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Myocardial Infarction Complicated by Conduction Defect
Symposium on Coronary Heart Disease
Myocardial Infarction Complicated by Conduction Defect Kenneth M. Rosen, M.D.,* Ali Ehsani, M.D.,** and Shahbudin H. Rahimtoola, MB., M.R.C.P.E.***
There have been several excellent reviews concerned with acute myocardial infarction and conduction defects.12, 30, 35, 41 In the present article, we will not duplicate these previous efforts, but will attempt to highlight the major features of acute myocardial infarction with complicating conduction disease. One of our major theses will be that myocardial infarction and heart block reflect two disease processes with different pathophysiology and clinical course, the first being diaphragmatic infarction (DMI) with compromised blood supply to the atrioventricular node, and the second being anterior infarction (AMI) with conduction disease involving primarily the intraventricular conduction system. The therapeutic implications of these two disease processes will be discussed.
ANATOMY, PATHOLOGY, AND PATHOPHYSIOLOGY The specialized cardiac conducting system consists of the sinoatrial node, the atrioventricular node, the bundle of His, the bundle branches, and the distal Purkinje network. The atrioventricular node possesses the property of slow conduction, allowing delay of ventricular contraction which enables the atria to contribute significantly to ventricular filling. The bundle of His and bundle branches are composed of rapidly conducting Purkinje tissue, allowing synchronous activation of both ventricles. From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital and the Department of Medicine, Abraham Lincoln School of Medicine, University of Illinois College of Medicine, Chicago, Illinois *Professor of Medicine and Chief, Cardiology Section, Abraham Lincoln School of Medicine, University of Illinois College of Medicine, Chicago **Cardiology Fellow, Cardiology Section, University of California, San Diego **"Professor of Medicine, University of Oregon Medical School, Portland Supported in part by Contract No. 71-2478, Myocardial Infarction Program, National Heart and Lung Institute, National Institutes of Health, Department of Health, Education and Welfare
Medical Clinics of North America- Vo!. 57, No. 1, January 1973
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Rosenbaum suggests that the intraventricular conduction system be considered trifascicular, consisting of the right bundle branch, the anterior division of the left bundle branch, and the posterior division of the left bundle branch. 34 Block of the right bundle branch produces the typical electrocardiogram of right bundle branch block (RBBB). Block of the anterior division of the left bundle branch (left anterior hemiblock, LAH) produces left axis deviation of -60° or greater, with aqRinlead I andanrS in lead In. Block of the posterior division of the left bundle branch (left posterior hemiblock, LP H) produces right axis deviation of +120 or greater with a rS pattern in lead I, and a qR pattern in lead In (Fig. 1). The QRS with either LAH or LPH is generally narrow. Right bundle branch block with left or right axis deviation suggests block of the right bundle branch with additional block in the anterior or posterior divisions of the left bundle branch respectively (Figs. 2A and 3A). Complete block of all three fascicles (trifascicular block) produces complete atrioventricular block (Figs. 2B and 3B). Cardiac cells having the ability to act as pacemakers demonstrate slow depolarization during diastole. 15 The presence of diastolic depolarization is a normal characteristic of cells comprising the sinoatrial node. Other areas of the heart in which pacemaker activity may also exist include ectopic atrial sites, the bundle of His, the bundle branches, and the distal Purkinje network. Under ordinary circumstances, the pacemaker functions of these areas are masked, since the sinoatrial node is the dominant pacemaker controlling the heart. Intrinsic rhythmicity decreases as one moves more distally in the conduction system. In the event of atrioventricular block, conduction tissue just distal to the site of block takes over pacemaker function. Therefore, with block at the atrioventricular node, escape rhythms appear to arise in the bundle of His, producing a relatively rapid escape rhythm with a narrow QRS. With trifascicular block, escape rhythms are idioventricular, arising distal to the sites of block. Idioventricular escape rhythms are characterized by a wide QRS and relatively slow rates (Figs. 2B and 3B). Heart block in myocardial infarction almost certainly reflects an interplay of both functional and structural abnormalities. Zipes reviewed a
Figure 1. Isolated left posterior hemiblock complicating nontransmural acute myocardial infarction. On January 9 normal axis is present. On January 11 the axis has shifted somewhat rightward. On January 12 the typical electrocardiographic findings of left posterior hemiblock (LPH) are seen. Note right axis deviation with an rS in I and a qR in Ill. On January 13 the axis has normalized, with reversion of the conduction defect.
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number of reflexes that could be evoked in acute infarction, producing sinus slowing and/or atrioventricular block. 4 ! These reflexes are protective in that they slow heart rates, minimizing oxygen needs of the ischemic myocardium. However, profound bradycardia can induce catastrophic decreases in coronary and/or systemic blood flow. Ischemia of the conduction system itself, can also impair conduction. The atrioventricular node is more sensitive than the His Purkinje system to ischemia.! A knowledge of the blood supply of the conduction system is useful in understanding the conduction defects seen with acute myocardial infarctionP' !8 The artery to the sinoatrial node arises from the proximal right coronary artery in about 55 per cent of patients, and from the left
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Figure 3. Acute anteroseptal infarction with right bundle branch block, left posterior hemiblock, and developing complete heart block. A, Intact conduction with right bundle branch block and left posterior hemiblock. Note abnormal right axis deviation with rS in I and qR in In. Also note the pattern of right bundle branch block in Vi' B, Complete heart block (trifascicular block), developing several days following the onset of myocardial infarction.
