Introduction Sodium-glucose cotransporter-2 inhibitors (SGLT2i) have emerged as a mainstay in therapy for all classes of heart failure. Heart failure with preserved ejection fraction (HFpEF), a class that was previously devoid of many treatment options, now has evidence for SGLT2i use in treatment. The hemodynamic effects of SGLT2i in HFpEF are not well described. We aimed to evaluate the hemodynamic effects of SGLT2i over a 6 month period. Hypothesis If an SGLT2i was started in patients with HFpEF and CardioMEMS pulmonary artery monitoring device, then real time reductions in pulmonary artery pressures would be seen. Methods We performed a single center retrospective analysis of 10 patients with the diagnosis of HFpEF in whom a CardioMEMS pulmonary artery monitoring device was implanted and either dapagliflozin or empagliflozin was prescribed. We collected baseline characteristics, heart failure regimen, renal function, body mass index (BMI) and pulmonary artery pressures over a 6-month period from starting SGLT2i. Baseline pulmonary pressures were measured via right heart catheterization or CardioMEMS device, and subsequent pressures were measured via remote monitoring via the CardioMEMS device. The Wilcoxon signed rank test was used to compare the median values of the baseline and six-month measures. Analysis was done using SAS Version 9.4 and a p-value < 0.05 was considered statistically significant. Institutional review board considered this project exempt. Results The average PA diastolic pressure before and after SLGT2i was 22mmHg and 19mmHg (p=0.5781), average PA systolic pressure was 59mmHg and 48 mmHg (p=0.0859), and mean PA pressure was 33.5mmHg and 31.5mmHg (p=0.1406). BMI prior to SGLT2i was 40.05 and 38.66 after (p=0.2754). Brain natriuretic peptide (BNP) was 258 and 87 (p=0.1602). There was no significant change in kidney function over the six months. Conclusion Our results did not show a statistically significant reduction in the pulmonary pressures after 6 months of therapy. However, the sample size was small and there was a trend in the reduction of pulmonary pressures over time. The BNP and BMI were also numerically lower after SGLT2i, however not statistically significant. Larger cohorts may reveal statistically significant reduction in pulmonary artery pressures in the HFpEF population.
Introduction: Coronary artery aneurysm (CAA) is a vessel dilation exceeding 1.5 times adjacent normal segments. We present a case of massive right coronary artery (RCA) aneurysm complicated by ST elevation (STE) myocardial infarction. Case Summary: An 87-year-old female with no significant medical history presented with chest pain. Vitals signs and physical exam were normal. A 12 lead EKG demonstrated STE in inferior leads. Coronary angiography revealed a large aneurysm of the RCA throughout its course (max diameter 20 mm) with TIMI I flow. In the mid RCA, there was a long filling defect with irregular borders consistent with a congealed, organized layered thrombus causing 90% stenosis. Percutaneous coronary intervention (PCI) was not pursued due severe aneurysmal dilation and risk for embolization. The proximal to mid left anterior descending artery (LAD) and abdominal aorta were also aneurysmal. The patient was deemed not to be a surgical candidate after a heart team discussion (STS risk of morbidity or mortality = 12.6%). Left ventricular ejection fraction was 60%. Chest pain resolved and patient was discharged on indefinite anticoagulation and antiplatelet therapy. Discussion: Giant CAAs are rare, with an incidence of 0.02%. Causes include atherosclerosis, Takayasu arteritis, Kawasaki disease, or congenital defects. Although mostly incidental, CAA can be complicated by thrombosis, embolization, fistulation, rupture, arrhythmia, or sudden death. Our patient had an acute RCA thrombus due to stasis and turbulent blood flow in the aneurysm. Localized CAA are treated with surgery or percutaneous coiling or stenting. However, PCI was not feasible in our patient due to risk of embolization and difficultly with stent apposition in the setting of a diffuse, giant-sized aneurysm. Conclusion: CAAs are rare but may cause grave complications. A heart team discussion is essential to guide appropriate medical, percutaneous, or surgical treatment based on vessel anatomy.
