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Acute effects of ethanol ingestion on signal-averaged electrocardiograms
Acute Mary
Effects of Ethanol Ingestion Electrocardiograms A. Cardy,
BS, Richard
on Signal-Averaged
L. Donnerstein, MD, Leslee F. Kelly, BA, Nathan MD Gia M. Palombo, BS, and Stanley J. Goldberg,
cute ethanol intoxication has been implicated as a cause of atria1 fibA rillation in otherwise healthy persons
50
H. Bittner,
1
( “Holiday Heart” syndrome) .I Studies have shown that signal-averaged P waves are of longer duration in patients prone to atrial fibrillation than in those without atria1 fibrillation.’ These 2 observations led us to investigate whether atria1 and ven.g tricular signal-averaged electrocardioE grams change after acute ingestion of eth5 *’ anol. ... loThe study group consisted of 8 women and 5 men ranging in age from 23 to 27 years. An experimental group of 10 sub0 ,11,,11,1,1111,1111, jects (6 women, 4 men) ingested ethanol. 150 0 50 2co Five of these experimental subjects and 3 Ti rtYZ(ms) other subjects later served as a control group and did not ingest alcohol. All sub- FIGURE 1. Example of signal-averaged P waves obtained at baseline (so/id iects were nonsmokers. had no recent ethheI and at an ethanol level of 0.075 g/dl (dashed he). gnol ingestion, had no; eaten for 4 hours ’ before the experiment, and had no evidence of car- were bandpass filtered from 30 to 300 Hz3 and amplidiac disease by history, physical examination, or fied 100,000 to 200,000 times for P waves and 10,000 echocardiography. Informed consent was obtained to 20,000 times for QRS complexes (Grass Instrubefore the study under a protocol approved by the ments, Quincy, Massachusetts). Signals were sampled Institutional Human Subjects Committee. at 2,000 Hz for 7.2 minutes using a 1Zbit analog-toSubjects in the experimental group drank a total of digital’ converter (MacAdios II, GW Instruments, 0.95 g/kg of body weight of ethanol. Ethanol was di- Cambridge, Massachusetts). Digital data were stored luted in 24 ounces of fruit punch and divided into 3 for later signal averaging on a Macintosh Quadra 950 equal portions for consumption at separate intervals. microcomputer (Apple Computers Inc., Cupertino, Subjects drank no other fluids during the study. Blood California). ethanol levels were estimated by analysis of expired Signal-averaged P waves and QRS complexes were air (Intoxilyzer 5000 CMI, Incorporated, Owensboro, compared by 2 investigators who were blinded to the Kentucky). Signal-averaged P waves and QRS com- other’s results. By superimposing the computer-genplexes were obtained in the study group at baseline (0 erated signal-averaged P waves (or QRS complexes) g/dl), at 0.025 2 0.005 g/d1 increasing ethanol levels, on the computer display (Figure l), differences beat 0.075 & 0.005 g/d1 peak ethanol levels, and at 0.025 tween waveforms were readily apparent. Statistical sig2 0.005 g/d1 decreasing ethanol levels. The control nificance from baseline was determined using a paired group drank only 8 ounces of fruit punch; signal-av- t test. Changes between the experimental group at eraging was performed before and 30 minutes after 0.025 g/d1 and the control group after fluid ingestion fluid ingestion. Thirty minutes was the average amount were compared with an unpaired t test. of time required for the experimental group to reach More than 200 beats were averaged for all studies, the 0.025 g/d1 increasing ethanol level. With subjects and noise levels after signal averaging were <0.3 relaxed in a supine position, recordings were obtained /JV in all cases. Results after signal averaging are in an electrically shielded room from electrodes kept summarized in Figure 2. Baseline signal-averaged Pin the lead II position throughout the study. Signals wave duration was 108 + 8.5 ms [SEMI and QRS duration was 90 2 7 ms. After ethanol ingestion, P waves were prolonged in 9 of 10 subjects, and QRS From the Department of Pediatrics, Steele Memorial Children’s Recomplexes in 10 of 10 subjects. In most subjects, search Center, Diamond Research laboratory, and University Heart increases relative to the baseline were greater as ethCenter, Tucson, Arizona. Dr. Donnersiein’s address is: Dept. of Peanol levels increased. In the control group, P waves diatrics, University of Arizona Health Sciences Center, Tucson, Ariwere prolonged in 7 of 8 subjects and QRS comzona 85724 Manuscrilst received Seotember 26. 1995: revised manuscript received and’accepted Jan&y 23, 1946 plexes in 8 of 8 subjects after fluid ingestion. How1356
01996 by Excerpto Medica, All rights reserved.
