Tako-tsubo cardiomyopathy
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Mr. Nine
Dec 15, 2009, 11:47:53 PM12/15/09
to Myanmar Journal of Surgery
Tako-tsubo cardiomyopathy is a potentially lifethreatening cardiac
syndrome characterized by transient left ventricular dysfunction,
without angiographically significant coronary artery stenosis. The
disease takes its name from the typical left apical ballooning
observed on end systolic left ventriculogram, which has the appearance
of a Tako-Tsubo, a term for an ancient device used in Japan to trap
octopuses in the sea. Other names, stress cardiomyopathy, tako-tsubo
cardiomyopathy, left ventricular apical ballooning syndrome, and
broken heart syndrome
are used interchangeably.
It is estimated that about 2% of patients presenting with suspected
acute coronary syndromes may actually have TTC.
Although initially reported only in Japan, it has been reported in
patients with diverse ethnic background from all over the world.
Clinical Features
The clinical presentation is identical to that of acute coronary
syndromes. The most frequent presentation is chest pain (66%),
followed by dyspnea (16%). Most patients have no prior cardiac
history. The trigger factor is an emotional
or physical stressor in 70% of cases.
Pathophysiology
Several mechanisms have been proposed to explain the underlying
pathophysiology of this syndrome. These include an acute and excessive
rise of catecholamine levels, calcium overload with direct myocyte
damage, estrogen depletion, multiple vessel epicardial coronary spasm
or diffuse microvascular spasm. Increased sympathetic tone with
elevated levels of plasma catecholamines and stress neuropeptides may
play an important role in the pathogenesis of myocardial stunning
following emotional and physical stress. Reduction of estrogen levels
may explain the high incidence of TTC in postmenopausal females.
Diagnosis
Electrocardiography (ECG) can be normal, or can have nonspecific ST-
and T-wave abnormalities. The most common ECG abnormality (in 70% of
cases) is ST-segment elevation in the anterior precordial leads.
Most patients with TTC have mildly elevated cardiac enzymes (including
creatine phosphokinase, Troponin I, and T levels) at the time of
presentation. These enzyme elevations, however, are much lower than
those typically observed with acute myocardial infarction.
The most specific diagnostic feature of this syndrome is the unusual
left ventricular contractile pattern in the absence of significant
coronary artery disease. The left ventriculogram frequently shows
akinesis or dyskinesis of the apical and midventricular segments with
hyperkinesis of the basal segments.
Treatment
The treatment of TTC is generally supportive in nature. The standard
supportive care for congestive heart failure with diuretics and
vasodilators remains largely empirical. For hemodynamically stable
patients, diuretics are
used to treat pulmonary congestion, and Angiotensin-converting enzyme
(ACE) inhibitors and beta-blockers are frequently used during the
period of LV recovery. Beta-adrenergic blockers are also useful in
suppressing ventricular arrhythmia. There is no consensus on how long
to continue these medications; it is probably safe to
stop them once LV function has completely recovered.
For hemodynamically unstable patients, the treatment includes
inotropic therapy, vasopressor support, and intra-aortic balloon
counterpulsation. Recent data implicate massive catecholamine release
as the pathogenesis of stress-induced myocardial stunning. Therefore,
it has been recommended to avoid the administration of exogenous
catecholamines and beta-agonists whenever possible and to rely on
mechanical circulatory support, e.g., intra-aortic balloon
counterpulsation.
Prognosis
In most patients, the left ventricular function returns to normal
within two weeks. The ECG abnormalities usually disappear completely
within six months. Complications like shock, followed by heart
failure, LV thrombus formation, dynamic LV outflow tract obstruction,
acute mitral valve regurgitation, and ventricular arrhythmias are seen
in 18% of cases.
Recurrence rate is only 3.5%.
Conclusion
Tako-tsubo cardiomyopathy (TTC) is an increasingly recognized
diagnosis. Its clinical presentation mimics the presentation of acute
STelevation myocardial infarction without concomitant epicardial
coronary artery disease.
Despite the initial dramatic presentation of this disease the
prognosis is quite favourable.
syndrome characterized by transient left ventricular dysfunction,
without angiographically significant coronary artery stenosis. The
disease takes its name from the typical left apical ballooning
observed on end systolic left ventriculogram, which has the appearance
of a Tako-Tsubo, a term for an ancient device used in Japan to trap
octopuses in the sea. Other names, stress cardiomyopathy, tako-tsubo
cardiomyopathy, left ventricular apical ballooning syndrome, and
broken heart syndrome
are used interchangeably.
It is estimated that about 2% of patients presenting with suspected
acute coronary syndromes may actually have TTC.
Although initially reported only in Japan, it has been reported in
patients with diverse ethnic background from all over the world.
Clinical Features
The clinical presentation is identical to that of acute coronary
syndromes. The most frequent presentation is chest pain (66%),
followed by dyspnea (16%). Most patients have no prior cardiac
history. The trigger factor is an emotional
or physical stressor in 70% of cases.
