Download TAKOTSUBO CARDIOMYOPATHY AFTER A POSITIVE

Acta Medica Mediterranea, 2013, 29: 191
TAKOTSUBO CARDIOMYOPATHY AFTER A POSITIVE EMOTIONAL STRESS
GIUSEPPINA NOVO1, EMANUELE GRASSEDONIO2, ANTONIO ROTOLO1, MARIANNA FIORE1, MARINELLA PUGLIESI1, RICCARDO DI
MICELI1, AMBRA LUPO1, SALVATORE GIAMBANCO1, MASSIMO MIDIRI2, SALVATORE NOVO1, PASQUALE ASSENNATO1
1
Chair and Division of Cardiology, University of Palermo - 2Department of Radiology Science, DIBIMEF, University of Palermo
[Cardiomiopatia Takotsubo insorta dopo una forte emozione]
ABSTRACT
Takotsubo cardiomyopathy, also known as transient left ventricular apical ballooning syndrome, is a cardiac syndrome mimicking an acute coronary syndrome and characterized by peculiar transient left ventricular wall motion in the absence of significant
coronary lesions at coronary angiography. The pathogenic mechanisms linking emotional stress to Takotsubo cardiomyopathy still
remain undefined. The onset of Takotsubo cardiomyopathy can be triggered by an acute, intense emotional stress. This is the first
report reporting that not only negative stress but also positive stressful event may precede the syndrome.
Key words: Takotsubo cardiomyopathy, emotional stress, left ventricular dysfunction, coronary syndrome.
Received March 07, 2013; Accepted March 25, 2013
Case report
A 60-year-old female was admitted to our
Department because of sudden onset chest pain
occurring after a surprise party in occurrence of her
birthday. The chest pain was associated with nausea, dizziness and syncope. Her cardiovascular risk
factors were female sex, cigarette smoking, and
dyslipidemia. Upon admission blood pressure was
100/60 mmHg, pulse rate was 60 beats/min, oxygen
saturation (O2 sat) was of 99%, blood glucose was
107mg/dl and glomerular filtration rate was of 134
ml/min/1,73mq. ECG showed sinus rhythm, firstdegree atrioventricular (AV) block, negative T
waves from V3 to V6 and in leads I, aVL, II, aVF.
Echocardiography revealed apical and mid segments akinesis with basal segments hypekinesis and
severely reduced left ventricular systolic (EF 25%)
(fig 1). Patient underwent coronary angiography
that showed arteries free of stenosis. Left ventriculography confirmed the characteristic morphology
of apical ballooning (fig 2). Laboratory analysis
showed a peak serum Troponin T level of 4,198
pg/dl disproportionate in relation to the extension of
wall motion abnormalities. Diagnosis of Takotsubo
Figure 1: Echocardiographic image showing apical and
mid segments akinesis with basal segments hypekinesis
and severely reduced left ventricular systolic activity (EF
25%).
Cardiomyophaty (TCM) was made according
to the Mayo Clinic 2008 criteria (1). Moreover a
gadolinium-enhanced cardiovascular magnetic resonance (CMR) at 1,5 Tesla was performed. The
scans evaluated myocardial morphology, function,
and late gadolinium enhancement (LGE) images
were adquired. The CMR showed midventricular
and apical LV dysfunction, absence of edema,
necrosis and fibrosis. All these data confirmed the
diagnosis of Takotsubo cardiomyopathy. The
patient was treated with beta blocker, diuretic,
statin, enoxaparin and aspirin.
192
At one months follow up echocardiography
was repeated and showed normalization of systolic
function (EF 55%) and wall motion normalities.
Figure 2: Ventriculography, systolic frame showing a
typical apical balooning with apical and mid segments
akinesia (panel 2 A) and diastolic frame (panel 2B).
Discussion
TCM is an increasingly recognized clinical
syndrome characterized by acute reversible ventricular dysfunction. It classically presents with signs
and symptoms similar to those of an acute coronary
syndrome (ACS), and the onset of symptoms are
usually triggered by an intense emotional or physical stress.
Diagnostic criteria proposed by researchers at
the Mayo Clinic are:
• transient hypokinesis, akinesis, or dyskinesis
in the left ventricular mid segments with or without
apical involvement; regional wall motion abnormalities that extend beyond a single epicardial vascular
distribution; and frequently, but not always, a
stressful trigger;
• the absence of obstructive coronary disease
or angiographic evidence of acute plaque rupture;
• new ECG abnormalities (ST-segment elevation and/or T-wave inversion) or modest elevation
in cardiac troponin;
• the absence of pheochromocytoma and
myocarditis(1).
Although the exact cause of the syndrome
remains unknown, many underlying mechanisms
have been proposed including diffuse epicardial
arteries spasm, coronary microcirculation dysfunction, catecholamines-induced myocardial dysfunction, and neurologically-mediated myocardial stunning(2,3). The most convincing hypothesis are the last
two. In fact emotional and physical stress can
induce an excitation of the limbic system.
Amygdalus and hippocampus are, with the insula
G. Novo, E. Grassedonio et Al
the principle brain areas, implicated in emotion and
memory. These areas play a central role in the control of cardiovascular function(4).
