HTN: Alcohol (2015)
Hering D, Kucharska W, Kara T, Somers VK, Narkiewicz K. Potentiated sympathetic and hemodynamic responses to alcohol in hypertensive vs. normotensive individuals. J Hypertens. 2011; 29 (3): 537-541.
PubMed ID: 21252702- Hypertensive patients with Stage One and Stage Two hypertension who were newly diagnosed, never treated for hypertension and free of any other diseases
- Hypertensive status confirmed by 24-hour blood pressure monitoring
- Controls not taking any medication or having any history of chronic diseases.
- Patients with white-coat hypertension
- Controls with masked hypertension.
- Recruitment: Methods not described
- Design: Randomized crossover trial
- Blinding used: Implied with measurements. Participants were blinded to which experimental session (alcohol vs. placebo) they were undergoing.
Intervention
- Effects of oral alcohol intake and placebo on blood pressure (BP), heart rate (HR) and muscle sympathetic nerve activity (MSNA) in hypertensive patients and normotensive controls were examined
- Two experimental sessions (an alcohol session and a vehicle session) were performed at the same time of day on two separate days in random order
- All studies were carried out in the morning after a standard light breakfast
- All participants were asked to abstain from alcohol for at least 36 hours
- After undergoing baseline measurements for 10 minutes, alcohol (1.0g per kg body weight diluted in 500ml of low-caloric orange juice) or vehicle (500ml of low-caloric orange juice) was administered orally over a period of 20 minutes
- 10-minute recordings were performed 10 minutes after completion of drinking either alcohol or placebo.
Statistical Analysis
- Results are expressed as means ±SEM
- Responses to alcohol were analyzed by repeated-measures analysis of variance (ANOVA) with time (before vs. during alcohol) as within-factor and group (hypertensive patients vs. normotensive controls) as between factor
- The P-values for differences within a session were obtained by post-hoc tests
- The key variable was the group-by-time interaction
- P<0.05 was considered significant.
Timing of Measurements
Baseline measurements were obtained before the experimental session, then the same parameters measured again 10 minutes after completion of drinking either alcohol or placebo.
Dependent Variables
- Systolic and diastolic blood pressure (SBP and DBP) measured continuously by the Finapres system
- Heart rate measured continuously from surface electrodes using a 12-lead switch box system
- MSNA measured continuously by obtaining multiunit recordings of postganglionic sympathetic nerve activity to muscle, measured from a muscle fascicle of the peroneal nerve posterior to the fibular head.
Independent Variables
Alcohol (1.0g per kg body weight diluted in 500ml of low-caloric orange juice) or vehicle (500ml of low-caloric orange juice) was administered orally over a period of 20 minutes.Control Variables
- Sex
- Age
- Absence of anti-hypertensive treatment
- Social drinking history.
Initial N
- 24
- Hypertensive patients: 13 (eight males and five females)
- Normotensive controls: 11 (six males and five females).
Attrition (Final N)
No attrition noted: 24 subjects as above.
Age
- 44±2 years for hypertensive patients
- 43±2 years for controls.
Ethnicity
Not described.
Other Relevant Demographics
All participants consumed alcoholic beverages socially (between 100g and 200g of alcohol a week, with the median of 150g in both groups).
Anthropometrics
Not described.
Location
Not described.
Key Findings
- Baseline MSNA and both office and ambulatory BP were significantly elevated in the hypertensive patients as compared to the controls
- There was no significant difference in office and asleep HR
- Hypertensive patients had faster awake HR.
Measurement | Controls | Hypertensive Patients | |
SBP (mmHg) | Office | 133±4 | 148±5** |
Awake | 123±3 | 146±5** | |
Asleep | 112±3 | 133±4** | |
DBP (mmHg) | Office | 75±3 | 87±4** |
Awake | 73±3 | 92±4** | |
Asleep | 66±3 | 81±3** | |
Heart Rate (bpm) | Office | 70±3 | 72±2 |
Awake | 76±3 | 86±3* | |
Asleep | 69±3 | 76±3 | |
MSNA (bursts per minute) | 28±2 | 38±2* |
*P<0.01
** P<0.001 vs. controls.
- Placebo had no significant effect on MSNA, BP or HR in either group
- In normotensive individuals, alcohol had no significant effect on blood pressure (SBP increased by 1±4mmHg). By contrast, SBP increased after alcohol in hypertensive patients by 24±6mmHg (P<0.001 vs. controls).
