Clinical Science (1994) 87, 225-230 (Printed in Great Britain)
225
Acute alcohol intake decreases short-term heart rate
variability in healthy subjects
Pekka KOSKINEN, Juha VlROLAlNEN and Markku KUPARI
Division of Cardiology, First Department of Medicine, Helsinki University Central Hospital,
Helsinki. Finland
(Received 12 November 1993/14 February 1994 accepted 18 March 1994)
1. The acute effects of a moderate dose of ethanol
(1 g/kg body weight) on heart rate and blood pressure
variability and baroreflex sensitivity were studied in
12 healthy male subjects in a juice-controlled experiment. Electrocardiographic and finger blood pressure
data were recorded and stored in a minicomputer
during 5 min of controlled breathing (15 cycleslmin)
and during deep breathing (5s inpiration, 5 s expiration, four cycles) before drinking and hourly
thereafter for 3h.
2. Mean breath alcohol concentration rose to
18.9 mg/100 ml. In the time domain analysis, the root
mean square difference of successive R-R interval
decreased significantly with ethanol as compared with
the juice experiment. The difference remained statistically significant even after adjustment for the shorter
R-R interval after alcohol. In the frequency domain
analysis the high-frequency (0.150.5 Hz) spectral
power showed a significant decrease after alcohol
intake. Also, the index of sensitivity of the baroreceptor reflex (square root of R-R interval power/
systolic blood pressure power) decreased significantly
in the high-frequency component. Ethanol did not
change finger systolic blood pressure, and power
spectral analysis did not show significant variability
in blood pressure.
3. These data indicate that acute intake of moderate
amounts of alcohol causes a significant decrease in
heart rate variability owing to diminished vagal
modulation of the heart rate.
INTRODUCTION
Cyclic variations in heart rate and blood pressure
reflect mainly the autonomic nervous system modulation of the circulatory system [ 1-31. Heart rate
variability is reduced in coronary heart disease and
has been proposed as a prognostically important
factor, particularly after myocardial infarction [4].
Recently, decreased heart rate variability has also
been reported in chronic alcoholics [S], and autonomic neuropathy has been linked with increased
mortality in an alcoholic population [6]. How
social drinking influences heart rate variability is
still poorly understood, although an acute postalcohol impairment has been reported in one study
[7]. The present study was designed to assess in
more detail the effects of acute alcohol intake on
short-term heart rate and blood pressure variability
in healthy subjects.
METHODS
Subjects
We studied 12 male subjects whose mean (SD)
age was 23.8 (1.5) years and weight was 74.5 (8.4) kg.
All were healthy according to history and clinical
examination, and none had abnormalities in the 12lead electrocardiogram. None of the subjects was on
regular drug therapy. Their weekly alcohol consumption averaged 77 g (range 20-150 g) of ethanol.
Two of them were regular cigarette smokers.
General study design
The subjects were studied in the afternoon in a
quiet and warm room in a research ward. They had
abstained from alcohol for at least 48h and had
fasted and refrained from coffee and tobacco for 4 h
or more before the study. All subjects took part in
two experiments, which were identical except that
on one occasion they drank ethanol (1 g/kg body
weight in juice, 15% w/v) and on the other the same
volume of juice. The order of the juice and ethanol
experiments was random. The experiments were
carried out at least 7 days apart. The study was
approved by the local ethics committee, and all
participants gave their informed consent.
Baseline recordings were carried out after a
30 min supine rest. The subjects then ingested either
ethanol or juice during 30min and the recordings
were repeated every hour for 3h. Brachial artery
pressure was recorded by the cuff method at baseline and every hour thereafter. Breath alcohol was
determined with a portable breath analyser (SD-2,
Lion Laboratories, Barry, South Glamorgan, U.K.)
Key words: alcohol, baroreflex, heart rate variability.
Correspondence: D r Pekka Koskinen, First Department of Medicine, Helsinki University Central Hospital, Haartmaninkatu 4, SF40290 Helsinki, Finland.
226
P. Koskinen et al.
at baseline and every hour during the ethanol
experiment.
Heart rate and blood pressure variability
The finger arterial pressure was monitored using
an Ohmeda 2300 Finapres device [8,9]. The finger
cuff was applied to the right thumb or middle finger
and the cuff was maintained at the midchest level.