Their excitation provokes the stimulation of
the medullary autonomic center, and then the excitation of pre and post-synaptic neurons leading to
the liberation of norepinephrine and its neuronal
metabolites. Adrenomedullary hormonal outflows
increase simultaneously and induce the liberation of
epinephrine. Epinephrine and norepinephrine reach
heart and blood vessel adrenoreceptors. The occupation of the B2 adrenoreceptors induces catecholamine toxicity in the cardiomyocytes. In fact
intense activation of beta(2)-adrenoceptors (B2AR)
by epinephrine trigger a switch in intracellular signal trafficking, from G(s) protein to G(i) protein.
This signaling protects against the pro-apoptotic
effects of B2AR stimulation but cause inotropic
effects. The apex is more responsive to catecholamine toxicity because of the higher density of
B2AR. Stimulation of sympathetic nervous termination, more represented at basal level, favor basal
segments hyperkinesis(5-7).
Several emotional or physical stressors such as
an unexpected death in the family, abuse, a quarrel,
acute diarrhea, and other precipitant stressors not
yet identified, may lead to the occurrence TCM(8,5).
According to our knowledge this is the first report
suggesting that the occurrence of TCM can be
related to negative physical or emotional stress, but
also to a sudden positive stress.
There are no specific guidelines for TCM
treatment because cardiac function is normalized
within a few weeks. The treatment of TCM remains
empirical(9,10). In the acute phase, therapy must be
individualized depending on hemodynamic situation. In stable conditions, it appears advantageous
to prevent excessive sympathetic activation by
combining alpha and beta blockade. Beta blockers
are used to treat dynamic left ventricular obstruction.
Conclusion
TCM is a cardiac syndrome usually triggered
by a negative acute physical or emotional stress.
This is the first case reporting the occurrence of
TCM after a positive emotional event.
Takotsubo cardiomyopathy after a positive emotional stress
193
References
1)
2)
3)
4)
5)
6)
7)
8)
9)
10)
Prasad A, Lerman A, Rihal CS. Apical ballooning syndrome (Tako-Tsubo or stress cardiomyopathy): a mimic
of acute myocardial infarction. Am Heart J 2008; 155:
408-417.
Fazio G, Sarullo FM, Novo G, Evola S, Lunetta M,
Barbaro G, Sconci F, Azzarelli S, Akashi Y, Fedele F,
Novo S. Tako-tsubo cardiomyopathy and microcirculation. J Clin Monit Comput 2010; 24: 101-105.
Novo S, Akashi Y, Arbustini E, Assennato P, Azzarelli
S, Barbaro G, Fazio G, Fedele F, Giordan M,
Mazzarotto P, Modena MG, Novo G, Parodi G,
Previtali M, Rapezzi C, Sconci F, Sganzerla P, Tona F,
Salerno-Uriarte JA. Takotsubo cardiomyopathy: a consensus document. G Ital Cardiol 2008; 9: 785-797.
Akashi YJ, Goldstein DS, Barbaro G, Ueyama T.
Takotsubo cardiomyopathy: a new form of acute,
reversible heart failure. Circulation 2008; 118: 27542762.
Tsuchihashi K, Ueshima K, Uchida T, Oh-mura N,
Kimura K, Owa M, Yoshiyama M, Miyazaki S, Haze
K, Ogawa H, Honda T, Hase M, Kai R, Morii I.
Transient left ventricular apical ballooning without
coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. Angina PectorisMyocardial Infarction Investigations in Japan. J Am
Coll Cardiol 2001; 38: 11-18.
Lyon AR, Rees PS, Prasad S, Poole-Wilson PA,
Harding SE. Stress (Takotsubo) cardiomyopathy--a
novel pathophysiological hypothesis to explain catecholamine-induced acute myocardial stunning. Nat
Clin Pract Cardiovasc Med 2008; 5: 22-29.
Paur H, Wright PT, Sikkel MB, Tranter MH, Mansfield
C, O'Gara P, Stuckey DJ, Nikolaev VO, Diakonov I,
Pannell L, Gong H, Sun H, Peters NS, Petrou M, Zheng
Z, Gorelik J, Lyon AR, Harding SE. High Levels of
Circulating
Epinephrine
Trigger
Apical
Cardiodepression in a β2-Adrenergic Receptor/GiDependent Manner: A New Model of Takotsubo
Cardiomyopathy. Circulation 2012; 126: 697-706.
Novo G, Ferro G, Fazio G, Coppola G, Ciaramitaro G,
Farinella M, Rotolo A, Caruso M, Ferrandes M,
Hoffmann E, Assennato P, Novo S. Takotsubo cardiomiopathy after acute diarrhea. Intern Med 2010; 49:
903-905.
Fazio G, Novo G, Barbaro G, Sutera L, Azzarelli S,
Palecek T, Di Gesaro G, Akashi Y, Novo S. Treatment
of Tako-tsubo cardiomyopathy. Int J Cardiol 2008; 129:
272-273.
Fazio G, Pizzuto C, Barbaro G, Sutera L, Incalcaterra
E, Evola G, Azzarelli S, Palecek T, Di Gesaro G,
Cascio C, Novo G, Akashi YJ, Novo S. Int J Cardiol.
Chronic pharmacological treatment in takotsubo cardiomyopathy 2008; 127: 121-123.
_________
Request reprints from:
Marianna Fiore
Via B. Ricasoli 1,
91022 Castelvetrano (TP)
(Italy)