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Benjamin D Horne

Publications and source records attributed to Benjamin D Horne.

At least 37 records · Page 2Linked to original sources
PubMed2005

Which white blood cell subtypes predict increased cardiovascular risk?

OBJECTIVES: We sought to determine the predictive ability of total white blood cell (WBC) count and its subtypes for risk of death or myocardial infarction (MI). BACKGROUND: An elevated WBC count has been associated with cardiovascular risk, but which leukocyte subtypes carry this risk is uncertain. METHODS: Consecutive patients without acute MI who were assessed angiographically for coronary artery disease (CAD) and were followed up long-term were studied. The predictive ability for death/MI of quartile (Q) 4 versus Q1 total WBC, neutrophil (N), lymphocyte (L), and monocyte (M) counts and N/L ratio were assessed using Cox regressions. RESULTS: A total of 3,227 patients was studied. Mean age was 63 years; 63% of patients were male, and 65% had CAD. In multivariable modeling entering standard risk factors, presentation, and CAD severity, the total WBC (hazard ratio [HR] 1.4, p = 0.01) and M (HR 1.3, p < 0.02) were weaker and N (HR 1.8, p < 0.001), L (HR 0.51, p < 0.001), and N/L ratio (HR 2.2, p < 0.001) were independent predictors of death/MI. When WBC variables were entered together, N/L ratio and M were retained as independent predictors. Risk associations persisted in analyses restricted to CAD patients or including acute MI patients. CONCLUSIONS: Total WBC count is confirmed to be an independent predictor of death/MI in patients with or at high risk for CAD, but greater predictive ability is provided by high N (Q4 >6.6 x 10(3)/microl) or low L counts. The greatest risk prediction is given by the N/L ratio, with Q4 versus Q1 (>4.71 versus <1.96) increasing the hazard 2.2-fold. These findings have important implications for CAD risk assessment.

Aged↗
PubMed2005

Effect of beta-blocker therapy on mortality rates and future myocardial infarction rates in patients with coronary artery disease but no history of myocardial infarction or congestive heart failure.

Beta-blocker therapy has been shown to benefit patients who have coronary artery disease and present with acute myocardial infarction (AMI) and/or congestive heart failure (HF). However, whether beta-blocker therapy provides a similar benefit in patients who have coronary artery disease but not AMI or HF is unknown. A population of 4,304 patients who did not have HF but did have angiographically confirmed coronary artery disease (>/=1 stenosis of >/=70%) without AMI at hospital presentation was evaluated. Baseline demographics, cardiac risk factors, clinical presentation, therapeutic procedures, and discharge medications were recorded. Patients were followed for a mean of 3.0 +/- 1.9 years (range 1 month to 6.9 years) for outcomes of all-cause death or AMI. Patients' average age was 65 +/- 11 years and 77% were men. Overall, 10% died and 5% had a nonfatal AMI. Discharge beta-blocker prescription was associated with an increased event-free AMI survival rate for all-cause death (no beta blocker 88.3%, beta blocker 94.5%, p <0.001) and death/AMI (no beta blocker 83.4%, beta blocker 89.2%, p <0.001) but not non-fatal AMI (no beta blocker 93.6%, beta blocker 94.1%, p = 0.60). After adjustment for 16 covariates, including statin prescription, angiotensin-converting enzyme inhibitor prescription, and type of baseline therapy, the effect of beta blockers on the combination end point of death/AMI was eliminated. However, the effect of beta blockers on death remained (hazard ratio 0.66, 95% confidence interval 0.47 to 0.93, p = 0.02). Thus, beta blockers are clearly indicated for most patients who have HF or AMI, and our results suggest that patients who have coronary artery disease without these conditions have approximately the same protective benefit against death. No effect was observed on longitudinal incidence of AMI or the combination of death/nonfatal MI.

Adrenergic beta-Antagonists↗
PubMed2005

Serum uric acid independently predicts mortality in patients with significant, angiographically defined coronary disease.

