Opportunities and Limitations in the Study of Transient Takotsubo Syndrome in Animal Models

Angelini, Paolo; Gamero, Maria T

doi:10.14740/jocmr4225

Cited by 2 publications

(3 citation statements)

References 26 publications

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“…It may help to determine whether a substantial rise in serum catecholamine levels at TTC onset identifies a potential predisposing or precipitating factor, but not in healthy people. 10 In addition, the frequent clinical use of dobutamine testing only rarely causes TTC. 13 In a cohort registry study of 1,016 patients with TTC, the mean heart rate of 86 ± 20.8 beats/min and systolic blood pressure of 131.8 ± 28 mmHg at clinical presentation did not suggest a credible catecholamine-surge state, 6 and Y-Hassan 14 proved that we cannot currently substantiate the presence of a catecholamine surge in TTC.…”

Section: Inadequacies Of the Catecholamine Stress Theorymentioning

confidence: 99%

“…Adequately designed animal experiments might apply to human cardiac endothelial dysfunction only if a preliminary endothelial dysfunctional state were added to the catecholamine model, for example by applying cardiac radiation. 10,14 Prolonged spasm has long been known to lead to the myocardial stunning that is presumably the essential mechanism for TTC. 1,10 For all these reasons, ACh testing of endothelial dysfunction may credibly identify the cause of stunning in TTC in specific circumstances.…”

Section: Inadequacies Of the Catecholamine Stress Theorymentioning

confidence: 99%

“…10,14 Prolonged spasm has long been known to lead to the myocardial stunning that is presumably the essential mechanism for TTC. 1,10 For all these reasons, ACh testing of endothelial dysfunction may credibly identify the cause of stunning in TTC in specific circumstances. 13,15…”

Section: Inadequacies Of the Catecholamine Stress Theorymentioning

confidence: 99%

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Pathophysiology of Takotsubo Cardiomyopathy: Reopened Debate

Angelini¹,

Uribe²,

Tobis

2021

Texas Heart Institute Journal

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Takotsubo cardiomyopathy (TTC), a persistently obscure dysfunctional condition of the left ventricle, is uniquely transient but nevertheless dangerous. It features variable ventricular patterns and is predominant in women. For 30 years, pathophysiologic investigations have progressed only slowly and with inadequate focus. It was initially proposed that sudden-onset spastic obliteration of coronary flow induced myocardial ischemia with residual stunning and thus TTC. Later, it was generally accepted without proof that, in the presence of pain or emotional stress, the dominant mechanism for TTC onset was a catecholamine surge that had a direct, toxic myocardial effect. We think that the manifestations of TTC are more dynamic and complex than can be assumed from catecholamine effects alone. In addition, after reviewing the recent medical literature and considering our own clinical observations, especially on spasm, we theorize that atherosclerotic coronary artery disease modulates and physically opposes obstruction during spasm. This phenomenon may explain the midventricular variant of TTC and the lower incidence of TTC in men. We continue to recommend and perform acetylcholine testing to reproduce TTC and to confirm our theory that coronary spasm is its initial pathophysiologic factor. An improved understanding of TTC is especially important because of the condition's markedly increased incidence during the ongoing COVID-19 pandemic.

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Section: Inadequacies Of the Catecholamine Stress Theorymentioning

confidence: 99%

Section: Inadequacies Of the Catecholamine Stress Theorymentioning

confidence: 99%