Supraventricular and Ventricular Arrhythmias in Acute Myocardial Infarction

Introduction

Cardiac rhythm abnormalities occur in 72% to 95% of patients with acute myocardial infarction (MI) ( Table 16.1 ). Because arrhythmias tend to occur early and before the patient receives medical attention, the incidence may even be higher. Mechanisms for the various arrhythmias seen in MI include reentry, automaticity, and triggered activity. These mechanisms may be exacerbated or caused by certain characteristics of the clinical course, such as infarct size, hemodynamic instability, electrolyte disturbances, use of inotropic agents, autonomic nervous system control and preexisting conduction system or rhythm disturbances. Arrhythmias may be asymptomatic but can also result in symptoms of palpitations, angina, syncope, heart failure, or cardiac arrest. Whether supraventricular or ventricular in origin, they require treatment, particularly when they perturb hemodynamic stability, provoke myocardial ischemia, or threaten to degenerate into life-threatening arrhythmias. Timely recognition and treatment decreases morbidity and mortality associated with MI. However, preemptive antiarrhythmic treatment has not been shown to be effective. This chapter reviews the mechanisms, diagnosis, and therapy for supraventricular and ventricular arrhythmias that occur in acute MI. Conduction disturbances in the setting of acute MI are discussed in Chapter 17 .

TABLE 16.1

Incidence of Arrhythmias in Acute Myocardial Infarction

Arrhythmia	Incidence (%)
Sinus bradycardia	10–55
First-degree AV block	4–15
Second-degree AV block
Mobitz type I	4–10
Multilevel AV block	2
Mobitz type II	Rare
Third-degree or complete AV block
Inferior infarction	12–17
Anterior infarction	5
Asystole	1–10
Sinus tachycardia	30
Premature atrial contractions	54
Supraventricular tachycardia	<5
Atrial fibrillation	2.3–21
Atrial flutter	1–2
Premature ventricular contractions	90–100
Accelerated idioventricular rhythm	8–20
Ventricular tachycardia	10–40
Ventricular fibrillation	4–18

AV, Atrioventricular.

Supraventricular Arrhythmias

Sinus Tachycardia

Sinus tachycardia in the setting of acute MI usually occurs in response to an increase in sympathetic tone and can be seen in up to 30% of cases. However, patients with isolated sinus tachycardia during acute MI fare more poorly than those without. Acutely, MI patients with sinus tachycardia have higher levels of cardiac biomarker release, a larger proportion of anterior and diffuse infarcts, and a higher incidence of recurrent chest pain. Sinus tachycardia has also been shown to be an independent predictor of post-MI complications and in-hospital mortality. Sinus tachycardia may be an early manifestation of heart failure and, in this setting, is a poor prognostic sign. Sinus tachycardia that persists beyond 4 hours may be suggestive of another underlying cause, which should prompt further evaluation. Left untreated, these culprits, such as fever, pericarditis, pain, heart failure, and anemia, can lead to increased myocardial oxygen demand. Specific therapy to lower the heart rate and decrease sympathetic tone, such as with β-blocker medications, may be helpful ( Table 16.2 ).

