Acute Effects of Low Doses of Alcohol on
Left Ventricular Function by Echocardiography
By CEDIAR E. DELGADO, M.D., NICHOLAS J. FORTLIN, M.D.,
AND
RICHARD S. Ross, M.D.
SUMMARY
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The ultrasound method for measuring the dimensions of the left ventricle was utilized to study the effect
of oral doses of alcohol on left ventricular function in normal volunteers. Systolic time intervals were also
measured. Seven subjects received 0.7 g/kg of ethanol (group I) and six subjects received 1.15 g/kg (group
II). The peak blood alcohol levels in the two groups were 75 mg/100 ml and 138 mg/100 ml respectively.
There was a 6% decrease in the fractional change in the minor axis of the left ventricle in group I patients
which resulted in a decrease in ejection fraction (P < 0.05). In group II patients, there was a 3% decrease in
the fractional change in the minor axis of the left ventricle, but the change in ejection fraction was not
significant. Since there was no significant difference between the physiological effects observed in groups I
and II, the two groups were combined. In the combined group, at 30 minutes after the ingestion of alcohol,
the heart rate was increased by 11 %, the fractional change in the minor axis of the left ventricle decreased by
6%c, the ejection fraction decreased by 4% (P < 0.01), and Ver decreased by 5%. These data suggest that in
normal subjects myocardial contractility is depressed following the ingestion of alcohol.
Additional Indexing Words:
Ethanol
Systolic time intervals
Ultrasound
PREVIOUS STUDIES in isolated heart muscle
fibers, 2 and in experimental animals3' 4'' suggest
that acute exposure to alcohol is associated with a
depression of myocardial contractility. In alcoholic
subjects without evidence of cardiac disease Regan et
al. reported that 12 oz of Scotch whiskey (162 ml
ethanol) ingested in two hours produced transient
depression of left ventricular function, evidenced by
elevation of left ventricular end-diastolic pressure,
and a simultaneous decrease in the stroke volume index.7 In normal volunteers the noninvasive systolic
time intervals method has been used by Ahmed et al.
in studies which showed that myocardial contractility
wvas depressed by 6 oz of Scotch whiskey (81 ml
ethanol) which produced blood levels from 75-110
mg/100 ml.8 The present study utilized echocardiography to record serial changes in ventricular function following acute alcohol ingestion in normal
human volunteers. The echocardiographic measurements of ventricular dimensions were compared with
systolic time intervals.
Subjects and Procedure
The subjects were ten normal volunteers, seven males and
three females (average age of 29.9 years, range from 22 to
31). They were infrequent users of alcohol and were studied
in the fasting condition after 20 minutes of rest in the supine
position. Two groups of experiments were conducted which
differed only in the alcohol dose. Group I, seven subjects, ingested 0.7 g of ethanol/kg of body weight in less than 30
min. Group II, six subjects, ingested 1.15 g of ethanol/kg in
less than 60 min. The alcohol was diluted in orange juice to
a total of 400 cc. The alcohol dosage corresponds to between
two and three drinks of Scotch whiskey (2 oz per drink), and
the blood levels are in the expected range for this dosage.
The dose of ethanol exceeds that usually consumed during
the course of "social" drinking, especially when the 30 to 60
minute period of administration is considered. Heart rate,
blood pressure, echocardiographic and systolic time interval
measurements were made two times during the control
period and every 30 minutes for the next three hours. A
blood sample was obtained for alcohol determinations at the
time of each set of measurements.
Echocardiography
Echocardiograms were obtained with a Smith-Kline
Ekoline 20A ultrasonoscope utilizing a 2.25 mHz focused
transducer. Recordings were made on a Cambridge multichannel photographic recorder at a paper speed of 50
mm/sec. Standard techniques were employed to obtain the
left ventricular minor axis dimension. The measurement of
left ventricular minor axis (S) was made on echocardiograms
which showed echoes from the mitral apparatus. This
precaution assured that serial records used for comparison
were obtained with the ultrasound beam crossing the ventri-
From the Cardiovascular Division, Department of Medicine, 'the
Johns Hopkins Mledical Institutions, Baltimore, Marvland.
