Background: Obesity has been associated with increased incidence and severity of various cardiovascular risk factors and increased risk for stroke. However, the evidence of its effect on outcomes in stroke victims have been equivocal. We aimed to investigate the distribution of BMI in a nation-wide cohort of individuals, admitted for a stroke, and the relationship between BMI and in-hospital mortality. Methods: Data from the U.S. National Inpatient Sample (NIS) was collected, to identify hospitalizations for stroke, between October 2015 and December 2016. The patients were sub-divided into six groups based on their BMI: underweight, normal weight, overweight, obese I, obese II and extremely obese groups. Various sociodemographic and clinical parameters were gathered, and incidence of mortality and the length of hospital stay were analyzed. Multivariable analysis was performed to identify independent predictors of in-hospital mortality. Results: A weighted total of 84,185 hospitalizations for stroke were included in the analysis. The approximate mean patients aged was 65.5 ± 31 years, the majority being female (55.3%) and white (63.1%). The overall in-hospital mortality during the study period was 3.6%. A reverse J-shaped relationship between the body mass index and in-hospital mortality was documented, while patients with elevated BMI showed significantly lower in-hospital mortality compared to the underweight and normal weight study participants, 2.8% vs. 7.4%, respectively, p < 0.001. Age and several comorbidities, as well as the Deyo Comorbidity Index, were found to predict mortality in a multivariable analysis. Conclusion: A reverse J-shaped relationship between body mass index and in-hospital mortality was documented in patients admitted for a stroke in the U.S. during the study period. The above findings support the existence of an “obesity paradox” in patients hospitalized following a stroke, similar to that described in other cardiovascular conditions.

Purpose: We report on the clinical course and management of patients supported with durable implantable LVADs who developed outflow graft obstructions at a large academic center. Methods: We performed a retrospective review of patients receiving LVAD support from 2012 through 2020. Patients who developed an outflow graft obstruction diagnosed by computed tomography angiography (CTA) or angiogram were identified, and patient characteristics and outcomes were reported. Results: Of the 324 patients supported by LVAD at our institution, 11 patients (3.4%) were diagnosed with outflow graft obstructions. The most common presentation was low flow alarms, which was present in 10/11 patients, and the remaining patient presented with lightheadedness. Patients had minimal LDH elevation with 8/11 presenting with less than 2-fold the upper limit of normal. Transthoracic echocardiograms were not diagnostic, but CTA enabled non-invasive diagnoses in 8/11 of the patients. Three patients with extrinsic compression of the outflow graft successfully underwent endovascular stent placement, and three patients with outflow cannula kinks received supportive care. Of the five patients diagnosed with intraluminal thromboses, one received a heart transplant, one underwent an outflow graft revision, and three received supportive care due to comorbidities. Conclusion: Outflow graft obstructions remain a rare, but serious complication. The true prevalence of this entity is likely underestimated due to the non-specific clinical presentation. CTA is a pivotal non-invasive diagnostic step. Patients with external compression were successfully treated with endovascular stenting.

Despite advancing technology, right heart failure after left ventricular assist device implantation remains a significant source of morbidity and mortality. With the UNOS allocation policy change, a larger proportion of patients proceeding to LVAD are destination therapy and consist of an overall sicker population. Thus, a comprehensive understanding of right heart failure is critical for ensuring the ongoing success of durable LVADs. The purpose of this review is to describe the effect of LVAD implantation on right heart function, review the diagnostic and predictive criteria related to right heart failure, and discuss the current evidence for management and treatment of post-LVAD right heart failure.

