Explore the vast range of titles available.

New generation of the most widely used devices for transcatheter aortic valve implantation have been recently introduced into practice. We compare the short-term outcomes of transcatheter aortic valve implantation with the Edwards SAPIEN S3 and the Medtronic Evolut-R. We performed a retrospective analysis from a single high-volume tertiary center. Valve Academic Research Consortium-2 criteria were used to define composite end points of device success and safety at 30 days. Study population included 232 patients implanted with the SAPIEN S3 (n = 124) and Evolut-R (n = 108). Device success reached 91.9% and 95.4% in the SAPIEN S3 and Evolut-R groups, respectively (p = 0.289). Postprocedural echocardiography showed greater aortic valve gradients (22.8 ± 7 vs 16 ± 9 mm Hg, p <0.001) among SAPIEN S3 group. Paravalvular leak of ≥ moderate severity was observed in 2.4% and 0% in the SAPIEN S3 and Evolut-R groups, respectively (p = 0.251). Similar rates of in-hospital complications, including major bleedings, vascular complications, and pacemaker implantations were recorded in both groups. At 30-day follow-up, the combined safety end point was reached in 5.6% and in 6.5% of patients in the SAPIEN S3 and Evolut-R groups, respectively (p = 0.790). During follow-up of 237 ± 138 days, all-cause mortality was higher in patients implanted with Evolut-R compared with SAPIEN S3 (7 vs 1 cases, respectively, p = 0.006), however, cardiovascular mortality was not significantly different between groups. In conclusions, in a single-center comparative analysis, comparable rate of device success as well as safety profile and long-term cardiovascular mortality were observed with the SAPIEN S3 and Evolut-R valves.

We have recently shown that the expression of the transient receptor potential vanilloid 2 channel, TRPV2, is upregulated in the peri-infarct zone 3-5 days following an acute myocardial infarction (AMI). Further analysis has demonstrated that invading monocytes maturing to macrophages merely harbor the documented elevated expression of this channel. Assess cardiac function in TRPV2-KO mice compared to TRPV2-WT following AMI and analyze the potential involvement of TRPV2-expressing macrophages in the recovery process. TRPV2-KO or WT mice were induced with AMI by ligation of the left anterior descending artery (LAD). In another set of experiments, TRPV2-KO mice induced with AMI, were intravenously (IV) injected with WT or TRPV2-KO peritoneal macrophages in order to directly assess the potential contribution of TRPV2-expressing macrophages to cardiac healing. Cardiac parameters were obtained by echocardiography 1 day and 30 days post infarction. The relative changes in the ejection fraction (EF) and additional cardiac parameters between baseline (day 1) and day 30 were calculated and statistical significance was determined (SPSS). The in vivo study showed that while EF was significantly decreased in the WT animals between baseline and day 30, EF was only slightly and insignificantly reduced in the KO animals. Likewise LVESD and LVESA were significantly modified exclusively in the WT animals. Moreover, intravenous administration of peritoneal WT macrophages, but not KO macrophages, significantly reduced survival of post-MI TRPV2-KO mice. The data suggest that knockout of the TRPV2 channel may attenuate macrophage-dependent pro-inflammatory processes and result in better cardiac recovery. TRPV2 may thus represent a novel therapeutic target for treatment of patients undergoing an acute MI.

Monoclonal antibody derivatives are promising drugs for the treatment of various diseases due to their high matrix metalloproteinases (MMP) active site specificity. We studied the effects of a novel antibody, SDS3, which specifically recognizes the mature active site of MMP9/2 during ventricular remodeling progression in a mouse model of chronic volume overload (VO). VO was induced by creating an aortocaval fistula (ACF) in 10- to 12-week-old C57BL male mice. The VO-induced mice were treated with either vehicle control (PBS) or with SDS3 twice weekly by intraperitoneal (ip) injection. The relative changes in cardiac parameters between baseline (day 1) and end-point (day 30), were evaluated by echocardiography. The effects of SDS3 treatment on cardiac fibrosis, cardiomyocyte volume, and cardiac inflammation were tested by cardiac staining with Masson's trichrome, wheat Germ Agglutinin (WGA), and CD45, respectively. Serum levels of TNFα and IL-6 with and without SDS3 treatment were tested by ELISA. SDS3 significantly reduced cardiac dilatation, left ventricular (LV) mass, and cardiomyocyte hypertrophy compared to the vehicle treated animals. The antibody also reduced the heart-to-body weight ratio of the ACF animals to values comparable to those of the controls. Interestingly, the SDS3 group underwent significant reduction of cardiac inflammation and pro-inflammatory cytokine production, indicating a regulatory role for MMP9/2 in tissue remodeling, possibly by tumor necrosis factor alpha (TNFα) activation. In addition, significant changes in the expression of proteins related to mitochondrial function were observed in ACF animals, these changes were reversed following treatment with SDS3. The data suggest that MMP9/2 blockage with SDS3 attenuates myocardial remodeling associated with chronic VO by three potential pathways: downregulating the extracellular matrix proteolytic cleavage, reducing the cardiac inflammatory responses, and preserving the cardiac mitochondrial structure and function.

