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Heart Block Complicating Acute Inferior Wall Myocardial Infarction* Prem K. Gupta, M.D.;"" Edgar Lichstein, M.D.;t and Kul D. Chuddu, M.D.S Heart block was noted in 60 (35 complete and 25 seconddegree) of 410 patients with acute inferior wall myocardial infarction. This group with heart Mock was compared to a control grow of 30 patients with acute inferior wall infarction without heart Mock. The incidences of prior myocardial infarction and hypertendon, in addition to the highest level of serum creatine phospholdnase and a maximum degree of !ST-segment elevation in the inferior leads, were all greater in patients with heart Mock, as compared to the controls. The incidences of various complications, including dizziness and syncope, transient hypotension, cardiogenic shock, and congestive heart failure, were also higher in the group with heart Mock, while sinus nodal disturbances and atrial arrhythmias occurred with equal frequency. The mortality in those with heart Mock was 28 percent compared to 13 percent for the control. It is concluded that patients with heart Mock complicating acute inferior myocardial infarction have a greater amount of myocardial necrosis, a higher incidence of complications, and a higher mortality. Insertion of a temporary pacemaker shoold be considered when spedllc indications are present and not rootineb. concerning heart block complicating acute Studies myocardial infarcti~n~-~O have emphasized the period of 1970 to 1974. Most patients were monitored in the coronary care unit for four to six days, except those who required longer periods because of various complications. Daily 12-lead electrocardiograms and determinations of serum creatine phosphokinase levels were performed during this period. In addition to constant electrocardiographicmonitoring and hourly rhythm strips, repeat ECGs were obtained whenever changes in atrioventricular conduction were noted. Patients in whom heart block appeared as a terminal event or transiently during cardiac resuscitation were not included in this study. A history of hypertension was recorded if the patient had previously had more than one blood-pressure determination greater than 160/90 mm Hg or if the patient was receiving antihypertensive medication. Diabetes mellitus was considered to be present if a fasting blood glucose level greater than 120 mg/100 ml had been recorded prior to hospitalization or if the patient was receiving antidiabetic medication. Previous myocardial infarction was diagnosed by the history of typical precordial pain and the presence of significant Q waves on the ECG. Serial 12-lead ECGs were reviewed for the maximum degree of ST-segment elevation in the inferior leads. In addition, rhythm strips were reviewed to determine the time of onset and the disappearance of heart block and to determine the presence of sinus nodal abnormalities and atrial arrhythmias. Maximum serum creatine phosphokinase values were recorded as multiples of the upper limit of normal for our laboratory. The presence of cardiogenic shock was recorded if the systolic blood pressure was persistently lower than 80 mm Hg and was accompanied by the clinical features of cool moist skin, mental confusion, and a fall in urinary output. A transient fall in blood pressure not accompanied by these clinical features and usually associated with bradyarrhythmias was classified as transient hypotension. Congestive heart failure was considered to be present if bilateral basal rales were heard which were not related to a history of chronic pulmonary disease and were accompanied by radiographic appearance of bundle-branch block and the higher mortality associated with anterior wall infarction, and the more benign prognosis of atrioventricular block associated with inferior wall myocardial infarction. The indications for insertion of a temporary pacemaker in patients with heart block complicating acute inferior wall myocardial infarction remain unsettled.7,8.12.1421.2e This study reports our experience with 60 patients with heart block complicating acute inferior wall myocardial infarction. Significant clinical features, serum creatine phosphokinase levels, ST-segment elevations, and