Publications by authors named "Usman A Tahir"

15 Publications

  • Page 1 of 1

Metabolomic Analysis of Coronary Heart Disease in an African American Cohort From the Jackson Heart Study.

JAMA Cardiol 2021 Dec 1. Epub 2021 Dec 1.

Division of Cardiovascular Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.

Importance: African American individuals have disproportionate rates of coronary heart disease (CHD) but lower levels of coronary artery calcium (CAC), a marker of subclinical CHD, than non-Hispanic White individuals. African American individuals may have distinct metabolite profiles associated with incident CHD risk compared with non-Hispanic White individuals, and examination of these differences could highlight important processes that differ between them.

Objectives: To identify novel biomarkers of incident CHD and CAC among African American individuals and to replicate incident CHD findings in a multiethnic cohort.

Design, Setting, And Participants: This analysis targeted plasma metabolomic profiling of 2346 participants in the Jackson Heart Study (JHS), a prospective population-based cohort study that included 5306 African American participants who were examined at baseline (2000-2004) and 2 follow-up visits. Replication of CHD-associated metabolites was sought among 1588 multiethnic participants from the Women's Health Initiative (WHI), a prospective population-based multiethnic cohort study of 161 808 postmenopausal women who were examined at baseline (1991-1995) and ongoing follow-up visits. Regression analyses were performed for each metabolite to examine the associations with incident CHD and CAC scores. Data were collected from the WHI between 1994 and 2009 and from the JHS between 2000 and 2015. All data were analyzed from November 2020 to August 2021.

Exposures: Plasma metabolites.

Main Outcomes And Measures: Incident CHD was defined as definite or probable myocardial infarction or definite fatal CHD in both the JHS and WHI cohorts. In the JHS cohort, silent myocardial infarction between examinations (as determined by electrocardiography) and coronary revascularization were included in the incident CHD analysis. Coronary artery calcium was measured using a 16-channel computed tomographic system and reported as an Agatston score.

Results: Among 2346 African American individuals in the JHS cohort, the mean (SD) age was 56 (13) years, and 1468 individuals (62.6%) were female. Among 1588 postmenopausal women in the WHI cohort, the mean (SD) age was 67 (7) years; 217 individuals (13.7%) self-identified as African American, 1219 (76.8%) as non-Hispanic White, and 152 (9.6%) as other races or ethnicities. In the fully adjusted model including 1876 individuals, 46 of 303 targeted metabolites were associated with incident CHD (false discovery rate q <0.100). Data for 32 of the 46 metabolites were available in the WHI cohort, and 13 incident CHD-associated metabolites from the JHS cohort were replicated in the WHI cohort. A total of 1439 participants from the JHS cohort with available CAC scores received metabolomic profiling. Nine metabolites were associated with CAC scores. Minimal overlap was found between the results from the incident CHD and CAC analyses, with only 3 metabolites shared between the 2 analyses.

Conclusions And Relevance: This cohort study identified metabolites that were associated with incident CHD among African American individuals, including 13 incident CHD-associated metabolites that were replicated in a multiethnic population and 9 novel metabolites that included N-acylamides, leucine, and lipid species. These findings may help to elucidate common and distinct metabolic processes that may be associated with CHD among individuals with different self-identified race.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1001/jamacardio.2021.4925DOI Listing
December 2021

Whole Genome Sequence Analysis of the Plasma Proteome in Black Adults Provides Novel Insights into Cardiovascular Disease.

Circulation 2021 Nov 24. Epub 2021 Nov 24.

Department of Exercise Science, University of South Carolina, Columbia, SC.

