Postgraduate Medicine
ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20
Arrhythmias and acute myocardial infarction Gregory A. Granrud MD & Pierce J. Vatterott MD To cite this article: Gregory A. Granrud MD & Pierce J. Vatterott MD (1991) Arrhythmias and acute myocardial infarction, Postgraduate Medicine, 90:6, 85-96, DOI: 10.1080/00325481.1991.11701102 To link to this article: http://dx.doi.org/10.1080/00325481.1991.11701102
Published online: 17 May 2016.
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Third of four articles on myocardial infarction
Arrhythmias and acute myocardial infarction Preview Intensive coronary care, cardiopulmonary resuscitation, betablocker therapy, and thrombolytic therapy have all helped reduce the morbidity and mortality rates of acute myocardial infarction (MI). However, electrical complications continue to pose a major threat to patients' recovery. In this article, Drs Granrud and Vatterott discuss the etiology and treatment of arrhythmias associated with acute Ml as well as risk assessment for future ventricular tachycardia and sudden death.
Gregory A Granrud, MD Pierce J. Vatterott, MD •:• The risk of cardiac arrhythmia is highest in the first few days after myocardial infarction (MI). However, because of the underlying cause or concomitant conditions, some patients are at risk for late complications and may benefit from prolonged monitoring and/or prophylactic therapy.
Bradycardias and acute inferior-wall MI The arterial supply to the sinus node usually arises from the proximal right coronary artery, which supplies the inferior lefr ventricle. Therefore, inferior MI often leads to sinus node dysfunction, which manifests as si-
nus bradycardia, sinus arrhythmia, sinus pauses, sinus node exit block, or emerging atrial fibrillation. Sinus node dysfunction is quite common (incidence, 25% to 40% 1) during the early phases of acute inferior Ml. However, by 4 hours after MI, only 15% to 20% of patients continue to have sinus node dysfunction. 1 Acute sinus bradyarrhythmia is related to cholinergic overload; the inferior and posterior walls of the left ventricle are richly endowed with cardiac vagal-afferent receptors, allowing overload. The Bezold-Jarisch reflex, manifested as reflex bradycardia and hypotension, characterizes this overload. 2 Reactive vagotonia (vasovagal reaction) may also occur as a result of painful stimuli, anxiety, use of sublingual nitroglycerin (Ni-
VOL 90/NO 6/NOVEMBER 1, 1991/POSTGRADUATE MEDICINE • ARRHYTHMIA& AND Ml
trostat) or intravenous nitroglycerin (Nitrostat N, Nitro-Bid N, Tridil), narcotic-induced nausea and vomiting, or intake of other potentially noxious substances. HEART BlOCK-With inferior MI, atrioventricular (AV) block is quite common; major AV block occurs in 15% to 33% of these patients. Characteristically, the QRS interval is narrow, reflecting intact sub nodal conduction. Of the major AV blocks, two thirds result in complete heart block. About half of these occur within the first 6 hours and 92% within 72 hours of Ml. Heart block occurring within the first 6 hours is generally abrupt and causes severe bradycardia. Parasympathetic tone is usually heightened, but it responds to atropine sulfate and resolves within 24 hours. Pacemaker therapy is rarely indicated for early heart block.H Heart block occurring more than 6 hours after MI generally develops slowly, often progressing through first-degree heart block and Mobitz type I AV block (ie, Wenckebach period) before ending in complete heart block. late heart block usually persists for more than 40 hours and is accompanied by a fairly adequate ventricular response.4 It is not vagally mediated; rather, it reflects ischemia or metabolic abnormalities of the AV node. AV block nearly always resolves in patients recovering from inferior MI, although recovery of AV conduction may take up to 16 days. 4 continued 85
Patients with bradycardia and inferior Ml who do not respond satisfactorily to medications may be candidates for temporary pacemaker therapy.
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Table 1. Indications for temporary pacemaker therapy In Inferior-wall myocardial infarction Profound asystolic spells related to sinus arrest or high-grade atrioventricular block that is unresponsive to medication Bradycardia-dependent heart failure, typically with ventricular response of 100 msec] on invasive electrophysiologic testing). If syncope develops in this highrisk group, full electrophysiologic examination is warranted. If a prolonged HV interval or infrahisian block during decremental atrial pacing is noted, permanent pacemaker therapy is recommended. (However, it is more likely that syncope is related to inducible paroxysmal ventricular tachyanhythmias.)
Tachyaudias and acute supraventriwlar MI Sinus tachycardia complicates acute MI in about 24% of cases. Possible causes include sympathetic overactivity; pain, anxiety; hypovolernia, congestive heart failure (CHF), atrial distention from fluid overload, and administration of such drugs as atropine and isoproterenol. Supra-
ventricular tachycardias (ie, atrial fibrillation or flutter, paroxysmal supraventricular tachycardia) often reflect left ventricular dysfunction and pending CHF. TREATMENT OF UNDERLYING
CAUSFS--Sinus and supraventricular tachycardias must be treated because of their deleterious effect on myocardial oxygen consumption, especially when regional myocardial blood flow is marginal. The first step is identification of potential causes. Anxiety and pain are best treated with anxiolytics or appropriate narcotics. Hypovolernia is managed with fluid replacement. If there are no signs of CHF, profound bradycardia, or other contraindications, beta-adrenergic blocking agents play an important role in limiting heart rate and preserving myocardial tissue. In most cases in which CHF is a concern, betablocker therapy should be guided by invasive hemodynarnic monitoring. Another option is the use of esmolol hydrochloride (Brevibloc), a shortacting class N beta blocker with an elimination half-life of9 minutes. It offers the opportunity to try beta blocker therapy and evaluate tolerance; however, expense is a concern. In a patient with impending CHF, warning atrial anhythrnias (eg, frequent premature atrial beats) are common. Such a warning is secondary to high ventricular end-diastolic pressures, which result in atrial distention. These patients often respond to diuretics. Some researchers have recommended prophylactic treatment with digitalis when atrial
continued on page 93 88
ARRHYTHMIA& AND Ml • VOL 90/NO 6/NOVEMBER 1, 1991/POSTGRADUATE MEDICINE
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Immediately after cardioversion, therapy to reverse patients' predisposition to atrial fibrillation or flutter should be initiated.
