right ventricular infarction with shock but without significant left ventricular infarction: a new...

Right ventricular infarction with shock but without significant left ventricular infarction: A new clinical syndrome

Neal Roberts, M.D.,* David G. Harrison, M.D.,* Keith A. Reimer, M.D., Ph.D.,** Barbara S. Crain, M.D., Ph.D.,** and Galen S. Wagner, M.D.* Durhum, N.C.

Patients with right ventricular infarction in the absence of left ventricular infarction have been reported in a number of autopsy series.le6 However, the clinical entity of combined left and right ventricular infarction characterized by right ventricular dysfunction has been widely recognized only since 1974.7 Cohn et al. performed both animal8 and clinical7 studies indicating a role for right ventricular function in the maintenance of left ventricular output. Subsequently Swan-Ganz catheterization of the right heart, radionuclide techniques, and echo- cardiography have facilitated the diagnosis of right ventricular infarction and have identified its common occurrence accompanying inferior left ventricular infarction?-12 Goldstein et all3 used mercury embolism of the right coronary artery to create a canine model of severe right ventricular infarction without septal or left ventricu1ar13 involvement. They found that cardiac output fell by one third. Prior to these studies, Starr et al.,14 Bakos,15 and others had shown the apparent absence of left ventricular failure after cauterization of the right ventricle in dogs.

In 1979 Coh# reviewed both autopsy17* l8 and clinical studies7* 11, 1g-21 and noted that as many as 8 % of patients with acute myocardial infarcts have a clinical course characterized by the effects of right ventricular involvement. however, he also con- cluded that right ventricular infarction occurs exclu-

From the Departments of Medicine* and Pathology,** Duke University Medical Center.

This work was supported in part by Contract HRA-230-76-0300 from the Health Resources Administration. Dept. of Health, Education, and Wel- fare, Bethesda, Md.; hy Research Grant HL-17670 from the National Heart. Lung, and Blood Institute, Bethesda, Md.; and by Grants from the Prudential Insurance Company of America. Newark. NJ.. and the Kaiser Family Foundation, Menlo Park, Calif.

Received for publication Nov. 30, 1984: revision received May 31, 1985: accepted July 1, 1985.

Reprint requests: Galen S. Wagner. M.D.. P.O. Box 31211, Duke University Medical Center. Durham, NC 27710.

sively in association with left ventricular inferior wall (posterior interventricular septum and adjacent free wall) involvement. Data supporting this conclu- sion came from the National Institutes of Health autopsy study,18 which demonstrated right ventricular infarction with 24 % of patients with left ventricular inferior infarcts. No patients with right ventricular infarcts without left ventricular involvement at postmortem examination were identified. In contrast, the present report documents the occurrence of cardiogenic shock due to right ventricular infarction without QRS change indicative of left ventricular involvement, and identifies by search of a computerized data bank an additional patient who met clinical criteria for this entity.

CLINICAL-PATHOLOGY STUDY

A 69-year-old woman with a history of hypertension and diabetes was admitted to the hospital with right upper abdominal pain of 2 days’ duration. She had no previous history suggesting cardiac, pulmonary, or renal disease. Physical examination revealed a lethargic female with systolic blood pressure of 70 mm Hg and a pulse rate of 40 to 48 bpm. Respirations were 18/min. and there was no dys- pnea. Jugular veins were distended to the mandible but there were neither rales nor a gallop rhythm present. The abdomen was tender in both upper quadrants.

Laboratory studies included a blood urea nitrogen (BUN) of 60. The chest x-ray examination showed clear lung fields and a normal heart size. The ECG (Fig. 1) showed sinus bradycardia with first-degree atrioventricular block. The QRS configuration was normal but there was ST segment elevation in leads II, III, aV,, and V, to Vs. Subsequently, right bundle branch block but no QRS changes suggesting myocardial infarction developed. The initial total creatine kinase was 735 IU/L, with a myocardial band fraction of 58 IU/L. Soon after hospital admission,

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1048 Roberts et al. November, 1985

American Heart Journal

CLINICAL- PATHOLOGY STUDY I CLINICAL STUDY

Fig. 1. The la-lead ECGs from the patient in the clinical-pathology study and those from the patient identified in the retrospective clinical study are shown. The cardiogram shown in the left-hand panel was taken on the autopsied patient’s first day of hospitalization. The right-hand panel shows a cardiogram from the second patient’s fourth day of hospitalization. The seven preceding cardiograms from this surviving patient showed similar QRS complexes with T wave inversions and ST segment elevations, but no distinct P wave. No abnormal QRS changes suggestive of myocardial infarction occurred in either patient during hospitalization following acute myocardial infarction. ST segment elevation appears in leads II, III, aVr, and V, to VB.

