Best Medication To Lower Diastolic Blood Pressure – Address correspondence to Maria H. Mehlum, Department of Geriatric Medicine, Oslo Ullevaal University Hospital, Kirkeveien 166, NO-0407 Oslo, Norway. E-mail
Stroke Prevention Research Unit, Nuffield Department of Clinical Neurology, John Radcliffe Hospital, University of Oxford, UK (P.M.R.)
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Blood pressure lowering drugs have different blood pressure lowering profiles. We investigated whether differences in mean and variability of blood pressure could explain differences in the risks of cardiovascular events and death among 15,245 high-risk hypertensive patients randomized to valsartan or amlodipine and followed for 4.2 years in the VALUE (valsartan antihypertensive long-term use evaluation) trial. We selected patients with ≥ 3 visits and performed a Cox regression analysis with mean blood pressure as a time-dependent covariate and visit-to-visit and within-visit blood pressure variability as the SD. Of 14,996 eligible patients, participants in the valsartan group had a 2.2 mm Hg higher mean systolic blood pressure. sl., higher systolic deviation from visit to visit by 1.4 mm Hg. sl. and higher systolic fluctuation during the visit by 0.2 mmHg. 0.0001). The higher risk of myocardial infarction and stroke in the valsartan group was reduced after adjustment for mean and variability of systolic blood pressure, with an HR of 1.19 (95% CI, 1.02-1.39) to 1.11 (0 .96-1.30 ) and with HR of 1.13 (0.96). –1.33) to 1.00 (0.85–1.18). The lower risk of congestive heart failure in the valsartan group was accentuated after adjusting for heart rate from 0.86 (0.74-1.00) to 0.76 (0.65-0.89). A smaller effect was observed for the risk of death from 1.01 (0.92–1.12) to 0.94 (0.85–1.04). In conclusion, the higher risk of myocardial infarction and stroke in patients randomized to valsartan compared to amlodipine was related to different blood pressure modulation profiles of the drugs. The risk of congestive heart failure was lower with valsartan, regardless of the less favorable blood pressure modulation profile.
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Despite findings in randomized controlled trials that drug classes have different effects on the prevention of cardiovascular events at the same level of reduction in mean arterial pressure.
One of the reasons for the different clinical effects may be that antihypertensive drugs affect the neurohumoral systems differently.
Or in patients with different blood pressure phenotypes. Another reason may be that they have different effects on blood pressure,
For example, greater between-visit blood pressure variability for a given reduction in mean blood pressure for angiotensin receptor blockers or β-blockers than for calcium channel blockers.
Is There A Cure For High Blood Pressure?
But the significance of blood pressure variability for the clinical effects of drugs has not been investigated.
The VALUE study compared treatment with the angiotensin receptor blocker valsartan and the calcium channel blocker amlodipine and provided an opportunity to evaluate the importance of the blood pressure lowering profiles of individual groups of drugs for their clinical effect.
To date, this study is the only large study comparing these 2 mainstays of hypertension treatment. We investigated whether differences in mean blood pressure or blood pressure variability, or both, could explain differences in the risks of myocardial infarction, stroke, congestive heart failure, and death between patients treated with the angiotensin receptor blocker valsartan or the calcium channel blocker amlodipine. VALUE test. The results refer to angiotensin receptor blockers and calcium channel blockers and do not necessarily reflect the general feature of antihypertensive agents. The aim was to identify patterns of blood pressure effect rather than the absolute magnitude of the differences.
The VALUE study was a multinational, randomized, controlled, double-masked comparison of valsartan with amlodipine in 15,245 patients with hypertension and at least 1 additional cardiovascular risk factor. Patients were randomly assigned to amlodipine 5 mg or valsartan 80 mg, and during the first 6 months the doses were increased and thiazide diuretics or other antihypertensives could be added to achieve a target blood pressure of <140/90 mmHg. The methods and main results of the VALUE study have been described previously.
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The trial was held in accordance with the Declaration of Helsinki. All patients provided written informed consent and the study protocol was approved by ethics committees in all participating countries. Data supporting the conclusions of this analysis are available from the corresponding author upon reasonable request.
