Hypertension and Heart Failure as Predictors of Mortality in an Adult Congenital Heart Defect Population

Early intervention to prevent premature mortality is vital for adults with congenital heart defects(CHD).Anatomic complexity and comorbid conditions are thought to contribute to CHD mortality.Since hypertension(HTN)and heart failure(HF)are the comorbid conditions among the most prevalent causes of death in the United States,and commonly accompany CHD,it is crucial to evaluate whether they are reliable predictors of mortality for adults with CHD(ACHD)independent of anatomic CHD complexity.A retrospective cross-sectional analysis of ACHD,aged 18–64,with concomitant HTN and/or HF and at least one health care encounter during 2008–2010 were assessed.Of 5,397 ACHD patients(18.3%HTN without HF,4.4%HF without HTN,8.3%with both),3.0%died(n=163)during the study period.Overall,the sample was 45.1%white,61.4%female,and 29.0%had a complex CHD.Among those who died,23.3%had HTN without HF,17.2%had HF without HTN,and 42.3%had both.Crude analyses revealed that older age,male gender,black race,and having public health insurance were associated with increased mortality during the three-year study period compared to ACHD patients who were younger,female gender,white race,and covered by private health insurance.ACHD patients diagnosed with non-complex CHD lesions(i.e.,shunts,valves,or shunts+valves)were at greater risk of dying compared to those with severe complex CHDs.When CHD type was assessed separately,those with valve lesions were more likely to die compared to those with complex CHD lesions.After adjustment for age,gender,race,insurance and CHD complexity,ACHD patients with HF,with or without HTN,were equally likely to die during the study period.However,ACHD patients with HF,without or without HTN,who had valve defects were more likely to die during the three-year study period compared to patients with complex CHDs.

Mitochondrial network in the heart

Mitochondria are subcellular organelles that provide energy for the cell.They form a dynamic tubular network and play an important role in maintaining the cell function and integrity.Heart is a powerful organ that supplies the motivation for circulation,thereby requiring large amounts of energy.Thus,the healthiness of cardiomyocytes and mitochondria is necessary for the normal cardiac function.Mitochondria not only lie in the center of the cell apoptotic pathway,but also are the major source of reactive oxygen species(ROS)generation.Mitochondrial morphological change includes fission and fusion that are regulated by a large number of proteins.In this review we discuss the regulators of mitochondrial fission/fusion and their association with cell apoptosis,autophagy and ROS production in the heart.