Takotsubo cardiomyopathy, also known as stress-induced cardiomyopathy or broken heart syndrome, is a type of temporary heart muscle dysfunction typically affecting postmenopausal women. It is often triggered by stressful events and presents similarly to a heart attack, with chest pain and elevated cardiac biomarkers. However, coronary angiography shows no blockages. The condition is caused by excessive sympathetic stimulation leading to myocardial stunning and dysfunction, particularly of the left ventricular apex. Most patients recover normal heart function within weeks with treatment focused on complications. While in-hospital mortality is similar to heart attacks, long-term prognosis is generally favorable though recurrences are possible.

1. TAKOTSUBOCARDIOMYOPATHY
Dr. Nurul Islam
Thesis part student, MD cardiology.
NHFH&RI

2. • First described in 1990 in Japan.
• Initially thought rare or specific to Japanese.
• In 2006, recognized as Primary Acquired Cardiomyopathy by American Heart
Association.
• Most are postmenopausal women (Mean age 66-80).

3. Theclassicfindingofapicalballooningwithpreservedbasalleftventricularsystolic
functionhasasimilarappearancetotheJapaneseoctopustrapofthesamename.

4. Also knownas-
• Broken Heart Syndrome
• Stress induced Cardiomyopathy
• Stress induced Myocardial Stunning
• Adrenergic Cardiomyopathy
• Neurogenic Stress Syndrome
• Ampulla Cardiomyopathy
• Apical Ballooning Syndrome
• Transient Cardiac Ballooning
• Artichoke Heart

5. Clinical Presentation:
• Indistinguishable from Acute Coronary Syndrome (ACS)
Chest Pain & Dyspnea
Elevated cardiac biomarkers
ECG changes
• Often stressful triggering event.
• Urgent CAG is required for a definitive diagnosis-ABSENCE of coronary
lesion.

6. Pathophysiology:
• Excessive sympathetic stimulation leads to myocardial stunning.
• Serum catecholamine levels are 2-3 times greater in TCM than MI .
• Similar left ventricular dysfunction has been described in the setting of
exogenous catecholamine use and other states of excess endogenous
catecholamine production such as pheochromocytoma.
• Takotsubo cardiomyopathy is also associated with coronary vasomotor
dysfunction at the epicardial and microvascular level with increased
vasoconstriction resulting in vasospasm and transient myocardial ischemia.

7. Cont.
• Additionally, systemic response to catecholamine surges includes
peripheral vasoconstriction resulting in an acute increase in left
ventricular afterload, which may further contribute to left ventricular
systolic dysfunction.
• The apex of the left ventricle has a higher proportion of β-adrenergic
receptors, which may account for the typical vulnerability of the left
ventricular apex to stress cardiomyopathy.
• Myocardial biopsies show direct catecholamine toxicity (contraction band
necrosis, inflammatory cell infiltration, localized fibrosis) .

8. Diagnosis:
• Stress cardiomyopathy is mostly diagnosed on clinical grounds.
• ECG findings Usually mimic those of an acute MI-
ST-segment elevation
 T-wave inversion.
• Echocardiography: Characteristic echocardiographic finding include
severe apical hypokinesis or akinesis with relatively preserved function of
the left ventricular base. Nonapical variants including mid-ventricular and
basal hypokinesis have been reported.
LVEF is typically severely reduced during the acute phase of stress cardiomyopathy.
In most patients, LVEF recovers within 4 to 6 weeks after acute presentation.

9. Cont.
• Cardiac MRI : shows no perfusion abnormalities and no evidence of
delayed gadolinium enhancement suggestive of scar.
• CAG: Because there is nearly complete overlap of clinical presentation
between acute MI and stress cardiomyopathy CAG is a required in all
cases to exclude a culprit coronary lesion.

10. Treatment:
• The underlying physical or emotional trigger should be identified and treated.
• In the acute phase of stress cardiomyopathy, treatment is targeted at
electrical and mechanical complications resulting from acute left ventricular
dysfunction such as VT, cardiogenic shock, and dynamic left ventricular
outflow tract obstruction using conventional therapies for these
complications.
• ACE inhibitors or ARB and β-blockers are widely used as in other cases of left
ventricular systolic dysfunction.
• Unfortunately, there is no proven therapy to prevent recurrence.

11. Prognosis:
• Historically, the prognosis of stress cardiomyopathy was felt to be
favorable when compared with acute MI. However, recent reports have
identified in-hospital mortality of nearly 2% to 7% for patients with stress
cardiomyopathy, which is similar to the inhospital mortality of patients
with ST-segment elevation MI.
• However, this relatively high in-hospital mortality of stress
cardiomyopathy may reflect that stress cardiomyopathy is often
associated with other non cardiac acute comorbid illnesses.
• The annual rate of recurrence of stress cardiomyopathy is about 1.5% to
2.9% per year with recurrences more common in patients younger than
50 years of age.
• There is no treatment for secondary prophylaxis that has proven to be
effective.

12. Thank you