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Biomedical subjects

Juan Pedro-Botet

Publications and source records attributed to Juan Pedro-Botet.

14 recordsLinked to original sources
PubMed2006

Subclinical carotid atherosclerosis in HIV-infected patients: role of combination antiretroviral therapy.

BACKGROUND AND PURPOSE: Whether or not combination antiretroviral therapy (CART) alone directly contributes to accelerating atherosclerosis in HIV-infected patients has not been studied in depth. This study aimed to ascertain the relationship between this therapy and subclinical carotid atherosclerosis according to cardiovascular risk. METHODS: Sixty-eight HIV-infected patients with < or =1 cardiovascular risk factors and 64 with > or =2 risk factors completed the study protocol consisting of clinical, laboratory, and vascular evaluation by carotid high-resolution B-mode ultrasonography. Univariate and multivariate logistic regression analyses were performed with the presence of subclinical carotid atherosclerosis, defined by carotid intima-media thickness >0.8 mm or the presence of plaque being the dependent variable. RESULTS: Among the 132 enrolled patients, 93 (70.5%) were on CART and 39 (29.5%) had never been on antiretroviral therapy. In accordance with cardiovascular risk stratification, subclinical carotid atherosclerosis was found in 26.6% (17 of 64 patients) of the very low-risk group (10-year coronary risk <5%), 35.3% (12 of 34 patients) of the low-risk group (10-year coronary risk between 5% and 9%) and 76.5% (26 of 34 patients) of the moderate/high-risk group (10-year coronary risk > or =10%). Thus, 55 (41.7%) of the 132 HIV-infected patients had subclinical carotid atherosclerosis, and independent variables associated with carotid atherosclerosis (odds ratio; 95% CI) were: CART exposure (10.5; 2.8 to 39) and 10-year coronary risk > or =10% (4.2; 1.5 to 12). In very low coronary risk patients (<5%), age (per 10-year increment: 4.01; 1.12 to 14.38), systolic blood pressure (per unit mm Hg 1.07; 1.01 to 1.14), and CART exposure (8.65; 1.54 to 48.54) were independently associated with subclinical carotid atherosclerosis. CONCLUSIONS: CART should be considered a strong, independent predictor for the development of subclinical atherosclerosis in HIV-infected patients, regardless of known major cardiovascular risk factors and atherogenic metabolic abnormalities induced by this therapy.

Anti-Retroviral Agents↗
PubMed2005

Hypertension in HIV-infected patients: prevalence and related factors.

BACKGROUND: Little is known about hypertension in the HIV-infected population. This study aimed to assess the prevalence of hypertension and related factors in HIV-infected patients. METHODS: In this prospective cross-sectional study, 710 HIV-infected patients (626 on combination antiretroviral therapy and 84 naive) managed at the outpatient clinic of a tertiary hospital during 2003 and 802 controls completed the study protocol consisting of medical examination and a 6-month follow-up period including three control visits. RESULTS: Hypertension prevalence was 13.1% in HIV-infected patients and 13.5% in the control group. Age (per 10-year increment) (odds ratio [OR]: 1.92; 95% confidence interval [CI]: 1.48-2.48), body mass index (OR: 1.18; 95% CI: 1.10-1.27), and lipoaccumulation pattern of fat redistribution (OR: 2.26; 95% CI: 1.20-4.24) were independently and significantly associated with the presence of hypertension in HIV-infected patients at logistic regression analysis. CONCLUSIONS: The present results suggest no meaningful difference in prevalence of hypertension between subjects with and without HIV infection. Thus, the influence of combination antiretroviral therapy appears to have little impact on the prevalence of hypertension.

Adult↗
PubMed2005

Metabolic syndrome among HIV-infected patients: prevalence, characteristics, and related factors.