Supported in part bh a grant from the LUnited States Bress ers'
Associationi. Dr. Delgado X as a Research Fellov, supported bh the
American Heart Association, \Iarvland Affiliate.
Address for reprints: Richard S. Ross, \1.D., Carnegie 568, The
Johns Hopkins Hospital, Baltimore, \larx land 21205.
Received November 11, 1974; accepted for publication
November 19, 1974.
Circulation, Volume 51, March 1975
cle in the same location on each occasion.9 End-diastolic
diameter (Sd) was measured at the onset of the QRS. Endsystolic diameter (S,) was measured from the peak systolic
535
DELGADO, FORTUIN, ROSS
5036
Table l
Systolic Time Intervals in Group I (0.7 g/kg)
Blood
alcohol
ml/100 ml
Control
30 min
60 min
90 min
120 min
150 min
180 min
74.48
76.29
68.07
62.28
61.20
3.63
-
-
10.45
06.21
06.99
10.20
08.29
07.17
Heart
rate
BP
syst
(mm Hg)
(beats/min)
39.7 - 2.3
66.6 3.3**
66.9 2.5*
64.3 2.7*
65.7 =3.4*
64.0 3.3
67.3 3.0**
111.7
114.3
109.0
108.7
107.6
109.7
109.7
-
-
4.5
4.3
4.2
4.5
3.8*
4.8
4.7*
BP
diast
(mm Hg)
SD
cm
68.6 3.1
71.1
3.1
70.0 2.7
69.7 2.7
66.9 2.4
69.7 3.7
68.8 i 3.1
0.16
4.81
4.80 0.16
4.80 0.17
4.81 i 0.16
4.78 0.16
4.73 0.16
4.76 0.17
Ss
cm
3.16
3.28
3.26
3.26
3.17
3.10
3.17
-
-
0.13
0.14
0.12
0.16
0.15
0.13
0.16
Mean values standard error are shown.
Statistical significance (paired t), *P < 0.05, **P < 0.01.
Abbreviations: SD = end-diastolic diameter; QS2 = electromechanical systole; Ss = end-systolic diameter; LVET = left venitricular
ejection time; E.F. ejection fraction; PEP = pre-ejection period; V,f = Mean velocity of circumferential fiber shortening.
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motion of the endocardial echo of the left ventricular
posterior wall to the left side of the interventricular septal
echo. An average of five beats was taken as the value for
each dimension. At the completion of the study the records
were coded. The minor axis dimension was measured independently by two observers without knowledge of the
conditions at the time of study.
Results
The blood alcohol values are listed in tables 1 and 2
and are plotted in figure 1. Subjects in group I ingested 0.7 g of ethanol/kg in less than 30 minutes and
Derived Echocardiographic Volumes and Contractility Indices
Ventricular volumes at end diastole and end systole were
calculated from V = 1.047 S3.` The stroke volume and ejection fraction were calculated from the end-diastolic and
The
systolic volumes. SV = EDV -ESV, EF = EDV
fractional change of the left ventricular minor axis during
systole (% A S) = Sd - S,/Sd.' The mean velocity of circumferential fiber shortening (Vcf) was calculated from
SdSd *dt ;" dt was the left ventricular ejection time
measured from the simultaneously recorded carotid pulse.
dS
Systolic Time Intervals
Systolic time intervals`2 13
were measured from
simultaneous recordings of the carotid pulse, electrocardiogram, and phonocardiogram from the third left intercostal space. The Cambridge multichannel system was
utilized for recording at a paper speed of 100 mm/sec. The
following measurements were made: electromechanical
systole (QS,) from the onset of the Q wave of the electrocardiogram to the first rapid deflection of the aortic component
of the second heart sound; left ventricular ejection time
(LVET) taken from the onset of the rapid upstroke of the
carotid pulse to the incisura of the dicrotic notch; preejection period (PEP) = QS2 - LVET. A mean value of five
beats was used as the value for each measurement. Blood
pressure was obtained by sphygmomanometer and heart
rate was measured directly from the electrocardiogram.
