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Background: The arrhythmic burden and cardiovascular risks of cardiac amyloidosis compared with other types of restrictive cardiomyopathies (RCM), such as hemochromatosis and cardiac sarcoid, have not been well characterized in the literature. An increase in emphasis on screening has resulted in more diagnoses of cardiac amyloidosis and a larger data pool to analyze the cardiovascular outcomes of this cardiomyopathy. Methods and results: We queried the National Inpatient Sample (NIS) database to identify all adult patients diagnosed with cardiac amyloidosis or other RCM between the years 2016 and 2019. Discharge-weighted analysis using survey regressions accounts for discharge weights and characteristics found to be significantly different between groups. A total sample size of 13 345 patients was obtained, including cardiac amyloidosis (N = 8365; 62.7%) and other RCM (N = 4980; 37.3%). Cardiac amyloidosis was associated with a significantly increased risk of stroke (Odds ratio = 3.91: 95% confidence interval = [2.15, 7.11], P

Cardiopulmonary exercise testing allows for a comprehensive assessment of the mechanism of exercise limitation in pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension. Competitive pathophysiologic mechanisms may affect the clinical interpretation of cardiopulmonary disease as they relate to dyspnea, leg fatigue, and exercise intolerance.

Objectives To construct a new scoring system utilizing biomarkers, vitals, and imaging data to predict 30-day mortality in acute pulmonary embolism (PE). Background Acute PE, a well-known manifestation of venous thromboembolic disease, is responsible for over 100,000 deaths worldwide yearly. Contemporary management algorithms rely on a multidisciplinary approach to care via PE response teams (PERT) in the identification of low, intermediate, and high-risk patients. The PESI and sPESI scores have been used as cornerstones of the triage process in assigning risk of 30-day mortality for patients presenting with acute PE; however, the specificity of these scoring systems has often come into question. Methods This study retrospectively analyzed 488 patients with acute PE who were managed at a tertiary care institution with either conservative therapy consisting of low molecular weight or unfractionated heparin, advanced therapies consisting of catheter directed therapies, aspiration thrombectomy, or a combination of these therapies, or surgical embolectomy. The CLOT-5 score was designed to include vital signs, biomarkers, and imaging data to predict 30-day mortality in patients presenting with acute PE. Results The CLOT-5 score had an area under the curve (AUC) of 0.901 with a standard error of 0.29, while the PESI and sPESI scores had an AUC and standard errors of 0.793 ±­ 0.43 and 0.728 ± 0.55, respectively. Conclusions When incorporated into the management algorithms of national PERT programs, the CLOT-5 score may allow for rapid and comprehensive assessment of patients with acute PE at high risk for clinical decompensation, leading to early escalation of care where appropriate.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a complication of incomplete resolution of acute pulmonary embolism. We hypothesize changes in CT Hounsfield Unit gradient (HU-Δ) created by the dispersion of IV contrast through the downstream blood pool correlate with cardiac index (CI). We sought to compare HU-Δ with invasively obtained CI. Methods: We completed a retrospective analysis of CTEPH patients in which individuals with low CI (2) were identified. Both absolute and fractional HU-Δ were derived from pulmonary CTA by subtracting the HU value of the left atrium (LA) and left ventricle (LV) from the main pulmonary artery (MPA) (absolute) and expressing them as a percentage of MPA-HU (fractional) on static axial images. These were compared between low and normal CI. Results: Of the 237 patients, 50.2% were female, 53.2% were White, 36.7% were Black. Hemodynamics were mean pulmonary artery (PA) pressure = 45.4 ± 11.2-mmHg, pulmonary vascular resistance = 9.2 ± 4.4-WU, CI = 2.05 ± 0.48-L/min/m2. There was a higher mean MPA-HU = 391.1 ± 113.6 than LA-HU = 251.6 ± 81. In patients with low CI, the HU-Δ was higher, HU-ΔMPA-LA was 148.9 ± 78.4 vs. 124.5 ± 77.2 (p = 0.02), and HU-ΔMPA-LV was 170.7 ± 87 vs. 140 ± 82 (p = 0.009). A HU-ΔMPA-LA = 118 had a sensitivity of 75.6% and specificity of 77% to detect low CI, AUC 0.61, p = 0.003. A HU-ΔPA-LV = 156 had a sensitivity of 77% and specificity of 53% to detect low CI, AUC = 0.62, p = 0.001. A fractional reduction HU-ΔMPA-LA of 35% had a sensitivity and specificity of 79% and 53%, respectively, to detect low CI (AUC 0.65, p < 0.001). A fractional reduction of the HU-ΔMPA-LV of 40% had a sensitivity and specificity of 80% and 55%, respectively, to detect low CI (AUC 0.65, p < 0.001). HU Δ were highly reproducible (Kappa = 0.9, p < 0.001, 95% CI 0.86–0.95). Conclusions: High HU Δ between MPA-LA and MPA-LV were associated with low CI in patients with CTEPH.