Plasma proteins are critical mediators of cardiovascular processes and are the targets of many drugs. Previous efforts to characterize the genetic architecture of the plasma proteome have been limited by a focus on individuals of European descent and leveraged genotyping arrays and imputation. Here we describe whole genome sequence analysis of the plasma proteome in individuals with greater African ancestry, increasing our power to identify novel genetic determinants. Proteomic profiling of 1,301 proteins was performed in 1852 Black adults from the Jackson Heart Study using aptamer-based proteomics (SomaScan). Whole genome sequencing association analysis was ascertained for all variants with minor allele count ≥ 5. Results were validated using an alternative, antibody-based, proteomic platform (Olink) as well as replicated in the Multi-Ethnic Study of Atherosclerosis and the HERITAGE Family Study. We identify 569 genetic associations between 479 proteins and 438 unique genetic regions at a Bonferroni-adjusted significance level of 3.8 × 10. These associations include 114 novel locus-protein relationships and an additional 217 novel sentinel variant-protein relationships. Novel cardiovascular findings include new protein associations at the gene locus including ZAP70 (sentinel single nucleotide polymorphism [SNP] rs7412-T, β = 0.61±0.05, p-value = 3.27 × 10) and MMP-3 (β = -0.60±0.05, p = 1.67 × 10), as well as a completely novel pleiotropic locus at the gene, associated with nine proteins. Further, the associations suggest new mechanisms of genetically mediated cardiovascular disease linked to African ancestry; we identify a novel association between variants linked to APOL1 associated chronic kidney and heart disease and the protein CKAP2 (rs73885319-G, β = 0.34±0.04, p = 1.34 × 10) as well as an association between ATTR amyloidosis and RBP4 levels in community dwelling individuals without heart failure. Taken together, these results provide evidence for the functional importance of variants in non-European populations, and suggest new biological mechanisms for ancestry-specific determinants of lipids, coagulation and myocardial function.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1161/CIRCULATIONAHA.121.055117DOI Listing
November 2021

Human plasma proteomic profiles indicative of cardiorespiratory fitness.

Nat Metab 2021 06 27;3(6):786-797. Epub 2021 May 27.

Division of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA.

Maximal oxygen uptake (VOmax) is a direct measure of human cardiorespiratory fitness and is associated with health. However, the molecular determinants of interindividual differences in baseline (intrinsic) VOmax, and of increases of VOmax in response to exercise training (ΔVOmax), are largely unknown. Here, we measure ~5,000 plasma proteins using an affinity-based platform in over 650 sedentary adults before and after a 20-week endurance-exercise intervention and identify 147 proteins and 102 proteins whose plasma levels are associated with baseline VOmax and ΔVOmax, respectively. Addition of a protein biomarker score derived from these proteins to a score based on clinical traits improves the prediction of an individual's ΔVOmax. We validate findings in a separate exercise cohort, further link 21 proteins to incident all-cause mortality in a community-based cohort and reproduce the specificity of ~75% of our key findings using antibody-based assays. Taken together, our data shed light on biological pathways relevant to cardiorespiratory fitness and highlight the potential additive value of protein biomarkers in identifying exercise responsiveness in humans.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1038/s42255-021-00400-zDOI Listing
June 2021

Multiomic Profiling in Black and White Populations Reveals Novel Candidate Pathways in Left Ventricular Hypertrophy and Incident Heart Failure Specific to Black Adults.

Circ Genom Precis Med 2021 06 21;14(3):e003191. Epub 2021 May 21.

Division of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Boston, MA (D.H.K., U.A.T., D.N., M.D.B., X.S., M.J.K., D.S., M.H., J.M.R., Z.-Z.C., D.E.C., B.P., J.G.W., R.E.G.).

Background: Increased left ventricular (LV) mass is associated with adverse cardiovascular events including heart failure (HF). Both increased LV mass and HF disproportionately affect Black individuals. To understand the underlying mechanisms, we undertook a proteomic screen in a Black cohort and compared the findings to results from a White cohort.

Methods: We measured 1305 plasma proteins using the SomaScan platform in 1772 Black participants (mean age, 56 years; 62% women) in JHS (Jackson Heart Study) with LV mass assessed by 2-dimensional echocardiography. Incident HF was assessed in 1600 participants. We then compared protein associations in JHS to those observed in White participants from FHS (Framingham Heart Study; mean age, 54 years; 56% women).