fibrillation or flutter occurs. However, because digitalis increases myocardial oxygen demand and may reach toxic levels in active infarction, we recommend that it be used only in patients who have ovett CHF or sustained tachyarrhythmias. 1REA1MENT OF TACHYCARDIAS--
Treatment of atrial fibrillation or flutter, as with other supraventricular tachycardias, depends on the patient's immediate status. If tachycardia causes hemodynamic compromise, dyspnea, or angina, immediate cardioversion is indicated. Immediately after cardioversion, therapy to reverse the patient's predisposition to atrial fibrillation or flutter should be initiated. This may include treatment of underlying CHF or electrolyte abnormalities. Therapy with procainamide hydrochloride (Pronestyl) (1 g administered intravenously over 20 to 40 minutes, followed by a drip of 1 to 3 mg/min) and digoxin helps prevent recurrence of atrial fibrillation and flutter. Patients can then be switched to oral class I agents, but their need for long-term therapy should be assessed before they are discharged from the hospital. If atrial fibrillation or flutter appears to be moderately well tolerated, treatment should be started with digoxin (0.5 mg administered intravenously, followed by 0.125 to 0.25 mg every 2 to 4 hours for a total dose of about 1.0 to 1.5 mg/24 hr). Therapy should be guided by the ventricular rate response to atrial fibrillation. In addition, therapy to reverse a patient's predisposition to atrial arrhythmias should be initiated
Gregory A. Granrud, MD Pierce J. Vatterott, MD Dr Granrud (left) and Dr Vatterott (right) are eo-directors of the St Paul Arrhythmia Center and staff physicians, St Paul Heart Clinic, St Paul. Among Dr Granrud's interests are invasive and interventional cardiology and treatment of sudden cardiac death. Some of Dr Vatterott's interests are electrophysiology, signal-averaged electrocardiography, antitachycardia devices, and pacemakers.
as described. If, after treatment of CHF, the patient remains in atrial fibrillation or flutter, intravenous procainamide should be started. Overdrive atrial pacing is a convenient alternative therapy for atrial flutter. Adenosine (Adenocard) is a new adjuvant drug for atrial tachyarrhythmia that has distinct benefits. Its side effects (ie, anxiety, chest discomfort, and flushing) are minimal and of brief duration. It is taken up and metabolized rapidly by nearly all living cells in the human body; thus, adenosine has few hemodynamic consequences. It provides a very
VOL 90/NO 6/NOVEMBER 1, 1991/POSTGRADUATE MEDICINE • ARRHYTHMIA$ AND Ml
short-acting block of the AV node and so terminates tachycardias involving the AV node. It gradually slows sinus tachycardia. Adenosine has diagnostic as well as therapeutic capabilities. In cases of atrial flutter, it provides a temporary AV block, thus allowing detection of atrial flutter waves that were not seen previously. Since adenosine is taken up by endothelium throughout the cardiovascular system, central line administration is more effective than peripheral administration. Adenosine can cause prolonged pauses. If the drug is given by central line, a dose of continued 93
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The substrate for ventricular arrhythmias in acute Ml is ischemic or necrotic myocardium.
3 mg should be used initially and the dose increased gradually in 3-mg increments to a maximum of 12 mg. Intravenous doses start at 6 mg. Doses greater than 12 mg are oflittle benefit. Concurrent use of theophylline inhibits adenosine's effectiveness.2" For short-term in-hospital therapy, the use of beta blockers, digoxin, calcium antagonists, or class lA agents (ie, disopyramide [Norpace], procainamide, and quinidine sulfate) may be of benefit. Given the results of the Cardiac Arrhythmia Suppression Trial/ 1 we do not recommend treatment with classIC agents (ie, encainide hydrochloride [Enkaid], flecainide acetate [Tambocor], and propafenone hydrochloride [Rythmol]).
