Abstract Awareness of racial/ethnic disparities represents a key challenge for healthcare systems that attempt to provide effective healthcare and to reduce existing inequalities in the use of and adherence to guideline-recommended cardiovascular drugs to improve clinical outcomes for cardiovascular disease (CVD). In this review, we describe important racial/ethnic differences between and within ethnic groups in the prevalence, risk factors, haemostatic factors, anti-inflammatory and endothelial markers, recurrence, and outcomes of CVD. We discuss important differences in the selection, doses, and response [efficacy and adverse drug reactions (ADRs)] in ethnically diverse patients treated with antithrombotics or lipid-lowering drugs. Differences in drug response are mainly related to racial/ethnic differences in the frequency of polymorphisms in genes encoding drug-metabolizing enzymes (DMEs) and drug transporters. These polymorphisms markedly influence the pharmacokinetics, dose requirements, and safety of warfarin, clopidogrel, and statins. This review aims to support a better understanding of the genetic differences between and among populations to identify patients who may experience an ADR or a lack of drug response, thus optimizing therapy and improving outcomes. The greater the understanding of the differences in the genetic variants of DMEs and transporters that determine the differences in the exposure, efficacy, and safety of cardiovascular drugs between races/ethnicities, the greater the probability that personalized medicine will become a reality.
We examined the role of gastric ammonia in the development of gastric lesions in rats. Exposure of the gastric mucosa to ammonia (30 mM) produced microscopic injury, but no macroscopic lesion was observed. However, exposure of the stomach to ammonia in rats subiected to ischemia resulted in macroscopic gastric lesions. The macroscopic lesions were markedly inhibited by pretreatment with taurine, a scavenger of hypochlorous acid (HOCl) and monochloramine (NH2Cl). These results indicate that ammonia is deleterious to gastric mucosa, and monochloramine may be involved in the pathogenesis of ammonia-induced mucosal lesions
BACKGROUND: Social influencers of health namely race ethnicity, and structural inequities are known to affect the incidence of out of hospital sudden death (OHSD).We sought to examine the association between social influencers of health and the incidence of OHSD in the diverse neighborhoods of New York City during the first wave of coronavirus disease 2019 (COVID-19) epidemic. METHODS:New York City ZIP-stratified data on OHSD were obtained from the Fire Department of New York during the first wave of COVID-19 epidemic (March 1 to April 10, 2019) and the same period in 2020.To assess associates of OHSD, ZIP code-specific sociodemographic characteristics for 8 491 238 New York City residents were obtained via the US Census Bureau's 2018 American Community Survey and the New York Police Department's crime statistics. RESULTS:Between March 1 and April 10, 2020, the number of OHSD rose to 4334 from 1112 compared with the year prior.Of the univariate ZIP code level variables evaluated, proportions of Black race, Hispanic/Latino ethnicity, single parent household, unemployed inhabitants, people completing less than high school education, inhabitants with no health insurance, people financially struggling or living in poverty, percent of noncitizens, and population density were associated with increased rates of OHSD within ZIP codes.In multivariable analysis, ZIP codes with higher proportions of inhabitants with less than high school education (P<0.001) and higher proportions of Black race (P=0.04) were independent predictors for increases in ZIP code rates of OHSD. CONCLUSIONS:Educational attainment and the proportion of Black race in New York City ZIP codes remained independent predictors of increased rates of ZIP code level OHSD during the COVID-19 outbreak even after controlling for 2019 rates.To facilitate health equity, future research should focus on characterizing the impacts of structural inequities while exploring strategies to mitigate their effects.