Results: In JHS, there were 110 proteins associated with LV mass and 13 proteins associated with incident HF hospitalization with false discovery rate <5% after multivariable adjustment. Several proteins showed expected associations with both LV mass and HF, including NT-proBNP (N-terminal pro-B-type natriuretic peptide; β=0.04; =2×10; hazard ratio, 1.48; =0.0001). The strongest association with LV mass was novel: LKHA4 (leukotriene-A4 hydrolase; β=0.05; =5×10). This association was confirmed on an alternate proteomics platform and further supported by related metabolomic data. Fractalkine/CX3CL1 (C-X3-C Motif Chemokine Ligand 1) showed a novel association with incident HF (hazard ratio, 1.32; =0.0002). While established biomarkers such as cystatin C and NT-proBNP showed consistent associations in Black and White individuals, LKHA4 and fractalkine were significantly different between the two groups.

Conclusions: We identified several novel biological pathways specific to Black adults hypothesized to contribute to the pathophysiologic cascade of LV hypertrophy and incident HF including LKHA4 and fractalkine.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1161/CIRCGEN.120.003191DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8497179PMC
June 2021

Genetic Risk Assessment for Atherosclerotic Cardiovascular Disease: A Guide for the General Cardiologist.

Cardiol Rev 2021 Mar 19. Epub 2021 Mar 19.

Department of Medicine Division of Cardiovascular Medicine Cardiovascular Institute, Beth Israel Deaconess Medical Center, Boston, MA.

Genetic testing for cardiovascular (CV) disease has had a profound impact on the diagnosis and evaluation of monogenic causes of CV disease, such as hypertrophic and familial cardiomyopathies, long QT syndrome, and familial hypercholesterolemia (FH). The success in genetic testing for monogenic diseases has prompted special interest in utilizing genetic information in the risk assessment of more common diseases such as atherosclerotic cardiovascular disease (ASCVD). Polygenic risk scores (PRS) have been developed to assess the risk of coronary artery disease (CAD) that now include millions of single-nucleotide polymorphisms (SNPs) that have been identified through genome-wide association studies (GWAS). While these PRS have demonstrated a strong association with CAD in large cross-sectional population studies, there remains intense debate regarding the added value that PRS contribute to existing clinical risk prediction models such as the pooled cohort equations (PCEs). In this review, we provide a brief background of genetic testing for monogenic drivers of CV disease and then focus on the recent developments in genetic risk assessment of ASCVD, including the use of PRS. We outline the genetic testing that is currently available to all cardiologists in the clinic and discuss the evolving sphere of specialized cardiovascular genetics programs (CVGPs) that integrate the expertise of cardiologists, geneticists, and genetic counselors. Finally, we review the possible implications that PRS and pharmacogenomic data may soon have on clinical practice in the care for patients with or at risk of developing ASCVD.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1097/CRD.0000000000000384DOI Listing
March 2021

Metabolomic Markers of Southern Dietary Patterns in the Jackson Heart Study.

Mol Nutr Food Res 2021 04 11;65(8):e2000796. Epub 2021 Mar 11.

Division of Cardiology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.

Scope: New biomarkers are needed that are representative of dietary intake.

Methods And Results: We assess metabolites associated with Southern dietary patterns in 1401 Jackson Heart Study participants. Three dietary patterns are empirically derived using principal component analysis: meat and fast food, fish and vegetables, and starchy foods. We randomly select two subsets of the study population: two-third sample for discovery (n = 934) and one-third sample for replication (n = 467). Among the 327 metabolites analyzed, 14 are significantly associated with the meat and fast food dietary pattern, four are significantly associated with the fish and vegetables dietary pattern, and none are associated with the starchy foods dietary pattern in the discovery sample. In the replication sample, nine remain associated with the meat and fast food dietary pattern [indole-3-propanoic acid, C24:0 lysophosphatidylcholine (LPC), N-methyl proline, proline betaine, C34:2 phosphatidylethanolamine (PE) plasmalogen, C36:5 PE plasmalogen, C38:5 PE plasmalogen, cotinine, hydroxyproline] and three remain associated with the fish and vegetables dietary pattern [1,7-dimethyluric acid, C22:6 lysophosphatidylethanolamine, docosahexaenoic acid (DHA)].

