Henry Ford Hospital Medical Journal

Volume 39 Number 3 Article 20

9-1991

Incomplete Versus Complete Myocardial Infarction

Mihai Gheorghiade

Sidney Goldstein

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Recommended Citation Gheorghiade, Mihai and Goldstein, Sidney (1991) "Incomplete Versus Complete Myocardial Infarction," Henry Ford Hospital Medical Journal : Vol. 39 : No. 3 , 263-264. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol39/iss3/20

This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Incomplete Versus Complete Myocardial Infarction

Mihai Gheorghiade, MD,* and Sidney Goldstein, MD*

Incomplete myocardial infarction (MI), when compared with a complete Ml. is characterized by a small infarct size and a large mass of viable hut jeopardized myocardium within the perfusion zone of the infarct-related vessel that is manifested ctinicalty hy early recurrent infarction. The pathophysiology involves earty spontaneous or thrombolytic reperfusion. Clinical (i.e., residual ischemia), electrocardiographic, and echocardiographic findings and magnitude of serum cardiac enzyme elevatitms should be taken into account in diagnosing an incomplete Ml. (Heniy Ford Hosp MedJ 1991;39:263-4)

he observation that the ischemic event associated with on the ECG may not properly identify patients with incomplete Tthrombotic occlusion of the coronary artery can be inter­ infarction. rupted with thrombolytic therapy has led to the recognition of a When applied to the individual patient, it is therefore more new ischemic syndrome, the incomplete myocardial infarction useful to divide postinfarction patients, regardless of whether or (MI) (1). These observations have also called our attention to the not they have spontaneous reperfusion or receive thrombolytic fact that early spontaneous reperfusion may occur in patients therapy, into those who have a completed versus incomplete MI. who experience a non-Q wave MI (2). These two clinical pre­ In determining the incompleteness of MI, a number of factors sentations of incomplete infarction identify patients with initial­ come into play. The presence of Q waves, the location of the ST ly small Mis who are at risk of early recurrence of myocardial and T-wave changes (5), and the degree of ST depression (17, ischemia involving a relatively large area of viable but jeopar­ 18) all are important. Peak serum creatine phosphokinase eleva­ dized myocardium in the infarct-related artery (3). tion may have significance in differentiation of the event. Small Patients recovering from a large but completed Ml have a elevations of creatine phosphokinase suggest an incompleted well-defined increased mortality related to the extent of myocar­ event (16,19). The magnitude of wall motion abnormality in the dium lost (4). In contrast, patients with an incomplete ischemic area of the infarct-related artery, evaluated either by echocardi­ event, despite an initial modest insult, are prone to reinfarction ography or angiography, provides important information as to shortly after their event, leading to a significant increase in mor­ the completeness of the MI. However, early reperfusion of the tality related to further tissue loss and recurrent ischemia (5). occluded artery is not always accompanied by immediate recov­ Patients who experienced early thrombolytic or spontaneous re­ ery of the contractile function in the infarct-related artery seg­ perfusion comprise the patient population of incomplete infarc­ ments (stunned myocardium). This condition in which the myo­ tion. Both groups of patients with incomplete infarction are cardium is viable but not contractile may persist much longer if bound together by the patent but diseased vessel, the high rate of the infarct-related artery is occluded or has a tight stenosis (hi­ early reinfarction, and a limited initial insult. bernating myocardium) (20,21). Identification of areas of viable Given the heterogeneity of the non-Q wave infarction group but not contractile myocardium (stunned or hibernating) may be (6) that includes patients with prior Q waves, different electro­ possible by observing functional recovery by two-dimensional cardiographic locations, and even normal ECGs (7), and the fact echocardiography during infusion of a small dose of dobuta­ that in patients receiving thrombolytic therapy the presence of Q mine (22,23). In addition, residual ischemia, spontaneous or pro­ waves does not always predict a completed event or transmural- voked in the area of the infarct-related artery, plays a pivotal role ity (8-10), it is not surprising that the ECG alone will not prop­ in identifying patients with an incomplete infarction (24). erly identify patients with an incomplete infarction (11-13). The In order to create a framework to describe the features of in­ frequent presence of a Q wave in the incomplete thrombolytic completeness of infarction, we propose the following: infarct is partially related to the duration of symptoms and the protocol demand for significant ST and T-wave changes before administering thrombolytic therapy (14,15). In addition, the ab­ sence of Q waves is not always correlated with a small or suben­ Submitted for publication: August 15. 1991, docardial MI, particularly if the myocardial segments are sup­ Accepled for publication: August 28, 1991, plied by the right or the circumflex coronary artery (16). In this *Heart and Vascular Institute, Division of Cardiovascular Medicine, Henry Ford Hospital, Address correspondence to Dr, Gheorghiade, Hean and Vascular Institute, Division of era of thrombolytic therapy, the absence or presence ofQ waves Cardiovascular Medicine, Henry Ford Hospilal, 2799 W Grand Blvd, Detroit, Ml 48202,

