Deep vein thrombosis (DVT) and pulmonary embolism (PE) are key complications of coronavirus disease 2019 (COVID-19). The study's primary outcome was assessing the utility of Wells DVT, Wells PE scores, and D-dimers in diagnosing DVT and PE. Secondary outcomes were the risk factors for the development of PE and DVT in COVID-19 patients. We compared COVID-19 patients with a positive and negative lower extremity (LE) duplex. A similar approach was made for patients who underwent imaging for PE. The prevalence of PE was 23.8% (26 out of 109 patients), and the prevalence of DVT was 33% (35 out of 106). A D-dimer of 500 ng/mL had a sensitivity of 95.6% and 93.7% for the diagnosis of PE and DVT, respectively. A Wells DVT score of 3 points had a specificity of 92.9% and sensitivity of 8.8% for DVT diagnosis in COVID-19. A Wells PE score of 4 had a specificity of 100% and a sensitivity of 20% for the diagnosis of PE. The combined approach of using a Wells DVT score of 3 in suspected DVT and a Wells PE score of 4 in suspected PE and D-dimers of 500 ng/ml has a sensitivity of 94.2% and 96.1%, respectively. In the suspected DVT group, male gender (OR 3.88, 95% CI 1.55-9.7, P=0.004), lower body mass index (BMI) (OR 0.92, 95% CI 0.86-0.99, P=0.037), antiplatelet use (OR 0.19, 95% CI 0.04-0.88, P=0.035), systolic blood pressure ≤100 mmhg (OR 4.96, 95% CI 1.37-17.86, P=0.014), absolute lymphocytes ≤1 (OR 2.57, 95% CI 1.07-6.12, P=0.033), D-dimer ≥500 ng/ml (OR 6.42, 95% CI 1.40-29.38, P=0.016), blood urea nitrogen (BUN) ≥20 mg/dl (OR 2.33, 95% CI 1.00-5.41, P=0.048), and intubation (OR 3.32, 95% CI 1.26-8.78, P=0.015) were found to be statistically significant for DVT. In the suspected PE group, history of cancer (OR 10.69, 95% CI 1.06-107.74, P=0.044), total WBC count (OR 1.07, 95% CI 0.95-1.21, P=0.032), platelets ≥ 400,000 (OR 5.13, 95% CI 1.79-14.68, P=0.002), D-dimer levels ≥ 500 ng/ml (OR 25.47, 95% CI 3.27-197.97, P=0.002), Wells PE score (OR 2.46, 95% CI 1.50-4.06, P<0.001), pulmonary embolism rule-out criteria (PERC) score (OR 1.79, 95% CI 1.05-3.05, P=0.054), and Sequential Organ Failure Assessment (SOFA) score (OR 1.91, 95% CI 1.16-3.12, P=0.002) were statistically significant. The combined approach of using a Wells DVT score of 3 in suspected DVT and Wells PE score of 4 in suspected PE and D-dimers of 500 ng/ml may be used to diagnose PE and DVT in COVID-19. Venous thromboembolism (VTE) occurrence in COVID-19 is associated with non-traditional risk factors such as intubation and higher severity of systemic inflammation, and these patients may benefit from more aggressive testing for VTE.

Background-Previous studies on coronavirus disease 2019 (COVID-19) were limited to specific geographical locations and small sample sizes. Therefore, we used the National Inpatient Sample (NIS) 2020 database to determine the risk factors for severe outcomes and mortality in COVID-19. Methods-We included adult patients with COVID-19. Univariate and multivariate logistic regression was performed to determine the predictors of severe outcomes and mortality in COVID-19. Results-1,608,980 (95% CI 1,570,803–1,647,156) hospitalizations with COVID-19 were included. Severe complications occurred in 78.3% of COVID-19 acute respiratory distress syndrome (ARDS) and 25% of COVID-19 pneumonia patients. The mortality rate for COVID-19 ARDS was 54% and for COVID-19 pneumonia was 16.6%. On multivariate analysis, age > 65 years, male sex, government insurance or no insurance, residence in low-income areas, non-white races, stroke, chronic kidney disease, heart failure, malnutrition, primary immunodeficiency, long-term steroid/immunomodulatory use, complicated diabetes mellitus, and liver disease were associated with COVID-19 related complications and mortality. Cardiac arrest, septic shock, and intubation had the highest odds of mortality. Conclusions-Socioeconomic disparities and medical comorbidities were significant determinants of mortality in the US in the pre-vaccine era. Therefore, aggressive vaccination of high-risk patients and healthcare policies to address socioeconomic disparities are necessary to reduce death rates in future pandemics.

