Abstract

First described in 1990 (1), takotsubo cardiomyopathy (TC), known also as “broken heart syndrome” and “stress-induced cardiomyopathy,” remains a perplexing pathophysiologic condition. This transient clinical disorder is classically precipitated by intense emotional stress and manifests with signs and symptoms mimicking acute coronary syndrome in the absence of angiographically evident coronary disease. The echocardiographic sine qua non of TC includes left ventricular (LV) systolic dysfunction with apical ballooning that spontaneously resolves on serial exams over days to weeks. From a mechanistic standpoint, most postulate that TC is the culmination of a “perfect storm,” encompassing an intricate interplay between neurohormonal and/or other physiologic stressors that incite a catecholamine surge in susceptible patients with predisposing cardiovascular risk factors and comorbidities (2, 3). In the current issue of Baylor Proceedings, Ravi and colleagues (4) describe one of the only reported cases of a donor heart with TC successfully used for cardiac transplantation. The donor, a 17-year-old female with no prior cardiac history, suffered brain death following a high-impact motor vehicle collision. A confirmatory coronary angiogram was not performed, but the echocardiographic findings were clearly indicative of TC, including both LV dysfunction and apical ballooning. The authors correctly surmised this was a reversible state and that once removed from the stressful catecholamine milieu of the donor, the heart function would normalize and the recipient would thrive. By the third postoperative day, this newly implanted heart exhibited no signs of TC and the patient had an uneventful course. While the authors should certainly be applauded for their courage and astute clinical judgment in this case, it is unfortunate to note that many, if not most, other transplant centers would likely have declined this donor heart offer. Such widespread reluctance is based largely on the prevalent concern that donor hearts with LV dysfunction will exhibit a greater proclivity for primary graft dysfunction following implantation. Such fears often persist, even when structural heart disease, such as coronary artery disease or valvular abnormalities, has been excluded as an etiologic factor. A number of studies examining outcomes of donor hearts with LV dysfunction would refute the notion that such hearts would have intrinsically worse outcomes (5–7). In a study by Mohamedali and colleagues (5) of 11 potential heart donors with compromised ejection fraction, LV systolic function normalized, regardless of the pattern of abnormalities. Similarly, in a Cleveland Clinic study of 50 donor hearts with >70 echocardiographic abnormalities (6), the vast majority exhibited normalized parameters following transplantation. When examining outcomes of “marginal donor hearts” in the alternative heart transplant program at Duke, we found no increased risk of subsequent graft dysfunction (7). These and other studies suggest that TC may very well be part of the spectrum of so-called neurogenic stress cardiomyopathy, an increasingly acknowledged phenomenon accompanying nearly 50% patients with brain death (8). The salient feature of this clinical entity is its reversibility, i.e., the spontaneous normalization of cardiac function. As such, potential heart donors exhibiting LV dysfunction should not be readily dismissed. Time permitting, serial echocardiographic evaluations should be conducted to document improvement. Conversely, the absence of structural heart disease, as confirmed by coronary angiography and echocardiography, along with the absence of cardiovascular risk factors, may itself justify acceptance for transplantation in many of these scenarios. Given the exponential growth in the number of patients with advanced heart failure and the purported shortage of donor organs, the therapeutic paradigm has increasingly evolved towards mechanical circulatory support to meet the growing demand. However, cardiac transplantation remains the gold standard therapy for these patients, and the oft-reported “shortage” of donor organs may be self-imposed, where clinically unfounded exclusion criteria are rampantly applied, thereby disqualifying many potentially viable donor hearts. In light of the published data, case reports such as this should not represent isolated aberrations in clinical practice, but a growing trend in our collective approach to heart donor selection.

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