Inc.
0002-9 149/96/$15.00 PII 50002.9149(96)00205-6
B. T
**
0.075
0.025
(Falling)
Ethanol Level (g/dl) FIGURE 2. Mean than es in signal-avemged P wave, top, and QRS complex ~J~$WIS (lower pane 0 at varying ethanol levels. Error bars = + 1 SEM ‘p . ,- l *pO.OS.
QRS
P Wave
EthXd
Fluid
Ethanol
Fluid
l&i
F&i
FIGURE 3. Comparison of changes in signal-avemged electrocardi mm dumtions in subjects drinking both ethanol and fluid and those drinking 7l uid alone. Error bars = + 1 SEM; ‘p
ever, changes relative to baseline were significantly greater in the experimental group than in the control group (Figure 3). . . .
The main findings from this study are that acute ethanol ingestion causes an increase in duration of
both atrial and ventricular signal-averaged electrocardiograms. These results are consistent with those of Gould et al,4 who used electrophysiology studies in humans to demonstrate that alcohol causes a delay in atrial conduction. Recent studies have shown that on signal-averaged electrocardiograms, patients prone to atrial fibrillation have au increase in duration of high-frequency, low-amplitude signals, particularly at the end of the P wave.’ It is possible that prolongation of these later components may contribute to dysrhythmias associated with Holiday Heart syndrome found in some patients after binge drinking. Several mechanisms have been offered to explain the effect of ethanol on the heart. Ethanol may have a direct or indirect effect on the myocardium. Indirectly it may stimulate the release of catecholamines, which have been shown to cause an increase in P-wave duration in otherwise healthy persons.‘95Acetaldehyde, a principal metabolite of ethanol, may also increase levels of circulating catecholamines both systemically and in the myocardium.’ Heavy ethanol consumption also causesthe release of plasma free fatty acids, which may be arrhythmogenic.’ We also found that fluid consumption alone (without ethanol) appearsto increase duration of both P-wave and QRS complex signal-averaged electrocardiograms but to a lesser magnitude than found with ethanol. This finding suggests that a patient’s fluid status should be considered when comparing the effects of medications on signal-averaged electrocardiograms. This factor could be particularly important in studies involving patients with congestive heart failure or receiving diuretic therapy. In conclusion, we found that acute ethanol ingestion causes prolongation of both atria1 and ventricular signal-averaged electrocardiograms. Acknowledgment: We wish to acknowledge the assistance of the Tucson Police Department and Nora Rankin for providing the Intoxilyzer 5000 for measurement of breath-ethanol levels.
1. Thornton JR. Atrial fibrillation in healthy non-alcoholic people after an alcoholic binge. Lancet 19X4:1013-1015. 2. Gondo N, Kumagai K, Matsuo K, Ogawa M, Annoura M, Moroe K, Arakawa K. The best criterion for discrimination between patients with and without paroxysmal atria1 fibrillation on signal-averaged electrocardiogram. An J Cardiol 1995;75:93-95. 3. Scott WA, Donnerstein RL. Alignment of P waves for signal averaging. PACE Pacing Clin Elecrrophysiol 1990; 13: 1559- 1562. 4. Gould L, Reddy CV, Becker W, Oh KC, Kim SG. Electrophysiologic properties of alcohol in man. J Electrocardiol 1978; 11:219-226. 5. Cheema A, Ahmed M, Kadish A, Goldberger J. Effects of autonomic changes on the signal averaged P wave duration (abstr) JAm Coil Cardiol1995:318A.