Abstract Background The impact of very low baseline levels of low-density lipoprotein cholesterol (LDL-C) on patients with coronary artery disease remains unclear. Therefore, we aimed to investigate the baseline characteristics and clinical outcomes of patients with low baseline LDL-C levels who had undergone coronary revascularization. Methods We enrolled 39439 patients of the pooled population from the CREDO-Kyoto registries Cohorts 1, 2, and 3. After excluding 6306 patients with missing baseline LDL-C data, the study population consisted of 33133 patients who had undergone their first coronary revascularization. We assessed the risk for mortality and cardiovascular events according to quintiles of the baseline LDL-C levels. Results Patients in the very low LDL-C quintile (< 85 mg/dL) had more comorbidities than those in the other quintiles. Lower LDL-C levels were strongly associated with anemia, thrombocytopenia, and end-stage renal disease. The cumulative 4-year incidence of all-cause death increased as LDL-C levels decreased (very low: 19.4%, low: 14.5%, intermediate: 11.1%, high: 10.0%, and very high:9.2%; P<0.001), which was driven by both the early and late events. After adjusting for baseline characteristics, the adjusted risks of the very low and low LDL-C quintiles relative to the intermediate LDL-C quintile remained significant for all-cause death (very low: HR 1.29, 95% CI 1.16-1.44, P<0.001; low: HR 1.15, 95% CI 1.03-1.29, P=0.01). There were no significant interactions between the association of LDL-C level with all-cause death and subgroup factors, such as lipid-lowering treatment at index hospitalization, age, sex, acute myocardial infarction presentation, and study cohort. The excess adjusted risks of the lowest LDL-C quintile relative to the intermediate LDL-C quintile were significant for clinical outcomes such as cardiovascular death (HR 1.17, 95% CI 1.01-1.35), non-cardiovascular death (HR 1.35, 95% CI 1.15-1.60), sudden death (HR 1.44, 95% CI 1.01-2.06), and heart failure admission (HR 1.11 95% CI 1.01-1.22), while there was no excess risk for the lowest LDL-C quintile relative to the intermediate LDL-C quintile for myocardial infarction and stroke. Conclusions Lower baseline LDL-C levels were associated with more comorbidities and a significantly higher risk of death, regardless of cardiovascular or non-cardiovascular causes, in patients who underwent coronary revascularization.
Background: Safety and efficacy of clopidogrel monotherapy after very short dual antiplatelet therapy (DAPT) is uncertain in patients undergoing complex percutaneous coronary intervention (PCI). Methods: We conducted a post hoc subgroup analysis based on the complexity of PCI in the STOPDAPT-2 trial (Short and Optimal Duration of Dual Antiplatelet Therapy-2), which randomly compared 1-month DAPT followed by clopidogrel monotherapy with 12-month DAPT after cobalt-chromium everolimus-eluting stent implantation. Complex PCI was defined as any of the following: 3 vessels treated, ≥3 stents implanted, ≥3 lesions treated, bifurcation with 2 stents, >60 mm total stent lengths, and target of chronic total occlusion. The primary end point was the composite of cardiovascular (cardiovascular death/myocardial infarction/definite stent thrombosis/stroke) and bleeding (TIMI [Thrombolysis in Myocardial Infarction] major/minor) end points. The major secondary end points were the cardiovascular and bleeding end points. Results: Among the 3009 study patients, there were 509 patients (16.9%) with complex PCI (1-month DAPT: N=245, and 12-month DAPT: N=264) and 2500 patients (83.1%) without complex PCI (1-month DAPT: N=1255, and 12-month DAPT: N=1245). There were no significant interactions between the complexity of PCI and the effects of 1-month DAPT versus 12-month DAPT on the primary end point (complex PCI: 1.67% versus 5.32%, hazard ratio, 0.30 [95% CI, 0.10–0.92], P =0.04, and noncomplex PCI: 2.50% versus 3.35%, hazard ratio, 0.75 [95% CI, 0.47–1.20], P =0.23; P interaction =0.14), and on the major secondary cardiovascular end point (complex PCI: 1.67% versus 3.04%, hazard ratio, 0.54 [95% CI, 0.16–1.79], P =0.31, and noncomplex PCI: 2.02% versus 2.39%, hazard ratio, 0.86 [95% CI, 0.50–1.47], P =0.58; P interaction =0.49). The cumulative 1-year incidence of the major secondary bleeding end point was significantly lower in the 1-month DAPT group than in the 12-month DAPT group regardless of the complexity of PCI (complex PCI: 0% versus 2.29%, log-rank P =0.02, and noncomplex PCI: 0.48% versus 1.38%, log-rank P =0.02). Conclusions: The effects of clopidogrel monotherapy after 1-month DAPT relative to 12-month DAPT for the primary and major secondary end points were comparable in complex PCI and noncomplex PCI without significant interactions. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT02619760.
High bleeding risk (HBR) and acute coronary syndrome (ACS) subtypes are critical in determining bleeding and cardiovascular event risk after percutaneous coronary intervention (PCI).