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circumflex artery in 45 peI\'Cent of patients. The artery to the atrioventricular node arises from the right coronary in about 90 per cent of patients, and from the left circumflex in only about 10 per cent. The atrioventricular nodal artery also supplies the His bundle and the very proximal bundle branches. Most of the bundle branch systems are supplied by the blood supply of the ventricular septum. The right bundle branch and the anterior fasicles of the left bundle branch are supplied by perforating branches of the left anterior descending coronary artery. The posterior fasicles of the left bundle branch possess a dual blood supply, receiving branches from both the anterior and posterior descending coronary arteries. One would predict from these anatomic considerations, that atrioventricular block complicating right coronary disease (DMI) would be atrioventricular nodal, and that block complicating disease of the anterior descending coronary artery (AMI) would involve the bundle branch system. Pathologic examinations in patients dying with acute myocardial infarction and heart block support these contentions. Sutton and Davies reported results of serial section of the conduction system in 29 patients dying with heart block and myocardial infarction.39 Twenty-four of their patients had DMI. In these, pathological examination revealed proximal occlusion of the coronary artery giving origin to the atrioventricular nodal artery. Major structural damage to the conduction system was absent in most, suggesting that ischemia was responsible for atrioventricular block. In contrast, 5 of their cases had extensive anteroseptal infarction. In these cases, the blood supply to the atrioventricular node was not compromised, but there was extensive destruction of the ventricular septum and bundle branches. Similar results were reported by Blondeau and their co-workers.3
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Figure 4. Complete heart block proximal to the bundle of His in acute diaphragmatic infarction. Shown are the simultaneous electrocardiogram and bundle of His electrogram. P waves and atrial electrograms are labeled P and QRS, and ventricular electrograms are labeled R. The continuous strips show complete atrioventricular dissociation with an atrial rate of 100 per min. and a ventricular rate of 48 per min. Note that block is above the bundle of His, since none of the P waves are followed by H potentials. Each QRS is preceded by an H potential, reflecting a junctional escape rhythm. Paper speed is 100 mm. per sec. (From Rosen, K. M., et al.: Circulation, 42:925, 1970, by permission of the American Heart Association.)
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Figure 5. Wenckebach periods proximal to the bundle of His in a patient with acute subendocardial infarction. Note progressive prolongation of the P-H interval (P-H intervals are listed on the illustration) with block of the third P wave proximal to the bundle of His. Atrial rate is 100 per min. The H-Q interval is 45 msec. and normal. (From Rosen, K. M., et al.: Circulation, 42:925,1970, by permission of the American Heart Association.)
Electrophysiologic studies also support the relationship of site of block and site of infarction. Electrograms can be recorded from the His bundle using an electrode catheter recording technique. 3 ! Our laboratory reported results of His bundle recording in eight patients with acute infarction and heart block. 33 Three patients with DMI and one patient with subendocardial infarction had block proximal to the bundle of His, suggesting an atrioventricular nodal site of block (Figs. 4 and 5). Intraventricular conduction was normal in these three patients. One patient with DMI had block in the His bundle. Three patients with AMI infarction had block distal to the His bundle, suggestive of trifasicular block (Fig. 6). Atrioventricular conduction in these latter 3 patients was normal.
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Figure 6. Complete heart block distal to the bundle of His in acute anteroseptal myocardial infarction. Complete atrioventricular dissociation is present with an atrial rate of 109 per min. and a ventricular rate of 36 per min. Note that each P wave is followed by a nonconducted H potential with a normal P-H interval of 104 msec. The QRS complexes are idioventricular, being wide and not preceded by H potentials. (From Rosen, K. M., et al.: Circulation, 42:925, 1970, by permission of the American Heart Association.)
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INCIDENCE Resnekov and Lipp reviewed the incidence of atrioventricular block in acute myocardial infarction, analyzing the incidence in 5160 patients reported from 17 medical centers. 30. The overall incidence of first degree block was 13 per cent, that of second degree block 5 per cent, and that of third degree block, 3 per cent. Approximately one third of patients with first degree block progress to more advanced forms of block, and approximately a third of the patients with second degree block progressed to more advanced block. DMI is a much more common cause of atrioventricular block than AMI.5, 7, 9, 23, 26 However, the mortality with DMI and heart block is much less than the mortality with AMI and heart block.5, 7, 20, 23, 26
DIAPHRAGMATIC INFARCTION In the typical case of DMI with conduction defect, the patient may have first, second, or third degree block at the time of admission. Approximately a third of the patients with first degree block progress to a more advanced form of block over the next 24 to 48 hours. In almost all patients with DMI and heart block, complete reversal of the conduction defect occurs generally within a week of admission, if the patient survives the infarction (Fig. 7).7,12,16,26 In rare cases, atrioventricular block secondary to DMI may be permanentY Progression and reversal of conduction disease in DMI is generally a gradual process, occurring over hours or days. Precipitous changes in heart rate are unusual. Most patients manifest Wenckebach periods (Mobitz type I block) at some point during the evolution of atrioventricular block (Fig. 7A).21 This reflects the atrioventricular nodal site of block, since Wenckebach periods are a typical manifestation of the depressed atrioventricular node. There are several features of DMI with atrioventricular block that appear directly related to the site of block. 7 , 9,12, 20-23,26,32,37 These are as follows: (1) QRS duration is narrow, this finding relating to the absence of intraventricular conduction disease and the presence of escape rhythms originating above the bifurcation of the His bundle. (2) Ventricular rates during complete block are usually relatively rapid (40 to 60 beats per min), also reflecting the proximal site of block and the relatively high origin of the escape rhythms. In addition, atrioventricular automaticity may be increased with resultant nonparoxysmal atrioventricular junctional tachycardia superimposed upon atrioven-
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Figure 7. Second degree atrioventricular block in diaphragmatic myocardial infarction. A, 4:3 Wenckebach periods noted on admission. B, Rhythm strip sevt:ral days later showing return of 1: 1 atrioventricular conduction. First degree atrioventricular block is still present.
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tricular block (ventricular rates of 60 to 100).29 (3) Stokes-Adams attacks are unusual in DMI, reflecting the relatively rapid ventricular rates and the reliability of the atrioventricular junctional escape pacemakers.