Tachycardias and acute ventricular MI The substrate for ventricular arrhythmias in acute Ml is ischemic or necrotic myocardium. Myocardial irritability is increased, and metabolic changes cause a decrease in fibrillation threshold. Early ECG monitoring has demonstrated that ventricular ectopic activity occurs within a few hours of acute Ml in almost 100% of patients. Although this high percentage is worrisome, it reflects, in part, the frequent finding of premature ventricular beats among the healthy population. In fact, the value of warning ventricular arrhythmias (ie, more than 5 premature ventricular beats per minute) is now in question. Many patients have warning arrhythmias without ventricular fib94
rillation and others have ventricular fibrillation without arrhythmias. FIBRILLATION-Ventricular fibrillation occurs in about 10% of patients during the first hour of symptoms, in 16% during the first 4 hours, and in 6% who survive to reach the coronary care unit. Ventricular tachycardia occurs in 3% to 15% of patients with acute Ml; it is usually self-limited and occurs in short runs. Ventricular fibrillation in Ml patients can be divided into distinct categones: • Primary ventricular fibrillation occurs suddenly during severe acute ischemia and is independent of cardiac failure. Therapy with lidocaine and beta blockers and reversal of ischemia have been shown to prevent primary ventricular fibrillation. • Secondary ventricular fibrillation occurs 1 to 6 weeks after MI. It may be drug-induced, due to pacing in or near an infarct wne, or agonal. Prognosis is extremely poor, even if ventricular arrhythmia is successfully treated, because arrhythmia is ofi:en a sign of severe underlying lefi: ventricular dysfunction. PROPHYLAXIs-The use oflidocaine for prophylaxis remains controversial, but there is no question that it is first-line therapy for ventricular tachyarrhythmias. The initial bolus is 1 mg/kg administered over a 1-minute period, followed by a drip of2 mg/min. A second bolus, at half dose, should be given 10 minutes later. Maintenance therapy should be reduced in patients prone to toxicity (eg, those with CHF, shock, ad-
vanced liver disease, or age greater than 70). During therapy, patients should be monitored for evidence of lidocaine toxicity. AV block with ventricular escape rhythm is an absolute contraindication to lidocaine therapy. Bretylium tosylate (Bretylol) and procainamide are also useful for adjunctive treatment of ventricular tachyarrhythmias in the coronary careumt. lREATMENT IN THE CORONARY
CARE UNIT-Attention
should be directed to vigorous correction of electrolyte imbalances, including hypokalernia and hypomagnesemia. Hypokalemia is a common complication in patients who are dehydrated, taking diuretics, or consuming excessive amounts of caffeine. Hypomagnesemia is common in patients who are malnourished or receiving diuretics, are alcoholic, have a malabsorptive state, or recently received aminoglycosides or cisplatin (Platinol). The increase in catecholamines resulting from infarction alone can cause hypomagnesemia. Patients receiving magnesium replacement therapy have fewer ventricular arrhythmias. 22 Studies have shown that magnesium sulfate can be administered safely during the early days of infarction and improves survival rates. 22 Clearly, monitoring the magnesium level is appropriate in acute Ml, and its repletion is strongly recommended. Standard replacement therapy is intravenous (piggyback) administration of2 to 4 g of magnesium over a 30- to GO-minute period.
ARRHYTHMIA& AND Ml • VOL 90/NO 6/NOVEMBER 1, 1991 /POSTGRADUATE MEDICINE
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Signal-averaged electrocardlography is a new high-resolution method that minimizes the level of noise that contaminates the periodic ECG signal.
Accelerated idioventricular rhythm occurs in about 30% of patients with acute MI, most often in the first 2 days after MI. It is equally common in anterior and inferior infarcts. Accelerated idioventricular rhythm probably results from enhanced automaticity of Purkinje fibers during acute MI. This slow ventricular rhythm often emerges during slowing of sinus rhythm.Acceleratedidioventricular rhythm is often associated with episodes of rapid ventricular tachycardia However, unlike rapid ventricular tachycardia, accelerated idioventricular rhythm is thought not to affect prognosis. The need for treatment of this rhythm is conrroversial. Beta-blocker therapy is often recommended. Signal-averaged electrocardiography can be very helpful in demonstrating the presence of a myocardial substrate that could suppon a more malignant ventricular arrhythmia. 23 Signal averaging of the surface ECG is a new noninvasive, highresolution, computerized method of analyzing standard ECGs and averaging multiple QRS complexes. It identifies patients at risk for ventricular tachycardia Signal averaging minimizes the level of noise that contaminates the periodic ECG signal and thereby exposes signals of the microvolt level normally hidden within noise.
Risk assessment for sudden death after MI Ventricular tachycardia and sudden death occur in 5% to 10% of pa-
Table 3. Comparison of value of monitoring methods used to predict arrhythmic events Method
Normal result No. of % arrhythmic events/No. of patients
Abnormal result* No. of % Pvalue arrhythmic events/No. of patients
SA ECG EF Halter SA ECG+ EF SA ECG + Halter EF +Halter SA ECG + EF + Halter
2/57 3/47 3/32 0/26 0/14 1/16 0/9
13/45 12/50 12/52 10/28 9/26 11/30 8/16
3.5 6.3 9.3 0 0 6 0
29 24 23 36 35 37 50
0.0003 0.01 0.09 0.0007 0.01 0.025 0.01
EF, ejection fraction; Holter, ambulatory continuous electrocardiographic monitoring; SA ECG, signal-averaged electrocardiography. ·Abnormal SA ECG = QRS duration > 114 msec, root mean square voltage < 20 11V. or low-amplitude signal > 38 msec; abnormal EF = < 40%; abnormal Holter = > 10 premature ventricular beats per hour. Adapted from Gomes et al."
