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Visual Abstract, Highlights • The impact of breastfeeding on prolactin, cellular immune activation, and myocardial recovery was analyzed in 100 women with peripartum cardiomyopathy • Cardiac function was assessed by echocardiography at presentation and at serial intervals over the first year postpartum • The levels of circulating prolactin were assessed by ELISA, and cellular immunophenotyping by flow cytometry, and compared between breastfeeding and nonbreastfeeding women • Prolactin levels were higher in breastfeeding women and correlated with significant increases in CD8+ T cells • Despite significantly higher prolactin levels and increased CD8+ cells, myocardial recovery was similar in breastfeeding and nonbreastfeeding women, Summary The etiology of peripartum cardiomyopathy remains unknown. One hypothesis is that an increase in the 16-kDa form of prolactin is pathogenic and suggests that breastfeeding may worsen peripartum cardiomyopathy by increasing prolactin, while bromocriptine, which blocks prolactin release, may be therapeutic. An autoimmune etiology has also been proposed. The authors investigated the impact of breastfeeding on cellular immunity and myocardial recovery for women with peripartum cardiomyopathy in the IPAC (Investigations in Pregnancy Associated Cardiomyopathy) study. Women who breastfed had elevated prolactin, and prolactin levels correlated with elevations in CD8+ T cells. However, despite elevated prolactin and cytotoxic T cell subsets, myocardial recovery was not impaired in breastfeeding women.

This pilot study used acoustic speech analysis to monitor patients with heart failure (HF), which is characterized by increased intracardiac filling pressures and peripheral edema. HF-related edema in the vocal folds and lungs is hypothesized to affect phonation and speech respiration. Acoustic measures of vocal perturbation and speech breathing characteristics were computed from sustained vowels and speech passages recorded daily from ten patients with HF undergoing inpatient diuretic treatment. After treatment, patients displayed a higher proportion of automatically identified creaky voice, increased fundamental frequency, and decreased cepstral peak prominence variation, suggesting that speech biomarkers can be early indicators of HF.

Background: We examined the effect of 4mg/day rosiglitazone (RSG) versus placebo (PLC) on rapid angiographic progression (RAP) of non-culprit coronary lesions (NCCL) in type 2 diabetes (DM 2). Methods: Using biomarkers and angiograms from 43 DM 2 enrolled in a randomized controlled double blind trial examining the effects of RSG or PLC on late loss after PCI, we investigated the effects of RSG on RAP of NCCL using logistic regression. All stenoses >=30% of vessel diameter were identified at baseline and quantified by QCA. Patients had 8 month angiography and biomarkers (HOMA (insulin resistance index), insulin, MMP-9, adiponectin (ADI), fibrinogen, hs-CRP, A1C, and LDL and HDL cholesterol) drawn at baseline and 4 months. RAP was defined as >=20% diameter reduction of pre-existing NCCL by QCA, or a new narrowing >=30% arising in a segment angiographically normal at baseline. Results: There were 52 NCCL in the RSG versus 56 in the PLC. 14.8 % (16/108) of lesions had RAP with 7/52 (13.5%) lesions progressing in RSG versus 9/56 (16.1%) in PLC, p=ns. RSG was not a predictor of RAP. Of the biomarkers and angiographic variables examined, hsCRP was the only predictor of RAP. Patients with a 120 day hsCRP above the 75th percent had an OR of 7.35 [2.35,23] for RAP versus those below. Interestingly, although RSG treatment lowered hsCRP at 4 months (RSG 2.03±2.8 mg/dl vs. Placebo 3.37±4.25, p=0.06), it did not decrease the likelihood of plaque progression in either the low or high hsCRP groups (see graph). LDL levels at this time were not different (RSG 74±23 mg/dl vs. PLC 89±32, p=ns). Conclusion: 120 day hsCRP is a predictor of RAP. Despite lowering 120d hsCRP, RSG did not lower the frequency of RAP.

The PARTNER trial demonstrated superior survival with transcatheter aortic valve replacement (TAVR) compared to standard therapy (ST) in inoperable patients with symptomatic, severe aortic stenosis (AS). We sought to evaluate the effect of left ventricular (LV) dysfunction on clinical outcomes and

The Placement of Aortic Transcatheter Valves (PARTNER) trial Cohort A demonstrated similar survival after transcatheter and surgical aortic valve replacement (TAVR and SAVR, respectively) in high-risk operable patients with symptomatic, severe aortic stenosis (AS). The impact of valve replacement