HIPK2 expression in the heart was significantly reduced in human end-stage ischemic cardiomyopathy in comparison to nonfailing myocardium, suggesting a clinical relevance of HIPK2 in cardiac biology.
Finally, although hematocrit increases with SGLT2 inhibitors might favorably affect patients with coronary artery disease, in DAPA-HF, the benefit of dapagliflozin was similar in patients with or without an ischemic cardiomyopathy; furthermore, increases in hematocrit do not favorably affect the clinical course of patients with heart failure.
Positive correlation was found between serum PACAP level and ejection fraction only in patients with heart failure due to ischemic cardiomyopathy but not in patients with primary dilated cardiomyopathy.
Confirmatory western bolt analysis demonstrated that SDHB was down-regulated in both ICM and DCM hearts, while UQCRQ, GLUT4 and adiponectin were up-regulated in ICM hearts.
The effects of a FXa inhibitor, rivaroxaban, were investigated in a new murine model of ischemic cardiomyopathy (ICM) using SR-BI KO/ApoeR61<sup>h/h</sup> mice (Hypo E mice) that developed MI by high-fat diet loading.
Selective Treg ablation in Foxp3-diphtheria toxin receptor mice with ischemic cardiomyopathy reversed LV remodeling and dysfunction, alleviating hypertrophy and fibrosis, while suppressing circulating CD4<sup>+</sup> T cells and systemic inflammation and enhancing tissue neovascularization.
Thus, we conclude that VPO1 is a crucial regulator of cardiac fibrosis after MI by mediating HOCl/Smad2/3 and ERK1/2 signaling pathways, implying a promising therapeutic target in ischemic cardiomyopathy.
Advancements in medical treatment, percutaneous interventions, and device therapy (ICD and CRTD) showed consistent reduction in mortality, mainly in survivors of SCD and in patients with ischemic cardiomyopathy and depressed left ventricular function.
In human hearts, we found that the mRNA level of splicing factor Rbfox1, but not Rbfox2, was downregulated in dilated cardiomyopathy, and CACNA1C mRNA level was dramatically decreased in the both of dilated and ischemic cardiomyopathy.
In African Americans, ischemic cardiomyopathy (ICM) and lack of therapy with an angiotensin-converting enzyme inhibitor (ACEI) or angiotensin II receptor blocker (ARB) were associated with increased mortality.
Our findings revealed an unexpected role of CRTH2 in promoting ER stress-induced cardiomyocyte apoptosis, suggesting that CRTH2 inhibition has therapeutic potential for ischemic cardiomyopathy.
Of the 5539 consecutive patients enrolled in the multicentre Défibrillateur Automatique Implantable-Prévention Primaire (DAI-PP) study (2002-12), 5485 patients (with information on underlying heart disease) were included in the present analysis: 2181 (39.8%) had NICM and 3304 (60.2%) had ICM.
Multivariable regression analyses revealed that IL-34 was remarkably associated with the presence and severity of ICM after adjusting for age, sex, conventional risk factors as well as medication [odds ratio (OR): 1.501, 95% confidence interval (CI): 1.249-1.803, <i>P</i> < 0.001, per SD increase].
Western blot analysis showed up-regulation of the full-length NOX4 in ischemic cardiomyopathy samples and confirmed presence of shorter isoforms both in control and failing samples with disease-associated expression pattern.
Histological analyses of myocardial biopsies from patients with various cardiomyopathies revealed that ESRRβ protein is absent from the nucleus of cardiomyocytes from patients with DCM but not other forms of cardiomyopathy (ischemic, hypertrophic, and arrhythmogenic right ventricular cardiomyopathy).