Cardiovascular and Aortic Wave Reflection Responses to Evening Binge Alcohol Consumption

Abstract

Evening binge alcohol consumption contributes to sleep disruption and autonomic dysregulation that persists into the following morning. However, its impact on morning-after arterial stiffness and aortic wave reflection remains unknown. Using a randomized, crossover, fluid-controlled design, we hypothesized that heart rate (HR), carotid-femoral pulse wave velocity (cfPWV), aortic augmentation index (AIx), and aortic pulsatile load (APL) would be increased acutely after binge drinking at night (study 1) and the morning-after binge drinking (study 2). Participants (n=33; 18 females, 15 males; age 25±1 years; BMI: 27±1 kg/m²) completed binge alcohol (4–5 drink equivalent) and fluid control protocols. Study 1 examined cardiovascular responses during resting baseline and within 30 minutes of evening alcohol consumption, while study 2 examined cardiovascular responses within 15 minutes of waking the morning-after binge alcohol or fluid control. In Study 1, HR and APL increased after the final dose of alcohol (p<0.001) but decreased with fluid control. In Study 2, morning HR (63±2 vs. 57±1 beats/min; p<0.001), APL (2060±82 vs. 1857±66 a.u.; p=0.012) and AIx normalized to 75 beats per minute (AIx@75) (6.5±2.4 vs. 2.9±2.5%; p=0.042) were increased, while unadjusted AIx was unchanged, after binge alcohol compared to fluid control. cfPWV was not altered by binge alcohol acutely (study 1) or the morning-after (study 2). Our results indicate evening binge alcohol consumption elicited acute increases of HR and APL and morning-after increases HR, APL, and AIx@75. These findings highlight physiological mechanisms that might contribute to well-documented associations between binge alcohol consumption and heightened cardiovascular risk.

INTRODUCTION

Alcohol consumption elicits a dose-dependent increase of systolic blood pressure in both males and females (1). Acute and chronic binge drinking have been associated with cardiovascular risks such as coronary and peripheral artery disease, hypertension, and stroke (2). Epidemiological studies have demonstrated that men should have ≤2 drinks per day and women should have ≤1 drink per day to reduce alcohol-related cardiovascular risk (3).

Our laboratory demonstrated that blood pressure reductions in response to an orthostatic challenge were exaggerated following binge alcohol intake (4). More recent studies have demonstrated how binge alcohol consumption alters cardiovascular and autonomic control (5–7). Specifically, binge alcohol consumption in the evening reduced cardiovagal baroreflex sensitivity during sleep (6) and contributed to increased muscle sympathetic nerve activity (MSNA) responses to the Valsalva maneuver the morning after alcohol consumption (7). Most recently, evening binge alcohol elicited an increase in morning-after sympathetic transduction to blood pressure when compared to fluid control, a finding that was documented both at rest and during a cold pressor test (5). While the autonomic responses to evening binge drinking are becoming more clear, acute and morning-after aortic wave reflection responses to evening binge alcohol consumption remain unknown.

Mahmud and Feely reported that carotid-femoral pulse wave velocity (cfPWV) and aortic augmentation index (AIx), a common indicator of aortic wave reflection, were elevated in males who chronically consumed excessive alcohol (8). More recent work has demonstrated an association between repeated binge drinking and elevated AIx (9), a clinically relevant finding given that AIx has been linked to mortality (10). Aortic pulsatile load (APL; aortic pulse pressure × heart rate) is yet another important cardiovascular risk factor that can increase pulsatile stress to end organs (11, 12). A study by Karatzi et al. (13) demonstrated that the acute consumption of a moderate dose of red wine decreased AIx and aortic blood pressure in adults with coronary artery disease. Despite these findings, it remains unclear how binge alcohol consumption impacts AIx and aortic blood pressure. The present study aimed to investigate the effects of evening binge alcohol consumption on acute and morning-after arterial stiffness and aortic wave reflection. We hypothesized that heart rate (HR), cfPWV, aortic augmentation index normalized to 75 heart beats per minute (AIx@75), and APL would be increased acutely (study 1) and the morning-after binge drinking when compared to fluid control (study 2).

METHODS

Participants

All studies were conducted at Michigan Technological University and Montana State University. Prior to any testing the Institutional Review Board at each institution approved the study in accordance with the Declaration of Helsinki. All participants were informed about the study design and risks. This study was part of a larger project where we have published autonomic and polysomnography sleep findings (5–7). From the sixty-nine adults who consented to participate in the study, forty-four completed at least the familiarization visit, and thirty-three participants completed all three study visits with arterial tonometry data as detailed in Figure 1.

