CLINICAL STUDIES
Early changes in left ventricular function in chronic asymptomatic alcoholics: relation to the duration of heavy drinking
Aleksandar M. Lazarevi , MD*,
Satoshi Nakatani, MD, PhD, FACC*,
Aleksandar N. Ne kovi, MD ,
Jelena Marinkovi, PhD,
Yoshio Yasumura, MD, PhD*,
Djordjo Stoji i, MD, PhD ,
Kunio Miyatake, MD, PhD, FACC*,
Milovan Boji, MD, PhD* and
Aleksandar D. Popovi, MD, PhD, FACC, FESC
* Cardiology Division, National Cardiovascular Center, Suita, Osaka, Japan
Cardiovascular Research Center, Dedinje Cardiovascular Institute, Belgrade University Medical School, Belgrade, Yugoslavia
Cardiology Division, Banja Luka Medical Center, Banja Luka University Medical School, Banja Luka, Republika Srpska, Bosnia and Herzegovina
Manuscript received August 5, 1999;
revised manuscript received November 16, 1999,
accepted January 7, 2000.
Reprint requests and correspondence: Dr. Satoshi Nakatani, Cardiology Division, National Cardiovascular Center, 5-7-1 Fujishiro-dai, Suita, 565-8565 Osaka, Japan
nakatas{at}hsp.ncvc.go.jp
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Abstract
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OBJECTIVES
This study sought to assess preclinical cardiac abnormalities in chronic alcoholic patients and possible differences among alcoholics related to the duration of heavy drinking.
BACKGROUND
Chronic excessive alcohol intake has been reported as a possible cause of dilated cardiomyopathy. However, before the appearance of severe cardiac dysfunction, subtle signs of cardiac abnormalities may be identified.
METHODS
We studied 30 healthy subjects (age 44 ± 8 years) and 89 asymptomatic alcoholics (age 45 ± 8 years, p = NS) divided into three groups, with short (S, 5–9 years, n = 31), intermediate (I, 10–15 years, n = 31) and long (L, 16–28 years, n = 27) duration of alcoholism. Transmitral early (E) and late (A) Doppler flow velocities, E/A ratio, deceleration time of E (DT) and isovolumic relaxation time (IVRT) were obtained. Left ventricular (LV) wall thickness and volumes were also determined by echocardiography, and LV mass and ejection fraction (EF) were calculated.
RESULTS
The alcoholics had prolonged IVRT (92 ± 11 vs. 83 ± 7 ms, p < 0.001), longer DT (180 ± 20 vs. 170 ± 10 ms, p < 0.01), smaller E/A (1.25 ± 0.34 vs. 1.40 ± 0.32, p < 0.05), larger LV volumes (73 ± 8 vs. 65 ± 7 ml/m2, p < 0.001 for end-diastolic volume index; 25 ± 4 vs. 21 ± 2 ml/m2, p < 0.001 for end-systolic volume index), higher LV mass index (92 ± 14 vs. 78 ± 8 g/m2, p < 0.001) and thicker posterior wall (9 ± 1 vs. 8 ± 1 mm, p < 0.001). Ejection fraction did not differ between the two groups (66 ± 4 vs. 67 ± 2%). Deceleration time of the early transmitral flow velocity was longer in groups L (187 ± 18 ms) and I (185 ± 16 ms) compared with group S (168 ± 17 ms, p < 0.001 for L and I vs. S), whereas A was higher in group L compared with S (43 ± 10 vs. 51 ± 10 cm/s, p < 0.005). Multiple regression analysis identified duration of heavy drinking as the most important variable affecting DT and A.
CONCLUSIONS
Left ventricular dilation with preserved EF and impaired LV relaxation characterized LV function in chronic asymptomatic alcoholic patients. It appeared that the progression of abnormalities in LV diastolic filling related to the duration of alcoholism.