various complications are compared to a group of control patients with inferior myocardial infarction without heart block. An attempt is made to clarify the indications and value of temporary-pacemaker insertion. Heart block was noted in 60 (35complete and 25 seconddegree) of the 410 patients with acute inferior-wall myocardial infarction seen in our coronary care unit during the "From the Department of Medicine, Division of Cardiology, Mount Sinai Ho ital Senices, City Hospital Center at E I m h m NY, an3 Mount Sinai School of Medicine, City University of New York, New York. ""Assistant Professor of Clinical Medicine. tAssociate Professor of Medicine. $Assistant Professor of Medicine. Manuscript received September 9; revision accepted December 1. Reprint requests: Dr. Cupta, Mt. Sinai Hospital S e d e s , 7901 Broadway, Elmhurst, New York 11373 CHEST, 69: 5, MAY, 1976 HEART BLOCK COMPLICATING ACUTE lWMl 589 Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/20980/ on 05/02/2017 of the upper limit of normal are shown in Figure 2. Time of Onset and Duration of Heart B b c k DIABETES HYPERENSION OLD M I FIGURE 1. Diabetes, hypertension, and old myocardial infaro tion ( MI) in patients with heart block ( HB ) and controls, Numbers in bars are numbers of patients. evidence of increasing pulmonary vascular congestion. Similar historic and clinical data were obtained on a control group of 30 patients with acute inferior wall my-dial infarction who did not show evidence of heart block. The incidence of heart block (second-degree and third-degree) in patients with acute inferior wall myocardial infarction was 15 percent. The average age of the patients with heart block (61 years) was similar to that of the control group (62 years), as was the malelfemale ratio ( 2 : l ) . The incidences of previous myocardial infarction, hypertension, and diabetes mellitus in the patients with heart block and the control group are shown in Figure 1. The maximum ST-segment elevation measured in millimeters in the inferior leads and the maximum serum creatine phosphokinase level expressed in multiples Heart block was present on admission or developed within 24 hours in 35 patients (early heart block) and appeared late (two to seven days after admission) in 25 patients (late heart block). Of the group with early heart block, the block was noted at the time of admission in 26 patients and appeared within 24 hours in nine patients. There were no deaths in ten of the patients with early heart block in whom the defect was transient ( a few minutes to one hour), while there were ten deaths in the remaining 25 patients with early heart block patients in whom the block lasted from two hours to 14 days. In the 25 patients with late block, the block lasted from two hours to 16 days, and seven deaths occurred in this group. The duration of block varied and was noted to be intermittent and unstable in 11 patients and present for more than six days in nine others. In four patients in whom the block was present transiently on admission, it reappeared on the third and fourth days of hospitalization. The incidences of various complications for those with heart block and the controls are shown in Figure 3. The greater incidences of transient hypotension and cardiogenic shock in the group with heart block were statistically significant ( P < 0.05). The mortality of 28 percent (17160) in the patients with heart block was higher than the 13 percent (4130) noted in the controls and was not affected by the degree of heart block. The 56-percent incidence (34160) atrial arrhythmias and sinus nodal abnormalities was similar to the 53-percent incidence ( 16/30) noted in the control group. Rate and Morphologic Appearance of Escape Rhythm ST SEGMENT SERUM CPK RGURE2. Maximum height of ST-segment elevation measured in millimeters and highest level of serum creatine phosphokinase ( CPK) measured in multiples of upper limit of normal. HB, heart block. The average rate of the escape rhythm in those patients with complete heart block was 45 beats per minute, with a range of 24 to 70 beats per minute. There was no relationship between the rate of this escape pacemaker and the morphologic appearance of the escape beats, the time