tients during the first year after infarction. Both ischemia and primary ventricular arrhythmias have a role in sudden death. Ischemic events are predicted by postinfarction exercise testing or coronary angiography; arrhythmic events are not. Gomes and associatei4 found that late potentials on the signal-averaged ECG, an ejection fraction less than 40%, and more than 10 premature ventricular beats per hour predict the occurrence of ventricular tachycardia and sudden death in the next year (table 3); the risk is 50% in patients with all three of these traits. Cripps and coworke~ 5 found that arrhythmic events are also predicted by a higher class of CHF on presentation at the coronary care unit. Heart rate vari-
V0L 90INO 6/NOVEMBER 1, 1991/POSTGRADUATE MEDtCINE • ARRHYTHMIAS AND Ml
ability, as demonstrated on ambulatory continuous ECG (Holter) monitoring, may also play a role. Physicians' ability to identify patients who are at increased risk for future arrhythmic events has improved more than their ability to treat such events. Empirical therapy with class I antiarrhythmics does not improve survival rates. Ar. this time, our recommendation for patients at moderate risk for future arrhythmic events is treatment with beta blockers and/or angiotensin-convening enzyme inhibitors. Physicians should plan for aggressive management of CHF (see related anicle on page 99), appropriate management of electrolyte status, and, when possible, reversal of ischemia. Abstract data suggested that empirical use of continued 95
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low-dose amiodarone (200 mglday) may be of benefit in patients with nonsustained ventricular tachycardia after MF6 Further studies are under way, including one in which choosing treatment on the basis of signalaveraged ECG late potentials, ejection fraction, and Holter monitoring results is being investigated. Patients should be referred for electrophysiologic evaluation when they have malignant ventricular arrhythrnias after MI, do not respond to appropriate medical management, and are judged to be at high risk by results of signal-averaged ECG, by the presence of symptoms of heart failure, and by their ejection fraction. Electrophysiologic testing may be used to guide future drug treatment and to determine whether patients would benefit from the use of such devices as an implantable cardiodefibrillator or a complex antitachycardia device.
Summary The most common arrhythmias associated with inferior-wall and anterior-wall myocardial infarction are bradycardia and supraventricular and ventricular tachycardia. Optimal treatment approaches are based on the pathophysiology of the infarct and the presence of contributing medical factors (eg, congestive heart failure, metabolic disorders). Temporary or permanent pacemaker therapy is hdpful in some patients. Sudden death due to arrhythmia after myocardial 96
infarction may be predicted and avoided in certain situations. IFUVI
Earn credit on this article. ~ See CME Quiz.
Address for correspondence: Gregory A Granrud, MD, St Paul Heart Clinic, 255 N SmithAve, Suite 100, St Paul, MN 55102.
References 1. O'Doherty M, Tayler DI, Quinn E, et al. Five hundred patients with myocardial infarction monitored within one hour of symptoms. BMJ (Clin Res) 1983;286(6375): 1405-8 2. Mark AL The Bezold-Jarisch reflex revisited: clinical implications of inhibitory reflexes originating in the hean. JAm Coli Cardiol1983; 1(1):90-102 3. Tans AC, Lie Kl, Durrer D. Clinical setting and prognostic significance of high degree AV block in acute inferior myocardial infarction: a study of 144 patients. Am Hean J 1980;99(1) :4-8 4. Feigl D, Ashkenazy J, Kishon Y. Early and late atrioventricular block in acute inferior myocardial infarction. JAm Coli Cardiol1984;4(1):35-8 5. Gerkin R, Desser KB, Benchimol A. Temporary pacemakers in acute myocardial infarction. Ariz Med 1982;39(8):515-7 6. Topol EJ, Goldschlager N, Ports TA, et al. Hemodynamic benefit of atrial pacing in right ventricular myocardial infarction. Ann Intern Med 1982;96(5):594-7 7. Sdarovsky S, Zafrir N, Strasberg B, et al. Ventricular fibrillation complicating temporary ventricular pacing in acute myocardial infarction: significance of right ventricular infarction. Am J Cardiol 1981:48(6):1160-6 8. Roos JC, Dunning AJ. Bundle branch block in acute myocardial infarction. Eur J Cardiol 1978; 6(6):403-24 9. Hindman MC, Wagner GS, JaRo M, et al. The clinical significance of bundle branch block complicating acute myocardial infarction. 2. Indications for temporary and permanent pacemaker insertion. Circulation 1978;58(4):689-99 10. Hindman MC, Wagner GS, JaRo M, et al. The clinical significance of bundle branch block complicating acute myocardial infarction. I. Clinical characteristics, hospital mottaliry, and one-year follow-up. Circulation 1978;58(4):679-88 11. Lamas GA, Muller JE, Turi 7£, et al. A simplified method to predict occurrence of complete heart block during acute myocardial infarction. Am J Cardioll986;57(15):1213-9