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Abbreviations and Acronyms
| | A | = peak late transmitral flow velocity | | DT | = deceleration time of the early transmitral flow velocity | | E | = peak early transmitral flow velocity | | EF | = ejection fraction | | I | = intermediate duration of alcoholism | | IVRT | = isovolumic relaxation time | | IVST | = diastolic interventricular septum thickness | | L | = long duration of alcoholism | | LV | = left ventricular | | LVDD | = left ventricular diastolic diameter | | PWT | = diastolic left ventricular posterior wall thickness | | S | = short duration of alcoholism |
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Chronic excessive alcohol consumption may lead to progressive and chronic cardiac dysfunction and can be a possible cause of dilated cardiomyopathy (1). During the progression of the disease, subtle signs of cardiac abnormalities may be identified, preceding the appearance of cardiac dysfunction (2). It would be clinically important to detect such subtle signs because early cessation of alcohol consumption may reverse left ventricular (LV) dysfunction (3). Numerous clinical studies that have examined the effect of chronic alcohol consumption on systolic and diastolic LV function have yielded conflicting results (2,4–11). Some authors (2,8) found impaired but others found well preserved LV systolic function (5–7). Similarly, normal (7,11) and impaired LV filling were reported (9,10). To some extent, this may be due to the different methods employed (12). Other possible reasons for these discrepancies may be different diagnostic criteria, failure to exclude other forms of heart disease, different age and differences in drinking histories (7).
To overcome these drawbacks, in this study all patients were carefully diagnosed by the specialists using the standard criteria, and, to assess a possible effect of duration of heavy drinking on LV function, we grouped the patients according to their drinking history. The purposes of this study were: - to detect preclinical cardiac abnormalities in chronic alcoholic patients using two-dimensional and Doppler echocardiography, and
- to evaluate possible differences in LV systolic and diastolic function related to the duration of heavy drinking.
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Methods
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Study patients.
Ninety-five consecutive male alcoholics, who were scheduled for admission to an inpatient alcohol dependence treatment program or admitted for detoxification to the Sections of Alcoholism, Institute for Mental Health, Belgrade, or Department of Psychiatry, Banja Luka Medical Center, between February 1995 and December 1997, were enrolled in the study. Entry criteria were: 1) positive diagnostic criteria for alcohol abuse established by the American Psychiatric Association (13), 2) age  60 years, 3) daily ethanol consumption  90 g, 4 days/week, 4) drinking history 5 years, 5) no history of hypertension or cardiac disease, 6) absence of signs and symptoms of cardiovascular, respiratory and metabolic disease, 7) no use of tricyclic antidepressants, and 8) normal sinus rhythm. Six patients with inadequate echocardiographic images were excluded from the study. The remaining 89 patients (ages 45 ± 8 years, range 23 to 60) represented the final study group. All patients with alcoholism, as well as their families or friends, were carefully questioned by experienced interviewers about the total duration of heavy alcohol drinking, the type and the amount of alcoholic drinks usually consumed per day and the duration of abstinence. Detoxification was considered as completed if the patient has stopped drinking and was free of alcohol withdrawal symptoms for more than 48 h. Daily ethanol consumption was obtained by converting the type and amount of alcoholic beverages into g of absolute ethanol (14). In advance of data collection, it was decided to divide alcoholic patients into three groups according to the duration of heavy drinking: short (S, drinking history 5–9 years), intermediate (I, drinking history 10–15 years) and long (L, drinking history >15 years) duration groups.
Thirty male healthy subjects (age 44 ± 8 years, range 25 to 58; p = NS vs. all alcoholic patients, groups S and I; p < 0.01 vs. group L) without drinking histories were studied as the control group. None of them had a history of hypertension nor any history, signs or symptoms of diabetes, cardiovascular or lung disease.
Echocardiograms.
Complete two-dimensional, M-mode and Doppler echocardiograms were recorded after detoxification, a mean of 19 days (range, 2 to 69 days) after the last drink. Examinations were performed with an Acuson 128 imaging system (Mountain View, California) or an Aloka 830 SSD (Tokyo, Japan) imaging system using 2.5 MHz transducers and were stored on 1/2-inch VHS videotapes for later analysis.
