Journal of internal medicine
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The prognosis of patients with congenital heart defects has improved significantly: more and more patients reach adulthood and old age. At the same time, the possibility of cardiovascular morbidity increases. The conventional risk factors for coronary artery disease are at least as high or even higher in patients than in the general population. ⋯ Fontan), the incidence of CAD might be lower, but it usually returns to the average level or higher after correction of the defect. Coronary artery disease is one of the most important reasons for mortality also in ACHD patients, and the consequences of a coronary event might be more fateful in a patient with a corrected congenital heart defect than in her/his peer. There should be a paradigm shift from operative mortality and short-term outcome to long-term morbidity and prevention of cardiovascular disease - a task that often has been forgotten during follow-up visits.
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Renin-angiotensin system (RAS) blockers are extensively used worldwide to treat many cardiovascular disorders, where they are effective in reducing both mortality and morbidity. These drugs are known to induce an increased expression of angiotensin-converting enzyme 2 (ACE2). ACE2 acts as receptor for the novel SARS coronavirus-2 (SARS-CoV-2) which raising the important issue of possible detrimental effects that RAS blockers could exert on the natural history and pathogenesis of the coronavirus disease-19 (COVID-19) and associated excessive inflammation, myocarditis and cardiac arrhythmias. We review the current knowledge on the interaction between SARS-CoV-2 infection and RAS blockers and suggest a scientific rationale for continuing RAS blockers therapy in patients with COVID-19 infection.
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One of the most frequent causes of cardiac embolism in cryptogenic stroke is a paradoxical embolus, which originate from systemic venous source though an unidentified patent foramen ovale (PFO). PFO is a common finding in the general population with a prevalence of 25% to 30%. Transcatheter PFO device closure is known to be feasible and safety treatment for such patients. ⋯ Based on these data, PFO device closure is recommended to carefully select cryptogenic stroke patients aged from 18 to 65 years, with a high probability of a causal role of the PFO in stroke events. However, it is still uncertain whether PFO closure is superior to oral anticoagulants therapy in these patients. Therefore, further prospective randomized trials are needed to address the efficacy of PFO device closure to oral anticoagulants therapy.
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The disproportionate obesity in African American (AA) women has a physiologic basis and can be explained by the interactive effects of insulin secretion, insulin clearance, insulin sensitivity and the glycaemic load of the diet. This review will present data supporting a physiologic basis for obesity propensity in obesity-prone AA women that resides in their unique metabolic/endocrine phenotype: high beta-cell responsiveness, low hepatic insulin extraction and relatively high insulin sensitivity, which together result in a high exposure of tissues and organs to insulin. When combined with a high-glycaemic (HG) diet (that stimulates insulin secretion), this underlying propensity to obesity becomes manifest, as ingested calories are diverted from energy production to storage. ⋯ Greater bioenergetic efficiency has been reported in AA and, via resultant oxidative damage, could plausibly contribute to insulin resistance. In summary, it is proposed here that a subset of AA women are predisposed to obesity due to a specific metabolic/endocrine phenotype. However, greater diabetes risk in AA has an independent aetiology based on impaired lipid storage and mitochondrial efficiency/oxidative stress.
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Type 2 diabetes is more common in non-Europeans and starts at a younger age and at lower BMI cut-offs. This review discusses the insights from genetic studies about pathophysiological mechanisms which determine risk of disease with a focus on the role of adiposity and body fat distribution in ethnic disparity in risk of type 2 diabetes. ⋯ One possible mechanism suggested by epidemiological studies is the role of ethnic difference in body fat distribution. Using genetic variants associated with an ability to store extra fat in a safe place, which is subcutaneous adipose tissue, we discuss how different ethnic groups could be genetically less susceptible to type 2 diabetes by developing a more favourable fat distribution.