Angiotensin II type 1 receptor antibodies (AT1R-Ab) are among the most investigated type of non-human leukocyte antigen antibodies in solid organ transplantation, particularly given its association with allograft dysfunction. Some prior studies have described the development of AT1R antibodies in patients with durable mechanical circulatory support (MCS); however, the role of temporary MCS in autoantibody development is still uncertain. Given that the current United Network For Organ Sharing (UNOS) allocation system prioritizes heart transplant recipients in cardiogenic shock requiring temporary MCS, we investigated the development of these antibodies in 10 patients with temporary MCS (Impella 5.5 n = 8, Intra-aortic balloon pump n = 2) listed for heart transplant. We found that 7 out of 8 (87.5%) patients supported with Impella developed AT1R-Ab, while the remaining 1 patient was borderline positive. Two patients supported with an intra-aortic balloon pump did not develop AT1R-Ab. We attribute this difference to the endothelial shear stress imparted by Impella devices, although more investigation is needed.

Preeclampsia is the most common cause of morbidity and mortality in pregnancy, the incidence being significantly higher in low-income countries with reduced access to health care. Women with preeclampsia are at a higher risk of developing cardiovascular disease with a poorer long-term outcome. Early recognition and treatment are key to improving short- and long-term outcomes. Approximately 3%–5% of pregnant women will develop preeclampsia, with potentially fatal outcomes. Despite ongoing research, the exact pathophysiologic mechanism behind its development remains unclear. In this brief report, we describe the potential role of natriuretic peptides as biomarkers in the imminent development of preeclampsia. In a retrospective manner, we analyzed changes in the left ventricular ejection fraction and left atrial volume and increases in natriuretic peptide in correlation with the development of preeclampsia. We found that three out of four patients developed a significant increase in natriuretic peptide, which correlated with the development of preeclampsia and/or peripartum cardiomyopathy. Significant increases in natriuretic peptides around the time of delivery might be a marker for the imminent development of preeclampsia. Close monitoring of natriuretic peptide levels in the peripartum period could give important insight into the imminent development of preeclampsia in high-risk patients. Close follow-up in specialized cardio-obstetric clinics is highly recommended.

Background Acute pulmonary embolism (PE) is a heterogeneous disease process with variable presentation and outcomes. The endogenous fibrinolytic system is a complex framework of regulatory pathways that maintains homeostasis by dissolving overabundant thrombi. We sought to investigate phenotypic profiles of the endogenous fibrinolytic system among patients presenting with acute PE and their impact on mortality. Methods We enrolled all consecutive patients with acute PE in our institutional Pulmonary Embolism Response Team registry. We collected blood samples at the time of PE diagnosis and analyzed concentrations of plasminogen activator inhibitor 1 (PAI-1), thrombin-activatable fibrinolysis inhibitor (TAFI), and alpha-2-antiplasmin (A2A). We assessed the association of concentration of fibrinolytic inhibitors and 1-year all-cause mortality and various echocardiographic markers of right ventricular (RV) dysfunction. Results There is significant variability of PAI-1, A2A, and TAFI concentrations across the spectrum of PE risk profiles with high PAI-1, low TAFI, and low A2A (herein referred to as a high-risk biomarker profile) correlating with worse PE severity. High-risk biomarker profile correlated with high-risk echocardiographic features of RV dysfunction, including increased RV/left ventricular (LV) ratio, low tricuspid annular plane systolic excursion, and low right ventricular outflow tract velocity time integral. Higher-risk biomarker profile was able to discriminate and independently identify patients at high risk of all-cause mortality (Group 2 HR 6 95% CI 1.3-27.8, Group 3 HR 12, 95% CI 1.7-86). Conclusions Further studies are needed to assess the exact pathophysiological link between fibrinolytic status and poor outcome after acute PE and to ascertain the impact of anti-inhibitors of the fibrinolytic system on response to therapy and outcomes after acute PE.