Figure 1.

Overview of the three study visits including the familiarization (FAM) visit and the two protocol visits (randomized with ~1 month between) where participants received either binge alcohol or placebo. A standardized breakfast was provided at 7:30 am and standardized lunch and dinner times are shown above. The arterial tonometry baseline was completed at ~4:15 pm. Tonometry was repeated 30 minutes after each drink consumption, and within 15 minutes of waking the following morning.

Participants were between the ages of 21 and 40 years, had a BMI of less than 35 kg/m², reported binge drinking at least once in the six months prior to the study, and did not have alcohol use disorder based on DSM-5 criteria. Participants were nonsmokers, not taking any cardiovascular medication, and had no history of asthma, diabetes, or autonomic dysfunction. Participants were given a ResMed nasal cannula and finger pulse oximeter device to use at home for one night to screen out moderate-to-severe obstructive sleep apnea. Prior to the laboratory visits, participants abstained from exercise and caffeine for a minimum of 12 hours, and alcohol for a minimum of 24 hours. All female participants had a regular ovarian cycle between 25 and 32 days and visited the lab in either the early follicular (n = 10) or mid-luteal (n = 8) phase of the ovarian cycle. Females were not on any type of contraceptive.

Protocol

For familiarization, participants arrived at the sleep lab at 9 pm. Familiarization did not include any alcohol or fluid control treatment. It was designed to familiarize the subjects with the polysomnography (PSG) process (7), overnight beat-to-beat blood pressure recordings from the Finapres NOVA (6), and aortic wave reflection / arterial stiffness measurements.

On experimental visits, participants reported to the laboratory for a standardized breakfast at 7:30 AM. After breakfast, they were given a box lunch to eat at 12:00 PM. Participants reported to the Sleep Research Laboratory at 4:00 PM. Urine samples were obtained to determine specific gravity as a marker of hydration status, and breathalyzer was taken to confirm absence of recent alcohol. Female subjects also took a pregnancy test to confirm that they were not pregnant per the inclusion criteria.

At approximately 4:10 PM, subjects had surface electrodes placed below the clavicle and the lower left rib cage to record electrical activity of the heart (electrocardiogram) when using the SphygmoCor CPVH system. Applanation tonometry was utilized to estimate central arterial blood pressure and arterial stiffness (more details in Measurements section below).

Dinner was provided at approximately 5:00 PM. At 8:00 PM, participants began the beverage consumption protocol. Binge drinking was defined as a male consuming 5 drinks or more, or a female consuming 4 drinks or more, within a 2-hour period (14). Therefore, oral alcohol (190-proof ethanol) was given in two divided doses of 1.0 g/kg of body weight for males, administered at 1-hour intervals (8 and 9 PM). Females received a reduced dose (0.85 g/kg) to evoke similar blood alcohol content between male and female participants. The alcohol beverage was diluted in a 1:3 mixture with cranberry juice or orange juice, depending on participant preference. The fluid control session consisted of the cranberry or orange juice in the same volume. Beverages were administered blind to participants, served in opaque lidded cups, and sprayed with an alcohol mist to maximize blinding effect. During both sessions, the drinks were divided into thirds, and participants had 5 min to consume each drink. The breathalyzer was administered in 15 min intervals from 8 to 11 PM. Aortic wave reflection and arterial stiffness measurements were repeated in 1-hour intervals at 8:45 and 9:45 PM as shown in Figure 1. At 9:15 PM, participants were instrumented with PSG as reported in our previous studies (6, 7).

Participants rested quietly in bed, with lights-out at 11:00 PM, and were provided an 8-hour sleep opportunity. Participants were woken up at 7:00 AM, and BrAC was assessed via breathalyzer, blood alcohol concentration via venous blood draw from the left arm, specific gravity via urine sample, and vascular stiffness via applanation tonometry on the right side of the body. PSG de-instrumentation followed the morning urine sample. The final aortic wave reflection and arterial stiffness measures began at approximately 7:15 AM.

