MMP-2 and sTNF-R1 Variability in Patients with Essential Hypertension: 1-Year Follow-Up Study.

The aim of this study is to analyze MMP-2 and sTNF-R1 variability, potent predictors of cardiovascular events, in stable hypertensive patients during a 12-month followup. 234 asymptomatic patients (age 60 ± 13, 136 male) out of 252 patients with essential hypertension were followed up. MMP-2 and sTNF-R1 were measured at baseline and after 12 months (stage I). To compare MMP-2 and sTNF-R1 levels over time interval, we used the statistical method of Bland-Altman. MMP-2 and sTNF-R1 reproducibility was good in our patients for the two intervals with a coefficient of reproducibility of 8.2% and 11.3%, respectively. The percentages of patients within 1.96 × standard deviation of the mean were 93.6% and 92.7%. An elevated coefficient of correlation was obtained for MMP-2, basal versus stage I (r = 0.55, P < 0.0001) and for sTNF-R1 (r = 0.75, P < 0.0001). There is good stability in MMP-2 and sTNF-R1 levels in a followup study of patients with stable hypertension. As a consequence, assessment of its concentrations may be a useful tool for monitoring the follow-up of these patients. Measured variations in MMP-2 and sTNF-R1 levels, exceeding 8.2% and 11.3%, respectively, may indicate an increase in cardiovascular risk, thus, could be used to optimizing treatment than blood pressure control alone.

Variability of NT-proBNP and its relationship with inflammatory status in patients with stable essential hypertension: a 2-year follow-up study.

BACKGROUND: The variability of NT-proBNP levels has been studied in heart failure, yet no data exist on these changes over time in hypertensive patients. Furthermore, studies on the relationship between natriuretic peptides and inflammatory status are limited. METHODOLOGY/PRINCIPAL FINDINGS: 220 clinically and functionally asymptomatic stable patients (age 59 ± 13, 120 male) out of 252 patients with essential hypertension were followed up, and NT-proBNP was measured at baseline, 12 and 24 months. No differences in NT-proBNP were found with respect to the basal stage in the hypertrophic group, but significant changes were found in non-hypertrophic subjects. The reproducibility of NT-proBNP measurements was better in patients with hypertrophy than in the non-hypertrophic group for the three intervals (stage I-basal; stage II-stage I; stage II-basal) with a reference change value of 34%, 35% and 41%, respectively, in the hypertrophic group. A more elevated coefficient of correlation was obtained in the hypertrophic group than in patients without hypertrophy: basal versus stage I (r = 0.79, p < 0.0001 and r = 0.59, p < 0.0001) and stage I versus stage II (r = 0.86, p < 0.0001 and r = 0.56, p < 0.0001). Finally, levels of NT-proBNP significantly correlated with sTNF-R1 (p < 0.0001) and IL-6 (p < 0.01) during follow-up. A multivariate linear regression analysis showed that sTNF-R1 is an independent factor of NT-proBNP. CONCLUSIONS/SIGNIFICANCE: This work shows that there is good stability in NT-proBNP levels in a follow-up study of asymptomatic patients with stable hypertension and left ventricular hypertrophy. As a consequence, assessment of NT-proBNP concentrations may be a useful tool for monitoring the follow-up of hypertensive patients with hypertrophy. Measured variations in peptide levels, exceeding 35% in a 12-month follow-up and 41% in a 24-month follow-up, may indicate an increase in cardiovascular risk, and therefore implies adjustment in the medical treatment. In addition, this study shows a link between neurohormonal and inflammatory activation in these patients.

Inflammatory activation and left ventricular mass in essential hypertension.

BACKGROUND: Inflammation is an independent risk factor for high blood pressure, and as a consequence inflammatory cytokines could be related with left ventricular hypertrophy (LVH). We sought to assess the association and predictive role of different cytokine levels with LVH in a group of patients with essential hypertension (HT). METHODS: We studied 251 asymptomatic hypertensive patients (142 with LVH and 109 without LVH), referred from 11 hospitals. A routine physical examination, laboratory analyses, and echo-Doppler study were performed. Plasma soluble tumor necrosis factor (TNF) receptors (sTNF-R1 and sTNF-R2), interleukin-6 (IL-6), and interleukin-1 receptor antagonist (IL-1ra) were centrally determined. RESULTS: Hypertensive patients with LVH had higher inflammatory cytokine levels than the group without hypertrophy (P < 0.001). Multivariate linear regression reported that sTNF-R1 (P < 0.01) was an independent predictor of left ventricular mass index (LVMI). All cytokines had significant area under the curves for detection of LVH, but sTNF-R1 has the highest area, 0.71 +/- 0.03 (P < 0.001). Finally, prevalence of LVH was increased in the group of patients with higher cytokine levels, and logistic regression analysis showed that sTNF-R1 (odds ratio = 2.59, 95% CI of 1.14-5.87) was an independent predictor of LVH. CONCLUSIONS: Cytokine levels were significantly correlated with LVMI in hypertensive patients. The sTNF-R1 was an independent predictor of LVMI. Plasma sTNF-R1 concentrations could be a predictive factor of LVH in patients with essential HT.

Obese and nonobese patients with essential hypertension show similar N-terminal proBNP plasma levels.

BACKGROUND: Multiple studies have focused on the influence of obesity on natriuretic peptide levels. However, the effect of obesity on amino-terminal propeptide of B-type natriuretic peptide (NT-proBNP) levels in hypertensive (HT) patients remains uncertain. METHODS: We studied 252 asymptomatic patients (60 +/- 13 years, 136 men) with essential HT. A routine physical examination, anthropometry, laboratory analyses, echo-Doppler study, and NT-proBNP level determination were performed. RESULTS: NT-proBNP levels were similar in both obese and nonobese HT (median 56 (25-130) pg/ml vs. median 51 (26-129) pg/ml, P = 0.488). No significant differences were found in obese or nonobese patients with left ventricular hypertrophy (LVH) (median 135 (73-425) pg/ml vs. median 151 (64-274) pg/ml, P = 0.597). The area under the curve was 0.89 +/- 0.03 for NT-proBNP to diagnose LVH in the obese HT patients and 0.88 +/- 0.03 in the nonobese. A logistic regression analysis showed that age, gender, and left ventricular mass index (LVMI) were independent predictors of NT-proBNP levels. Body mass index (BMI) was not significantly associated with NT-proBNP in LVH HT patients. CONCLUSIONS: Obesity is not statistically associated with NT-proBNP levels in HT asymptomatic patients. The same results were observed in our group of patients with LVH. These data are in contrast with those previously found in heart failure, and raise questions about the role of obesity per se as primary cause of decreased NT-proBNP levels in other pathophysiological conditions.