Stress Cardiomyopathy Diagnosis and Treatment: JACC State-of-the-Art Review

Horacio Medina de Chazal, Marco Giuseppe Del Buono, Lori Keyser-Marcus, Liangsuo Ma, F Gerard Moeller, Daniel Berrocal, Antonio Abbate, Horacio Medina de Chazal, Marco Giuseppe Del Buono, Lori Keyser-Marcus, Liangsuo Ma, F Gerard Moeller, Daniel Berrocal, Antonio Abbate

Abstract

Stress cardiomyopathy is an acute reversible heart failure syndrome initially believed to represent a benign condition due to its self-limiting clinical course, but now recognized to be associated with a non-negligible rate of serious complications such as ventricular arrhythmias, systemic thromboembolism, and cardiogenic shock. Due to an increased awareness and recognition, the incidence of stress cardiomyopathy has been rising (15-30 cases per 100,000 per year), although the true incidence is unknown as the condition is likely underdiagnosed. Stress cardiomyopathy represents a form of neurocardiogenic myocardial stunning, and while the link between the brain and the heart is established, the exact pathophysiological mechanisms remain unclear. We herein review the proposed risk factors and triggers for the syndrome and discuss a practical approach to diagnosis and treatment of the patients with stress cardiomyopathy, highlighting potential challenges and unresolved questions.

Keywords: Takotsubo; cardiomyopathy; stress.

Copyright © 2018 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Figures

FIGURE 1. Acute Treatment of Patients With…
FIGURE 1. Acute Treatment of Patients With Stress Cardiomyopathy and Hemodynamic Compromise
In patients with no hemodynamic instability and pulmonary congestion, treatment is directed to relief congestion with diuretic agent and vasodilators. Arterial vasodilators and β-adrenergic blockers are useful especially if hypertension is present. For patients with hemodynamic instability (hypotension/shock), treatment depends on the presence of LVOTO obstruction. In the absence of LVOTO, inotropic agents, and if not sufficient, mechanical left ventricular assist devices (IABP, Impella) should be considered. In the presence of LVOTO, intravenous fluids and low dose of short-acting β-adrenergic blockers (i.e., esmolol or metoprolol) may be used with caution to reduce the LVOTO or peripherally active vasopressor drugs (i.e., phenylephrine or vasopressin) to maintain adequate perfusion pressure as a temporizing solution to LVOTO resolution or mechanical support. Extracorporeal membrane oxygenation is used as a mechanical cardiac assist device for refractory cases of stress cardiomyopathy with LVOTO or biventricular failure. ACEinh = angiotensin-converting enzyme inhibitors; ARB = angiotensin II receptor blockers; ARN = angiotensin II receptor blocker neprilysin inhibitors; ECMO = extracorporeal membrane oxygenation; IABP = intra-aortic balloon pump; ISDN = isosorbide dinitrate; LVOTO = left ventricular out flow tract obstruction.
CENTRAL ILLUSTRATION. Pathophysiology of Stress Cardiomyopathy
CENTRAL ILLUSTRATION. Pathophysiology of Stress Cardiomyopathy
In a predisposed individual, who may have enrichment in NPY/norepinephrine granules and risk factors for endothelial dysfunction, an intense stimulation for an adrenergic stimulation may be sufficient to trigger stress cardiomyopathy in response to emotional or physical stress. Stress-related neuropeptides stored in the pre-synaptic terminations of postganglionic neurons at level of CANS may suddenly spill at myocardial level, and through a direct catecholamine toxicity and/or microvascular dysfunction, explain the prevailing theory of a neurogenic-mediated mechanism of myocardial stunning. Medina de Chazal, H. et al. J Am Coll Cardiol. 2018;72(16):1955–71.

Source: PubMed

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