Acute electrocardiographic pseudoinfarction pattern in the setting of diabetic ketoacidosis and severe hyperkalemia

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1086 Sweterlitsch and Murphy

aVF was observed during the procedure. No complications were encountered during and after procedure. Corticosteroid therapy 10 to 30 rag/day (prednisone for 6 months) was begun, with resultant normalization of the erythrocyte sedimentation rate. Follow-up treadmill testing 2 months after the procedure revealed electrocardiographic changes during moderate exercise (Bruce stage 5, 50 mph at a grade of 18%) and associated significant ST segment depressio n of 2 to 4 m m in leads II, III, aVF, and V2 to V6. Follow-up coronary angiography 27 months after the PTCA revealed no evidence ofrestenosis of the left coronary artery (Fig. 1, C). The post-PTCA clinical course was uncomplicated, and the patient has had no symptoms over a 2-year period after balloon angioplasty. Recently, balloon angioplasty of the aorta in Takayasu's arteritis has produced good results both immediately after the procedure and on long-term follow u p . 4 No aneurysm at the site of angioplasty was found in these patients. Markedly thickened vessel wall resulting from inflammatory fibrosis of all three layers as observed in Takayasu's arteritis could reduce the risk of future aneurysm formation. 5 To our knowledge this is the first case of PTCA for coronary artery stenosis in Takayasu's arteritis. Hitherto, PTCA in Kawasaki disease has been reported. One patient with Kawasaki disease who had undergone PTCA for coronary artery stenosis died of obstruction of the left coronary artery immediately after balloon rupture caused by a high inflating pressure occurred. Two other patients underwent successful dilation. 6, 7 Acute obstruction is an inherent risk of PTCA and can be deleterious in left coronary artery main stem lesions. However, recent results of aortocoronary bypass grafting have not been satisfactory. Ohara et al. s reported a low graft patency rate (50%) in their six patients undergoing aortoc0ronary bypass grafting. Cippiano et al.9 stated that it was difficult to construct proximal anastomoses of the grafts because of extremely thickened aortic wall, and inflammation of the aortic wall may have contributed to the late proximal occlusion of bypass grafts. This case suggests that PTCA may well be an effective alternative method to aortocoronary bypass surgery for coronary artery stenosis in Takayasu's arteritis. REFERENCES

1. Lupi-Herrera E, Sanchez-Torres G, Marcushamer J, Mispireta J, Horwitz S, Vela JE. Takayasu's arteritis: clinical study of 107 cases. Am Heart J 1977;93-94-103 2. Suzuki A, Kitamura T, Ona Y, Takayashi N, Naito Y, Koh Y. Indication of aortocoronary bypass for coronary arterial obstruction due to Kawasaki disease. Heart Vessels 1985;1:94-100 3. Morgan JM, Honey M, Gray HH, Belcher P, Paneth M. Angina pectoris in a case of Takayasu's disease: revascularization by coronary osteoplasty and bypass grafting. Eur Heart J 1987;8:1354-7 4. Tyagi S, Kaul VA~ Nair M, Sethi KK, Arora R, Khalilullah M. Balloon angioplasty of the aorta in Takayasu's arteritis: initial and long term results. Am Heart J 1992;124:876-82 5. Viramani R, Lande A, McAllster HA. Pathological aspects of Takayasu's arteritis. In: Lande A, Berkmen YM, McAllister HA, editors. Aortitis: clinical, pathologic and radiographic aspects. New York: Raven, 1986:56-63 6. Echigo S. PTCA. In Abstracts of the Third International Kawasaki Disease symposium. Tokyo, 64 7. Ino T, Nishmote N, Akimoto K, Park I, Shmajaki S, Yabuta K,