the patient’s blood pressure fell to 60 mm Hg systolic. Dopamine was administered without improvement, but volume administration resulted in stabilization of the blood pressure at 130/80. Subsequently, hypotension recurred, the urine output decreased, and she became obtunded. A Swan- Ganz catheter was inserted, demonstrating a pulmonary artery pressure of 30/15 mm Hg with a pulmonary capillary wedge pressure of 15 mm Hg and cardiac output of 2.6 L/min. A right atrial pressure measurement was not obtained. Hypotension, meta- bolic acidosis, and oliguria persisted despite volume, isoproterenol, and dobutamine infusions. Over the next 3 days creatine kinase myocardial band remained present. The serum glutamic oxaloacetic transaminase @GOT) and lactic dehydrogenase (LDH) were elevated to 5,560 and 8,140, respective- ly, with LDHl > LDH2. No improvement in cardiac output could be sustained and the patient died 11 days after admission.

At autopsy, the heart weighed 293 gm. The coronary arterial system was right-dominant, i.e., the posterior descending artery was a branch of the right coronary artery. However, only the medial aspect of the inferior (posterior) wall of the left ventricle and the posterior 25% to 30% of the interventricular septum were supplied by the right coronary artery;

the posterolateral aspect of the left ventricle was supplied by branches of the circumflex artery. A postmortem arteriogram demonstrated a complete occlusion of the proximal right coronary artery. Serial sections through this artery revealed an orga- nized thrombus superimposed on an old 60% ath- erosclerotic occlusion just distal to the origin of the sinus node artery. The left main and circumflex coronary arteries were less than 25% occluded and the left anterior descending artery, its major diago- nal branch, and marginal branches of the left circumflex artery were normal. Secondary to the occlusion of the right coronary artery was extensive infarction of the right ventricle, which histologically was of various ages, from 24 hours to about 2 weeks old. Patchy necrosis was present throughout, involving at least 50% of the right ventricular myocardi- urn. The left ventricular component of the infarct was minimal and appeared to be about 2 weeks old.

The proportion of the left ventricle supplied by the right coronary artery was defined from postmortem angiograms, and the amount of necrosis in the left ventricular component of the infarct was quan- tified by computerized planimetry, with techniques described by Savage et aLz2 Although the right coronary artery supplied approximately 20% of the

Volume 110 Number 5

q Infarct 1 Mural Thrombus

q RC Vascular Bed

Right ventricular infarction 1049

Fig. 2. Diagram of serial cross-sectional slices of the ventricles of the heart from the patient in the clinical-pathology study. The slices were viewed from the base of the heart with the right ventricle to the left and the posterior (inferior) wall toward the top of the diagram. The slices are labeled from base to apex. The dominant right coronary artery supplied much of the right ventricle and the medial half of the posterior wall of the left ventricle. By histologic analysis, there was extensive necrosis throughout most of the right ventricle, but the left ventricular comnonent of the infarct consisted of only small scattered foci of necrosis within the right coronary vascular bed.

myocardium of the left ventricle, the left ventricular component of the infarct consisted of only scattered necrotic foci totalling about 1% of the volume. The right and left ventricular distributions of the infarct are illustrated in Fig. 2. In addition, focal acute and organizing contraction band necrosis was noted in several regions of the left ventricle not correspond- ing to any vascular distribution, suggestive of a catecholamine effect. There also was acute necrosis in the right atrium, involving the sinus node. There was severe right ventricular and right atria1 dilata- tion indicative of severe right-sided cardiac failure. Large mural thrombi were present in the right ventricle and right atrium and a small thrombus was also present in the left atrium. The cardiac valves were normal.

The general autopsy revealed severe passive congestion and central necrosis of the liver, moderate congestion of the lungs with bilateral pleural effu- sions, and acute renal tubular necrosis.

RETROSPECTIVE CLINICAL STUDY

Methods. A retrospective clinical study was subsequently designed to determine if there were other patients with myocardial infarcts with shock, and hemodynamic characteristics suggesting right ven-

tricular infarction in the absence of QRS changes indicating left ventricular infarction. The clinical characteristics of the autopsied patient suggested guidelines for identification of surviving patients with right ventricular infarction alone. These included (1) transiently elevated total creatine kinase and creatine kinase myocardial band; (2) diffuse transient ST elevation without QRS changes indicative of left ventricular infarction on the ECG; (3) normal left ventricular function; (4) hemodynamic evidence of right ventricular dysfunction; and (5) cardiogenic shock.

