Blood pressure-lowering activity of statins: a systematic literature review and meta-analysis of placebo-randomized controlled trials.

PURPOSE: To investigate the blood pressure (BP)-lowering effects of statins by conducting a systematic review and meta-analysis of placebo-randomized controlled trials (RCTs). METHOD: We conducted a meta-analysis of placebo RCTs reporting antihypertensive effects of statins therapy. We only included RCTs that did not allow for concomitant antihypertensive therapy, or clearly stated that antihypertensive therapy was fixed throughout the study period. RESULTS: Our meta-analysis included 46 placebo RCTs, including 53 group comparisons and a total of 49,087 participants (24,589 participants in the statin groups and 24,498 participants in the placebo group). Subgroup analysis, based on use of concomitant antihypertensive, was performed. The meta-analysis showed that statin reduced systolic BP by - 1.6 mmHg (95% CI: - 2.50 to - 0.60), and diastolic BP by - 0.96 mmHg (95% CI: - 1.36 to - 0.56). Although the presence of concomitant antihypertensive therapy diluted the BP lowering effect of statins, it remained statistically significant and independent of the lipid-lowering activity. Furthermore, the BP -lowering effect of the statins was independent of the dose or type of statin (p > 0.05). CONCLUSION: Our results strengthen the evidence for pleiotropic effects of statins on BP that are independent of their lipid-lowering activity, supporting their beneficial role in hypertensive patients with dyslipidemia.

2024 Recommendations for Validation of Noninvasive Arterial Pulse Wave Velocity Measurement Devices.

BACKGROUND: Arterial stiffness, as measured by arterial pulse wave velocity (PWV), is an established biomarker for cardiovascular risk and target-organ damage in individuals with hypertension. With the emergence of new devices for assessing PWV, it has become evident that some of these devices yield results that display significant discrepancies compared with previous devices. This discrepancy underscores the importance of comprehensive validation procedures and the need for international recommendations. METHODS: A stepwise approach utilizing the modified Delphi technique, with the involvement of key scientific societies dedicated to arterial stiffness research worldwide, was adopted to formulate, through a multidisciplinary vision, a shared approach to the validation of noninvasive arterial PWV measurement devices. RESULTS: A set of recommendations has been developed, which aim to provide guidance to clinicians, researchers, and device manufacturers regarding the validation of new PWV measurement devices. The intention behind these recommendations is to ensure that the validation process can be conducted in a rigorous and consistent manner and to promote standardization and harmonization among PWV devices, thereby facilitating their widespread adoption in clinical practice. CONCLUSIONS: It is hoped that these recommendations will encourage both users and developers of PWV measurement devices to critically evaluate and validate their technologies, ultimately leading to improved consistency and comparability of results. This, in turn, will enhance the clinical utility of PWV as a valuable tool for assessing arterial stiffness and informing cardiovascular risk stratification and management in individuals with hypertension.

Postprandial effect of dietary fat quantity and quality on arterial stiffness and wave reflection: a randomised controlled trial.

BACKGROUND: Arterial stiffness is a component of vascular function and an established risk factor for cardiovascular disease. There is a lack of conclusive evidence on the effect of a meal rich in monounsaturated fat (MUFA) compared with an isoenergetic meal rich in saturated fat (SFA) on postprandial vascular function and specifically on arterial stiffness. METHODS: Twenty healthy, non-smoking males (BMI 24 ± 2 kg/m2; age 37.7 ± 14.4 y) participated in this single-blind, randomised, cross-over dietary intervention study. Each subject was randomised to receive a high-fat test-meal (3 MJ; 56 ± 2 g fat) at breakfast on 2 separate occasions, one rich in oleic acid (MUFA-meal) and one rich in palmitic acid (SFA-meal), and the meals were isoenergetic. Blood pressure (BP), arterial stiffness (PWV) and arterial wave reflection (augmentation index, AIx) were measured using applanation tonometry at baseline and every 30 minutes up to 4 hours after the ingestion of the test-meals. RESULTS: All subjects completed both arms of the dietary intervention. There was no significant difference in BP parameters, PWV or AIx at baseline between the two treatments (P > 0.05). There was a significant increase in brachial and aortic BP, mean arterial pressure (MAP), heart rate and PVW (time, P < 0.05) over the four hours after consumption of the fat-rich test-meal although the increase in PWV was no longer significant when adjusted for the increase in MAP. There was no difference in PWV between the two treatments (treatment*time, P > 0.05). There was a significant reduction in AIx (time, P < 0.05) over the four hour postprandial period although this was no longer significant when adjusted for the increase in heart rate and MAP (time, P > 0.05). There was no difference in AIx between the two treatments (treatment*time, P > 0.05). However, the reduction in heart rate corrected augmentation index (AIx75) was significant when corrected for the increase in MAP (time, P < 0.01) with no differential effect of the treatments (treatment*time, P > 0.05). CONCLUSIONS: This study has demonstrated a BP dependent increase in PWV and a decrease in arterial wave reflection in the four hour period in response to a high-fat meal. There was no evidence however that replacement of some of the SFA with MUFA had a differential effect on these parameters. The study highlights the need for further research to understand the effects of the substitution of SFA with MUFA on non-serum, new and emerging risk factors for CVD such as arterial stiffness.