ANTERIOR MYOCARDIAL INFARCTION AMI is associated with a much higher incidence of intraventricular conduction defects than is DMI, presumably reflecting involvement of the ventricular septum.8. 13.23.33.38 The intraventricular conduction defects seen range from the relatively minor fascicular blocks to complete heart block secondary to necrosis of the trifascicular conduction septum. Fasicular Blocks and Bundle Branch Block The most common conduction defect complicating acute myocardial infarction is LAH.8. 24 Mariott reported a series of 250 patients with acute infarction, with an incidence of LAH of 15.2 per cent. 24 In most cases, the site of infarction was anterior. Isolated LPH is a much rarer defect. Several features of LAH complicating acute infarction are worth noting. These are as follows: (1) LAH does not generally progress to complete atrioventricular block, but remains as an isolated finding which mayor may not regress. 24 (2) Mortality in patients with infarction and LAH appears to be somewhat higher than patients with uncomplicated infarction (25 per cent).8 (3) LAH may mask diaphragmatic infarction because the rS pattern in lead III due to LAH may mask the presence of pathologic Q waves. 34 The incidence of bundle branch block in acute infarction varies from approximately 7 to 13 per cent of cases. 16 . 27 The mortality in these cases, is much higher than in the uncomplicated infarction, approximating 50 per cent. This mortality reflects the extent of the infarction necessary to compromise conduction in the bundle branches. Bifascicular Block and Complete Heart Block Characteristically, when heart block complicates AMI, electrocardiograms taken prior to the onset of atrioventricular block reveal evidence of involvement of two of the three fascicles of the conduction system (bifascicular block),13· 38 The specific conduction defects associated with high risk of heart block in AMI include right bundle branch block with left axis deviation (RBBB with LAH) (Fig. 2A), right bundle branch block with right axis deviation (RBBB with LP H) (Fig. 3A), alternating bundle branch block, and first degree atrioventricular block with bundle branch block. Godman and co-workers reported 100 patients with myocardial infarction and one of the above patterns (out of a total series of 1,809 patients),13 The most common abnormality in the 100 patients was RBBB with LAH, seen in 51 of the patients. The incidence of heart block in the 100 patients was 47 per cent. The overall mortality was very high, being 85 per cent in the patients developing heart block. Scanlon et al. reported a similar series of 28 patients with myocardial infarction. 36
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The incidence of heart block in their series was somewhat less, being only 21 per cent. The clinical features of heart block complicating AMI relate to both the site of block (distal to H) and the extensive myocardial infarction necessary to compromise conduction in both bundle branch systems. 12 . 13. 21. 23. 26. 38 Characteristic features of heart block and AMI include the following: (1) The paroxysmal onset of atrioventricular block. 38 These patients usually manifest intact conduction with bifasicular block prior to development of complete and sudden atrioventricular block (Figs. 2A, 2B, 3A, and 3B). Paroxysmal atrioventricular block appears to reflect sudden failure of the remaining functioning fasicle. The paroxysmal nature of block reflects the tendency of conduction to be all or none in the His-Purkinje system. Also typical of AMI with bifascicular block is the development of Mobitz type 11 atrioventricular block (second degree block without progressive prolongation of PR intervals prior to the dropped beat).21 Type 11 block in AMI often heralds the development of more advanced conduction disturbance. (2) Idioventricular escape rhythms characterized by wide QRS complexes and very slow rates. Stokes-Adams attacks are frequent in AMI with heart block because of the unreliability and slow rates of the idioventricular rhythms. (3) Very high mortality from heart failure and cardiogenic shock, reflecting the extensive infarction necessary to impair conduction in both bundle branch systemsP SUBENDOCARDIAL INFARCTION, PRINZMET AL'S ANGINA, ATYPICAL CASES Atrioventricular block complicating coronary disease may also occur both with subendocardial infarction and with Prinzmetal's angina (atypical angina with ST elevations).4.12 We have recorded His bundle electrograms in one case of each (Fig. 5). The site of block was proximal to the His bundle in both, suggesting atrioventricular nodal ischemia as the mechanism of block. 33 Therefore, these cases appear to resemble DMI with heart block. We would like to inject a note of caution into the discussion at this point, and that is that exceptions to the dictum that block in DMI is always atrioventricular nodal, and that block in AMI is always in the bundle branch system, probably occur. The reasons for this are as follows: (1) In 10 per cent of patients, the atrioventricular node is supplied by a branch of the left coronaryP' 18 In these cases, occlusion of the left coronary proximal to the atrioventricular nodal artery could produce block at the atrioventricular node. (2) The atrioventricular nodal artery supplies the His bundle and the proximal bundle branchesP' 18 We have reported one case of DMI with block in the His bundle. Since both right and left bundle branch block can occur with DMI, there is no reason why bilateral bundle branch block could not also occur. (3) In chronic coronary disease, development of collateral circulation is frequent. In such cases, one coronary could supply both the atrioventricular node and the
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bundle branches. Occlusion of that coronary could produce block at one or more sites. Although recording of His bundle electrograms is the most accurate guide to site of bloek, in these atypical cases QRS duration may be used as a guide to the site ofblock.31- 33 Narrow QRS complexes suggest a proximal site ofblbckandwide QRS complexes suggest a distal site of block.