TABLE 16.2

Antiarrhythmic Agents for Acute Myocardial Infarction ^a

Class	Drug	Indications	Dosage	Elimination Half-Life	Adverse Effects
IA	Procainamide	AVRT, VT	Intravenous: 15 mg/kg at 20 mg/min (load), then 1–6 mg/min (maintenance) Oral: 50 mg/kg/day in 4 divided doses	2.5–4.7 h	Hematologic: marrow suppression, lupus-like illness; proarrhythmia; hypotension (with intravenous infusion)
IB	Lidocaine	VT, PVCs, in setting of ischemia	Intravenous: 1 mg/kg bolus, then 1–4 mg/min (maintenance)	1.5–2 h	CNS: drowsiness, agitation, disorientation, tremulousness
II	Esmolol	Short-term rate control of AF, AFL; treatment of AVNRT, AVRT, MAT	Intravenous: 500 µg/kg over 1 min (load), then 50 µg/kg/min (maintenance)	2 min	Hypotension; CNS: dizziness, somnolence, headache; bronchospasm at higher doses
	Metoprolol	Rate control of AF, AF; treatment of AVNRT, MAT	Oral: 25–100 mg q6h Intravenous: 5 mg every 5–15 min up to 15 mg	3–4 h	As above
	Atenolol	As above	Oral: 25–200 mg qd ^b	6–7 h	As above
	Propranolol	As above	Intravenous: 0.5–3 mg, repeat in 2–5 min, then q4h Oral: 10–30 mg q6–8h	2 h (initial dose); 3, 4–6 h	As above; bronchospasm owing to β ₂ -antagonist activity
III	Amiodarone	VT, VF	Oral: 800–1600 mg/day for 1–3 wk (load), 200–400 mg qd (maintenance) Intravenous: 150 mg/min over 10 min, then 1 mg/min for 8 h, then reduce to 0.5 mg/min (maintenance)	9–11 days	Conduction disturbances: sinus bradycardia, heart block; abnormalities of thyroid function, liver function; pulmonary toxicity; hypotension more likely to occur with intravenous administration
IV	Diltiazem	Rate control of AF, AFL; treatment of AVNRT, MAT	Intravenous: 0.25 mg/kg over 2 min; if no response in 15 min, 0.35 mg/kg over 2 min, then 5–15 mg/h (maintenance) Oral: 30–125 mg tid, 120–300 mg CD qd	3.5–10 h	Hypotension; potentiation of sinus node dysfunction
	Verapamil	As above	Intravenous: 5–10 mg, may repeat in 15–30 min with 10 mg Oral: 80–120 mg q6–8h or 120–240 mg SR q12–24h	Intravenous: 2 h Oral: 4.5–12 h	Cardiac effects: congestive heart failure owing to negative inotropic effect, hypotension; gastrointestinal effects: constipation
Other	Digoxin	Rate control of AF, AFL; treatment of AVNRT	Intravenous/oral: 0.5 mg (initial), 0.25 mg q4–8h to total of 1 mg (load); 0.125–0.375 mg qd (maintenance) ^b	Intravenous: 30 min Oral: 34–44 h	Toxic side effects: nausea, accelerated functional rhythm, high-grade AV block
	Adenosine	Termination of AVNRT, AVRT, occasionally MAT, and exercise-mediated VT	Intravenous: 6 mg rapid bolus, may repeat with 12 mg in 1 min, then 18 mg	9.5 sec	Dyspnea, chest pain, flushing, sinus tachycardia
	Magnesium	Torsades de pointes	Intravenous: 1–2 g (load); 1–7.5 mg/min (maintenance) ^b		Hypotension

AF, Atrial fibrillation; AFL, atrial flutter; AT, atrial tachycardia; AV, atrioventricular; AVNRT, atrioventricular nodal reentry tachycardia; AVRT, atrioventricular reentry tachycardia; CD, controlled delivery; CNS, central nervous system; MAT, multifocal atrial tachycardia; PVCs, premature ventricular contractions; SR, sustained release; VF, ventricular tachycardia; VT, ventricular tachycardia.

a Dosages and indications listed are based on current practice standards and therefore are subject to change in the future.

b Dosage should be adjusted in the presence of renal insufficiency.

Atrial Arrhythmias

Atrial arrhythmias occur in 20% to 54% of patients with acute MI overall and in about 11% to 20% of patients with acute MI and cardiogenic shock. Patients with inferior MI in particular are more likely to develop atrial arrhythmias early in their clinical course, whereas patients with anterior MI tend to manifest atrial arrhythmias anywhere from 12 hours to days after MI onset. Several factors have been implicated in the pathogenesis of atrial arrhythmias, including atrial distention from either left ventricular (LV) or right ventricular (RV) dysfunction, pericarditis, or atrial infarction.

In a small series of patients with documented inferior MI, Rechavia and colleagues found a significantly higher occurrence of premature atrial contractions and atrial fibrillation in patients with RV dysfunction. It is unclear if this was because of atrial distention or atrial infarct; other studies have suggested that both factors may, in fact, play a role. Atrial arrhythmias that occur late in the clinical course have been attributed to LV dysfunction. In these patients, treatment of congestive heart failure may prevent recurrences.