BACKGROUND: Uric acid is a nontraditional risk factor implicated in the development of coronary artery disease (CAD). This study prospectively evaluated the predictive value of serum uric acid (SUA) levels for mortality after angiographic diagnosis of CAD. METHODS: Blood samples were collected from 1,595 consecutive, consenting patients with significant, angiographically defined CAD (stenosis 70%). Baseline and procedural variables were recorded and levels of SUA were measured. Patients were followed to death or to the time of contact (mean 2.6 years, range 1.8-5.0 years). RESULTS: Patients averaged 65 +/- 11 years of age, 78% were male and 170 subjects died during the follow-up period. In univariate analysis of prospectively defined quintiles, SUA predicted all-cause mortality (fifth quintile vs. first four quintiles: hazard ratio 1.9, p < 0.001). In multivariable Cox regression controlling for 20 covariables, independent predictive value for mortality was retained by SUA (hazard ratio 1.5, confidence interval 1.02-2.1, p = 0.04). In subgroup analysis based on diuretic use status, SUA independently predicted mortality among patients not using diuretics, while SUA was not a significant predictor of mortality among those who used diuretics. CONCLUSIONS: In patients with significant, angiographically defined CAD, SUA predicted mortality independent of traditional risk factors. This suggests that elevated SUA may be a risk factor for mortality in patients with significant cardiovascular disease and may be a stronger secondary than primary risk factor in CAD.

Aged↗
PubMed2005

Comparison of differing C-reactive protein assay methods and their impact on cardiovascular risk assessment.

A medium-sensitivity assay for C-reactive protein (CRP) was compared with a high-sensitivity, enhanced immunoturbidimetric assay in 803 angiographically studied patients. Different absolute CRP values were found by the assays, but there was a high correlation by quartile rank and similar predictive values for death and myocardial infarction. This suggests that the conclusions of previous studies performed using the medium-sensitivity assay are still valid but that cross-study comparisons should use percentile rank.

Blood Chemical Analysis↗
PubMed2005

Characterization of linkage disequilibrium structure, mutation history, and tagging SNPs, and their use in association analyses: ELAC2 and familial early-onset prostate cancer.

In association analyses, it is critical that informative single-nucleotide polymorphisms (SNPs) be selected for study and utilized appropriately. We sequenced 38 kb, including exons of ELAC2, promoter region and conserved upstream intergenic sequences. A comprehensive characterization of linkage disequilibrium (LD) structure and mutation history was performed using our principal components analysis (PCA) method and a phylogenetic analysis. We identified a complex pattern of LD structure consistent with the occurrence of both recombination and mutation events within ELAC2. Four overlapping and noncontiguous LD groups were defined. Eight tagging SNPs (tSNPs) were identified, accounting for over 90% of the genetic variation of the 19 total variants. We tested associations between familial early-onset prostate cancer (PRCA) and each variant independently and in haplotypes. We performed these tests using all 19 variants and the 8 tSNPs; the results using tSNP haplotypes accurately represent the association evidence for the full haplotypes. We observed increased evidence for association when SNPs were analyzed in haplotypes. The phylogenetic analysis indicated three haplotypes, clustered farthest from the root-node, all of which were found more often in cases than controls. These three haplotypes together showed the best evidence of association with familial, early-onset PRCA (P=0.0024; odds ratio=2.23; 95% CI, 1.33-3.74), indicating possible allelic heterogeneity. Our results suggest that 8 tSNPs are required to comprehensively assess associations in ELAC2, and that haplotypes should be considered for analysis, and that a knowledge of mutation history may be helpful in parsing allelic heterogeneity and suggesting combinations of haplotypes to be tested.

Aged↗
PubMed2005

Candidate gene susceptibility variants predict intermediate end points but not angiographic coronary artery disease.