American Heart Journal

Yamaguchi H. Percutaneous transluminal coronary angioplasty for Kawasaki disease: a case report and literature review. Pediatr Cardiol 1991;12:33-5 8. OharaK, KasegawaH, AndeT. Surgicaltreatment for coronary artery disease associated with aortitis syndrome. Jpn J Thorac Surg 1986; 39:423-31 9. Cippiano PR, Silverman JF, Perlroth MG. Coronary arterial narrowing in Takayasu's aortitis. Am J Cardiol 1977;39:744-50

Acute electrocardiographic pseudoinfarction pattern in the setting of diabetic ketoacidosis and severe hyperkalemia Eric M. Sweterlitsch, MD, and Gerald W. Murphy, MD, Rochester, N.Y. The electrocardiographic abnormalities commonly associated with hyperkalemia have been well described. Much less recognized is the uncommon occurrence of ST segment elevation, particularly in the precordial leads, which is electrocardiographically indistinguishable from acute myocardial infarction. Often associated with this abnormality is an intraventricular conduction delay with morphologic characteristics similar to those of right bundle-branch block. This abnormality has been described in the setting of severe hyperkalemia in patients with end-stage renal disease and once before in the setting of diabetic ketoacidosis (DKA). This abnormality is quite distinct from the electrocardiographic (ECG) abnormalities usually described in the setting of hyperkalemia and is easily mistaken for an acute anterior myocardial infarction. In the era of thrombolytic therapy this abnormality may expose the patient to unnecessary drug treatments or invasive medical procedures that carry significant risk of complications. Therefore we present this case of pseudoinfarction pattern in the setting of DKA and severe hyperkalemia to alert practicing physicians to this unusual phenomenon. Case R e p o r t . T. M. is a 46-year-old man with a history of insulin-dependent diabetes mellitus since the age of 18 years. He presented to the emergency department of our hospital on Feb. 24, 1995 with DKA and initially a suspected acute myocardial infarction. Complications of his diabetes included two episodes of DKA in the past and mild nephropathy and retinopathy. The patient abused alcohol, but the medical history was otherwise unremarkable, and specifically no history of cardiac disease or anginal symptoms was present. On presentation the patient was obfunded, but his wife gave a history of several days of nauFrom the Cardiology Unit, Department of Medicine, University of Rochester School of Medicine and Dentistry. Supported in part by NHLBI training grant HL0722OD-17. Reprint requests: Eric Sweterlitsch, MD, Allen Medical Building, 200 S. Wenona, Bay City, MI 48706. Am Heart J 1996;132:1086-9. Copyright © 1996 by Mosby-Year Book, Inc. 0002-8703/96/$5.00 + 0 4]4]73661

Volume 132~ Number 5 American Heart Journal

~UJ~r'~T~#Ch and Murphy

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Fig. 2. ECG on presentation to emergency department. There is marked change from baseline with ST segment elevation in anteroseptal leads consistent with acute myocardial infarction. In addition, there is now intraventricular conduction delay with morphologic characteristics similar to right bundle-branch block.

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November 1996 American Heart Journal

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sea, vomiting, and viral-like symptoms. No history of chest pain, dyspnea, or other symptoms suggestive of myocardial ischemia was present. Because of progressive mental status changes over a 2-day period, he was brought to the emergency department by his wife. Outpatient medications included only insulin. On physical examination he was a ketotic, obtunded man with blood pressure 130/ 70, pulse 130, respiration 38, and temperature 37.6 ° C. The skin was pale with poor turgor. Mucus membranes were dry. Cardiac examination revealed a regular tachycardia with no murmur, gallop, or rub. Lungs were clear to auscultation. Abdominal examination was unremarkable. No peripheral cyanosis or edema was seen. Distal pulses were equal and intact in all extremities. On neurologic examination the patient could not follow commands but was moving all extremities, and no focal motor defects were noted. Deep tendon reflexes were equal, and Babinski reflexes were downgoing bilaterally. Laboratory examination revealed findings consistent with severe DKA. Serum chemistries ~vere sodium, 132 meq/L, potassium, 7.9 meq/L, chloride, 93 meq/L, bicarbonate, <5 meq/L, blood urea nitrogen, 58 mg/dl, creatinine, 2.8 mg/dl, glucose, 1586 mg/dl, calcium, 10.2 mg/dl, phosphate, 9.3 mg/dl, and magnesium, 2.5 mg/dl. Arterial blood gas was pH, 6.97, Pcou, 8, and PO2, 153 on 4 L/min O2 via nasal cannula. The complete blood cell count was white blood cell count, 24,000/pL, hemoglobin, 15.6 gm/dl, and platelet estimation, normal. Chest radiography revealed no cardiomegaly or congestive heart failure. The patient's baseline ECG obtained approximately 1 year before admission is displayed in Fig. 1 and revealed normal sinus rhythm, rate 89, and lef~

