Increased thickness and stiffness of large arteries may contribute to why aging is the most important risk for cardiovascular diseases. Arterial stiffness, intimal medial thickness, and alcohol intake were measured in 563 subjects. A U-shaped relation was found between alcohol intake and a stiffness index, with the lowest index in moderate drinkers, which may partially explain the relation between alcohol and cardiovascular disease.
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- Cardiology and Cardiovascular Medicine
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Effect of light-to-moderate alcohol consumption on age-associated arterial stiffening. / Hougaku, Hidetaka; Fleg, Jerome L.; Lakatta, Edward G.; Scuteri, Angelo; Earley, Christopher J.; Najjar, Samer; Deb, Saswata; Metter, E. Jeffrey.In: American Journal of Cardiology, Vol. 95, No. 8, 15.04.2005, p. 1006-1010.
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TY - JOUR
T1 - Effect of light-to-moderate alcohol consumption on age-associated arterial stiffening
AU - Hougaku, Hidetaka
AU - Fleg, Jerome L.
AU - Lakatta, Edward G.
AU - Scuteri, Angelo
AU - Earley, Christopher J.
AU - Najjar, Samer
AU - Deb, Saswata
AU - Metter, E. Jeffrey
N1 - Funding Information: Hidetaka Hougaku MD, PhD d Jerome L. Fleg MD b Edward G. Lakatta MD b Angelo Scuteri MD, PhD e Christopher J. Earley MD, PhD c Samer Najjar MD b Saswata Deb BA f E. Jeffrey Metter MD a ⁎ firstname.lastname@example.org a Clinical Research Branch, National Institute on Aging, National Institutes of Health, Baltimore, Maryland b Laboratory of Cardiovascular Science, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, Maryland c Department of Neurology, Johns Hopkins Bayview Medical Center, Baltimore, Maryland d Osaka University Graduate School of Medicine, Osaka, Japan e Dipartimento Cardio-Geriatrico, INRCA, Rome, Italy f University of Toronto MD Program, Toronto, Ontario, Canada ⁎ Dr. Metter's address is: Clinical Research Branch, National Institute on Aging, Intramural Research Program, NIA-ASTRA, Harbor Hospital, 5th Floor, 3001 South Hanover Street, Baltimore, Maryland 21225 Increased thickness and stiffness of large arteries may contribute to why aging is the most important risk for cardiovascular diseases. Arterial stiffness, intimal medial thickness, and alcohol intake were measured in 563 subjects. A U-shaped relation was found between alcohol intake and a stiffness index, with the lowest index in moderate drinkers, which may partially explain the relation between alcohol and cardiovascular disease. This study examines the hypothesis that moderate alcohol consumption reduces arterial stiffness and wall thickness, particularly in older adults. We performed common carotid artery (CCA) ultrasound in apparently healthy volunteers from the Baltimore Longitudinal Study of Aging, 1 whose alcohol intake is routinely assessed by questionnaire. Carotid intimal medial thickness (IMT) was measured, and carotid diameter changes were used to calculate an arterial stiffness index. 2,3 The Baltimore Longitudinal Study of Aging is a cohort of community-dwelling, predominantly white, college-educated volunteers who are examined biennially with medical, physiologic, and psychologic studies. 1 From February 1994 to January 2000, 774 subjects underwent carotid duplex ultrasonography. Subjects were selected based on scheduling availability and availability of the technician to do the study. Of this sample, 563 subjects (276 men, 287 women; aged 60.1 ± 16.2 years [mean ± SD]) had adequate studies and had no significant carotid artery disease. The research protocol was approved by the Johns Hopkins Bayview Institutional Review Board, and signed informed consent was obtained from all participants. The investigation conformed to the principles outlined in the Declaration of Helsinki. The CCA was examined bilaterally by high-resolution B-mode ultrasonography with a linear array 5- to 10-MHz duplex-type scanner (Ultramark 9 HDI, Advanced Technology Laboratories, Bothell, Washington) by a trained sonographer. As previously reported, 3 a region approximately 1.5 cm proximal to the bulge of bifurcation was