THERAPY OF MYOCARDIAL INFARCTION WITH CONDUCTION DISTURBANCE Pharmacologic Therapy Atropine has- been used suocessfully in patients with acute myocardial infarction and bradyarrhythmia. 40 One to 2 mg. of atropine intravenous produces a vagolytic action, improving atrioventricular nodal conduction and increasing sinus rate. Heart block in DMI may be reversed with atropine, In addition, atropine may increase the rate of atrioventricular junctional escape rhythms. Atropine is ineffective in complete bilateral bundle branch block since the site of blook as well as the escape pacemakers are not under significant parasympathetic control. Atropine can also paradoxically worsen atrioventricular block in both DMI and AMI by increasing atrial rates and thus the number of impulses bombarding the site of block. IO With repetitive concealed conduction, this could produce more advanced degrees.ofblock, and.slower ventricular rates. Isoproterenol, apotent beta stimulator, may facilitate conduction in both the atrioventricular node and the His-Purkinje system. In addition, isoproterenol may increase the rates of both atrioventricular junctional and idioventricular escape rhythms. Unfortunately, isoproterenol, by increasing both con tractility and ventricular rate, may increase the oxygen demands of ischemic myocardium, increasing infarct size. Isoproterenol also increases ventricular irritability with risk of ventricular premature beating and ventricular fibrillation. We would recommend that isoproterenol be used only. as emergency therapy in symptomatic bradyarrhythmia, until less hazardous therapy can be initiated. Other agents used in treatment of myocardial infarction with heart block include steroids and the use of polarizing solutions (glucose, insulin, and potassium).25 The slow action of these together with the spontaneous reversibility of conduction disturbance in myocardial infarction, make evaluation of their effectiveness very difficult. It is our opinion, that the value of either steroids or polarizing solution in myocardial infarction with heart block is unproven, and we would not recommend their use. Pacing In experienced hands, transvenous pacing can be accomplished in patients with myocardial infarction with low morbidity.2 Lassers and co-workers demonstrated that ventricular pacing in patients with heart block and myocardial infarction increased cardiac
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output. 22 However, they also noted that tension time index, a measure of myocardial oxygen needs, was also correspondingly increased. It was implied, that pacing increased myocardial oxygen needs. This could be hazardous in patients with acute myocardial infarction, since it could increase infarct size. Thus, pacing may produce both beneficial and possibly hazardous effects. It is impossible to measure the effectiveness of ventricular pacing in improving the mortality of myocardial infarction and heart block, with the data presently available. Mortality with and without pacing varies tremendously from series to series.O;-7. 9. 12. 14. 19.20.26.28.37 In general, mortality is lower in DMI with and without pacing, and higher in AMI, with and without pacing. We prefer therapeutic recommendations based on the site of infarction and the hemodynamic status of the patient.
Inferior Infarction In DMI with first degree atrioventricular block, no specific therapy is necessary. Most of these patients do not develop progression of their conduction disease. Those that do progress, do so in stages, allowing ample time for specific therapy. In DMI with second or third degree block, therapy should be dependent upon both the ventricular rate and the hemodynamic status of the patient. If ventricular rates are less than 50 per min, or if there is evidence of either heart failure or cardiogenic shock, then increase of heart rate with specific therapy is indicated. Atropine can be tried first. If both ventricular rate and hemodynamic status do not improve, transvenous pacing is indicated. It should be remembered that heart block in DMI is generally reversible, so that pacing should be avoided in the stable patient with heart rates of 50 or above. Anterior Infarction Current literature suggests that either first degree block or LAH complicating AMI do not imply a risk of progression of conduction disease. No specific therapy is indicated in these patients. In AMI with intact conduction and bifasicular block, we would recommend prophylactic pacing if this can be accomplished by a physician skilled in pacemaker implantation, and if this can be done in or close to the coronary care unit. Prophylactic pacing of these patients is controversial, and if pacing cannot readily be accomplished, it is also reasonable to just carefully monitor this group of patientsP In AMI with either second or third degree block, we would recommend ventricular pacing. Mortality will be extremely high in this group, with or without pacing. However, an occasional patient is salvageable, so that active therapy is indicated. In the future, this group of patients may become candidates for saphenous bypass and infarctectomy in addition to pacing. Atypical Cases The occasional patient with AMI, heart block, and narrow QRS, presumably has atrioventricular nodal block, and should be managed as
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recommended for DMI. The occasional patient with DMI, heart block, and a wide QRS, should be managed as a patient with AMI and heart block. In these cases, His bundle recording, if available, can provide accurate delineation of the site of block. 31-33
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27. Norris, R. M., and Croxson, M. S.: Bundle branch block in acute myocardial infarction. Amer. Heart J., 79:728, 1970. 28. Paulk, E. A., and Hurst, J. W.: Complete heart block in acute myocardial infarction. A clinical evaluation of the intracardiac bipolar catheter pacemaker. Amer. J. Cardio!., 17:695,1966. 29. Pick, A., and Dominguez, P.: Nonparoxysmal A· V nodal tachycardia. Circulation, 16: 1022, 1957. 30. Resnekov, L., and Lipp, H.: Pacemaking and acute myocardial infarction. Prog. Cardiovasc. Dis., 14:475, 1972. 31. Rosen, K. M.: The contribution of His bundle recording to understanding of cardiac conduction in man. Circulation, 43:961, 1971. 32. Rosen, K. M., Gunnar, R. M., and Rahimtoola, S. H.: Site and type of second degree atrioventricular block. Chest, 61 :99, 1972. 33. Rosen, K. M., Loeb, H. S., Chuquimia, R., et al.: Site of heart block in acute myocardial infarction. Circulation, 42:925, 1970. 34. Rosenbaum, M. B., Elizari, M. V., and Lazzari, J. 0.: The Hemiblocks. Oldsmar, Florida, Tampa Tracings, 1970. 35. Rotman, M., Wagner, G. S., and Wallace, A. G.: Bradyarrhythmias in acute myocardial infarction. Circulation, 45:703, 1972. 36. Scanlon, P. J., Pryor, R., and Blount, S. G.: Right bundle-branch block associated with left superior or inferior intraventricular block. Associated with acute myocardial infarction. Circulation, 42:1135,1970. 37. Scott, M. E., Geddes, J. S., Patterson, G. C., et a!.: Management of complete heart block complicating acute myocardial infarction. Lancet, 2:1382,1967. 38. Stock, R. J., and Macken, D. L.: Observations on heart block during continuous electrocardiographic monitoring in myocardial infarction. Circulation, 38:993, 1968. 39. Sutton, R., and Davies, M.: The conduction system in acute myocardial infarction complicated by heart block. Circulation, 38:987, 1968. 40. Thomas, M., and Woodgate, D.: Effect of atropine on bradycardia and hypotension in acute myocardial infarction. Brit. Heart J., 28:409, 1966. 41. Zipes, D. P.: The clinical significance of bradycardic rhythms in acute myocardial infarc· tion. Amer. J. Cardio!., 24:814, 1969. Cook County Hospital 1825 West Harrison Street Chicago, Illinois 60612
Myocardial Infarction Complicated by Conduction Defect Kenneth M. Rosen, M.D.,* Ali Ehsani, M.D.,** and Shahbudin H. Rahimtoola, MB., M.R.C.P.E.***
There have been several excellent reviews concerned with acute myocardial infarction and conduction defects.12, 30, 35, 41 In the present article, we will not duplicate these previous efforts, but will attempt to highlight the major features of acute myocardial infarction with complicating conduction disease. One of our major theses will be that myocardial infarction and heart block reflect two disease processes with different pathophysiology and clinical course, the first being diaphragmatic infarction (DMI) with compromised blood supply to the atrioventricular node, and the second being anterior infarction (AMI) with conduction disease involving primarily the intraventricular conduction system. The therapeutic implications of these two disease processes will be discussed.
