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Background: Coronavirus disease 2019 (COVID-19) triggers multiple components of the immune system and causes inflammation of endothelial walls across vascular beds, resulting in respiratory failure, arterial and venous thrombosis, myocardial injury, and multi-organ failure leading to death. Early in the COVID-19 pandemic, aspirin was suggested for the treatment of symptomatic individuals, given its analgesic, antipyretic, anti-inflammatory, anti-thrombotic, and antiviral effects. This study aimed to evaluate the association of aspirin use with various clinical outcomes in patients hospitalized for COVID-19., Methods: This was a retrospective study involving patients aged ≥ 18 years and hospitalized for COVID-19 from March 2020 to October 2020. Primary outcomes were acute cardiovascular events (ST elevation myocardial infarction (STEMI), type 1 non-ST elevation myocardial infarction (NSTEMI), acute congestive heart failure (CHF), and acute stroke) and death. Secondary outcomes were respiratory failure, need for mechanical ventilation, and acute deep vein thrombosis (DVT)/pulmonary embolism (PE)., Results: Of 376 patients hospitalized for COVID-19, 128 were taking aspirin. Significant proportions of native Americans were hospitalized for COVID-19 in both aspirin (22.7%) and non-aspirin (24.6%) groups. Between aspirin and non-aspirin groups, no significant differences were found with regard to mechanical ventilator support (21.1% vs. 15.3%, P = 0.16), acute cardiovascular events (7.8% vs. 5.2%, P = 0.32), acute DVT/PE (3.9% vs. 5.2%, P = 0.9), readmission rate (13.3% vs. 12.9%, P = 0.91) and mortality (23.4% vs. 20.2%, P = 0.5); however, the median duration of mechanical ventilation was significantly shorter (7 vs. 9 days, P = 0.04) and median length of hospitalization was significantly longer (5.5 vs. 4 days, P = 0.01) in aspirin group compared to non-aspirin group., Conclusion: No significant differences were found in acute cardiovascular events, acute DVT/PE, mechanical ventilator support, and mortality rate between hospitalized COVID-19 patients who were taking aspirin compared to those not taking aspirin. However, larger studies are required to confirm our findings., Competing Interests: Authors have no conflict of interest to declare., (Copyright 2024, Vinod et al.)

Background: Impaired renal function has been shown in previous studies to be an independent predictor of cardiovascular adverse events amongst patients admitted for percutaneous coronary intervention (PCI) following ST-segment elevation myocardial infarction (STEMI). This study investigates the impact of admission serum creatinine (SCr) on major cardiovascular outcomes among STEMI patients undergoing PCI., Methods: A retrospective study of patients admitted for PCI following STEMI was conducted using the National Cardiovascular Database Action Registry (NCDR) at Cleveland Clinic Akron General (CCAG) Hospital. The primary outcome was a composite of major clinical events: cardiogenic shock, atrial fibrillation, ventricular tachycardia/fibrillation, heart failure, bleeding and mechanical ventilation. SCr was an independent and continuous variable., Results: A total of 656 patients included in the study with the diagnosis of STEMI who subsequently underwent primary PCI. Patients with eGFR < 60 mL/min/1.73 m 2 on admission had an increased incidence of cardiogenic shock (P = 0.001), bleeding (P < 0.001), heart failure (P < 0.0005) and higher mortality rates (P = 0.0005). Furthermore, in the setting of STEMI, elevated SCr was also associated with an increased risk of developing major adverse events like cardiogenic shock (P = 0.05), bleeding (P = 0.05), and heart failure (P = 0.005)., Conclusions: In the setting of STEMI, elevated SCr and eGFR < 60 mL/min/1.73 m 2 was associated with an increased risk of developing major adverse events including cardiogenic shock, bleeding and heart failure., Competing Interests: The authors have no conflict of interest to declare

Heart and kidney failure continued to be of increasing prevalence in today's society, and their comorbidity has synergistic effect on the morbidity and mortality of patients. Cardiorenal syndrome (CRS) is a complex disease with multifactorial pathophysiology. Better understanding of this pathophysiological network is crucial for the successful intervention to prevent advancement of the disease process. One of the major factors in this process is neurohormonal activation, predominantly involving renin-angiotensin-aldosterone system (RAAS) and arginine vasopressin (AVP). Heart failure causes reduced cardiac output/cardiac index (CO/CI) and fall in renal perfusion pressures resulting in activation of baroreceptors and RAAS, respectively. Activated baroreceptors and RAAS stimulate the release of AVP (non-osmotic pathway), which acts on V 2 receptors located in the renal collecting ducts, causing fluid retention and deterioration of heart failure. Effective blockade of AVP action on V 2 receptors has emerged as a potential treatment option in volume overload conditions especially in the setting of hyponatremia. Vasopressin receptor antagonists (VRAs), such as vaptans, are potent aquaretics causing electrolyte-free water diuresis without significant electrolyte abnormalities. Vaptans are useful in hypervolemic hyponatremic conditions like heart failure and liver cirrhosis, and euvolemic hyponatremic conditions like syndrome of inappropriate anti-diuretic hormone secretion. Tolvaptan and conivaptan are pharmaceutical agents that are available for the treatment of these conditions., Competing Interests: Authors have no conflicts of interest to declare.