Conclusion: Twelve metabolites are discovered and replicated in association with dietary patterns detected in a Southern U.S. African-American population, which could be useful as biomarkers of Southern dietary patterns.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/mnfr.202000796DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8192080PMC
April 2021

Proteomic profiling reveals biomarkers and pathways in type 2 diabetes risk.

JCI Insight 2021 03 8;6(5). Epub 2021 Mar 8.

Cardiovascular Institute.

Recent advances in proteomic technologies have made high-throughput profiling of low-abundance proteins in large epidemiological cohorts increasingly feasible. We investigated whether aptamer-based proteomic profiling could identify biomarkers associated with future development of type 2 diabetes (T2DM) beyond known risk factors. We identified dozens of markers with highly significant associations with future T2DM across 2 large longitudinal cohorts (n = 2839) followed for up to 16 years. We leveraged proteomic, metabolomic, genetic, and clinical data from humans to nominate 1 specific candidate to test for potential causal relationships in model systems. Our studies identified functional effects of aminoacylase 1 (ACY1), a top protein association with future T2DM risk, on amino acid metabolism and insulin homeostasis in vitro and in vivo. Furthermore, a loss-of-function variant associated with circulating levels of the biomarker WAP, Kazal, immunoglobulin, Kunitz, and NTR domain-containing protein 2 (WFIKKN2) was, in turn, associated with fasting glucose, hemoglobin A1c, and HOMA-IR measurements in humans. In addition to identifying potentially novel disease markers and pathways in T2DM, we provide publicly available data to be leveraged for insights about gene function and disease pathogenesis in the context of human metabolism.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1172/jci.insight.144392DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8021115PMC
March 2021

Metabolomic Profiles and Heart Failure Risk in Black Adults: Insights From the Jackson Heart Study.

Circ Heart Fail 2021 01 19;14(1):e007275. Epub 2021 Jan 19.

Division of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA (U.A.T., D.H.K., T.Z., D.N., D.E.C., J.M.R., Z.-Z.C., B.P., M.D.B., X.S., C.S., J.G.W., R.E.G.).

Background: Heart failure (HF) is a heterogeneous disease characterized by significant metabolic disturbances; however, the breadth of metabolic dysfunction before the onset of overt disease is not well understood. The purpose of this study was to determine the association of circulating metabolites with incident HF to uncover novel metabolic pathways to disease.

Methods: We performed targeted plasma metabolomic profiling in a deeply phenotyped group of Black adults from the JHS (Jackson Heart Study; n=2199). We related metabolites associated with incident HF to established etiological mechanisms, including increased left ventricular mass index and incident coronary heart disease. Furthermore, we evaluated differential associations of metabolites with HF with preserved ejection fraction versus HF with reduced ejection fraction.

Results: Metabolites associated with incident HF included products of posttranscriptional modifications of RNA, as well as polyamine and nitric oxide metabolism. A subset of metabolite-HF associations was independent of well-established HF pathways such as increased left ventricular mass index and incident coronary heart disease and included homoarginine (per 1 SD increase in metabolite level, hazard ratio, 0.77; =1.2×10), diacetylspermine (hazard ratio, 1.34; =3.4×10), and uridine (hazard ratio, 0.79; , 3×10). Furthermore, metabolites involved in pyrimidine metabolism (orotic acid) and collagen turnover (-methylproline) among others were part of a distinct metabolic signature that differentiated individuals with HF with preserved ejection fraction versus HF with reduced ejection fraction.

Conclusions: The integration of clinical phenotyping with plasma metabolomic profiling uncovered novel metabolic processes in nontraditional disease pathways underlying the heterogeneity of HF development in Black adults.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1161/CIRCHEARTFAILURE.120.007275DOI Listing
January 2021

MTORC1-Regulated Metabolism Controlled by TSC2 Limits Cardiac Reperfusion Injury.

Circ Res 2021 03 6;128(5):639-651. Epub 2021 Jan 6.

Division of Cardiology, Department of Medicine, The Johns Hopkins Medical Institutions, Baltimore, MD (C.U.O., S.J., S.M., B.L.D.-E., A.C., M.I.G., N.P., M.J.R., D.A.K.).