BRIEF REPORTS 1357
Effects of Ethanol Ingestion Electrocardiograms A. Cardy,
BS, Richard
on Signal-Averaged
L. Donnerstein, MD, Leslee F. Kelly, BA, Nathan MD Gia M. Palombo, BS, and Stanley J. Goldberg,
cute ethanol intoxication has been implicated as a cause of atria1 fibA rillation in otherwise healthy persons
50
H. Bittner,
1
( “Holiday Heart” syndrome) .I Studies have shown that signal-averaged P waves are of longer duration in patients prone to atrial fibrillation than in those without atria1 fibrillation.’ These 2 observations led us to investigate whether atria1 and ven.g tricular signal-averaged electrocardioE grams change after acute ingestion of eth5 *’ anol. ... loThe study group consisted of 8 women and 5 men ranging in age from 23 to 27 years. An experimental group of 10 sub0 ,11,,11,1,1111,1111, jects (6 women, 4 men) ingested ethanol. 150 0 50 2co Five of these experimental subjects and 3 Ti rtYZ(ms) other subjects later served as a control group and did not ingest alcohol. All sub- FIGURE 1. Example of signal-averaged P waves obtained at baseline (so/id iects were nonsmokers. had no recent ethheI and at an ethanol level of 0.075 g/dl (dashed he). gnol ingestion, had no; eaten for 4 hours ’ before the experiment, and had no evidence of car- were bandpass filtered from 30 to 300 Hz3 and amplidiac disease by history, physical examination, or fied 100,000 to 200,000 times for P waves and 10,000 echocardiography. Informed consent was obtained to 20,000 times for QRS complexes (Grass Instrubefore the study under a protocol approved by the ments, Quincy, Massachusetts). Signals were sampled Institutional Human Subjects Committee. at 2,000 Hz for 7.2 minutes using a 1Zbit analog-toSubjects in the experimental group drank a total of digital’ converter (MacAdios II, GW Instruments, 0.95 g/kg of body weight of ethanol. Ethanol was di- Cambridge, Massachusetts). Digital data were stored luted in 24 ounces of fruit punch and divided into 3 for later signal averaging on a Macintosh Quadra 950 equal portions for consumption at separate intervals. microcomputer (Apple Computers Inc., Cupertino, Subjects drank no other fluids during the study. Blood California). ethanol levels were estimated by analysis of expired Signal-averaged P waves and QRS complexes were air (Intoxilyzer 5000 CMI, Incorporated, Owensboro, compared by 2 investigators who were blinded to the Kentucky). Signal-averaged P waves and QRS com- other’s results. By superimposing the computer-genplexes were obtained in the study group at baseline (0 erated signal-averaged P waves (or QRS complexes) g/dl), at 0.025 2 0.005 g/d1 increasing ethanol levels, on the computer display (Figure l), differences beat 0.075 & 0.005 g/d1 peak ethanol levels, and at 0.025 tween waveforms were readily apparent. Statistical sig2 0.005 g/d1 decreasing ethanol levels. The control nificance from baseline was determined using a paired group drank only 8 ounces of fruit punch; signal-av- t test. Changes between the experimental group at eraging was performed before and 30 minutes after 0.025 g/d1 and the control group after fluid ingestion fluid ingestion. Thirty minutes was the average amount were compared with an unpaired t test. of time required for the experimental group to reach More than 200 beats were averaged for all studies, the 0.025 g/d1 increasing ethanol level. With subjects and noise levels after signal averaging were <0.3 relaxed in a supine position, recordings were obtained /JV in all cases. Results after signal averaging are in an electrically shielded room from electrodes kept summarized in Figure 2. Baseline signal-averaged Pin the lead II position throughout the study. Signals wave duration was 108 + 8.5 ms [SEMI and QRS duration was 90 2 7 ms. After ethanol ingestion, P waves were prolonged in 9 of 10 subjects, and QRS From the Department of Pediatrics, Steele Memorial Children’s Recomplexes in 10 of 10 subjects. In most subjects, search Center, Diamond Research laboratory, and University Heart increases relative to the baseline were greater as ethCenter, Tucson, Arizona. Dr. Donnersiein’s address is: Dept. of Peanol levels increased. In the control group, P waves diatrics, University of Arizona Health Sciences Center, Tucson, Ariwere prolonged in 7 of 8 subjects and QRS comzona 85724 Manuscrilst received Seotember 26. 1995: revised manuscript received and’accepted Jan&y 23, 1946 plexes in 8 of 8 subjects after fluid ingestion. How1356
01996 by Excerpto Medica, All rights reserved.
