De novo recurrent SCAD invariably affected new segments distinct from previously dissected segments.

Conservative therapy is typically recommended for patients with spontaneous coronary artery dissection (SCAD). However, percutaneous coronary intervention (PCI) may have to be pursued in cases of ongoing ischemia or hemodynamic instability. There is early and increasing interest in using cutting balloon (CB) angioplasty to fenestrate the false lumen to allow communication and back-bleed of intramural hematoma into the true lumen. We report a successful case of CB angioplasty for SCAD without the need for stenting, and provide a review of the published experience and recommendation for technical approaches with this strategy.

No abstract

Background: Transcatheter aortic valve replacement (TAVR) can be an effective option for high-risk Aortic Regurgitation (AR) patients. Although international experiences of TAVR for AR are published, U.S. data are limited. This study sought to report the short-term outcomes of TAVR in AR in the U.S. population. Methods: Study cohorts were derived from the Nationwide Inpatient Sample (NIS) and Nationwide Readmissions Database (NRD) 2016-17. TAVR and AR were identified using ICD-10-CM-codes. The key outcomes were all-cause mortality, disabling stroke, valvular complications, complete heart block (CHB)/permanent pacemaker placement (PPM), open-heart surgery, acute kidney injury (AKI) requiring dialysis, and vascular complications. Multivariate logistic regression was used to adjust for confounders.Results: 915 patients from the NIS (male-71%, age ≥65-84.2%) and 822 patients from the NRD (male-69.3%, age ≥65-80.5%) underwent TAVR for AR. The median length of stay (LOS) was 4 days for both cohorts. In-hospital mortality was 2.7%, and 30-day mortality was 3.3%. Disabling strokes were noted in 0.6% peri-procedurally and 1.8% at 30-days. Valve-related complications were 18-19% with paravalvular leak (4-7%) being the most common. Approximately 11% of patients developed CHB and/or needed PPM in both cohorts. In NRD, 2.2% of patients required dialysis for

Genetic variants have been described for a range of G protein-coupled receptors (as well as for G proteins) linked to adenylyl cyclase. Furthermore, expression of these variants resulted in alterations in receptor-mediated activation of adenylyl cyclase, as well as alterations in more "downstream" effector pathways mediated by cyclic adenosine monophosphate. However, the identification of dysfunctional variants of adenylyl cyclase has been far more limited. Screening a region of the molecule that we recently demonstrated to be critical in regulation of enzyme activity, we have identified a missense single-nucleotide variant at amino acid 674 of human adenylyl cyclase isoform VI. In a population of 286 healthy white subjects, this variant has an allelic frequency of 3.1% (although 0/90 nonwhite subjects had this variant). Expression of this variant of adenylyl cyclase VI (whether expressed as the S674 human adenylyl cyclase VI [ADCY6] or the S686 ADCY6 rat analog) is characterized by a significant decrease in stimulated adenylyl cyclase activity (forskolin-stimulated activity of the S674 human ADCY6 variant was decreased to 56% +/- 6% of the activity of the A674 variant [mean +/- SEM]; n = 9; P = .004). Furthermore, subjects with the S674 variant demonstrated a significantly higher lymphocyte count (2.68 +/- 4.13 x 10(3)/mm3 versus 1.90 +/- 0.72 x 10(3)/mm3, P = .019). Paralleling this phenotype, expression of the variant was associated with attenuation of the forskolin-mediated reduction in cell growth rate to 64% +/- 5% of the effect seen with expression of the wild-type ADCY6 (n = 4; P = .001). In summary, these data demonstrate an unappreciated variant of adenylyl cyclase isoform VI that has a functional impact on both enzyme activity and cyclic adenosine monophosphate-mediated regulation of cell growth.

No abstract

No abstract

Background: The current literature focuses on the risk of infective endocarditis (IE) following transcatheter aortic valve implantation (TAVI). However, the risk of IE in patients waiting for TAVI is not well-studied. We present a unique case of a patient waiting for TAVI with decompensated heart failure who was found to have a large mitral vegetation, and consider risk factors for the development of IE in this population. Case description: We report the case of an 85-year-old male with severe aortic stenosis and recurrent small bowel angiodysplasias, requiring frequent blood transfusions and intravenous iron. He presented to a peripheral hospital in decompensated heart failure. Transfer was arranged to our center to expedite TAVI, under the premise that worsening aortic stenosis precipitated his decompensated state. Prior to TAVI, an echocardiogram was done, and demonstrated a 30 × 18 mm mass on the mitral valve with anterior leaflet perforation and severe mitral regurgitation. The findings were consistent with IE, and the TAVI was cancelled. Despite antibiotic therapy, the patient unfortunately deteriorated and palliative care was provided. Conclusions: This case highlights the need for further research regarding the risk of IE in patients waiting for TAVI. Current literature focuses on the development and management of IE following TAVI. Clinicians must understand that TAVI candidates have multiple risk factors for IE, including valvular disease, age, and comorbidities. IE should be considered as a possible cause for decompensated heart failure in patients awaiting TAVI.