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The Unrecognized Prevalence of Primary Aldosteronism

Author/s: 
Brown, JM, Siddiqui, M, Calhoun, DA, Carey, RM, Hopkins, PN, Williams, GH, Vaidya, A

Background:

Primary aldosteronism is a nonsuppressible renin-independent aldosterone production that causes hypertension and cardiovascular disease.

 

Objective:

To characterize the prevalence of nonsuppressible renin-independent aldosterone production, as well as biochemically overt primary aldosteronism, in relation to blood pressure.

 

Design:

Cross-sectional study.

 

Setting:

4 U.S. academic medical centers.

 

Participants:

Participants with normotension (n = 289), stage 1 hypertension (n = 115), stage 2 hypertension (n = 203), and resistant hypertension (n = 408).

 

Measurements:

Participants completed an oral sodium suppression test, regardless of aldosterone or renin levels, as a confirmatory diagnostic for primary aldosteronism and to quantify the magnitude of renin-independent aldosterone production. Urinary aldosterone was measured in participants in high sodium balance with suppressed renin activity. Biochemically overt primary aldosteronism was diagnosed when urinary aldosterone levels were higher than 12 µg/24 h.

 

Results:

Every blood pressure category had a continuum of renin-independent aldosterone production, where greater severity of production was associated with higher blood pressure, kaliuresis, and lower serum potassium levels. Mean adjusted levels of urinary aldosterone were 6.5 µg/24 h (95% CI, 5.2 to 7.7 µg/24 h) in normotension, 7.3 µg/24 h (CI, 5.6 to 8.9 µg/24 h) in stage 1 hypertension, 9.5 µg/24 h (CI, 8.2 to 10.8 µg/24 h) in stage 2 hypertension, and 14.6 µg/24 h (CI, 12.9 to 16.2 µg/24 h) in resistant hypertension; corresponding adjusted prevalence estimates for biochemically overt primary aldosteronism were 11.3% (CI, 5.9% to 16.8%), 15.7% (CI, 8.6% to 22.9%), 21.6% (CI, 16.1% to 27.0%), and 22.0% (CI, 17.2% to 26.8%). The aldosterone–renin ratio had poor sensitivity and negative predictive value for detecting biochemically overt primary aldosteronism.

 

Limitation:

Prevalence estimates rely on arbitrary and conventional thresholds, and the study population may not represent nationwide demographics.

 

Conclusion:

The prevalence of primary aldosteronism is high and largely unrecognized. Beyond this categorical definition of primary aldosteronism, there is a prevalent continuum of renin-independent aldosterone production that parallels the severity of hypertension. These findings redefine the primary aldosteronism syndrome and implicate it in the pathogenesis of “essential” hypertension.

 

Primary Funding Source:

National Institutes of Health.

Keywords 
primary aldosteronism hypertension cardiovascular disease

The Effect of Aged Garlic Extract on the Atherosclerotic Process - A Randomized Double-Blind Placebo-Controlled Trial

Author/s: 
Wlosinska, M., Nilsson, A., Hlebowicz, J., Hauggaard, A., Fakhro, M., Lindstedt, S.

Background: One of the most serious secondary manifestations of Cardiovascular Disease (CVD) is coronary atherosclerosis. This study aimed to evaluate whether aged garlic extract (AGE) can influence coronary artery calcification (CAC) and to predict the individual effect of AGE using a standard process for data mining (CRISP-DM).

Method: This was a single-center parallel randomized controlled study in a university hospital in Europe. Patients were randomized, in a double-blind manner, through a computer-generated randomization chart. Patients with a Framingham risk score ≥ 10 after CT scan (n = 104) were randomized to an intake of placebo or AGE (2400 mg daily) for 1 year. Main outcome measures were changes in CAC score and secondary outcome measures changes in blood pressure, fasting blood glucose, blood lipids and inflammatory biomarkers.

Result: 104 patients were randomized and 46 in the active group and 47 in the placebo group were analyzed. There was a significant (p < 0.05) change in CAC progression (OR: 2.95 [1.05-8.27]), blood glucose (OR: 3.1 [1.09-8.85]) and IL-6 (OR 2.56 [1.00-6.53]) in favor of the active group. There was also a significant (p = 0.027) decrease in systolic blood pressure in the AGE group, from a mean of 148 (SD: 19) mmHg at 0 months, to 140 (SD: 15) mmHg after 12 months. The AGE Algorithm, at a selected probability cut-off value of 0.5, the accuracy score for CAC progression was 80%, precision score of 79% and recall score 83%. The score for blood pressure was 74% (accuracy, precision and recall). There were no side-effects in either group.

Conclusions: AGE inhibits CAC progression, lowers IL-6, glucose levels and blood pressure in patients at increased risk of cardiovascular events in a European cohort. An algorithm was made and was used to predict with 80% precision which patient will have a significantly reduced CAC progression using AGE. The algorithm could also predict with a 74% precision which patient will have a significant blood pressure lowering effect pressure using AGE.

