IMPORTANCE Little is known about cardiac adverse events among patients with nonobstructive coronary artery disease (CAD). OBJECTIVE To compare myocardial infarction (MI) and mortality rates between patients with nonobstructive CAD, obstructive CAD, and no apparent CAD in a national cohort. DESIGN, SETTING, AND PARTICIPANTS Retrospective cohort study of all US veterans undergoing elective coronary angiography for CAD between October 2007 and September 2012 in the Veterans Affairs health care system. Patients with prior CAD events were excluded. EXPOSURES Angiographic CAD extent, defined by degree (no apparent CAD: no stenosis >20%; nonobstructive CAD: ≥1 stenosis ≥20% but no stenosis ≥70%; obstructive CAD: any stenosis ≥70% or left main [LM] stenosis ≥50%) and distribution (1,2, or 3 vessel). MAIN OUTCOMES AND MEASURES The primary outcome was 1-year hospitalization for nonfatal MI after the index angiography. Secondary outcomes included 1-year all-cause mortality and combined 1-year MI and mortality. RESULTS Among37 674 patients, 8384 patients (22.3%) had nonobstructive CAD and 20 899 patients (55.4%) had obstructive CAD. Within 1 year, 845 patients died and 385 were rehospitalized for MI. Among patients with no apparent CAD, the 1-year MI rate was 0.11% (n = 8, 95% CI, 0.10%–0.20%) and increased progressively by 1-vessel nonobstructive CAD, 0.24% (n = 10, 95% CI, 0.10%–0.40%); 2-vessel nonobstructive CAD, 0.56% (n = 13, 95% CI, 0.30%–1.00%); 3-vessel nonobstructive CAD, 0.59% (n = 6, 95% CI, 0.30%–1.30%); 1-vessel obstructive CAD, 1.18% (n = 101, 95% CI, 1.00%–1.40%); 2-vessel obstructive CAD, 2.18% (n = 110, 95% CI, 1.80%–2.60%); and 3-vessel or LM obstructive CAD, 2.47% (n = 137, 95% CI, 2.10%–2.90%). After adjustment, 1-year MI rates increased with increasing CAD extent. Relative to patients with no apparent CAD, patients with 1-vessel nonobstructive CAD had a hazard ratio (HR) for 1-year MI of 2.0 (95% CI, 0.8–5.1); 2-vessel nonobstructive HR, 4.6 (95% CI, 2.0–10.5); 3-vessel nonobstructive HR, 4.5 (95% CI, 1.6–12.5); 1-vessel obstructive HR, 9.0 (95% CI, 4.2–19.0); 2-vessel obstructive HR, 16.5 (95% CI, 8.1–33.7); and 3-vessel or LM obstructive HR, 19.5 (95% CI, 9.9–38.2). One-year mortality rates were associated with increasing CAD extent, ranging from 1.38% among patients without apparent CAD to 4.30% with 3-vessel or LM obstructive CAD. After risk adjustment, there was no significant association between 1- or 2-vessel nonobstructive CAD and mortality, but there were significant associations with mortality for 3-vessel nonobstructive CAD (HR, 1.6; 95% CI, 1.1–2.5), 1-vessel obstructive CAD (HR, 1.9; 95% CI, 1.4–2.6), 2-vessel obstructive CAD (HR, 2.8; 95% CI, 2.1–3.7), and 3-vessel or LM obstructive CAD (HR, 3.4; 95% CI, 2.6–4.4). Similar associations were noted with the combined outcome. CONCLUSIONS AND RELEVANCE In this cohort of patients undergoing elective coronary angiography, nonobstructive CAD, compared with no apparent CAD, was associated with a significantly greater 1-year risk of MI...
