Effects of low-dose aspirin on blood pressure and endothelial function of treated hypertensive hypercholesterolaemic subjects.

The main objective of this study was to assess whether aspirin 100 mg QD can improve blood pressure (BP) control and endothelial function in subjects with arterial hypertension (AH) and hypercholesterolaemia. In total, 21 patients of both sexes (52.1+/-11.5 years) with treated AH and hypercholesterolaemia on antihypertensive and statin therapy were included in the treatment group. In the control group, 20 matched patients of both sexes (51.3+/-12.7 years), but without statin therapy, were recruited. Treatment group subjects received aspirin (100 mg QD) for a duration of 12 weeks at randomization (Treatment phase-1), followed by single blind matching placebo for 12 weeks (Placebo phase) and then again received aspirin (100 mg QD) for an additional 12 weeks (Treatment phase-2). The control group participated in Treatment phase-1, but did not continue Placebo phase and Treatment phase-2. At randomization and at the end of each study phase, mean 24-h systolic BP (SBP) and diastolic BP (DBP) were assessed by 24-h ambulatory blood pressure monitoring (ABPM) and endothelium-dependent (flow mediated, FMD) and -independent (nitroglycerin induced, NTG) vasodilatations of brachial artery were measured using high-resolution ultrasound. In Treatment phase-1, reduction of SBP and DBP (DeltaSBP 5.7+/-2.6 mmHg, P=0.008; DeltaDBP 3.8+/-1.7 mmHg, P=0.014) and improvement of FMD (4.1+/-0.6%, P=0.019), in Placebo phase an elevation of SBP and DBP (DeltaSBP -6.2+/-2.9 mmHg, P=0.002; DeltaDBP -4.2+/-1.9 mmHg, P=0.031) and worsening of FMD (-3.8+/-0.9%, P=0.027), and in Treatment phase-2 reduction of SBP and DBP (DeltaSBP 4.9+/-2.3 mmHg, P=0.005; DeltaDBP 4.1+/-1.3 mmHg, P=0.024) and improvement of FMD (4.5+/-1.3%, P=0.009) were observed in the treatment Group but not in the control group. Addition of low-dose aspirin to antihypertensive medications and statins in hypertensive and hypercholesterolaemic subjects can reduce both SBP and DBP by improvement of endothelial function.

The different patterns of blood pressure elevation by rofecoxib and nabumetone.

Hypertension and knee osteoarthritis (OA) are frequent comorbidities. Nonsteroidal anti-inflammatory drugs (NSAIDs) are often used to relieve pain in such patients. In the last decade selective NSAIDs are used more commonly since they lead to less gastrointestinal complications. As has been shown, the treatment with NSAIDs may cause a mild rise of arterial blood pressure (BP). The influence of selective NSAIDs on BP, particularly in hypertensive patients has still to be investigated. The aim of this study was to determine arterial BP changes in patients suffering from stable arterial hypertension and knee OA and treated with rofecoxib or nabumetone. Two groups of patients with knee OA and stable arterial hypertension received either 25 mg rofecoxib once daily or namebutone 2000 mg once daily during the first week of treatment and 1000 mg for the following 3 weeks. Twenty-four hour arterial BP monitoring was performed prior to initiation of treatment and at the end of a 4-week period. The results were that no changes were found in the mean systolic and diastolic characteristics of BP in the rofecoxib treatment group during day time (delta systolic BP -0.4 mm Hg and delta diastolic BP -0.4 mm Hg), while nocturnal BP increased significantly: delta systolic BP +15.7 mm Hg and delta diastolic BP +8.5 mm Hg. The mean systolic arterial pressure in the nabumeton group raised delta systolic BP 2.9 mm Hg in the daytime and 5 mm Hg during the night-time after the treatment. The mean diastolic arterial pressure also rose delta diastolic 3.2 mm Hg and 4.9 mm Hg at day and night hours respectively. In conclusion rofecoxib treatment did not change arterial BP during day time hours, however, there was a distinct increase in night-time systolic and diastolic BP leading to a disappearance of the physiological diurnal variation. Nabumetone caused a moderate increase of day and night BP, without changes in biological diurnal variation.

The effect of fish oil on hypertension, plasma lipids and hemostasis in hypertensive, obese, dyslipidemic patients with and without diabetes mellitus.

We have recently reported that dietary fish oil supplementation (n-3) polyunsaturated fatty acid (PUFA) led to a reduction in blood pressure (BP) and serum triglycerides (TG), in addition to the normalization of the hypercoagulable state in subjects with obesity, hypertension and dyslipidemia without diabetes mellitus (OHD-DM). The aim of the present study was to explore the mechanism of this amelioration by comparing the previous results to those obtained from 19 subjects who, in addition to the conditions described above, also suffer from diabetes mellitus (OHD+DM) and proteinuria. In both the non-diabetic and diabetic groups, a similar reduction was observed in BP (from 158.7/80.8 to 146/72.9 mmHg, and from 157.6/83.2 to 141.9/75.6 mmHg, respectively, P<0.001) and TG levels (from 159.2 to 108.0 mg/dl and from 208.7 to 153.1 mg/dl, respectively, P<0.001). However, a favorable reduction in hemostasis parameters (platelet aggregation on extracellular matrix and (alpha2-antiplasmin) was only seen among the nondiabetic patients (from 12.1+/-4.9 to 4.2+/-3.2%, P<0.001). This difference may stem from a less efficient exchange between n-3 and n-6 PUFA in serum phospholipid of the OHD+DM patients. Overall, this 13-day fasting/refeeding method developed by us has proven to cause the rapid exchange of arachidonic acid for eicosapentaenoic acid. It appears to be an effective regimen for the reduction of cardiovascular risk factors (BP, TG and hemostatic variables) in OHD-DM patients and to a lesser extent in OHD+DM patients.