Impact of the 2017 ACC/AHA guideline on the prevalence of elevated blood pressure and hypertension: a cross-sectional analysis of 10 799 individuals.

OBJECTIVES: To assess the effect of the 2017 American College of Cardiology and the American Heart Association (ACC/AHA) hypertension guideline on the prevalence of elevated blood pressure (BP) and hypertension and the initiation of antihypertensive treatment, as well as the level of adherence to the BP target in the Saudi population. DESIGN: A cross-sectional study. PARTICIPANTS: A total of 10 799 adults (≥18 years old), with three BP readings during 2017-2020 from the Saudi Biobank was used. PRIMARY OUTCOME: Hypertension was defined using three sources: the Joint National Committee 7 Blood Pressure Guideline (JNC-7) guideline (systolic BP (SBP)≥140 or diastolic BP (DBP)≥90 mm Hg), the 2017 ACC/AHA guideline (SBP≥130 or DBP≥80 mm Hg) and a self-reported hypertension diagnosis. RESULTS: The prevalence of hypertension, according to the JNC-7 guideline, was 14.49% (95% CI 14.37 to 14.61), and the 2017 ACC/AHA, 40.77% (95% CI 40.60 to 40.94), a difference of 26.28%. Antihypertensive medication was recommended for 24.84% (95% CI 24.69 to 24.98) based on the JNC-7 guideline and 27.67% (95% CI 27.52 to 27.82) using the 2017 ACC/AHA guideline. Lifestyle modification was recommended for 13.10% (95% CI 12.47 to 13.74) of patients with hypertension who were not eligible for a pharmacological intervention, based on the 2017 ACA/AHA guideline. For patients with prescribed antihypertensive medication, 49.56% (95% CI 45.50 to 53.64) and 27.81% (95% CI 24.31 to 31.59) presented with a BP reading above the treatment goal, based on the 2017 ACA/AHA and JNC-7 guidelines, respectively. Using the two definitions, the risk factors were older age, male gender, diabetes diagnosis, increased body mass index, waist circumference and waist-to-hip ratio. CONCLUSIONS: According to the 2017 ACC/AHA guideline, the prevalence of hypertension has increased significantly, but there was only a small increase in the proportion of patients recommended for antihypertensive treatment. A large proportion of patients with prescribed antihypertensive medication, had a BP above the target. Unless public health prevention efforts are adopted, the increased prevalence of elevated BP and hypertension will increase cardiovascular disease.

Prevalence and clinical correlates of ambulatory blood pressure phenotypes in a Saudi hypertensive population.

International Guidelines recommend ambulatory blood pressure monitoring (ABPM) for the management of hypertension. ABPM phenotypes predict outcomes independent of office blood pressure (BP). The authors explored the prevalence and clinical correlates of ABPM phenotypes and relationship with office BP in Saudi patients (n = 428, mean age 53.5 ± 14.6, 55% male) referred to a Specialist Hypertension clinic in Riyadh, Saudi Arabia. ABPM phenotypes included sustained normotension (27%), masked hypertension, MHT(32%), sustained hypertension, SHT(52%), and white coat hypertension(2.6%). MHT was more prevalent using asleep than 24-hours (26.4% vs 12.9%, P < .01) or awake BP (26.4% vs 8.5%, P < .001) and observed in 85% of pre-hypertensive patients. Isolated nocturnal hypertension was more prevalent in MHT vs SHT (70% vs 30%, P < .001). Office BP overestimated control rates compared with ABPM (48% vs 12.9%, P < .001). Our study shows that one in three Saudi patients will be managed inappropriately if office BP alone was relied upon for management of hypertension.

