Diagnostic Dilemma: Takotsubo Cardiomyopathy Versus Acute Coronary Syndrome

ABSTRACT: Takotsubo cardiomyopathy is a kind of non-ischemic cardiomyopathy characterized by transient apical ballooning of the heart. This often results from sudden, temporary weakening of the myocardium. Initially defined in the absence of coronary artery disease, it has since expanded to involve patients with coronary artery disease. This inclusion is not free of challenges now faced at distinguishing between the two when they occur concomitantly, impacting the therapeutic interventions. We present a case of takotsubo cardiomyopathy with simultaneous coronary artery disease that responded well to conservative management and resulted in complete recovery of the patient. This reiterates the principle that a case-by-case evaluation of patients with takotsubo cardiomyopathy with underlying coronary artery disease needs to be made before an individualized therapeutic approach can be taken.

J INVASIVE CARDIOL 2014;26(6):E82-E84

Key words: takutsubo cardiomyopathy, concomitant disease

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Takotsubo cardiomyopathy (TC), initially described over two decades ago in the form of a few case reports to explain transient apical ballooning in the absence of significant coronary artery disease (CAD),^1-3 has since evolved to include subjects with CAD.⁴ According to recent reports, the prevalence of various degrees of CAD in patients with this syndrome ranged from 10%-60%.^5,6  This increased recognition of the coexistence of CAD and TC brings with it diagnostic and therapeutic challenges, especially in early stages of presentation. In this case report, we seek to highlight the diagnostic dilemma and therapeutic challenges encountered in a patient presenting to the emergency room with chest pain when CAD coexisted with TC.

Case Report. An 80-year-old Caucasian woman with a history of hypertension and anxiety was admitted to the emergency department after initial presentation to her primary care physician with chest pain. Electrocardiogram (ECG) showed 1 mm ST-segment elevations in leads II, III, aVF, V3, V4, and V5 (Figure 1). A two-dimensional echocardiogram showed dyskinetic left ventricular apex and akinetic periapical segments along with hyperdynamic basal segments with an ejection fraction of 48% (Figure 2). The cardiac enzymes were mildly elevated, with a peak troponin I of 4.93 ng/mL. The patient was initially treated with beta-blockers, heparin, clopidogrel, atorvastatin, and aspirin, and was taken immediately for cardiac catheterization. Angiography revealed 50% proximal heavily calcified lesion of the left anterior descending (LAD) coronary artery and an 80% occlusive lesion at the trifurcation of the septal perforator and the diagonal branch of the LAD (Figure 3). The right coronary artery was a dominant vessel, with a proximal 50% focal calcified lesion. Left ventriculogram showed hyperdynamic basal, inferior, and anterior segments with dyskinetic anterolateral, apical, and inferior walls (Figure 4). Subsequently, the patient was placed on conservative medical therapy with uneventful hospital stay and then discharged. Repeat echocardiogram and ECG performed 3 weeks later showed resolution of wall-motion abnormalities and normalization of ejection fraction, along with resolution of ST-T changes, respectively (Figures 5 and 6). 

Discussion. It is often difficult to differentiate TC from acute ST-elevation myocardial infarction (STEMI) on initial presentation. The ECG classically mimics STEMI and is usually accompanied by elevation of myocardial enzymes, resulting in immediate cardiac catheterization. However, in the absence of CAD on angiogram along with apical ballooning, the diagnosis of TC is free of any ambiguity. With early recognition and supportive care, TC is reversible and carries very good prognosis.  However, if the angiogram reveals significant CAD with high-grade lesion, it can lead to uncertainty and confusion and can pose a challenge to distinguish between the two. Furthermore, it is also difficult as the patients with TC are usually 60-70 years old and frequently have hypertension, diabetes, tobacco abuse, and dyslipidemia, all of which are causative agents for CAD.⁷ Accurate diagnosis of TC not only has broader therapeutic and prognostic implications, it is also necessary to avoid unwarranted invasive interventions and potential harm to the patient.

Although multiple criteria have been proposed to diagnose TC, some of them clinical^8,9 and others ECG based,¹⁰ all of them require the absence of CAD. However, this does not have to be an absolute criterion when reviewing former literature. Although TC manifests as regional wall-motion abnormality that extends beyond the territory of a single coronary vessel, this disease entity has been reported with underlying CAD as well. A Japanese case series of more than 90 patients with TC reported the incidence of concomitant CAD to be ~10%, with CAD defined as >75% stenosis of a major epicardial coronary artery.⁵ Another case series comprised of 7 patients reported the incidence of TC along with at least 1 epicardial coronary artery stenosis to be >50%.⁴

Unfortunately, to date, we don’t have prespecified criteria to clearly diagnose TC in the presence of CAD. Hence, as in our case, we are still dependent on basic clinical skills and have to bank on every aspect of the case to arrive at the correct diagnosis. Certain key pointers, such as recent history of emotional or physical stress, wall-motion abnormalities out of proportion to cardiac enzyme elevation or in territory that cannot be explained by anatomic lesion, and absence of unstable plaque or thrombosis (either angiographically or by intravascular ultrasound) can be very useful.

 Similarly, in our patient, despite the presence of underlying CAD, ST-T wave changes on ECG, and echocardiographic findings of apical ballooning, cardiac catheterization did not reveal a potential culprit lesion, unstable plaque, or thrombosis. The decision was made to withhold any percutaneous intervention since the atherosclerotic lesion was considered to be present chronically and not contributing to acute presentation.

Conclusion. We propose that it is usually difficult to differentiate acute coronary syndrome from TC upon presentation, but the mere presence of significant atherosclerotic coronary lesion on cardiac catheterization should not be construed as primary underlying etiology. Significant CAD and TC may coexist without a direct causal association and a case-by-case evaluation seems more prudent.

References

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From the ¹Department of Internal Medicine, and ²Division of Cardiovascular Medicine, University of Louisville, Louisville, Kentucky.

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.

Manuscript submitted September 12, 2013, provisional acceptance given September 16, 2013, final version accepted September 23, 2013.

Address for correspondence: Sohail Ikram, MD, 401 E Chestnut St, Suite 310, Louisville, KY 40202. Email: s.ikram@louisville.edu