Takotsubo-like Cardiomyopathy Research Articles

Effects of metoprolol on epinephrine-induced takotsubo-like left ventricular dysfunction in non-human primates

Takotsubo cardiomyopathy, alternatively known as stress cardiomyopathy, is an increasingly recognized clinical syndrome characterized by acute reversible apical ventricular dysfunction. To elucidate the mechanism, we tried to make a new model of takotsubo-like cardiomyopathy in non-human primates. Echocardiography revealed that repeated intravenous infusion of epinephrine overdose in cynomolgus monkeys induced takotsubo-like cardiomyopathy, which is characterized by progressive left ventricle and depressed systolic function with severe hypokinesis in apical regions and hyperkinesis in the basal region. Although this cardiac dysfunction almost normalized after a month even without any treatment, metoprolol, a beta-blocker, improved the decreased ejection fraction earlier than in the control. Luxol fast blue staining, which is useful for estimating myocytolysis, showed that increased myocytolysis was observed in the apical ventricle of the epinephrine-infused heart. Metoprolol diminished epinephrine-induced cardiomyocytolysis. To explain the mechanism of takotsubo myopathy and the effect of metoprolol, gene expressions in apical or basal ventricle were compared. Heart failure-related genes, such as brain natriuretic peptide, connective tissue growth factor and osteopontin; calcium signaling-related genes, such as ryanodine receptor 2, sarcoendoplasmic reticulum Ca(2+)-ATPase 2A2 and adenylate cyclase 7; renin-angiotensin system-related genes, such as angiotensinogen, angiotensin II receptor, type 1 and type 2; and mitochondria-related genes, such as peroxisome proliferator-activated receptor-gamma co-activator-1alpha, cytochrome c and transcription factor A mitochondrial, were significantly changed at the apical ventricle rather than at the basal ventricle. The changes of some genes improved with metoprolol treatment. These results indicate that this model is valuable in understanding the pathogenesis of takotsubo cardiomyopathy and the effectivity of beta-blockers.

Apical thrombus in a patient with Takotsubo-like cardiomyopathy: another brick in the wall of knowledge

Apical thrombus in a patient with Takotsubo-like cardiomyopathy: another brick in the wall of knowledge

Takotsubo-Like Cardiomyopathy in a 17-Year-Old Male with a Pheochromocytoma

We report a case of a 17-year-old adolescent male with Takotsubo-like cardiomyopathy in the setting of pheochromocytoma who presented with hematemesis, hypertension, and pallor. Takotsubo-like cardiomyopathy is rarely reported in the pediatric population, and this is the first report in the pediatric literature of Takotsubo-like cardiomyopathy associated with both pheochromocytoma and an elongated course of the left anterior descending coronary artery.

Typical and atypical takotsubo-like cardiomyopathy as a manifestation of pheochromocytoma

Typical and atypical takotsubo-like cardiomyopathy as a manifestation of pheochromocytoma

Noninvasive Detection of Takotsubo Cardiomyopathy Using Multi-detector Row Computed Tomography

We present a 60-year-old woman with chest pain preceded by emotional stress. Trans-thoracic echocardiography demonstrated localized left ventricular hypokinesis around the apical area. Multi-detector row computed tomography (MDCT) revealed no significant stenosis in the coronary arteries, which comfirmed Takotsubo-like cardiomyopathy. We show here the usefulness of MDCT for the noninvasive differentiation of Takotsubo cardiomyopathy from acute coronary syndrome.

“Broken Heart Syndrome” After Separation (From OxyContin)

We describe a 61-year-old woman with "broken heart syndrome" (Takotsubo-like cardiomyopathy) after abrupt postsurgical withdrawal of OxyContin. Her medical history was remarkable for long-term opiold dependence associated with the treatment of multi-Joint degenerative osteoarthritis. The patient presented to the emergency department 1 day after discharge from the hospital following total knee arthroplasty revision with acute-onset dyspnea and mild chest pain. She had precordial ST-segment elevation characteristic of acute myocardial infarction and elevated cardiac biomarkers. Emergency coronary angiography revealed no major coronary atherosclerosis. However, the left ventricular ejection fraction was severely decreased (26%), and new regional wall motion abnormalities typical of broken heart syndrome were noted. In addition to resuming her opioid therapy, she was treated supportively with bilevel positive airway pressure, diuretic therapy, morphine, aspirin, metoprolol, enalaprilat, intravenous heparin, nitroglycerin infusion, and dopamine infusion. Ventricular systolic function recovered completely by the fourth hospital day. To our knowledge, broken heart syndrome after opioid withdrawal has not been reported previously in an adult. Our case illustrates the importance of continuing adequate opiate therapy perioperatively in the increasing number of opioid-dependent patients to prevent potentially life-threatening complications such as broken heart syndrome.