“Normal left ventricular function” is defined as both a left ventricular ejection fraction of at least 50 % and entirely normal left ventricular contraction on biplane left ventriculogram. Patients with these features would be considered to have “probable right ventricular infarction without significant left ventricular infarction” if pulmonary emboli, acute pericardial tamponade, and chronic constrictive pericarditis were excluded.

A computerized data bank storing the history, physical examination, and laboratory results of each patient undergoing cardiac catheterization at Duke University Hospital and the Durham Veterans Administration HospitaP was searched to identify

1050 Roberts et al. November, 1985


Table 1. Clinical characteristics of patients with predominant right ventricular infarction

ECG at time Total Total LDH LV ejection of event CK CK-MB SGQT LDH isoenzymes RAMIPCWP fraction

Patient from ST elevation Vi-V,, clinical-pathology study II, III, aV, 375 58 5, 5560 8140 1>2 --/15

Patient from clinical study ST elevation Vi-V, 213 21 oo 63 361 2>1 17117 64’,$

ECG = electrocardiogram; CK = creatine kinase; CK-MB = creatine kinase, myocardial specific fraction; SGOT = serum glutamic oxaloacetic transaminase; LDH = lactic dehydrogenase; RAM = right atria1 mean pressure; PCWP = pulmonary capillary wedge pressure; LV = left ventricle.

any patients with the above characteristics during the g-month period preceding the admission of the patient identified by the clinical-pathology study. One hundred sixty-seven patients with a previous history of a myocardial infarct had received a cardiac catheterization during this period, and their computerized records form the basis for this report.

Results. Of the 167 catheterized patients with a history of a myocardial infarct, 24 had at least one coronary artery with stenosis of at least 75 % , but no wall motion abnormality on biplane left ventriculogram and no QRS changes on serial ECGs (Table I). Only one of these 24 patients met all of the above criteria for presumptive evidence of right ventricular infarction without significant left ventricular involvement. The clinical characteristics of this patient are compared with those of the patient identified by the clinical-pathology study in Table I and their ECGs are shown in Fig. 1.

The patient was a 54-year-old woman who had experienced several weeks of exertional chest pain preceding the more severe pain which prompted admission to a coronary care unit. She had no rales, murmurs, or ventricular gallops on physical examination. The ECG showed transient ST elevation in leads V, to V, (Fig. 1). No QRS changes developed. A ventilation-perfusion lung scan revealed no evidence of pulmonary emboli. Third-degree atrioventricular block and cardiogenic shock developed during the first day. Temporary right ventricular pacing and a dopamine infusion failed to raise the systolic pressure above 70 mm Hg, but rapid infusion of normal saline resulted in an increase in the blood pressure to 130/80 mm Hg. On the fifth day a cardiac catheterization was performed to clarify the unusual clinical picture (see Table I). A dominant right coronary artery system was demonstrated. Though the posterolateral aspect of the left ventricle was supplied by the right coronary artery, retrograde

filling of this segment occurred during the left coronary injection.

COMMENTS

Significance of right ventricular infarction. The failure to lower cardiac output with right ventricular cautery in dogs14, I5 and the strong association of right ventricular infarction with inferior left ventricular infarction at autopsy’8’ 24 have suggested that (1) right ventricular infarction occurs only as an exten- sion of left ventricular infarction25 and that (2) right ventricular infarction has hemodynamic significance only in the setting of such biventricular involvement. In contrast, this report demonstrates that right ventricular infarction can (1) occur with minimal septal or left ventricular free wall involvement, (2) need not be associated with either septal or inferior wall QRS changes on the ECG, and (3) can result in cardiogenic shock. These findings are consistent with the 34% fall in cardiac output found in the canine model of right ventricular infarction3 which employed coronary emboli rather than cautery.12 They are also consistent with the results of earlier large autopsy series*e5 as well as with the report of Chou et al.,26 in which one of 11 patients with right ventricular infarction presented with ST segment elevation but no QRS change on the ECG.