OBJECTIVE: To assess the prevalence in HIV-infected patients of the metabolic syndrome as defined by the National Cholesterol Education Program, i.e., three or more of the following components: abdominal obesity, hypertriglyceridemia, low HDL cholesterol, high blood pressure, and high fasting glucose. RESEARCH DESIGN AND METHODS: In this cross-sectional study, 710 HIV-infected patients managed at the outpatient clinic of a tertiary hospital during 2003 completed the study protocol consisting of a medical examination and laboratory analysis after a 12-h overnight fast. RESULTS: Metabolic syndrome prevalence was 17% and increased from 5.1% among HIV-infected patients under age 30 years to 27.0% for those aged 50-59 years. Age (per 10-year increment) (odds ratio [OR] 1.41 [95% CI 1.12-1.77]), BMI (1.27 [1.19-1.36]), past and present protease inhibitor exposure (2.96 [1.03-3.55] and 4.18 [1.4-12.5], respectively) were independently associated with the metabolic syndrome on logistic regression analysis. Furthermore, only stavudine (d4T) (1.74 [1.01-2.98]) and lopinavir/ritonavir (2.46 [1.28-4.71]) were associated with the metabolic syndrome after adjustment for age and BMI. CONCLUSIONS: The prevalence of metabolic syndrome among these HIV-infected patients is similar to that previously reported in uninfected individuals. Of specific concern is the association of protease inhibitor exposure with the metabolic syndrome and, more specifically, with exposure to stavudine and lopinavir/ritonavir when individual antiretroviral drugs were analyzed.

Adult↗
PubMed2004

[Clinical autopsy: a useful tool in the emergency department of teaching hospitals].

BACKGROUND AND OBJECTIVE: We aimed to know the usefulness of clinical autopsy at the medical room of an emergency department in a teaching hospital. PATIENTS AND METHOD: Retrospective study of clinical autopsies performed in the emergency department of a teaching hospital between 1995 and 2000. We explored the correlation between clinical emergency and autopsy diagnosis. RESULTS: The number of deaths was 1,484 (0.9%) among 165,662 patients attended in the emergency medical room in the study period. Of 281 autopsies (18.9%), 227 (15.3%) were judicial. Only 54 clinical autopsies (3.6%) were included. Dyspnea and chest pain, the two more frequent guide symptoms, were in concordance with the two more prevalent initial clinical diagnoses: respiratory and cardiovascular diseases. 38.9% (21 cases) of autopsies agreed with the clinical diagnosis and 14.8% (8 cases) did not agree with it. 25.9% (14 cases) of autopsies were diagnostic since the clinical diagnosis, both initial and final, was unknown. Moreover, 14.8% (8 cases) autopsies were explanatory. Furthermore, 5.6% (3 cases) of autopsies were undetermined. With regard to the main cause of death, there were 9 (16.7%) cases of previously unknown neoplasms. CONCLUSIONS: The results of the present study confirm the need and usefulness of autopsy in patients dying in the medical room of emergency departments, as well as the crucial role of the clinico-pathological exercise in the definitive diagnosis of the postmortem examination.

Aged↗
PubMed2004

[Cardiovascular disease in HIV-infected patients on highly active antiretroviral therapy].

BACKGROUND AND OBJECTIVE: Our goal was to assess the main characteristics of cardiovascular disease in HIV-infected patients on highly active antiretroviral therapy (HAART). PATIENTS AND METHOD: Retrospective analysis of the clinico-epidemiological characteristics of 16 HIV-infected patients treated with HAART who had suffered a cardiovascular event from a 1,459 patients' cohort. RESULTS: Clinical presentation of cardiovascular disease was an acute coronary syndrome in 12 cases, ischemic stroke in 2 and peripheral vascular disease in 2. Patients included in the study had a mean of 3.2 cardiovascular risk factors, smoking and low HDL levels being the more prevalent risk factors. Eight (50%, 95% CI, 25-75%) patients fulfilled the criteria of metabolic syndrome. The mean CD4 count was 548 x 10(6)/l. CONCLUSIONS: HIV-infected patients on HAART ha-ve a high cardiovascular risk. A strict management of modifiable risk factors must be warranted in these patients.

Adult↗
PubMed2004

Significance of high density lipoprotein-cholesterol in cardiovascular risk prevention: recommendations of the HDL Forum.