In this system the cuff pressure equals arterial blood
pressure, and the monitor displays arterial blood
pressure waveform and numerical readings. Heart
rate was monitored using a bipolar lead producing
a tall positive R-wave. Heart rate and blood pressure variation was studied during 5-7 min of
controlled breathing ( 15 respiratory cycles/min) and
during deep breathing (four successive deep respiratory cycles, 5 s inspiration and 5 s expiration). A
metronome, giving a signal with a frequency of l/s,
was used to help the subjects breath regularly.
During both controlled and deep breathing, continuous electrocardiographic and finger arterial pressure signals were stored in an IBM PC/ATcompatible microcomputer through an analog-todigital converter (sampling frequency 200 Hz, amplitude resolution 12 bits).
Analyses of heart rate and blood pressure variations were performed with a commercially available
computer program (CAFTS, Medikro Inc., Kuopio,
Finland) [lo]. A stationary segment of the graphical
displays of the beat-to-beat R-R intervals and finger
arterial pressure were selected for analysis. The
program calculates the mean R-R interval, the root
mean square difference of successive R-R intervals
and the mean systolic and diastolic blood pressure,
and produces power spectral density functions of
R-R intervals and blood pressure using autoregressive modelling (model order 18). During the deep
breathing experiment it calculates the ratio of the
longest expiratory R-R interval to the shortest
inspiratory R-R interval. The power of R-R intervals and systolic and diastolic blood pressure were
determined over all frequencies from 0.00 Hz to
0.5 Hz (total power) and separately in the low- (0.W
0.06 Hz), medium- (0.07-0.14 Hz) and high- (0.150.5 Hz) frequency bands. The repeatability of the
measurements and a more detailed description of
the analysis have been published elsewhere [lo, 1 I].
The R-R interval-systolic arterial pressure relationship was used as an index of baroreceptor reflex
sensitivity [I21 and computed both in the mediumand high-frequency bands as: (R-R interval power/
systolic blood pressure power)’’2. Although our
method did not allow measurement of the coherence
function of R-R interval and systolic blood pressure
variations, previous studies [12,131 have shown a
high coherence between them around medium- and
high-frequency regions regardless of whether blood
pressure was measured invasively or by Finapres, as
in our study.
Since many of the variables studied are heart-
Table I. Spearman rank correlation coefficients between R-R interval and other measured variables. MF/HF denotes the ratio of R-R
interval power in the medium-frequency band to that in the high-frequency
band. The coefficients are derived from data acquired at baseline of the
juice and ethanol experiments (n = I1 in both; P<O.O5 when the coefficient
is >0.591).
R-R interval
Juice expt.
Root mean square of
R-R interval difference
Ratio of expiratory t o inspiratory R-R
interval during deep breathing
R-R interval power
0.00-0.5HZ
Ethanol expt.
0.630
0.516
0.151
- 0.056
0.553
0.329
0.655
0.392
0.501
0.298
0.501
0.503
(total)
O.oo-O.06 Hz
(low)
0.074).
14 Hz
(medium)
0. I 5 4 5 Hz
(high)
MF/HF
-0.310
0.042
rate-dependent [14], adjustment for R-R interval
was performed when appropriate. The root mean
square difference of successive R-R intervals and the
ratio of expiratory to inspiratory R-R interval
during deep breathing were divided by the mean
R-R interval. The power spectral data were adjusted
by the method of Hayano et al. [l5]. The results are
given for both unadjusted and adjusted data. Correlations between R-R interval and other variables
using baseline data of both experiments are given in
Table 1.
Statistical analysis
Since the subjects served as their own controls,
the results of the juice and ethanol experiments were
compared by analysis of variance for repeated measures without a grouping factor, but using time and
treatment (i.e. juice or ethanol) as within-subject
factors. Many of the variables were right-skewed,
and logarithmic transformation was performed
before the analyses if the Kolmogorow-Smirnov
one-sample test detected non-normal distribution in
a continuous variable. Normally distributed variables are given as mean (SD), and those with nonnormal distribution as median (range). The significant level was set at P<O.O5.
RESULTS
The mean (SD) volume of juice and ethanol the
subjects drank was 497 (57) ml. During ethanol
ingestion their breath alcohol level rose to 18.9mg/
100m1, 14.7mg/100ml and 12.6mg/100ml after 1 h,
2 h and 3 h, respectively.