atrial enlargement but otherwise was unremarkable. The ECG on presentation is displayed in Fig. 2 and shows marked changes from the patient's baseline ECG. There is sinus tachycardia and P waves with morphologic characteristics unchanged from baseline. Of note is the appearance of marked ST segment elevation in the anteroseptal leads consistent with acute myocardial infarction. No Q waves are present. An intraventricular conduction delay similar to a right bundle-branch block with delayed rightward voltage is also present. Initially the diagnosis was DKA and probable acute anteroseptal myocardial infarction. There was additional concern over the development of a new intraventricular conduction delay in the setting of ischemia. Because of the patient's severe metabolic derangements, specific therapy for his suspected myocardial infarction was withheld, and he was immediately treated with high doses of intravenous fluids and insulin. In addition, a small dose of intravenous sodium bicarbonate was administered. The patient was admitted to the cardiac care unit, where the next determination of serum electrolytes revealed sodium, 147 meq/L, potassium, 3.8 meq/L, chloride, 114 meq/L, bicarbonate <5 meq/L, blood urea nitrogen, 52 mg/dL, creatinine, 2.4 mg/dl, and glucose, 858 rag/ dl, and arterial blood gaswas pH, 7.12, PCo2, 12, and Po2, 112. An ECG obtained at this time is displayed in Fig. 3 and shows complete resolution of both the anterosepta] ST segment elevation and the intraventricular conduction delay. Findings on this tracing are suggestive of hypokalemia including slight shortening of the PR segment and prolongation of the QT interval with more prominent U waves consistent with the absolute hypokalemia found i n DKA. Follow-up ECGs showed no fur-

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Khan and Chou

American Heart Journal

ther evolutionary ST changes or Q waves. The patient was treated in the usual manner for his DKA. Serial creatinine kinase determinations remained within normallimits, and no other evidence of myocardial infarction was found. The patient was treated successfully for DKA, but his recovery was prolonged because of the development of delirinm tremens 3 days into the hospitalization. However, no clinical symptoms of angina were seen. When he had stabilized medically, a rest thallium/exercise sestamibi SPECT myocardial perfusion scan was performed on March 17, 1995. He exercised for 7 minutes, 25 seconds on a standard Bruce protocol, achieving a rate-pressure product of 24,300. The electrocardiogram and exercise sestamibi images were normal, and no evidence of previous myocardial infarction was found on the resting thallium images. Comments This case report graphically illustrates an unusual reversible electrocardiographic abnormality that may occur in the setting of severe hyperkalemia and may be confused with acute myocardial infarction. Although an ischemic basis for these findings cannot be completely excluded, the rapid reversal of the abnormalities with currection of the patient's metabolic status and the lack of clinical evidence of ischemia or infarction make this diagnosis very unlikely. Furthermore the normal resting thallium and stress sestamibi images serve to further exclude ischemia as a diagnosis. Hyperkalemia has profound effects on myocardial conduction, membrane depolarization, and consequently on the surface ECG. The earliest change that typically occurs in hyperkalemia is symmetric peaking of T waves and occasional shortening of the QT interval. ST segment depression rather than elevation is well described. Reduction in P-wave amplitude and eventual disappearance of the P wave is characteristic. This latter finding may coexist with preserved conduction of impulses from the sinoatrial node to the atrioventricular node (sinoventricular rhythm), although varying degrees of atrioventricular block may occur. With more severe hyperkalemia, widening of the QRS occurs and various forms of intraventricular conduction delay result, which may resemble right bundle-branch block, left bundle-branch block, or be nonspecific. In end-stage hyperkalemia a "sine wave" ECG may be found. Although intraventricular conduction delay as found in this patient is well described in the presence of hyperkalemia, the precordial ST segment elevation or "pseudoinfarction pattern" has been less frequently reported. Levine et al.1 describe identical electrocardiographic abnormalities or "dialysable currents of injury" in four patients with end-stage renal disease and severe hyperkalemia. These described changes may have also been associated with other metabolic abnormalities found in renal failure. More recently 2 similar ECG findings were described in a 45year-old patient with nonrenal failure and DKA in which the ECG abnormalities rapidly resolved with treatment of the DKA and hyperkalemia. A similar ECG pattern has been described in a patient with severe hyperkalemia as a complication of ]ymphosarcomas and again was rapidly reversible on correction of the hyperkalemia and acidosis. The electrophysiologic mechanism for these unusual electrocardiographic abnormalities is unclear. Hyperkalemia is known to cause a decrease in resting membrane poten-