Rationale: The mTORC1 (mechanistic target of rapamycin complex-1) controls metabolism and protein homeostasis and is activated following ischemia reperfusion (IR) injury and by ischemic preconditioning (IPC). However, studies vary as to whether this activation is beneficial or detrimental, and its influence on metabolism after IR is little reported. A limitation of prior investigations is their use of broad gain/loss of mTORC1 function, mostly applied before ischemic stress. This can be circumvented by regulating one serine (S1365) on TSC2 (tuberous sclerosis complex) to achieve bidirectional mTORC1 modulation but only with TCS2-regulated costimulation.

Objective: We tested the hypothesis that reduced TSC2 S1365 phosphorylation protects the myocardium against IR and is required for IPC by amplifying mTORC1 activity to favor glycolytic metabolism.

Methods And Results: Mice with either S1365A (TSC2; phospho-null) or S1365E (TSC2; phosphomimetic) knockin mutations were studied ex vivo and in vivo. In response to IR, hearts from TSC2 mice had amplified mTORC1 activation and improved heart function compared with wild-type and TSC2 hearts. The magnitude of protection matched IPC. IPC requited less S1365 phosphorylation, as TSC2 hearts gained no benefit and failed to activate mTORC1 with IPC. IR metabolism was altered in TSC2, with increased mitochondrial oxygen consumption rate and glycolytic capacity (stressed/maximal extracellular acidification) after myocyte hypoxia-reperfusion. In whole heart, lactate increased and long-chain acylcarnitine levels declined during ischemia. The relative IR protection in TSC2 was lost by lowering glucose in the perfusate by 36%. Adding fatty acid (palmitate) compensated for reduced glucose in wild type and TSC2 but not TSC2 which had the worst post-IR function under these conditions.

Conclusions: TSC2-S1365 phosphorylation status regulates myocardial substrate utilization, and its decline activates mTORC1 biasing metabolism away from fatty acid oxidation to glycolysis to confer protection against IR. This pathway is also engaged and reduced TSC2 S1365 phosphorylation required for effective IPC. Graphic Abstract: A graphic abstract is available for this article.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1161/CIRCRESAHA.120.317710DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8257748PMC
March 2021

Proteomic Profiling in Biracial Cohorts Implicates DC-SIGN as a Mediator of Genetic Risk in COVID-19.

medRxiv 2020 Jun 11. Epub 2020 Jun 11.

COVID-19 is one of the most consequential pandemics in the last century, yet the biological mechanisms that confer disease risk are incompletely understood. Further, heterogeneity in disease outcomes is influenced by race, though the relative contributions of structural/social and genetic factors remain unclear. Very recent unpublished work has identified two genetic risk loci that confer greater risk for respiratory failure in COVID-19: the ABO locus and the 3p21.31 locus. To understand how these loci might confer risk and whether this differs by race, we utilized proteomic profiling and genetic information from three cohorts including black and white participants to identify proteins influenced by these loci. We observed that variants in the ABO locus are associated with levels of CD209/DC-SIGN, a known binding protein for SARS-CoV and other viruses, as well as multiple inflammatory and thrombotic proteins, while the 3p21.31 locus is associated with levels of CXCL16, a known inflammatory chemokine. Thus, integration of genetic information and proteomic profiling in biracial cohorts highlights putative mechanisms for genetic risk in COVID-19 disease.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1101/2020.06.09.20125690DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7302224PMC
June 2020

Omics and Cardiometabolic Disease Risk Prediction.

Annu Rev Med 2020 01;71:163-175

Division of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA; email:

Risk assessments are integral for the prevention and management of cardiometabolic disease (CMD). However, individuals may develop CMD without traditional risk factors, necessitating the development of novel biomarkers to aid risk prediction. The emergence of omic technologies, including genomics, proteomics, and metabolomics, has allowed for assessment of orthogonal measures of cardiometabolic risk, potentially improving the ability for novel biomarkers to refine disease risk assessments. While omics has shed light on novel mechanisms for the development of CMD, its adoption in clinical practice faces significant challenges. We review select omic technologies and cardiometabolic investigations for risk prediction, while highlighting challenges and opportunities for translating findings to clinical practice.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1146/annurev-med-042418-010924DOI Listing
January 2020

Massive pulmonary embolism: embolectomy or extracorporeal membrane oxygenation?

