MadSci Network: Medicine

Re: what are signals that induce broken heart syndrome?

Date: Sun Mar 13 18:39:10 2005
Posted By: Jens Peter Bork, M.D., Internal Medicine, Erlangen University Hospital
Area of science: Medicine
ID: 1108853222.Me

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 [1] 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

[1] 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
[2] 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. 
[3] Villareal RP, Achari A, Wilansky S, Wilson JM. Anteroapical stunning
and left ventricular outflow tract obstruction. Mayo Clin Proc 2001;76:79-83.
[4] Brandspiegel HZ, Marinchak RA, Rials SJ, Kowey PR. A broken heart.
Circulation 1998;98:1349-1349.
[5] 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.
[7] 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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