BACKGROUND: Moderate-sized studies have suggested that variants of candidate genes can influence laboratory markers of coronary artery disease (CAD), but whether they predict parallel changes in clinical CAD risk is unknown. METHODS: We studied a single nucleotide polymorphism (SNP) from each of the 5 candidate genes for intermediate (laboratory) and clinical (angiographic CAD) end points in a large cohort of patients. The 5 gene SNPs were cholesteryl ester transfer protein (CETP) TaqIB (N = 3219), ATP-binding cassette (ABCA1) G596A (N = 3302), lipoprotein lipase (LPL) HindIII (N = 909), plasminogen activator inhibitor, type 1 (PAI1), 4G/5G (N = 1142), and hepatic lipase (HL) C-541T (N = 4704). Intermediate outcomes were high-density lipoprotein cholesterol (HDL-C) and triglycerides (TGs). Cases had 1- to 3-vessel CAD (> or = 70% stenosis); controls had angiographically normal coronaries. RESULTS: Cholesteryl ester transfer protein predicted HDL (mean, B1B1 35.0 mg/dL, B2B2 38.6 mg/dL; P < .001) but not CAD (B1B1 74%, B2B2 70%; adjusted P = .35, odds ratio [OR] = 0.89). ABCA1 predicted HDL (mean, GG = 36.4 mg/dL, AA = 39.2 mg/dL; P = .02) but not CAD (GG 74%, AA 75%; adjusted P = .96, OR = 0.99). HL predicted HDL (CC 37.1 mg/dL, TT 40.9 mg/dL; P = .002) but not CAD (CC 71%, TT 68%, adjusted P = .66, OR = 0.94). LPL predicted TG (median: [++] 134, [--] 98 mg/dL; P < .001) but not CAD ([++] 79%, [--] 79%; adjusted P = .99, OR = 1.00). PAI1 predicted TG (median, 4G4G 130 mg/dL, 5G5G 148 mg/dL; P = .16), but not CAD (4G4G 77%, 5G5G 76%; adjusted P = .62, OR = 1.11). CONCLUSIONS: Five SNPs predicted differences in risk-related lipids but not angiographic CAD. These discrepancies suggest that genetic determinants of CAD are complex and intermediate phenotypes are poor surrogates. These findings have important implications for future directions in genetic research.

ATP Binding Cassette Transporter 1↗
PubMed2005

Improved long-term survival associated with stent deployment during percutaneous coronary interventions: results from a registry of 3399 patients.

INTRODUCTION: The use of stents in percutaneous coronary intervention (PCI) improves procedural success and reduces restenosis. However, few studies have had a sufficient sample size or adequate follow-up to determine whether this advantage results in a positive effect on mortality. METHODS: A total of 3399 patients undergoing PCI (stented [with dual antiplatelet therapy]: n = 2456, nonstented [balloon PCI or rotational atherectomy]: n = 942) at a single institution from 1994 to 2001 were followed up prospectively (43 +/- 22 and 54 +/- 25 months, respectively) for acute and long-term clinical outcomes. RESULTS: Angiographic success (< 50% residual stenosis) (99.7% vs 97.7%, P < .001) and acute gain (3.02 +/- 0.55 vs 2.08 +/- 0.62 mm, P < .001) were both greater for stented lesions. Likewise, procedural complications of death (0.04% vs 0.4%, P = .02) and dissection (4.9% vs 8.0%, P = .001) were lower in the stent group, as were rates of 6-month clinical restenosis (10.3% vs 16.3%, P < .001). Eight-year mortality (12.0% vs 18.2%, hazard ratio = 0.78, P = .009) was lower among the stent group, as was long-term major adverse cardiac events (36.2% vs 50.6%, P < .001), but no difference in long-term myocardial infarction was found (6.5% vs 7.6%, P = .28). In multivariable Cox regression, stent use (hazard ratio = 0.76, 95% CI [0.58-0.99], P = .04) remained associated with significantly reduced mortality. CONCLUSION: This large prospective study demonstrates that, in addition to a general improvement in procedural success and a reduced need for repeat revascularization, the use of stents with dual antiplatelet therapy was associated with a significant reduction in long-term mortality. Consideration should be given for the use of stents whenever feasible during PCI.

Angioplasty, Balloon, Coronary↗
PubMed2005

Early postoperative use of unfractionated heparin or enoxaparin is associated with increased surgical re-exploration for bleeding.