Curr Opin Crit Care 2019 12;25(6):630-637

Division of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.

Purpose Of Review: To highlight updates on the use of extracorporeal membrane oxygenation (ECMO) and surgical embolectomy in the treatment of massive pulmonary embolism.

Recent Findings: Outcomes for surgical embolectomy for massive pulmonary embolism have improved in the recent past. More contemporary therapeutic options include catheter embolectomy, which although offer less invasive means of treating this condition, need further study. The use of ECMO as either a bridge or mainstay of treatment in patients with contraindications to fibrinolysis and surgical embolectomy, or have failed initial fibrinolysis, has increased, with data suggesting improved outcomes with earlier implementation in selected patients.

Summary: Although surgical embolectomy continues to be the initial treatment of choice in massive pulmonary embolism with contraindications or failed fibrinolysis, the use of ECMO in these high-risk patients provides an important tool in managing this often fatal condition.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1097/MCC.0000000000000660DOI Listing
December 2019

Predictors of Mortality in Light Chain Cardiac Amyloidosis with Heart Failure.

Sci Rep 2019 06 12;9(1):8552. Epub 2019 Jun 12.

Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, USA.

Cardiac involvement in systemic amyloidosis (AL) occurs in ~50% of all AL patients. However once symptomatic heart failure develops, therapeutic options are limited thereby conferring a poor overall prognosis. The median survival is <6 months when AL patients are untreated for the underlying plasma cell dyscrasia. We thus sought to identify risk factors of increased mortality in treatment-naïve, AL cardiac amyloidosis with heart failure. Patients with biopsy-proven AL cardiac amyloid, who presented with heart failure and did not received prior AL treatment, were enrolled between 2004-2014, at the initial visit to the Amyloidosis Center at Boston University Medical Center. Routine laboratory tests, physical examination and echocardiography data were collected. There were 165 predominantly white (76.4%), and male (61%) patients, with a mean age of 61.6 ± 9.5 years. Median survival was 10.9 months (95% CI 6.2-14.7). By multivariate analysis increased relative wall thickness (RWT) [HR 6.70; 95% CI 2.45-18.30), older age (HR 1.04; 95% CI 1.01-1.06), higher New York Heart Association (NYHA) functional class (HR 1.50; 95% CI 1.02-2.2), log brain natriuretic peptide (BNP) levels (HR 1.45; 95% CI 1.15-1.81) and C-reactive protein (CRP) levels (HR 1.02; 95% CI 1.00-1.04) were significant predictors for increased mortality. In conclusion, in treatment-naïve, AL cardiac amyloidosis patients with heart failure symptoms who lack these high-risk features may have a better outcome. These findings might allow for better risk stratification although outcomes are still poor.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1038/s41598-019-44912-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6561903PMC
June 2019

Individualizing dual antiplatelet therapy duration after percutaneous coronary intervention: from randomized control trials to personalized medicine.

Expert Rev Cardiovasc Ther 2017 Sep 9;15(9):681-693. Epub 2017 Aug 9.

a Smith Center for Outcomes Research in Cardiology , Beth Israel Deaconess Medical Center , Boston , MA , USA.

Introduction: Improved stent technologies have lead to reduced minimum durations of dual antiplatelet therapy (DAPT) to prevent stent thrombosis. However, the anti-ischemic benefits seen in extended DAPT in both stent and non-stent related lesions have called into question the optimum duration of DAPT after stent placement. Areas covered: We review the evidence for varying durations of DAPT after drug eluting stent placement including for patients on oral anticoagulation; decision tools available for clinicians to optimize patient selection for extended therapy and insight into application of these risk assessment tools in clinical practice. Expert commentary: The use of risk assessment tools in optimizing DAPT duration after stent placement provides an opportunity for improved outcomes by means of a personalized approach to care while allowing clinicians to engage with patients in shared-decision making.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1080/14779072.2017.1362980DOI Listing
September 2017
-->