ANATOMY, PATHOLOGY, AND PATHOPHYSIOLOGY The specialized cardiac conducting system consists of the sinoatrial node, the atrioventricular node, the bundle of His, the bundle branches, and the distal Purkinje network. The atrioventricular node possesses the property of slow conduction, allowing delay of ventricular contraction which enables the atria to contribute significantly to ventricular filling. The bundle of His and bundle branches are composed of rapidly conducting Purkinje tissue, allowing synchronous activation of both ventricles. From the Department of Adult Cardiology, Hektoen Institute for Medical Research of the Cook County Hospital and the Department of Medicine, Abraham Lincoln School of Medicine, University of Illinois College of Medicine, Chicago, Illinois *Professor of Medicine and Chief, Cardiology Section, Abraham Lincoln School of Medicine, University of Illinois College of Medicine, Chicago **Cardiology Fellow, Cardiology Section, University of California, San Diego **"Professor of Medicine, University of Oregon Medical School, Portland Supported in part by Contract No. 71-2478, Myocardial Infarction Program, National Heart and Lung Institute, National Institutes of Health, Department of Health, Education and Welfare
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Rosenbaum suggests that the intraventricular conduction system be considered trifascicular, consisting of the right bundle branch, the anterior division of the left bundle branch, and the posterior division of the left bundle branch. 34 Block of the right bundle branch produces the typical electrocardiogram of right bundle branch block (RBBB). Block of the anterior division of the left bundle branch (left anterior hemiblock, LAH) produces left axis deviation of -60° or greater, with aqRinlead I andanrS in lead In. Block of the posterior division of the left bundle branch (left posterior hemiblock, LP H) produces right axis deviation of +120 or greater with a rS pattern in lead I, and a qR pattern in lead In (Fig. 1). The QRS with either LAH or LPH is generally narrow. Right bundle branch block with left or right axis deviation suggests block of the right bundle branch with additional block in the anterior or posterior divisions of the left bundle branch respectively (Figs. 2A and 3A). Complete block of all three fascicles (trifascicular block) produces complete atrioventricular block (Figs. 2B and 3B). Cardiac cells having the ability to act as pacemakers demonstrate slow depolarization during diastole. 15 The presence of diastolic depolarization is a normal characteristic of cells comprising the sinoatrial node. Other areas of the heart in which pacemaker activity may also exist include ectopic atrial sites, the bundle of His, the bundle branches, and the distal Purkinje network. Under ordinary circumstances, the pacemaker functions of these areas are masked, since the sinoatrial node is the dominant pacemaker controlling the heart. Intrinsic rhythmicity decreases as one moves more distally in the conduction system. In the event of atrioventricular block, conduction tissue just distal to the site of block takes over pacemaker function. Therefore, with block at the atrioventricular node, escape rhythms appear to arise in the bundle of His, producing a relatively rapid escape rhythm with a narrow QRS. With trifascicular block, escape rhythms are idioventricular, arising distal to the sites of block. Idioventricular escape rhythms are characterized by a wide QRS and relatively slow rates (Figs. 2B and 3B). Heart block in myocardial infarction almost certainly reflects an interplay of both functional and structural abnormalities. Zipes reviewed a
Figure 1. Isolated left posterior hemiblock complicating nontransmural acute myocardial infarction. On January 9 normal axis is present. On January 11 the axis has shifted somewhat rightward. On January 12 the typical electrocardiographic findings of left posterior hemiblock (LPH) are seen. Note right axis deviation with an rS in I and a qR in Ill. On January 13 the axis has normalized, with reversion of the conduction defect.
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number of reflexes that could be evoked in acute infarction, producing sinus slowing and/or atrioventricular block. 4 ! These reflexes are protective in that they slow heart rates, minimizing oxygen needs of the ischemic myocardium. However, profound bradycardia can induce catastrophic decreases in coronary and/or systemic blood flow. Ischemia of the conduction system itself, can also impair conduction. The atrioventricular node is more sensitive than the His Purkinje system to ischemia.! A knowledge of the blood supply of the conduction system is useful in understanding the conduction defects seen with acute myocardial infarctionP' !8 The artery to the sinoatrial node arises from the proximal right coronary artery in about 55 per cent of patients, and from the left
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circumflex artery in 45 peI\'Cent of patients. The artery to the atrioventricular node arises from the right coronary in about 90 per cent of patients, and from the left circumflex in only about 10 per cent. The atrioventricular nodal artery also supplies the His bundle and the very proximal bundle branches. Most of the bundle branch systems are supplied by the blood supply of the ventricular septum. The right bundle branch and the anterior fasicles of the left bundle branch are supplied by perforating branches of the left anterior descending coronary artery. The posterior fasicles of the left bundle branch possess a dual blood supply, receiving branches from both the anterior and posterior descending coronary arteries. One would predict from these anatomic considerations, that atrioventricular block complicating right coronary disease (DMI) would be atrioventricular nodal, and that block complicating disease of the anterior descending coronary artery (AMI) would involve the bundle branch system. Pathologic examinations in patients dying with acute myocardial infarction and heart block support these contentions. Sutton and Davies reported results of serial section of the conduction system in 29 patients dying with heart block and myocardial infarction.39 Twenty-four of their patients had DMI. In these, pathological examination revealed proximal occlusion of the coronary artery giving origin to the atrioventricular nodal artery. Major structural damage to the conduction system was absent in most, suggesting that ischemia was responsible for atrioventricular block. In contrast, 5 of their cases had extensive anteroseptal infarction. In these cases, the blood supply to the atrioventricular node was not compromised, but there was extensive destruction of the ventricular septum and bundle branches. Similar results were reported by Blondeau and their co-workers.3
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Figure 4. Complete heart block proximal to the bundle of His in acute diaphragmatic infarction. Shown are the simultaneous electrocardiogram and bundle of His electrogram. P waves and atrial electrograms are labeled P and QRS, and ventricular electrograms are labeled R. The continuous strips show complete atrioventricular dissociation with an atrial rate of 100 per min. and a ventricular rate of 48 per min. Note that block is above the bundle of His, since none of the P waves are followed by H potentials. Each QRS is preceded by an H potential, reflecting a junctional escape rhythm. Paper speed is 100 mm. per sec. (From Rosen, K. M., et al.: Circulation, 42:925, 1970, by permission of the American Heart Association.)