How to check whether a blood pressure monitor has been properly validated for accuracy.

Hypertension guidelines recommend that blood pressure (BP) should be measured using a monitor that has passed validation testing for accuracy. BP monitors that have not undergone rigorous validation testing can still be cleared by regulatory authorities for marketing and sale. This is the situation for most BP monitors worldwide. Thus, consumers (patients, health professionals, procurement officers, and general public) may unwittingly purchase BP monitors that are non-validated and more likely to be inaccurate. Without prior knowledge of these issues, it is extremely difficult for consumers to distinguish validated from non-validated BP monitors. For the above reasons, the aim of this paper is to provide consumers guidance on how to check whether a BP monitor has been properly validated for accuracy. The process involves making an online search of listings of BP monitors that have been assessed for validation status. Only those monitors that have been properly validated are recommended for BP measurement. There are numerous different online listings of BP monitors, several are country-specific and two are general (international) listings. Because monitors can be marketed using alternative model names in different countries, if a monitor is not found on one listing, it may be worthwhile cross-checking with a different listing. This information is widely relevant to anyone seeking to purchase a home, clinic, or ambulatory BP monitor, including individual consumers for use personally or policy makers and those procuring monitors for use in healthcare systems, and retailers looking to stock only validated BP monitors.

Ambulatory arterial stiffness index, pulse wave velocity and augmentation index--interchangeable or mutually exclusive measures?

BACKGROUND: The ambulatory arterial stiffness index (AASI) has been proposed as a novel measure of arterial stiffness and has been prospectively shown to predict stroke and cardiovascular death, but not cardiac death. This index has prompted considerable controversy as to whether it is a true measure of arterial stiffness. OBJECTIVE AND METHODS: The present study aimed to examine three different measures of arterial stiffness - pulse wave velocity (PWV; Complior), wave reflection [augmentation index (AIx)] and AASI - in a large hypertensive population, comparing their determinants and intercorrelations, both unadjusted and adjusted for confounders, and using Bland-Altman analysis to determine 95% confidence intervals for the ability of the AASI to predict PWV, the proposed gold standard of arterial stiffness. RESULTS: The AASI correlated univariately with both PWV and the AIx in individuals overall (r = 0.28 for PWV and r = 0.24 for AIx; both P < 0.001) and in those with untreated or treated hypertension. Adjustment for age in the current study negated entirely the positive correlation between the AASI, PWV and AIx. Additional adjustment for confounders did not significantly alter these nonsignificant relationships. Furthermore, the 95% prediction limits for the AASI to predict PWV were +/- 4.18 m/s and for the AASI to predict AIx were +/- 25.4%, suggesting that the methods would not be interchangeable in a clinical setting. Direct comparative studies would be required to establish the relative predictive strength of each measure and whether combining measures can provide additional risk prediction. Until such data become available, we propose that the measures should not be considered interchangeable.

Beta-blockers reduce aortic stiffness in hypertension but nebivolol, not atenolol, reduces wave reflection.

BACKGROUND: There is conflicting information with regard to the effect of beta-blockers on arterial stiffness and wave reflection. We compared a vasodilating beta-blocker, nebivolol, with atenolol. METHODS: We randomized 40 subjects with untreated hypertension (mean +/- s.e.m. systolic/diastolic blood pressure (BP) of 160 +/- 3/98 +/- 1 mm Hg, age 49 +/- 1 years) 16 of whom were women, to atenolol 50 mg or nebivolol 5 mg daily for 4 weeks. Arterial stiffness was assessed in terms of carotid-femoral pulse wave velocity (PWV, Complior) and arterial wave reflection (augmentation index (AIx) by applanation tonometry, Sphygmocor). RESULTS: Both beta-blockers produced an equal reduction in brachial BP but aortic pulse pressure (PP) was reduced to a greater extent by nebivolol (P < 0.05). PWV was decreased significantly by both therapies (nebivolol: from 11.5 +/- 0.5 to 9.9 +/- 0.5 m/s; atenolol: from 11.1 +/- 0.4 to 9.8 +/- 0.4 m/s; P < 0.01) but only nebivolol significantly reduced AIx (from 35 +/- 5 to 28 +/- 2%, P < 0.05). In addition, whereas PP amplification (PP, mm Hg) decreased with atenolol therapy (from 10 +/- 1 to 7 +/- 1, P < 0.01), it increased with nebivolol therapy (from 8 +/- 1 to 14 +/- 3, P < 0.01). Atenolol reduced heart rate to a greater extent than nebivolol did (14 +/- 3/min reduction by atenolol vs. 8 +/- 2/min reduction by nebivolol, P < 0.05). There was no difference between the two treatments in respect of the effect on transit time. CONCLUSION: The beta-blockers, atenolol and nebivolol, have a similar effect in reducing arterial stiffness in the large elastic aorta, largely secondary to BP reduction. Nebivolol, in contrast to atenolol, has an effect on small muscular arteries, increasing PP amplification and reducing wave reflection, possibly because of increased levels of nitric oxide (NO). Such ancillary properties may impart important distinct hemodynamic effects, and therefore beta-blockers cannot be regarded as a homogeneous group.

