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Background Right ventricular (RV) dilation has been used to predict adverse outcomes in acute pulmonary conditions. It has been used to categorize the severity of novel coronavirus infection (COVID-19) infection. Our study aimed to use chest CT-angiogram (CTA) to assess if increased RV dilation, quantified as an increased RV:LV (left ventricle) ratio, is associated with adverse outcomes in the COVID-19 infection, and if it occurs out of proportion to lung parenchymal disease. Results We reviewed clinical, laboratory, and chest CTA findings in COVID-19 patients (n = 100), and two control groups: normal subjects (n = 10) and subjects with organizing pneumonia (n = 10). On a chest CTA, we measured basal dimensions of the RV and LV in a focused 4-chamber view, and dimensions of pulmonary artery (PA) and aorta (AO) at the PA bifurcation level. Among the COVID-19 cohort, a higher RV:LV ratio was correlated with adverse outcomes, defined as ICU admission, intubation, or death. In patients with adverse outcomes, the RV:LV ratio was 1.06 ± 0.10, versus 0.95 ± 0.15 in patients without adverse outcomes. Among the adverse outcomes group, compared to the control subjects with organizing pneumonia, the lung parenchymal damage was lower (22.6 ± 9.0 vs. 32.7 ± 6.6), yet the RV:LV ratio was higher (1.06 ± 0.14 vs. 0.89 ± 0.07). In ROC analysis, RV:LV ratio had an AUC = 0.707 with an optimal cutoff of RV:LV ≥ 1.1 as a predictor of adverse outcomes. In a validation cohort (n = 25), an RV:LV ≥ 1.1 as a cutoff predicted adverse outcomes with an odds ratio of 76:1. Conclusions In COVID-19 patients, RV:LV ratio ≥ 1.1 on CTA chest is correlated with adverse outcomes. RV dilation in COVID-19 is out of proportion to parenchymal lung damage, pointing toward a vascular and/or thrombotic injury in the lungs.

Aims Accurate blood pressure (BP) measurement in continuous‐flow ventricular assist device (CF‐VAD) patients is imperative to reduce stroke risk. This study assesses the accuracy of the Doppler opening pressure method compared with the gold standard arterial line method in CF‐VAD patients. Methods and results In a longitudinal cohort of HeartMate II and HVAD patients, arterial line BP and simultaneously measured Doppler opening pressure were obtained. Overall correlation, agreement between Doppler opening pressure and arterial line mean vs. systolic pressure, and the effect of arterial pulsatility on the accuracy of Doppler opening pressure were analysed. A total of 1933 pairs of Doppler opening pressure and arterial line pressure readings within 1 min of each other were identified in 154 patients (20% women, mean age 55 ± 15, 50% HeartMate II and 50% HVAD). Doppler opening pressure had good correlation with invasive mean arterial pressure (r = 0.742, P

Introduction: Post-capillary pulmonary hypertension (PH) is diagnosed with rest hemodynamics and requires management of left heart disease. However, in subclinical PH and mixed PH (mixed pre- and post-capillary), it is imperative to identify a predominant post-capillary phenotype with exercise (aka. Pulmonary venous hypertension). Hypothesis: In suspected subclinical and mixed PH, greater left atrial volume index (LAVI; >35) and E/E’ (>8) on echocardiogram can reliably predict a predominant post-capillary PH with exercise, assessed with invasive cardiopulmonary exercise testing (iCPET). Methods: We reviewed clinical, echocardiographic and iCPET data for 37 patients undergoing exercise right heart catheterization and then analyzed the data with receiver operator curve (ROC) and area under the curve (AUC) analysis to estimate the different echo parameters to identify post-capillary PH. Results: Within the cohort, mean age (± SD) was 63.6±11.3 years, and 19 subjects were female (51%). On ROC analysis, LAVI and E/E’ had high predictive ability to identify a pulmonary venous hypertension response with exercise (AUC=0.860, p=0.003 for LAVI, and AUC=0.788, p=0.014) with optimal cut-offs identified as: LAVI >35 and E/E’ >8. These variables also notably had a significant association with PCWP/CO>2. To understand the hemodynamics associated with these differentiable echo features, we divided the overall cohort (n=37) into 2 groups: group 1 ( Abnormal-LA group ) =LAVI>35 and/or E/E’ >8, group 2 ( Normal-LA group )=LAVI≤ 34 and E/E’≤8. The LAVI in group 1 vs group 2 was: 44.3±15.2 vs 23.1±4.4 (p Conclusions: Among individuals with suspected PH, LAVI>35 and E/E’ >8 are reliable non-invasive markers to identify post-capillary PH. In a patient with a new diagnosis of PH based on screening echocardiogram, LAVI≤ 34 and E/E’≤8 may identify a patient who is likely to benefit from PH drugs.