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Electrophysiologic studies also support the relationship of site of block and site of infarction. Electrograms can be recorded from the His bundle using an electrode catheter recording technique. 3 ! Our laboratory reported results of His bundle recording in eight patients with acute infarction and heart block. 33 Three patients with DMI and one patient with subendocardial infarction had block proximal to the bundle of His, suggesting an atrioventricular nodal site of block (Figs. 4 and 5). Intraventricular conduction was normal in these three patients. One patient with DMI had block in the His bundle. Three patients with AMI infarction had block distal to the His bundle, suggestive of trifasicular block (Fig. 6). Atrioventricular conduction in these latter 3 patients was normal.
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INCIDENCE Resnekov and Lipp reviewed the incidence of atrioventricular block in acute myocardial infarction, analyzing the incidence in 5160 patients reported from 17 medical centers. 30. The overall incidence of first degree block was 13 per cent, that of second degree block 5 per cent, and that of third degree block, 3 per cent. Approximately one third of patients with first degree block progress to more advanced forms of block, and approximately a third of the patients with second degree block progressed to more advanced block. DMI is a much more common cause of atrioventricular block than AMI.5, 7, 9, 23, 26 However, the mortality with DMI and heart block is much less than the mortality with AMI and heart block.5, 7, 20, 23, 26
DIAPHRAGMATIC INFARCTION In the typical case of DMI with conduction defect, the patient may have first, second, or third degree block at the time of admission. Approximately a third of the patients with first degree block progress to a more advanced form of block over the next 24 to 48 hours. In almost all patients with DMI and heart block, complete reversal of the conduction defect occurs generally within a week of admission, if the patient survives the infarction (Fig. 7).7,12,16,26 In rare cases, atrioventricular block secondary to DMI may be permanentY Progression and reversal of conduction disease in DMI is generally a gradual process, occurring over hours or days. Precipitous changes in heart rate are unusual. Most patients manifest Wenckebach periods (Mobitz type I block) at some point during the evolution of atrioventricular block (Fig. 7A).21 This reflects the atrioventricular nodal site of block, since Wenckebach periods are a typical manifestation of the depressed atrioventricular node. There are several features of DMI with atrioventricular block that appear directly related to the site of block. 7 , 9,12, 20-23,26,32,37 These are as follows: (1) QRS duration is narrow, this finding relating to the absence of intraventricular conduction disease and the presence of escape rhythms originating above the bifurcation of the His bundle. (2) Ventricular rates during complete block are usually relatively rapid (40 to 60 beats per min), also reflecting the proximal site of block and the relatively high origin of the escape rhythms. In addition, atrioventricular automaticity may be increased with resultant nonparoxysmal atrioventricular junctional tachycardia superimposed upon atrioven-
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tricular block (ventricular rates of 60 to 100).29 (3) Stokes-Adams attacks are unusual in DMI, reflecting the relatively rapid ventricular rates and the reliability of the atrioventricular junctional escape pacemakers.
ANTERIOR MYOCARDIAL INFARCTION AMI is associated with a much higher incidence of intraventricular conduction defects than is DMI, presumably reflecting involvement of the ventricular septum.8. 13.23.33.38 The intraventricular conduction defects seen range from the relatively minor fascicular blocks to complete heart block secondary to necrosis of the trifascicular conduction septum. Fasicular Blocks and Bundle Branch Block The most common conduction defect complicating acute myocardial infarction is LAH.8. 24 Mariott reported a series of 250 patients with acute infarction, with an incidence of LAH of 15.2 per cent. 24 In most cases, the site of infarction was anterior. Isolated LPH is a much rarer defect. Several features of LAH complicating acute infarction are worth noting. These are as follows: (1) LAH does not generally progress to complete atrioventricular block, but remains as an isolated finding which mayor may not regress. 24 (2) Mortality in patients with infarction and LAH appears to be somewhat higher than patients with uncomplicated infarction (25 per cent).8 (3) LAH may mask diaphragmatic infarction because the rS pattern in lead III due to LAH may mask the presence of pathologic Q waves. 34 The incidence of bundle branch block in acute infarction varies from approximately 7 to 13 per cent of cases. 16 . 27 The mortality in these cases, is much higher than in the uncomplicated infarction, approximating 50 per cent. This mortality reflects the extent of the infarction necessary to compromise conduction in the bundle branches. Bifascicular Block and Complete Heart Block Characteristically, when heart block complicates AMI, electrocardiograms taken prior to the onset of atrioventricular block reveal evidence of involvement of two of the three fascicles of the conduction system (bifascicular block),13· 38 The specific conduction defects associated with high risk of heart block in AMI include right bundle branch block with left axis deviation (RBBB with LAH) (Fig. 2A), right bundle branch block with right axis deviation (RBBB with LP H) (Fig. 3A), alternating bundle branch block, and first degree atrioventricular block with bundle branch block. Godman and co-workers reported 100 patients with myocardial infarction and one of the above patterns (out of a total series of 1,809 patients),13 The most common abnormality in the 100 patients was RBBB with LAH, seen in 51 of the patients. The incidence of heart block in the 100 patients was 47 per cent. The overall mortality was very high, being 85 per cent in the patients developing heart block. Scanlon et al. reported a similar series of 28 patients with myocardial infarction. 36