An 80-year-old man with severe nonischemic cardiomyopathy status post left ventricular assist device (LVAD) placement 11 years prior presented for recurrent LVAD alarms from internal driveline fracture. Given his partial myocardial recovery and his preference to avoid surgical procedures, percutaneous LVAD decommissioning was performed by occlusion of the outflow graft and subsequently driveline removal. (Level of Difficulty: Advanced.)

We present the characteristics and outcomes of the first 2 cases of catheter-directed thrombolysis performed in patients presenting with coronavirus disease-2019 (COVID-19)-related iliocaval thrombosis. (Level of Difficulty: Beginner.)

Acute pulmonary embolism (PE) is a potentially life-threatening manifestation of venous thromboembolic disease. Severe acute respiratory syndrome-coronavirus-2, a novel coronavirus that causes coronavirus disease-2019 (COVID-19), has been associated with an increased risk of thrombosis. We describe the therapeutic challenges of 3 patients presenting with PE and suspected or confirmed COVID-19. (Level of Difficulty: Beginner.)

Background: Anticoagulation (AC) adherence after acute pulmonary embolism (PE) is vital to prevent mortality and future recurrence of venous thromboembolism (VTE). We aimed to analyze factors affecting AC adherence after acute PE. Methods: Consecutive adult patients with CT angiography or V/Q scan confirmed acute PE were included in a single-center retrospective study from April 2016 to May 2020. Adherence data, including AC refill dates, were collected from pharmacies, and adherence measures including Continuous Measure of Medication Acquisition (CMA), Proportion of Days Covered (PDC), and Optimal Medication Adherence (OMA) were calculated per standardized formulas. Univariable and multivariable linear and logistic regression was used to analyze different variables affecting AC adherence. Results: A total of 118 out of 144 patients had sufficient follow-up data to measure adherence and were included in the final analysis. Mean age was 60 ± 15 years, with 64 (54.2%) women; 70 (59.3%) White, 26 (22%) African American, 13 (11%) Hispanic; 58 (49.2%) patients had private insurance, 48 (40.7%) Medicare, 11 (9.3%) Medicaid. Type of AC comprised of 57 (48.3%) apixaban, 17 (14.4%) rivaroxaban, 8 (6.8%) warfarin, 6 (5.1%) enoxaparin, and 30 (25.4%) patients with changing AC. In univariable regression, African American and Medicaid-insured patients had significantly lower adherence, while advancing age, apixaban usage, and 30-day follow-up clinic visit showed a higher adherence. However, in multivariable regression, African American race (PDC -0.135, p = 0.006, CI (−0.231, −0.040) | OMA Adjusted OR 0.166, p = 0.030, CI (0.033, 0.837)) and other non-White, non-Hispanic races (PDC -0.314, p = 0.009, CI (−0.548, −0.080)) were associated with lower AC adherence. Conclusion: In our study, African American and other minority race patients showed lower AC adherence after hospital admission for acute PE. Further studies are needed to address underlying contributors and improve adherence in this population.