The purpose of this review is to provide an update on cardiac sarcoidosis (CS) and to discuss the current recommendations and progress in diagnosis and management of this disease. Sarcoidosis is a multisystem granulomatous disease of unknown etiology. Cardiac involvement is seen in at least 25% and is associated with poor prognosis. Manifestations of cardiac sarcoidosis (CS) can vary from presence of silent myocardial granulomas, which may lead to sudden death, to symptomatic conduction abnormalities, ventricular arrhythmias, and heart failure. We discuss newer imaging modalities such as cardiac magnetic resonance imaging and positron emission tomography in conjunction with clinical criteria increasingly used for diagnosing and prognosticating patients with CS. Immunosuppression (primarily corticosteroids) is recommended for treatment of CS; however, its efficacy has never been proven in prospective randomized studies. The role of imaging to guide the use of immunotherapy is unknown. Cardiac sarcoidosis continues to challenge clinicians due to its protean presentations, lack of diagnostic standards, and data for risk stratification and treatment. There is a need for prospective, randomized controlled trials to understand how best to diagnose and treat cardiac sarcoidosis.

This study investigated the association between left ventricular ejection fraction (LVEF) and the risk of ventricular arrhythmias (VA), heart transplantation, and death in cardiac sarcoidosis (CS). We identified 110 CS patients meeting 2014 Heart Rhythm Society (HRS) diagnostic criteria with baseline LVEF35% (n = 32) or ≥35% (n = 78). The primary end point was sustained VA or sudden cardiac death (SCD), and secondary end points included risk of heart transplantation, death, or a composite. Logistic regression determined risk factors for VA/SCD, and Cox proportional hazards regression analysis was performed for secondary end points. Receiver operating curve analysis determined the best discrimination point of LVEF for each end point; sensitivity analyses evaluated the effects of higher LVEF on each end point. Over a follow-up of 2.6 (range 1.0 to 5.8) years, 49 (44.5%) CS patients experienced VA/SCD, including 19 of 32 (59.4%) with LVEF35%, and 30 of 78 (38.5%) with LVEF ≥35%. After adjustment, LVEF35% was not significantly associated with an increased risk of VA/SCD compared with LVEF ≥35% (odds ratio 1.3, 95% confidence intervals 0.5 to 3.7). Although LVEF35% was associated with an increased risk of heart transplantation and death (28.1% vs 12.8%, p = 0.05), this was not significant after adjustment (hazard ratio 1.7, 95% confidence intervals 0.5 to 9.0, p = 0.53). In conclusion, patients with CS experience high rates of VA, SCD, and heart transplantation, even when LVEF is mildly impaired or normal. Patients with LVEF35% are at particularly elevated risk of VA/SCD. Our findings highlight the imperative to investigate arrhythmia risk in all patients with CS, even in the setting of an otherwise reassuring LVEF.

