Obesity is common in heart failure (HF) and associated with improved outcomes, often termed the “obesity paradox”. Although fat distribution varies by sex, the role of obesity in the outcomes of women compared to men with HF has not been well-studied. In a cohort of advanced systolic HF patients followed at a single university center, 2718 patients had body mass index (BMI) measured at baseline and 469 HF patients had waist circumference (WC) measured at baseline. Elevated BMI was defined as ≥25 kg/m2. High WC was defined as ≥88 cm in women and ≥102 cm in men. The primary outcome was death, urgent heart transplant, or ventricular assist device placement. Mean age was 53.0 ± 12.4, 25% of subjects were women, and LVEF was 22.9 ± 7.19. In men, 2-year event-free survival was better for high vs. normal BMI (63.2 vs. 53.5% p<0.001) and for high vs. normal WC (78.8% vs. 63.1%, p=0.01). In women, 2-year event-free survival was better in elevated vs. normal BMI groups (67.1% vs. 56.6%, p=0.01), but similar in WC groups. In multivariate analyses, normal BMI and normal WC were associated with higher risk of primary outcome in both men (BMI 1.34, WC 2.02) and women (BMI 1.38, WC 2.99). In advanced HF, high BMI and WC were associated with improved outcomes in both sexes. Further investigation of the interaction between body composition and sex in HF outcomes is warranted.
BackgroundCardiovascular progenitor cells (CPCs) have been identified within the developing mouse heart and differentiating pluripotent stem cells by intracellular transcription factors Nkx2.5 and Islet 1 (Isl1). Study of endogenous and induced pluripotent stem cell (iPSC)-derived CPCs has been limited due to the lack of specific cell surface markers to isolate them and conditions for their in vitro expansion that maintain their multipotency.Methodology/Principal FindingsWe sought to identify specific cell surface markers that label endogenous embryonic CPCs and validated these markers in iPSC-derived Isl1+/Nkx2.5+ CPCs. We developed conditions that allow propagation and characterization of endogenous and iPSC-derived Isl1+/Nkx2.5+ CPCs and protocols for their clonal expansion in vitro and transplantation in vivo. Transcriptome analysis of CPCs from differentiating mouse embryonic stem cells identified a panel of surface markers. Comparison of these markers as well as previously described surface markers revealed the combination of Flt1+/Flt4+ best identified and facilitated enrichment for Isl1+/Nkx2.5+ CPCs from embryonic hearts and differentiating iPSCs. Endogenous mouse and iPSC-derived Flt1+/Flt4+ CPCs differentiated into all three cardiovascular lineages in vitro. Flt1+/Flt4+ CPCs transplanted into left ventricles demonstrated robust engraftment and differentiation into mature cardiomyocytes (CMs).Conclusion/SignificanceThe cell surface marker combination of Flt1 and Flt4 specifically identify and enrich for an endogenous and iPSC-derived Isl1+/Nkx2.5+ CPC with trilineage cardiovascular potential in vitro and robust ability for engraftment and differentiation into morphologically and electrophysiologically mature adult CMs in vivo post transplantation into adult hearts.
Several risk models for HF mortality have been recently developed and show variable levels of success as evidenced by c-statistics ranging from 0.63 to 0.78. [4][5][6][7][8] The Seattle Heart Failure Model (SHFM) 9 and the Heart Failure Survival Score (HFSS) 10 are 2 generally accepted models used to predict risk in patients with advanced HF. Although these models have been previously validated in several HF cohorts, recent studies suggest that these risk models may not apply to the modern era of patients with advanced HF referred to HF treatment centers for heart transplant and VAD evaluation. 11,12 In addition, many of these models were developed and validated in selective cohorts of patients from clinical trials and may not have equal use in nontrial real-world patients.Because women are not as well represented in most clinical trials compared with men, 13 risk models derived without validation in sex-specific cohorts may not have the same predictive accuracy as sex-specific HF risk models in providing effective risk stratification. Men and women with advanced HF present with different baseline characteristics. Women tend to have better systolic function, higher rates of hypertension, and lower rates of ischemic pathogenesis of cardiomyopathy.14-16 The purpose of this study was to develop sex-specific risk prediction tools in patients with advanced HF, with the hypothesis that sex-specific risk models would be more accurate in predicting outcomes in advanced HF. Original Article© 2013 American Heart Association, Inc. Background-Risk stratification is an integral component of clinical decision making in heart failure (HF). Women with HF have unique characteristics compared with men, and it is unknown whether common prognostic factors are equally useful in both populations. We aimed to investigate whether sex-specific risk models are more accurate for risk prediction in patients with advanced HF. Methods and Results-Patients with advanced HF referred to University of California, Los Angeles (UCLA; n=2255), were stratified by sex into derivation (referred in [2000][2001][2002][2003][2004][2005][2006][2007] and validation (referred in 2008-2011) cohorts. Cox regression analysis was used to ascertain key variables predictive of the primary end point of death/urgent transplantation/ ventricular assist device in the derivation cohorts and confirmed in the validation cohorts in men, women, and the total population. Women were younger, with higher ejection fraction and better event-free survival. Despite differences in baseline characteristics, the 4 strongest predictors of outcome in both women and men, as well as in the total cohort, were B-type natriuretic peptide, peak oxygen consumption by cardiopulmonary exercise testing (pkVO 2 ), New York Heart Association (NYHA) classification, and use of angiotensin-converting enzyme inhibitor or angiotensin receptor blocker. In addition, the UCLA model performed better than the Seattle Heart Failure Model (SHFM) and the Heart Failure Survival Score (HFSS) in our cohort...
Rathke's cleft cysts (RCC) are benign cystic lesions of the sella resulting from incomplete obliteration of Rathke's cleft. Symptomatic lesions often require surgical decompression, which is often amenable to a transnasal, transsphenoidal (TNTS) approach. We report our experience with marsupialization of RCC and describe a novel technique to promote re-epithelization of the cyst cavity. Retrospective review. Tertiary academic medical center. Patients who underwent TNTS for RCC between 2007 and 2015. Demographics, lesion characteristics, and reconstruction and treatment outcomes. In total, 52 patients were identified. The mean age was 41 ± 18 years. The mean RCC size was 13 ± 5 mm. Intraoperative cerebrospinal fluid (CSF) leak was encountered in 14 (27%) patients; all were repaired. There were six complications (12%) and no deaths. Mean follow-up was 20 ± 18 months, with five (10%) recurrences. RCC size was associated with intraoperative CSF leak ( = 0.04). In 12 patients, the marsupialized cyst cavity was lined with a free mucosal graft (FMG) to promote healing and re-epithelialization. The TNTS approach is safe and effective in surgical decompression of RCC. Lining the exposed cyst cavity with an FMG is a simple intervention without added morbidity that may promote formation of an epithelialized tract. Not applicable.
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