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The incidence of heart block in their series was somewhat less, being only 21 per cent. The clinical features of heart block complicating AMI relate to both the site of block (distal to H) and the extensive myocardial infarction necessary to compromise conduction in both bundle branch systems. 12 . 13. 21. 23. 26. 38 Characteristic features of heart block and AMI include the following: (1) The paroxysmal onset of atrioventricular block. 38 These patients usually manifest intact conduction with bifasicular block prior to development of complete and sudden atrioventricular block (Figs. 2A, 2B, 3A, and 3B). Paroxysmal atrioventricular block appears to reflect sudden failure of the remaining functioning fasicle. The paroxysmal nature of block reflects the tendency of conduction to be all or none in the His-Purkinje system. Also typical of AMI with bifascicular block is the development of Mobitz type 11 atrioventricular block (second degree block without progressive prolongation of PR intervals prior to the dropped beat).21 Type 11 block in AMI often heralds the development of more advanced conduction disturbance. (2) Idioventricular escape rhythms characterized by wide QRS complexes and very slow rates. Stokes-Adams attacks are frequent in AMI with heart block because of the unreliability and slow rates of the idioventricular rhythms. (3) Very high mortality from heart failure and cardiogenic shock, reflecting the extensive infarction necessary to impair conduction in both bundle branch systemsP SUBENDOCARDIAL INFARCTION, PRINZMET AL'S ANGINA, ATYPICAL CASES Atrioventricular block complicating coronary disease may also occur both with subendocardial infarction and with Prinzmetal's angina (atypical angina with ST elevations).4.12 We have recorded His bundle electrograms in one case of each (Fig. 5). The site of block was proximal to the His bundle in both, suggesting atrioventricular nodal ischemia as the mechanism of block. 33 Therefore, these cases appear to resemble DMI with heart block. We would like to inject a note of caution into the discussion at this point, and that is that exceptions to the dictum that block in DMI is always atrioventricular nodal, and that block in AMI is always in the bundle branch system, probably occur. The reasons for this are as follows: (1) In 10 per cent of patients, the atrioventricular node is supplied by a branch of the left coronaryP' 18 In these cases, occlusion of the left coronary proximal to the atrioventricular nodal artery could produce block at the atrioventricular node. (2) The atrioventricular nodal artery supplies the His bundle and the proximal bundle branchesP' 18 We have reported one case of DMI with block in the His bundle. Since both right and left bundle branch block can occur with DMI, there is no reason why bilateral bundle branch block could not also occur. (3) In chronic coronary disease, development of collateral circulation is frequent. In such cases, one coronary could supply both the atrioventricular node and the
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bundle branches. Occlusion of that coronary could produce block at one or more sites. Although recording of His bundle electrograms is the most accurate guide to site of bloek, in these atypical cases QRS duration may be used as a guide to the site ofblock.31- 33 Narrow QRS complexes suggest a proximal site ofblbckandwide QRS complexes suggest a distal site of block.
THERAPY OF MYOCARDIAL INFARCTION WITH CONDUCTION DISTURBANCE Pharmacologic Therapy Atropine has- been used suocessfully in patients with acute myocardial infarction and bradyarrhythmia. 40 One to 2 mg. of atropine intravenous produces a vagolytic action, improving atrioventricular nodal conduction and increasing sinus rate. Heart block in DMI may be reversed with atropine, In addition, atropine may increase the rate of atrioventricular junctional escape rhythms. Atropine is ineffective in complete bilateral bundle branch block since the site of blook as well as the escape pacemakers are not under significant parasympathetic control. Atropine can also paradoxically worsen atrioventricular block in both DMI and AMI by increasing atrial rates and thus the number of impulses bombarding the site of block. IO With repetitive concealed conduction, this could produce more advanced degrees.ofblock, and.slower ventricular rates. Isoproterenol, apotent beta stimulator, may facilitate conduction in both the atrioventricular node and the His-Purkinje system. In addition, isoproterenol may increase the rates of both atrioventricular junctional and idioventricular escape rhythms. Unfortunately, isoproterenol, by increasing both con tractility and ventricular rate, may increase the oxygen demands of ischemic myocardium, increasing infarct size. Isoproterenol also increases ventricular irritability with risk of ventricular premature beating and ventricular fibrillation. We would recommend that isoproterenol be used only. as emergency therapy in symptomatic bradyarrhythmia, until less hazardous therapy can be initiated. Other agents used in treatment of myocardial infarction with heart block include steroids and the use of polarizing solutions (glucose, insulin, and potassium).25 The slow action of these together with the spontaneous reversibility of conduction disturbance in myocardial infarction, make evaluation of their effectiveness very difficult. It is our opinion, that the value of either steroids or polarizing solution in myocardial infarction with heart block is unproven, and we would not recommend their use. Pacing In experienced hands, transvenous pacing can be accomplished in patients with myocardial infarction with low morbidity.2 Lassers and co-workers demonstrated that ventricular pacing in patients with heart block and myocardial infarction increased cardiac
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output. 22 However, they also noted that tension time index, a measure of myocardial oxygen needs, was also correspondingly increased. It was implied, that pacing increased myocardial oxygen needs. This could be hazardous in patients with acute myocardial infarction, since it could increase infarct size. Thus, pacing may produce both beneficial and possibly hazardous effects. It is impossible to measure the effectiveness of ventricular pacing in improving the mortality of myocardial infarction and heart block, with the data presently available. Mortality with and without pacing varies tremendously from series to series.O;-7. 9. 12. 14. 19.20.26.28.37 In general, mortality is lower in DMI with and without pacing, and higher in AMI, with and without pacing. We prefer therapeutic recommendations based on the site of infarction and the hemodynamic status of the patient.