identified, and the maximum (systolic) and minimum (diastolic) diameters were measured visually using electrocardiographic timing. The measurements were averaged from 3 different cardiac cycles from the right and left CCA. Blood pressure was measured after 15 minutes of lying in the quiet room using a Critikon Dinamap 1846SX/P version 085 (Tampa, Florida). Stiffness of the CCA was evaluated by the stiffness index as (stiffness index = ln (systolic blood pressure/diastolic blood pressure)/(Δd/diastolic diameter]), where Δd/diastolic diameter is the strain calculated as the difference between systolic and diastolic carotid diameters (Δd) divided by the diastolic diameter. 4 The intrarater correlation between repeated stiffness measurements from 10 subjects was 0.96 (p <0.01), with similar averages for the 2 sets of readings (6.37 ± 2.59 vs 6.43 ± 2.58, p = NS), and met Bland-Altman criteria for reproducibility. 5 The IMT of the carotid far wall was evaluated as the distance between the luminal-intimal interface and the medial-adventitial interface from 5 contiguous sites at 1-mm intervals in the right and left CCAs, and the average of the 10 measurements was used for analyses. The intrarater correlation between repeated IMT measurements from 10 subjects was 0.96 (p <0.01), with similar averages for the 2 sets of readings (0.47 ± 0.13 vs 0.45 ± 0.12 mm, p = NS), 2 and met Bland-Altman criteria for reproducibility. 5 Alcohol intake was assessed by written questions addressing the unit consumption of beer, spirits, and wine, the 3 major types of alcoholic beverage. A unit was defined as 12 oz of beer, 2 oz of spirits, or 4 to 5 oz (1 glass) of wine/day. Consumption was graded by categorizing frequency of use into 7 responses: never (≤1 to 2 U/month), ≤2 U/week, 1 to 2 U every other day, 1 to 2 U/day, 3 to 4 U/day, or ≥5 U/day. Total alcohol consumption was estimated by converting these 7 responses into units per week for each beverage and adding the values. For example, when a participant drank 2 U of beer every other day, 2 U of spirits/week, and no wine, the total estimated alcohol intake was 6.75 U/week (5.5 for beer + 1.25 for spirits + 0 for wine). Total alcohol intake was used to divide participants into 3 groups: nondrinkers (<1 U/week), moderate drinkers (1 to 9.9 U/week), and heavy drinkers (≥10 U/week). To evaluate the reliability of the cross-sectional estimates of alcohol intake, we compared these cross-sectional estimates to the averaged longitudinal alcohol intake data in 192 patients who were evaluated over at least a 10-year period (mean 12.3 years, range 10.0 to 33.3) with 5.5 ± 0.9 observations per subject. A paired t test revealed no significant difference between the cross-sectional alcohol intake (4.8 ± 7.3 U/week) and the averaged intake (5.0 ± 6.2 U/week), with a correlation of 0.89 (p <0.01). Other potential determinants of vascular stiffness examined included age, gender, smoking status, serum total cholesterol, fasting blood glucose, mean blood pressure, pulse pressure, and body mass index. Total physical activity per day 6 and years of formal education were assessed by questionnaire. Subjects were diagnosed as having hypertension if casual blood pressure was ≥140/90 mm Hg in a sitting position or they were taking antihypertensive medication. A total of 184 subjects were hypertensive, and 94 subjects had elevated blood pressure. Coronary heart disease was diagnosed by history of angina pectoris, myocardial infarction, or significant Q waves on an electrocardiogram at rest (Minnesota Code 1:1 or 1:2). Stroke was diagnosed by a clinical evaluation of history, physical examination, and medical records, where available. Coronary heart disease was evident in 38 subjects. Statistical analyses were performed using the Statistical Package of the Social Sciences (SPSS) version 8.0 for Windows (SPSS, Inc., Chicago, Illinois). Subject characterization by group is presented as mean ± SD in the text and tables, and as means ± SEs in the figures. One-way analysis of variance was used for comparisons of normally distributed data among alcohol usage groups and a chi-square test for the distribution of categorical factors