Pathophysiology of Takotsubo Syndrome

被引:518
作者
Pelliccia, Francesco [2 ]
Kaski, Juan Carlos [3 ]
Crea, Filippo [4 ]
Camici, Paolo G. [1 ,5 ]
机构
[1] Univ Vita Salute San Raffaele, Via Olgettina 58, I-20132 Milan, Italy
[2] Sapienza Univ, Dept Cardiovasc Sci, Rome, Italy
[3] St Georges Univ London, Mol & Clin Sci Res Inst, London, England
[4] Catholic Univ, Inst Cardiol, Rome, Italy
[5] Osped San Raffaele, Milan, Italy
关键词
autonomic nervous system; cardiomyopathies; catecholamines; coronary circulation; heart diseases; ischemic heart disease; Takotsubo cardiomyopathy; CORONARY MICROVASCULAR DYSFUNCTION; TAKO-TSUBO CARDIOMYOPATHY; SYMPATHETIC-NERVOUS-SYSTEM; HEART-FAILURE; STRESS CARDIOMYOPATHY; SUBARACHNOID HEMORRHAGE; CLINICAL-FEATURES; EMOTIONAL-STRESS; TC-99M-TETROFOSMIN; CATECHOLAMINE;
D O I
10.1161/CIRCULATIONAHA.116.027121
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Originally described by Japanese authors in the 1990s, Takotsubo syndrome (TTS) generally presents as an acute myocardial infarction characterized by severe left ventricular dysfunction. TTS, however, differs from an acute coronary syndrome because patients have generally a normal coronary angiogram and left ventricular dysfunction, which extends beyond the territory subtended by a single coronary artery and recovers within days or weeks. The prognosis was initially thought to be benign, but subsequent studies have demonstrated that both short-term mortality and long-term mortality are higher than previously recognized. Indeed, mortality reported during the acute phase in hospitalized patients is approximate to 4% to 5%, a figure comparable to that of ST-segment-elevation myocardial infarction in the era of primary percutaneous coronary interventions. Despite extensive research, the cause and pathogenesis of TTS remain incompletely understood. The aim of the present review is to discuss the pathophysiology of TTS with particular emphasis on the role of the central and autonomic nervous systems. Different emotional or psychological stressors have been identified to precede the onset of TTS. The anatomic structures that mediate the stress response are found in both the central and autonomic nervous systems. Acute stressors induce brain activation, increasing bioavailability of cortisol and catecholamine. Both circulating epinephrine and norepinephrine released from adrenal medullary chromaffin cells and norepinephrine released locally from sympathetic nerve terminals are significantly increased in the acute phase of TTS. This catecholamine surge leads, through multiple mechanisms, that is, direct catecholamine toxicity, adrenoceptor-mediated damage, epicardial and microvascular coronary vasoconstriction and/or spasm, and increased cardiac workload, to myocardial damage, which has a functional counterpart of transient apical left ventricular ballooning. The relative preponderance among postmenopausal women suggests that estrogen deprivation may play a facilitating role, probably mediated by endothelial dysfunction. Despite the substantial improvement in our understanding of the pathophysiology of TTS, a number of knowledge gaps remain.
引用
收藏
页码:2426 / 2441
页数:16
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