Reverse Takotsubo cardiomyopathy: a comprehensive review

Abstract

Takotsubo cardiomyopathy (TTC) was first described in Japan in the 1980s. It is described as an acute but often reversible left ventricular (LV) dysfunction mainly triggered by emotional or physical stress.Multiple variants of TTC have been reported including reverse Takotsubo cardiomyopathy (rTTC) which is a variant characterized by the basal akinesis/hypokinesis associated with apical hyperkinesis that resolves spontaneously. The hallmark of rTTC is a clinical presentation similar to an acute coronary syndrome (ACS), with no evident obstructive coronary artery disease. The incidence of TTC is estimated to be 2% of all troponin-positive patients presenting with suspected ACS. The proportion of patients presenting with the rTTC variant out of all TTC patients in published literature has been variable, ranging from 1-23%.Reverse Takotsubo has been associated with younger age, less decrease in left ventricular ejection fraction (LVEF), and more neurological disease compared to the TTC. While the exact mechanism of rTTC is unknown, hypothesized mechanisms include catecholamine cardiotoxicity, coronary artery spasm, coronary microvasculature impairment, and estrogen deficiency. Patients with rTTC typically present with chest pain and/or dyspnea after an emotional or physically stressful event. rTTC can also be triggered by intracranial hemorrhage, general anesthesia, or neurological conditions. Diagnosis of rTTC requires the presence of LV basal hypokinesis/akinesis, new electrocardiogram (EKG) abnormalities or elevated cardiac troponin, and absence of obstructive coronary disease, pheochromocytoma, or myocarditis. Management of rTTC is similar to that of TTC, which is predominantly supportive with the treatment of complications. The recurrence rate of rTTC is around 10%. The most common complications of rTTC include myocarditis, pleural and pericardial effusions, and development of LV thrombi. The best predictors of mortality include decreased LVEF, development of atrial fibrillation, and neurologic disease.

Catecholamine-induced reverse takotsubo cardiomyopathy

“…11 This can be associated with dynamic electrocardiographic changes, ranging from transient ST elevations at onset subsequently transitioning to deep T-wave inversions followed by late normalization of T-waves. 3,5,[13][14][15][16][17] In contrast, patients with reverse TC usually present at a younger age and often have an emotional or physical trigger leading to basal and/or midventricular hypokinesis but preserved apical contractility, as seen in our patient. 18 Reverse TC is also typically more likely to be complicated by pulmonary edema and cardiogenic shock.…”

“…18 Reverse TC is also typically more likely to be complicated by pulmonary edema and cardiogenic shock. 5,19 The plausible underlying mechanisms for TC are sympathetic hyperactivity, multivessel transient coronary vasospasm, 8 estrogen deficiency, 9,17 and microcirculatory dysfunction. 5,9,20,21 There is a near-complete resolution of myocardial dysfunction in most patients usually within a few weeks.…”

“…5,19 The plausible underlying mechanisms for TC are sympathetic hyperactivity, multivessel transient coronary vasospasm, 8 estrogen deficiency, 9,17 and microcirculatory dysfunction. 5,9,20,21 There is a near-complete resolution of myocardial dysfunction in most patients usually within a few weeks. The reverse pattern TC coupled with a very rapid resolution of ventricular dysfunction in our young male patient further supports the causation related to an inadvertent high-dose epinephrine administration.…”

“…Reverse TC is a rare variant usually seen in young patients, which presents with mid to basal ballooning instead of the classical apical ballooning. 5 We present a rare case of iatrogenic epinephrine-induced reverse TC in a young man who presented with anaphylaxis triggered by a spider bite.…”

Broken Heart Syndrome Secondary To Liver Abscess

“…The exact mechanism leading to TTCM remains unknown. However, catecholamine-induced cardiotoxicity, microvascular dysfunction, stimulus trafficking, coronary vasospasm, and estrogen deficiency are the most prominent theories described behind its occurrence [10][11]. Several studies have shown that serum catecholamine levels are elevated during the acute phase of TTCM [2][3].…”