The effect of contrast media (CM), delivered prior to- and during transcatheter aortic valve implantation (TAVI), on kidney function, following the procedure, is debatable. Consequently, the performance of CM-based, acute kidney injury (AKI) risk prediction models is also questionable. We retrospectively studied 210 patients that underwent TAVI. We recorded the dose of CM used prior and during TAVI, calculated the results of different AKI risk assessment models containing a CM module, and tested their association with AKI after the procedure. AKI was diagnosed in 38 patients (18.1%). The baseline estimated glomerular filtration rate (eGFR) was lower in the AKI+ group compared to AKI− group (51 ± 19.3 versus 64.5 ± 19 mL/min/1.73 mr², respectively). While the dose of CM delivered prior to TAVI, during TAVI or the cumulative amount of both did not differ between the groups, the results of all tested risk models were higher in AKI+ patients. However, by multivariable analysis, only eGFR had a consistent independent association with AKI. We suggest that the dose of CM delivered prior or during TAVI is not associated with AKI and that the predictive power of CM based AKI risk models is, in all probability, limited to eGFR alone.

Background: Decreased peak oxygen consumption during exercise (peak Vo₂) is a well-established prognostic marker for mortality in ambulatory heart failure. After heart transplantation, the utility of peak Vo₂ as a marker of post-transplant survival is not well established. Methods and Results: We performed a retrospective analysis of adult heart transplant recipients at the Hospital of the University of Pennsylvania who underwent cardiopulmonary exercise testing within a year of transplant between the years 2000 to 2011. Using time-to-event models, we analyzed the hazard of mortality over nearly two decades of follow-up as a function of post-transplant percent predicted peak Vo₂ (%Vo₂). A total of 235 patients met inclusion criteria. The median post-transplant %Vo₂ was 49% (IQR 42 to 60). Each standard deviation (±14%) increase in %Vo₂ was associated with a 32% decrease in mortality in adjusted models (HR 0.68, 95% CI 0.53 to 0.87, p = 0.002). A %Vo₂ below 29%, 64% and 88% predicted less than 80% survival at 5, 10, and 15 years, respectively. Conclusions: Post-transplant peak Vo₂ is a highly significant prognostic marker for long-term post-transplant survival. It remains to be seen whether decreased peak Vo₂ post-transplant is modifiable as a target to improve post-transplant longevity.

Introduction: The contribution of chronotropic incompetence to reduced exercise tolerance after a heart transplant is well known, but its role as a prognostic marker of post-transplant mortality is unclear. The aim of this study is to examine the relationship between post-transplant heart rate response (HRR) and survival. Methods: We performed a retrospective analysis of all adult heart transplant recipients at the University of Pennsylvania between the years 2000 and 2011 who underwent a cardiopulmonary exercise test (CPET) within a year of transplant. Follow-up time and survival status were observed through October 2019, using data merged from the Penn Transplant Institute. HRR was calculated by subtracting the resting HR from the peak exercise HR. The association between HRR and mortality was analyzed using Cox proportional hazard models and Kaplan–Meier analysis. The optimal cut-off point for HRR was generated by Harrell’s C statistic. Patients with submaximal exercise tests were excluded, defined by a respiratory exchange ratio (RER) cut-off of 1.05. Results: Of 277 patients with CPETs performed within a year post-transplant, 67 were excluded for submaximal exercise. In the 210 included patients, the mean follow-up time was 10.9 years (Interquartile range (IQR) 7.8–14). Resting HR and peak HR did not significantly impact mortality after adjusting for covariates. In a multivariable linear regression analysis, each 10-beat increase in heart rate response was associated with a 1.3 mL/kg/min increase in peak VO₂ and a 48 s increase in the total exercise time. Each beat/min increase in HRR was associated with a 3% reduction in the hazard of mortality (HR 0.97; 95% CI 0.96–0.99, p = 0.002). Using the optimal cut-off point generated by Harrell’s C statistic, survival was significantly higher in patients with an HRR > 35 beats/min compared to those with an HRR < 35 beats/min (log rank p = 0.0012). Conclusion: In heart transplant patients, a low HRR is associated with increased all-cause mortality and decreased exercise capacity. Additional studies are needed to validate whether targeting HRR in cardiac rehabilitation may improve outcomes.