Despite efforts at early revascularization in acute coronary syndrome and advancing technologies in the field of temporary mechanical circulatory support (TMCS), the mortality from cardiogenic shock (CS) remains very high. Treatment of these patients involves understanding the trajectory of the condition and making complex decisions regarding the appropriate selection of medical and device therapies. The current definition of CS is not universally applicable and defines shock in absolute terms. CS should be thought of as a continuum rather than a binary diagnosis and is best defined as a clinical syndrome of tissue hypoperfusion resulting from cardiac dysfunction. Early intervention with appropriate timing and selection of apposite TMCS device may be the key to improving outcomes. TMCS device selection is a complex process requiring consideration of the severity of CS, patient-specific risks, technical limitations, overall goals of care, and assessment of futility of care. In this review, we discuss identification and pathophysiology of CS, and critically review acute management strategies, both medical and mechanical therapies and outline areas that need further investigation.

BACKGROUND: Cardiac magnetic resonance (CMR) techniques permit quantification of the myocardial extracellular volume fraction (ECV), representing a surrogate marker of reactive interstitial fibrosis, and late gadolinium enhancement (LGE), representing replacement fibrosis or scar. ECV and LGE have been independently linked with heart failure (HF) events. In deriving ECV, coronary artery disease (CAD) type LGE, but not non-CAD type LGE, has been consistently excluded. We examined the associations between LGE, global ECV derived from myocardial tissue segments free of any detectable scar, and subsequent HF events. METHODS: Mid short-axis T1 maps were divided into 6 cardiac segments, each classified as LGE absent or present. Global ECV was derived from only segments without LGE. ECV was considered elevated if >30%, the upper 95% bounds of a reference group without known cardiac disease (n=28). Patients were divided into 4 groups by presence of elevated ECV and of any LGE. Subsequent HF hospitalization and any death were ascertained. Their relationship with ECV was examined separately and as a composite with Cox proportional hazard models. RESULTS: Of 1,604 serial patients with T1 maps, 1,255 were eligible after exclusions and followed over a median 26.3 (interquartile range 15.9–37.5) months. Patients with elevated ECV had increased risk for death (hazard ratio [HR] 2.45, 95% confidence interval [CI] 1.76–3.41), HF hospitalization (HR 2.45, 95% CI 1.77–3.40), and a combined endpoint of both outcomes (HR 2.46, 95% CI 1.94–3.14). After adjustments for covariates including LGE, the relationship persisted for death (HR 1.82, 95% CI 1.28–2.59), hospitalization (HR 1.60, 95% CI 1.12–2.27), and combined endpoints (HR 1.73, 95% CI 1.34–2.24). CONCLUSIONS: ECV measures of diffuse myocardial fibrosis were associated with HF outcomes, despite exclusion of replacement fibrosis segments from their derivation and even among patients without any scar. ECV may have a synergistic role with LGE in HF risk assessment.

Cancer and cardiovascular disease are the leading causes of mortality in the USA. In this review, we highlight these shared disease pathways and provide a framework for a systems-based approach to reduce overall risk burden. From traditional risk factors such as age and tobacco use to more recently recognized entities including clonal hematopoiesis, we are gaining insights into shared mechanisms. Because of these overlapping risks, providers on each level of patient care (primary care providers, cardiologists, oncologists) need to recognize and reduce these underlying risk factors. There is significant overlap in the epidemiology and risk factors for the development of cardiovascular disease and cancer, providing opportunities for joint risk factor modification.

Purpose The resistance compliance (RC) time describes the relationship between the pulmonary vascular resistance (PVR) and the pulmonary artery compliance (PAC) reflecting right ventricular (RV) afterload. Increased left atrial pressure shifts this relationship, lowering PAC for any given PVR leading to ventricular-arterial uncoupling and increased RV afterload. We hypothesize that decreased RC time is associated with increased in-hospital mortality due to poor right heart compensation in acute shock. Methods Admission right heart catheterization (RHC) data were analyzed in consecutive patients from 2014 to 2016 with cardiogenic shock as defined by a cardiac index Results We studied 235 patients with 265 unique encounters, where 15.3% died during the hospitalization. The mean RC time in our study sample was 0.33 (SD ±0.21). The hazard ratio (HR) for in-hospital mortality risk with the RC time was 0.161 (p-value = 0.07). Compared to the highest tertile, the lowest tertile of RC time was associated with increased mortality (HR 0.323, p-value = 0.045). The mortality risk persisted when adjusted for the RAP (HR 0.344, p-value = 0.056). The mean PAPi was 3.08 (SD ±3.79). The HR of in-hospital mortality with the PAPi was 0.806 (p-value = 0.166). Compared to the highest tertile, the lowest tertile of PAPi was associated with an increased mortality (HR 0.382, p-value = 0.045). This association was non-significant when adjusted for the RAP (HR 0.461, p-value = 0.202). Conclusion We demonstrate that a low RC time and increased RV afterload is associated with increased mortality in patients admitted with cardiogenic shock. In contrast to the PAPi, this association is independent of right atrial pressure, suggesting that the RC time may be a better marker of outcomes independent of central venous pressure. Further studies are needed to evaluate the role of these markers in cardiogenic shock.