The results of heart rate variability analyses in the
time and the frequency domains are shown in
Alcohol and heart rate variability
227
Table 2. Heart rate variability indices in the time domain during controlled breathing (I5 cycles/min) and deep
breathing (four cycles, 5 s inspiration, 5 s expiration) in 12 healthy subjects drinking ethanol (Ig/kg body weight) or
juice. The values are mean (SD) o r median (range). F and P values, denoting the significance of the difference between juice and
ethanol experiments, are derived from analysis of variance for repeated measures. F' and P' denote the significance of the difference
after adjustment for R-R interval. Root mean square R-R interval difference data were log-transformed before analysis.
Time
Oh
R-R interval (ms)
Juice
Ethanol
Ih
Zh
loel
( 149)
3h
I060
I064
(163)
I083
(143)
96 I
919
(149)
983
( 189)
( 122)
(89)
(144
(zz-lel)
47
(2C-214)
56
(23-173)
34
50
31
40
(iciis)
(IC67)
(16124)
Ratio of expiratory to inspiratory R-R interval
during deep breathing
Juice
1.52
(0.29)
Ethanol
I.59
1.52
(0.27)
I .54
I .55
(0.30)
I .46
(0.20)
I .59
(0.29)
I.so
(0.17)
(0.30)
Tables 2 and 3, respectively. Ethanol decreased the
mean R-R interval significantly. The root mean
square difference of successive R-R intervals decreased significantly during the ethanol experiment
compared with the juice experiment, and the difference between the treatments remained statistically
significant after adjustment for the increased heart
rate. During ethanol intake, the ratio of expiratory
to inspiratory R-R interval during deep breathing
was lower than during juice ingestion. The difference between the treatments was not statistically
significant when adjusted for R-R interval.
In the frequency domain analyses, the total R-R
interval power decreased more during ethanol than
during juice ingestion. Adjustment for R-R interval
changes reduced the difference. The power of the
high-frequency component of R-R interval decreased more during ethanol than during juice ingestion. Also, the medium-frequency component power
decreased during both experiments, more so during
ethanol ingestion. The ratio of the medium- to the
high-frequency component was not different
between the experiments. The changes in the power
of the low-frequency component are less important
since the data acquisition time was too short to
include rhythmic alterations occurring in this
component.
Table 4 and Fig. 1 show the changes in the
baroreceptor reflex control of heart rate. The index
of the baroreceptor reflex sensitivity decreased
slightly during ethanol ingestion in the mediumfrequency band and significantly in the highfrequency band as compared with the juice
experiment.
Finger arterial systolic or diastolic pressure did
not differ between the experiments. During juice
P
f'
P'
4.097
0.014
1.279
0.298
1061
Root mean square R-R interval difference (ms)
Juice
57
(2617 I)
Ethanol
66
(22-192)
(0.28)
f
5.754
7.798
4.679
0.003
<0.001
0.008
ingestion, the mean fSD systolic pressure was 130f
11, 136+13, 131+10and 135f12mmHgat Oh, l h ,
2 h and 3 h, respectively, and the diastolic pressure
was 64 f8, 69 f8, 69 f6 and 67 f 11 mmHg, respectively. During ethanol ingestion systolic and diastolic blood pressures were 130f 12, 130k 13, 131 f 15,
130f16 and 6 2 f l 1 , 6 5 k 8 , 66f7, 64f8mmHg,
respectively. The spectral power analysis of the
finger systolic blood pressure did not show significant differences in the short-term variation between
the two experiments (Table 5).
DISCUS90N
Acute intake of socially acceptable amounts of
alcohol resulted in a significant decrease in shortterm heart rate variability in healthy subjects. A
significant suppression of R-R interval variability,
even after adjustment for the faster heart rate during
the ethanol experiment, was found in the time
domain analyses. In the power spectral density
analysis, a significantly lowered high-frequency component was observed during ethanol ingestion,
although this difference lost significance after adjustment for heart rate. Ethanol also decreased the
index of the baroreceptor reflex sensitivity in the
high-frequency component.
Although most of the heart rate variability indices
are rate-dependent, the question of whether to
adjust for heart rate or not in the analyses is problematic. For example, vagal inhibition decreases both
heart rate variation and R-R interval length. Thus
the decrease in heart rate variation can be a direct
consequence of vagal inhibition, an indirect effect
of reduced R-R interval, or both. By adjusting for
P. Koskinen et al.
Table 3. Heart rate variability indices in the frquency domain during ethanol (Ig/kg body weight) and juice
experiments (controlled breathing at I5 cycla/min). The valuer are median (range). MF/HF is the percentage of R-R interval
power in the medium-frequency band of that in the high-frequency band. F and P values denote the difference between ethanol and
juice experiments, Data were log-transformed before analysis. In F' and PI adjustment for R-R interval was performed.