12. Hynes JK, Holmes DR Jr, Harrison CE. Five-year experience with temporary pacemaker therapy in the coronary care unit. Mayo Clin Proc 1983;58(2): 122-6 13. Falk RH, Zoll PM, Zoll RH. Safery and efficacy of noninvasive cardiac pacing: a preliminary repott. N EnglJ Med 1983;309(19):1166-8 14. Lie Kl, Wellens HJ, Schuilenhurg RM, et al. Factors influencing prognosis of bundle branch block complicating acute antero-septal infarction: the value of His bundle recordings. Circulation 1974;50(5):935-41 15. Atkins JM, Leshin SJ, Blomqvist G, et al. Ventricular conduction blocks and sudden death in acute myocardial infarction: potential indications for pacing. N EnglJ Med 1973;288(6):281-4 16. Waugh RA, Wagner GS, Haney TL, et al. Immediate and remote prognostic significance of fascicular block during acute myocardial inl3.rction. Circulation 1973:47(4):765-75 17. Hauer RN, Lie Kl, Liem KL, et al. Longterm prognosis in patients with bundle branch block complicating acute antetoseptal infarction. Am J Cardiol 1982;49(7): 1581-5 18. Ginks WR, Sutton R, Oh W, et al. Longterm prognosis after acute anterior infarction with atrioventricular block. Br Hearr J 1977;39(2): 186-9 19. Waters DD, Mizgala HF. Long-term prognosis of patients with incomplete bilateral bundle branch block complicating acute myocardial infarction: role of cardiac pacing. Am J Cardiol 1974; 34(1):1-6 20. DiMarco JP, Sellers TD, Berne RM, et al. Adenosine: electrophysiologic effects and therapeutic use for terminating paroxysmal supraventricular tachycardia. Circulation 1983;68(6):1254-63 21. Cardiac Arrhythmia Suppression Trial (CAST) Investigators. Preliminary report: effect of encainide and flecainide on mottaliry in a randomized trial of arrhythmia suppression after myocardial infarction. N Engl J Med 1989:321 :406-12 22. Keren A, Tziwni D. Magnesium therapy in ventricular arrhythmias. PACE 1990;13(7):937-45 23. Vaneron PJ, Hammill SC, Bailey KR, et al. Signal-averaged electrocardiography: a new noninvasive test to identifY patients at risk for ventricular arrhythmias. Mayo Clin Proc 1988;63(9):931-42 24. Gomes JA, Wmters SL, Stewart D, et al. A new noninvasive index to predict sustained ventricular tachycardia and sudden death in the first year after myocardial infarction: based on signal-averaged electrocardiogram, radionuclide ejection fraction and Holter monitoring. ] Am CoU Gudiol 1987; 10(2):349-57 25. Cripps T, Bennett D, Camm J, et al. Prospective evaluation of clinical assessment, exercise testing and signal-averaged electrocardiogram in predicting outcome after acute myocardial infarction. Am J Cardiol 1988;62( 15):995-9 26. Burkart F, Pfuterer M, Kiowski W, et al. Improved survival of patients with asymptomatic ventricular arrhythmias after myocardial infarction with amiodarone: a randomized, controlled trial. Circulation 1989;80(4 Suppl):IIll9
ARRHYTHMJAS AND Ml • VOL 90/NO 6/NOVEMBER 1, 1991 /POSTGRADUATE MEDICINE
ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20
Arrhythmias and acute myocardial infarction Gregory A. Granrud MD & Pierce J. Vatterott MD To cite this article: Gregory A. Granrud MD & Pierce J. Vatterott MD (1991) Arrhythmias and acute myocardial infarction, Postgraduate Medicine, 90:6, 85-96, DOI: 10.1080/00325481.1991.11701102 To link to this article: http://dx.doi.org/10.1080/00325481.1991.11701102
Published online: 17 May 2016.
Submit your article to this journal
View related articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ipgm20 Download by: [University of Technology Sydney]
Date: 23 July 2016, At: 01:03
Symposium
Downloaded by [University of Technology Sydney] at 01:03 23 July 2016
Third of four articles on myocardial infarction
Arrhythmias and acute myocardial infarction Preview Intensive coronary care, cardiopulmonary resuscitation, betablocker therapy, and thrombolytic therapy have all helped reduce the morbidity and mortality rates of acute myocardial infarction (MI). However, electrical complications continue to pose a major threat to patients' recovery. In this article, Drs Granrud and Vatterott discuss the etiology and treatment of arrhythmias associated with acute Ml as well as risk assessment for future ventricular tachycardia and sudden death.
Gregory A Granrud, MD Pierce J. Vatterott, MD •:• The risk of cardiac arrhythmia is highest in the first few days after myocardial infarction (MI). However, because of the underlying cause or concomitant conditions, some patients are at risk for late complications and may benefit from prolonged monitoring and/or prophylactic therapy.