Measurements

Arterial Tonometry

Applanation tonometry recording occurred with subjects lying down in a relaxed supine position on a bed within the sleep lab with the palm of their right hand supinated using a SphygmoCor CPVH system (n=23; Michigan Tech University) or SphygmoCor XCEL system (n=10; Montana State University). Measurements were collected for pulse wave analysis (PWA), including aortic augmentation index (AIx) and AIx normalized to 75 heart beats (AIx@75), by placing the SphygmoCor tonometry probe directly on the radial artery and flattening the artery against the underlying connective tissue and bone (15). Recordings were taken for 10 full and consistent cardiac cycles to ensure an accurate waveform was recorded. Acceptable recordings required an operator index of 75 or higher on the SphygmoCor software. The SphygmoCor XCEL system uses a standard brachial blood pressure cuff to measure blood pressure and capture a brachial waveform. This waveform is then used to estimate the aortic waveform and AIx.

Carotid femoral pulse wave velocity (cfPWV), an estimate of central arterial stiffness, was recorded using the femoral artery and carotid artery sites. These sites were palpated and marked with tape or a marker dot, respectively. The straight-line distance of each of these sites relative to the suprasternal notch of the sternum was measured and recorded to the closest millimeter. The three electrodes used for the electrocardiogram were used for recording R waves. These recorded R-waves were gated to the pulses recorded at the carotid and femoral sites to calculate the time it takes a pulse wave to arrive at each specified site. PWV was determined simply by the time it takes a pulse to reach each of the sites. With the SphygmoCor XCEL system cfPWV was measured by placing the tonometer at the carotid pulse site, similar to the SphygmoCor CPVH system, and simultaneously captured the femoral pulse waveform with a leg cuff placed at the upper thigh. The distance between pulse sites was measured and used to calculate the velocity of the pressure wave, and the suprasternal notch was used to estimate the location of the aorta.

Data Analysis

Duplicate recordings were taken and averaged for analysis of PWA and PWV recordings. Data were deemed acceptable if the recordings of cfPWV were within 1 m/s of each other. If the first two measurements did not meet this criterion an additional measurement was completed and the closest two readings within 1 m/s were averaged.

Statistical Analyses

Statistical data analyses were completed using SPSS. For Study 1, repeated measures analysis of variance (ANOVA) was conducted to assess changes in all cardiovascular variables using condition (alcohol and placebo) and time (pre-dinner baseline, post drink 1, and post drink 2) as within-subjects factors. These variables include systolic arterial pressure, diastolic arterial pressure, mean arterial pressure, HR, aortic pulse pressure, APL, AIx, AIx@75, and cfPWV. We had quality recordings for 31 participants for aPP, APL, AIx and AIx@75 during the morning after fluid control and alcohol and for 28 participants for cfPWV due to not having an average of two acceptable recordings at each of the time points for all participants. Each of these variables was checked for a normal distribution using the Shapiro-Wilk test. Mauchly’s Test of Sphericity was performed for each variable to determine if sphericity could be assumed. When sphericity was violated, the Greenhouse-Geisser method was used to determine the adjusted p-value. Post-hoc paired t-tests with Bonferroni corrections were utilized for the comparisons across three time points (i.e., baseline, drink 1, and drink 2) for variables with a significant condition × time interaction. For Study 2, we utilized paired t-tests to compare the variables listed above on the morning-after binge alcohol and morning-after fluid control. We also utilized a repeated measures ANOVA model with condition as the within-subjects factor (fluid control vs. binge alcohol) and biological sex as the between-subjects factor (male vs. female) which we report in Supplemental Table S1. Data were considered significantly different when p<0.05. Results are reported as mean ± standard error.

RESULTS

Participant Characteristics

Participants (18 females and 15 males) were 25±1 years with an average body mass index (BMI) of 27±1 kg/m². Age (27 ± 2 vs. 23 ± 1 years), BMI (27±1 kg/m² vs. 27±1 kg/m²), seated systolic arterial pressure (108 ± 2 vs. 112 ± 2 mmHg), and seated diastolic arterial pressure (72 ± 2 vs. 71 ± 2 mmHg) were not different between females and males, respectively. In contrast, females (69 ± 2 beats/min) had a significantly higher resting seated heart rate when compared to males (60 ± 3 beats/min; p=0.006).

Acute Effects of Evening Binge Alcohol on Arterial Stiffness

Table 1 demonstrates that acute HR and APL responses differed between alcohol and fluid control (condition × time: P < 0.001 for both). Specifically, HR and APL decreased after the first fluid control dose and remained reduced throughout the fluid control session. In contrast, HR and APL were elevated after the 2^nd dose of alcohol. Mean arterial pressure, aPP, AIx, Aix@75, and cfPWV were not different between alcohol and fluid control conditions (Table 1). The BrAC was 0.044 ± 0.002 % 30 minutes after dose 1 of alcohol and 0.092 ± 0.003 % 30 minutes after dose 2 of alcohol, while BrAC was 0.000 ± 0.000 after each fluid control dose.