Background Prior studies have shown that late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) and fluorodeoxyglucose (FDG) positron emission tomography (PET) confer incremental risk assessment in patients with cardiac sarcoidosis (CS). However, the incremental prognostic value of the combined use of LGE and FDG compared to either test alone has not been investigated, and this is the aim of the present study. Methods Retrospective observational study of 56 symptomatic patients with high clinical suspicion for CS who underwent LGE-CMR and FDG-PET and were followed for the occurrence of death and/or malignant ventricular arrhythmias (VA). Results The combination of PET and CMR yielded the following groups: 1) LGE-negative/normal-PET (n=20), 2) LGE-positive/abnormal-FDG (n=20), and 3) LGE-positive/normal FDG (n=16). After a median follow-up of 2.6years (IQR 1.2–4.1), 16 patients had events (7 deaths, 10 VA). All, but 1, events occurred in patients with LGE. LGE-positive/abnormal-FDG (7 events, HR 10.1 [95% CI 1.2–84]; P =0.03) and LGE-positive/normal-FDG (8 events, HR 13.3 [1.7–107]; P =0.015) patients had comparable risk of events compared to the reference LGE-negative/normal-PET group. In adjusted Cox-regression analysis, presence of LGE (HR 18.1 [1.8–178]; P =0.013) was the only independent predictor of events. Conclusion CS patients with LGE alone or in association with FDG were at similar risk of future events, which suggests that outcomes may be driven by the presence of LGE (myocardial fibrosis) and not FDG (inflammation).

Background— Increased left ventricular myocardial thickness (LVMT) is a feature of several cardiac diseases. The purpose of this study was to establish standard reference values of normal LVMT with cardiac magnetic resonance and to assess variation with image acquisition plane, demographics, and left ventricular function. Methods and Results— End-diastolic LVMT was measured on cardiac magnetic resonance steady-state free precession cine long and short axis images in 300 consecutive participants free of cardiac disease (169 women; 65.6±8.5 years) of the Multi-Ethnic Study of Atherosclerosis cohort. Mean LVMT on short axis images at the mid-cavity level was 5.3±0.9 mm and 6.3±1.1 mm for women and men, respectively. The average of the maximum LVMT at the mid-cavity for women/men was 7/9 mm (long axis) and 7/8 mm (short axis). Mean LVMT was positively associated with weight (0.02 mm/kg; P =0.01) and body surface area (1.1 mm/m 2 ; P P P =0.01), and lower left ventricular stroke volume (−0.01 mm/mL; P Conclusions— Normal values for wall thickness are provided for middle-aged and older subjects. Normal LVMT is lower for women than men. Observed values vary depending on the imaging plane for measurement.

