Background In this systematic review and meta-analysis, we aimed to investigate the correlation of D-dimer levels measured on admission with disease severity and the risk of death in patients with coronavirus disease 2019 (COVID-19) pneumonia. Materials and methods We performed a comprehensive literature search from several databases. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were followed in abstracting data and assessing validity. Quality assessment was performed using the Newcastle-Ottawa quality assessment scale (NOS). D-dimer levels were pooled and compared between severe/non-severe and surviving/non-surviving patient groups. Weighted mean difference (WMD), risk ratios (RRs) and 95% confidence intervals (CIs) were analyzed. Results Thirty-nine studies reported on D-dimer levels in 5750 non-severe and 2063 severe patients and 16 studies reported on D-dimer levels in 2783 surviving and 697 non-surviving cases. D-dimer levels were significantly higher in patients with severe clinical status (WMD: 0.45 mg/L, 95% CI: 0.34–0.56; p < 0.0001). Non-surviving patients had significantly higher D-dimer levels compared to surviving patients (WMD: 5.32 mg/L, 95% CI: 3.90–6.73; p < 0.0001). D-dimer levels above the upper limit of normal (ULN) was associated with higher risk of severity (RR: 1.58, 95% CI: 1.25–2.00; p < 0.0001) and mortality (RR: 1.82, 95% CI: 1.40–2.37; p < 0.0001). Conclusion Increased levels of D-dimer levels measured on admission are significantly correlated with the severity of COVID-19 pneumonia and may predict mortality in hospitalized patients.

Objective COVID-19 is a disease with high mortality, and risk factors for worse clinical outcome have not been well-defined yet. The aim of this study is to delineate the prognostic importance of presence of concomitant cardiac injury on admission in patients with COVID-19. Methods For this multi-center retrospective study, data of consecutive patients who were treated for COVID-19 between 20 March and 20 April 2020 were collected. Clinical characteristics, laboratory findings and outcomes data were obtained from electronic medical records. In-hospital clinical outcome was compared between patients with and without cardiac injury. Results A total of 607 hospitalized patients with COVID-19 were included in the study; the median age was 62.5 ± 14.3 years, and 334 (55%) were male. Cardiac injury was detected in 150 (24.7%) of patients included in the study. Mortality rate was higher in patients with cardiac injury (42% vs. 8%; P < 0.01). The frequency of patients who required ICU (72% vs. 19%), who developed acute kidney injury (14% vs. 1%) and acute respiratory distress syndrome (71%vs. 18%) were also higher in patients with cardiac injury. In multivariate analysis, age, coronary artery disease (CAD), elevated CRP levels, and presence of cardiac injury [odds ratio (OR) 10.58, 95% confidence interval (CI) 2.42–46.27; P < 0.001) were found to be independent predictors of mortality. In subgroup analysis, including patients free of history of CAD, presence of cardiac injury on admission also predicted mortality (OR 2.52, 95% CI 1.17–5.45; P = 0.018). Conclusion Cardiac injury on admission is associated with worse clinical outcome and higher mortality risk in COVID-19 patients including patients free of previous CAD diagnosis.

We investigated whether the neutrophil to lymphocyte ratio (NLR) can predict stent thrombosis (STh) and high mortality rate in patients with ST-segment elevation myocardial infarction (STEMI). We analyzed data of 102 patients with STh and 450 patients with STEMI admitted to 2 high volume hospitals. Preprocedural NLR was significantly higher in patients with STh (P < .001). There was a significantly higher mortality rate in patients with high NLR during hospitalization (P < .001). Also, in the STh group there was a significantly higher mortality rate in patients with high NLR (P < .001). In receiver-operating characteristic analysis, NLR >4.8 had 56% sensitivity and 68% specificity for predicting STh. The NLR >4.9 had 70% sensitivity and 65% specificity for predicting in-hospital mortality. On multivariate regression analysis, NLR was found to be significantly related to STh. In patients with STEMI, preprocedural high NLR is associated with both STh and higher mortality rates.

COVID-19 patients with cardiac involvement have a high mortality rate. The aim of this study was to investigate the echocardiographic features in COVID-19 patients between severe and non-severe groups.For this single-center study, data from patients who were treated for COVID-19 between March 25, 2020 and April 15, 2020 were collected. Two-dimensional echocardiography (2DE) images were obtained for all patients. Patients were divided into two groups based on the severity of their COVID-19 infections. 2DE parameters indicating right ventricular (RV) and left ventricular (LV) functions were compared between the two groups.A total of 90 patients hospitalized for COVID-19 were included in this study. The mean age of the severe group (n = 44) was 63.3 ± 15.7 years, and 54% were male. The mean age of non-severe group (n = 46) was 49.7 ± 21.4 years, and 47% were male. In the severe group, RV and LV diameters were larger (RV, 36.6 ± 5.9 mm vs. 33.1 ± 4.8 mm, p = 0.003; LV 47.3 ± 5.8 mm vs. 44.9 ± 3.8 mm, p = 0.023), the LE ejection fraction (LVEF) and the RV fractional area change (RV-FAC) were lower (LVEF, 54.0 ± 9.8% vs. 61.9 ± 4.8%, p < 0.001; RV-FAC, 41.4 ± 4.1% vs. 45.5 ± 4.5%, p < 0.001), and pericardial effusions were more frequent (23% vs. 0%) compared to patients in the non-severe group. A multiple linear regression analysis determined that LVEF, right atrial diameter, high-sensitivity troponin I, d-dimer, and systolic pulmonary artery pressure, were independent predictors of RV dilatation.The results demonstrate that both right and left ventricular functions decreased due to COVID-19 infection in the severe group. 2DE is a valuable bedside tool and may yield valuable information about the clinical status of patients and their prognoses.