The new European Society of Cardiology guidelines reclassified heart failure according to left ventricular ejection fraction, recognizing patients with mid-range EF (mrEF; 40% to 49%) as a distinct group. We sought to investigate the clinical profile, in-hospital outcomes, and long-term mortality of ST-elevation myocardial infarction (STEMI) patients treated with primary percutaneous coronary intervention who had mrEF. We conducted a retrospective study of 2,086 consecutive patients with STEMI between December 2007 and June 2016 who underwent primary percutaneous coronary intervention and had a comprehensive echocardiographic examination performed within 72 hours of hospital admission. Patients were stratified according to their left ventricular ejection fraction–mrEF (40% to 49%), reduced EF (rEF; <40%), and preserved EF (pEF; ≥50%) groups and evaluated for baseline characteristics, in-hospital outcomes, as well as for long-term mortality. A total of 858 of 2,086 patients (41%) had mrEF, 215 of 2086 (10%) had rEF, and 1,013 of 2,086 (48%) had pEF. Patients with mrEF had nearly similar baseline co-morbidities and similar 30-day mortality compared with patients with pEF (2% vs 1%, p = 0.17). In a univariate analysis, long-term mortality was higher compared with those with pEF (9.8% vs 7.2%, p <0.01). In a multivariate Cox regression model, mrEF was independently associated with increased long-term mortality risk compared with pEF (hazard ratio 1.4, 95% CI 1.02 to 1.93, p = 0.04). In conclusion, among STEMI patients, those with mrEF at presentation constitute a distinct group in terms of baseline characteristics, in-hospital outcomes, and long-term mortality.

[This corrects the article DOI: 10.1371/journal.pone.0231202.].[This corrects the article DOI: 10.1371/journal.pone.0231202.].

Various physical, emotional, and extrinsic triggers have been attributed to acute coronary syndrome. Whether a correlation can be drawn between identifiable ischemic triggers and the nature of coronary artery disease (CAD) still remains unclear. In the present study, we evaluated the correlation between triggered versus nontriggered ischemic symptoms and the extent of CAD in patients with ST-segment elevation myocardial infarction (STEMI). We conducted a retrospective, single-center observational study including 1,345 consecutive patients with STEMI, treated with primary percutaneous coronary intervention. Acute physical and emotional triggers were identified in patients' historical data. Independent predictors of multivessel CAD were determined using a logistic regression model. A potential trigger was identified in 37% of patients. Physical exertion was found to be the most dominant trigger (65%) followed by psychological stress (16%) and acute illness (12%). Patients with nontriggered STEMI tended to be older and more likely to have co-morbidities. Patients with nontriggered STEMI showed a higher rate of multivessel CAD (73% vs 30%, p <0.001). In a multivariate regression model, nontriggered symptoms emerged as an independent predictor of multivessel CAD (odds ratio 8.33, 95% CI 5.74 to 12.5, p = 0.001). No specific trigger was found to predict independently the extent of CAD. In conclusion, symptoms onset without a recognizable trigger is associated with multivessel CAD in STEMI. Further studies will be required to elucidate the putative mechanisms underlying ischemic triggering.

Early recognition of deteriorating left ventricular function plays a key prognostic role in patients with aortic stenosis (AS). First-phase ejection fraction (EF1), the ejection fraction (EF) up to time of maximal contraction, has been suggested for detection of early left ventricular dysfunction in patients with AS with preserved EF. This work aims to evaluate the predictive value of EF1 for assessment of long-term survival in patients with symptomatic severe AS and preserved EF who undergo transcatheter aortic valve implantation (TAVI). We included 102 consecutive patients (median age 84 years [interquartile range 80 to 86 years]) who underwent TAVI between 2009 and 2011. Patients were retrospectively stratified into tertiles by EF1. Device success and procedural complications were defined according to the Valve Academic Research Consortium-3 criteria. Mortality data were retrieved from a computerized interface of the Israeli Ministry of Health. Baseline characteristics, co-morbidities, clinical presentation, and echocardiographic findings were similar among groups. The groups did not differ significantly regarding device success and in-hospital complications. During a potential follow-up period of >10 years, 88 patients died. Kaplan–Meier analysis (log-rank p = 0.017) followed by multivariable Cox regression analysis showed that EF1 predicted long-term mortality independently, either as continuous variable (hazard ratio 1.04, 95% confidence interval 1.01 to 1.07, p = 0.012) or for each decrease in tertile group (hazard ratio 1.40, 95% confidence interval 1.05 to 1.86, p = 0.023). In conclusion, low EF1 is associated with a significant decrease in adjusted hazard for long-term survival in patients with preserved EF who undergo TAVI. Low EF1 might delineate a population at great risk who would benefit from prompt intervention.