- The alcohol-related increase in HR was similar in hypertensive and normotensive individuals
- MSNA increased after alcohol in controls by 83±34% (P<0.01 vs. baseline). MSNA did not change significantly after alcohol in hypertensive patients (16±7%, not significant) despite a profound BP increase, which would be expected to inhibit sympathetic activity.
Effects of Alcohol in Normotensive and Hypertensive Individuals
Measurement | Normotensive Controls | Hypertensive Patients | Interaction Group x Time P-value |
||
Before | After | Before | After | ||
SBP (mmHg) | 133±4 | 135±7 | 149±7 | 173±8 | <0.001 |
DBP (mmHg) | 77±2 | 81±4 | 89±5 | 104±5 | <0.001 |
HR (bpm) | 73±3 | 80±3 | 74±3 | 83±4 | Not significant |
MSNA (bursts/minute) | 25±4 | 35±4 | 38±4 | 41±4 | 0.09 |
Integrated MSNA (%) | 100 | 183±34 | 100 | 116±7 | 0.03 |
- Pressor responses to acute alcohol consumption are potentiated in hypertensive patients compared with normotensive controls. Vasoconstrictor sympathetic tone is not suppressed in hypertensive patients after alcohol, despite the enhanced pressor response.
- Sympathetic neural mechanisms might contribute to both alcohol-related blood pressure increases and cardiovascular events in hypertensive patients.
Government: | National Institute of Health, European Union InGenious, Foundation for Polish Science |
- This study assessed the short-term effects of relatively high dose of alcohol (1.0g per kg of weight). This level of alcohol exposure might reflect the equivalent of binge drinking.
- Strengths of this study
- Randomized, placebo-controlled study design
- Not confounded by anti-hypertensive treatment.
- Limitations of this study
- ?Relatively small number of subjects
- Lack of additional measures of sympathetic tone such as plasma noradrenaline concentrations
- Most hypertensive patients were overweight or obese and the effect of alcohol may be different in normal-weight hypertensive patients (anthropometric measures for participants not described)
- Limited to middle-aged patients.
Quality Criteria Checklist: Primary Research
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Relevance Questions | |||
1. | Would implementing the studied intervention or procedure (if found successful) result in improved outcomes for the patients/clients/population group? (Not Applicable for some epidemiological studies) | Yes | |
2. | Did the authors study an outcome (dependent variable) or topic that the patients/clients/population group would care about? | Yes | |
3. | Is the focus of the intervention or procedure (independent variable) or topic of study a common issue of concern to dieteticspractice? | Yes | |
4. | Is the intervention or procedure feasible? (NA for some epidemiological studies) | Yes | |
Validity Questions | |||
1. | Was the research question clearly stated? | Yes | |
1.1. | Was (were) the specific intervention(s) or procedure(s) [independent variable(s)] identified? | Yes | |
1.2. | Was (were) the outcome(s) [dependent variable(s)] clearly indicated? | Yes | |
1.3. | Were the target population and setting specified? | No | |
2. | Was the selection of study subjects/patients free from bias? | ??? | |
2.1. | Were inclusion/exclusion criteria specified (e.g., risk, point in disease progression, diagnostic or prognosis criteria), and with sufficient detail and without omitting criteria critical to the study? | Yes | |
2.2. | Were criteria applied equally to all study groups? | Yes | |
2.3. | Were health, demographics, and other characteristics of subjects described? | Yes | |
2.4. | Were the subjects/patients a representative sample of the relevant population? | ??? | |
3. | Were study groups comparable? | ??? | |
3.1. | Was the method of assigning subjects/patients to groups described and unbiased? (Method of randomization identified if RCT) | Yes | |
3.2. | Were distribution of disease status, prognostic factors, and other factors (e.g., demographics) similar across study groups at baseline? | ??? | |
3.3. | Were concurrent controls or comparisons used? (Concurrent preferred over historical control or comparison groups.) | Yes | |
3.4. | If cohort study or cross-sectional study, were groups comparable on important confounding factors and/or were preexisting differences accounted for by using appropriate adjustments in statistical analysis? | N/A | |
3.5. | If case control study, were potential confounding factors comparable for cases and controls? (If case series or trial with subjects serving as own control, this criterion is not applicable.) | N/A | |
