Post-dilatation trepidation: Post-dil is "no big dil".

Selective stent post-dilatation (PD) in a cohort of STEMI patients did not affect major adverse cardiac events but it did decrease device-oriented composite events, a secondary composite end point of less clear significance. This study suggests that selective stent PD in STEMI does not increase the incidence of acute no-reflow or long-term adverse clinical events. In primary PCI for STEMI, if the stent appears under-expanded, then PD, perhaps guided by intravascular imaging (which was not reported in this study), is reasonable.

Brief Report: Oxidative Stress Mediates Cardiomyocyte Apoptosis in a Human Model of Danon Disease and Heart Failure.

Danon disease is a familial cardiomyopathy associated with impaired autophagy due to mutations in the gene encoding lysosomal-associated membrane protein type 2 (LAMP-2). Emerging evidence has highlighted the importance of autophagy in regulating cardiomyocyte bioenergetics, function, and survival. However, the mechanisms responsible for cellular dysfunction and death in cardiomyocytes with impaired autophagic flux remain unclear. To investigate the molecular mechanisms responsible for Danon disease, we created induced pluripotent stem cells (iPSCs) from two patients with different LAMP-2 mutations. Danon iPSC-derived cardiomyocytes (iPSC-CMs) exhibited impaired autophagic flux and key features of heart failure such as increased cell size, increased expression of natriuretic peptides, and abnormal calcium handling compared to control iPSC-CMs. Additionally, Danon iPSC-CMs demonstrated excessive amounts of mitochondrial oxidative stress and apoptosis. Using the sulfhydryl antioxidant N-acetylcysteine to scavenge free radicals resulted in a significant reduction in apoptotic cell death in Danon iPSC-CMs. In summary, we have modeled Danon disease using human iPSC-CMs from patients with mutations in LAMP-2, allowing us to gain mechanistic insight into the pathogenesis of this disease. We demonstrate that LAMP-2 deficiency leads to an impairment in autophagic flux, which results in excessive oxidative stress, and subsequent cardiomyocyte apoptosis. Scavenging excessive free radicals with antioxidants may be beneficial for patients with Danon disease. In vivo studies will be necessary to validate this new treatment strategy.

Removal of Impella® 2.5 while maintaining vascular access: a solution to a vascular quandary.

Cardiogenic shock (CS) in the setting of acute myocardial infarction is associated with high in-hospital mortality rates. Society guidelines provide a Class Ib recommendation for the use of hemodynamic support devices in patients with CS following ST-elevation myocardial infarction. Exchanging of hemodynamic support devices is often complicated by inability to maintain percutaneous vascular access upon device removal in the setting of anticoagulation. This report highlights one potential solution to the dilemma of maintaining vascular access following removal of an Impella® 2.5 mechanical support device to allow safe transition to a TandemHeart system in a patient with refractory CS.

Late presenting, contained rupture of the superficial femoral artery following atherectomy and stenting: case report and literature review.

Excisional atherectomy alone or followed by stenting is considered an appropriate treatment strategy for patients with lifestyle-limiting claudication due to obstructive infra-inguinal peripheral arterial disease (Ramaiah et al., J Endovasc Ther 2006;13:592-6021). We present a case of a 69-year-old man with eccentric severely calcified disease of the superficial femoral artery (SFA) treated with excisional atherectomy followed by stenting with an interwoven nitinol stent. The procedure was complicated by extravascular stent migration associated with a contained rupture presenting 30 days after the intervention. The complication was successfully treated with a stent graft. Although rare, pseudoaneurysms have been reported at the site of prior atherectomy; however, this case is the first description of a contained rupture post atherectomy associated with erosion of a nitinol stent into an extra-luminal position. The mechanism and management of this complication are discussed.

Investigating intestinal permeability and gut microbiota roles in acute coronary syndrome patients.

