Search PubMed⌕ Search

Biomedical subjects

Juan P Zambrano

Publications and source records attributed to Juan P Zambrano.

10 recordsLinked to original sources
PubMed2006

Evaluation of comorbidity scores to predict all-cause mortality in patients with established coronary artery disease.

BACKGROUND: To assess the value of scores based on the presence of comorbid conditions for mortality risk-stratification in patients with coronary artery disease (CAD) METHODS: We prospectively followed 305 males with CAD undergoing coronary angiography for 58 months. We correlated the modified Charlson Index (MCI) and the recently proposed CAD-specific index (CSI) with the risk of all-cause mortality. RESULTS: The odds ratio (OR) for death increased by 31% per point increase in the MCI (95% CI=17-46%; p<0.0001). The OR for death increased by 16% per point increase in the CSI (95% CI=8.5-25%; p<0.0001). In logistic regression models that adjusted for age, left ventricular ejection fraction, and the number of vessels involved with CAD, both the MCI and the CSI were the strongest predictors of mortality according to the chi2 value for each term, with the MCI having the highest value. The adjusted OR per point increase in the MCI was 1.32 (95% CI=1.17-1.48; p<0.0001); the corresponding adjusted OR per point increase in the CSI was 1.17 (95% CI=1.09-1.26; p<0.0001). The model including the MCI had a slightly higher chi2 value (45.1 vs. 39.1) and area under the receiver operator characteristic curve (0.742 vs. 0.727) than the model including the CSI. CONCLUSION: The MCI and the newly proposed CSI are powerful tools to predict all-cause mortality in patients with established CAD. Although the CSI was not superior to the MCI, its simplicity might make it useful in populations with a low prevalence of comorbidities not included in this score.

Cause of Death↗
PubMed2005

Ability of serum to decrease cellular acylCoA:cholesterol acyl transferase activity predicts cardiovascular outcomes.

BACKGROUND: We evaluated whether cholesterol efflux activity of serum is associated with the presence of angiographic coronary artery disease (CAD) and the risk of major adverse cardiovascular events (MACE) and death. METHODS AND RESULTS: We studied 168 men undergoing coronary angiography. Cholesterol efflux activity was measured in vitro by incubation of patient serum with human skin fibroblasts and defined as the ability of serum to decrease the pool of cholesterol available for esterification by the acylCoA:cholesterol acyl transferase (ACAT) reaction. We evaluated whether this activity was associated with the presence of CAD and the risk of MACE and death during a 4.5-year follow-up. Serum-induced changes in ACAT activity did not correlate with HDL levels or the presence of CAD. Patients in the highest tertile of change in ACAT activity had a significantly higher risk for MACE (HR, 2.15; 95% CI, 1.36 to 3.39; P=0.001) and death (HR, 2.23; 95% CI, 1.17 to 4.26; P=0.01). These correlations were independent of other risk markers including LDL, HDL, and C-reactive protein levels. CONCLUSIONS: Serum-induced depletion of cellular cholesterol available for esterification by ACAT was a strong, independent predictor of MACE and death. We speculate that the ability of serum to decrease ACAT activity depends on ATP binding cassette transporter A1 (ABCA1)-mediated efflux. Furthermore, serum samples that induce larger changes in ACAT activity contain increased levels of HDL particles that preferentially interact with ABCA1 and that these particles accumulate in the serum of patients because of low activity of ABCA1 in vivo preventing or limiting the extent of apoA-I lipidation.

Aged↗
PubMed2005

Relation between ascending aortic pressures and outcomes in patients with angiographically demonstrated coronary artery disease.

We prospectively followed 324 men, who underwent coronary angiography, for 1,161 +/- 418 days. We analyzed the association between ascending aortic pressures measured during cardiac catheterization and the risk of all-cause mortality and a combined end point of major adverse cardiovascular events (MACEs), including unstable angina pectoris, myocardial infarction, coronary revascularization, stroke, or death. Pulse pressure significantly predicted MACEs (hazard ratio [HR] per 10 mm Hg increase 1.09, 95% confidence interval [CI] 1.002 to 1.17, p = 0.04). Diastolic blood pressure (BP) inversely correlated with the risk of MACEs (HR per 10 mm Hg increase 0.85, 95% CI 0.74 to 0.98, p = 0.02). These correlations remained significant after adjusting for other predictors and potential confounders. The association between lower diastolic BP with the risk of MACEs was more pronounced in patients with triple-vessel coronary artery disease (p for interaction = 0.03). Peripheral diastolic BP (but not pulse pressure) correlated inversely with the risk of MACEs (HR 0.87 per 10 mm Hg increase, 95% CI 0.75 to 0.998, p = 0.047). Aortic pulse pressure significantly predicted death (HR per 10 mm Hg increase 1.18, 95% CI 1.05 to 1.33, p = 0.004), and aortic diastolic BP correlated inversely with the risk of death (HR 0.76, 95% CI 0.62 to 0.94, p = 0.01).

Aorta↗
PubMed2005

Correlation between apoptotic endothelial microparticles and serum interleukin-6 and C-reactive protein in healthy men.

Inflammation has been associated with increased cardiovascular risk, and endothelial cell (EC) apoptosis has been implicated in atherogenesis. The correlation between circulating concentrations of interleukin-6 (IL-6), C-reactive protein (CRP), and endothelial microparticles (EMPs) expressing an apoptotic (EMP31) or activation (EMP62E) phenotype in 20 middle-aged healthy men was investigated. IL-6 was significantly correlated with EMP31 (r = 0.6, p = 0.004), which persisted after adjusting for body mass index and CRP. CRP was significantly correlated with body mass index (r = 0.49, p = 0.02) but not with EMP31 or EMP62E. EC apoptosis is associated with IL-6 levels in men and might be partially responsible for the increased cardiovascular risk associated with subclinical inflammation.