Premature Atrial Contraction

Premature atrial contractions are the most common atrial arrhythmias, occurring in 54% of patients with acute MI. They may result from heightened sympathetic tone exacerbated by pain or anxiety, atrial distention, pericarditis, atrial infarction, or atrial ischemia. Although premature atrial contractions may precipitate other atrial arrhythmias, they are usually of little clinical significance and are not associated with increased mortality. Thus suppressive treatment is not indicated.

Paroxysmal or Persistent Supraventricular Tachycardia

Paroxysmal atrial tachycardia and reentrant supraventricular tachycardia are relatively rare in acute MI, occurring in less than 5% of patients. Most of these arrhythmias are transient. However, a rapid ventricular response can be highly symptomatic and hemodynamically compromising. Management of these arrhythmias should first be directed at controlling the ventricular rate and initiated promptly, such as with intravenous β-blockers or calcium channel blockers (see Table 16.2 ). These agents or adenosine may also terminate persistent tachyarrhythmias if the atrioventricular (AV) node is an integral part of the reentry circuit. While adenosine may also terminate atrial tachycardia, it may result in atrial fibrillation (AF). All of these agents should be administered with caution in acute MI, being mindful of associated hypotension or congestive heart failure.

In patients with hemodynamic instability, urgent synchronized direct current (DC) cardioversion is usually the safest and most expedient method to terminate the arrhythmia. Treating underlying heart failure may help to prevent recurrence. Treatment of supraventricular tachycardia in the unstable patient is also reviewed in Chapter 25 .

Atrial Fibrillation

AF occurs frequently in acute MI patients, affecting from 2.3% to 21% of hospitalized patients. In approximately one-third of patients, AF is a preexisting condition, while new-onset AF occurs in the other two-thirds of these patients. Age, tachycardia at the time of clinical presentation, a history of AF, congestive heart failure, and both systolic and diastolic LV dysfunction are independent predictors for the development of AF in acute MI. Patients are also more likely to have had preexisting atrial arrhythmias, prior MI, or coronary artery disease, hypertension, diabetes mellitus, and more extensive myocardial damage at the time of presentation. The incidence of post-MI AF has declined markedly due in large part to the broad utilization of reperfusion strategies as well as commonly used medications, such as β-blockers, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers.

AF impacts patient outcomes in the acute MI setting. While some studies suggest a negative prognostic impact of AF, other studies have disputed this. A meta-analysis of 43 studies that evaluated the impact of AF on mortality in MI patients found an increased odds ratio (OR) for mortality if patients developed new-onset (OR, 1.37) or had prior AF (OR, 1.28). The increased mortality risk was true even after controlling for age, diabetes mellitus, hypertension, prior MI, heart failure, and coronary revascularization in patients with new-onset AF. The increase in mortality held true for short-, mid- and long-term outcomes (out to 1 year) and included both sudden and nonsudden cardiac death. Serrano and coworkers investigated the short- and long-term outcomes of patients with supraventricular arrhythmias after MI. Although patients with arrhythmias during the late phase of MI (12 hours to 4 days) had significantly higher mortality rates at 1 month and 47 months, mortality was only shown to correlate with the extent of coronary artery disease. In another study, mortality was higher for patients with new-onset AF that developed 30 days or later after their MI (hazard ratio [HR], 2.58; 95% confidence interval [CI], 2.21–3.00 vs. HR, 1.81; 95% CI, 0.45–2.27 for AF between 3 and 30 days, and HR, 1.63; 95% CI, 1.37–1.93 for AF within 2 days). AF is also associated with a higher rate of reinfarction, cardiogenic shock, heart failure, asystole, and recurrent AF.

Patients with AF can develop symptoms from the loss of atrial contribution to cardiac output and impaired LV filling, as well as rapid ventricular rates. In patients with cardiogenic shock, increases in pulmonary capillary wedge pressure and left atrial pressure can contribute to the development of AF. Other contributing factors can include atrial ischemia or infarction, LV dysfunction causing hemodynamic instability, and autonomic nervous system disturbances. In hemodynamically unstable patients, synchronized DC cardioversion can and should be utilized to promptly restore sinus rhythm. For stable patients, β-blockers or calcium channel blockers can be intravenously administered to control ventricular rates. Cardioversion may occur spontaneously; if not, synchronized DC cardioversion should be considered.