The major limitation of the present report is the retrospective nature of both the clinical-pathologic and clinical studies. Since the entity of right ventricular infarction without significant left ventricular infarction had not been previously emphasized, important noninvasive studies of right ventricular function as well as special ECG lead recordings27 were omitted. However, the anatomic documenta- tion of the location and extent of the infarct at postmortem examination establishes the existence of this entity. The incidence of this type of infarction can only be determined by a careful prospective

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Number 5 Right ventricular infarction 1051

Outcome Coronary anatomy

Died with shock (1) Total proximal right coronary artery stenosis

(2) 25”( left coronary artery stenosis

Alive and well (3) Right dominant system (1) Total proximal right coronary

artery stenosis (2) 50”CI circumflex stenosis (3) Right dominant system

trial in which all patients with acute infarcts which are not accompanied by new QRS changes have careful evaluation of the presence and extent of both right and left ventricular involvement.

ECG diagnosis of right ventricular infarction. The recognition of right ventricular infarction without QRS change should alter the approach to clinical diagnosis of right ventricular infarction. Clinicians have relied on inferior left ventricular infarction, usually diagnosed by ECG, as their cue to suspect the presence of right ventricular infarction.12z I*, 27, 28 Even when physical findings such as Kussmaul’s sign have been primary criteria for diagnosis of right ventricular infarction, inferior infarction on ECG has been considered a prerequisite.2g However, in a recent study by Geft et aL30 5 of 69 patients (7%) with ST segment elevations in the right precordial leads and no ECG evidence of inferior infarction had right ventricular infarction documented by angio- graphic and scintigraphic studies. Pulmonary emboli and chronic obstructive pulmonary disease, with attendant pulmonary hypertension, have been suggested as factors which might create a higher risk of right ventricular infarction.17,31 Studies of experimental animals have suggested that right ventricular infarction is more common in the presence of right ventricular hypertrophy,32 but a postmortem study failed to confirm this association in humans.18 There was no evidence of either significant inferior left ventricular involvement or right ventricular hypertrophy in the patient in the clinical-pathology study in the present report.

Both the patient in the clinical-pathology study and the one identified from the search of the data bank represent another clinical setting which sug- gests the presence of right ventricular infarction without significant left ventricular involvement. These patients had myocardial infarcts without QRS changes on the ECG but with severe hypotension. The absence of significant left ventricular infarction seen at autopsy in the first patient and a

normal left ventriculogram in the second eliminate the possibility of extensive subendocardial involvement of the left ventricle. Previous studies,33-35 have shown that a myocardial infarct which does not significantly alter a normal QRS complex usually does not alter left ventricular function. Consequent- ly, a patient who has clinical evidence of a decreased cardiac output in the presence of a persistently normal QRS complex has one of two rare entities: circumferential extensive left ventricular infarction or right ventricular infarction without significant left ventricular infarction. Swan-Ganz catheterixa- tion should permit prompt diagnosis.

Prognosis of right ventricular infarction. The prognosis of patients with left ventricular infarcts with a low cardiac output has been evaluated in groups with and without right ventricular involvement. In one series31 the mortality in the presence of right ventricular involvement was 40 % . However, in most studies, survival rates have been higher when right ventricular involvement was present than when the low cardiac output state was due solely to left ventricular dysfunction.lO, lfi. x Variations in left ventricular factors may determine the prognosis when the infarction is biventricular. However, the two patients described in the present study demonstrate that either fatal or nonfatal cardiogenic shock can result when only the right ventricle is significantly involved.

Treatment of right ventricular infarction. The clinical course experienced by these two patients does not suggest any change in the treatment of right ventricular infarction. The hemodynamic treatment of right ventricular infarcts is well established and includes volume infusion, inotropes, vasodilators, and atrial pacing.16s 37-3g Anticoagulation is usually not considered to be indicated. However, a large right ventricular mural thrombus was found at postmortem examination in the present clinical- pathology study. WadelI has observed that pulmonary emboli are ninefold more common in the presence of right ventricular infarction than with left ventricular infarction alone. Coma-Canella et al.31 reported 10 patients with hemodynamically defined right ventricular infarcts, one of whom died of pulmonary emboli. This observation and other experience40 have prompted the suggestion that routine anticoagulation should follow the diagnosis of right ventricular infarction.31 The importance of thromboembolic complications in right ventricular infarction should be established in future studies.

