|MadSci Network: Medicine|
Dear EC, thank you for your question regarding the „broken heart syndrome“, which – judging from a result of a Google search – created quite a lot of media attention in the United States. The attention results from the fact that in a recent publication  in the New England Journal of Medicine (NEJM), one of the top medical publications in the world, doctors from Johns Hopkins University were the first to demonstrate that not only is there a demonstrable decline in cardiac function in some people under severe emotional stress (this had already been documented in earlier publications, see [2-7]); they could also show one possibility how the syndrome might be caused. So, if you want to know the exact technical answer to your question, go to your University’s library and read the article. Meanwhile, I’ll summarize it for you: First, the number of patients was small (19; all female, most around 60). Also, this was not a rigorous study with a formal protocol predefining inclusion/exclusion criteria or specifying procedures in advance. This means that the results of the investigation have to be taken with a grain of salt or two: The investigation was a done with a somewhat unclear problem in mind („there’s this thing about emotional stress weakening the heart and mimicking acute coronary syndrome. Shouldn’t we look a little closer at these patients to see what it’s all about?”), and the authors report what they found when they took a good, close look (this is called an observational study). Their study generated a sound, workable hypothesis but is by no means a definitive study on the problem, only a good (quite good, in fact) start. All patients were evaluated with an array of modern imaging techniques: coronary angiography, serial echocardiography, and some also with nuclide ventricular imaging, cardiac MRI and a biopsy from the heart muscle. Not every pt. received every investigation, but then again, it was not a formal study: In principle, patient care dictated what investigations a patient should receive, not a study protocol. What is new about this study (and thus might merit the publication in such a prominent journal) was the fact that there was an investigation into the levels of several stress-related hormones: Catecholamines (e.g., adrenaline and noradrenaline) and their metabolites, and neuropeptide Y. Brain natriuretic peptide (BNP) was also investigated as an indirect measure of cardiac failure. The remarkable result was that in all patients there was clear evidence of myocardial damage in the ECG. Moreover, the various imaging techniques, especially echocardiography, confirmed this, showing that the heart as a whole pumped with sharply reduced strength; that in some patients some regions of the heart did not contract as well as others; and that the areas of the heart showing the least contraction were similar in all patients. The clinical picture was sometimes severe - One patient even survived a cardiac arrest, and two had to be supported with an aortic balloon pump to maintain adequate blood pressure. In some of the patients, biopsies of the cardiac muscle were taken showing an inflammatory infiltrate, but only one of them had evidence of some, if little, muscle cell necrosis. Importantly, virtually all these changes were fully reversible on repeat examinations over a short period (last follow-up was 21 days after hospital admission), and there was never any evidence of gross myocardial necrosis – the heart muscle was severely damaged and weakened, but not killed. It fits well into this picture that none of the patients except one had evidence of significant coronary arteriosclerosis on coronary angiography. What the authors had shown at this point was that emotional stress can cause very real, tangible damage to the heart which follows a certain clinical pattern and which is fully reversible after only a short time. But you were asking for mechanisms... The most important part was the assessment of catecholamine levels – they were shown to be increased several-fold, and it is likely they were responsible for the myocardial damage. The authors posit three possible mechanisms: Spasm of the large coronary arteries resulting in diminished, but non-lethal oxygen supply to the muscle cells; spasm occurring in the small vessels; and direct damage to the cells, e.g. by local production of free radicals or intracellular calcium overload. All these effects have previously been documented in different circumstances. Which of these processes is predominant in causing the „new“ syndrome – termed stress cardiomyopathy (Greek for „ailment of the heart muscle“) is unclear. The authors close their paper with a sentence you could put under most good scientific papers, „.... a more complete understanding of [...] this syndrome awaits further research“. How true! Sincerely yours, Jens Peter Bork References:  Wittstein I. S., Thiemann D. R., Lima J. A.C., Baughman K. L., Schulman S. P., Gerstenblith G., Wu K. C., Rade J. J., Bivalacqua T. J., Champion H. C.: Neurohumoral Features of Myocardial Stunning Due to Sudden Emotional Stress. N Engl J Med 2005; 352:539-548  Kawai S, Suzuki H, Yamaguchi H, et al. Ampulla cardiomyopathy (`Takotsubo' cardiomyopathy) -- reversible left ventricular dysfunction: with ST segment elevation. Jpn Circ J 2000;64:156-159.  Villareal RP, Achari A, Wilansky S, Wilson JM. Anteroapical stunning and left ventricular outflow tract obstruction. Mayo Clin Proc 2001;76:79-83.  Brandspiegel HZ, Marinchak RA, Rials SJ, Kowey PR. A broken heart. Circulation 1998;98:1349-1349.  Tsuchihashi K, Ueshima K, Uchida T, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. J Am Coll Cardiol 2001;38:11-18.  Kurisu S, Sato H, Kawagoe T, et al. Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction. Am Heart J 2002;143:448-455.
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