Effects of amlodipine and lisinopril on intima-media thickness in previously untreated, elderly hypertensive patients (the ELVERA trial) Terpstra, W.; May, J.; Smit, Andries J.; de Graeff, Pieter A.; Meyboom-de Jong, B.; Crijns, H.

BackgroundSeveral clinical studies have evaluated the association between galectin‐3 levels and outcome in patients with heart failure (HF). However, little is known about the predictive value of repeated galectin‐3 measurements. This study evaluates the prognostic value of repeated time‐dependent galectin‐3 measurements in acute HF patients.Methods and ResultsIn the TRIUMPH (Translational Initiative on Unique and Novel Strategies for Management of Patients with Heart Failure) clinical cohort study, 496 acute HF patients were enrolled in 14 hospitals in The Netherlands, between 2009 and 2014. Repeated blood samples (7) were drawn during 1‐year follow‐up. Associations between repeated biomarker measurements and the primary end point were assessed using a joint model. Median age was 74 years and 37% were women. The primary end point, composite of all‐cause mortality and HF rehospitalization, was reached in 188 patients (40%), during a median follow‐up of 325 days (interquartile range 85–401). The median baseline galectin‐3 level was 24 ng/mL (interquartile range 18–34). The mean number of galectin‐3 measurements available per patient was 4.3. After adjustment for clinical factors and N‐terminal pro‐brain natriuretic peptide, there was a weak association between baseline galectin‐3 and risk of the primary end point. When repeated measurements were taken into account, the adjusted hazard ratio per 1 SD increase of the galectin‐3 level (on the log2 scale) at any time point increased to 1.67 (95% confidence interval, 1.24–2.23, P<0.001). After additional adjustment for repeated N‐terminal pro‐brain natriuretic peptide measurements, the association remained statistically significant.ConclusionsRepeated galectin‐3 measurements appeared to be a strong predictor of outcome in acute HF patients, independent of N‐terminal pro‐brain natriuretic peptide. Hence, galectin‐3 may be helpful in clinical practice for prognostication and treatment monitoring.

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In hypertension, both reduced vascular supply and increased cardiac demand contribute to the development of (silent) myocardial ischemia. Our aim was to determine the prevalence of ST-segment depression and to analyze contributing factors in asymptomatic, previously untreated, older hypertensives. From a population survey, in 184 patients with mild hypertension (4 times systolic blood pressure >/=160 mm Hg and/or diastolic blood pressure >/=95 mm Hg), 60 to 75 years of age, cardiovascular end-organ damage was measured. Episodes of ST-segment depression were measured by 48-hour ambulatory Holter monitoring and were observed in 21 hypertensives (12%). They showed a significantly higher combined far-wall intima-media thickness of carotid and femoral arteries and more arterial plaques as measured by B-mode ultrasound compared with hypertensives without ST depression (0.00098+/-0.00021 versus 0.00088+/-0.00016 mm and 5.2+/-3.7 versus 3.7+/-2.8 plaques, P<0.05, respectively), whereas left ventricular mass index was not different (111+/-18 versus 104+/-24 g/m(2); P=0.18, respectively). In hypertensives with transient ST-segment depression, a significant relation was found between left ventricular mass and ischemic burden (r=0.51, P=0.02). Approximately 1 of 8 unselected and previously untreated older hypertensives show asymptomatic ST-segment depression, suggestive of silent myocardial ischemia. These data suggest that vascular factors mainly determine the occurrence of ischemic ST-segment depression and cardiac factors determine the ischemic burden in older hypertensives.