Broken heart syndrome pdf
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Transcript of Broken heart syndrome pdf
Presenter :- DR.Rajesh M. Dandale Università degli Studi di Verona
A 64 year-old post-menopausal female presented with
sudden onset of chest discomfort which started after
she experienced severe emotional stress. She was
transported to Department of Cardiology by Emergency
Service. The pain resolved with administration of
sublingual nitroglycerin during transportation .
She was dyslipidemic, non diabetic, non HTN, no P/H
of MI.
No history of similar episodes in other family
members.
Initial electrocardiogram revealed sinus bradycardia with
diffuse ST – segement elevation, QRS and and QT interval
prolongation.
CK-MB -13,5 ug/L. Troponin I- 1.02 ug/L (ULN: <0.5).
Chest X-ray: WNL
Akinetic apical and anteroseptal wall with reduction in EF. Minimal MR
1. Acute coronary syndrome?
2. Aborted myocardial infarction? (no detectable
myocardial injury)
3. Myocarditis?
4. Myocardial dysfunction?
5. Apical ballooning syndrome?
In hospital day 4,ECG and cardiac biomarker normalized,
TTE after 7 days show no RWM abnormality and EF-60%
Patient was discharged from hospital with healthy condition,
advised for regular follow up.
Tako-Tsubo cardiomyopathy
Apical ballooning syndrome
Stress cardiomyopathy
Ampulla cardiomyopathy
Neurological cardiomyopathy (stunning)
Broken heart syndromeInt J Cardiol 2007;116:405
Synonyms for same clinical syndrome
Cardiac Syndrome – defined as presence of transient left ventricular apical ballooning after ACS in patients with angiographically normal coronary arteries. Iga reported first case. Described in 1990 by Sito et al, as Tako-Tsubo cardiomyopathy.
Named after the octopus trapping pot with a round bottom and narrow neck, which resembles the end systolic left ventriculogramin these patients.
Sporadic cases found around world.
In 2006 , the American Heart association included ABS into its classification of cardiomyopathy as a primary acquired cardiomyopathy.
Circ.2006;113:1807-16.
1-2% of ACS / MI
AHA-732.000 hospital discharges with diagnosis of
AMI /year so annual rate of ABS may be 7.000-14.000
cases.
Worldwide, the incidence of ABS appeared to be on
the rise- recent advances in the work-up of patients with
chest pain.
Am Heart J 2008;155:408-17.
Circulation 2008;118:2754-2762.
Postmenopausal women
88.8% (Gianni et al.14 major studies involving
286 patients), mean age 58-75 yrs- suggest
hormonal predisposition -further investigation to
find out potential mechanisms
Underlying hormonal predisposition-research
Genetic contribution- ( Pison et al. 2 middle-
aged sisters involvement)
Cardiovasc Drug Ther 2008;22:71-77
Eur Heart J 2006;27:1523-9
Chest pain at rest- 50-60%
Dyspnea
Pulmonary edema
Ischemic changes on ECG- diffuse T-wave inversion and
QT prolongation( myocardial stunning)
Elevated cardiac biomarkers
Hypotension
2/3 presented after emotional/physical stressful condition
(“broken heart” syndrom)
Am Heart J 2008;155:408-17.
MC- ST-segment elevation-mimicking STEMI
Typically in precordial leads, but it maybe seen in the
inferior and lateral leads. Non-specific T-wave abnormality,
new bundle branch block and in some cases ECG may be
normal at presentation.
Resolution of ST-segment elevation, development of diffuse
and often deep T-wave inversion that involves most leads.
Resolution occur within 4-6 weeks
Am Heart J 2008;155:408-17
Am. Heart J 2008;155:408-17
Coronary angiography- normal coronary arteries /mild atherosclerosis,
Left ventriculography- hypokinesia, akinesia or even dyskinesia of the mid and or apical segment of LV.
TTE-RW abnormality is beyond the distribution of single coronary artery (30% right ventricle shows similar RWA)
Magnetic resonance- extent of the RWM abnormality and differentiating myocardial infarction and myocarditis.
Circulation . 2008;118:2754-2762.