Clinical visits were made monthly during the first 6 months and then every 6 months, but for a maximum of 72 months (17 visits). Blood pressure was measured in the morning, 24 hours after the last dose. Measurements were taken 3 times during each visit with the patient seated, after 5 minutes of rest, using a calibrated standard sphygmomanometer or a validated digital device. The average blood pressure at each visit was determined as the average of all 3 measurements. We defined blood pressure variability as the SD of mean blood pressure across all visits (between-visit blood pressure variability) and as the SD of 3 blood pressure measurements at each visit averaged across all visits (within-visit variability). . We also calculated the coefficient of variation.
In this analysis, we included patients with 3 or more visits from baseline to 60 months (visits 1–15), as only 187 patients (1.2%) had follow-up visits at 60 months ( Fig. 1 ). In addition, we defined a target population of patients who received valsartan or amlodipine alone (with or without diuretics) and who were not abstinent from treatment for a total of more than 30 days (Figure 1). To avoid the effect of high blood pressure decline and variability during the dose titration period, we also defined a population of patients who had no cardiovascular events during the first 6 months and assessed the significance of mean blood pressure and blood pressure variability over 6 months. forward for the risk of future events (Figure 1).
Finally, we defined a population of patients without cardiovascular events during the first 18 months to evaluate the effect of mean blood pressure and blood pressure variability during the first 18 months on the risk of events after 18 months (Figure 1).
Mechanism(s) Of Systolic Blood Pressure Reduction And Drug Therapy In Hypertension
For this analysis, we used the primary endpoints of the components in the VALUE study (nonfatal or fatal myocardial infarction, stroke, and congestive heart failure) and death as defined in the primary report.
Stroke included ischemic stroke, hemorrhagic stroke, and unclassified stroke, and congestive heart failure included chronic congestive heart failure requiring hospitalization. We counted the first occurrence of each endpoint, but each patient could contribute to all endpoints. Because myocardial infarction and heart failure are closely related, we included only congestive heart failure events that were not preceded by myocardial infarction.
The main analysis included all patients with 3 or more visits from baseline to 60 months. We compared baseline characteristics and blood pressure profiles during follow-up in the 2 treatment groups using t-tests and X
Tests for continuous and categorical variables, or Cardiovascular events were analyzed by time to first event using Cox regression models. We examined the effect of medications on blood pressure by stepwise adjustment for mean systolic blood pressure, systolic blood pressure variability, and clinical risk factors. The goal was to detect patterns of effect rather than magnitude, meaning that P values of differences in effects were not of particular interest. First, we adjusted for mean blood pressure, then for visit or within-visit blood pressure variability, then for mean blood pressure and both forms of blood pressure variability, and finally for all risk factors, including clinical risk factors: age, sex, history of myocardial infarction , history of transient ischemic attack (TIA)/stroke, history of peripheral artery disease, left ventricular hypertrophy and history of atrial fibrillation. Mean systolic blood pressure was analyzed as a continuous variable.
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To account for possible changes in mean pressure over time, it was entered into the model as a segmented time-dependent variable,
Meaning that the average blood pressure at each time point was determined as the average of all 3 measurements at the previous visit. Visit-to-visit variability in systolic blood pressure was entered into the model as a categorical variable in SD quintiles, using the lowest quintile category as the reference category to account for possible non-linear effects on events.
The proportional hazards assumption was tested using the log minus log for each variable in the model.
We repeated the analyzes using mean blood pressure, defined as the average of all visits, analyzed as an ordinal, time-independent continuous variable, which reduces the measurement error associated with using mean blood pressure for individual visits in time-dependent analyses. We also repeated the analysis using visit-to-visit blood pressure variability as a continuous variable and using the coefficient of variation as a measure of blood pressure variability.
Hypertension And Hypotension Notes: Diagrams & Illustrations
We also performed a sensitivity analysis of alternative patient samples. We first performed the analysis in the target population of patients who received valsartan or amlodipine alone (with or without diuretics) and who were not abstinent for more than 30 days overall. Second, we repeated the analysis in patients without cardiovascular events during the first 6 months and evaluated the effect of mean blood pressure and blood pressure variability from month 6. Third, we repeated the analysis in patients without events during the first 18 months and evaluated the effect of blood pressure during the first 18 months on
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