Abstract Background Loeys-Dietz syndrome (LDS) is a heritable disorder that presents with thoracic aortic aneurysm and/or dissection caused by a mutation in one of the transforming growth factor-B receptor or ligand genes. It is associated with widespread familial arterial aneurysm and rupture. Case summary We present a case of a 70-year-old male with a family history of heritable thoracic aortic aneurysm disease who presented to the emergency department with chest pain. His presenting electrocardiogram was significant for ST elevation in the inferior leads with complete heart block. Computed tomography-angiography was done to rule out aortic dissection, which was negative for aortic dissection but did reveal 3.9 cm infrarenal abdominal aortic aneurysm and 2.7 cm bilateral iliac artery aneurysms. He was then taken for invasive angiography and was found to have aneurysmal dilation of the entire right coronary artery measuring up to 6 mm with 100% occlusion secondary to thrombus in the distal segment. He was found to have obstructive disease in the left anterior descending artery and first and second obtuse marginals (OMs). Genetic testing performed confirmed a pathogenic mutation in the TGFBRI gene (TGFBRI c.934G > A p.Gly312Ser) consistent with the diagnosis of LDS. Discussion Although LDS is known to cause arterial aneurysms throughout the arterial tree, there have been no other cases of primary coronary aneurysms reported in this patient population. This case represents the first description of a patient with genetically confirmed LDS presenting with coronary artery aneurysm.
The prevalence of different cancers after heart transplant (HT) is unclear due to small and conflicting prior studies. Herein, we report a systematic review and meta-analysis to highlight the prevalence and pattern of malignancies post-HT. We conducted an extensive literature search on PubMed, Scopus, Cochrane databases for prospective or retrospective studies reporting malignancies after HT. The proportions from each study were subjected to random effects model that yielded the pooled estimate with 95% confidence intervals (CI). Fifty-five studies comprising 60,684 HT recipients reported 7759 total cancers during a mean follow-up of 9.8 ± 5.9 years, with an overall incidence of 15.3% (95% CI = 12.7%-18.1%). Mean time from HT to cancer diagnosis was 5.1 ± 4 years. The most frequent cancers were gastrointestinal (7.6%), skin (5.7%), and hematologic/blood (2.5%). Meta-regression showed no association between incidence of cancer and mean age at HT (coeff: -0.008; P = 0.25), percentage of male recipients (coeff: -0.001; P = 0.81), donor age (coeff: -0.011; P = 0.44), 5-year (coeff: 0.003; P = 0.12) and 10-year (coeff: 0.02; P = 0.68) post-transplant survival. There is a substantial risk of malignancies in HT recipients, most marked for gastrointestinal, skin, and hematologic. Despite their occurrence, survival is not significantly impacted.
Penetrating aortic ulcer (PAU) is an important, albeit, rarer cause of embolization to internal organs and distal extremities. Embolization occurs as a result of the disruption of cholesterol deposition in the wall of the aorta by a PAU. The classic presentation of cholesterol embolization syndrome (CES) includes pain, pallor, poikilothermia, paresthesia, and paralysis with intact pulses. The patient will classically have livedo reticularis or "blue toes." We present a case of a patient who presented to the emergency department with the complaint of a painful, blue toe. The patient had intact distal pulses on exam with the distal 2/3 of the first toe having a markedly blue/black color with livedo reticularis spreading proximally on the other 1/3 of the toe. CT angiogram with runoff to the lower extremities revealed a 3.6-cm infrarenal abdominal aortic aneurysm with a 5-mm penetrating aortic ulcer with a three-vessel runoff to the distal lower extremities. The diagnosis of CES secondary to a PAU was made. While thrombotic embolization from PAU causing acute limb ischemia is less common, it is well described. In contrast, cholesterol embolization from PAU remains a rare phenomenon without adequate treatment options.
Rituximab is a chimeric monoclonal antibody against the protein CD20 which is predominantly found on the surface of B cells. Malignant B cells express higher levels of CD20. Rituximab not only induces cellular apoptosis but also down regulates the B cell receptor and mediates antibody dependent