Blood Alcohol Determinations
Ethanol concentrations were determined in all serum
samples by gas-liquid chromatography under the direction
of Dr. Esteban Mezey at the Alcoholism Research Unit of
the Baltimore City Hospitals.'4
Statistics
The results were analyzed by the Student's paired t-test.
(.3
-.
MINUTES
MEASUREMENTS
xx X
(-HEART RATE
X
X
X
X
X
X
-PLOOD? PRESSURE
-ECHOCARD/OGRA PH/C
LEFT VENTRICULAR MINOR AXIS
Y-SYSTOLIC TIME INTERVALS
Figure 1
Blood alcohol levels. Mean values ± standard error are shown.
Solid line = group I (0.7 g/kg); Broken line = Group II (1.15
g/kg). Ingestion period presented at bottom left: Group I = 0.7
glkg in less than 30 minutes. Group II = 1.15 g/kg in less than 60
minutes.
Circulation, Volume 51, March 1975
537
EFFECT OF ALCOHOL ON LV FUNCTION
SD-SS
0.34
0.32
0.32
0.33
0.33
0.34
0.33
Vef
E.F.
SD
0.02
0.02*
0.02**
0.02
0.03
0.02
0.02
0.71
0.02
0.68 0.02*
0.68 0.02*
0.68 0.03
0.69 0.04
0.71
0.03
0.69 l 0.03
cire/sec
1.10
1.05
1.06
1.06
1.09
1.13
1.09
-
-
f
0.04
0.04
0.05
0.05
0.08
0.07
0.07
QS2
msec
LVET
mseC
417.0 8.2
411.3 - 10.7
409.3 £ 8.1
412.3 7.6
409.4
7.7
413.0 7.1
419.7 - 7.8
310.4
7.4
303.0 9.3
300.4 - 7.8*
304.3 W 7.5*
305.3 8.0
303.9 1 8.6
305.8 ± 9.8
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following this a mean peak blood alcohol level of 75
mg/100 ml was attained at between 30-60 minutes.
The blood alcohol concentration fell slowly and 70%
of the peak concentration was still present at the end
of three hours. Subjects in group II received the larger
dose (1.15 g/kg) over a longer period (60 min) and in
this group the mean peak blood alcohol value of 138
mg/100 ml was reached at 60 minutes. At 30 minutes
the mean value was 86 mg/100 ml. At the end of three
hours the blood level was 80% of the peak value.
The physiological observations are presented in
tables 1, 2, and 3 for the low dose group, the high dose
group, and total group, respectively. In group I, the
low dose group (table 1), the heart rate increased from
60 beats/min to a value of 67 beats/min at 30 and 60
minutes. This 12% change was significant (P < 0.01)
and persisted throughout the period of observation.
There was a 6% decrease in the fractional change of
the left ventricular minor axis %,\ S, as measured by
the echocardiographic method (P < 0.01), and this
resulted in a 4% decline in ejection fraction. Both
measurements had returned to control values by 90
minutes. The changes in QS2, LVET, and PEP were
small and of borderline significance (P < 0.05)
throughout the period of observation despite the 12%
increase in heart rate.
In group II, the high dose group (table 2), the heart
rate increased by 8% at 30 minutes, but the change
did not achieve statistical significance. The fractional
change in the minor axis %/S decreased by 3% at 60
minutes (P < 0.05). The associated decrease in ejection fraction did not achieve significance. The mean
velocity of circumferential fiber shortening decreased
from 1.22 ± 0.06 to 1.19 ± 0.06 circumferences/sec
at 60 minutes (P < 0.001). There were no significant
changes in the systolic time intervals. Thus, although
the group II subjects ingested a larger quantity of
alcohol over a longer time and had higher blood
levels, the changes in heart rate and contractility were
similar in direction, but smaller than in the group I
subjects.