Biomarkers↗
PubMed2005

Elevation of endothelial microparticles, platelets, and leukocyte activation in patients with venous thromboembolism.

OBJECTIVES: The purpose of this research was to determine the levels of platelet, leukocyte, and endothelial activation and markers of cellular interactions in patients with venous thromboembolism (VTE). BACKGROUND: The details of interactions between endothelium, platelets, and leukocytes in VTE are not well understood. METHODS: We studied 25 patients with VTE and compared 25 healthy controls. We used flow cytometry to measure: 1) endothelial microparticles (EMP) identified by CD31+/CD42b- (EMP(31)) or E-selectin (EMP(62E)); 2) platelet microparticles (CD31+/CD42b+); 3) surface expression of P-selectin in platelets and CD11b in leukocytes; 4) EMP-monocyte conjugates (percentage of monocytes positive for E-selectin); and 5) platelet-leukocyte conjugates (PLC) expressed as percentage of leukocytes positive for CD41. RESULTS: Patients with VTE had marked elevations of EMP(31) (2,193 vs. 383 counts/microl; p = 0.003), EMP(62E) (368 vs. 223 counts/microl; p = 0.001), and EMP-monocyte conjugates (3.3% vs. 2.5%; p = 0.002), as well as increased activation of platelets (35.2 vs. 5.0 fluorescence intensity units for P-selectin; p < 0.0001) and leukocytes (13.9 vs. 7.7 U for CD11b; p = 0.004). Also elevated in VTE were PLC (61.7% vs. 39.6%; p = 0.01). Expression of CD11b in leukocytes strongly correlated with PLC (r = 0.74; p < 0.0001). CONCLUSIONS: Marked activation of endothelium, platelets, and leukocytes occurs in VTE, and VTE, or the accompanying inflammatory process, involves the release of EMP and formation of EMP-monocyte conjugates and PLC. These findings support prior studies suggesting that release of EMP and their binding to monocytes are key events in thrombogenesis. Our findings also support the concept that the formation of PLC regulates leukocyte activation and participates in linking thrombosis with inflammation.

Biomarkers↗
PubMed2005

Aortic pressure augmentation predicts adverse cardiovascular events in patients with established coronary artery disease.

Pulse pressure (PP), a marker of arterial stiffness, predicts cardiovascular risk. We aimed to determine whether augmentation pressure (AP) derived from the aortic pressure waveform predicts major adverse cardiovascular events (MACE) and death independently of PP in patients with established coronary artery disease (CAD). We prospectively followed-up 297 males undergoing coronary angiography for 1186+/-424 days. Ascending aortic pressure tracings obtained during catheterization were used to calculate AP (difference between the second and the first systolic peak). Augmentation index (AIx) was defined as AP as a percentage of PP. We evaluated whether AP and AIx can predict the risk of MACE (unstable angina, acute myocardial infarction, coronary revascularization, stroke, or death) and death using Cox regression. All models evaluating AP included PP to assess whether AP adds to the information already provided by PP. Both AP and AIx significantly predicted MACE. The hazard ratio (HR) per 10 mm Hg increase in AP was 1.20 (95% confidence interval [CI], 1.08 to 1.34; P<0.001); the HR for each 10% increase in AIx was 1.28 (95% CI, 1.11 to 1.48; P=0.004). After adjusting for other univariate predictors of MACE, age, and other potential confounders, AP remained a significant predictor of MACE (HR per 10 mm Hg increase=1.19; 95% CI, 1.06 to 1.34; P=0.002), as did AIx (adjusted HR, 1.28; 95% CI, 1.09 to 1.50; P=0.003). AP was a significant predictor of death (HR per 10 mm Hg increase=1.18; 95% CI, 1.02 to 1.39; P=0.03). Higher AIx was associated with a trend toward increased mortality (HR=1.22; 95% CI, 0.98 to 1.52; P=0.056). Aortic AP predicts adverse outcomes in patients with CAD independently of PP and other risk markers.

Aged↗
PubMed2005

Usefulness of C-reactive protein as an independent predictor of death in patients with ischemic cardiomyopathy.

The usefulness of serum C-reactive protein, an inflammatory marker, to predict mortality risk in patients who have ischemic cardiomyopathy was investigated. C-reactive protein was measured in 123 men who underwent cardiac catheterization and were noted to have left ventricular ejection fraction <or=45% and significant angiographic coronary artery disease. They were prospectively followed for 3 years. Higher levels of C-reactive protein were associated with increased mortality rate. This correlation was independent of other prognostic factors, such as age, ejection fraction, symptoms of severe congestive heart failure, use of angiotensin-converting enzyme inhibitors, and use of beta blockers.

Biomarkers↗
PubMed2003

Noncompaction of the ventricular myocardium: the use of contrast-enhanced echocardiography in diagnosis.

We describe a case of noncompaction of the ventricular myocardium diagnosed in the preoperative evaluation of a patient undergoing renal transplantation. Ventricular noncompaction is characterized by numerous prominent trabecular recesses with intratrabecular blood from the ventricular cavity. Color Doppler was suggestive of intramyocardial flow. With contrast-enhanced echocardiography the endocardial borders were clearly demarcated, allowing for visualization of trabecular recesses and intratrabecular flow. Contrast-enhanced echocardiography facilitates the diagnosis of noncompaction of the ventricular myocardium, circumventing the need for invasive diagnostic testing.

Cardiomyopathies↗