Pathophysiology
Several mechanisms have been proposed to explain the underlying
pathophysiology of this syndrome. These include an acute and excessive
rise of catecholamine levels, calcium overload with direct myocyte
damage, estrogen depletion, multiple vessel epicardial coronary spasm
or diffuse microvascular spasm. Increased sympathetic tone with
elevated levels of plasma catecholamines and stress neuropeptides may
play an important role in the pathogenesis of myocardial stunning
following emotional and physical stress. Reduction of estrogen levels
may explain the high incidence of TTC in postmenopausal females.
Diagnosis
Electrocardiography (ECG) can be normal, or can have nonspecific ST-
and T-wave abnormalities. The most common ECG abnormality (in 70% of
cases) is ST-segment elevation in the anterior precordial leads.
Most patients with TTC have mildly elevated cardiac enzymes (including
creatine phosphokinase, Troponin I, and T levels) at the time of
presentation. These enzyme elevations, however, are much lower than
those typically observed with acute myocardial infarction.
The most specific diagnostic feature of this syndrome is the unusual
left ventricular contractile pattern in the absence of significant
coronary artery disease. The left ventriculogram frequently shows
akinesis or dyskinesis of the apical and midventricular segments with
hyperkinesis of the basal segments.
Treatment
The treatment of TTC is generally supportive in nature. The standard
supportive care for congestive heart failure with diuretics and
vasodilators remains largely empirical. For hemodynamically stable
patients, diuretics are
used to treat pulmonary congestion, and Angiotensin-converting enzyme
(ACE) inhibitors and beta-blockers are frequently used during the
period of LV recovery. Beta-adrenergic blockers are also useful in
suppressing ventricular arrhythmia. There is no consensus on how long
to continue these medications; it is probably safe to
stop them once LV function has completely recovered.
For hemodynamically unstable patients, the treatment includes
inotropic therapy, vasopressor support, and intra-aortic balloon
counterpulsation. Recent data implicate massive catecholamine release
as the pathogenesis of stress-induced myocardial stunning. Therefore,
it has been recommended to avoid the administration of exogenous
catecholamines and beta-agonists whenever possible and to rely on
mechanical circulatory support, e.g., intra-aortic balloon
counterpulsation.
Prognosis
In most patients, the left ventricular function returns to normal
within two weeks. The ECG abnormalities usually disappear completely
within six months. Complications like shock, followed by heart
failure, LV thrombus formation, dynamic LV outflow tract obstruction,
acute mitral valve regurgitation, and ventricular arrhythmias are seen
in 18% of cases.
Recurrence rate is only 3.5%.
Conclusion
Tako-tsubo cardiomyopathy (TTC) is an increasingly recognized
diagnosis. Its clinical presentation mimics the presentation of acute
STelevation myocardial infarction without concomitant epicardial
coronary artery disease.
Despite the initial dramatic presentation of this disease the
prognosis is quite favourable.
အာကာ လြင္
Dec 16, 2009, 12:33:28 AM12/16/09
to mjsu...@googlegroups.com
plse reply me , what are the difference between acute coronary syndrome and Tako-tsubo cardiomyopathy?
.,why is it called life threatening cardiac syndrome ?
,if ECG shows normal, what is the most significant investigation to diagnose this disease?
,Is this disease related with hereditary factors and genetic factors?
,Is it more common in male or female / what decade is it more common occuring in ?
--
စိတ္က်န္းမာခ်မ္းသာၾကပါေစ။
ေလးစားစြာျဖင္႕
အာကာ( Kaungkinsky)
.,why is it called life threatening cardiac syndrome ?
,if ECG shows normal, what is the most significant investigation to diagnose this disease?
,Is this disease related with hereditary factors and genetic factors?
,Is it more common in male or female / what decade is it more common occuring in ?
--
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စိတ္က်န္းမာခ်မ္းသာၾကပါေစ။
ေလးစားစြာျဖင္႕
အာကာ( Kaungkinsky)
mr. pearl
Dec 16, 2009, 2:09:14 AM12/16/09
to mjsu...@googlegroups.com
it is a very interesting topic as we haven't heard it before
thank for yr sharing
as usual, plz fufil my curiosity
wishing u able to present more!!!
thank for yr sharing
as usual, plz fufil my curiosity
- firstly,how do u think, is it more common in patient with pheochromocytoma(in which high level of catecholamines) or not?
- secondly,what are the physical stressors? do u mean extreme noise or intense light?
- thirdly,are all kinds of catecholamines involved ?(if not,which one is the dominant agent)
- and finally,in case of haemodynamically unstable patient,what kind of inotropic should we use?(as in broken heart syndrome,digoxin can't be used as it can rise Ca+level)
wishing u able to present more!!!
On Wed, Dec 16, 2009 at 7:47 AM, Mr. Nine <medica...@gmail.com> wrote:
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