Introduction The pathophysiology of pulmonary embolism (PE) represents complex, multifactorial processes involving blood cells, vascular endothelium, and the activation of inflammatory pathways. Platelet (P), endothelial (E), and leukocyte (L)-selectin molecules may play an important role in PE pathophysiology. We aimed to profile the biomarkers of inflammation, including selectins in PE patients, and compare them to healthy individuals. Materials and methods 100 acute PE patients and 50 controls were included in this case control study. ELISA methods were used to quantify levels of selectins, inflammatory, and hemostatic biomarkers. Results In PE patients, levels of selectin molecules as compared to controls convey increased P-selectin levels (95 ng/mL vs 40 ng/mL, p

Pulmonary embolism (PE) clinical manifestations vary widely, and that scope is not fully captured by current all-cause mortality risk models. PE is associated with inflammatory, coagulation, and hemostatic imbalances so blood cellular indices may be prognostically useful. Complete blood count (CBC) data may improve current risk models like the simplified pulmonary embolism severity index (sPESI) for all-cause mortality, offering greater accuracy and analytic ability. Acute PE patients (n = 228) with confirmatory diagnostic imaging were followed for all-cause mortality. Blood cellular indices were assessed for association to all-cause mortality and were supplemented into sPESI using multivariate logistic regression. Multiple blood cellular indices were found to be significantly associated with all-cause mortality in acute PE. sPESI including red cell distribution width, hematocrit and neutrophil-lymphocyte ratio had better predictive ability as compared to sPESI alone (AUC: 0.852 vs 0.754). Blood cellular indices contribute an inflammatory and hemodynamic perspective not currently included in sPESI. CBC with differential is a widely used, low-cost test that can augment current risk stratification tools for all-cause mortality in acute PE patients.

The complex pathophysiology of pulmonary embolism (PE) involves hemostatic activation, inflammatory processes, cellular dysfunction, and hemodynamic derangements. Due to the heterogeneity of this disease, risk stratification and diagnosis remains challenging. Biochip-array technology provides an integrated high throughput method for analyzing blood plasma samples for the simultaneous measurement of multiple biomarkers for potential risk stratification. Using biochip-array method, this study aimed to quantify the inflammatory biomarkers such as interleukin (IL)-1α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, vascular endothelial growth factor (VEGF), interferon gamma (IFN-γ), tumor necrosis factor alpha (TNF-α), monocyte chemoattractant protein-1 (MCP-1), and epidermal growth factor (EGF) in 109 clinically confirmed PE patients in comparison to the control group comprised of plasma samples collected from 48 healthy subjects. Cytokines IL-4, IL-6, IL-8, IL-10, IL-1β, and MCP-1 demonstrated varying level of significant increase ( P < 0.05) in massive-risk PE patients compared to submassive- and low-risk PE patients. The upregulation of inflammatory cytokines in PE patients observed in this study suggest that inflammation plays an important role in the overall pathophysiology of this disease. The application of biochip-array technology may provide a useful approach to evaluate these biomarkers to understand the pathogenesis and risk stratification of PE patients.

Pulmonary embolism (PE) patients have an increased prevalence and incidence of atrial fibrillation (AF). Because comorbid AF increases risk of morbidity and mortality, we sought to investigate the role of thrombo-inflammatory biomarkers in risk stratifying patients who experience an acute PE episode. Study participants were enrolled from a Pulmonary Embolism Response Team (PERT) registry between March 2016 and March 2019 at Loyola University Medical Center and Gottlieb Memorial Hospital. This cohort was divided into 3 groups: PE patients with a prior diagnosis of AF (n = 8), PE patients with a subsequent diagnosis of AF (n = 11), and PE patients who do not develop AF (n = 71). D-Dimer, CRP, PAI-1, TAFIa, FXIIIa, A2A, MP, and TFPI were profiled using the ELISA method. All biomarkers were significantly different between controls and PE patients ( P < 0.05). Furthermore, TFPI was significantly elevated in PE patients who subsequently developed AF compared to PE patients who did not develop AF (157.7 ± 19.0 ng/mL vs. 129.0 ± 9.3 ng/mL, P = 0.0386). This study suggests that thrombo-inflammatory biomarkers may be helpful in indicating an acute PE episode. Also, elevated TFPI levels may be associated with an increased risk of developing AF after a PE.