Coronavirus disease 2019 (COVID-19) infection is associated with troponin elevation, which is associated with increased mortality. However, it is not clear if troponin elevation is independently linked to increased mortality in COVID-19 patients. Although there is considerable literature on risk factors for mortality in COVID-19-associated myocardial injury, the Global Registry of Acute Coronary Events (GRACE), Thrombolysis in Myocardial Infarction (TIMI), and Sequential Organ Failure Assessment (SOFA) scores have not been studied in COVID-19-related myocardial injury. This data is important in risk-stratifying COVID-19 myocardial injury patients. Of the 1,500 COVID-19 patients admitted to our hospitals, 217 patients who had troponin levels measured were included. Key variables were collected manually, and univariate and multivariate cox regression analysis was done to determine the predictors of mortality in COVID-19-associated myocardial injury. The differences in clinical profiles and outcomes of COVID-19 patients with and without troponin elevation were compared. Mortality was 26.5% in the normal troponin group and 54.6% in the elevated troponin group. Patients with elevated troponins had increased frequency of hypotension (p = 0.01), oxygen support (p < 0.01), low absolute lymphocyte (p < 0.01), elevated blood urea nitrogen (p < 0.01), higher C-reactive protein (p < 0.01), higher D-dimer (p < 0.01), higher lactic acid (p < 0.01), and higher Quick SOFA (qSOFA), SOFA, TIMI, and GRACE (all scores p < 0.01). On univariate cox regression, troponin elevation (hazard ratio (HR) = 1.85, 95% confidence interval (CI) = 1.18-2.88, p < 0.01), TIMI score >3 (HRv = 1.79, 95% CI = 1.11-2.75, p = 0.01), and GRACE score >140 (HR = 2.27, 95% CI = 1.45-3.55, p < 0.01) were highly associated with mortality, whereas cardiovascular disease (HR = 1.40, 95% CI = 0.89-2.21, p = 0.129) and cardiovascular risk factors (HR = 1.15, 95% CI = 0.73-1.81, p = 0.52) were not. After adjusting for age, use of a non-rebreather or high-flow nasal cannula, hemoglobin <8.5 g/dL, suspected or confirmed source of infection, and qSOFA and SOFA scores (HR = 1.18, 95% CI = 1.07-1.29, p < 0.01) were independently associated with mortality, whereas troponin (HR = 1.08, 95% CI = 0.63-1.85, p = 0.76), TIMI score (HR = 1.02, 95% CI = 0.99-1.06, p = 0.12) and GRACE scores (HR = 1.01, 95% CI = 0.99-1.02, p = 0.10) were not associated with mortality. Our study shows that troponin, GRACE score, and TIMI score are not independent predictors of mortality in COVID-19 myocardial injury. This may be because troponin elevation in COVID-19 patients may be related to demand ischemia rather than acute coronary syndrome-related. This was shown by the association of troponin with a higher degree of systemic inflammation and end-organ dysfunction. Therefore, we recommend SOFA scores in risk-stratifying COVID-19 patients with myocardial injury.

Introduction: Spontaneous coronary artery dissection (SCAD) is a common cause of Myocardial infarction (MI) in women less than 50 years of age (1). SCAD has a high recurrent rate, and beta blockers are the only drug shown to reduce the recurrence of SCAD. However, in our clinical practice, we could not use beta-blockers in some of our patients due to sinus bradycardia of unclear cause. Therefore, we planned to study if SCAD could cause Bradycardia. Purpose: To determine if Bradycardia is associated with SCAD. Methodology: Utilising the National Inpatient Sample (NIS) from 2016 to 2020, we performed a multivariable logistic regression analysis to determine if SCAD was independently associated with Bradycardia (ICD-10 code R0.01) among adults. SCAD was defined as coronary artery dissection (ICD-10 code I25.42) after excluding patients who had PCI. Results: A- A total of 2,561,434 (95% CI 2,526,646-2,596,222) weighted hospitalisations with Bradycardia and 18,049 (95% CI 17,288-18,811) with SCAD was included. Bradycardia was present in 5.2% (95% CI 4.6-6) of patients with SCAD and 1.7% (95% 1.7-1.7) in patients without SCAD. After adjusting for relevant causes of Bradycardia, SCAD was highly associated with Bradycardia (OR 3.04, 95% CI 2.61-3.55). Among all the risk factors studied, SCAD showed the 2nd highest strength of association (Table 1). Discussion: We report the first described association of SCAD with Bradycardia in literature. Although the prevalence of Bradycardia with SCAD in our study is only 5.2%, Bradycardia is frequently not coded, and we suspect the true frequency of Bradycardia in SCAD is much higher. The exact mechanism for this association is unclear. Although the frequency of beta-blocker use is not available in our study, several other conditions, such as ischemic heart disease and cardiomyopathy, which involve more frequent beta-blocker use, did not show a degree of association as strong as SCAD with bradycardia. Therefore, we hypothesize Bradycardia could be from SCAD itself, and the current ongoing BA-SCAD (Beta-blockers and Antiplatelet agents in patients with Spontaneous Coronary Artery Dissection) trial could shed light on this association (2).

Background: Many arrhythmias are known to be triggered by hormonal imbalances. Polycystic ovarian syndrome (PCOS) is a common hormonal imbalance seen in reproductive aged women. There is sparse literature linking PCOS to increased risk of atrial fibrillation (1). We hypothesise that PCOS could also be associated with Supraventricular tachycardia (SVT) Purpose: To determine if PCOS is a risk factor for SVT and Atrial fibrillation/flutter (AF/AFL). Methods: Utilising the National Inpatient Sample (NIS) of the years 2015-2020, We performed a multivariable logistic regression analysis to determine if PCOS was independently associated with SVT and AF/AFL. The NIS is the largest publicly available database of United States containing data on upto 7 million hospital visits per year. Results: From the years 2015 to 2020, PCOS was present in 367,375 adult patients and SVT was observed in 965, 799 patients. After adjusting for relevant risk factors, PCOS was associated with increased odds of SVT (OR 1.23, 95% CI 1.12-1.36, P<0.001) (Table 1). However, PCOS was not associated with increased odds of atrial fibrillation and atrial flutter (OR 0.72, 95% CI 0.66-0.77, P<0.001) Conclusion: SVTs have been clinically observed to be more frequent in the luteal phase of the menstrual cycle due to low estrogen. The high androgen/estrogen ratio seen in PCOS may result in a similar increased risk of SVT in PCOS patients. PCOS is known to increase P wave maximum duration and dispersion, indicating abnormal atrial conduction (2). The negative association between AF/AFL is likely because PCOS is seen more commonly in younger patients, and AF/AFL is a disease of older adults. We recommend further studies in PCOS women to confirm our findings and characterise the mechanisms of SVT.