of occurrence of heart block, the associated complications, or the mortality. The escape beats were wide in seven patients (Table 1). In three of these patients, bundle-branch block was not present in the conducted beats, and the morphologic appearance of the escape beats was consistent with right bundle-branch block and left anterior hemiblock, suggesting an escape focus in the posterior division of the left bundle branch (Fig 4). A His-bundle electrogram recorded in one of these patients showed a markedly prolonged atrioHis (A-H) interval, in addition to block distal to the 600 GUPTA, UCHSTEIN, CHADDA Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/20980/ on 05/02/2017 CHEST, 69: 5, MAY, 1976 CHF MORTALITY HYFOTENSION FIGURE 3. Incidences of various complications in patients with heart block (HB)and controla. Numbers in bars are numbers of patients. CHF, congestive heart failure. a SmCQeL His-bundle potential (Fig 5). One of these patients died, and two survived. The four remaining patients with wide escape beats all had evidence of bundlebranch block during periods of normal conduction. In one patient, who ultimately survived, a pattern of right bundle-branch block was present during normal conduction and in the escape beats. In the remaining three patients, the morphologic appearance of the escape complex was different from that of the normally conducted beats, and all three died, despite pacemaker insertion. An additional patient developed trifascicular block manifested by periods of right bundle-branch block and left posterior hemiblock and of left bundle-branch block. Ventricular asystole occurred, requiring insertion of a temporary pacemaker. A permanent pacemaker was inserted at four weeks after hospitalization, but the patient died suddenly of a possible arrhythmia at seven weeks. Mode of Death Seventeen patients in the group with heart block died. The cause of death was cardiogenic shock in 11 patients; death occurred within the &st 24 hours in seven of these and occurred between the third and Table 14Irmocteri.tia of Patient. Showiw wile Ewope Beds* Patient 1 SinukConducted QRS Normal Escape &RS Outcome RBBB and LAH Survived (shock) RBBB and LAH Died (shock) 3 Normal RBBB and LAH Survived 4 RBBB RBBB survived 5 RBBB LBBB Died (CHF) 6 RBBB and LAEI RBBB and LPH; RBBB and LAB; Died (shock) LBBB 7 RBBB and LAH; Wide LPH Died (shock) *RBBB, Right bundle-branch block; LAH, left anterior hemiblock; LBBB, left bundle-branch block; LPH, left posterior hemiblock; and CHF, congestive heart failure. CHEST, 69: 5, MAY, 1976 Frcm 4. Selected leads from ECGs (case 1, Table 1). A. At time of admission. Note sinus rhythm with changes of acute inferior-wall myocardial infarction B. Recorded soon after admission. Note complete heart block with QRS morphologic appearance suggestive of right bundle-branch block and left anterior hemiblock. HEART BLOCK COMPUCATIWG ACUTE lWMl 601 Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/20980/ on 05/02/2017 I f A-H = 190-220 Msec 1 I I FIGURE5. His-bundle electrograrns (HBE) (case 1, Table 1 ) . Complete heart block is present, and block occurs distal to His-bundle potential. Atrio-His interval (A-H) is prolonged and ranges from 190 to 220 msec. the seventh days of hospitalization in the remaining four. All of these 11 patients had heart block, and six had temporary pacemakers at the time of their death. In the remaining five, there was not adequate time for pacemaker insertion. Cardiac rupture was the cause of death in one additional patient, who died on the eighth day of hospitalization. In the remaining five patients, death occurred from other causes between the fifth and 35th days of hospitalization. In four of these patients, heart block was not present when the patients were discharged from the coronary care unit, but in the three instances in which death was sudden, it is not known whether the mechanism was recurrent block or ventricular fibrillation. Indications for Pacemaker Insertion Temporary transvenous pacemakers were inserted in 31 patients (eight with second-degree and 23 with comple'te heart block). The various indications for pacemaker insertion were as follows: atropine-resistant symptomatic bradyarrhythmia, 19 