Coronavirus disease 2019 (COVID-19) is a debilitating viral infection and, to date, 628,903 people have died from it, numbers that cannot yet be compared to the 50 million who died in the 1918 flu pandemic. As COVID-19 became better understood, cardiovascular manifestations associated with it were identified. This led to a complete healthcare restructuring with virtual clinics and changes to the triaging of critically ill patients. There are a lot of questions over how COVID-19 affects patients with heart failure (HF) as this condition is a leading cause of cardiovascular death. This review describes the cardiovascular implications of COVID-19 and new practices surrounding the use of telehealth to follow up and triage patients with HF. Current practices supported by medical societies, the role of angiotensin-converting enzyme inhibitors and, finally, a brief note regarding the management of advanced HF patients will also be discussed.

The interplay between vitamin D, the renin–angiotensin system (RAS), and collagen remodeling has been implicated in the pathogenesis of various cardiovascular diseases. This study sought to explore this relationship in atrial fibrillation (AF) by profiling plasma levels of 25-hydroxyvitamin D, RAS biomarkers, and collagen remodeling biomarkers using the enzyme-linked immunosorbent assay method. We hypothesized that 25-hydroxyvitamin D levels would inversely correlate with RAS biomarkers and that levels of RAS and collagen remodeling biomarkers would positively correlate with each other. Although our AF cohort (n = 37) did not exhibit decreased 25-hydroxyvitamin D levels compared to normal controls (n = 26), these levels inversely correlated with renin (Spearman r = −0.57, P = 0.005). Renin levels were elevated in patients with AF compared to normal controls (1233 ± 238 ng/mL vs 401 ± 27 ng/mL, P = 0.0002) and positively correlated with levels of matrix metalloproteinase 1 (MMP-1; Spearman r = 0.89, P = 0.01) and MMP-2 (Spearman r = 0.82, P = 0.03). These data suggest that 25-hydroxyvitamin D may influence RAS activation, and renin may help mediate the collagen remodeling process in AF. Understanding mediators of RAS dysregulation in AF may elucidate targets for therapeutic intervention to prevent collagen remodeling.

The aim of this study was to investigate the utility of the neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) to predict all-cause mortality in patients presenting with acute pulmonary embolism (PE). Three hundred consecutive patients with acute PE between March 2016 and December 2018 were retrospectively analyzed. We identified 191 patients who met the study inclusion criteria. Twenty-eight patients died during the study period. There was a significant difference in PLR, but not NLR, between patients with low risk, submassive, and massive risk PE ( P = .02 and P = .58, respectively, by the Kruskal-Wallis test). Elevated NLR and PLR were associated with all-cause mortality ( P < .01 and P < .01, respectively). Neutrophil-to-lymphocyte ratio of 5.46 was associated with all-cause mortality with sensitivity of 75.0% and specificity of 66.9% (area under the curve [AUC]: 0.692 [95% confidence interval, CI]: 0.568-0.816); P < .01). Platelet-to-lymphocyte ratio of 256.6 was associated with all-cause mortality with sensitivity of 53.6% and specificity of 82.2% (AUC: 0.693 [95% CI: 0.580-0.805]; P < .01). Neutrophil-to-lymphocyte ratio and PLR are simple biomarkers that are readily available from routine laboratory values and may be useful components of PE risk prediction models.

Intermediate-risk pulmonary embolism (PE) has variable outcomes. Current risk stratification models lack the positive predictive value to identify patients at highest risk of PE-related mortality. We identified intermediate-risk PE patients who underwent catheter-based interventions and right heart catheterization (RHC) and identified those with low cardiac index (CI < 2.2 L/min/m 2 ). We utilized regression models to identify echocardiographic predictors of low CI and Kaplan Meier curve to evaluate PE-related mortality when stratified by the echocardiographic predictor. Of 174 intermediate-risk PE patients, 41 underwent RHC. Within this cohort, 46.3% had low CI. Univariable linear regression identified right ventricular outflow tract velocity time integral (RVOT VTI), right/left ventricular ratio, S prime, inferior vena cava diameter, and pulmonary artery systolic pressure as potential predictors of low CI. Multivariable linear regression identified RVOT VTI as significant predictor of low CI (β coefficient 0.124, 95% confidence interval [CI]: 0.01-0.24, P = .034). Right ventricular outflow tract velocity time integral