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Stress-Induced Cardiomyopathy Presenting as Shock.

ABSTRACT: Stress-induced cardiomyopathy has become a more recognized and reported entity. It can be caused by emotional or physical stress, which causes excessive catecholamine release. Typically, the clinical course is benign with conservative treatment being effective. However, stress-induced cardiomyopathy can be fatal. A 41-year-old female presented with cardiogenic shock followed by sudden back pain. Initial echocardiographic finding showed severely decreased ejection fraction with akinesia at all mid-to-apical walls with relatively preserved basal wall contractility. The coronary artery was intact on coronary angiography. Cardiac resuscitation and extra-corporeal membrane oxygenation was needed to manage the cardiogenic shock. Recovery was complete after 2 weeks.

SUBMITTER: Yoo TK

PROVIDER: S-EPMC4828422 | biostudies-literature | 2016 Mar

REPOSITORIES: biostudies-literature

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Stress-Induced Cardiomyopathy Presenting as Shock.

Yoo Tae Kyung TK Lee Jong-Young JY Sung Ki-Chul KC Oh Sam Sae SS Song Young Seok YS Lee Seung Jae SJ Ko Kyung Jin KJ

Journal of cardiovascular ultrasound 20160324 1

Stress-induced cardiomyopathy has become a more recognized and reported entity. It can be caused by emotional or physical stress, which causes excessive catecholamine release. Typically, the clinical course is benign with conservative treatment being effective. However, stress-induced cardiomyopathy can be fatal. A 41-year-old female presented with cardiogenic shock followed by sudden back pain. Initial echocardiographic finding showed severely decreased ejection fraction with akinesia at all mi ...[more]

PMID: 27081451

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Project description:BACKGROUND:Myocarditis is inflammation of the heart muscle that can follow various viral infections. Why children only rarely develop life-threatening acute viral myocarditis (AVM), given that the causal viral infections are common, is unknown. Genetic lesions might underlie such susceptibilities. Mouse genetic studies demonstrated that interferon (IFN)-?/? immunity defects increased susceptibility to virus-induced myocarditis. Moreover, variations in human TLR3, a potent inducer of IFNs, were proposed to underlie AVM. OBJECTIVES:This study sought to evaluate the hypothesis that human genetic factors may underlie AVM in previously healthy children. METHODS:We tested the role of TLR3-IFN immunity using human induced pluripotent stem cell-derived cardiomyocytes. We then performed whole-exome sequencing of 42 unrelated children with acute myocarditis (AM), some with proven viral causes. RESULTS:We found that TLR3- and STAT1-deficient cardiomyocytes were not more susceptible to Coxsackie virus B3 (CVB3) infection than control cells. Moreover, CVB3 did not induce IFN-?/? and IFN-?/?-stimulated genes in control cardiomyocytes. Finally, exogenous IFN-? did not substantially protect cardiomyocytes against CVB3. We did not observe a significant enrichment of rare variations in TLR3- or IFN-?/?-related genes. Surprisingly, we found that homozygous but not heterozygous rare variants in genes associated with inherited cardiomyopathies were significantly enriched in AM-AVM patients compared with healthy individuals (p = 2.22E-03) or patients with other diseases (p = 1.08E-04). Seven of 42 patients (16.7%) carried rare biallelic (homozygous or compound heterozygous) nonsynonymous or splice-site variations in 6 cardiomyopathy-associated genes (BAG3, DSP, PKP2, RYR2, SCN5A, or TNNI3). CONCLUSIONS:Previously silent recessive defects of the myocardium may predispose to acute heart failure presenting as AM, notably after common viral infections in children.

Dataset Information

Stress-Induced Cardiomyopathy Presenting as Shock.

Publications

Stress-Induced Cardiomyopathy Presenting as Shock.

Similar Datasets

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