte imbalance, effects of antiarrhythmic medications, or other metabolic derangements; it is usually associated with decreased LV systolic function and portends a poor prognosis. Sustained monomorphic ventricular tachycardia (VT), occurring early or late during the hospital course, is not common but implies a fixed arrhythmogenic substrate and a propensity for recurrence after dismissal. An invasive electrophysiologic study can be justified in these patients before discharge from the hospital.
++
The clinical practice guidelines recommend the following29:
+
Class I
Sustained (> 30 seconds or causing hemodynamic collapse) polymorphic VT should be treated with an unsynchronized electric shock with an initial monophasic shock energy of 200 J; if unsuccessful, a second shock of 200 to 300 J should be given, and, if necessary, a third shock of 360 J. (Level of Evidence: B)
Episodes of sustained monomorphic VT associated with angina, pulmonary edema, or hypotension (blood pressure less than 90 mm Hg) should be treated with a synchronized electric shock of 100 J of initial monophasic shock energy. Increasing energies may be used if not initially successful. Brief anesthesia is desirable if hemodynamically tolerable. (Level of Evidence: B)
Sustained monomorphic VT not associated with angina, pulmonary edema, or hypotension (blood pressure < 90 mm Hg) should be treated with:
Amiodarone: 150 mg infused over 10 minutes (alternative dose 5 mg/kg); repeat 150 mg every 10 to 15 minutes as needed. Alternative infusion: 360 mg over 6 hours (1 mg/min), then 540 mg over the next 18 hours (0.5 mg/min). The total cumulative dose, including additional doses given during cardiac arrest, must not exceed 2.2 g over 24 hours. (Level of Evidence: B)
Synchronized electrical cardioversion starting at monophasic energies of 50 J (brief anesthesia is necessary). (Level of Evidence: B)
Class IIa
It is reasonable to manage refractory polymorphic VT by:
Aggressive attempts to reduce myocardial ischemia and adrenergic stimulation, including therapies such as β-adrenoceptor blockade, intraaortic balloon pump use, and consideration of emergency PCI/coronary artery bypass graft surgery. (Level of Evidence: B)
Aggressive normalization of serum potassium to greater than 4.0 mEq/L and of magnesium to greater than 2.0 mg/dL. (Level of Evidence: C)
If the patient has bradycardia to a rate less than 60 beats/min or long QTc, temporary pacing at a higher rate may be instituted. (Level of Evidence: C)
Class IIb
It may be useful to treat sustained monomorphic VT not associated with angina, pulmonary edema, or hypotension (blood pressure <90 mm Hg) with a procainamide bolus and infusion. (Level of Evidence: C)
Class III
The routine use of prophylactic antiarrhythmic drugs (ie, lidocaine) is not indicated for suppression of isolated ventricular premature beats, couplets, runs of accelerated idioventricular rhythm, and nonsustained VT. (Level of Evidence: B)
The routine use of prophylactic antiarrhythmic therapy is not indicated when fibrinolytic agents are administered. (Level of Evidence: B)
Treatment of isolated ventricular premature beats, couplets, and nonsustained VT is not recommended unless they lead to hemodynamic compromise. (Level of Evidence: A)
+++
Implantable Cardiac Defibrillator
++
Several trials have demonstrated a mortality benefit with the use of implantable cardiac defibrillators (ICDs) as primary prevention for sudden cardiac death in patients with chronic ischemic cardiomyopathy. The DINAMIT (Defibrillator in Acute Myocardial Infarction Trial) investigated the used of ICD therapy early after AMI. In this study, 674 patients within 6 to 40 days after an AMI with subsequent LV dysfunction (ejection fraction < 35%) were randomized to ICD therapy or placebo. After a median follow-up period of 30 months, there was no significant difference in the mortality between the two groups. These results were somewhat surprising given that the highest incidence of sudden cardiac death in the VALIANT trial occurred during the first 3 months after myocardial infarction.147
++
AMI patients with LV dysfunction should not receive an ICD during the early period for prophylactic indications. ICD therapy is recommended in those who have recurrent sustained episodes of VT during the post–myocardial infarction period. A repeat assessment of LV dysfunction 30 to 40 days after the acute event should be performed, and those with an ejection fraction less than 35% should receive an ICD. Antiarrhythmic therapy has not been demonstrated to prevent sudden cardiac death in the post–myocardial infarction setting in patients without sustained ventricular arrhythmias.
++
STEMI patients with abnormal LV function who are not candidates for ICD implantation remain at risk for sudden cardiac death due to arrhythmia. The use of a home automated external defibrillator was studied in the HATS (Home Use of Automated External Defibrillators for Sudden Cardiac Arrest) trial.196 The study randomized 7001 post-STEMI patients to one of two responses should cardiac arrest occur at home: conventional emergency medical service response with home cardiopulmonary resuscitation versus the use of an automated external defibrillator (AED) followed by the conventional response. Of the 450 patients who died after home cardiac arrest, there was no difference in survival between conventional resuscitation and home AED use (6.5% vs 6.4%; P = .77). At this time, data do not support the recommendation for routine AED access at home. Currently these patients may be considered for wearable defibrillators. However, more data are needed, and an ongoing trial is under way in patients with reduced LV ejection fraction and AMI (VEST; ClinicalTrials.gov identifier: NCT01446965). A scientific statement also provides impetus for more data on use of wearable defibrillators.197
++
The clinical practice guidelines recommend the following29:
+
Implantable Cardioverter-Defibrillator Therapy Before Discharge
Class I
Implantable cardioverter-defibrillator (ICD) therapy is indicated before discharge in patients who develop sustained VT/VF [ventricular fibrillation] more than 48 hours after STEMI, provided the arrhythmia is not due to transient or reversible ischemia, reinfarction, or metabolic abnormalities. (Level of Evidence: B)
Assessment of Risk for SCD: Recommendation
Class I
Patients with an initially reduced LVEF [LV ejection fraction] who are possible candidates for ICD therapy should undergo reevaluation of LVEF 40 or more days after discharge (Level of Evidence: B)
+++
Cardiac Rehabilitation
++
Rehabilitation after myocardial infraction is an important aspect of secondary prevention and is described in Chap. 45.