Biomedical subjects

Benjamin D Horne

Publications and source records attributed to Benjamin D Horne.

59 records · Page 4Linked to original sources

PubMed2002

C-reactive protein and angiographic coronary artery disease: independent and additive predictors of risk in subjects with angina.

OBJECTIVES: The objective of this study was to determine the prognostic value of C-reactive protein (CRP) independent of coronary angiographic findings. BACKGROUND: High sensitivity CRP, a marker of inflammation, predicts risk of cardiovascular events. However, it is uncertain whether it remains predictive once angiographic findings are considered. METHODS: A total of 2,554 patients with angina but without acute myocardial infarction (MI) were studied angiographically; 1,848 patients had coronary artery disease (CAD) and 706 patients did not. Coronary artery disease was quantified in five ways and combined for a CAD score. C-reactive protein was measured and patients were followed for up to five years for death or MI. RESULTS: C-reactive protein correlated with the extent of CAD, but correlation coefficients were low (0.02 to 0.08). Of angiographic measures, the CAD score best predicted future events (hazard ratio [HR] = 1.8 [1.2 to 2.6], p = 0.004, for CAD score > 4). C-reactive protein > or = 1.0 mg/dl was predictive in both patients without CAD (HR = 2.3 [0.9 to 5.5], p = 0.07) and with CAD (HR = 2.1 [1.5 to 3.1], p = 0.0001). Multivariate adjustment resulted in little change in HR. C-reactive protein retained predictive value within each quintile of CAD score. C-reactive protein and CAD independently and additively contributed to the risk prediction: low CRP and lowest CAD score was associated with lowest risk, and high CRP and highest CAD score was associated with the highest risk, with a 10-fold difference between extremes (2.5% vs. 24%). CONCLUSIONS: C-reactive protein correlates with extent of CAD, but the degree of correlation is low. Severity/extent of CAD and CRP are independent and additive predictors of risk. Therapy should target CRP-associated risk as well as angiographically evident stenosis.

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PubMed2002

Usefulness of high-sensitivity C-reactive protein in predicting long-term risk of death or acute myocardial infarction in patients with unstable or stable angina pectoris or acute myocardial infarction.

High-sensitivity C-reactive protein (CRP), proposed as a new coronary risk marker, may reflect either an acute phase reaction or the level of chronic inflammation. Thus, CRP may be less predictive of long-term outcomes when measured after acute myocardial infarction (AMI) than after unstable angina pectoris (UAP) or stable angina pectoris (SAP). A total of 1,360 patients with severe coronary artery disease (>/=1 stenosis >/=70%) had CRP levels obtained at angiography. Presenting diagnoses were SAP (n = 599), UAP (n = 442), or AMI (n = 319). During follow-up (mean 2.8 years), death or nonfatal AMI (D/AMI) occurred in 19.5%, 16.1%, and 17.2% (p = NS) with SAP, UAP, and AMI, respectively. Corresponding median CRP levels were 1.31, 1.27, and 2.50 mg/dl (p <0.001). For the overall cohort, increasing age, low ejection fraction, revascularization, and elevated CRP were the strongest of 6 independent predictors for D/AMI. Among those presenting with SAP, CRP levels above the first tertile were associated with an adjusted hazard ratio of 1.8 (95% confidence interval [CI] 1.2 to 2.8, p <0.009) for D/AMI. After UAP, the hazard ratio was 2.7 (95% CI 1.4 to 5.0, p <0.002). However, when measured during hospitalization for AMI, CRP was not predictive of long-term outcome (hazard ratio 1.0 [95 % CI 0.5 to 1.7] p = 0.86). In conclusion, predischarge CRP levels are higher after AMI than after UAP or SAP. However, whereas CRP is strongly predictive of long-term D/AMI for patients presenting with SAP or UAP, it is not predictive shortly after AMI, suggesting that measurements should be delayed until the acute phase reaction is over and levels have returned to baseline.

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PubMed2002

Lack of association of Helicobacter pylori infection with coronary artery disease and frequency of acute myocardial infarction or death.

