Blood Pressure In Untreated Hypertensive Patients Research Articles

Acute effects of continuous and interval aerobic exercise on 24-h ambulatory blood pressure in long-term treated hypertensive patients

Background Despite antihypertensive therapy, it is difficult to maintain optimal systemic blood pressure (BP) values in hypertensive patients (HPT). Exercise may reduce BP in untreated HPT. However, evidence regarding its effect in long-term antihypertensive therapy is lacking. Our purpose was to evaluate the acute effects of 40-minute continuous (CE) or interval exercise (IE) using cycle ergometers on BP in long-term treated HPT. Methods Fifty-two treated HPT were randomized to CE ( n = 26) or IE ( n = 26) protocols. CE was performed at 60% of reserve heart rate (HR). IE alternated consecutively 2 min at 50% reserve HR with 1 min at 80%. Two 24-h ambulatory BP monitoring were made after exercise (postexercise) or a nonexercise control period (control) in random order. Results CE reduced mean 24-h systolic (S) BP (2.6 ± 6.6 mm Hg, p = 0.05) and diastolic (D) BP (2.3 ± 4.6, p = 0.01), and nighttime SBP (4.8 ± 6.4, p < 0.001) and DBP (4.6 ± 5.2 mm Hg, p = 0.001). IE reduced 24-h SBP (2.8 ± 6.5, p = 0.03) and nighttime SBP (3.4 ± 7.2, p = 0.02), and tended to reduce nighttime DBP ( p = 0.06). Greater reductions occurred in higher BP levels. Percentage of normal ambulatory BP values increased after CE (24-h: 42% to 54%; daytime: 42% to 61%; nighttime: 61% to 69%) and IE (24-h: 31% to 46%; daytime: 54% to 61%; nighttime: 46% to 69%). Conclusion CE and IE reduced ambulatory BP in treated HPT, increasing the number of patients reaching normal ambulatory BP values. These effects suggest that continuous and interval aerobic exercise may have a role in BP management in treated HPT.

Aspirin Administered at Bedtime, But Not on Awakening, Has an Effect on Ambulatory Blood Pressure in Hypertensive Patients

The purpose of this research was to investigate in untreated hypertensive patients the effects on ambulatory blood pressure (BP) of aspirin (ASA) administered at different times of the day. Previous studies have shown that ASA produces an administration time-dependent inhibition of angiotensin II. Low-dose ASA has also been shown to reduce BP when administered before bedtime, as opposed to upon awakening, in normotensive and hypertensive volunteers, and in pregnant women at high risk for preeclampsia. We studied 328 untreated patients with grade 1 hypertension, 44.0 +/- 12.6 years of age, randomly divided into three groups: nonpharmacological hygienic-dietary recommendations, the same recommendations and ASA (100 mg/day) on awakening, or the same recommendations and ASA before bedtime. Blood pressure was measured every 20 min during the day and every 30 min at night for 48 consecutive h before and after 3 months of intervention. After three months of nonpharmacological intervention, there was a small and nonsignificant reduction of BP (<0.2 mm Hg; p = 0.648). Blood pressure was slightly elevated after aspirin on awakening (2.6/1.6 mm Hg in the 24-h mean of systolic/diastolic BP; p = 0.002). A significant BP reduction, however, was observed in the patients who received aspirin before bedtime (6.8/4.6 mm Hg in systolic/diastolic BP; p < 0.001). This prospective trial documents a significant administration time-dependent effect of low-dose ASA on BP in untreated hypertensive patients. The timed administration of low-dose ASA could provide a valuable approach, beyond the secondary prevention of cardiovascular disease, in the added BP control of patients with mild essential hypertension.

Administration-time dependent influence of aspirin on blood pressure in previously untreated hypertensive patients

Several studies have shown statistically significant circadian rhythms in thromboxane and prostacyclin production, circulating platelets, platelet aggregation, clotting and fibrinolytic inhibitors, circulating angiotensin II, angiotensin sensitivity, and the inhibition of platelet aggregation produced by aspirin (ASA). Moreover, ASA exhibits a faster drug-disappearance rate when administered during the morning as compared to the evening. Despite this evidence, previous studies on the potential influence of ASA on blood pressure (BP) have not taken into consideration the chronopharmacological effects of nonsteroidal antiinflammatory drugs. This pilot study investigates the effects of ASA on BP in untreated hypertensive patients who received ASA at different times of the day according to their rest-activity cycle. We studied 78 patients with mild hypertension (36 men), 43.5±11.4 (mean±SD) years of age, divided in 3 groups: non-pharmacological hygienic-dietary recommendations (HDR); HDR and ASA (100 mg/day) on awakening; or HDR and ASA before bedtime. BP and heart rate (HR) were measured every 20 minutes during the day (07:00 to 23:00 hours) and every 30 minutes at night for 48 consecutive hours before and after 3 months of intervention. The circadian pattern of BP in each group was established by population multiple-component analysis [Fernandez & Hermida. Chronobiol Int. 1998;15:191-204]. After 3 months of non-pharmacological intervention, there was a small and non-significant reduction of BP (1.2 mm Hg for systolic BP, 1.4 mm Hg for diastolic BP; P=0.264). There was no effect of ASA on BP when given on awakening (P=0.211). A BP reduction was, however, highly significant when ASA was given before bedtime (decrease of 7.6 and 6.1 mm Hg in systolic and diastolic BP, respectively; P<0.001). There was no significant change in HR in any group. Results indicate a statistically significant administration-time dependent effect of low-dose ASA on BP in untreated patients with mild hypertension. In any trial of ASA effects, inquiries about the time when subjects took the drug are indicated and may account for discrepancies in the literature. Moreover, the influence of ASA on BP demonstrated here indicates the need to identify and control for ASA effects in patients using this drug before or during their participation in antihypertension medication trials. DGES, PM98-0106; PGICT00-PXI-32205PN; University of Vigo.