Henry Ford Hosp Med J—Vol 39, Nos 3 & 4, 1991 Incomplete Versus Complete MI—Gheorghiade & Goldstein 263 I. Suspect incomplete infarction when: 6, Gibson RS, Non-Q-wave myocardial infarction: Diagnosis, prognosis, and 1. A. Non-Q wave without thrombolytic therapy, or management. Curt ProbI Cardiol 1988;13:8-72. 7, Boden WE, Kleiger RE, Gibson RS, et al. Favourable long term prognosis B. Q or non-Q wave with thrombolytic therapy. in patients with non-Q wave acute myocardial infarction not associated with spe­ 2. Small elevation usually less than 500 lU/L of the cre­ cific electrocardiographic changes, Br HeartJ 1989:61:396-402, atine phosphokinase. 8, Rogers WJ. Bourge RC, Papapietro SE. et al. Variables predictive of good 3. A. Angiographic or echocardiographic evidence of pre­ functional outcome following thrombolytic therapy in the Thrombolysis in served function in the infarct-related area, or Myocardial Infarction phase II (TIMI II) pilot study. Am J Cardiol 1989:63:503- 12, B. Angiographic or echocardiographic evidence of a 9, Califf RM. O'Neil W. Stack RS. et al. Failure of simple clinical measure­ large area of viable but noncontractile myocardium (stunned or ments to predict perfusion status after intravenous tftromtxjiysis, Ann Intem Med hibernating myocardium) identified by low-dose dobutamine 1988:108:658-62, infusion. 10, Jaffe AS. Sobel BE. Thrombolysis with tissue-type plasminogen activator 4. Residual ischemia present (postinfarction angina or ex­ in acute myocardial infarction: Potentials and pitfalls, JAMA 1986:255:237-9, ercise-induced ischemia). 11, Stone PH. Raabe DS. Jaffe AS. et al. Prognostic significance of location and type of myocardial infarction: Independent adverse outcome associated with II. Complete infarction: anterior location, J Am Coll Cardiol 1988:11:453-63, 1. Persistent Q waves. 12, Ross J Jr, Gilpin EA, Madsen EB. et al, A decision scheme for coronary 2. Major elevation of serum creatine phosphokinase. angiography after acute myocardial infarction. Circulation 1989;79:292-303, 3. No evidence of residual ischemia. 13, Benhorin J, Moss AJ. Oakes D. et al. The prognostic significance of first myocardial infarction type (Q wave versus non-Q wave) and Q wave location, J 4. Large area of ventricular akinesis in infarct-related ar­ Am Coll Cardiol 1990:15:1201-7, tery resulting from irreversibly damaged myocardium. 14, Mikell FL, Petrovich J. Snyder MC. etal. Reliability of Q-wave formation The criteria proposed are not rigid but require physician inter­ and QRS score in predicting regional and global left ventricular performance in pretation. A definition of the completeness of the infarction, tak­ acute myocardial infarction and successful reperfusion. Am J Cardiol 1986:57: ing these factors into consideration, is more complex than the 923-6, simple presence or absence of a Q wave. For example, the pa­ 15, Schweitzer P, The electrocardiographic diagnosis of acute myocardial in­ farction in the thrombolytic era. Am Heart J 1990:119:642-54. tient with a Q wave MI with small elevation of the creatine ki­ 16, Gib.son RS. Beiler GA, Gheorghiade M. et al. The prevalence and clinical nase serum level and preserved wall motion in the infarct-re­ significance of residual myocardial ischemia 2 weeks after uncomplicated non- lated area by echocardiography will be assigned to the incom­ Q wave infarction: A praspective natural history study. Circulation 1986:73: plete MI group. On the other hand, the patient with a non-Q 1186-98, wave infarct who has a high total creatine kinase serum level and 