Background Pulmonary hypertension (PH) is associated with increased morbidity across the cardiopulmonary disease spectrum. Based largely on expert consensus opinion, PH is defined by a mean pulmonary artery pressure (mPAP) ≥25 mmHg. Although mPAP levels below this threshold are common among populations at risk for PH, the relevance of mPAP <25 mmHg to clinical outcome is unknown. Methods and Results We analyzed retrospectively all US veterans undergoing right heart catheterization (RHC)(2007–2012) in the Veterans Affairs health care system (N=21,727; 908 day median follow-up). Cox proportional hazards models were used to evaluate the association between mPAP and outcomes of all-cause mortality and hospitalization, adjusted for clinical covariates. When treating mPAP as a continuous variable, the mortality hazard increased beginning at 19 mmHg (HR=1.183, 95% CI [1.004–1.393]) relative to 10 mmHg. Therefore, patients were stratified into three groups: referent (≤18 mmHg; N=4,207), borderline PH (19–24 mmHg; N=5,030), and PH (≥25 mmHg; N=12,490). The adjusted mortality hazard was increased for borderline PH (HR=1.23, 95% CI [1.12–1.36], P<0.0001) and PH (HR=2.16, 95% CI [1.96–2.38], P<0.0001) compared to the referent group. The adjusted hazard for hospitalization was also increased in borderline PH (HR=1.07, 95% CI [1.01–1.12], P=0.0149) and PH (HR=1.15, 95% CI [1.09–1.22], P<0.0001). The borderline PH cohort remained at increased risk for mortality after excluding the following high-risk subgroups: patients with pulmonary artery wedge pressure >15 mmHg, pulmonary vascular resistance ≥3.0 Wood units, or inpatient status at the time of RHC. Conclusions These data illustrate a continuum of risk according to mPAP level, and that borderline PH is associated with increased mortality and hospitalization. Future investigations are needed to test the generalizability of our findings to other populations and study the effect of treatment on outcome in borderline PH.
BackgroundRecent evidence supports that the maternal gut microbiota impacts the initial infant gut microbiota. Since the gut microbiota may play a causal role in the development of obesity, it is important to understand how pre-pregnancy weight and gestational weight gain (GWG) impact the gut microbiota of mothers at the time of delivery and their infants in early life. In this study, we performed 16S rRNA gene sequencing on gut microbiota samples from 169 women 4 days after delivery and from the 844 samples of their infants at six timepoints during the first 2 years of life. We categorized the women (1) according to pre-pregnancy body mass index into overweight/obese (OW/OB, BMI ≥ 25) or non-overweight/obese (BMI < 25) and (2) into excessive and non-excessive GWG in the subset of mothers of full-term singleton infants (N = 116). We compared alpha diversity and taxonomic composition of the maternal and infant samples by exposure groups. We also compared taxonomic similarity between maternal and infant gut microbiota.ResultsMaternal OW/OB was associated with lower maternal alpha diversity. Maternal pre-pregnancy OW/OB and excessive GWG were associated with taxonomic differences in the maternal gut microbiota, including taxa from the highly heritable family Christensenellaceae, the genera Lachnospira, Parabacteroides, Bifidobacterium, and Blautia. These maternal characteristics were not associated with overall differences in the infant gut microbiota over the first 2 years of life. However, the presence of specific OTUs in maternal gut microbiota at the time of delivery did significantly increase the odds of presence in the infant gut at age 4–10 days for many taxa, and these included some lean-associated taxa.ConclusionsOur results show differences in maternal gut microbiota composition at the time of delivery by pre-pregnancy weight and GWG, but these changes were only associated with limited compositional differences in the early life gut microbiota of their infants. Further work is needed to determine the degree to which these maternal microbiota differences at time of birth with OW/OB and GWG may affect the health of the infant over time and by what mechanism.Electronic supplementary materialThe online version of this article (10.1186/s40168-017-0332-0) contains supplementary material, which is available to authorized users.
Objective Inadequate immunoregulation and elevated inflammation may be risk factors for posttraumatic stress disorder (PTSD), and microbial inputs are important determinants of immunoregulation; however, the association between the gut microbiota and PTSD is unknown. This study investigated the gut microbiome in a South African sample of PTSD-affected individuals and trauma-exposed (TE) controls, to identify potential differences in microbial diversity or microbial community structure. Methods The Clinician Administered Posttraumatic Stress Disorder Scale for DSM-5 (CAPS-5) was used to diagnose PTSD according to DSM-5 criteria. Microbial DNA was extracted from stool samples obtained from 18 individuals with PTSD and 12 TE control participants. Bacterial 16S ribosomal RNA (rRNA) gene V3/V4 amplicons were generated and sequenced. Microbial community structure, alpha-diversity, and beta-diversity were analyzed; random forest analysis was used to identify associations between bacterial taxa and PTSD. Results There were no differences between PTSD and TE control groups in alpha- or beta-diversity measures (e.g., alpha-diversity, Shannon index, t = 0.386, P = .70; beta diversity, based on analysis of similarities (ANOSIM), Bray Curtis test statistic = −0.033, P = .70); however, random forests analysis highlighted three phyla as important to distinguish PTSD status: Actinobacteria, Lentisphaerae, and Verrucomicrobia. Decreased total abundance of these taxa was associated with higher PTSD CAPS scores (r = −.387, P = .035). Conclusions In this exploratory study, measures of overall microbial diversity were similar among individuals with PTSD and TE controls; however, decreased total abundance of Actinobacteria, Lentisphaerae, and Verrucomicrobia was associated with PTSD status.
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