Left ventricular end-diastolic and end-systolic volumes and ejection fraction (EF) were determined from the apical two-chamber view, using the single plane area-length formula according to the recommendations of the American Society of Echocardiography (15). Left ventricular mass was determined by the formula: LV mass = 0.8 {1.04 [(LVDD + IVST + PWT)3 – LVDD3]} + 0.6 g, where LVDD = LV diastolic diameter, IVST = diastolic interventricular septal thickness and PWT = diastolic LV posterior wall thickness (16). Measurements of the IVST, LVDD and PWT were performed according to the recommendations of the American Society of Echocardiography (17). Left ventricular volumes and mass were normalized for the body surface area and expressed as indexes. Transmitral flow recordings were obtained after quiet expiration from the apical four-chamber view, with the pulsed Doppler sample volume placed at the level of the mitral leaflet tips. Peak early (E) and late (A) transmitral flow velocities, E wave deceleration time (DT) and E/A ratio were determined. The isovolumic relaxation time (IVRT) was measured by positioning the continuous wave Doppler cursor between the mitral valve and LV outflow. Measurements were performed in three consecutive beats and averaged.
Laboratory analysis.
All alcoholics underwent laboratory tests within 72 h of admission that included: hemoglobin, serum cholesterol and total triglycerides, alanin-aminotransferase, aspartate-aminotransferase and gamma-glutamyltransferase.
Statistical analysis.
Chi-square test was used for comparison of nonparametric data and t test was used to compare continuous variables. Analysis of variance was used to compare the differences among the three alcoholic groups and the control group, with individual group comparisons analyzed by the Bonferonni’s test. Analysis of covariance was used to determine the significance of duration of heavy drinking on transmitral flow velocities independent of the effect of age. Stepwise multiple linear regression analysis was used to evaluate the effects of several independent variables (age, heart rate, transitory hypertension and details related to the drinking histories: duration of heavy drinking, quantity of daily ethanol consumption and duration of abstinence) on LV volumes, EF and Doppler indexes in alcoholics, each considered separately as a dependent variable. Univariate linear regression analysis was used to correlate the duration of heavy drinking and echocardiographic parameters. Significance was established at p < 0.05.
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Results
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Patient’s characteristics.
Table 1 lists characteristics of all subjects. There were no differences in heart rate, systolic and diastolic blood pressures between control subjects and the patients. Control subjects had larger body surface area. Duration of heavy drinking varied from 5 to 28 years, with the length of the last drinking period ranging from two to 300 weeks. The average daily ethanol consumption was estimated at 252 g (range 174 to 464 g). Among the three alcoholic groups and controls, we found no differences in heart rate, systolic and diastolic blood pressures.
Although all of the alcoholics did not have a history of hypertension, transitory hypertension was observed during hospital stay in 16/31 patients in group S (52%), in 16/31 patients in group I (52%) and in 16/27 patients in group L (59%, p = NS vs. S and I).
Two-dimensional and M-mode echocardiographic measurements.
Two-dimensional and M-mode echocardiographic data are shown in Table 2. Left ventricular volume indexes and mass index were higher in alcoholics. However, EF did not differ between the control subjects and the alcoholics. Left ventricular posterior wall was thicker in alcoholics, and there was no difference in the interventricular septal thickness. Left ventricular mass index (except for group S) and LV volume indexes (except end-systolic volume index for group I) were higher in alcoholic groups compared with controls, but comparable among the alcoholics. There were no differences in EF among the alcoholic groups and controls.
Since the group L patients were the oldest, there might be some effect of aging on LV dysfunction in this group. In order to assess a potential effect of early aging in response to alcohol, we performed additional analysis, which showed no correlation between the age and EF in any of the three alcoholic groups (r = –0.03, p = 0.9, r = –0.06, p = 0.7 and r = –0.08, p = 0.7, for groups S, I and L, respectively).
Doppler LV diastolic filling parameters.
