TAKOTSUBO CARDIOMYOPATHY (Stress induced cardiomyopathy or Transient Apical ballooning syndrome or Broken Heart Syndrome)

"Dil e nada tujhe hua kya hai,
Akhir is dard ki dawa kya hai"
                - Mirza Ghalib

76 Y F admitted with severe chest pain, which started 4 hours back after hearing news of her sister's death. She  had no history of coronary artery disease. Evaluation suggested BP 90/50 and HR of 100. JVP was not elevated, no murmur heard, chest auscultation revealed vesicular sounds, and extremities were warm.
EKG showed ST elevation with T inversion in anterior leads. Cardiac enzymes were mildly raised.
Echo showed left ventricle apical akinesia  with hypercontractile basal wall. Abnormal dilatation of LV was seen during systole.
Emergency coronary angiography revealed normal coronaries.

TAKOTSUBO CARDIOMYOPATHY :

CLINICAL PRESENTATION  is similar to acute myocardial infarction with substernal chest pain and dyspnoea. EKG mimics ST elevation or T wave inversion, most commonly in anterior leads. Cardiac enzymes are mildly elevated.

ECHOCARDIOCARDIOGRAPHY shows depressed contractility of mid/apical segment and increased contractility of basal segment of LV, producing a balloon like appearance of distal ventricle during systole.
This resembles Japanese octopus trap called TAKOTSUBO.

CORONARY ANGIOGRAPHY typically reveals normal coronaries.

Patients are typically postmenopausal women.
Precipitating factors are acute medical illness or intense emotional or physical stress like death of relative, catastrophic medical diagnosis, financial loss,  natural disaster, domestic voilence.

PATHOPHYSIOLOGY is probably related to hyperadrenergic state, causing high myocardial catecholamine levels, leading to myocyte calcium overload and myocardial stunning.

TREATMENT is supportive.
Beta blocker, ace inhibitors, diuretic along with intravascular volume optimization is the standard therapy.
In case of shock, ionotropes should be used cautiously or better avoided, as it may worsen shock by hyperkinetic movement of basal portion of heart, leading to systolic anterior motion (SAM) of anterior mitral leaflet, causing left ventricular outflow tract obstruction.
Alpha agonist like phenylephrine should be considered. By increasing afterload, it causes left ventricular  dilatation, decrease in SAM of anterior mitral leaflet and lowering of LV outflow tract gradient,  thereby improving hemodynamics.
Aspirin may be added for atherosclerosis risk factor.
Anticoagulation should be considered until LV contractility improves.

Takotsubo cardiomyopathy is associated with good outcome. In almost all cases LV function begins to improve within days, and completely recovers to normal in weeks to months. In hospital mortality has been reported from zero to eight percent.
Follow up has shown that in ninety percent patient don't have recurrence.

Other conditions associated with ST segment changes with reversible cardiomyopathy without coronary artery disease-  Prinzmetal angina, cocain abuse, pheochromocytoma, acute brain injury.