BACKGROUND: A variety of indications (eg, prosthetic heart valves, atrial fibrillation, etc.) exist for the use of unfractionated heparin (UFH) and enoxaparin (ENOX) in the early postoperative period following open-heart surgery. However, the overall postoperative risk for hemorrhage from the use of UFH and ENOX are not known. METHODS: From 1998 to 2001, 2,977 consecutive open-heart or valve surgery patients were retrospectively evaluated. Postoperatively, 2,037 received no UFH or ENOX, 579 received intravenous UFH, and 361 received ENOX. Baseline characteristics were collected, patients who required surgical re-exploration for postoperative bleeding and time between surgery and re-exploration were followed-up. RESULTS: Average patient ages were 64 +/- 13, 65 +/- 12, and 68 +/- 10 years receiving none, UFH (p < 0.01 vs none), and ENOX (p < 0.01 vs none; p < 0.01 vs UFH), respectively. Rates of surgical re-exploration were 2.7% for none, 7.8% for UFH, and 8.9% for ENOX (vs none, adjusted hazard ratio = 2.8; p < 0.001 for UFH; hazard ratio = 3.3; p < 0.001 for ENOX). Males were also at higher risk for re-exploration (hazard ratio = 1.4; p = 0.07). For those requiring re-exploration, the interval between surgery and first re-exploration was prolonged (> 4 days) among those receiving ENOX (37.5%, odds ratio = 36.7; p = 0.001) and UFH (20.0%, odds ratio = 14.7; p = 0.01) compared with none (1.8%). Prolonged times with ENOX had a greater proportion of prolonged times than UFH (odds ratio = 2.5; p = 0.09). CONCLUSIONS: Early postoperative use of ENOX and UFH is associated with a significant increase in re-exploration for postoperative bleeding, often at a significantly delayed time period after the initial surgery. This delay was especially common with ENOX suggesting the need for prospective studies.

Aged↗
PubMed2005

The role of a common adenosine monophosphate deaminase (AMPD)-1 polymorphism in outcomes of ischemic and nonischemic heart failure.

BACKGROUND: A common variant of the adenosine monophosphate deaminase (AMPD)-1 gene (C34T) results in enzymatic inactivity and may increase adenosine in cardiac muscle and confer cardioprotection through ischemic preconditioning. METHODS AND RESULTS: We hypothesized that AMPD1 carriers with ischemic heart failure (HF) in the Beta-Blocker Evaluation of Survival Trial (BEST) might have a relative survival advantage. Patients (n = 1038, 20% black) with ischemic (58%) and nonischemic (42%) HF were followed for an average of 2.0 years for cardiovascular mortality. DNA was purified from blood using phenol/chloroform. Genotyping was performed by polymerase chain reaction with 5' exonuclease chemistry. Differences in survival were assessed by comparing Kaplan-Meier curves with the log-rank test. Genotype frequencies differed by ethnicity (P < .001) but not by disease etiology. AMPD1 genotype did not significantly modify survival in the entire study population (hazard ratio [HR] = 0.91, 95% CI = 0.61-1.37), among ischemics (HR = 0.73, CI = 0.44-1.22, P = .23), or ischemic non-blacks (HR = 0.74, CI = 0.44-1.24, P = .25). Genotype did not modify the effect of bucindolol on mortality. CONCLUSIONS: Results of this study failed to confirm a reported survival benefit among HF patients carrying the AMPD1 T-allele. However, further studies in larger, more homogeneous populations should explore the possibility of a modest survival advantage for patients with ischemic HF.

AMP Deaminase↗
PubMed2005

Atrial dimensions in health and left ventricular disease using cardiovascular magnetic resonance.

BACKGROUND: Cardiovascular magnetic resonance (CMR) has superior spatial resolution compared with echocardiography, but assessment of normal measurements has lagged behind its increasing clinical application. We assessed atrial size by CMR in healthy and diseased subjects to determine normal adult ranges. METHODS: Twenty normal adults and 20 cardiac patients with hypertrophic or dilated cardiomyopathy were studied. Four and two chamber left and four chamber right atrial areas and left and right atrial depths were measured and compared, and a normal range for these measures was proposed. RESULTS: Normal four-chamber left and right atrial systolic areas each averaged 21 cm2. Average depths were 53 and 52 cm, respectively. For both the left and right atrium, a systolic area of < 24 cm2 included the upper 95th percentile of the normal range and (especially for the left atrium) best separated normal from abnormal hearts. For atrial depth, a systolic value of < 58 cm best distinguished normal from abnormal and also included the upper 95th percentile of the normal range. CONCLUSIONS: Normal ranges for 1- and 2-dimensional left and right atrial size by CMR are proposed. These values are in general greater than those reported for echocardiography.

Adolescent↗
PubMed2004

Frequency of elevation of C-reactive protein in atrial fibrillation.

