Corresponding Author:
Dr. Eduardo J. De Marchena, M.D., F.A.C.C
Division of Cardiology, Department of Medicine, University of Miami
Miller School of Medicine
1400 NW 10th Ave, Dominion Tower, Suite 206A, Miami,
FL 33136
Fax: 205-243-2138; Phone: 305-243-5535
Email:
emarchen@med.miami.edu
Number of Authors: 2
Number of Words: 835
Number of References: 13
Number of Tables/Figures: 0
Data Availability Statement: The data that support the findings
of this study are available from the corresponding author, upon
reasonable request.
Funding Statement: “ Funding: None”
Conflict of Interest Statement: “Conflict of Interest: None”
Institutional Review Board Approval or Waiver: N/A
Informed Consent (or waiver): N/A
Clinical Trial registration : N/A
“Takotsubo cardiomyopathy”, also known as “broken heart syndrome”
and “stress cardiomyopathy” was first identified in the Japanese
population in 1990 as a transient non-ischemic cardiomyopathy
predominantly affecting post-menopausal females [1]. Patients
presented with features similar to an acute myocardial infarction with a
characteristic wall motion abnormality of a hyperkinetic base with
hypokinesis/akinesis and ballooning of the mid–apical segments; the
diagnosis was not confirmed until coronary angiography was performed and
ruled out significant underlying coronary artery disease. This syndrome
was subsequently recognized to have a global presence after a case
series of 19 patients from Baltimore presenting in a similar fashion to
their Asian counterparts was published in the New England Journal of
Medicine [2, 3]. A preceding stressful event in the form of a
physical and/or emotional trigger is commonly associated with this
cardiomyopathy, particularly in certain high-risk patient groups like
post-menopausal women and patients with underlying psychiatric or
neurological disorders [1]. Stress cardiomyopathy likely results
from neuro-cardiogenic stunning through epicardial and/or
micro-circulatory dysfunction after an extreme stressor leads to an
increased spillover of catecholamines and stress-related neuropeptides
in the neuro-cardiac axis [1, 4]. Takotsubo cardiomyopathy still,
however, continues to be an under-diagnosed and poorly understood
disease process.
Physical triggers for this cardiomyopathy can range from acute medical
conditions like a cerebral bleed, sepsis, acute respiratory failure,
pheochromocytoma to patients dealing with stressors in the post-surgical
setting. Takotsubo cardiomyopathy has been previously described in the
literature extensively in association with various intermediate-high
risk non-cardiac surgeries like gastrectomy, head and neck
reconstructive surgery, lung lobectomy, carotid endarterectomy, and
liver transplantation [5-9]. However, other than a few isolated case
reports describing the development of stress cardiomyopathy after mitral
valve replacement, the data is sparse for patients undergoing cardiac
surgery [10-12]. In this issue of the Journal of Cardiac
Surgery , a case-control comparison from a single-center experience by
Kim et al analyzes patients who develop Takotsubo cardiomyopathy
following cardiac surgery retrospectively and identifies factors that
increase the risk of cardiomyopathy through their case-control
comparison. The overall incidence of Takotsubo cardiomyopathy in this
study for all patients undergoing cardiopulmonary bypass is low at 0.9%
(total of 52 cases)— patients undergoing coronary artery bypass
surgery or cardiac transplantation were excluded from this analysis. The
average time to development of this cardiomyopathy was 4-5 days after
surgery and the mean period for myocardial recovery was estimated at 7
months, which is longer than what has been noted in prior literature for
Takotsubo cardiomyopathy [13]. Interestingly, the majority of
patients (approx. 69%) who had developed Takotsubo cardiomyopathy had
undergone mitral valve surgery, which is in line with prior published
case reports. No significant differences in the cardiopulmonary bypass
or aortic cross-clamping times were noted between the cases and the
controls. Further, based on the multivariate analysis, the use of
inotropes or vasopressors was positively associated with the development
of stress cardiomyopathy.
Cardiac surgery can be a source of extreme physical stress for the body
through multiple mechanisms— it can induce systemic inflammation and a
catecholaminergic surge through cardiopulmonary bypass, direct handling
of the myocardial tissue can cause direct toxicity and can also induce
inflammation, patients after cardiac surgery are commonly subjected to
use of multiple inotropes and vasopressors to counteract vasoplegia—it
is surprising that the development of stress or Takotsubo cardiomyopathy
in this setting is not seen more often. It is possible that limited
access to diagnostic modalities in the post-cardiotomy period (limited
electrocardiograms and trans-thoracic echocardiogram windows due to open
chest cavity) leads to underdiagnosis of stress cardiomyopathy in this
patient population.
To conclude, this case-control study will serve as the first step to
help establish the phenomenon of post-cardiotomy Takotsubo syndrome,
however, further research with longer follow-up data and prospective
study design would help address our knowledge gaps in the
pathophysiology of this disease process. Further studies are needed to
investigate the increased predisposition of Takotsubo cardiomyopathy
with mitral valve replacement surgeries compared to other cardiac
surgeries. While no difference in the relative frequencies of mitral
stenosis or mitral regurgitation as the predominant etiology for mitral
valve surgery was noted between the cases and controls in this analysis,
further research is needed to explore if the afterload mismatch in
patients with long-standing or very severe mitral regurgitation
predisposes them to a stress cardiomyopathy syndrome after mitral valve
surgery. The association of catecholamine use (particularly epinephrine
and dobutamine based on the multivariate analysis in this study) with
increased predisposition to post-cardiotomy stress cardiomyopathy also
warrants further research to address if the association is merely
correlational or causative. Finally, the relationship of the extent and
types of cardioprotective strategies with the incidence of post-op
Takotsubo syndrome would also need to be studied.
Management of Takotsubo syndrome is radically different from other
etiologies for cardiogenic shock in the post-op setting— hence, timely
diagnosis of post-cardiotomy Takotsubo syndrome is essential— this
study would help the cardiac intensivists and cardiac surgeons identify
patients at high risk for this phenomenon and aid timely detection and
appropriate management of Takotsubo syndrome in the post-op period.