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Lupus myopericarditis as a preceding stressor for takotsubo cardiomyopathy.

Takotsubo cardiomyopathy (TC), also known as stress-induced cardiomyopathy or apical ballooning syndrome or broken heart syndrome, produces transient systolic dysfunction of the left ventricular apical and/or mid segments in the absence of significant coronary artery disease (1-4). Common triggering factors are acute medical illness and severe emotional or physical stress, such as domestic violence, arguments, the unexpected death of relatives, catastrophic medical diagnoses, devastating financial or gambling losses, and natural disasters (1-4). We herewith report a case of TC where the likely preceding stressor was chest discomfort from a preceding lupus myopericarditis, highlighting the association of these two syndromes.

CASE REPORT

A 61-year-old African American woman with systemic hypertension and systemic lupus erythematosus presented to the hospital with the chief complaint of moderate to severe pleuritic chest discomfort. Chest pain had been present for 1 week and had worsened a day before presentation to the hospital. The pain was stronger when lying flat and improved when sitting upright or leaning forward. She also reported mild arthralgias and fatigue. Prior to arrival, she presented to an outside hospital where an electrocardiogram demonstrated diffuse ST-segment elevation and an elevated serum cardiac troponin level (0.8 ng/mL). She was treated with aspirin, clopidogrel, and heparin and referred to our facility for cardiac catheterization. Upon arrival, her vital signs were within normal limits, and an electrocardiogram demonstrated diffuse ST-segment elevations. Cardiac angiography revealed a 50% to 60% narrowing (diameter reduction) of the left anterior descending coronary artery, and a ventriculogram revealed severe apical ballooning/hypokinesis and basal hyperkinesis with an estimated left ventricular ejection fraction of 25%, consistent with a takotsubo pattern (Figure 1). Physical examination disclosed a facial rash and a pericardial rub. A detailed review of systems revealed no preceding emotional stressor. Preceding the pleuritic chest pain, however, the patient's lupus had flared, which she found annoying and stressful.

The troponin I level was 2.24 ng/mL (normal: 0.00-0.03 ng/mL); creatine kinase MB index, 10.3% (0.0-2.5%); and creatine kinase MB, 15.6 U/L (0.0-5.0 ng/mL). Brain natriuretic peptide was 173 pg/mL (0-99 pg/mL), and her thyroid function profile was within reference range. A chest radiograph revealed mild enlargement of the cardiac silhouette. The initial 12-lead electrocardiogram demonstrated diffuse ST elevation and PR depression (except aVR and V1, where it showed PR elevation) (Figure 2). Subsequent tracings obtained after 12 hours and 18 hours revealed PR segment normalization (Figure 3), and after 30 hours, diffuse T wave inversions (Figure 4) (5, 6).

The patient was hemodynamically stable and was placed on aspirin 325 mg 3 times a day, colchicine 0.6 mg twice a day, atorvastatin, carvedilol, and lisinopril. Her home dose of prednisone (10 mg daily) was continued for underlying lupus (7). The patient was discharged 3 days later with complete resolution of her symptoms. A transthoracic echocardiogram performed prior to discharge (2 days after cardiac catheterization) demonstrated significant improvement in the left ventricular ejection fraction (now 50%--55%) and only mild apical ballooning in ventricular systole, with hypokinesis of the apex and the distal third of the anterior wall.

DISCUSSION

There have been at least seven reports of patients with TC associated with pericarditis. Of these, at least three cases reported pericarditis preceding the development of TC, while three other reports suggested the possible occurrence of pericarditis in the resolution phase of TC and one report did not specify the onset of pericarditis with respect to TC (8-15). We believe that our patient had pericarditis before the development of TC. TC was likely due to an intense sympathetic stimulation resulting from pericarditis-induced severe chest discomfort. In cases where TC is the primary pathology, pericarditis may result secondary to the extension of the myocardial inflammation to the overlying pericardium, considering the inflammatory hypothesis for TC. One may also argue that such a coexistent association may actually represent a perimyocarditis variant manifesting as transient ST elevation on electrocardiogram and elevated cardiac biomarkers (16, 17).

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The coexistence or association between TC and acute pericarditis or myopericarditis can have several diagnostic and therapeutic implications. First, this association challenges the current existing Mayo Clinic criteria for the diagnosis of TC and suggests a call for their revision (18). Given now several reported cases of TC pericarditis, it is important that one should not completely exclude the diagnosis of TC if pericarditis or myopericarditis coexist, as advocated by the current diagnostic criteria. These two conditions do not need to be mutually exclusive and in fact can be present simultaneously. Additionally, two important management considerations should be made because the electro-cardiographic presentation in some cases may masquerade as ST-segment--elevation myocardial infarction (STEMI). Such patients (TC with coexistent pericarditis), if treated with thrombolytic therapy for suspected STEMI at centers unable to perform primary percutaneous coronary intervention, may be exposed to a potential hazard of hemorrhagic tamponade. This may be an even bigger problem in developing countries where thrombolytic therapy is employed routinely for management of suspected STEMI. Also, the TC-pericarditis association emphasizes that a careful clinical history and ventriculography during cardiac catheterization should be routinely employed in such patients presenting with ST-segment elevation, especially if the electro cardiogram and echocardiographic features are more suggestive of TC, to avert the need for unnecessary thrombolytic therapy and to avoid missing a more serious diagnosis of STEMI. The association also calls for a cautionary use of anticoagulants and glycoprotein Ilb/IIIa inhibitors in cases of TC when coexistent pericarditis is present (15).

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Acute pericarditis and Dressler syndrome have been reported as possible complications of TC (9, 10). Conversely, acute pericarditis complicated by TC has been reported on at least three occasions (11--13), where pericarditis was the primary pathology. Systemic lupus erythematosus presenting with myopericarditis and associated with TC as a complication is the first such case reported, to the best of our knowledge.

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(3.) Dote K, Sato H, Tateishi H, Uchida T, Ishihara M. Myocardial stunning due to simultaneous multivessel coronary spasms: a review of 5 cases. J Cardiol 1991; 21(2):203-214.

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(17.) Bybee KA, Kara T, Prasad A, Lerman A, Barsness GW, Wright RS, Rihal CS. Systematic review: transient left ventricular apical ballooning: a syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med 2004; 141(11):858-865.

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From the Department of Cardiovascular Medicine, Hartford Hospital, University of Connecticut School of Medicine, Hartford, Connecticut. Corresponding author: Lovely Chhabra, MD, Department of Cardiovascular Medicine, Hartford Hospital, University of Connecticut School of Medicine, 80 Seymour Street, Hartford, CT 06106 (e-mail: lovids@hotmail.com).
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Author:Chhabra, Lovely; Khalid, Nauman; Kluger, Jeffrey; Spodick, David H.
Publication:Baylor University Medical Center Proceedings
Article Type:Case study
Geographic Code:1USA
Date:Oct 1, 2014
Words:1554
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