Inferior Infarction In DMI with first degree atrioventricular block, no specific therapy is necessary. Most of these patients do not develop progression of their conduction disease. Those that do progress, do so in stages, allowing ample time for specific therapy. In DMI with second or third degree block, therapy should be dependent upon both the ventricular rate and the hemodynamic status of the patient. If ventricular rates are less than 50 per min, or if there is evidence of either heart failure or cardiogenic shock, then increase of heart rate with specific therapy is indicated. Atropine can be tried first. If both ventricular rate and hemodynamic status do not improve, transvenous pacing is indicated. It should be remembered that heart block in DMI is generally reversible, so that pacing should be avoided in the stable patient with heart rates of 50 or above. Anterior Infarction Current literature suggests that either first degree block or LAH complicating AMI do not imply a risk of progression of conduction disease. No specific therapy is indicated in these patients. In AMI with intact conduction and bifasicular block, we would recommend prophylactic pacing if this can be accomplished by a physician skilled in pacemaker implantation, and if this can be done in or close to the coronary care unit. Prophylactic pacing of these patients is controversial, and if pacing cannot readily be accomplished, it is also reasonable to just carefully monitor this group of patientsP In AMI with either second or third degree block, we would recommend ventricular pacing. Mortality will be extremely high in this group, with or without pacing. However, an occasional patient is salvageable, so that active therapy is indicated. In the future, this group of patients may become candidates for saphenous bypass and infarctectomy in addition to pacing. Atypical Cases The occasional patient with AMI, heart block, and narrow QRS, presumably has atrioventricular nodal block, and should be managed as
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recommended for DMI. The occasional patient with DMI, heart block, and a wide QRS, should be managed as a patient with AMI and heart block. In these cases, His bundle recording, if available, can provide accurate delineation of the site of block. 31-33
REFERENCES 1. Bagdonas, A. A., Stuckey, J. H., Piera, J., etal.: Effects of ischemia and hypoxia on the specialized conducting system of the canine heart. Amer. Heart J., 61 :206, 1961. 2. Beregovich, J., Fenig, S., Lasser, J., and Alien, D.: Management of acute myocardial infarction complicated by advanced atrioventricular block. Amer. J. CardioL 23:54, 1969. 3. Blondeau, M., Rizzon, M., and Lenegre, J.: Les troubles de la conduction auriculo-ventriculaire dans l'infarctus myocardique recent. 11. Etude anatomique. Arch. Mal Coeur, 54: 1104, 1961. 4. Botti, R. E.: A variant form of angina pectoris with recurrent transient complete heart block. Amer. J. CardioL, 17:443, 1966. 5. Brown, R. W., Hunt, D., and Sloman, J. G.: The natural history of atrioventricular conduction defects in acute myocardial infarction. Amer. Heart J., 78:460, 1969. 6. Bruce, R. A., Blackmon, J. R., Cobb, L. A., and Dodge, H. T.: Treatment of asystole or heart block during acute myocardial infarction with electrode catheter pacing. Amer. Heart J., 69:460, 1965. 7. Cohen, D. B., Doctor, L., and Pick, A.: The significance of atrioventricular block complicating acute myocardial infarction. Amer. Heart J., 55:215,1958. 8. Col, J. J., and Weinberg, S. L.: The incidence and mortality of intraventricular conduction defects in acute myocardial infarction. Amer. J. CardioL, 29:344, 1972. 9. Courter, S. R., Moffat, J., and Fowler, N. 0.: Advanced atrioventricular block in acute myocardial infarction. Circulation, 27:1034, 1963. 10. Danzig, R., Alpern, H., and Swan, H. J. C.: The significance of atrial rate in patient with atrioventricular conduction abnormalities complicating acute myocardial infarction. Amer. J. CardioL, 24:707, 1969. 11. Davies, M. J.: Pathology of conducting tissue of the heart. New York, Appleton-CenturyCrofts, 1971. 12. Friedberg, C. K., Cohen, H., and Donoso, E.: Advanced heart block as a complication of acute myocardial infarction. Role of pacemaker therapy. Prog. Cardiovasc. Dis., 10:466, 1968. 13. Godman, M. J., Alpert, B. A., and Juliab., D. G.: Bilateral bundle-branch block complicating acute myocardial infarction. Lancet, 2:345, 1971. 14. Hatie, L., and Rokseth, R.: Conservative treatment of AV block in acute myocardial infarction. Results in 105 consecutive patients. Brit. Heart J., 33:595,1971. 15. Hoffman, B. F., and Cranefield, P. F.: Electrophysiology of the Heart. New York, McGrawHill, 1960. 16. Hunt, D., and Sloman, G.: Bundle-branch block in acute myocardial infarction. Brit. Med. J., 1 :85, 1969. 17. James, T. N., and Burch, G. E.: Blood supply of the human intraventricular septum. Circulation, 1 7: 391, 1958. 18. James, T. N.: Anatomy of the coronary arteries in health and disease. Circulation, 32: 1 020, 1965. 19. Julian, D. G., Lassers, B. W., and Godman, J. J.: Ann N. Y. Acad. ScL, 167:911, 1969. 20. Kostuk, W. J., and Beanlands, D. S.: Complete heart block associated with acute myocardial infarction. Amer. J. Cardiol., 26:380, 1970. 21. Langendorf, R., and Pick, A.: Atrioventricular block, type 11 (Mobitz). Its nature and clinical Significance. Circulation, 38:819, 1968. 22. Lassers, B. W., Anderton, J. L., George M., et aL: Hemodynamic effects of artifical pacing in complete heart block complicating acute myocardial infarction. Circulation, 38:308, 1968. 23. Lim, C. H., Toh, C. C. S., and Low, L. P.: Atrioventricular and associated intraventricular conduction disturbances in acute myocardial infarction. Brit. Heart J., 33:947, 1971. 24. Marriott, H. J. L., and Hogan, P.: Hemiblock in acute myocardial infarction. Chest, 58: 342, 1970. 25. Mittra, B.: Potassium, glucose, and insulin in treatment of heart block after myocardial infarction. Lancet, 2:1438, 1966. 26. Norris, R. M.: Heart block in posterior and anterior myocardial infarction. Brit. Heart J., 31 :352, 1969.
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