R-R interval power (ms')
Time. ..Oh
Ih
2h
3h
3765
(548-16221)
2358
(7759453)
3538
(602-19 178)
I860
(579-6999)
268 I
I292
I552
(I 18-4951)
823
(1 0 7 4 4 )
861
41 I
( 106-2486)
350
F
P
F'
PI
2.758
0.058
1.050
0.383
0.398
0.690
2.764
0.057
2.606
0.068
1.627
0.202
4.139
0.014
2.705
0.061
0.259
0.855
1.185
0.331
0.00-0.5 Hz (total)
3556
(1037-19438)
4229
(642-1 8 973)
Juice
Ethanol
(1041-21697)
2426
(72044531)
0.00-0.06Hz (low)
883
(200-4994)
I181
( 166-3951)
Juice
Ethanol
0.07-0).14Hz (medium)
Juice
Ethanol
0.15-0.5Hz (high)
Juice
Ethanol
MF/HF (%)
Juice
Ethanol
(82-323 I)
796
( 123-3187)
(204-2I 727)
848
( 101-5076)
595
(I643521)
833
(67-41SO)
801
(843-2795)
397
(82-21 99)
573
(57-3675)
272
(10-1 107)
I957
(668-1 0 923)
I764
(367-10 870)
1444
(423-1 0 480)
1291
(323-5219)
I222
(427-1 2 097)
930
(41-1802)
I395
(537-16 322)
I I85
(324-5 153)
31
(I1-55)
33
(I 6202)
36
(10-71)
29
(I2-79)
34
(13-61)
31
( 16-76)
31
( 11-54)
30
(534302)
(643)
Table 4. Power spectral analysis of baroreceptor reflex sensitivity in
the medium- and high-frequency bands during juice and ethanol
(Ig/kg body weight) ingestion. Data are median (range). f and P denote
the significance of difference between juice and ethanol experiments. Data
were log-transformed before analysis.
Baroreceptor reflex
sensitivity (ms/mmHg)t
Time ...Oh
Ih
2h
F
P
3h
0.07-0.014Hz (medium)
Juice
Ethanol
0.15-0.5Hz (high)
Juice
Ethanol
I3
(9-26)
I5
(7-25)
13
(74)
12
(7-37)
20
19
18
I4
(6-53)
(745)
I2
2.283
10
(2-15)
23
18
( ~ 5 5 ) (10-65) (10-54) (8-57)
19
I4
I2
16
(11-51)
(9-33)
(3-23)
0.097
(7-26)
4.990
0.006
(74)
tlndex of the baroreceptor reflex sensitivity = (R-R interval power/systolic
blood pressure)'/'.
the changing R-R interval one may inappropriately
diminish the direct effect of vagal inhibition on
heart rate variation. There seems to be no consensus
on the matter, but most authors [2,5,8,16], do not
adjust power spectral data for heart rate although
there are exceptions [ l l , 151. Because our experience
0
I
2
3
Time (h)
Fig. 1. Median of the index of brroreceptor reflex sensitivity
(square root of R-R interval power/systolic blood pressure power)
in the high-frequency component of the spectral power analysis
The
M o r e and after ethanol (Ig/kg body weight; m) or juice (0).
difference between the experiments was statistically significant (P= 0.006).
[ l l ] suggests a close relationship between R-R
interval and heart rate variability indices, we chose
to report both adjusted and unadjusted results.
The acute alcohol-induced changes in heart rate
Alcohol and heart rate variability
229
Table 5. Power spectral analysis of finger systolic arterial pressure during juice and ethanol (Ig/kg body weight)
ingestion. The values are median (range). F and P denote the significance of difference between juice and ethanol experiments. Data
were log-transformed before analysis.