Bradycardias and acute inferior-wall MI The arterial supply to the sinus node usually arises from the proximal right coronary artery, which supplies the inferior lefr ventricle. Therefore, inferior MI often leads to sinus node dysfunction, which manifests as si-
nus bradycardia, sinus arrhythmia, sinus pauses, sinus node exit block, or emerging atrial fibrillation. Sinus node dysfunction is quite common (incidence, 25% to 40% 1) during the early phases of acute inferior Ml. However, by 4 hours after MI, only 15% to 20% of patients continue to have sinus node dysfunction. 1 Acute sinus bradyarrhythmia is related to cholinergic overload; the inferior and posterior walls of the left ventricle are richly endowed with cardiac vagal-afferent receptors, allowing overload. The Bezold-Jarisch reflex, manifested as reflex bradycardia and hypotension, characterizes this overload. 2 Reactive vagotonia (vasovagal reaction) may also occur as a result of painful stimuli, anxiety, use of sublingual nitroglycerin (Ni-
VOL 90/NO 6/NOVEMBER 1, 1991/POSTGRADUATE MEDICINE • ARRHYTHMIA& AND Ml
trostat) or intravenous nitroglycerin (Nitrostat N, Nitro-Bid N, Tridil), narcotic-induced nausea and vomiting, or intake of other potentially noxious substances. HEART BlOCK-With inferior MI, atrioventricular (AV) block is quite common; major AV block occurs in 15% to 33% of these patients. Characteristically, the QRS interval is narrow, reflecting intact sub nodal conduction. Of the major AV blocks, two thirds result in complete heart block. About half of these occur within the first 6 hours and 92% within 72 hours of Ml. Heart block occurring within the first 6 hours is generally abrupt and causes severe bradycardia. Parasympathetic tone is usually heightened, but it responds to atropine sulfate and resolves within 24 hours. Pacemaker therapy is rarely indicated for early heart block.H Heart block occurring more than 6 hours after MI generally develops slowly, often progressing through first-degree heart block and Mobitz type I AV block (ie, Wenckebach period) before ending in complete heart block. late heart block usually persists for more than 40 hours and is accompanied by a fairly adequate ventricular response.4 It is not vagally mediated; rather, it reflects ischemia or metabolic abnormalities of the AV node. AV block nearly always resolves in patients recovering from inferior MI, although recovery of AV conduction may take up to 16 days. 4 continued 85
Patients with bradycardia and inferior Ml who do not respond satisfactorily to medications may be candidates for temporary pacemaker therapy.
Downloaded by [University of Technology Sydney] at 01:03 23 July 2016
Table 1. Indications for temporary pacemaker therapy In Inferior-wall myocardial infarction Profound asystolic spells related to sinus arrest or high-grade atrioventricular block that is unresponsive to medication Bradycardia-dependent heart failure, typically with ventricular response of 100 msec] on invasive electrophysiologic testing). If syncope develops in this highrisk group, full electrophysiologic examination is warranted. If a prolonged HV interval or infrahisian block during decremental atrial pacing is noted, permanent pacemaker therapy is recommended. (However, it is more likely that syncope is related to inducible paroxysmal ventricular tachyanhythmias.)
Tachyaudias and acute supraventriwlar MI Sinus tachycardia complicates acute MI in about 24% of cases. Possible causes include sympathetic overactivity; pain, anxiety; hypovolernia, congestive heart failure (CHF), atrial distention from fluid overload, and administration of such drugs as atropine and isoproterenol. Supra-
ventricular tachycardias (ie, atrial fibrillation or flutter, paroxysmal supraventricular tachycardia) often reflect left ventricular dysfunction and pending CHF. TREATMENT OF UNDERLYING
CAUSFS--Sinus and supraventricular tachycardias must be treated because of their deleterious effect on myocardial oxygen consumption, especially when regional myocardial blood flow is marginal. The first step is identification of potential causes. Anxiety and pain are best treated with anxiolytics or appropriate narcotics. Hypovolernia is managed with fluid replacement. If there are no signs of CHF, profound bradycardia, or other contraindications, beta-adrenergic blocking agents play an important role in limiting heart rate and preserving myocardial tissue. In most cases in which CHF is a concern, betablocker therapy should be guided by invasive hemodynarnic monitoring. Another option is the use of esmolol hydrochloride (Brevibloc), a shortacting class N beta blocker with an elimination half-life of9 minutes. It offers the opportunity to try beta blocker therapy and evaluate tolerance; however, expense is a concern. In a patient with impending CHF, warning atrial anhythrnias (eg, frequent premature atrial beats) are common. Such a warning is secondary to high ventricular end-diastolic pressures, which result in atrial distention. These patients often respond to diuretics. Some researchers have recommended prophylactic treatment with digitalis when atrial
continued on page 93 88
ARRHYTHMIA& AND Ml • VOL 90/NO 6/NOVEMBER 1, 1991/POSTGRADUATE MEDICINE
Downloaded by [University of Technology Sydney] at 01:03 23 July 2016
Immediately after cardioversion, therapy to reverse patients' predisposition to atrial fibrillation or flutter should be initiated.
fibrillation or flutter occurs. However, because digitalis increases myocardial oxygen demand and may reach toxic levels in active infarction, we recommend that it be used only in patients who have ovett CHF or sustained tachyarrhythmias. 1REA1MENT OF TACHYCARDIAS--
Treatment of atrial fibrillation or flutter, as with other supraventricular tachycardias, depends on the patient's immediate status. If tachycardia causes hemodynamic compromise, dyspnea, or angina, immediate cardioversion is indicated. Immediately after cardioversion, therapy to reverse the patient's predisposition to atrial fibrillation or flutter should be initiated. This may include treatment of underlying CHF or electrolyte abnormalities. Therapy with procainamide hydrochloride (Pronestyl) (1 g administered intravenously over 20 to 40 minutes, followed by a drip of 1 to 3 mg/min) and digoxin helps prevent recurrence of atrial fibrillation and flutter. Patients can then be switched to oral class I agents, but their need for long-term therapy should be assessed before they are discharged from the hospital. If atrial fibrillation or flutter appears to be moderately well tolerated, treatment should be started with digoxin (0.5 mg administered intravenously, followed by 0.125 to 0.25 mg every 2 to 4 hours for a total dose of about 1.0 to 1.5 mg/24 hr). Therapy should be guided by the ventricular rate response to atrial fibrillation. In addition, therapy to reverse a patient's predisposition to atrial arrhythmias should be initiated
Gregory A. Granrud, MD Pierce J. Vatterott, MD Dr Granrud (left) and Dr Vatterott (right) are eo-directors of the St Paul Arrhythmia Center and staff physicians, St Paul Heart Clinic, St Paul. Among Dr Granrud's interests are invasive and interventional cardiology and treatment of sudden cardiac death. Some of Dr Vatterott's interests are electrophysiology, signal-averaged electrocardiography, antitachycardia devices, and pacemakers.