Classical situation:- a postmenopausal woman
In intensive care unit:-
Mayo clinic criteria-1. Transient hypokinesis, akinesis, or dyskinesis of the left ventricular mid
segments with or without apical involvement; the regional wall motion abnormalities extend beyond a single epicardial vascular distribution; a stressful trigger is often, but not always present.
2. Absence of obstructive coronary disease or angiographic evidence of acute plaque rupture.
3. New electrocardiographic abnormalities (either ST-segment elevation and/or T-wave inversion) or modest elevation in cardiac troponin.
4. Absence of: Pheochromocytoma Myocarditis
American Heart Journal Volume 155, Isssue3, March 2008,408-417
Emotional or physical stress
Sepsis-pathogen induced pro-inflammatory immune response
Critical illness
Subarachnoid hemorrage
Fig. from Am. Heart J 2008;155:408-17
Rare cases precipitated by
1. Hypoglycemia
2. Hyperthyroidism
3. Cocaine
4. Alcohol withdrawal
5. Pneumothorax
6. Subdural hematoma
All these associated with increased sympathetic drive.
Heterogeneous condition, which lacks a disease specific
etiology.
Catecholamine –mediated toxicity- increases in sympathetic
tone following a stressful event and could result in direct
cardio toxicity.
Multi-vessel epicardial coronary artery spasm
Microvascular dysfunction
Spontaneous aborted myocardial infarction
Cardiovasc Drugs Ther 2008; 22:71-77
Myocarditis
A lack of supporting histological and microbiological evidence
Mild interstitial fibrosis and limited mononuclear cellular
infiltration- ABS
Gadolinium-enhanced MRI studies failed to detect regional T2
enhancement, indicating inflammation and necrosis seen in
myocarditis
JACC, 2003;41:737-42.
Elevated circulating catecholamine-( Wittstein et al. 13 ABS and 7 MI),
1) levels remained dramatically raised even after cardiac function was
restored. 2) not every patient with ABS shows elevated catecholamine. 3)
all patients had suffered emotional stress prior to the cardiac event.
Kurisu et al.`s (30pt) six had normal serum nonadrenaline
One review mention 74.3% had elevated nonadrenaline
Disease affecting catecholamine levels (pheocromocytona, subarachnoid
hemorrage) can cause reversible LV dysfunction.
Sepsis and respiratory faillure- increase sympathetic
Anaphalaxis –histamine- adrenal medulla-catecholamine
Wealth of evidence point towards a pathogenic role for catecholamine in
ABS though exact nature remain unclear.
Cardiovasc Drugs Ther 2008;22:71-77Elevated catecholamine levels in ABS is a result of the disease process or is it the cause ???????????
Based on the 201Tl images, myocardial perfusion did not seem to be severely impaired even in
the acute phase, whereas fatty acid metabolism was profoundly depressed in the apical
myocardium in parallel with myocardial contraction abnormalities. The defective uptake seen on
both BMIPP and 201Tl improved within 3 weeks. However, the MIBG images showed that
sympathetic denervation persisted for 1 year after onset, which suggests that the primary cause of
AB cardiomyopathy is a disturbance of the cardiac sympathetic innervations.
Owa et al. serial SPECT scan
Functional sympathetic innervations- 123 I-MIBG
Fatty acid metabolism(C function)- 123 I- BMIPP
Myocardial perfusion- 201 Thallium scan
Sympathetic dysfunction and transiently disturbed cardiac function in the presence of normal
perfusion.
Jpn Circ J 2002;66:712-3.
Contraction-band necrosis is the classic histological finding in
catecholamine excess induced cardiovascular injury; seen in
pheochromocytoma and subarachnoid hemorrhage,
Only one patient of TTS studied by Wittstein et al.
Recently published Inverted TT syndrome case report -shows same
findings
Akashi et al. 7/ 5 biopsies -fatty infiltration-1;mild interstitial fibrosis-1;
small num of mononuclear cells (chronic myocarditis)-2; last patient
shows only adipose tissue
Int. Journal of cardiology 2010 Vol.8:no. 1
TCM: Pathological Insight from a
fatal case
Triphenyl tetrazolium chloride staining
Very strong C4d staining along the microvasculature and in the rare myocytes
with contraction band suggest that there was recent activation of the
complement cascade which is likely secondary to subendocardial ischemia due
to catecholamine surge.