3.6. | If diagnostic test, was there an independent blind comparison with an appropriate reference standard (e.g., "gold standard")? | N/A | |
4. | Was method of handling withdrawals described? | Yes | |
4.1. | Were follow-up methods described and the same for all groups? | Yes | |
4.2. | Was the number, characteristics of withdrawals (i.e., dropouts, lost to follow up, attrition rate) and/or response rate (cross-sectional studies) described for each group? (Follow up goal for a strong study is 80%.) | Yes | |
4.3. | Were all enrolled subjects/patients (in the original sample) accounted for? | Yes | |
4.4. | Were reasons for withdrawals similar across groups? | N/A | |
4.5. | If diagnostic test, was decision to perform reference test not dependent on results of test under study? | N/A | |
5. | Was blinding used to prevent introduction of bias? | Yes | |
5.1. | In intervention study, were subjects, clinicians/practitioners, and investigators blinded to treatment group, as appropriate? | Yes | |
5.2. | Were data collectors blinded for outcomes assessment? (If outcome is measured using an objective test, such as a lab value, this criterion is assumed to be met.) | Yes | |
5.3. | In cohort study or cross-sectional study, were measurements of outcomes and risk factors blinded? | N/A | |
5.4. | In case control study, was case definition explicit and case ascertainment not influenced by exposure status? | N/A | |
5.5. | In diagnostic study, were test results blinded to patient history and other test results? | N/A | |
6. | Were intervention/therapeutic regimens/exposure factor or procedure and any comparison(s) described in detail? Were interveningfactors described? | Yes | |
6.1. | In RCT or other intervention trial, were protocols described for all regimens studied? | Yes | |
6.2. | In observational study, were interventions, study settings, and clinicians/provider described? | N/A | |
6.3. | Was the intensity and duration of the intervention or exposure factor sufficient to produce a meaningful effect? | Yes | |
6.4. | Was the amount of exposure and, if relevant, subject/patient compliance measured? | Yes | |
6.5. | Were co-interventions (e.g., ancillary treatments, other therapies) described? | No | |
6.6. | Were extra or unplanned treatments described? | No | |
6.7. | Was the information for 6.4, 6.5, and 6.6 assessed the same way for all groups? | Yes | |
6.8. | In diagnostic study, were details of test administration and replication sufficient? | N/A | |
7. | Were outcomes clearly defined and the measurements valid and reliable? | Yes | |
7.1. | Were primary and secondary endpoints described and relevant to the question? | Yes | |
7.2. | Were nutrition measures appropriate to question and outcomes of concern? | N/A | |
7.3. | Was the period of follow-up long enough for important outcome(s) to occur? | ??? | |
7.4. | Were the observations and measurements based on standard, valid, and reliable data collection instruments/tests/procedures? | Yes | |
7.5. | Was the measurement of effect at an appropriate level of precision? | Yes | |
7.6. | Were other factors accounted for (measured) that could affect outcomes? | No | |
7.7. | Were the measurements conducted consistently across groups? | Yes | |
8. | Was the statistical analysis appropriate for the study design and type of outcome indicators? | Yes | |
8.1. | Were statistical analyses adequately described and the results reported appropriately? | Yes | |
8.2. | Were correct statistical tests used and assumptions of test not violated? | Yes | |
8.3. | Were statistics reported with levels of significance and/or confidence intervals? | Yes | |
8.4. | Was "intent to treat" analysis of outcomes done (and as appropriate, was there an analysis of outcomes for those maximally exposed or a dose-response analysis)? | N/A | |
8.5. | Were adequate adjustments made for effects of confounding factors that might have affected the outcomes (e.g., multivariate analyses)? | No | |
8.6. | Was clinical significance as well as statistical significance reported? | Yes | |
8.7. | If negative findings, was a power calculation reported to address type 2 error? | N/A | |
9. | Are conclusions supported by results with biases and limitations taken into consideration? | Yes | |
9.1. | Is there a discussion of findings? | Yes | |
9.2. | Are biases and study limitations identified and discussed? | Yes | |
10. | Is bias due to study's funding or sponsorship unlikely? | Yes | |
10.1. | Were sources of funding and investigators' affiliations described? | Yes | |
10.2. | Was the study free from apparent conflict of interest? | Yes | |