Inflammation has been implicated in the pathogenesis of cardiovascular diseases. C-reactive protein (CRP), a marker of systemic inflammation, predicts the risk of coronary events and stroke. Atrial fibrillation (AF) is associated with atrial structural changes that may have an inflammatory basis. We tested the hypothesis that CRP is a risk factor for AF. Subjects were those included in the database registry of the Intermountain Heart Collaborative Study from 1994 to 2001. Patients who had >or=1 electrocardiogram that demonstrated AF formed the disease group (n = 347), and those who had neither electrocardiographic nor clinical evidence for AF comprised the control group (n = 2,449). Logistic regression assessed the quartile (Q) of CRP and 13 other clinical and angiographic predictors of AF. Average age was 63 +/- 12 years, 33% were women, and 61% had advanced coronary artery disease. Patients who had AF were older (by 7 years) and more frequently had a history of heart failure than did controls (41% vs 9%). CRP was higher in patients who had AF than in controls (p <0.001). Q-CRP was a univariable predictor of AF (odds ratio 1.39/Q, 95% confidence interval 1.25 to 1.55, p <0.001). Adjusting for age and heart failure decreased the predictive value of Q-CRP to 1.20/Q (95% confidence 1.07 to 1.34, p = 0.002), whereas further adjustment for 11 other variables had little additional effect (odds ratio 1.19/Q, 95% confidence interval 1.06 to 1.33, p = 0.003). Thus, high levels of CRP independently predicted an increased risk of AF among a large, prospectively studied patient cohort that was assessed angiographically. Increased CRP is a new risk marker for AF propensity, and testing therapies that target inflammation should be considered.

Aged↗
PubMed2004

Early effects of statins in patients with coronary artery disease and high C-reactive protein.

Statins improve survival in patients with coronary artery disease, especially those with elevated C-reactive protein (CRP). Although some randomized studies have shown a delay in statin-related survival advantage of up to 2 years, recent studies demonstrated early (<2 months) survival benefit in certain patient groups. We hypothesized that this early benefit relates to baseline CRP concentration. Patients (n = 2,924) with significant, angiographically defined coronary artery disease (>/=70% stenosis in >/=1 coronary artery) were followed for an average of 2.4 years after discharged on a statin prescription. CRP was divided into tertiles (<1.2, 1.2 to 1.7, >1.7 mg/dl), and Kaplan-Meier methods were used to determine timing of statin benefit in both the overall population and a propensity score-matched subgroup. Cox regressions (multivariable and propensity score approaches) were used to predict mortality. Statins were prescribed for 28.4% of patients. In the first CRP tertile, no early statin benefit was observed (adjusted hazard ratio 0.69, 95% confidence interval [CI] 0.30 to 1.6, p = 0.39), and survival curves separated after >2 years. However, in the second and the third tertiles, statin survival curves separated much earlier ( approximately 3 months and 1 week, respectively) and statins predicted improved survival (second tertile: hazard ratio 0.63, 95% CI 0.32 to 1.2, p = 0.17; third tertile: hazard ratio 0.35, 95% CI 0.18 to 0.67, p = 0.002). Propensity score analysis confirmed both statin benefit and early timing. Thus, statin use in patients with high CRP provides not only a larger but also a significantly earlier absolute survival benefit than statin use in patients with lower CRP. This provides further evidence of an anti-inflammatory effect of statins.

Aged↗
PubMed2004

Sex- and age-related differences in the prognostic value of C-reactive protein in patients with angiographic coronary artery disease.

PURPOSE: To determine whether sex and age affect serum C-reactive protein level and its prognostic value in patients with coronary artery disease. METHODS: In a consecutive series of 2254 patients with angiographically defined coronary artery disease, baseline C-reactive protein and predictive value for incident death or nonfatal myocardial infarction by sex and age (<55 and > or =55 years) were compared. C-reactive protein levels were measured by fluorescence polarization immunoassay with use of a medium-sensitivity method. Patients were followed for a mean (+/-SD) of 3.1 +/- 2.2 years. Comparisons used ln-transformed C-reactive protein and linear and time-to-event regression analyses, adjusting for confounders. RESULTS: Overall, women had higher geometric mean C-reactive protein levels than did men (1.47 vs. 1.30 mg/dL, P <0.001), even after adjustment for age, hyperlipidemia, diabetes, prior myocardial infarction, body mass index, and heart failure (P = 0.002). High C-reactive protein levels were associated with increased mortality or myocardial infarction among men (adjusted hazard ratio [HR] = 1.9; 95% confidence interval [CI]: 1.5 to 2.3) but not among women (HR = 1.0; 95% CI: 0.69 to 1.4). Among patients aged <55 years, C-reactive protein level was similarly predictive in men and women (HR = 2.2 vs. 2.7), whereas in patients > or =55 years of age, it remained predictive for men (HR = 1.8; 95% CI: 1.5 to 2.3) but not women (HR = 0.93; 95% CI: 0.63 to 1.4). CONCLUSION: We found that the prognostic value of C-reactive protein in coronary artery disease patients varied by sex and age. This sex-age interaction may have important implications for C-reactive protein-based secondary risk assessment and requires further investigation.