17, Schechtman KB, Capone RJ, Kleiger RE, et al, Ri.sk stratification of pa­ tients with non-Q wave myocardial infarction: The critical role of ST segment by echocardiography akinetic wall in the infarct-related artery depression. Circulation 1989:80:1148-58, with no residual ischemia will be assigned as one with com­ 18, Boden WE, Gib,son RS, Schechtman KB, etal, ST segment shifts are poor pleted Ml. predictors of subsequent Q wave evolution in acute myocardial infarction: A nat­ It is clear that reperfusion, either therapeutic or spontaneous, ural history study of early non-Q wave infarction. Circulation 1989:79:537-48, 19, Garabedian HD, Gold HK, Yasuda T et al. Detection of coronary artery often leaves the artery with surprisingly little angiographic evi­ reperfusion with creatine kinase-MB determinations during thrombolytic ther­ dence of luminal narrowing (25). It is therefore important to re­ apy: Cortelation with acute angiography, J Am Coll Cardiol 1988:11:729-34, alize that therapy of the incomplete infarction lies in the realm of 20, Braunwald E, Kloner RA, The stunned myocardium: Prolonged, post- prevention of a recurrent thrombogenic and reocclusive process. ischemic ventricular dysfunction. Circulation I982;66:l 146-9, This may have a mechanical answer in surgical or intracoronary 21, Bolli R, Mechanism of myocardial "stunning," Circulation 1990:82:723- approach, but more than likely will be successfully approached 38, 22, Pierard LA, De Landsheere CM, Berthe C, Rigo P, Kulbertus HE, Identifi­ by pharmacologic interference of the thrombotic processes. cation of viable myocardium by echocardiography during dobutamine infusion in patients with myocardial infarction after thrombolytic therapy: Comparison with positron emission tomography, J Am Coll Cardiol 1990:15:1021-31, References 23, Barilla F, Gheorghiade M, Alam M, Khaja F, Goldstein S, Low-dose 1, Schaer DH. Ross AM. Wasserman AG, Reinfarction. recurtent angina, and dobutamine in patients with acute myocardial infarction identifies viable but not reocclusion after thrombolytic therapy. Circulation I987:76(suppl II):II-57-62, contractile myocardium and predicts the magnitude of improvement in wall mo­ 2, Roberts R, Recognition, pathogenesis, and management of non-Q-wave in­ tion abnormalities in response to coronary revascularization. Am Heart J 1991; farction. Mod Concepts Cardiovasc Dis I987;56:17-21. 122:1.522-31. 3, Bissett JK. Malts J. Sharma B. Program on Surgical Control for Hyperlipi- 24, Gibson RS. Young PM. Boden WE. Schechtman K. Roberts R. and the demia-Study Group (POSCH). Residual myocardial jeopardy in patients with Diltiazem Reinfarction Study Group, Prognostic significance and beneficial ef­ Q-wave and non-Q-wave infarctions, Br Heart J 1987:58:460-4, fect of diltiazem on the incidence of early recurtent ischemia after non-Q-wave 4, The Multicenter Postinfarction Research Group, Risk stratification and sur­ myocardial infarction: Results from the multicenter Diltiazem Reinfarction vival after myocardial infarction, N Engl J Med 1985:309:331-6, Study, Am J Cardiol 1987:60:203-9, 5, Kao W. Khaja F, Goldstein S. Gheorghiade M, Cardiac event rate following 25, Epstein SE, Quyymi AA, Bonow RO, Sudden cardiac death without wam­ non-Q-wave myocardial infarction and the significance of its anterior location, ing: Possible mechanisms and implications for screening asymptomatic popula­ AmJCardiol 1989:64:1236-42, tions, N Engl J Med 1989:321:320-4,

264 Henry Ford Hosp Med J—Vol 39, Nos 3 & 4. 1991 Incomplete Versus Complete MI—Gheorghiade & Goldstein