or alcohol intake. Correlations between variables were examined using Pearson's correlation for normally distributed data and Spearman's correlation coefficients for other data. SPSS general linear modeling was used to assess the relation between alcohol groups and the carotid stiffness index or IMT, adjusting for age, pulse pressure, total cholesterol, fasting plasma glucose, body mass index, gender, and smoking status. Bonferroni's method was used for post hoc analysis. The resulting models were used to adjust the carotid stiffness index and IMT for these risk factors. A 2-tailed p value <0.05 was considered statistically significant. Total alcohol intake was 0 to 44.3 U/week. Means for men and women were 5.3 ± 7.4 and 3.6 ± 6.0 U/week, whereas medians were 1.50 and 0.75 U/week, respectively. gives subject characteristics by alcohol intake category. In general, heavy drinkers were older and more likely to be men than the nondrinkers and moderate drinkers. Thirty-three percent of subjects drank wine (≥1U/week), significantly higher than the percentage who consumed beer (22.4%, p <0.01) or spirits (27.4%, p <0.05). Those with higher beer consumption were more likely to be younger (p <0.05) and men (p <0.01). Participants with higher spirits consumption were more likely to be older (p <0.01), men (p <0.05), smokers (p <0.05), and to have a higher pulse pressure (p <0.05). Table 1 A U-shaped relation was found between alcohol intake and the arterial stiffness index, with the lowest index in moderate drinkers (1 to 9.9 drinks/week) ( Alcohol intake was an independent determinant of arterial stiffness, after controlling for age, gender, pulse pressure, total cholesterol, fasting plasma glucose, body mass index, and smoking status (p <0.01; and Figure 1 ). Table 2 Figure 1 ). Adding or substituting mean blood pressure, or systolic and diastolic blood pressures, or including heart rate did not change the relation between alcohol use and either arterial stiffness or IMT. These relations were also observed when participants taking antihypertensive drugs or those with coronary heart disease and/or a history of stroke were excluded. Similar U-shaped relations were observed in men and women, in subjects aged <50 and ≥50 years old, or across groups stratified by mean blood pressure (<90 and ≥90 mm Hg, respectively, p <0.05). Similarly, a U-shaped relation between alcohol intake and IMT was observed (p <0.01; . However, the relation did not persist after adjusting for other cardiovascular risk parameters ( Figure 2 ) Figure 2 and Table 2 ). To investigate whether the alcohol effect differed in older versus younger patients, subjects were grouped based on age (50% reduction in the age-associated increase in stiffness index for older compared with younger moderate drinkers. No age group difference was found in the relation between alcohol intake and IMT after adjustment for other risk factors ( Figure 3 ) Figure 4 ). To examine whether there was a differential effect of beer, spirits, or wine on arterial stiffness, subjects were identified who reported using primarily a single beverage type and not >1 U/week of other beverages. By multiple regression analysis, beer, spirits, and wine consumption were each an independent predictor of the stiffness index (each p <0.05) but not IMT after adjusting for standard risk parameters. In these predominantly healthy volunteers, a U-shaped relation was found between alcohol intake and carotid arterial stiffness, with the lowest stiffness occurring in patients consuming approximately 1 drink/day. Moderate alcohol consumption appeared to attenuate the age-associated increase in arterial stiffness, independent of the other cardiovascular risk factors examined and was similar for the 3 main types of alcoholic beverages: beer, wine, and spirits. Aging adversely alters the arterial tree 7 and many cardiovascular risk parameters. 