Although the natural history of aortic stenosis (AS) depends on the severity of symptoms, the prognostic significance of AS clinical progression in patients who underwent aortic valve replacement is less clear. Here, we studied the correlation between the severity of AS presenting symptoms and survival after transcatheter aortic valve implantation (TAVI). We evaluated long-term survival of a consecutive cohort of severe AS patients (n = 862, mean Society of Thoracic Surgeons score 4.16 ± 2.9) who underwent transfemoral TAVI from 2009 to 2016. Patients were classified as having severe symptoms (i.e., angina, syncope, or heart failure, n = 424) or mild symptoms (i.e., dizziness, fatigue, effort dyspnea, chest discomfort, n = 438). No differences in device success nor in-hospital complications were found between groups. During a median follow-up of 2.84 (1.9 to 4.5) years, survival at 1, 3, and 5 years in the entire cohort, was 89% ± 1.1%, 75% ± 1.6%, and 59% ± 2.1%, respectively. Severe symptoms were associated with higher mortality (hazard ratio 1.54, 95% confidence intervals 1.230 to 1.939, p <0.001). The 1-, 3-, and 5-year survival was 94% ± 1.9%, 81% ± 3.3%, and 71% ± 4.3% in patients with angina, 92% ± 3.3%, 75% ± 5.6%, and 56% ± 8.2% in patients with syncope and 77% ± 3%, 54% ± 3.7%, and 41% ± 4.1% in patients with heart failure, respectively, (p <0.001). Heart failure symptoms emerged as independent predictor of mortality (hazard ratio 1.66, 1.28 to 2.17, p <0.001), regardless of left ventricular ejection fraction. The severity of AS symptoms affects survival after TAVI and overt heart failure independently predicts early mortality. Early intervention after diagnosis of severe AS is crucial to reduce the unfavorable effects of clinical progression on survival after TAVI.

Objective: To test the hypothesis that B-type natriuretic peptide (BNP) acts as a potent vasculogenic agent by enhancing the number, proliferation, adhesion, and migration of endothelial progenitor cells (EPCs). Background: BNP is a neurohormonal peptide that predicts outcome and used for treatment in chronic heart failure patients. It has been shown to promote angiogenesis in experimental animals. EPCs have been demonstrated to contribute to postnatal angiogenesis and vasculogenesis. Methods: The number of EPC colony forming units (CFU) and levels of N-terminal ProBNP were assayed in patients with severe, yet controlled, New York Heart Association (NYHA) II–IV heart failure. The in vitro effects of BNP on early EPC-CFU numbers, proliferation, migration, adhesive, and vascular tube formation capacities were studied using human and murine systems. The effects of in vivo BNP administration on Sca-1/Flk-1 progenitors and on vasculogenesis in the hindlimb ischemia model were then assayed in wild-type mice. Results: A significant correlation was found between circulating N-terminal ProBNP levels and EPC-CFU numbers. We observed a dose-dependent effect of BNP on the numbers of CFU and proliferation capacity of human EPCs as well as on their adhesive, migratory, and tube formation properties, in vitro . Systemic BNP administration to mice led to a significant increase in bone marrow Sca-1/Flk-1 EPCs and improvement in blood flow and capillary density in the ischemic limbs of mice. Conclusions: BNP promotes vessel growth by increasing the number of endothelial progenitors and enhancing their functional properties. These provasculogenic properties of BNP could account for some of its beneficial effects in chronic heart failure patients and may be harnessed for the purpose of improving collateral formation in ischemic subjects.

Transcatheter aortic valve implantation (TAVI) has been widely used for the treatment of aortic stenosis. Most pivotal studies of TAVI included patients with a mean age of over 80 years old. Many young patients may also be considered for TAVI because of severe co-morbidities. We sought to describe a group of patients undergoing TAVI at an age below 70 and to compare them with older patients undergoing the procedure. This study included 1,324 consecutive patients from a 3-center TAVI registry from 2008 to 2014. Patients were divided according to age into 3 groups: patients aged 70 years and below, patients between the ages of 71 and 80, and patients 81 years and older. Patients in the younger group had higher body mass index (p <0.001), higher proportion of previous stroke (p = 0.05), peripheral vascular disease (p = 0.03), and diabetes mellitus (p <0.001). Thirty percent of patients in the younger group had functional class IV. Corticosteroids treatment was 5-fold higher in the younger group (p <0.001). Average valve area was lower in the older group (p = 0.004). Thirty-day mortality was similar between the 3 groups. We found no difference in the rate of in-hospital complications. One-year all-cause mortality rate of patients aged 70 years, 71 to 80 years, and >80 years was 7.6%, 7.5%, and 12.6%, respectively, p = 0.01. In conclusion, younger patients undergoing TAVI exhibited higher prevalence of risk factors and co-morbidities that probably explain the decision to perform TAVI rather than surgical aortic valve replacement. Nevertheless, the 1-year mortality of these patients was significantly lower than in older patients.