Hematologic parameters such as mean platelet volume (MPV), red cell distribution width (RDW), and neutrophil to lymphocyte (N/L) ratio are associated with increased cardiovascular risk. We investigated the effect of atorvastatin on hematologic parameters in patients with hypercholesterolemia. A total of 79 patients with hypercholesterolemia and 47 normocholesterolemic healthy participants were included. Patients with hypercholesterolemia received 10 to 80 mg/d atorvastatin during a 24-week period. Hematologic parameters were measured at baseline and after 6 months. Atorvastatin treatment produced a significant decrease in MPV levels (9.3 ± 1.3 vs 9.1 ± 1.2 fL, P = .008) and platelet count (259 ± 61 vs 248 ± 51 10(9)/L, P = .005). The N/L ratio decreased significantly after atorvastatin treatment from 2.9 ± 1.2 to 2.6 ± 1.1, (P = .014). The RDW and platelet distribution width levels were not different among the study groups, before and after treatment. Atorvastatin may beneficially reduce MPV levels and N/L ratio. This antiplatelet and anti-inflammatory effect of atorvastatin treatment could play a role in reducing cardiovascular risk.

CIN was observed in 20.5% of patients. Advanced age, male gender, elevated creatinine, uric acid and phosphate levels, and low glomerular filtration rate were correlated with the development of CIN. Correlation analysis also showed a significant association between the ALP level and the development of CIN (126.1 ± 144.9 vs. 97.2 ± 46.9, p = 0.004). Univariate regression analysis also showed the impact of ALP on the development of CIN (OR 1.004, 95% CI 1.001–1.007, p = 0.02). Conclusions: Our outcomes indicate a possible active role of ALP in the mechanism of CIN. An elevated ALP level may predict the development of CIN.

We searched PubMed, Embase, Web of Science, and Cochrane Library up to October 2015 for eligible studies. We selected studies with fQRS defined with 12-lead ECG during the index hospitalization of STEMI/NSTEMI. Primary outcomes were in-hospital and long-term cardiovascular events. In-hospital mortality was significantly higher in fQRS (+) group (99/733; 13.5%) compared to fQRS (-) group (47/1293; 3.6%) (OR 4.03 95% CI 1.81-8.94; P = 0.0006). Long-term mortality rate was higher in fQRS (+) group (89/473; 18.8%) compared to fQRS (-) group (54/1009; 5.3%) (OR 3.93 95% CI 1.92-8.05; P = 0.0002). In addition the frequency of long-term MACE was higher in fQRS (+) group (46.9%) compared to fQRS (-) group (14.6%) (OR 5.13 95% CI 2.77-9.51; P < 0.00001) CONCLUSION: Presence of fQRS on admission ECG was found to be predictor of mortality, MACE, deterioration of LV function, and presence of multivessel disease in patients with STEMI and NSTEMI.

Contrast-induced nephropathy (CIN) accounts for 10% of hospital-acquired renal failure, causes a prolonged in-hospital stay and represents a powerful predictor of poor clinical outcome. The underlying mechanism of the CIN development remains unclear and seems to be multifactorial. The potential link between platelet indices such as mean platelet volume (MPV) and platelet distribution width (PDW) with CIN is unknown. Herein, we aimed to investigate the correlation between MPV and PDW levels with the development of CIN. The incidence of CIN (20.5%) was prospectively evaluated in 430 patients with diagnosis of acute coronary syndrome. Initial creatinine (1.13 ± 0.25 vs. 1.05 ± 0.27 mg/dl, P = 0.01) and PDW (40.1 ± 20.2 vs. 34.5 ± 19.9%, P = 0.02) levels and the total volume of contrast media used (121 ± 61 vs. 94 ± 42 ml, P = 0.01) were higher in patients who developed CIN. MPV was similar between the two groups (P = 0.80). In a univariate regression analysis, age, increased creatinine, uric acid, phosphate, PDW levels and higher total volume of contrast media used were significantly correlated with CIN incidence. However, in a multivariate analysis, only total volume of CM used [odds ratio (OR) 1.011, 95% confidence interval (CI) 1.006-1.016; P = 0.01], increased age (OR 1.026, 95% CI 1.00-1.052; P = 0.05) and increased PDW levels (OR 1.009, 95% CI 1.00-1.022; P = 0.04) remained as the independent predictors of CIN. Among platelet indices, PDW, but not MPV, was associated with CIN development. The clinical significance of such link remains unclear, but may indicate involvement of platelet activation in CIN pathogenesis.