History of gestational hypertension is associated with the metabolic syndrome and masked hypertension but not arterial stiffness in women with essential hypertension.

The underlying mechanisms of subsequent increased risk of cardiovascular disease with a history of gestational hypertension (GH) are not known. Untreated hypertensive women (n=155, age 43+/-1 years) underwent ambulatory blood pressure (BP) monitoring and assessment of aortic pulse wave velocity (PWV) and augmentation index (AIx). Despite identical clinic BP readings, the group of women with GH (n=54) had higher (P=.002) ambulatory daytime systolic BP levels and a greater number of extreme nocturnal dippers (P=.005) than the group without GH. Women with GH had higher body mass index (P=.003), greater waist circumference (P=.02), higher levels of triglycerides (P=.002), lower levels of high-density lipoprotein cholesterol (P=.004), a higher prevalence of the metabolic syndrome (P<.05) and microalbuminuria (P=.004), higher plasma renin activity (P=.03), and higher aldosterone levels (P=.01). There was no significant difference in PWV and AIx between the 2 groups. The higher prevalence of the metabolic syndrome, microalbuminuria, masked hypertension, and activation of the renin-angiotensin-aldosterone system but not arterial stiffness may explain the subsequent propensity to high BP and cardiovascular disease in women with GH.

Circadian blood pressure variation: relationship between dipper status and measures of arterial stiffness.

BACKGROUND: Compared with dippers, hypertensive individuals with a nondipping nocturnal blood pressure (BP) profile have more target organ damage and a worse cardiovascular prognosis, potentially mediated through arterial stiffness. OBJECTIVE: To examine arterial stiffness and dipping in a population of 314 untreated hypertensive individuals, mean age 48 +/- 8 years, 55% men. METHODS: Dipping was defined as a 10-20% fall in nocturnal BP; extreme dipping as greater than 20%, nondipping as less than 10%, and reverse-dipping as 0% at most fall in nocturnal BP. Aortic pulse wave velocity (PWV) (Complior) and augmentation index (Sphygmocor) were measured. RESULTS: Groups did not differ by age, gender, 24-h or daytime mean BP, body mass index, smoking, cholesterol, glucose, renin or aldosterone. The relationship between PWV and dipper-status was J-shaped, with extreme-dippers and reverse-dippers having the highest PWV. Nondippers and reverse-dippers had significantly higher age and sex-adjusted PWV compared with dippers. Following multivariate adjustment for age, gender, mean arterial pressure, heart rate and smoking, reverse-dippers had significantly higher PWV than either dippers or nondippers (P = 0.005 and P = 0.006, respectively). Dipper status was not associated with augmentation index. CONCLUSIONS: A reverse-dipper pattern, corresponding to the 95% percentile of the night: day BP ratio on ambulatory BP monitoring, identifies a population group with increased PWV. This difference could not be explained by the measured risk factors. Reverse-dippers had significantly less day: night variability in heart rate and wider pulse pressures at night than any of the other groups, suggesting altered sympathetic tone at night as a potential mechanism.

Comparison of echocardiographic measures of left ventricular diastolic function in early hypertension.