Table 1.

Supine Evening Alcohol and Fluid Control Values for Time by Condition (n=33).

							Time x Cond
Variable	Base	FC 1	FC 2	Base	Alc 1	Alc 2	P-Value
MAP (mmHg)	81 ± 1	80 ± 1	82 ± 1	79 ± 2	79 ± 2	79 ± 1	0.159
HR (bpm)	63 ± 2	61 ± 2*	60 ± 2*	62 ± 2	62 ± 2	65 ± 2*	<0.001
aPP (mmHg)	33 ± 1	32 ± 1	32 ± 1	33 ± 1	33 ± 1	33 ± 1	0.527
APL (a.u.)	2070 ± 80	1950 ± 85*	1918 ± 72*	1989 ± 86	2056 ± 73	2142 ± 78*	<0.001
AIx (%)	9 ± 3	6 ± 3	9 ± 3	11 ± 2	5 ± 3	6 ± 3	0.349
AIx@75 (%)	3 ± 3	−1 ± 3	1 ± 3	4 ± 2	−1 ± 3	2 ± 3	0.986
cfPWV (m/s)	4.8 ± 0.1	5.0 ± 0.1	5.1 ± 0.1	4.9 ± 0.1	4.9 ± 0.1	5.0 ± 0.1	0.211

MAP, supine brachial mean arterial pressure; HR, supine heart rate; aPP, aortic pulse pressure; APL, aortic pulsatile load (HR x aPP); AIx, aortic augmentation index; AIx@75, aortic augmentation index normalized to heart rate of 75 beats per minute (bpm); cfPWV, carotid-femoral pulse wave velocity; Base, baseline preceding either fluid control or alcohol; FC, fluid control; Alc, alcohol.

^*P < 0.05 vs. FC1 or BA1 (i.e., baseline) with post-hoc paired T-test.

Effects of Evening Binge Alcohol Consumption on Next-Morning Arterial Stiffness

Table 2 demonstrates that mean arterial pressure, aortic pulse pressure, AIx, and cfPWV were similar on the morning after fluid control compared to the morning after binge alcohol. In contrast, Figure 2 demonstrates that HR (63±2 vs. 57±1 beats/min; p<0.001), APL (2060±82 vs. 1857±66 a.u.; p=0.012) and AIx@75 (6.5±2.4 vs. 2.9±2.5%; p=0.042) were significantly elevated the morning-after binge alcohol when compared to the fluid control condition. Finally, supplemental Table S1 shows results of our additional analysis including biological sex as a key variable.

Table 2.

Supine Morning Alcohol vs. Fluid Control Values (n=33).

Variable	FC Morning	Alc Morning	P-Value
MAP (mmHg)	81 ± 1	80 ± 1	0.833
HR (bpm)	57 ± 1	63 ± 2*	<0.001
aPP (mmHg)	33 ± 1	34 ± 1	0.543
APL (a.u.)	1857 ± 66	2060 ± 82*	0.012
AIx (%)	12.4 ± 2.2	13.5 ± 2.1	0.424
AIx@75 (%)	2.9 ± 2.5	6.5 ± 2.4*	0.042
cfPWV (m/s)	5.1 ± 0.1	5.3 ± 0.1	0.076

MAP, supine brachial mean arterial pressure; HR, supine heart rate; aPP, aortic pulse pressure; APL, aortic pulsatile load (HR x aPP); AIx@75, aortic augmentation index normalized to heart rate of 75 beats per minute (bpm); cfPWV, carotid-femoral pulse wave velocity. FC, fluid control; Alc, alcohol.

^*P < 0.05. Note: n=31 for aPP, APL, AIx and AIx@75; n = 28 for cfPWV.

Figure 2.

Morning after heart rate (panel A), aortic pulsatile load (panel B), and aortic augmentation index (AIx) normalized to 75 beats per minute (panel C) responses to fluid control (blue) and alcohol (red); n=33 for all. ***P<0.001, *P<0.05 based on paired t-test results comparing the morning responses.