Trial registration: Clinical trials NCT03860350, retrospectively registered (1/32019).

Keywords: Aged garlic extract; Blood pressure; CRISP-DM; Calcium score; Data mining; Data science; Double-blinded; Placebo-controlled.

Keywords 
aged garlic extract placebo controlled

Cardiovascular Events and Mortality in White Coat Hypertension: A Systematic Review and Meta-analysis

Author/s: 
M.G., Cohen, J.B., Lotito, M.J., Denker, M.G., Cohen, D.L., Townsend, R.R.

BACKGROUND:

The long-term cardiovascular risk of isolated elevated office blood pressure (BP) is unclear.

PURPOSE:

To summarize the risk for cardiovascular events and all-cause mortality associated with untreated white coat hypertension (WCH) and treated white coat effect (WCE).

DATA SOURCES:

PubMed and EMBASE, without language restriction, from inception to December 2018.

STUDY SELECTION:

Observational studies with at least 3 years of follow-up evaluating the cardiovascular risk of WCH or WCE compared with normotension.

DATA EXTRACTION:

2 investigators independently extracted study data and assessed study quality.

DATA SYNTHESIS:

27 studies were included, comprising 25 786 participants with untreated WCH or treated WCE and 38 487 with normal BP followed for a mean of 3 to 19 years. Compared with normotension, untreated WCH was associated with an increased risk for cardiovascular events (hazard ratio [HR], 1.36 [95% CI, 1.03 to 2.00]), all-cause mortality (HR, 1.33 [CI, 1.07 to 1.67]), and cardiovascularmortality (HR, 2.09 [CI, 1.23 to 4.48]); the risk of WCH was attenuated in studies that included stroke in the definition of cardiovascular events(HR, 1.26 [CI, 1.00 to 1.54]). No significant association was found between treated WCE and cardiovascular events (HR, 1.12 [CI, 0.91 to 1.39]), all-cause mortality (HR, 1.11 [CI, 0.89 to 1.46]), or cardiovascular mortality (HR, 1.04 [CI, 0.65 to 1.66]). The findings persisted across several sensitivity analyses.

LIMITATION:

Paucity of studies evaluating isolated cardiac outcomes or reporting participant race/ethnicity.

CONCLUSION:

Untreated WCH, but not treated WCE, is associated with an increased risk for cardiovascular events and all-cause mortality. Out-of-office BP monitoring is critical in the diagnosis and management of hypertension.

PRIMARY FUNDING SOURCE:

National Institutes of Health.

Keywords 
blood pressure stroke cardiovascular

Impact of High Volume Energy Drink Consumption on Electrocardiographic and Blood Pressure Parameters: A Randomized Trial

Author/s: 
Kaul, Sanjay, Shah, S.A., Szeto, A.H., Farewell, Raechel, Shek, Allen, Fan, Dorothy, Quach, K.N., Bhattacharyya, Mouchumi, Elmiari, Jasmine, Chan, Winny, O'Dell, Kate, Nguyen, Nancy, McGaughey, T.J., Nasir, J.M.

Abstract

Background

Energy drinks have been linked to an increase in emergency room visits and deaths. We aim to determine the impact of energy drinks on electrocardiographic and hemodynamic parameters in young healthy volunteers.

Methods and Results

A randomized, double‐masked, placebo‐controlled, crossover study was conducted in healthy volunteers. Participants consumed 32 oz of either energy drink A, energy drink B, or placebo within 60 minutes on 3 study days with a 6‐day washout period in between. The primary end point of QTc interval and secondary end points of QT interval, PR interval, QRS duration, heart rate, and brachial and central blood pressures were measured at baseline, and every 30 minutes for 240 minutes. A repeated‐measures 2‐way analysis of variance was performed with the main effects of intervention, time, and an interaction of intervention and time. Thirty‐four participants were included (age 22.1±3.0 years). The interaction term of intervention and time was statistically significant for Bazett's corrected QT interval, Fridericia's corrected QT interval, QT, PR, QRS duration, heart rate, systolic blood pressure, diastolic blood pressure, central systolic blood pressure, and central diastolic blood pressure (all P<0.001). The maximum change from baseline in Bazett's corrected QT interval for drinks A, B, and placebo were +17.9±13.9, +19.6±15.8, and +11.9±11.1 ms, respectively (P=0.005 for ANOVA) (P=0.04 and <0.01, respectively compared with placebo). Peripheral and central systolic and diastolic blood pressure were statistically significantly different compared with placebo (all P<0.001).

Conclusion

Energy drinks significantly prolong the QTc interval and raise blood pressure.

Keywords 
energy drinks blood pressure Heart Rate hemodynamics electrocardiography
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