Inc.
0002-9 149/96/$15.00 PII 50002.9149(96)00205-6
B. T
**
0.075
0.025
(Falling)
Ethanol Level (g/dl) FIGURE 2. Mean than es in signal-avemged P wave, top, and QRS complex ~J~$WIS (lower pane 0 at varying ethanol levels. Error bars = + 1 SEM ‘p . ,- l *p
QRS
P Wave
EthXd
Fluid
Ethanol
Fluid
l&i
F&i
FIGURE 3. Comparison of changes in signal-avemged electrocardi mm dumtions in subjects drinking both ethanol and fluid and those drinking 7l uid alone. Error bars = + 1 SEM; ‘p
ever, changes relative to baseline were significantly greater in the experimental group than in the control group (Figure 3). . . .
The main findings from this study are that acute ethanol ingestion causes an increase in duration of
both atrial and ventricular signal-averaged electrocardiograms. These results are consistent with those of Gould et al,4 who used electrophysiology studies in humans to demonstrate that alcohol causes a delay in atrial conduction. Recent studies have shown that on signal-averaged electrocardiograms, patients prone to atrial fibrillation have au increase in duration of high-frequency, low-amplitude signals, particularly at the end of the P wave.’ It is possible that prolongation of these later components may contribute to dysrhythmias associated with Holiday Heart syndrome found in some patients after binge drinking. Several mechanisms have been offered to explain the effect of ethanol on the heart. Ethanol may have a direct or indirect effect on the myocardium. Indirectly it may stimulate the release of catecholamines, which have been shown to cause an increase in P-wave duration in otherwise healthy persons.‘95Acetaldehyde, a principal metabolite of ethanol, may also increase levels of circulating catecholamines both systemically and in the myocardium.’ Heavy ethanol consumption also causesthe release of plasma free fatty acids, which may be arrhythmogenic.’ We also found that fluid consumption alone (without ethanol) appearsto increase duration of both P-wave and QRS complex signal-averaged electrocardiograms but to a lesser magnitude than found with ethanol. This finding suggests that a patient’s fluid status should be considered when comparing the effects of medications on signal-averaged electrocardiograms. This factor could be particularly important in studies involving patients with congestive heart failure or receiving diuretic therapy. In conclusion, we found that acute ethanol ingestion causes prolongation of both atria1 and ventricular signal-averaged electrocardiograms. Acknowledgment: We wish to acknowledge the assistance of the Tucson Police Department and Nora Rankin for providing the Intoxilyzer 5000 for measurement of breath-ethanol levels.
1. Thornton JR. Atrial fibrillation in healthy non-alcoholic people after an alcoholic binge. Lancet 19X4:1013-1015. 2. Gondo N, Kumagai K, Matsuo K, Ogawa M, Annoura M, Moroe K, Arakawa K. The best criterion for discrimination between patients with and without paroxysmal atria1 fibrillation on signal-averaged electrocardiogram. An J Cardiol 1995;75:93-95. 3. Scott WA, Donnerstein RL. Alignment of P waves for signal averaging. PACE Pacing Clin Elecrrophysiol 1990; 13: 1559- 1562. 4. Gould L, Reddy CV, Becker W, Oh KC, Kim SG. Electrophysiologic properties of alcohol in man. J Electrocardiol 1978; 11:219-226. 5. Cheema A, Ahmed M, Kadish A, Goldberger J. Effects of autonomic changes on the signal averaged P wave duration (abstr) JAm Coil Cardiol1995:318A.
BRIEF REPORTS 1357