patients; shock, 11 patients; hypotension, eight patients; congestive heart failure, 17 patients; prolonged asystole, two patients; control of atrial and ventricular arrhythmia, five patients; and wide escape beats, seven patients. In many patients, two or more of these indications existed simultaneously. Ventricular fibrillation occurred in three patients during pacemaker insertion, and in each case, successful defibrillation was achieved. The reported incidence of heart block complicating acute myocardial infarction ranges from 1.5 per~ l ~ variation is due in cent to 18 p e r ~ e n t . ~ * " ' *This part to inclusion of both anterior and inferior wall infarctions in some of the reports and the lack of constant monitoring in earlier series. The incidence of 15 percent in our series is less than the incidences of 26 percent and 27 percent reported by ~thers.~,ll Our finding of a higher incidence of prior myocardial infarction in the group with heart block, as compared to the controls, suggests more extensive coronary arterial disease and is similar to other reported r e ~ u l t s . ~ . ~ , ~ The magnitude of ST-segment elevation and the levels of serum creatine phospholdnase have been correlated with the extent of myocardial n e ~ r o s i s . ~The ~ 3 ~elevation of both of these parameters in our group of patients with heart block is in agreement with the concept that patients with heart block complicating acute inferior-wall myocardial infarction have a greater amount of myocardial damage. This may also explain the higher incidences of congestive heart failure and shock and the higher mortality in patients with heart block. Onset and Duration of Heart Block The time of onset and the duration of block in acute inferior wall myocardial infarction have no uniform pattern.5*9.11.12.20 We observed block within the &st 24 hours following admission in 58 percent (35160) of our cases, which is similar to the experience of The duration of heart block varied markedly in our series and lasted from a few minutes to 16 days. Persistence of heart block to this degree was noted by Norrisl' and by Kostuk and Beanlands,12 but not by Simon et a1.20 It appears that different mechanisms may be in operation, producing heart block with different times of onset and different periods of duration. Heart block occumng early and transiently during periods of chest pain might be related to inappropriate vagal tone; or transient ischemia of the atrioventricular node might occur, as is seen in patients 602 GUPTA, LICHSTEIN, CHADDA Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/20980/ on 05/02/2017 CHEST, 69: 5, MAY, 1976 with Prinzmetal's angina and heart b l o ~ k . In ~~,~~ ples of this discrepancy are the exceptionally low those patients with heart block appearing later and mortality of 20 percent without pacing described by Jackson and Bashour," while Rotman et all3 relasting for longer periods of time, edema and inflammation of the atrioventricular node is likely. ported a 30 percent mortality despite pacing. In the Massive necrosis of the atrioventricular node has series of Friedberg et al,9 three deaths were related been demonstrated in patients with block who died to Stokes-Adams attacks, and it was thought that pacemaker therapy might have been useful. Other of cardiogenic shock.' This concept of different investigatorssg.%have reported beneficial effects of mechanisms may explain the reappearance of block pacing in patients who had experienced syncope. on the third and fourth days of hospitalization in It is our policy to insert a temporary pacemaker in four of our patients who showed transient block at a patient with heart block only if symptoms are the time of admission. Kostuk and bean land^'^ present. These symptoms include dizziness or synfound, as we did, that patients with early and trancope, hypotension, cardiogenic shock, and congessient block had a more benign prognosis. tive heart failure. In addition, we insert a pacemaker Significance of Wide Escape Beats if sigdicant ventricular arrhythmias requiring overdrive are present, or if the patient is completely The site of block in acute inferior wall myocardial asymptomatic and there is complete heart block infarction has been localized to the region of the with a wide QRS escape complex. atrioventricular node or within the His bundle.2728 Although the majority of these patients show narrow ACKNOWLEDGMENT: We are grateful to Mr. Manuel escape beats, a small percentage does show an esBeckeman for the art work and to Mrs. Frances Schlesinger a p e rhythm with a wide QRS c ~ m p l e x . In ~ ~the ~ ~ ' ~ for secretarial assistance. study by Lie et a1,28 12 out of 35 patients admitted REFERENCES with heart block complicating acute inferior-wall infarction showed a wide QRS esdape complex. 