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Abstract Introduction The majority of studies evaluating the effect of myocardial injury on the survival of COVID-19 patients have been performed outside of the United States (U.S.). These studies have often utilized definitions of myocardial injury that are not guideline-based and thus, not applicable to the U.S. patient population. Methods The current study is a two-part investigation of the effect of myocardial injury on the clinical outcome of patients hospitalized with COVID-19. The first part is a retrospective analysis of 268 patients admitted to our healthcare system in Toledo, Ohio, U.S.; the second part is a systematic review and meta-analysis of all similar studies performed within the U.S. Results In our retrospective analysis, patients with myocardial injury were older (mean age 73 vs. 59 years, P 0.001), more likely to have hypertension (86% vs. 67%, P 0.005), underlying cardiovascular disease (57% vs. 24%, P 0.001), and chronic kidney disease (26% vs. 10%, P 0.004). Myocardial injury was also associated with a lower likelihood of discharge to home (35% vs. 69%, P 0.001), and a higher likelihood of death (33% vs. 10%, P 0.001), acute kidney injury (74% vs. 30%, P 0.001), and circulatory shock (33% vs. 12%, P 0.001). Our meta-analysis included 12,577 patients from 8 U.S. states and 55 hospitals who were hospitalized with COVID-19, with the finding that myocardial injury was significantly associated with increased mortality (HR 2.43, CI 2.28–3.6, P 0.0005). The prevalence of myocardial injury ranged from 9.2 to 51%, with a mean prevalence of 27.2%. Conclusion Hospitalized COVID-19 patients in the U.S. have a high prevalence of myocardial injury, which was associated with poorer survival and outcomes.

Abstract Introduction The cause-and-effect relationship of QTc prolongation in Coronavirus disease 2019 (COVID-19) patients has not been studied well. Objective We attempt to better understand the relationship of QTc prolongation in COVID-19 patients in this study. Methods This is a retrospective, hospital-based, observational study. All patients with normal baseline QTc interval who were hospitalized with the diagnosis of COVID-19 infection at two hospitals in Ohio, USA were included in this study. Results Sixty-nine patients had QTc prolongation, and 210 patients continued to have normal QTc during hospitalization. The baseline QTc intervals were comparable in the two groups. Patients with QTc prolongation were older (mean age 67 vs. 60, P 0.003), more likely to have underlying cardiovascular disease (48% versus 26%, P 0.001), ischemic heart disease (29% versus 17%, P 0.026), congestive heart failure with preserved ejection fraction (16% versus 8%, P 0.042), chronic kidney disease (23% versus 10%, P 0.005), and end-stage renal disease (12% versus 1%, P

Background: Balloon angioplasty is the standard endovascular treatment for symptomatic infrapopliteal peripheral artery disease (PAD). However, recent trials have studied the effectiveness of drug-eluting stents (DES) for infrapopliteal PAD. Objective: This study investigated the use of DES compared with standard endovascular techniques for treatment of infrapopliteal artery disease. Methods: This is a comprehensive systematic review and meta-analysis of 9 recent randomized controlled trials. The primary clinical outcome assessed was primary patency. The secondary outcomes were target lesion revascularization (TLR), major limb amputation, and all-cause mortality. Results: A total of 945 patients met the inclusion criteria. Patients treated with DES were found to have increased primary patency than control at maximum follow-up (hazard ratio [HR] 2.17, 95% confidence interval [CI] 1.58-2.97, P < .0001, I2 = 62%). A similar result was seen in the subgroup of patients with critical limb ischemia (HR 2.58, 95% CI 1.49-4.49, P = .0008, I2 = 75%). DES were associated with significantly lower rates of TLR than control at maximum follow-up (HR 0.48, 95% CI 0.33-0.68, P < .0001; I2 = 11%). There was no statistical difference between DES versus control in rates of major limb amputation and mortality. Conclusions: DES have superior primary patency and TLR rates with no difference in amputation and all-cause mortality rates compared with conventional endovascular therapies in patients with infrapopliteal PAD.

Paraoxonase-1 (PON-1) is a hydrolytic enzyme associated with HDL, contributing to its anti-inflammatory, antioxidant, and anti-atherogenic properties. Deficiencies in PON-1 activity result in oxidative stress and detrimental clinical outcomes in the context of chronic kidney disease (CKD). However, it is unclear if a decrease in PON-1 activity is mechanistically linked to adverse cardiovascular events in CKD. We investigated the hypothesis that PON-1 is cardioprotective in a Dahl salt-sensitive model of hypertensive renal disease. Experiments were performed on control Dahl salt-sensitive rats (SSMcwi, hereafter designated SS-WT rats) and mutant PON-1 rats (SS-Pon1em1Mcwi, hereafter designated SS-PON-1 KO rats) generated using CRISPR gene editing technology. Age-matched 10-week-old SS and SS-PON-1 KO male rats were maintained on high-salt diets (8% NaCl) for five weeks to induce hypertensive renal disease. Echocardiography showed that SS-PON-1 KO rats but not SS-WT rats developed compensated left ventricular hypertrophy after only 4 weeks on the high-salt diet. RT-PCR analysis demonstrated a significant increase in the expression of genes linked to cardiac hypertrophy, inflammation, and fibrosis, as well as a significant decrease in genes essential to left ventricular function in SS-PON-1 KO rats compared to SS-WT rats. A histological examination also revealed a significant increase in cardiac fibrosis and immune cell infiltration in SS-PON-1 KO rats, consistent with their cardiac hypertrophy phenotype. Our data suggest that a loss of PON-1 in the salt-sensitive hypertensive model of CKD leads to increased cardiac inflammation and fibrosis as well as a molecular and functional cardiac phenotype consistent with compensated left ventricular hypertrophy.

Vascular calcification (VC) is one of the major causes of cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD). VC is a complex process expressing similarity to bone metabolism in onset and progression. VC in CKD is promoted by various factors not limited to hyperphosphatemia, Ca/Pi imbalance, uremic toxins, chronic inflammation, oxidative stress, and activation of multiple signaling pathways in different cell types, including vascular smooth muscle cells (VSMCs), macrophages, and endothelial cells. In the current review, we provide an in-depth analysis of the various kinds of VC, the clinical significance and available therapies, significant contributions from multiple cell types, and the associated cellular and molecular mechanisms for the VC process in the setting of CKD. Thus, we seek to highlight the key factors and cell types driving the pathology of VC in CKD in order to assist in the identification of preventative, diagnostic, and therapeutic strategies for patients burdened with this disease.