Left ventricular (LV) diastolic dysfunction identifies patients at risk of developing heart failure and may be common in patients with hypertension. The prevalence of LV diastolic dysfunction in patients with newly diagnosed hypertension was compared using criteria provided by the Canadian Consensus, European Study Group, and American Medical Association guidelines. One hundred twenty patients with newly diagnosed untreated hypertension (mean age 46.9 +/- 2.1 years; 62 men, 58 women) with increased blood pressure (clinic >140/90 mm Hg, daytime ambulatory >135/85 mm Hg) underwent comprehensive 2-dimensional echocardiography. Transmitral inflow velocities were measured using pulse-wave Doppler with and without Valsalva's maneuver, and a comprehensive assessment of tissue Doppler velocities was performed. The prevalence of LV diastolic dysfunction varied according to criteria used. There was a high prevalence of LV diastolic dysfunction (59%; n = 71) using Canadian Consensus guidelines; 27% of patients (n = 32) had a pseudonormal pattern unmasked using Valsalva's maneuver and 32% (n = 39) had impaired relaxation at rest. Significantly fewer patients (10%; n = 12) had this diagnosis using European or American Medical Association guidelines (23%; n = 27). Using tissue Doppler imaging (early-late diastolic velocity ratio <1), the prevalence of LV diastolic dysfunction was 59% (n = 71), identical to findings using the Canadian Consensus guidelines. In conclusion, current national consensus guidelines defining LV diastolic dysfunction varied widely and underdiagnosed LV diastolic dysfunction in patients with newly diagnosed hypertension. Tissue Doppler imaging assessment is a rapidly and widely available tool that is as sensitive as the most stringent national guidelines and should be systematically incorporated into a more comprehensive assessment of LV diastolic dysfunction in this population.

Choice of first antihypertensive: simple as ABCD?

BACKGROUND: The AB/CD British Hypertension Society guidelines predict that the blood-pressure response to antihypertensive agents A (angiotensin-converting enzyme inhibitors and angiotensin receptor blockers) or B (beta blockers) drugs is better in those aged<55 years, whereas that to agents C (calcium channel blockers) or D (diuretics) agents is better in those aged>or=55 years. METHODS: We conducted a cohort study of 175 consecutive, untreated, hypertensive whites (55% men), aged 19 to 80 years and prospectively randomized to either A/B or C/D antihypertensive agents, and in whom there was no compelling reason to choose a particular drug. Blood pressure (BP) was measured using a semiautomated device (Omron 705CM, Tokyo, Japan) at baseline and 4 weeks after therapy in a single, blind fashion. RESULTS: There was no difference in baseline BP (mean+/-SEM, A/B, 163+/-2/97+/-1 v C/D, 163+/-2/95+/-1 mm Hg). Whereas the A/B drugs were more effective in younger than older patients, expressed as percentage of reduction (13%+/-1%/12%+/-1% v 8.5%+/-1%/7%+/-1%, P<.01), as absolute reduction, or by classification of mean+/-SEM blood pressure into stages of hypertension, the C/D drugs were no more effective than A/B drugs in those aged>55 years. CONCLUSIONS: The arbitrary choice of age 55 years to predict the response to antihypertensive agents in a white population is not supported by our data. A prospective, multicenter study is required to underpin guideline recommendations in relation to using age as a determinant for choice of a particular antihypertensive drug in defined hypertensive populations.

Advanced glycation end-products and arterial stiffness in hypertension.

BACKGROUND: The formation of advanced glycation end-products is associated with arterial stiffness in experimental models and alagebrium (formerly known as ALT-711), an advanced glycation end-product cross-link breaker, has been shown to reduce arterial stiffness in elderly subjects. METHODS: We related plasma concentrations of advanced glycation end-products (AGEs), measured using a noncompetitive immunoassay, and markers of aortic stiffness-pulse wave velocity (PWV) and augmentation index (AIx), a measure of aortic wave reflection-in 46 subjects, aged 47 +/- 2 years, comprising 30 untreated hypertensive and 16 normotensive subjects. Results were analyzed using univariate and multiple logistic regression analysis. RESULTS: Plasma AGEs were significantly higher in hypertensive than in normotensive subjects (7.8 +/- 1 v 3 +/- 1 mug/ml; P < .0001). There was a significant relationship between plasma AGEs and aortic PWV (r = 0.49, P < .01), but not with AIx. In a stepwise regression model age, plasma AGE levels, smoking status, and total cholesterol explained 67% of the variability in PWV. For AIx, the only variables that entered the model were age, gender, and heart rate (R(2) = 0.53, P < .0001) with no contribution from plasma AGEs. CONCLUSIONS: Concentration of plasma AGEs is significantly higher in hypertensive than in normotensive subjects and related to aortic stiffness independent of age and blood pressure, with no relationship with aortic wave reflection. Plasma AGEs may play a blood pressure-independent role in large but not small vessel remodeling in essential hypertension.