as described. If, after treatment of CHF, the patient remains in atrial fibrillation or flutter, intravenous procainamide should be started. Overdrive atrial pacing is a convenient alternative therapy for atrial flutter. Adenosine (Adenocard) is a new adjuvant drug for atrial tachyarrhythmia that has distinct benefits. Its side effects (ie, anxiety, chest discomfort, and flushing) are minimal and of brief duration. It is taken up and metabolized rapidly by nearly all living cells in the human body; thus, adenosine has few hemodynamic consequences. It provides a very
VOL 90/NO 6/NOVEMBER 1, 1991/POSTGRADUATE MEDICINE • ARRHYTHMIA$ AND Ml
short-acting block of the AV node and so terminates tachycardias involving the AV node. It gradually slows sinus tachycardia. Adenosine has diagnostic as well as therapeutic capabilities. In cases of atrial flutter, it provides a temporary AV block, thus allowing detection of atrial flutter waves that were not seen previously. Since adenosine is taken up by endothelium throughout the cardiovascular system, central line administration is more effective than peripheral administration. Adenosine can cause prolonged pauses. If the drug is given by central line, a dose of continued 93
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The substrate for ventricular arrhythmias in acute Ml is ischemic or necrotic myocardium.
3 mg should be used initially and the dose increased gradually in 3-mg increments to a maximum of 12 mg. Intravenous doses start at 6 mg. Doses greater than 12 mg are oflittle benefit. Concurrent use of theophylline inhibits adenosine's effectiveness.2" For short-term in-hospital therapy, the use of beta blockers, digoxin, calcium antagonists, or class lA agents (ie, disopyramide [Norpace], procainamide, and quinidine sulfate) may be of benefit. Given the results of the Cardiac Arrhythmia Suppression Trial/ 1 we do not recommend treatment with classIC agents (ie, encainide hydrochloride [Enkaid], flecainide acetate [Tambocor], and propafenone hydrochloride [Rythmol]).
Tachycardias and acute ventricular MI The substrate for ventricular arrhythmias in acute Ml is ischemic or necrotic myocardium. Myocardial irritability is increased, and metabolic changes cause a decrease in fibrillation threshold. Early ECG monitoring has demonstrated that ventricular ectopic activity occurs within a few hours of acute Ml in almost 100% of patients. Although this high percentage is worrisome, it reflects, in part, the frequent finding of premature ventricular beats among the healthy population. In fact, the value of warning ventricular arrhythmias (ie, more than 5 premature ventricular beats per minute) is now in question. Many patients have warning arrhythmias without ventricular fib94
rillation and others have ventricular fibrillation without arrhythmias. FIBRILLATION-Ventricular fibrillation occurs in about 10% of patients during the first hour of symptoms, in 16% during the first 4 hours, and in 6% who survive to reach the coronary care unit. Ventricular tachycardia occurs in 3% to 15% of patients with acute Ml; it is usually self-limited and occurs in short runs. Ventricular fibrillation in Ml patients can be divided into distinct categones: • Primary ventricular fibrillation occurs suddenly during severe acute ischemia and is independent of cardiac failure. Therapy with lidocaine and beta blockers and reversal of ischemia have been shown to prevent primary ventricular fibrillation. • Secondary ventricular fibrillation occurs 1 to 6 weeks after MI. It may be drug-induced, due to pacing in or near an infarct wne, or agonal. Prognosis is extremely poor, even if ventricular arrhythmia is successfully treated, because arrhythmia is ofi:en a sign of severe underlying lefi: ventricular dysfunction. PROPHYLAXIs-The use oflidocaine for prophylaxis remains controversial, but there is no question that it is first-line therapy for ventricular tachyarrhythmias. The initial bolus is 1 mg/kg administered over a 1-minute period, followed by a drip of2 mg/min. A second bolus, at half dose, should be given 10 minutes later. Maintenance therapy should be reduced in patients prone to toxicity (eg, those with CHF, shock, ad-
vanced liver disease, or age greater than 70). During therapy, patients should be monitored for evidence of lidocaine toxicity. AV block with ventricular escape rhythm is an absolute contraindication to lidocaine therapy. Bretylium tosylate (Bretylol) and procainamide are also useful for adjunctive treatment of ventricular tachyarrhythmias in the coronary careumt. lREATMENT IN THE CORONARY
CARE UNIT-Attention
should be directed to vigorous correction of electrolyte imbalances, including hypokalernia and hypomagnesemia. Hypokalemia is a common complication in patients who are dehydrated, taking diuretics, or consuming excessive amounts of caffeine. Hypomagnesemia is common in patients who are malnourished or receiving diuretics, are alcoholic, have a malabsorptive state, or recently received aminoglycosides or cisplatin (Platinol). The increase in catecholamines resulting from infarction alone can cause hypomagnesemia. Patients receiving magnesium replacement therapy have fewer ventricular arrhythmias. 22 Studies have shown that magnesium sulfate can be administered safely during the early days of infarction and improves survival rates. 22 Clearly, monitoring the magnesium level is appropriate in acute Ml, and its repletion is strongly recommended. Standard replacement therapy is intravenous (piggyback) administration of2 to 4 g of magnesium over a 30- to GO-minute period.