DISCUSSION

This is the first study to examine both the acute and morning-after aortic cardiovascular responses to evening binge alcohol consumption. First, we document that evening binge alcohol consumption elicits acute increases HR and APL. Second, we demonstrate that evening binge alcohol consumption also increases HR and APL the morning-after binge alcohol consumption. Third, while aortic wave reflection was not altered by acute alcohol consumption, AIx@75 was higher the morning-after binge alcohol consumption when compared to the morning-after fluid control. These findings advance our understanding of the potential deleterious impacts of binge alcohol consumption on aortic wave reflection, providing new mechanistic insights into the known associations between binge drinking and cardiovascular disease.

Previous studies have reported that moderate doses of red wine can acutely decrease AIx and aortic blood pressure (8, 13). In contrast, our results demonstrate that binge drinking acutely increases HR and APL. APL is a combination of HR and aortic pulse pressure, and increases in APL can contribute to excess pulsatile stress on end organs such as the brain and kidneys (11, 12). These results are consistent with the recommendations that men should not consume more than two alcohol drinks per day, and that women should not have more than one alcohol drink per day (3). The significant reduction of APL and HR after the fluid control in our participants is consistent with prior studies that have reported decreases in HR after fluid loading (16, 17).

The findings of Study 2 build upon prior literature that has focused on chronic alcohol behaviors (5, 7, 18), and to our knowledge the present study is the first to report increases in HR, APL, and AIx@75 the morning-after binge alcohol consumption. These findings are clinically relevant considering the well-documented risks for early morning adverse cardiovascular events (19). Increases of HR and APL contribute to pulsatile stress, which can contribute to end-organ damage (12). Increases in AIx@75 are associated with increased afterload on the heart and risk for cardiac hypertrophy (20), and such increases have been linked to an increased risk of mortality, especially in men (10). The increases in morning-after AIx@75 within the present study align with previous work showing that those who drank three or more drinks per day had higher AIx values than those who abstained from drinking (21). Such increases of AIx, especially if repeated over time, could contribute to the significant increases in cfPWV (i.e., aortic arterial stiffness) that has been shown in previous studies with chronic binge drinkers (9, 22). Our results demonstrated no change in cfPWV after a single night of binge drinking (p=0.076). Additionally, it is worth noting that aPP and AIx can be associated with both forward and backward traveling pressure waves within the arterial tree, but aPP may have a higher association with the forward waves (23) while AIx may have a higher relationship to the backward waves (24). Larger epidemiological cohorts have identified backward reflection magnitude as a key predictor of all-cause mortality in clinical CVD populations (25). While we have kept our results focused on AIx@75, APL, and cfPWV within the present brief report, the relationship with alcohol consumption, and forward and backward wave reflection represents an important area of future research.

Limitations

The present study was restricted to healthy young adults (age 21–40 years). Age has an impact on cardiovascular health, including blood pressure, AIx, and cfPWV. Future projects should consider responses to binge alcohol in midlife and older adults, as well as adults with heightened cardiovascular risk factors. As highlighted previously, existing literature alludes to sex specific recommendations of alcohol consumption and mortality risk associated with aortic wave reflection. During our statistical analyses, we included biological sex as an additional variable, but did not detect any condition × time × sex interactions. However, we may not have had sufficient statistical power to fully assess the role of biological sex, and additional work on understudied female binge drinkers may be warranted. A recent report suggests binge drinking has dramatically increased in women over the past decade, including to levels where the prevalence of binge drinking in young women (18–25 years) has surpassed the prevalence in age-matched men (26).

In summary, evening binge alcohol consumption elicits acute increases of HR and APL, and increases HR, APL, and AIx@75 the morning-after binge drinking. These findings have potential serious health consequences, as the augmented aortic wave reflections could serve as triggers for the already heightened early morning risk of cardiovascular events such as myocardial infarction and stroke (19, 27). Such increases may also contribute to the long-term risk of hypertension, cardiovascular disease, and mortality associated with binge alcohol consumption (1–3, 5, 17, 28, 29).

Supplementary Material

Supplemental Table S1: 10.6084/m9.figshare.29622572.v1

NEW AND NOTEWORTHY.

Increases in aortic wave reflection and aortic pulsatile load are known contributors to hypertension, cardiovascular risk, and pulsatile stress to end organs. To our knowledge, this is the first study to demonstrate that evening binge alcohol consumption increases heart rate, aortic pulsatile load, and aortic augmentation index the following morning when compared to fluid control. These findings highlight the deleterious overnight cardiovascular effects of binge alcohol consumption in young adults.