C4d staining of a right ventricular endomyocardial biopsy may be used as
diagnostic tool to better predict the presence of injury??
The Int. Journal of Cardiology vol.8.
Positive C4d staining
Central hypothesis is challenged by the gender discrepancy.
If this is the predominant mechanism, one would expect a similar
incidence in men and women.
In fact, males have a greater adrenergic response to mental stress.
In women, estrogen plays a protective role on the vascular bed from the
adverse effects of catecholamine surge.
So relative deficiency of estrogen after menopause may predispose them to
ABS
A possible animal model of a
‘Tako-Tsubo’ cardiomyopathyUeyama et al.
• Characteristic LV apical ballooning in 8/10 rat subjected to the stress of
remaining immobilized on their back for 30 mins.
• Pre-administration of alfa/beta blockers (but no CCB/NTG), averted
anticipated ventricular dysfunction.
• Anatomical variation in (high) apical adrenergic receptor density may
explain the largely apical involvement.
• Basal myocardium has a somewhat higher norepinephrine content and
greater density of sympathetic nerves than apical.
Circ J 2002; 66: 712–713.
Adrenergic receptor activation is central to the etiology of ABS
The available pathophysiological information indicates that the
apical ballooning syndrome is result of toxic high local
concentration of catecholamine, not coronary artery or microvascular
disease.
Individual differences in the anatomy of cardiac sympathetic
innervation or the distributions of adrenoceptors might result in the
involvement of a variety of left ventricular myocardial segments.
In typical ballooning , high conc. of norepinephrine might evoke
basal hyperkinesia.
Elevated catecholamine level and adrenergic receptor
hypersensitivity is most accepted theory
In absence of significant comorbidities, prognosis is good.
The systolic dysfunction and RWM abnormalities are
transient and resolve completely within days to few weeks
(4-8 week). This is such a uniform finding.
In hospital mortality is very low (1-2%)
Long term survival is similar to that of the general age-
matched population.
Rate of recurrence is not > 10%
Complications are heart failure, ventricular arrhythmias,
LV free wall rupture, mural thrombus formation
JACC 2007; 50:448-52
Presumed to be suffering from an acute coronary syndrome and immediate
appropriate management should follow.
Aspirin, B-blockers and diuretics
Short term anticoagulation to prevent mural thrombus is indicated
B-blocker continued indefinitely due to the chance of a late recurrence
Due to prolonged QT interval leads to arrhythmia- VT- magnesium sulfate (if
cQT>600mSec)
Estrogen treatment – animal model
No specific treatment for left ventricular failure- cardiac function normalized within few weeks.
B-blockers (Sotalol) prolongs QT interval, potentiate adverse effect of high conc. of catecholamine at alfa receptors
ABS has high risk of cardiac rupture, it is still controversial whether to treat with aspirin /heparin
Ann Intern Med 2004;141:858-5
Circulation 2005; 111:388-90
A very small proportion of the population appears to be at
risk for ABS, suggesting a role for genetic predisposition
Whether estrogen replacement therapy will help to reduce
incidence and recurrence of ABS
Investigate the distribution of the adrenergic receptor that
may explain the segmental involvement
Only 30% of cases involve right ventricle
The recurrence rate is low despite the repeated exposure to
stressful events over lifetime
Need to establish a registry for ABS to investigate natural
history and to conduct randomized trials
Take home message
• ABS is not a rare entity. Represents 1-2 % of ACS.
• Prognosis is good, complete recovery within days to weeks, < 10% recurrence.
• Initial management should be directed towards the treatment of MI with continuous ECG monitoring, administration of aspirin, heparin and B-blockers. Consider diuretics and ACE-inhibitors in patients presenting with heart failure .
• Confirmation of diagnosis- particularly important if fibrinolytic therapy is being consider for presumed diagnosis of STEMI.
• Free wall rupture, severe MR, ventricular arrhythmia are rare but fatal complications.
• In the absence of contraindication, chronic B-blocker therapy will aim to reducing likelihood of a recurrent episodes.
• On the basis of rat immobilization model, supplementation of
estrogen in postmenopausal women might be protective.
• Annual clinical follow-up is advisable as natural history of
ABS remains unknown.
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