Choice of first antihypertensive--are existing guidelines ignored?

AIMS: To determine adherence to hypertension guidelines in relation to age and diabetes. METHODS: The Irish HSE-PCRS prescribing database identified patients initiating antihypertensive monotherapy in 2005. Logistic regression predicted the likelihood of therapy according to guidelines. RESULTS: The odds ratio (OR) of receiving therapies according to the guideline recommendations in those <55 years vs. > or =55 years was 1.31 (95% CI 1.26, 1.37). Diabetics were more likely than nondiabetics to receive antihypertensives other than beta-adrenoceptor blockers (OR 2.97, 95% CI 2.74, 3.21). CONCLUSIONS: Our findings show some adherence to the guidelines in relation to age but selective prescribing of antihypertensives for diabetics.

Aldosterone-to-renin ratio, arterial stiffness, and the response to aldosterone antagonism in essential hypertension.

BACKGROUND: Some 10% to 15% of hypertensive patients have hyperaldosteronism, an increased ambulant aldosterone-to-renin ratio. As aldosterone reduces arterial compliance, we examined the relationship between aldosterone-to-renin ratio, aortic blood pressure (BP), arterial stiffness, and the effect of spironolactone in a hypertensive population. METHODS: In 24 untreated patients (mean age 51 +/- 2 years, 10 women), we assessed arterial stiffness by augmentation index-height of the late systolic peak in the aorta, pulse pressure (Sphygmocor), and aortic pulse wave velocity (Complior). RESULTS: There were significant positive correlations between the aldosterone-to-renin ratio and aortic systolic pressure, aortic pulse pressure, and augmentation index and negative correlations with pulse pressure amplification, but none with brachial BP or pulse wave velocity. After randomization in a cross-over design to 50 mg of spironolactone or 2.5 mg of bendroflumetazide for 4 weeks with washout period of 1 month, both drugs significantly reduced brachial BP, but only spironolactone reduced (P < .001) pulse wave velocity and augmentation index, which remained significant when corrected for its greater reduction in mean BP. There were significant (P < .001) positive correlations between the ratio and decrease in aortic systolic (r = 0.78), mean (r = 0.75), diastolic BP (r = 0.66), aortic pulse pressure (r = 0.69, augmentation index (r = 0.64) and with, brachial systolic pressure (r = 0.66), brachial pulse pressure (r = 0.44, P < .05) and pulse pressure amplification (r = 0.46, P < .05). Such relationships were not found with pulse wave velocity. CONCLUSIONS: The aldosterone-to-renin ratio may have an important role in determining arterial stiffness, particularly wave reflection and aortic systolic pressure and is of predictive value for the responsiveness to spironolactone. Aldosterone antagonism has BP-independent effects on arterial stiffness.

Adiponectin and arterial stiffness.

BACKGROUND: Adiponectin, an anti-inflammatory adipocytokine, is reduced in hypertension, diabetes, and coronary artery disease (CAD). Arterial stiffness, as aortic pulse wave velocity (PWV) in hypertension and diabetes, and as augmentation index (AIx) in CAD, is independently associated with cardiovascular mortality. We explored the relationship between adiponectin and arterial stiffness in essential hypertension. METHODS: Seventy-six untreated patients, 34 women, aged 47 +/- 1 years, mean +/- SEM with essential hypertension, had blood pressure (BP), carotid-femoral PWV, AIx plasma adiponectin, and proinflammatory cytokine C-reactive protein (CRP) measured using ELISA technique after an overnight fast. Results were analyzed using univariate and multiple logistic regression analysis. RESULTS: There was a significant positive relationship between log adiponectin and AIx (r = 0.33, P < .005) and plasma HDL-cholesterol (r = 0.40, P < .001). In contrast there were significant negative relationships with PWV (r = -0.24, P < .05), transit time (r = -0.37, P < .001), and pulse pressure amplification (r = -0.30, P < .005) in addition to waist circumference, waist-to-hip ratio, height, and weight. In a stepwise regression model, the independent predictors of AIx were heart rate, height, mean arterial pressure, age, and gender (R2= 0.69, P < .0001) with no contribution from adiponectin. However, for PWV (R2= 0.59, P < .0001) the independent determinants were mean arterial pressure, age, and adiponectin. CONCLUSIONS: These results show a divergent relationship between adiponectin and arterial stiffness, negative for PWV, and positive for wave reflection (AIx). Anthropomorphic factors, particularly height, weight, and heart rate may influence the relationship to the latter. Adiponectin is an independent predictor of aortic PWV but not of AIx.