8–11 The salutary effect of moderate alcohol intake on age-associated changes in arterial stiffness suggests that alcohol retards the process of arterial wall remodeling that occurs with aging. Moderate alcohol intake was also associated with lower carotid IMT; however, this effect was not independent of other risk factors ( Figure 2 ). Previous studies have demonstrated that the lowest risk of atherosclerotic disease varied from <1 to 2 U of alcohol per day. 12–14 Thus, the optimal alcohol intake for reducing arterial stiffness is similar to that associated with the lowest cardiovascular risk. The lower stiffness in older subjects with moderate alcohol use was accompanied by lower systolic and pulse pressures, which might attenuate the left ventricular wall thickening that occurs with aging. These effects may lessen the risk for cardiovascular disease associated with an aging vascular tree. The relation between arterial stiffness and pulse pressure raises the question of whether the alcohol effect on stiffness is due to an effect on blood pressure. However, alcohol use had an independent effect on stiffness, after adjusting for pulse pressure or mean blood pressure ( Table 2 ). The effect of alcohol had the same U-shaped relation when blood pressure was used to divide subjects into 2 groups. Few previous studies have evaluated the relation between alcohol intake and arterial stiffness. Sehested et al 15 reported that acute intake of alcohol reduced pulse-wave velocity and increased blood flow 30 minutes after administration, whereas Fazio et al 16 found that acute elevation of serum alcohol levels to about 0.3 g/L caused a decrease in shear stress, arterial diameter pulsatility, and elastic modulus. Mahmud and Feely 17 found that the ingestion of a single alcoholic drink caused an immediate reduction of arterial stiffness and pressure, but long-term excessive use increased stiffness. The differences in the acute responses between the 2 studies suggest that the acute impact of alcohol is dynamic and may vary over different circulating concentrations of alcohol. Sierksma et al 18,19 found a J-shaped relation between alcohol intake and pulse wave velocity in men and women. The Atherosclerosis Risk in Community (ARIC) study did not find any effects of regular alcohol intake on arterial stiffness in subjects aged 45 to 64 years, 20 which was similar to our findings in subjects <55 years old. The benefit of alcohol in subjects ≥55 years old (mean 71.6 ± 9.9) but not in younger patients in our study may be explained by higher stiffness in the older group and that arterial stiffening accelerates after age 50 to 60, that is, blood vessels in younger patients are still overall compliant, so alcohol will not exert a significant effect. The association of light-to-moderate daily alcohol consumption with lower carotid arterial stiffness, but not IMT, in healthy community-dwelling volunteers may contribute to its protective effect on cardiovascular risk through favorable modulation of age-related changes in the arterial tree, leading to more elastic, less stiff arteries. Copyright: Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2005/4/15
Y1 - 2005/4/15
N2 - Increased thickness and stiffness of large arteries may contribute to why aging is the most important risk for cardiovascular diseases. Arterial stiffness, intimal medial thickness, and alcohol intake were measured in 563 subjects. A U-shaped relation was found between alcohol intake and a stiffness index, with the lowest index in moderate drinkers, which may partially explain the relation between alcohol and cardiovascular disease.
AB - Increased thickness and stiffness of large arteries may contribute to why aging is the most important risk for cardiovascular diseases. Arterial stiffness, intimal medial thickness, and alcohol intake were measured in 563 subjects. A U-shaped relation was found between alcohol intake and a stiffness index, with the lowest index in moderate drinkers, which may partially explain the relation between alcohol and cardiovascular disease.
UR - http://www.scopus.com/inward/record.url?scp=16844384611&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=16844384611&partnerID=8YFLogxK
U2 - 10.1016/j.amjcard.2004.12.051
DO - 10.1016/j.amjcard.2004.12.051
M3 - Article
C2 - 15820179
AN - SCOPUS:16844384611
VL - 95
SP - 1006
EP - 1010
JO - American Journal of Cardiology
JF - American Journal of Cardiology
SN - 0002-9149
IS - 8