Age Factors↗
PubMed2004

Evidence for a heritable component in death resulting from aortic and mitral valve diseases.

BACKGROUND: Cardiac valvular diseases contribute to >42,000 deaths yearly in the United States, but the role of genetics in these deaths is unknown. This study evaluated the familiality of death resulting from aortic, mitral, and all valvular diseases using a population-based genealogy linked to death records. METHODS AND RESULTS: The Utah Population Database contains >2 million individual records with genealogy data and 250,000 linked death certificates. Nonrheumatic aortic (n=932), mitral (n=1165), and all valvular (n=2504) disease deaths and rheumatic heart disease deaths (n=4713) were studied. Familial relative risks (FRRs) were assessed for first- and second-degree relatives. Familiality was also evaluated with the genealogical index of familiality, which considers all relationships in the Utah Population Database. FRRs were increased only for mitral valve death in both first-degree (FRR, 2.55; P<0.0001) and second-degree (FRR, 1.67; P<0.0001) relatives. Genealogical index of familiality analysis showed significant excess relatedness for all groups (P<0.001). Genealogical index of familiality results (P<0.001) for early age at death cases showed higher mean relatedness, a common characteristic of heritable disorders. Excess familiality extended to distant relatives for mitral (second-degree relatives) and aortic (beyond second-degree relatives) valve death. CONCLUSIONS: Deaths resulting from nonrheumatic mitral and aortic diseases clustered among both close and distant relatives, especially among early age at death cases, suggesting a significant genetic component in death resulting from valvular diseases. Future studies should focus on gene discovery.

Adult↗
PubMed2004

Improvements in 1-year cardiovascular clinical outcomes associated with a hospital-based discharge medication program.

BACKGROUND: Despite recent advances in the treatment and prevention of cardiovascular disease, a treatment gap for secondary prevention medications still exists. OBJECTIVE: To develop and implement a program ensuring appropriate prescription of aspirin, statins, beta-blockers, angiotensin-converting enzyme inhibitors, and warfarin at hospital discharge. DESIGN: A nonrandomized before-after study comparing patients hospitalized before (1996-1998) and after (1999-2002) implementation of a discharge medication program (DMP). Patients were followed for up to 1 year. SETTING: The 10 largest hospitals in the Utah-based Intermountain Health Care system. PATIENTS: In the pre-DMP and DMP time periods, 26,000 and 31,465 patients, respectively, were admitted to cardiovascular services (n = 57,465). MEASUREMENTS: Prescription of indicated medications at hospital discharge; postdischarge death or readmission. RESULTS: By 1 year, the rate of prescription of each medication increased significantly to more than 90% (P < 0.001); this rate was sustained. At 1 year, unadjusted absolute event rates for readmission and death, respectively, were 210 per 1000 person-years and 96 per 1000 person-years before DMP implementation and 191 per 1000 person-years and 70 per 1000 person-years afterward. Relative risk for death and readmission at 30 days decreased after DMP implementation; hazard ratios (HRs) for death and readmission were 0.81 (95% CI, 0.73 to 0.89) and 0.92 (CI, 0.87 to 0.99) (P < 0.001 and P = 0.017, respectively). At 1 year, risk for death continued to decrease (hazard ratio, 0.79 [CI, 0.75 to 0.84]; P < 0.001) while risk for readmission stabilized (hazard ratio, 0.94 [CI, 0.90 to 0.98]; P = 0.002), probably because survivors had more opportunities to be readmitted. LIMITATIONS: The study design was observational and nonrandomized, and the authors could not control for potential confounders or determine the extent to which secular trends accounted for the observed improvements. CONCLUSIONS: A relatively simple quality improvement program aimed at enhancing the prescription of appropriate discharge medications among cardiovascular patients is feasible and can be sustained within an integrated multihospital system. Such a program may be associated with improvements in cardiovascular readmission rates and mortality.