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tial, which in turn leads to a slowed inward sodium current and a delay in conduction in all cardiac tissues, although the endocardial tissues including the His-Purkinje system appear to be the most sensitive to these effects. This sensitivity may lead to dispersion of myocardial repolarization, which can explain peaking of the T waves. Abnormalities in phase 2 of the action potential are thought to be responsible for the ST segment depression that is oi~n encountered. In this patient with marked hyperkalemia and metabolic acidosis, the appearance of anteroseptal ST segment elevation was present with an intraventricular conduction delay similar to right bundle-branch block. It is debatable whether the ST elevation is a primary repolarization abnormality or an artifact caused by melding of the terminal R' of the QRS with the T wave. The fact that identical ECG changes have been previously observed in DKA and that these abnormalities are unusual in the presence of hyperkalemia alone raises the question of whether acidosis or another metabolic abnormality specific to DKA may play a contributory role. It is possible that the more severe hyperkalemia or the presence of acidosis as found in this case causes the epicardial myocardial tissue to become relatively more sensitive to these metabolic derangements, leading to anterior ST segment elevation. The metabolically induced ECG abnormalities in this patient, although uncommon, have been described previously. However, in a review of standard ECG texts 12 of 17 had no mention of this abnormality. This unusual manifestation of hyperkalemia should be noted for its possible confilsion with acute anteroseptal myocardial infarction. This misdiagnosis might occur even in the setting of known hyperkalemia because of the unusual characteristics of the electrocardiographic changes. REFERENCES

1. Levine HD, Wanzer SH, Merrill JP. Dialyzable currents of injury in potassium intoxication resembling acute myocardial infarction or pericarditis. Circulation 1956;13:29-36. 2. Kamimura M, Hancock EW. Acute MI pattern in diabetic ketoacidosis. Hospital Practice 1992;27:28-30. 3. Burris AC, Chung EI~L Pseudomyocardial infarction associated with acute bifasicular block due to hyperkalemia. Cardiology 1980;65:115-20.

Right ventricular infarction mimicking acute anteroseptal left ventricular infarction Zia U. Khan, MD, and Te-Chuan Chou, MD Cincinnati, Ohio The electrocardiographic (ECG) diagnosis of right ventricular infarction in association with acute inferior myocarFrom the Division of Cardiology, Department of Medicine, University of Cincinnati College of Medicine. Reprint requests: Zia U. Khan, MD, Division of Cardiology, University of Louisville Health Science Center, ACB, 3rd Floor, 550 S. Jackson St., Louisville, KY 40292. Am Heart J 1996;132:1089-93. Copyright © 1996 by Mosby-Year Book, Inc. 0002-8703/96/$5.00 + 0 414/73662