We investigated the association between Helicobacter pylori (H. pylori) infection and coronary artery disease (CAD) in 2 study populations: (1) a cross-sectional study to determine risk of having CAD, and (2) a longitudinal study to determine risk of acute myocardial infarction (AMI) or death over a mean follow-up period of 3 years in patients with angiographically documented CAD. Blood samples were tested for serum immunoglobulin G antibodies to H. pylori and C-reactive protein (CRP) levels. Study 1: Of 391 patients (62% men, mean age 57 years), 41% had antibodies to H. pylori. CAD prevalence was 70% in H. pylori seropositive patients and 59% in seronegative patients (p = 0.03). Elevated CRP levels (>0.5 mg/dl) were significantly higher in patients with than without CAD (p = 0.02). By univariate analysis, CAD prevalence significantly increased stepwise depending on H. pylori seropositivity and elevated CRP levels (p = 0.008). Significance was lost after adjustment for traditional risk factors. Further analyses revealed that age was the critical confounder. Study 2: Of 929 patients (77% men, mean age 65 years), 56% had antibodies to H. pylori. By univariate analysis, the incidence of AMI or death was 22% in H. pylori seropositive patients and 18% in seronegative patients (p = 0.1). The adjusted hazard ratio of AMI or death for H. pylori seropositivity was 1.12 (95% confidence interval 0.81 to 1.54). Our data suggest that prior infection with H. pylori is not a major factor determining either risk of CAD, AMI, or death in patients with CAD.

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PubMed2002

Impact of renal failure on the risk of myocardial infarction and death.

BACKGROUND: It is unclear whether pre-existing cardiovascular disease or predisposition of the uremic state leads to the high cardiovascular morbidity and mortality associated with renal failure. We examined whether renal failure independently increases the risk of myocardial infarction and death. METHODS: A total of 8600 patients with variable glomerular filtration rate (GFR) at the time of coronary angiography participated in the Intermountain Heart Study. Coronary disease was defined as >or=70% stenosis. Modification of Diet in Renal Disease formula was used to calculate glomerular filtration rate (GFR). Cox regression models were used to compare outcomes. RESULTS: The mean GFR was 71 +/- 24 mL/min. There were 1320 (15%) deaths, 657 (9%) myocardial infarctions and 1776 (21%) death or myocardial infarctions over 3.2 +/- 1.9 years. Compared to the highest GFR quartile, the lowest GFR quartile (mean GFR 41 +/- 14 mL/min) was associated with higher risk for myocardial infarction (RR 1.43, 95% CI 1.15 to 1.78), death (RR 2.77, 95% CI 2.32 to 3.30) and death/myocardial infarction (RR 2.13, 95% CI 1.85 to 2.45) in multivariable models adjusted for age, sex, hypertension, hyperlipidemia, smoking, family history of coronary disease and diabetes. Even after further adjustment for coronary angiographic data and the choice of initial therapy, lowest GFR quartile was associated with increased risk of myocardial infarction (RR 1.51, 95% CI 1.21 to 1.88), death (RR 2.60, 95% CI 2.18 to 3.10) and death/myocardial infarction (RR 2.08, 95% CI 1.80 to 2.39). CONCLUSIONS: Even moderate renal failure increases the risk of myocardial infarction and death independent of clinical variables, baseline angiographic evidence of coronary disease and therapy.

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PubMed2002

Greater pathogen burden but not elevated C-reactive protein increases the risk of clinical restenosis after percutaneous coronary intervention.

BACKGROUND: Restenosis after percutaneous coronary intervention (PCI) constitutes a serious complication in the treatment of cardiovascular disease, but known risk factors do not fully account for the observed restenosis risk. Preliminary studies of infection or inflammation in restenosis report varied results. We tested whether C-reactive protein (CRP) or pathogen burden (seropositivity to 0, 1, 2, or 3 pathogens, of Chlamydia pneumoniae [Cpn], cytomegalovirus [CMV], or Helicobacter pylori [Hpy]) predict clinical restenosis after percutaneous coronary intervention (PCI). METHODS: Blood samples were collected from 415 patients undergoing PCI, and levels of plasma CRP and antibodies to Cpn, CMV, and Hpy were measured. The patient's medical history, demographics, and procedural data were recorded. Patient end points were determined for as long as 6 months as a means of evaluating the incidence of clinical restenosis and major adverse cardiac events. RESULTS: The average patient age was 62 years, and 80% of patients were male. Fifty-eight patients (14%) experienced clinical restenosis, whereas 17 patients (4%) died or had an acute myocardial infarction. After adjusting for 19 possible predictors, we found the pathogen burden (P-trend =.04, adjusted odds ratio [OR] 1.5 per number of pathogens) and minimum luminal diameter (P =.003, OR 1.8 per mm decrease) to be significant predictors of clinical restenosis. Male sex was a nonsignificant predictor of restenosis (P =.06, OR 2.2), but CRP was not significant after adjustment (P-trend =.10, OR 0.73 per tertile). CONCLUSION: Pathogen burden was associated with clinical coronary restenosis, an association that deserves further exploration and evaluation. CRP, a marker of inflammation, was not associated with an increased risk of restenosis.

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