Cardiovascular Diseases↗
PubMed2004

Which features of the metabolic syndrome predict the prevalence and clinical outcomes of angiographic coronary artery disease?

BACKGROUND: The prevalence of the metabolic syndrome (MS) is growing. The Adult Treatment Panel (ATP) III provided a uniform definition of MS but no information on its predictive ability. METHODS: We tested the ability of MS and its components to predict angiographic coronary artery disease (CAD) and incident death/myocardial infarction (D/MI) over 2.8 +/- 2.3 years in a large cohort of patients undergoing angiography. ATP-III criteria were used for fasting glucose (FG), triglyceride (TG), high-density lipoprotein cholesterol (HDL), and blood pressure (BP); body mass index (BMI) >27 kg/m(2) was used as a surrogate for waist circumference. RESULTS: 3,128 subjects were studied; 65% had advanced CAD (>/=70% stenosis), and 35%, no CAD. MS was present in 64% (high FG 40%; high TG 52%; low HDL 71%; high BP 76%; high BMI 58%). Presence of CAD was predicted by MS [adjusted odds ratio (OR) = 1.30, 95% CI 1.10-1.55, p = 0.003] and, individually, by high FG (OR = 1.90, CI 1.63-2.23) and low HDL (OR = 1.38, CI 1.18-1.62). In multivariable modeling, CAD was predicted by high FG (OR = 1.80, CI 1.51-2.16) and low HDL (OR = 1.57, CI 1.31-1.89) as well as by age, gender, family history, smoking, and LDL cholesterol (all p < 0.001). For secondary risk of incident D/MI, only high FG of MS features was predictive (adjusted hazard ratio 1.46, CI 1.17-1.82, p = 0.001), and this risk was carried by diabetes (adjusted hazard ratio 1.71, p < 0.001); other predictors were age, heart failure, revascularization strategy, renal insufficiency, prior MI, and number of diseased vessels. CONCLUSION: MS has primary predictive ability for CAD, carried primarily by high FG and low HDL. Secondary predictive ability of MS features for clinical outcomes, in the setting of established CAD, is carried by diabetes alone. Dysglycemia deserves specific attention as a target for prevention and treatment.

Aged↗
PubMed2004

Effect of folic acid fortification of food on homocysteine-related mortality.

PURPOSE: In 1998, the Food and Drug Administration mandated the fortification of food products with folic acid. The effect of this rule on mortality associated with homocysteine levels in patients with coronary artery disease is unknown. METHODS: We studied 2481 consecutive patients with coronary artery disease who underwent coronary angiography between 1994 and 1999, and who had baseline homocysteine measurements and at least 2 years of follow-up. Patients were divided into prefortification (1994 to 1997, n = 1595) and postfortification (1998 to 1999, n = 886) groups, as well as classified based on baseline homocysteine levels (normal to low, intermediate, and high). Homocysteine levels were measured by fluorescence polarization immunoassay. Mortality was determined by telephone survey or from a national Social Security database or hospital records. RESULTS: After implementation of the fortification rule, median homocysteine levels declined from 13.8 to 12.3 micromol/L (P <0.001), and the proportion of patients with high homocysteine levels (>15 micromol/L) decreased from 41% (n = 650) to 28% (n = 249) (P <0.001). Overall, homocysteine was a modest risk factor for mortality (adjusted relative risk [RR] = 1.03 per micromol/L; 95% confidence interval [CI]: 1.01 to 1.05; P = 0.006). There was no significant interaction between fortification status and homocysteine category with mortality (P for interaction = 0.85). Two-year mortality was reduced minimally (7.8% [n = 124] to 7.2% [n = 64]; RR = 0.93; 95% CI: 0.68 to 1.27; P = 0.63; adjusted RR = 0.97; 95% CI: 0.68 to 1.40), but was consistent with the expectation of a modest reduction in homocysteine levels. CONCLUSION: Homocysteine is an independent, graded risk factor for mortality. Homocysteine levels decreased modestly after the fortification of food with folic acid, but the effects on mortality were minor and likely attributable to other factors, indicating the need for more aggressive measures to reduce homocysteine-associated cardiovascular risk.

Aged↗