Despite considerable public awareness and technological advances that foster early diagnosis and aggressive therapeutic interventions, heart failure, which results as a final outcome from an underlying cardiovascular disorder remains a critical and an unsolved problem. Among the various cardiomyopathies, Dilated cardiomyopathy with an obscure etiology is known to be the leading cause of heart failure and sudden cardiac death among young adults and children. Studies related to the molecular basis of the condition have implicated oxidative stress pathways, apart from primary disease causing sarcomeric, cytoskeletal and mitochondrial gene mutations in the disease onset. The present study aims to evaluate the role of oxidative stress markers in 97 DCM patients and 105 control individuals to identify specific electromorphic association of superoxide dismutase, catalase and alpha-1-antitrypsin with the disease. Our study has revealed an association of SODA2, catalase HPII and AAT 'M' and 'Z' alleles with DCM, thereby resulting in inefficient scavenging of the free radicals, which may confer decreased protection against oxidative stress induced tissue injury in the disease pathogenesis. The involvement of SOD and AAT in apoptotic pathway and as immunomodulators is also emphasized.
Purpose: This study was to assess the feasibility and cardio-protective effects of biocompatible silicon built restraint device (ASD) in rat's heart failure (HF) model. Background: Ventricle restraint therapy (VRT) is a well-established and promising approach for management of advanced-stage dilated HF. Previous VRT devices offer a subjective level of restraint to the dilated heart muscles. However, the impact of the restraint nature, mesh tubular design and biocompatibility of VRT devices is not well investigated. Method: The performance and compliance of ASD were determined in vitro by adopting a pneumatic drive and ball burst test. SD rats were grouped into four (n=24); control, HF, ASD+HF and CSD+HF groups, respectively. HF was induced by left anterior descending artery ligation in all groups except the control group. ASD and CSD devices were implanted in the heart of ASD+HF and CSD+HF groups respectively. Results: The functional and expansion ability of ASD was observed to be safer and suitable to attenuate ventricular remodeling. ASD treated rats showed normal heart rhythm which was validated by a smooth -ST and asymmetrical T-wave. Hemodynamic parameters, and systolic and diastolic functions improved in the ASD+HF group and reduction in ventricular wall stress indicated reverse remodeling. Furthermore BNP values were reduced in ASD+HF group which confirmed ASD feasibility and reverse remodeling at a molecular level. ASD+HF group also showed no fibrosis thus proposing that ASD has its significant curative effects on the heart muscles. Conclusion: ASD was found to be a promising restraint therapy than the previously standard restraint therapies.
Heart failure, the one, and only cardiovascular disease is the primary cause of mortality and morbidity with increasing incidence and possess a considerable economic burden. The abrasions seen after Isoprenaline treatment are even more severe than those induced by epinephrine or norepinephrine. This severeness implies that the administration of Isoprenaline diminishes the efficacy of cardiac muscle cells and causes complex biochemical and structural alterations leading to cell damage and necrosis. Moreover, the abrasions demonstrated that ACE inhibitors reduce blood pressure, enhance left ventricular hypertrophy, decrease morbidity and mortality in cardiac failure, and inhibit progression to explicit cardiac failure in patients with depressed ventricular function or myocardial infarction. On the other hand, Beta-blockers decrease heart rate, lower blood pressure and cardiac contractility prominent to diminished oxygen consumption which may, in turn, stimulate the metoprolol-induced enhancement in function and structure.
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