Background Heart transplant remains the definitive therapy for advanced heart failure patients but is limited by organ availability. We identified a large number of donor hearts from our organ procurement organization (OPO) being exported to other regions. Methods We engaged a multidisciplinary team including transplant surgeons, cardiologists, and our OPO colleagues to identify opportunities to improve our center-specific organ utilization rate. We performed a retrospective analysis of donor offers before and after institution of a novel review process. Results Each donor offer made to our program was reviewed on a monthly basis from July 2013 to June 2014 and compared with the previous year. This review process resulted in a transplant utilization rate of 28% for period 1 versus 49% for period 2 ( P = .007). Limiting the analysis to offers from our local OPO changed our utilization rate from 46% to 75% ( P = .02). Transplant volume increased from 22 to 35 between the 2 study periods. Thirty-day and 1-year mortality were unchanged over the 2 periods. A total of 58 hearts were refused by our center and transplanted at other centers. During period 1, the 30-day and 1-year survival rates for recipients of those organs were 98% and 90%, respectively, comparable with our historical survival data. Conclusions The simple process of systematically reviewing donor turndown events as a group tended to reduce variability, increase confidence in expanded criteria for donors, and resulted in improved donor organ utilization and transplant volumes.

Antibody-mediated rejection (AMR) of the cardiac allograft is a poorly defined and challenging diagnosis for transplant recipients and their clinicians. Although even its very existence in heart transplantation was debated until relatively recently, improved immunopathologic and serological techniques to detect myocardial capillary complement deposition and circulating anti-HLA (human leukocyte antigen) antibodies have led to the detection of a spectrum of newly uncovered immunologic changes that characterize AMR. The earliest standardized clinical and pathological criteria for the diagnosis of AMR in heart transplantation became available in 2004, the result of a task force assembled by the International Society for Heart and Lung Transplantation (ISHLT). In 2006, the criteria were refined by the ISHLT Immunopathology Task Force (Table 1). These revisions provide 4 categories of diagnostic criteria: clinical, histopathologic, immunopathologic, and serological assessment.1 Despite these published criteria, currently >50% of heart transplant centers make the diagnosis of AMR based on cardiac dysfunction and the lack of cellular infiltrates on the heart biopsy (preconference survey included in the ISHLT consensus article).2 More recently, the ISHLT Consensus Conference on AMR has redefined the pathological diagnosis of AMR.3 The 2013 ISHLT “Working Formulation for the Standardization of Nomenclature in the Pathologic Diagnosis of Antibody-Mediated Rejection in Heart Transplantation” was published in December 2013. This document provided an update to the 2010 consensus conference.4 It is anticipated that this update to the definition of AMR will reduce variations in the diagnosis of AMR, providing a platform for the development of standardized therapies. The goal of the present scientific statement is to provide the heart transplant professional with an overview of the current status of the diagnosis and treatment of AMR in the cardiac allograft based on recent consensus conferences and the published literature. We include recommendations to facilitate evolving standardization and strategies …

Primary cardiac tumors are far rarer than tumors metastatic to the heart. Angiosarcoma is the primary cardiac neoplasm most frequently detected; lymphomas constitute only 1% of primary cardiac tumors. We present the case of a 55-year-old woman with a recently diagnosed intracardiac mass who was referred to our institution for consideration of urgent orthotopic heart transplantation. Initial images suggested an angiosarcoma; however, a biopsy specimen of the mass was diagnostic for diffuse large B-cell lymphoma. The patient underwent chemotherapy rather than surgery, and she was asymptomatic 34 months later. We use our patient's case to discuss the benefits and limitations of multiple imaging methods in the evaluation of cardiac masses. Certain features revealed by computed tomography, cardiac magnetic resonance, and positron emission tomography can suggest a diagnosis of angiosarcoma rather than lymphoma. Cardiac magnetic resonance and positron emission tomography enable reliable distinction between benign and malignant tumors; however, the characteristics of different malignant tumors can overlap. Despite the great usefulness of multiple imaging methods for timely diagnosis, defining the extent of spread and the hemodynamic impact, and monitoring responses to treatment, we think that biopsy analysis is still warranted in order to obtain a correct histologic diagnosis in cases of suspected malignant cardiac tumors.

Radiation recall phenomenon is a tissue reaction that develops within a previously irradiated area, precipitated by the subsequent administration of certain chemotherapeutic agents. It commonly affects the skin, but can also involve internal organs with functional consequences. To our best knowledge, this phenomenon has never been reported as a complication on the heart and should be consider as a potential cause of cardiotoxicity.