Because of this lack of significant difference
Circulation, Volume 51, March 1975
-
PEP
106.6
108.3
108.9
108.0
104.1
109.1
113.8
-
-
i
PEP/ET
3.2
4.4
4.1
4.4
3.8
3.7
4.1
0.01
0.34
0.36 i 0.02
0.02
0.36
0.36 0.02
0.35 0.02
0.36 - 0.02
0.38 - 0.02
between the physiological effects observed in the two
groups, the two groups I and II were combined and
the results of this combined group are presented in
table 3 and plotted in figure 2. Heart rate increased by
11% from 62 to 68 beats/min at 30 minutes
(P < 0.001) and remained significantly elevated
*p<.05
**O<.01
N=/3SL/IBJECS
.75
k
.74,
K-
.73.
T
.72
.7/
70-
/.204.
*~
//
Wi /05
'I
,.*
,*
..
1.
/10+
11
_
/00*.
K
70+
654
60'
t
Cn
/20+
//0'
180
i
i
~
i
i
i
60
,
.
.
.
C
30
60
90
A
/20
/50
/30
TIME (Minutes)
Figure 2
Effects of Alcohol on Indices of Cardiac Function, total group. Time
in minutes is shown on the abcissa. C = control values. Ejection
fraction = ratio of stroke volume to end-diastolic volume.
V( = velocity of circumferential fiber shortening. PEP= preejection period.
DELGADO, FORTUIN, ROSS
538
Table 2
Systolio Time Intervals in Group II (1.15 g/kg)
Blood
alcohol
Control
30 min
60 min
90
120
150
180
min
min
min
min
Mean values
86.50
137.55
126.32
130.06
117.52
110.42
-
-
-
21.08
07.72
13.31
16.78
12.25
12.03
BP
syst
(mm Hg)
Heart
rate
(beats/min)
ml/100 ml
65.0
70.7
67.7
68.3
67.7
64.8
66.3
-
-
118.8
120.0
115.7
114.3
115.2
114.5
112.8
3.0
3.9
4.2
4.9
5.6
5.6
4.7
-
-
6.1
6.5
7.9
6.4
7.3
7.3*
5.2*
BP
diast
(mm Hg)
75.3
75.8
74.0
-
-
73.2
72.0
72.0 71.5 -
3.5
4.0
4.3
3.9
3.9
4.0
3.1
SD
cm
Ss
cm
4.99 - 0.13
4.99 - 0.12
5.00 - 0.11
0.13*
4.91
0.13
4.97
4.97 - 0.13
0.11*
4.89
3.10
0.15
3.17 0.16
3.16 i 0.13
3.16
0.12
3.07 i 0.14
:3.12
0.14
3.09 i 0.14
standard error are preseinted.
Statistical significance (paired t), *P < 0.05, **P < 0.01, ***P < 0.001.
For abbreviations see table 1.
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Table 3
Combined Group (13 Subjects)
Heart
rate
(beats/min)
Control
30 mi'
60 min
90 min
120 miii
150 min
180 mill
61.8
68.5
67.2
66.2
66.6
64.4
66.8
-
-
2.0
2.5***
2.2**
2.6*
3.0*
3.0
2.7*
BP
syst
(mm Hg)
115.4
116.9
112.8
111.3
111.1
112.0
111.2
-
-
3.8
3.7
4.2
3.7
3.9
4.1
3.4
BP
diast
SD
(mm Hg)
71.8
73.3
71.8
71.3
69.2
70.7
70.1
-
-
cm
2.6
2.0
2.4
2.3
2.2
2.6
2.1
4.91 - 0.11
4.89 - 0.10
4.89 - 0.11
4.86 - 0.10
4.87 - 0.11
4.84 - 0.11
4.83 - 0.10
SD-SS
Ss
cm
3.14 3.23 3.21 3.21 3.13 3.11 )
3.13 -
SD
0.10
0.10*
0.09
0.10
0.10
0.09
-. 10
0.366
0.34 0.34 0.34 O
0.35 -
0.35
0.35
-
0.01
0.01*
0.01**
0.01*
0.02
0.01
0.01
Mean values - standard errors are showis.
