Right Atrial Mass Biopsy Using Endobronchial Forceps.

A 72-year-old male with past medical history of complete heart block status post pacemaker in 2019, renal cell carcinoma, and thyroid cancer presented with a 4-cm right atrial mass incidentally found on routine transthoracic echocardiography. Cardiovascular computed tomography angiogram revealed an infiltrative mildly enhancing soft-tissue density along the right and left atrioventricular grooves, anterior interventricular groove, interatrial septum, free wall of the right ventricle, and right atria. Transesophageal echocardiography at the time of the cardiac biopsy revealed a heterogeneous mass extending along the interatrial septum into the superior vena cava, which appeared partially occluded, as well as probable involvement of the aortic root. After several attempts with traditionally used devices, an endobronchial alligator forceps was used to biopsy the right atrial mass under intracardiac echocardiographic guidance, with no complications.

Outcomes of Radial Versus Femoral Access in Patients With Severe Aortic Stenosis Undergoing Percutaneous Coronary Intervention Prior to Transcatheter Aortic Valve Replacement.

BACKGROUND: The safety and feasibility of radial access in patients undergoing percutaneous coronary intervention (PCI) prior to transcatheter aortic valve replacement (TAVR) has not been studied. METHODS: This study included consecutive patients who underwent PCI within 30 days before TAVR at Mayo Clinic. Vascular access was left to the discretion of the operator. Baseline demographics, procedural data, PCI outcomes, and subsequent transfemoral TAVR outcomes were extracted from patient charts. RESULTS: A total of 331 patients were included in this study, with 107 patients undergoing PCI via radial access (rPCI), and 224 via femoral access (fPCI). Mean age was 80.6 years and 35.6% were females (35.5% rPCI vs 35.3% fPCI). More patients in the fPCI group had previous coronary artery bypass graft surgery (13.1% rPCI vs 34.4% fPCI; P<.001). Fluoroscopy time (13.36 minutes vs 18.86 minutes; P<.001) and contrast use (115 mL vs 140 mL; P<.01) were lower in the rPCI group than in the fPCI group. Crossover rate from radial to femoral was 6.5%. There were more access-site hematomas in the fPCI group (2.8% rPCI vs 14.3% fPCI; P<.001), with no statistically significant rate of other access-related complications. There was no difference in stroke, myocardial infarction, cardiac arrest, or unplanned surgery. There was no difference in bleeding or stroke between both groups during subsequent transfemoral TAVR. CONCLUSION: Radial access for pre-TAVR PCI is feasible and safe and is associated with a lower rate of access-site hematoma. This study supports the increased use of transradial access for pre-TAVR PCI.

Removal of Abnormal Myofilament O-GlcNAcylation Restores Ca2+ Sensitivity in Diabetic Cardiac Muscle.

Contractile dysfunction and increased deposition of O-linked ß-N-acetyl-d-glucosamine (O-GlcNAc) in cardiac proteins are a hallmark of the diabetic heart. However, whether and how this posttranslational alteration contributes to lower cardiac function remains unclear. Using a refined ß-elimination/Michael addition with tandem mass tags (TMT)-labeling proteomic technique, we show that CpOGA, a bacterial analog of O-GlcNAcase (OGA) that cleaves O-GlcNAc in vivo, removes site-specific O-GlcNAcylation from myofilaments, restoring Ca(2+) sensitivity in streptozotocin (STZ) diabetic cardiac muscles. We report that in control rat hearts, O-GlcNAc and O-GlcNAc transferase (OGT) are mainly localized at the Z-line, whereas OGA is at the A-band. Conversely, in diabetic hearts O-GlcNAc levels are increased and OGT and OGA delocalized. Consistent changes were found in human diabetic hearts. STZ diabetic hearts display increased physical interactions of OGA with α-actin, tropomyosin, and myosin light chain 1, along with reduced OGT and increased OGA activities. Our study is the first to reveal that specific removal of O-GlcNAcylation restores myofilament response to Ca(2+) in diabetic hearts and that altered O-GlcNAcylation is due to the subcellular redistribution of OGT and OGA rather than to changes in their overall activities. Thus, preventing sarcomeric OGT and OGA displacement represents a new possible strategy for treating diabetic cardiomyopathy.

Cardiac troponin I Pro82Ser variant induces diastolic dysfunction, blunts ß-adrenergic response, and impairs myofilament cooperativity.

Troponin I (TnI) variant Pro82Ser (cTnIP82S) was initially considered a disease-causing mutation; however, later studies suggested the contrary. We tested the hypothesis of whether a causal link exists between cTnIP82S and cardiac structural and functional remodeling, such as during aging or chronic pressure overload. A cardiac-specific transgenic (Tg) mouse model of cTnIP82S was created to test this hypothesis. During aging, Tg cTnIP82S displayed diastolic dysfunction, characterized by longer isovolumetric relaxation time, and impaired ejection and relaxation time. In young, Tg mice in vivo pressure-volume loops and intact trabecular preparations revealed normal cardiac contractility at baseline. However, upon ß-adrenergic stimulation, a blunted contractile reserve and no hastening in left ventricle relaxation were evident in vivo, whereas, in isolated muscles, Ca(2+) transient amplitude isoproterenol dose-response was blunted. In addition, when exposed to chronic pressure overload, Tg mice show exacerbated hypertrophy and decreased contractility compared with age-matched non-Tg littermates. At the molecular level, this mutation significantly impairs myofilament cooperative activation. Importantly, this occurs in the absence of alterations in TnI or myosin-binding protein C phosphorylation. The cTnIP82S variant occurs near a region of interactions with troponin T; therefore, structural changes in this region could explain its meaningful effects on myofilament cooperativity. Our data indicate that cTnIP82S mutation modifies age-dependent diastolic dysfunction and impairs overall contractility after ß-adrenergic stimulation or chronic pressure overload. Thus cTnIP82S variant should be regarded as a disease-modifying factor for dysfunction and adverse remodeling with aging and chronic pressure overload.