In the approach to lipid-related risk factors for cardiovascular diseases, serum high density lipoprotein-cholesterol (HDL-C) levels bear a particular significance as this lipoprotein is considered to be an antiatherogenic factor mainly, but not only, because of its influence and impact on reverse cholesterol transport. Hence the need and requirement to consider serum HDL-C levels for both primary and secondary prevention of cardiovascular disease. A particularly important aspect is the association of the 'low HDL syndrome' with the metabolic syndrome. These factors force us to consider serum HDL-C level as a therapeutic target by itself, or even in association with low density lipoprotein-cholesterol (LDL-C) levels when the latter are increased. This review stresses the aspects connecting serum HDL-C levels and cardiovascular risk, and looks at the populations that should be considered amenable to therapeutic management because of low serum HDL-C levels. We review therapeutic strategies, both pharmacological and nonpharmacological. The aim of this review is to present therapeutic management recommendations for correcting the proportion of cardiovascular risk that is attributable to changes in HDL-C. Serum HDL-C levels of >40 mg/dL must be a therapeutic target in primary and secondary prevention. This goal is particularly important in patients with low serum HDL-C levels and ischemic heart disease (IHD) or its equivalents, even if the therapeutic target for serum LDL-C levels (<100 mg/dL) has been achieved. The first choice for this clinical condition is fibric acid derivates. The same therapeutic option should be considered in patients without IHD with low serum HDL-C levels and high cardiovascular risk (>20%), hypertriglyceridemia, type 2 diabetes mellitus, or metabolic syndrome.

Bezafibrate↗
PubMed2003

Differences between genotyping and phenotyping methods for assessing apolipoprotein(a) size polymorphisms.

The aim of the present study was to analyze, on a double-blind basis, the relationships between the apolipoprotein(a) (apo(a)) gene and protein size polymorphisms in healthy volunteers (n = 99) and patients with premature myocardial infarction (n = 91). Apo(a) genotypes were determined by pulse-field electrophoresis and phenotypes were separated by sodium dodecyl sulfate-agarose gel electrophoresis. Results showed that phenotyping overestimated apo(a) size with respect to genotyping (mean (SD) = 3.7 (3.4) kringle units; p < 0.001) in subjects with a double-band genotype, although both measurements were highly correlated (r = 0.83; p < 0.001). We also observed that the protein band in subjects with a single-band phenotype was related more closely to the smallest allele than to the largest allele band. The correlation of plasma lipoprotein(a) (Lp(a)) concentration was stronger with the phenotype than with the genotype. We hypothesize that post-translational modifications in the apo(a) molecule may be the most plausible explanation for the discrepancies observed. In conclusion, the present study highlights the dissimilarities between phenotyping and genotyping methods for the measurement of apo(a) size and suggests that laboratories should carefully consider these relationships and the transfer of results between such methodologies.

Age of Onset↗
PubMed2002

Heterozygous apolipoprotein (a) status and protein expression as a risk factor for premature coronary heart disease.

Exactly how apolipoprotein a [APO(a)] isoform size affects the degree of cardiovascular risk associated with high lipoprotein a [LP(a)] levels is not fully understood. Using a sodium dodecyl sulfate-agarose APO(a) & LP(a) phenotyping method, we assessed the role of APO(a) size heterogeneity according to the number of kringle 4 repeats and the differential APO(a) protein expression in 91 male Spanish patients with premature coronary heart disease (CHD) compared with 99 healthy Spanish men. CHD patients had significantly increased median plasma LP(a) levels (0.31 g/L) and a higher percentage of subjects with LP(a) levels of 0.30 g/L or greater (51%) than controls (0.15 g/L and 23%, respectively). Patients with the double-band phenotype had significantly higher plasma LP(a) levels (median 0.37 g/L) compared with those expressing a single-band phenotype (median 0.20 g/L; P =.018) and with their corresponding controls (median 0.15 g/L; P <.001). The double-band phenotype and LP(a) values of 0.30 g/L or greater had a significant association with CHD (odds ratio [OR] 6.47, 95% confidence interval [CI] 2.51-16.7), stronger than that observed for the entire group (OR 4.19, 95% CI 1.97-8.90). The adjusted OR for the APO(a) protein pattern that equally expressed both isoforms indicates an independent association with premature CHD (OR 3.33; 95% CI 1.08-10.3). These results suggest that APO(a) phenotyping might be used in subjects with hyperlipoproteinemia a as a powerful marker to assess the risk of premature CHD because heterozygous status, mainly when both isoforms are equally expressed, is associated with higher cardiovascular risk.

Apolipoproteins A↗