Statistical analysis (paired t), *P < 0.05, **P < 0.01, ***P < 0.001.
throughout the period of observation. The echocardiographic measurement of the fractional change in
the minor axis %zAS was significantly decreased by 6%
at 30, 60, and 90 minutes (P < 0.01). This resulted in
a 4% decrease in ejection fraction which was significant at 30, 60, and 90 minutes. The mean velocity of
circumferential fiber shortening (VCf) decreased by 5%
during the same 30-90 minute period (P < 0.01). All
echocardiographic indices of contractility returned to
baseline by 120 minutes. There were no significant
changes in systolic time intervals QS2 and LVET when
groups I and II were analyzed together, as in table III.
The PEP was increased at 180 minutes, but this
change was of only borderline significance (P < 0.05).
Discussion
The direct measurement of the dimensions of the
left ventricle by ultrasound has provided evidence of
depression of myocardial contractility in normal
volunteers following the ingestion of alcohol. The
fractional change in the minor axis of the left ventricle
in systole was decreased significantly at 30 and 60
minutes following the ingestion of alcohol. The in-
dices of myocardial contractility derived from the
measurement of the minor axis also showed depression. The changes were small (5-12%) in these
healthy, young subjects but assume more significance
when it is recognized that they occurred at a time
when the heart rate was increased. An increase rather
than a decrease in contractility would have been expected in healthy young subjects and, therefore, these
small changes assume more significance if the association with increased heart rate is considered.`5 18, 17
'The effect of increased heart rate must also be considered in interpretation of the systolic time intervals.12 In this study there was no large change in these
indices, but the improvement which would have been
expected with tachycardia failed to occur. Ahmed et
al., in a similar study, demonstrated decreased contractility as evidenced by increases in PEP and
PEP/LVET in a group of normal volunteers.8
Previous studies had reported an increase in heart
rate and cardiac output and no impairment of the
response to exercise following alcohol ingestion.'8 19
These studies had been interpreted as indicating that
alcohol had no significant effects on the normal heart.
Circulation, Volume 51, March 1975
EFFECT OF ALCOHOL ON LV FUNCTION
SD-SS
SD
E.F.
0.02
0.02
0.01*
0.02
- 0.02
0.38 0.01
0.37 - 0.02
0.02
0.76
0.75 (0.02
0.75a 0.01
0.73 0.02
0.77 0.02
0.75
0.02
0.75 = 0.02
0.38
0.37
0.37
0.36
0.39
-
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E.F.
0.02
0.73
4 .71 0.02**
0.02**
0.71
0.02**
0.70
0.73
0.02
0.02
0.73
0.72
0.02
V Cf
cire/sec
1.16
0.04
1.10
0.04**
1.12
0.04*
1.11 (0.04*
1.135 0.06
1.17
0.04
1.14
0.05
V'f
circ/sec
1.22
0.06
1.17 & 0.07
0.06***
1.19
0.04
1.17
1.22
0.08
1.22 - 0.06
1.19 - 0.08
S.V.
92.1
5.6
87.6 5.3
6.1
89.1
85.6 -).3
.5.4
89.7
88.5 , .8
86.0 , .2
539
QS2
msec
409.8 - 7.5
413.2 - 10.5
414.2 - 13.6
412.8 - 15.7
420.2 - 16.0
409.7 - 14.2
413.2 - 11.6
QS
mseC
413.7
413.1
411.35
412.3
414.4
411.5
417.4
-
-
The current studies lead to another conclusion in that
they confirm in man the effects of alcohol on contractility which have been observed in isolated heart
muscle fibers and in both anesthetized and conscious
intact animals. In these animal and in vitro studies
concentrations of alcohol similar to those found in the
blood of the subjects in the current study produced a
reduction in contractility. The current study and that
of Ahmed et al. demonstrate the direct effect of
alcohol on the contractility of the normal human
myocardium. These minor changes in contractility do
not, however, impair the function of the heart as a
pump. Presumably, compensatory mechanisms are
responsible for the preservation of over-all circulatory
function in the presence of decreased contractility.
