an abnormal DSE can reliably predict the development of CAV or risk of death on follow up. Hypothesis: We hypothesize that among patients with cardiac transplantation, abnormal DSEs are not predictive of CAV or survival upon follow up. Methods: We retrospectively examined all patients who received a heart transplant at our institution between 2004-2013 (n = 192) if they had at least one DSE (6, 18 or 30 months posttransplant) followed by a coronary angiogram (annually) and excluded those with no DSEs (n = 62) or no follow up angiograms (n = 50). Baseline characteristics were examined at the time of transplant and DSE results were categorized as normal or abnormal (if they were suggestive of coronary disease). Cox regression models were used to examine the disease-free survival according to DSE result and adjusted for age, sex and subsequent DSE test results (time-dependent covariate). Results: A total of 80 patients were included with mean age 54 ± 27 (23% women). Upon follow up, mean 77 ± 31 months, 26 patients developed CAV and 10 patients died. A total of 187 DSEs were performed; 85% of these studies achieved adequate level of stress (>85% of agepredicted heart rate). Only 7 patients had abnormal DSE results. Of those who had an abnormal DSE test, none died and 4 developed CAV. Of the other 22 patients who developed CAV, 4 died. These 22 patients had a total of 50 DSE studies, 90% of which were adequate. Average left ventricular ejection fraction (EF) over the study period as determined by transthoracic echocardiogram did not differ significantly in patients who developed CAV compared to those who did not develop CAV on follow up (63.4 ± 5.5 vs 62.9 ± 6.0; P > .05). Overall, DSE tests had a sensitivity of 12.5% and a specificity of 93.8% for detection of CAV. An abnormal DSE test neither predicted the development of CAV (hazard ratio [HR] 1.38 with 95% confidence interval [CI] 0.52, 3.68) nor death (HR 1.70, 95% CI 0.34, 8.48). Conclusions: Abnormal DSE tests have a low sensitivity for diagnosis of CAV and do not predict the risk of CAV or death upon follow up. As such, we question the appropriateness of DSEs to be used as a screening test to detect CAV in cardiac transplant recipients.

Heart failure (HF) is a major cause of morbidity and mortality worldwide, and the burden of HF continues to rise. There has been an interest in sodium-glucose co-transporter-2 (SGLT2) inhibitors for their role in reducing HF hospitalizations in pivotal trials. Since these agents were approved by the Food and Drug Administration for the management of diabetes mellitus, multiple small trials and analyses have tried to explain the underlying beneficial mechanisms in HF. In this review, we discuss different mechanisms by which SGLT2 inhibitors play hemodynamic, metabolic, and cellular roles in different HF phenotypes. We also address issues pertaining to the safety of these relatively newer agents. KEY MESSAGES 1. SGLT2 inhibitors are associated with a reduction in HF hospitalizations in both diabetics and non-diabetics. 2. The beneficial role of SGLT2 inhibitors in reducing HF hospitalization is observed among participants with established cardiovascular disease/HF and at-risk population. 3. SGLT2 inhibitors pose an important role in renal protection, another mechanism by which these medications can be helpful in HF patients

Background: Intravenous unfractionated heparin (IV-UFH) has been the mainstay for bridging therapy, and for the treatment of suspected device hemolysis/thrombosis in patients with continuous-flow left ventricular assist devices (CF-LVADs). Significant levels of discordance between activated partial thromboplastin time (aPTT) and antifactor Xa (anti-FXa) levels have been reported in CF-LVAD patients. We sought to compare alternate monitoring protocols while on IV-UFH therapy in patients with CF-LVADs. Methods: Consecutive patients implanted with CF-LVAD and treated with IV-UFH had simultaneous measurement of aPTT, activated clotting time (ACT), R time (measured by thromboelastography), and anti-FXa. All patients were managed by targeting anti-FXa levels while on IV-UFH therapy. Results: 20 patients were enrolled. Poor relationship between anti-FXa and ACT was found (R 2 = 0.24); however, stronger relationship was found between aPTT and ACT (R 2 = 0.55). While Anti-FXa was in therapeutic range, aPTT was supra-therapeutic, thus ACT was <250 sec. The relationship between anti-FXa and R time was also limited (R 2 = 0.38); and it was similar to the relationship between aPTT and R time (R 2 = 0.45). Conclusion: Levels of aPTT and R time were disproportionately prolonged as compared to anti-FXa and ACT levels. Despite anti-FXa levels being in the therapeutic range, both aPTT and R time were supra-therapeutic, and the ACT <250 sec. Use of alternate monitoring protocols to guide IV-UFH therapy may lead to different estimates of heparin concentration in the same patient. In light of the early risk of device thrombosis, re-examination of bridging protocols while on IV-UFH therapy are necessary.