ARRHYTHMIA& AND Ml • VOL 90/NO 6/NOVEMBER 1, 1991 /POSTGRADUATE MEDICINE
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Signal-averaged electrocardlography is a new high-resolution method that minimizes the level of noise that contaminates the periodic ECG signal.
Accelerated idioventricular rhythm occurs in about 30% of patients with acute MI, most often in the first 2 days after MI. It is equally common in anterior and inferior infarcts. Accelerated idioventricular rhythm probably results from enhanced automaticity of Purkinje fibers during acute MI. This slow ventricular rhythm often emerges during slowing of sinus rhythm.Acceleratedidioventricular rhythm is often associated with episodes of rapid ventricular tachycardia However, unlike rapid ventricular tachycardia, accelerated idioventricular rhythm is thought not to affect prognosis. The need for treatment of this rhythm is conrroversial. Beta-blocker therapy is often recommended. Signal-averaged electrocardiography can be very helpful in demonstrating the presence of a myocardial substrate that could suppon a more malignant ventricular arrhythmia. 23 Signal averaging of the surface ECG is a new noninvasive, highresolution, computerized method of analyzing standard ECGs and averaging multiple QRS complexes. It identifies patients at risk for ventricular tachycardia Signal averaging minimizes the level of noise that contaminates the periodic ECG signal and thereby exposes signals of the microvolt level normally hidden within noise.
Risk assessment for sudden death after MI Ventricular tachycardia and sudden death occur in 5% to 10% of pa-
Table 3. Comparison of value of monitoring methods used to predict arrhythmic events Method
Normal result No. of % arrhythmic events/No. of patients
Abnormal result* No. of % Pvalue arrhythmic events/No. of patients
SA ECG EF Halter SA ECG+ EF SA ECG + Halter EF +Halter SA ECG + EF + Halter
2/57 3/47 3/32 0/26 0/14 1/16 0/9
13/45 12/50 12/52 10/28 9/26 11/30 8/16
3.5 6.3 9.3 0 0 6 0
29 24 23 36 35 37 50
0.0003 0.01 0.09 0.0007 0.01 0.025 0.01
EF, ejection fraction; Holter, ambulatory continuous electrocardiographic monitoring; SA ECG, signal-averaged electrocardiography. ·Abnormal SA ECG = QRS duration > 114 msec, root mean square voltage < 20 11V. or low-amplitude signal > 38 msec; abnormal EF = < 40%; abnormal Holter = > 10 premature ventricular beats per hour. Adapted from Gomes et al."
tients during the first year after infarction. Both ischemia and primary ventricular arrhythmias have a role in sudden death. Ischemic events are predicted by postinfarction exercise testing or coronary angiography; arrhythmic events are not. Gomes and associatei4 found that late potentials on the signal-averaged ECG, an ejection fraction less than 40%, and more than 10 premature ventricular beats per hour predict the occurrence of ventricular tachycardia and sudden death in the next year (table 3); the risk is 50% in patients with all three of these traits. Cripps and coworke~ 5 found that arrhythmic events are also predicted by a higher class of CHF on presentation at the coronary care unit. Heart rate vari-
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ability, as demonstrated on ambulatory continuous ECG (Holter) monitoring, may also play a role. Physicians' ability to identify patients who are at increased risk for future arrhythmic events has improved more than their ability to treat such events. Empirical therapy with class I antiarrhythmics does not improve survival rates. Ar. this time, our recommendation for patients at moderate risk for future arrhythmic events is treatment with beta blockers and/or angiotensin-convening enzyme inhibitors. Physicians should plan for aggressive management of CHF (see related anicle on page 99), appropriate management of electrolyte status, and, when possible, reversal of ischemia. Abstract data suggested that empirical use of continued 95
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low-dose amiodarone (200 mglday) may be of benefit in patients with nonsustained ventricular tachycardia after MF6 Further studies are under way, including one in which choosing treatment on the basis of signalaveraged ECG late potentials, ejection fraction, and Holter monitoring results is being investigated. Patients should be referred for electrophysiologic evaluation when they have malignant ventricular arrhythrnias after MI, do not respond to appropriate medical management, and are judged to be at high risk by results of signal-averaged ECG, by the presence of symptoms of heart failure, and by their ejection fraction. Electrophysiologic testing may be used to guide future drug treatment and to determine whether patients would benefit from the use of such devices as an implantable cardiodefibrillator or a complex antitachycardia device.
Summary The most common arrhythmias associated with inferior-wall and anterior-wall myocardial infarction are bradycardia and supraventricular and ventricular tachycardia. Optimal treatment approaches are based on the pathophysiology of the infarct and the presence of contributing medical factors (eg, congestive heart failure, metabolic disorders). Temporary or permanent pacemaker therapy is hdpful in some patients. Sudden death due to arrhythmia after myocardial 96
infarction may be predicted and avoided in certain situations. IFUVI
Earn credit on this article. ~ See CME Quiz.
Address for correspondence: Gregory A Granrud, MD, St Paul Heart Clinic, 255 N SmithAve, Suite 100, St Paul, MN 55102.
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