Does aldosterone-to-renin ratio predict the antihypertensive effect of the aldosterone antagonist spironolactone?

BACKGROUND: The recognition that some 10% to 15% of the hypertensive population may have aldosterone excess has increased the frequency of measurement of the aldosterone-to-renin ratio (ARR) and the use of aldosterone antagonists. Whether this ratio will predict the blood pressure (BP) response to spironolactone is not clear. METHODS: We correlated the BP response to spironolactone 50 mg/day to baseline ARR in 69 hypertensive patients (mean [+/-SD] age 57 +/- 2 years, 65% male), consisting of 39 subjects with long-standing hypertension (4.0 +/- 0.2 years) whose hypertension was uncontrolled on at least three antihypertensive medications and 30 previously untreated patients who were randomized in a cross-over design to receive either spironolactone 50 mg/day or bendroflumethiazide 2.5 mg/day for 4 weeks. RESULTS: After 4 weeks of spironolactone, BP in patients with never-treated hypertension was reduced by 18 +/- 3 / 11 +/- 1 mm Hg. There was a highly significant correlation between log ARR and the fall in systolic BP (r = 0.69, P < .001) and diastolic BP (r = 0.45, P < .05). Nine of ten patients with low renin activity (< or =0.5 ng/mL/h) showed a >20-mm Hg fall in systolic BP. No such correlations were seen when BP was reduced by bendroflumethazide 2.5 mg. For patients with resistant hypertension, despite a BP reduction of 28 +/- 3 / 13 +/- 2 mm Hg after 14 weeks of spironolactone, there was no relationship between the reduction in BP and the ARR; however, subjects with pretreatment potassium <4.0 mmol/L had a greater response than those with levels > or =4.0 mmol/L (34 +/- 3 / 16 +/- 2 v 20 +/- 6 / 8 +/- 3 mm Hg, P < .05) CONCLUSIONS: Based on the study results, ARR and low renin activity may predict the response to spironolactone in never-treated hypertensive patients but not in patients taking antihypertensive drugs, possibly because of the effect of these agents on ARR. In such patients a trial of spironolactone is required to assess the BP response.

Taking blood pressure -- no laughing matter!

BACKGROUND: Humour is used commonly to relax subjects when their blood pressure is being measured. However the short-term effect of laughter on blood pressure is not described. METHODS: Sixteen normotensive volunteers had blood pressure measured using a validated automated oscillometric sphygmomanometric device (Omron 705 CP) as control and during three episodes of laughter while viewing a humorous sit-com video. RESULTS: Blood pressure was stable in the control period. There was a significant rise (P<0.01) in systolic blood pressure from 115 mmHg (108-121, mean 95% confidence interval) to 127 mmHg (120-135) during laughing. The increase in diastolic pressure 71 (67-74) to 73 (69-77) mmHg was not significant. CONCLUSION: Laughing has an acute effect on systolic blood pressure. Patients should not be encouraged to laugh when their blood pressure is being measured.

Reduction in arterial stiffness with angiotensin II antagonist is comparable with and additive to ACE inhibition.

We measured the effects of angiotensin II blockade on arterial stiffness, augmentation index (AI%), pulse wave velocity (PWV), and blood pressure (BP) in 12 hypertensive patients (mean 49 +/- 11 years) in a 4-week, randomized, cross-over study comparing valsartan 160 mg/day with captopril 100 mg/day, with a 2-week washout period. Subsequently both therapies were combined. Reductions in PWV and AI% remained significant when corrected for BP. Combined therapy reduced PWV and AI% (P < .05) more than monotherapy, even when corrected for BP. The study shows that angiotensin receptor antagonists reduce arterial stiffness in hypertension comparable with and possibly additive to angiotensin converting enzyme inhibition.