1 Kerr JDO: Heart block in coronary thrombosis. Lancet 2: 19681969, 1937 Kostuk and Beanlands12 noted four patients with a 2 Master AM, Dack S, JafFe HL: Bundle branch and wide QRS escape rhythm and observed that their intraventricular blodc in acute coronary artery occlusion. mortality was similar to those with narrow escape Am Heart J 16:283-308, 1939 beats. Earlier studies by Lassers and Julian8 and by 3 Penton GB, Miller H, Levine SA: Some clinical features Friedberg et ale found a higher mortality in those of complete heart b l d . Circulation 13:801-824, 1956 4 Cohen DB, Doctor L, Pick A: The significance of ahiopatients with wide escape beats. We believe that the ventricular block complicating acute myocardial infarcmechanisms producing a wide QRS complex relate tion. Am Heart J 55:215-219, 1958 to mortality rather than the QRS width alone. Prog5 Courter SR, Moffat J, Fowler NO: Advanced atriovennosis in patients with prior bundle-branch block tricular block in acute myocardial infarction. Circulation who develop block at the atrioventricular node is 27:1034-1042, 1963 6 Julian DG, Valentine PA, Miller GG: Disturbance of rate similar to those with narrow escape beats; however, rhythm and conduction in acute myocardial infarction. if the escape beats are wide as a result of acute Am J Med 37:915-927, 1964 trifascicular block, the mortality increases sign$7 Paulk EA Jr, Hurst JW: Complete heart block in acute cantly and resembles those with anterior myocardial myocardial infarction: A clinical evaluation of the intrainfarction and trifascicular block.519 Those patients cardiac bipolar catheter pacemaker. Am J Cardiol 17:695706, 1966 who do not have bundle-branch block in sinus beats 8 Lassers BW, Julian DG: Artificial pacing in management but show wide escape beats during heart block are of complete heart block complicating acute myocardial most likely to have block in the area of the His infarction. Br Med J 2: 142-148, 1968 bundle and show a variable p r o g n o s i ~ . ~ ~ ~ ~ ~ 9 Friedberg CK, Cohen H, Donoso E: Advanced heart The benefit of routine pacemaker therapy for pablock as complication of acute myocardial infarction: Role of pacemaker therapy. Prog Cardiovasc Dis 10:466-481, tients with heart block complicating inferior wall 1968 infarction has not been established.§ There does not 10 Brown RW, Hunt D, Sloman JG: The natural history of appear to be a direct relationship between a policy atrioventricular conduction defect in myocardial infarcof pacemaker insertion and mortality. The death tion. Am Heart J 78:460-466, 1969 rates of 40 percent7 and 45 percent12were noted by 11 Nonis RM: Heart block in posterior and anterior infarction. Br Heart J 31352-356,1969 groups who implanted pacemakers in all patients 12 Kostuk WJ, Beanlands DS: Complete heart block assowith block, while mortalities of 37 percent,' 39 perciated with .acute myocardial infarction. Am J Cardiol cent,5 and 44 percent9 were reported by groups who 26:380-384, 1970 did not use prophylactic pacemakers. Further exam13 Rotman M, Wagner GS, Wallace AG: Bradyarrhythmias $References 7,8, 12,14,15,21,22,32,33. CHEST, 69: 5, MAY, 1976 in acute myocardial infarction. Circulation 45:703-722, 1972 HEART BLOCK COMPLICATING ACUTE lWMl 603 Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/20980/ on 05/02/2017 14 Jackson AE, Bashour FA: Cardiac arrhythmias in acute myocardial infarction: 1. Complete heart block and its natural history. Dis Chest 51:31-38, 1967 15 Waugh RA, Wagner GS, Haney TL, et al: Immediate and remote prognostic significance of fascicular block during acute myocardial infarction. Circulation 47:765-775, 1973 16 Godman