Systolic arterial
pressure power (mmHn’)
Time.. .Oh
Ih
2h
3h
18
(8-32)
16
(7-50)
(3-24)
7
(436)
F
P
0.016
0.997
0.149
0.929
0.096
0.962
1.525
0.226
O.OO-O.5 Hz (total)
Juice
21
19
(W
Ethanol
(1347)
23
(S57)
18
( E l 17)
IS
(6-38)
17
(8-35)
14
(3-29)
13
(346)
9
(3-31)
10
(1-86)
6
(2-28)
6
(3-27)
3
(1-7)
3
(1-12)
3
2
(1-10)
2
(1-7)
2
5
(3-10)
4
(2-14)
4
(3-16)
4
(1-1 I)
4
(2-12)
5
(3-1 I)
0.004.06HZ (low)
Juice
Ethanol
0.07-0.14Hz (medium)
Juice
Ethanol
O . I M . 5 H z (high)
Juice
Ethanol
(14
2
(1-14)
5
(2-19)
variability observed in this study can be explained
by acute inhibition of the vagal modulation of heart
period. The high-frequency component (0.15-0.5 Hz)
of the R-R interval spectrum during controlled
breathing is mainly under vagal control and fast
changes in its power are produced by alterations of
vagal modulation [2]. Other parameters that affect
the high-frequency component, e.g. atrial stretch
caused by venous return and reflexes originating
from the respiratory tract, play a minor role. The
root mean square difference of successive R-R intervals correlates highly with the high-frequency spectral component, implying vagal control of this variable also. The power of the medium-frequency
component (0.07-0.014 Hz), on the other hand, is
believed to depend on both parasympathetic and
sympathetic inflows [2]. However, in supine rest the
parasympathetic system may also dominate the
control in this frequency band [16). Thus, inhibition
of the parasympathetic system can also explain the
decrease in the power of the medium-frequency
component in the present study.
Acute ethanol ingestion has been reported to
increase the concentrations of circulating catecholamines [17] and therefore its acute effects on cardiovascular control systems are frequently attributed to
activation of the sympatho-adrenergic system. However, some more recent studies have found no effect
of acute ethanol intake on the adrenergic system
when measuring plasma catecholamines and lymphocytic B-adrenergic receptor density in healthy
subjects [181. Activation of the sympatho-adrenergic
system by the tilt test, for example, results in a
II
(13
2
(1-10)
4
(2-23)
decrease in the high-frequency component and,
unlike our results, an increase in the mediumfrequency component [19]. On the other hand,
studies in chronic alcoholics have shown that longterm alcohol abuse can cause autonomic neuropathy with vagal damage as one of its main features
[20,21]. The present findings suggest that the
changes evoked acutely by moderate alcohol intoxication in the cardiovascular control are also vagally
mediated.
Long-term alcohol use elevates blood pressure
and hypertension is prevalent among chronic
drinkers [22]. Impaired baroreceptor reflex sensitivity has been found in hypertensive patients [23]
and in ethanol-induced hypertension in rats [24].
Animal studies have also shown that the impairment in baroreceptor reflex sensitivity related to
ethanol can be found even before the rise in blood
pressure occurs [25]. Because we did not find a
significant elevation in blood pressure after acute
ethanol ingestion, the decrease in the index of the
baroreceptor reflex sensitivity in the high-frequency
component during ethanol ingestion was mainly due
to the reduced R-R interval variability.
Diminished heart rate variability and depressed
baroreflex sensitivity are markers of poor prognosis
in post-infarction patients [4,26]. The incidence of
ventricular fibrillation and sudden death are
increased in these patients. Acute arrhythmias are
not uncommon among alocholics either. The
mechanism of sudden death is not clear, but since
the post-mortem studies frequently fail to detect
coronary atherosclerosis or myocardial infarction,
230
P. Koskinen et al.
the deaths have been attributed to malignant ventricular arrhythmias [27]. Disturbed balance between
the sympathetic and parasympathetic systems may
render the heart vulnerable to arrhythmias,
especially in patients whose chronic alcohol abuse
has already injured the myocardium and caused a
substrate for arrhythmias. Johnson and Robinson
[ 6 ] have reported mortality data in chronic alcoholics in relation to autonomic nervous dysfunction.
They found a significantly higher mortality in chronic alcoholics with autonomic neuropathy than in
the general population. The deaths were mainly
cardiovascular in origin. In addition, altered balance
between the sympathetic and parasympathetic
systems may play a role in initiation of less malignant cardiac arrhythmias, like atrial fibrillation,
often associated with ethanol [28].
In conclusion, these results suggest that acute
alcohol intake reduces short-term heart rate variability and depresses the index of the baroreceptor
reflex sensitivity in healthy subjects, and that these
changes are due to inhibited parasympathetic
control of the heart.
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ACKNOWLEDGMENT
This work was supported by the Foundation for
Alcohol Research, Finland and the Finnish Cardiac
Society.
REFERENCES