All evidence suggests that alcohol acts as a direct
depressant of myocardial cell function. An alternative
explanation, proposed by Regan, was that the effect
was related to the change in plasma osmolarity and
plasma volume.3 Ahmed gave normal volunteers
alcohol and an isosmotic, isocaloric, isovolumic
sucrose solution orally and measured systolic time inCirculation, Volume 51, March 1975
LVET
PEP
msec
msec
8.7
- 11.2
- 12.9
- 13.1
316.8 - 15.2
306.7 - 12.3
311.3 - 10.8
309.8
314.2
312.2
305.8
-
LVET
msec
3.4
7.3
7.3
7.9
8.2
7.3
6.7
310.2 .).4
308.2
7.1
303.8
7.2
305.()0 7.0
,31 0.6 ( 8.0
303.2
7.0
7.0
308.7
100.0
101.0
102.0
107.0
103.3
103.0
103.7
-
-
-
PEP/ET
2.7
1.1
3.5
3.1
1.7
2.1
2.;
PEP
103.3
2.2
104.9 + 2.6
2.8
105.7
2.6
107.4
2.1
103.7
106.3 - 2.3
108.7 - 2.7*
0.33
0.01
0.32 - 0.01
0.33 - 0.02
0.35 - 0.01*
0.33 - 0.01
0.34 - 0.01
0.34 - 0.01
=
PEP/ET
0.33 0.34 0.35 0.33 0.33)0.33 0.35 -
0.009
0.012
0.014
0.011*
0.011
0.011*
0.014
tervals.8 Alcohol depressed and the sucrose increased
contractility, and therefore increased osmolarity cannot be the explanation for the contractility changes
seen after oral alcohol administration.
The lack of correlation between the blood alcohol
concentration and the cardiac effects presents a
problem in interpretation. In the first place, there was
no significant difference between the hemodynamic
effects of the two dose levels. Furthermore, the
hemodynamic changes persisted for only 30 to 60
minutes, yet the blood alcohol remained elevated
throughout the entire three hours of the experiment.
In the low dose group, changes in ventricular function
are seen at 30 and 60 minutes when the mean blood
alcohol levels were between 70 and 80 mg/100 ml.
Much higher blood levels between 110 and 120
mg/100 ml were present at 120, 150 and 180 minutes
in the high dose group (II) and no alteration in cardiac
function was apparent at that time. These observations could be explained by postulating that the
time and concentration characteristics of the build up
of blood alcohol in the blood during the first 30 to 60
DELGADO, FORTUIN, ROSS
5040
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minutes determine the degree of myocardial depressioIn and that the blood levels at later points in time
are unimportant. It also appears that within those
dosage ranges, the higher dose is not associated with a
larger effect. This suggests that a threshold level is
reached which produces depression of function, and
this in turn initiates a compensatory reaction which
restores the homeostasis.
A similar lack of correlation of blood level and effect
was observed by Juchems who found that normal
volunteers ingesting 0.9 to 1.9 ml/kg of ethanol
evidenced a 13% increase in heart rate at blood levels
of 85 mg/100 ml.20 No further increase in heart rate
was observed with blood alcohol levels above 100
mg/100 ml. A similar effect was observed by Conway
who found no correlation between blood alcohol
levels and hemodynamic changes in eight patients
with coronary artery disease.2' Both differing absorption and the compensatory responses of the autonomic
nervous system have been suggested as responsible for
this lack of relationship between dose and effect. Lack
of absorption cannot be a factor in the current study
and in others in which direct measurements of blood
alcohol have been made. The compensatory response
of the autonomic nervous system probably provides a
better explanation. The role of the autonomic nervous
system has been investigated by Wong4 who studied
the effect of alcohol with and without beta blockade in
anesthetized dogs. Her results show that the depressant effects of ethanol are greater in animals with
autonomic blockade by atropine and propranolol.4
Horwitz and associates were not able to demonstrate
an effect of autonomic blockade in modifying the
response to ethanol in conscious dogs, but they used a
smaller dose of propranolol than in Dr. Wong's study.5
Acknowledgment
The authors would like to acknowledge the assistance of Dr.
Esteban Mezey of the Baltimore City Hospitals who arranged to
have the blood alcohol levels measured in his laboratory. The
authors also wish to express their appreciation to Mrs. Susan V.
Livengood, Technical Director of The Graphics Laboratory, for her
assistance in the conduct of these studies.