Background: Acute Coronary Syndrome (ACS) is a leading cause of morbidity and mortality. Perturbed gut- microbiota (dysbiosis) and increased intestinal permeability (leaky-gut) with translocation of bacterial antigens, play critical role in obesity and metabolic syndrome, which are also major ACS risk factors. Additionally, Trimethylamine-N-Oxide (TMAO), a metabolite produced by phylum Proteobacteria in gut is implicated in developing ACS. As Proteobacteria is a major source of translocated antigen lipopolysaccharides (LPS), we hypothesized that ACS patients have leaky-gut condition characterized by dysbiosis with increased Proteobacteria, leading to elevated blood levels of TMAO and LPS. Methods: In a pilot case-control study, we enrolled 19 ACS patients (within 72-h of cardiac events) and 19 healthy-controls. Gut barrier function was determined using lactulose-to-mannitol urinary excretion ratio (L/M ratio). Stool microbiome composition was examined using16S sequencing and predictive functional analysis for LPS biosynthesis pathway by PICRUSt tool. Serum TMAO and LPS levels were measured. Results: ACS patients had increased Gammaproteobacteria compared to controls:1.8 ±3.0 vs. 0.2 ±0.4% (P =0.04). Though Proteobacteria level was increased but not statistically significant: 4.1 ±3.8 vs. 2.1 ±1.7% (P =0.056). L/M-ratio was three times higher in ACS patients; 0.06 ±0.07 vs 0.023 ±0.02, (P =0.014). Surprisingly, there was no difference in the mean serum LPS or TMAO levels. However, PICRUSt analysis indicated increased Proteobacteria population increasingly contributed to LPS biosynthesis in ACS patients only. Conclusions: ACS patients likely to have leaky-gut and perturbed gut microbiota. Further studies are required to precisely define the role of dysbiosis in ACS.

Unusual congenital coronary artery anomaly in a young adult presenting as sudden cardiac arrest.

A previously asymptomatic young female with no previous medical or cardiac history collapsed during indoor exercise. A portable automatic external defibrillator showed a shockable rhythm. She received multiple electrical shocks with return to normal sinus rhythm without ischaemic ECG changes. Her troponin level was mildly elevated. A transthoracic echocardiogram revealed moderately reduced left ventricular ejection fraction with global hypokinesis. During emergent coronary angiography, the left main coronary artery could not be found. The right coronary artery was normal with robust collaterals to the entire left coronary circulation extending to the left main coronary artery, but did not fill the ostium. Coronary CT angiogram confirmed nearly complete absence of the left main coronary artery ostium. A diagnosis of left main coronary artery atresia was made. Patient underwent successful two vessel coronary artery bypass grafting. She continues to do well 1 year postoperatively.

Impact of ranolazine on coronary microvascular dysfunction (MICRO) study.

BACKGROUND: Patients with angina and coronary microvascular dysfunction, without evidence of structural or epicardial coronary disease (Type I CMVD) remain without evidence based treatment options. Previous work has demonstrated that ranolazine can improve angina frequency and stability among patients with Type 1 CMVD; however, the mechanism remains unclear. Therefore, the objective of this pilot project was to assess the impact of ranolazine on Type I CMVD as measured using an invasive tool to measure global resistance (index of microcirculatory resistance (IMR)). METHODS: Patients with Type 1 CMVD diagnosed using IMR were enrolled and treated with ranolazine 1000mg BID. Coronary angiography and IMR were performed at baseline and on treatment after four weeks. The primary outcome measure was change in IMR pre- and post-treatment. Secondary outcome measures, improvement in angina and activity level, were assessed using the Seattle Angina Questionnaire (SAQ), Duke Activity Status Index (DASI) and Metabolic equivalent for Task (MET) scores. RESULTS: A total of 7 patient were enrolled and completed the study. Mean age was 57.6±7.5, 43% were female and 43% were Hispanic. Mean baseline IMR was 37.25±16.27 which decreased to 19.48±5.69 (p=0.02; (-48% Δ) after treatment with ranolazine. Four of the five SAQ domains improved on treatment with significant improvement in physical limitation (p=0.001), angina frequency (p=0.04), angina stability (p=0.05) and disease perception (p=0.001). Non-significant improvements in activity were also seen in both the DASI and MET scores. CONCLUSION: Among patients with Type 1 CMVD, our pilot data suggest favorable changes in IMR, anginal symptoms and activity status with ranolazine treatment. These findings support further evaluation of the effects of ranolazine on microcirculatory function and angina symptoms in a larger cohort of patients with Type 1 CMVD.