Effect of short-term NSAID use on echocardiographic parameters in elderly people: a population-based cohort study.

BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) are associated with an increased risk of heart failure. NSAIDs inhibit the synthesis of renal prostaglandin, which results in a higher total blood volume, cardiac output and preload. The association between recent start of NSAIDs in elderly people and echocardiographic parameters was investigated. METHODS: In the Rotterdam Study, a population-based cohort study, the effect of NSAIDs on left ventricular end-systolic dimension, left ventricular end-diastolic dimension, fractional shortening and left ventricular systolic function was studied in all participants for whom an echocardiogram was available (n=5307). NSAID use was categorised as current NSAID use on the date of echocardiography, past use and never used before echocardiography during the study period. Current use was divided into short-term NSAID use (≤ 14 days) and long-term NSAID use (> 14 days). Associations between drug exposure and echocardiographic measurements were assessed using linear and logistic regression analyses. RESULTS: Current NSAID use for < 14 days was associated with a significantly higher left ventricular end-systolic dimension (+1.74 mm, 95% CI 0.20 to 3.28), left ventricular end-diastolic dimension (+3.69 mm, 95% CI 1.08 to 6.31) and significantly lower fractional shortening (-6.03%, 95% CI -9.81% to -2.26%) compared with non-users. Current NSAID use for > 14 days was associated with a higher left end-diastolic dimension (+1.96 mm, 95% CI 0.82 to 3.11) but there was no change in the other echocardiographic parameters. CONCLUSION: This study is the first to investigate the association between NSAIDs and echocardiographic parameters and suggests that there is a transient effect of short-term use of NSAIDs on the left ventricular dimension and function of the heart.

Genetic variation in the fibrinogen-alpha and fibrinogen-gamma genes in relation to arterial stiffness: the Rotterdam Study.

OBJECTIVE: Arterial stiffness increases with age and predicts cardiovascular disease. Fibrinogen is an acute-phase protein and some studies showed an association with arterial stiffness. We studied genetic variation in the fibrinogen-alpha (FGA) and fibrinogen-gamma (FGG) genes, by means of single nucleotide polymorphisms (FGA: -58 G/A, 1374 G/A, 1526 T/C, 312 Thr/Ala, and FGG: 4288 G/A, 6326 G/A, 7792 T/C) and resultant haplotypes in relation to arterial stiffness. METHODS: The present study (n = 3891) was embedded in the Rotterdam Study. Associations of the fibrinogen level, genotypes and haplotypes with aortic stiffness (pulse wave velocity), carotid stiffness (distensibility coefficient) and pulse pressure were investigated in men and women by analyses of variance, linear regression and by haplotype analyses. Analyses were adjusted for age, mean arterial pressure, heart rate, known cardiovascular risk factors and atherosclerosis. RESULTS: Genotype analyses yielded associations of FGA-58 G/A (P = 0.040, for trend) and FGA-1526 T/C (P = 0.004, for trend) with the fibrinogen levels, but no consistent associations with arterial stiffness, in women. FGA-haplotype 4 was associated with the fibrinogen level (P = 0.02) in women. FGA-haplotype 3 and FGG-haplotype 2 were associated with aortic stiffness (P = 0.05) in women. No associations were found in men. CONCLUSION: Findings indicate that the fibrinogen level and genetic variation in the FGA and FGG genes may influence arterial stiffness in women.

Antihypertensive treatment is associated with improved left ventricular geometry: the Rotterdam Study.

PURPOSE: Left ventricular hypertrophy (LVH) increases the risk of cardiovascular disease. We evaluated the association between antihypertensive therapy and echocardiographically determined LVH. METHODS AND RESULTS: The Rotterdam Study is a population-based prospective cohort study among 7983 participants aged 55 years or over. Echocardiography was performed in 2823 participants. The study population consisted of 740 participants with grade 1 hypertension or antihypertensive monotherapy, without heart failure. Of these, 646 had an adequate echocardiogram for analysis of relative wall thickness (RWT) and 642 for left ventricular mass index. Participants were followed from 1 January 1991 until the date of echocardiography, between September 1992 and June 1993. Outcome measures were defined as being in the highest gender-specific quintile of left ventricular mass index and as having a RWT higher than 0.43. A Cox regression model with duration of use of antihypertensives defined as time-dependent covariates was used for data-analysis. Antihypertensive treatment lowered the risk of increased left ventricular mass index (RR 0.6, 95%CI 0.4-0.9). ACE-inhibitors, diuretics and beta-blockers all showed a risk reduction. Use of antihypertensives was also associated, although non-significantly, with a decrease of high RWT (RR 0.8, 95%CI 0.6-1.0). ACE-inhibitors, beta-blockers and calcium antagonists showed similar risk reductions, while diuretics seemed to increase the risk, possibly by reducing left ventricular end diastolic diameter. CONCLUSIONS: The use of antihypertensive drugs is associated with a decreased risk of echocardiographically determined LVH in a population-based setting.