SUMMARY

Right ventricular infarction has been described as concurrent with infarction involving the inferior

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Sanders AO: Coronary thrombosis with complete heart-block and relative ventricular tachycardia: A case report. AM HEART J 6:820, 1930-31. Lisa JB, Ring A: Myocardial infarction or gross fibrosis, analysis of 100 necropsies. Arch Intern Med 50:131, 1932. Bean WB: Infarction of the heart. III. Clinical course and morphological findings. Ann Intern Med 12:71, 1938. Yater WM, Traum AH, Brown WG, Fitzgerald RP, Geisler MA. Wilcox BB: Coronarv arterv disease in men einhteen to thirty-nine years of age. AM HE&T J 36:683, 1948.- Wartman SB, Hellerstein HK: The incidence of heart disease in 2,000 consecutive autopsies. Ann Intern Med 26:41, 1948. Horan LG, Flowers NC, Harelda CJ: Relation between right ventricular mass and cavity size: an analysis of 1500 human hearts. Circulation 64:135, 1981. Cohn JN, Guiha NH, Broder MI, Limas CJ: Right ventricular infarction: clinical and hemodynamic features. Am J Cardiol 33:209, 1974. Guiha NH, Limas CJ, Cohn JN: Predominant right ventricular dysfunction after right ventricular destruction in the dog. Am J Cardiol 33:254, 1974. Lore11 B, Gold HK, Pohost GM, Dinsmore RE, Leinbacb RC, Hutter AM, DeSanctis RW: Right ventricular infarction: Clinical features, emphasizing its resemblance to cardiac tamponade (abstr). Am J Cardiol 41:409, 1978. Lore11 B, Leinbach RC, Pohost GM, Gold HK, Dinsmore RE, Hutter AM, Pastore JO, DeSanctis RW: Right ventricular infarction: Clinical diagnosis and differentiation from cardiac tamponade and pericardial constriction. Am J Cardiol 43:i65, 1979. Sharpe DN, Botvinick EH, Shames DM, Schiller NB, Massie BM, Chatterjee K, Parmley WW: The noninvasive diagnosis of right ventricular infarction. Circulation 57:483, 1978. Jensen DP, Goolsby JP, Oliva PB: Hemodynamic pattern

1052 Roberts et al.

(posterior) aspect of the left ventricular free wall and adjacent interventricular septum. Patients with right ventricular infarction typically show the ECG changes of inferior infarction in leads II, III, and aV,. This report describes two patients with right ventricular infarction but without changes in the QRS complex of the ECG, indicating an inferior infarct of the left ventricle.

An autopsy-proven infarct of the right ventricular free wall with neither QRS nor other clinical evidence of left ventricular involvement was responsi- ble for cardiogenic shock and death in one patient. This observation led to a review of a computerized data bank containing records of patients who had undergone cardiac catheterization to determine if there were other patients with clinical criteria suggesting right ventricular infarction without QRS changes of left ventricular infarction. One of the 167 patients with a history of a myocardial infarction also met the following clinical criteria: (1) transiently elevated total creatine kinase and creatine kinase myocardial band, (2) diffuse ST segment elevation without QRS changes indicative of left ventricular infarction on the ECG; (3) normal left ventricular function; (4) hemodynamic evidence of right ventricular dysfunction; and (5) cardiogenic shock.

REFERENCES

13.

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16.

17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

27.

28.

29.

