Rev Cardiovasc Med
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Meta Analysis
Serum albumin in patients undergoing transcatheter aortic valve replacement: A meta-analysis.
Transcatheter aortic valve replacement is becoming a more common therapeutic option for the treatment of aortic stenosis in patients at high risk for invasive surgery, but detecting which patients will benefit clinically can be challenging. Hypoalbuminemia is a useful prognostic marker for chronic inflammation in this population. We carried out a systematic review and meta-analysis of studies evaluating the prognostic value of serum albumin level in patients undergoing transcatheter aortic valve replacement. ⋯ A sub-group analysis of eight studies reporting adjusted hazard ratios indicated that low serum albumin was independently correlated with increased post-operative mortality. The hazard ratio of mortality risk associated with each 1 g/dL increment in serum albumin level was 0.46, suggesting a potential dose-response relationship between increased serum albumin level and increased survival rate in patients undergoing transcatheter aortic valve replacement. This meta-analysis provides strong evidence for the utility of serum albumin as a prognostic marker in aortic stenosis patients undergoing transcatheter aortic valve replacement, with low serum albumin levels (2.5-3.5 g/dL) suggesting poor prognosis.
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Myocardial ischemia-reperfusion (I/R) injury is leading cause of death worldwide. miR-34a-5p was up-regulated in myocardial ischemia-reperfusion injury rats. We aim to explore how miR-34a-5p inhibition protected myocardium against I/R injury in both cell and animal models. In vivo rat and in vitro cell model were firstly constructed. quantitative real-time polymerase chain reaction was employed to investigate expression of miR-34a-5p and its target genes. ⋯ In in vitro cell model, miR-34a-5p inhibitor also promoted cell proliferation, inhibited cell apoptosis and reactive oxygen species accumulation through targeting Notch Receptor 1 signaling. Our results revealed that miR-34a-5p knocking down attenuated myocardial I/R injury by promoting Notch Receptor 1 signaling-mediated inhibition of reactive oxygen species accumulation and cell apoptosis. Hence, miR-34a-5p might be a potential target for treatment of myocardial ischemia-reperfusion injury.
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In this systematic review, we sought to summarize the 3 recent sodium-glucose cotransporter 2 inhibitor (SGLT2i) trials (Dapagliflozin Effect on CardiovasculAR Events (DECLARE-TIMI 58), Canagliflozin Cardiovascular Assessment Study (CANVAS) Program, and Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes (EMPA-REG OUTCOME)) and to explore the potential causes for their different results. We found that the major adverse cardiovascular event rates per 1000 patient-years for drug and placebo, as well as the corresponding relative risk reductions, were 22.6, 24.2, 7%; 26.9, 31.5, 14%; 37.4, 43.9, 14% for DECLARE-TIMI 58, CANVAS, and EMPA-REG OUTCOME, respectively. DECLARETIMI 58 had the fewest cardiorenal events (across treatment and control arms) and EMPA-REG OUTCOME the most. ⋯ Therefore, the DECLARE-TIMI 58 study cohort had higher eGFR (mean eGFR 85.2 mL/min/1.73 m2 compared to 76.5 and 74 in CANVAS and EMPAREG OUTCOME, respectively); this may have caused the difference in results. Additionally contributing to the high event rate in EMPA-REG OUTCOME was the requirement of prior confirmed cardiovascular disease (CVD), resulting in 99.2% of patients with CVD compared to only 65.6% and 40.6% in CANVAS and DECLARE-TIMI 58, respectively (which did not require CVD). In conclusion, there is a need for large-scale studies of SGLT2i with matching inclusion/exclusion criteria and appropriate endpoints to ensure a truly direct comparison of the drugs.
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A rapid diagnosis of ST-segment elevation myocardial infarction (STEMI) is mandatory for optimal treatment of an acute coronary syndrome. However, a small number of patients with suspected STEMI are afflicted with other medical conditions. ⋯ These conditions include coronary vasospasm, Takotsubo cardiomyopathy, coronary arteritis/aneurysm, myopericarditis, Brugada syndrome, left bundle branch block, early repolarization, aortic dissection, infective endocarditis with root abscess, subarachnoid hemorrhage, ventricular aneurysm after transmural myocardial infarction, and hemodynamically significant pulmonary embolism with right ventricular strain. Herein, we present several STEMI mimickers.
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Hyperkalemia is defined as serum potassium concentrations elevated above the upper limit of normal (> 5.0 mEq/L). It has become more common in cardiovascular practice due to the growing population of patients with chronic kidney disease and the broad application of drugs that modulate renal elimination of potassium by reducing production of angiotensin II (angiotensin-converting enzyme inhibitors, direct renin inhibitors, β-adrenergic receptor antagonists), blocking angiotensin II receptors (angiotensin receptor blockers), or antagonizing the action of aldosterone on mineralocorticoid receptors (mineralocorticoid receptor antagonists). The risk of hyperkalemia is a major limiting factor for the use of these disease-modifying drugs in both acute and chronic cardiorenal syndromes. ⋯ Novel oral therapies in development for both acute and extended use in the management of hyperkalemia include patiromer sorbitex calcium and sodium zirconium cyclosilicate. Important biochemical differences between these compounds result in unique product profiles and electrolyte outcomes in patients treated for hyperkalemia. This review highlights the major mechanisms of hyperkalemia and key results from randomized trials in a range of clinical scenarios in patients with, and at risk for, hyperkalemia.