MJ, Lassers BW, Julian DG: Complete bundlebranch block complicating acute myocardial infarction. N Engl J Med 282237-240, 1970 17 Scheidt S, Killip T: Bundle branch block complicating acute myocardial infarction. JAMA 222:919-924, 1972 18 Atkins JM, Leshin SJ, Blomgvist G, et al: Ventricular conduction blocks and sudden death in acute myocardial infarction and potential indications for pacing. N Engl J Med 288:281-284, 1973 19 Scheinman M, Brenman B: Clinical and anatomic implications of intraventricular conduction blocks in acute myocardial infarction. Circulation 46:753-760, 1972 20 Simon AB, Steinke WE, Curry JJ: Atrioventricular block in acute myocardial infarction. Chest 62: 156-161, 1972 21 Chatteqee K, Harris A, Leatharn A: The risk of pacing after infarction and current recommendations. Lancet 2: 1061-1063, 1969 22 Schluger J, Iraj I, Edson JN: Cardiac pacing in acute myocardial infarction complicated by complete heart block. Am Heart J 80: 116124, 1970 23 Maroko PR, Libby P, Covell JW, et al: Precordial S-T segment elevation mapping: An atraumatic method for assessing alterations in the extent of myocardial ischemic injury. Am J Cardiol29:223-230, 1972 24 Sobel BE, Bresnaman GF, Shell WE, et al: Estimation of infarct size in man and its relation to prognosis. Circulation 46:640-648, 1972 25 Prinzmetal M, Kennamer R, Merliss R, et al: Angina 26 27 28 29 30 31 32 33 34 pectoris: 1. A variant form of angina pectoris. Am J Med 27:375-388, 1959 Botti R: A variant form of angina pectoris with recurrent transient complete heart block. Am J Cardiol 17:443-446, 1966 Rosen KM, Loeb HS, Chuquimia R, et al: Site of heart block in acute myocardial infarction. Circulation 42:925933, 1970 Schuilenburg RM, Durrer D: Conduction disturbances located within the His bundle. Circulation 45:612-628, 1972 Lie KI, Wellens HJ, Schuilenburg RM, et al: Mechanism and significance of widened QRS complexes during complete atrioventricular block in acute inferior myocardial infarction. Am J Cardiol33:833-839, 1974 Schamroth L, Ziady F, deKock J: Acute inferior wall myocardial infarction associated with complete atrioventricular block and left posterior hemiblock. Br Heart J 37:471-474, 1975 Bashour TT,Fahdul H, Cheng TO: Complete heart block with normal QRS duration occurring distal to the His bundle in acute inferior myocardial infarction. J Electrocardiography 8: 185-190, 1975 Sutton R, Chattejee K: Heart block in myocardial infarction. Lancet 1:94, 1968 Beregovich J, Fenig S, Lasser J, et al: Management of acute myocardial infarction complicated by advanced atrioventricular .block: Role of artificial pacing. Am J Cardiol23 :54-65, 1969 Bruce RA, Blackmon JR, Cobb LA, et al: Treatment of asystole or heart block during acute myocardial infarction with electrode catheter pacing. Am Heart J 69:460-469, 1965 Modern Wood Engraving Apart from lithography and etching, the post-war period saw the rebirth of wood engraving, especially in Switzerland. In 1953, an international society of wood engravers was founded in Zurich, under the name of Xylon. This group looks back to fifteenth-century engraving, especially colored wood engraving, for its members d o not want just "grim black and white." In the introduction of the catalogue at the exhibition at Vienna in October 1961, they pointed out that wood engraving should draw its inspiration from the Gargas cave in the Pyrenees, "where you can see imprints of mutilated hands done with a primitive paint made of iron oxide and animal fat." In spite of their manifesto, several artists hesitated between nineteenth-century traditionalism and the influence of Gauguin, but there are among them marked personalities like HR Bosshard (born in 1929 in Zurich), Werner H o h a n n (born in 1935 in Affoltem), and Heinz Keller (born in 1928 in Wintherthur). Nearly all of them are Expressionists, for wood does not lend itself well to Abstract art, and moreover, they say their forebears of the fifteenth century had such power of expression that they were the ancestors of modem Expressionism. AdhBmar, J: Twentieth-Century Graphics, New York, Praeger, 1971 604 GUPTA, LICHSTEIN, CHADDA Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/20980/ on 05/02/2017 CHEST, 69: 5, MAY, 1976