Atrial flutter is relatively rare in acute MI, occurring in only 1% to 2% of patients. When it occurs, 2 : 1 conduction is often present and ventricular rate control may be difficult. DC cardioversion or pace termination, when available, can be utilized to terminate the tachycardia. Amiodarone may be used in an attempt to treat or prevent recurrence of atrial fibrillation or flutter, though it has the potential to cause hypotension. In patients with hemodynamic compromise, rate-lowering agents are often precluded by their negative inotropic effect. Class IC antiarrhythmic medications, such as flecainide and propafenone, are contraindicated in acute MI patients and their use is to be avoided. Antiplatelet agents do not prevent or reduce the risk of thromboembolism in patients with AF. Therapeutic anticoagulation should be considered to reduce the long-term risk of thromboembolism in patients meeting current guideline criteria without contraindications.

Ventricular Arrhythmias

Ventricular tachyarrhythmias are potentially the most dangerous arrhythmias associated with acute MI, occurring in 10% to 50% of patients. These arrhythmias are observed more frequently soon after the onset of MI. In experimental animals, factors that determine the occurrence of ventricular arrhythmias include the size of the ischemic area, psychological stress, preconditioning, increased heart rate, and autonomic nervous system influences. The combination of ischemia and sympathetic stimulation is more arrhythmogenic than either factor alone.

Considerable evidence indicates that factors that influence arrhythmias in experimental models also influence the occurrence of ventricular arrhythmias in humans. The incidence of ventricular tachyarrhythmias is related to infarct size and the presence of heart failure. Patients with an absolute increase in sympathetic tone or decreased vagal efferent activity are at an increased risk of sudden cardiac death due to ventricular arrhythmias. Acute MI causes several changes in the autonomic nervous system that may facilitate the initiation of ventricular arrhythmias. Activation of cardiac mechanoreceptors and cardiopulmonary and carotid baroreceptors results in increased circulating catecholamine levels and increased efferent sympathetic activity. Ischemic damage to cardiac adrenergic neurons results in the release of catecholamines as well. Transmural MI denervates viable myocardium distal to the infarct site. Ischemic and denervated viable myocardium is hypersensitive to circulating catecholamines. Sympathetic stimulation also enhances automaticity in the Purkinje fibers. These effects result in inhomogeneities of repolarization and enhance automaticity.

Electrolyte abnormalities, including hypokalemia and hypomagnesemia, are potentially correctable causes of ventricular arrhythmias in acute MI. Hypokalemia is an independent risk factor for ventricular arrhythmias early in MI. Hypomagnesemia often accompanies hypokalemia and may result in polymorphic ventricular tachycardia (VT). Coronary reperfusion may cause isolated premature ventricular contractions, accelerated idioventricular rhythm (AIVR), VT, or ventricular fibrillation (VF), presumably by enhancing automaticity of ischemic myocardium. The severity of the arrhythmia induced by reperfusion is related to the duration of myocardial ischemia.

The circulating effects of certain antiarrhythmic drugs at the time of MI may also facilitate initiation and maintenance of ventricular arrhythmias. This proarrhythmic effect is thought to occur because of changes in the electrophysiologic action of the drugs in the setting of myocardial ischemia. In the Cardiac Arrhythmia Suppression Trial (CAST), the use of class IC antiarrhythmic drugs given to patients both early and late after prior MI (6 days to 2 years) for the treatment and suppression of premature ventricular beats ultimately lead to increased mortality and sudden cardiac death.

Ventricular Premature Beats

Ventricular premature beats (VPBs) occur in almost all patients with acute MI and are rarely a cause of myocardial ischemia or systemic hypotension. Previously, these beats were thought to potentially trigger VT or VF. Data from animal models and human studies indicate that frequent and complex ectopy is neither a sensitive nor specific predictor for the development of sustained ventricular tachyarrhythmias early after MI.

The incidence of frequent VPB and the R-on-T phenomenon is similar between patients who develop VF and those who do not. Studies of animals and humans have shown that most VT episodes and 41% to 45% of VF episodes are initiated by late-coupled VPBs (after the T wave), suggesting that early beats are not required to initiate the arrhythmia. VF occurs in the absence of preceding ventricular ectopy in 40% to 83% of patients.

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