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resembling pericardial constriction after acute inferior myocardial infarction with right ventricular infarction. Am J Cardiol 42:858, 1978. Goldstein JA, Vlahakes GJ, Verrier ED, Schiller NB, Tyberg JV, Ports TA, Parmley WW, Chatterjee K: The role of right ventricular systolic dysfunction and elevated intrapericardial pressure in the genesis of low output in experimental right ventricular infarction. Circulation 65:513, 1982. Starr I, Jeffers WA, Meade RH Jr: The absence of conspicu- ous increments of venous pressure after severe damage to the right ventricle of the dog, with a discussion of the relation between clinical congestive failure and heart disease. AM HEART J 26:291, 1943. Bakos ACP: The question of the function of the right ventricular myocardium: An experimental study. Circulation 1:724, 1950. Cohn JN: Right ventricular infarction revisited. Am J Cardiol 43:666, 1979. Wade WG: The pathogenesis of infarction of the right ventricle. Br Heart J 21:545, 1959. Isner JM, Roberts WC: Right ventricular infarction compli- cating left ventricular infarction secondary to coronary artery disease. Am J Cardiol 43:885, 1978. Wackers FJT, Lie KI, Sokole EB, Res J, van der Schoot JB, Durrer D: Prevalence of right ventricular involvement in inferior wall infarction assessed with myocardial imaging with thalium-201 and technetium-99m pyrophosphate. Am J Cardiol 42:358, 1978. Rigo P, Murray M, Taylor DR, Weisfeldt ML, Kelly DT, Strauss HW, Pitt B: Right ventricular dysfunction by gated scintiphotography in patients with acute inferior myocardial infarction. Circulation 52:268, 1975. Rotman M, Ratliff NB, Hawley J: Right ventricular infarction: A haemodynamic diagnosis. Br Heart J 36:941, 1974. Savaee RM. Wagner GS. Ideker RE. Podolskv SA. Hackel DB: Correlation-of post mortem anatomic &dings with electrocardiographic changes in patients with myocardial infarction. Circulation 55:279, 1977. Rosati RA, McNeer JF, Starmer CF, Mittler BS, Morris JM, Wallace AG: A new information system for medical practice. Arch Intern Med 135:1017, 1975. Ratliff NB, Hackel DB: Combined right and left ventricular infarction: Pathogenesis and clinicopathologic correlation. Am J Cardiol 45:217, 1980. Isner JM, Roberts WC: Right ventricular infarction compli- cating left ventricular infarction: A complication exclusively of posterior wall infarction (abstr). Am J Cardiol 41:409, 1978. Chou T, van der Bel-Kahn J, Allen J, Brockmeier L, Fowler NO: Electrocardiographic diagnosis of right ventricular infarction. Am J Med 70:1175, 1981. Myers GB, Klein HA, Hiratzka T: IV. Correlation of electrocardiographic and pathologic findings in infarction of the interventricular septum and right ventricle. AM HEART J 37:720, 1949. Croft CH, Nicod P, Corbett JR, Lewis SE, Huxley R, Willerson JT, Rude RE: Detection of acute right ventricular infarction by right precordial electrocardiography. Am J Cardiol 50:421, 1982. Dell’Italia LJ, Starling MR, O’Rourke RA: Physical examination for exclusion of hemodynamically important right ventricular infarction. Ann Intern Med 99:544, 1983.

30. Geft IL, Shah PK, Rodriguea L, Hulse S, Maddahi 3, Berman DS, Ganz W: ST elevations in leads V, to V, may be caused by right coronary artery occlusion and acute right ventricular infarction. Am J Cardiol 53:991, 1984.

31. Coma-Canella I, Lopez-Sendon J, Game110 C: Low output syndrome in right ventricular infarction. AM HEART J 96:613, 1979.

32. Peter RH, Ramo BW, Ratliff N, Morris JJ Jr: Collateral vessel development after right ventricular infarction in the pig. Am J Cardiol 29:56, 1972.

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33. Palmeri ST, Harrison DG, Upton MT: The EKG prediction of left ventricular ejection fraction following myocardial infarction (abstr). Circulation 60:11-187, 1979.

34. Askenazi J, Parisi AF, Cohn PF, Freedman WB, Braunwald E: Value of the QRS complex in assessing left ventricular ejection fraction. Am J Cardiol 41:494, 1978.

35. Roark SF, Ideker RE, Wagner GS, Alonso DR, Bishop SP, Bloor DM, Bramlet DA, Edwards JE, Fallon JT, Gottlieb Gd, Hackel DB, Phillips HR, Reimer KA, Rogers WJ, Ruth WK, Savage RM. White RD. Selvester RH: Evaluation of a QRS scoring system for estimating myocardial infarct size. -111. Correlation with quantitative anatomic findings for inferior infarcts. Am J Cardiol 51:382, 1983.

36. Iqbal MZ, Liebson PR, Messer JV: Right ventricular infarct. Cardiovasc Rev Rep 1:693, 1979.

37. Crexells C, Chatterjee K, Forrester JS, Dikshit K, Swan JHC: Optimal level of filling pressure in the left side of the heart in acute myocardial infarction. N Engl J Med 269:1263, 1973.

38. Clark G, Strauss HD, Roberts R: Dobutamine vs furosomide in the treatment of cardiac failure due to right ventricular infarction. Chest 77:220, 1980.

39. Top01 EJ, Goldschlager N, Ports TA, Dicarlo LA Jr, Schiller NB, Botvinick EH, Chatterjee K: Hemodynamic benefit of atria1 pacing in right ventricular infarction. 4nn Intern Med 96:594, 1982.

40. Trigano JA: Infarctus du coeur dreit. Semeiologie et incidence therapeutique. Coeur Med Interne 17:43, 1978.

right ventricular infarction with shock but without significant left ventricular infarction: a new...

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