References
1. Si'.\N JF Jo, MASOx- DT, BEISER GD, GOLD HK: Actions of
ethanol on the contractile state of normal and failing cat
papillary muscle. (abstr) Clin Res 16: 249, 1968
2. GixiFxo AL, GINMENo MF, WEBB TL: Effect of ethanol on
cellular membrane potential and contractility of isolated rat
atrium. Am J Physiol 203: 194, 1962
3. Ri(.vx TJ, KoiioXE\ii)is G, MOS HOS CB, OLDEwL-RTEIElHA,
i ii s'n PH, HELLEMS HK: The acute metabolic and
hemodynamic responses of the left ventricle to ethanol. J
Clin Invest 45: 270, 1966
4. Wom;. M: Depression of cardiac performance by ethanol
unmasked during autonomic blockade. Am Heart J 86: 508,
1973
5. Houvii<Rllz LD, AiKINS JM: Acute effects of ethanol on left
ventricular performance. Circulation 49: 124, 1974
6. WEBBo WR, DFEFEILI IV: Ethyl alcohol and the cardiovascular
system. JAMA 191: 1055, 1965
7. R(.sx TJ, LE\-INSoN GE, OLDEWUOTEL HA, FRAN\K MJ, WEISSE
AB, Mos( iios CB: Ventricular function in non-cardiacs with
alcoholic fatty liver: Role of ethanol in the production of cardiomyopathy. J Clin Invest 48: 397, 1969
8. AilxIFo) SS, LFvisoN\ GE, REG.s-\ TJ: Depression of myocardial
contractilitv with low doses of ethanol in normal man. Circulation 48: 378, 1973
9. Fooi l L-i\ NJ, Hooi) WP, SHIE1MMN. ME, CRAIoF E:
Determination of left ventricular volumes by ultrasound.
Circulation 44: 575, 1971
10. PONIB0 JF, Tiioo BL, RUSSEL L RO: Left ventricular volumes
and ejection fraction by echocardiography. Circulation 43:
480, 1970
11. FooTUIN NJ, HooD WP, CSAIGE E: Evaluation of left
ventricular function by echocardiography. Circulation 46:
26, 1972
12. Wi ii EO AM, H sims WS, SC HOENFELD CD: Bedside technics
for the evaluation of ventricular function in man. Am J Cardiol 23: 577, 1969
13. Wi issi I AM, HAsIIIs VWS, SCHOENFELD CD: Systolic time
intervals in heart failure in man. Circulation 37: 149, 1968
14. NlizF.- S, ToBAN F: Rates of ethanol clearance and activities of
the ethanol-oxidizing enzymes in chronic alcoholic patients.
Gastroenterology 61: 707, 1971
15. D\s)Eii EM: Left ventricular pressure-volume alterations and
regional disorders of contraction during myocardial ischemia
induced by atrial pacing. Circulation 42: 1111, 1970
16. M( L,xURIN LP, ROLETir EL, GoossMiAN W: Impaired left
ventricular relaxation during pacing-induced ischemia. Am J
Cardiol 32: 751, 1973
17.
BIT xxx SLI) E, SONNENBLICK EH, Ross J Jo, GLICK G, EisTEIN
SE: Analysis of the cardiac response to exercise. Circ Res
20-21 (suppl I): 1-44, 1967
18. Ri-- DP, JAIx AC, DoYLE JT: Acute hemodynamic effects of
ethanol on normal human volunteers. Am Heart J 78: 592,
1969
19. Bio\i(;\iSi G, SALIIN B, MI41I HELI, JH: Acute effects of ethanol
ingestion on the response to submaximal and maximal exercise in man. Circulation 42: 463, 1970
20. J( hF Xi! R, KLOBE R: Hemodynamic effects of ethyl alcohol in
man. Am Heart J 78: 133, 1969
21. CONx\\ s N: Hemodynamic effects of alcohol in patients with
coronary heart disease. Br Heart J 30: 638, 1968
Circulation, Volume 51, March 1975
Acute effects of low doses of alcohol on left ventricular function by echocardiography.
C E Delgado, N J Gortuin and R S Ross
Circulation. 1975;51:535-540
doi: 10.1161/01.CIR.51.3.535
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