Doppler LV diastolic filling variables, except E and A, showed differences between controls and all alcoholics; IVRT and DT were longer and E/A was smaller in alcoholics (Table 3). When we compared these data among controls and the alcoholic groups, we found the tendencies of gradual prolongation of IVRT and DT, increase in A and decrease in E/A as the drinking history became longer. Since patients in group L were the oldest and age was known to affect LV diastolic function, we performed correction for age with analysis of covariance. After correcting for age we found longer DT (control subjects 170 ± 17, group S 168 ± 17, group I 185 ± 16, group L 187 ± 18 ms, F = 10, p < 0.001; p < 0.001 for groups L and I vs. control subjects and group S) and larger A (control subjects 43 ± 10, group S 43 ± 10, group I 47 ± 10, group L 51 ± 10, F = 4, p = 0.01, p < 0.005 for L vs. control subjects and p < 0.01 for L vs. group S) in patients with a longer history of heavy drinking, and IVRT was significantly longer in group S compared with control subjects (91 ± 11 vs. 83 ± 10, p < 0.005). Peak early transmitral flow velocity did not change substantially after correction for age. E/A ratio in group L increased slightly after correcting for age but still tended to decrease with the prolonged drinking history.
Early signs of cardiac abnormalities in chronic alcoholism.
In order to establish the earliest detectable change by echocardiography (LV volume changes or LV filling impairment), we assessed the differences in echocardiographic parameters among controls and the three alcoholic groups. The difference between group S and controls was significant for LV volumes (74 ± 8 vs. 65 ± 7 mL/m2, p < 0.005 for end-diastolic volume index, 25 ± 4 vs. 21 ± 2 mL/m2, p < 0.005 for end-systolic volume index) (Table 2) and IVRT (91 ± 11 vs. 83 ± 10 ms, p < 0.005) after correcting for age, whereas no difference was found in other Doppler indexes (Fig. 1), LV mass (86 ± 18 vs. 79 ± 8 ms, p = NS) and EF (66 ± 3 vs. 67 ± 2 ms, p = NS) (Table 2). Comparison between group I and control subjects included additional increase in LV mass (94 ± 15 vs. 79 ± 15 g/m2, p < 0.001) (Table 2) and prolongation of DT in group I (185 ± 16 vs. 170 ± 17 ms, p < 0.001) (Fig. 1). When we compared group L and control subjects, besides the forementioned differences, we found a significant increase in A and lower E/A ratio in alcoholics compared with control subjects (51 ± 10 vs. 43 ± 10 cm/s2, p < 0.005) (Fig. 1). Thus, the echocardiographic changes in chronic alcoholics were seen in the following order: first, increase in LV volume and prolongation of IVRT; second, increase in LV mass and prolongation of DT; last, increase in A and decrease in E/A ratio (Table 2, Fig. 1).
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Figure 1 Doppler left ventricular diastolic filling variables in four groups after correcting for age. IVRT = isovolumic relaxation time (A); DT = deceleration time of the early transmitral flow velocity (B); E = peak early transmitral flow velocity (C); A = peak late transmitral flow velocity (D); E/A ratio (E). Group S = alcoholic patients with short duration of heavy drinking; Group I = alcoholic patients with intermediate duration of heavy drinking; Group L = alcoholic patients with long duration of heavy drinking. Data presented are mean value ± SD.
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Impact of patients’ characteristics on echocardiographic parameters.
The impact of several independent variables: age, heart rate, transitory hypertension and details related to drinking histories (duration of heavy drinking, quantity of daily ethanol consumption and duration of abstinence) on echocardiographic parameters each considered separately as a dependent variable was analyzed by multivariate linear regression analysis. Left ventricular end-systolic volume index, EF and IVRT were not affected by any of the independent variables mentioned above. Left ventricular end-diastolic volume index was influenced by transitory arterial hypertension (p = 0.04) and duration of abstinence (p = 0.01). Deceleration time of the early transmitral flow velocity was affected only by total duration of heavy drinking (p = 0.01). Peak early transmitral flow velocity was influenced by patient age (p = 0.0004), transitory hypertension (p = 0.001) and total duration of heavy drinking (p = 0.02), while A was determined predominantly by the duration of heavy drinking (p = 0.00001) and heart rate (p = 0.00001), with a minor impact from transitory hypertension (p = 0.03). Finally, E/A ratio was determined by age (p = 0.00001) and heart rate (p = 0.0007).
To demonstrate the effect of heavy drinking on echocardiographic abnormalities more precisely, we assessed the univariate correlations between the duration of heavy drinking and echocardiographic parameters. No significant correlations were found between the duration and LV volume indexes, EF and LV mass index. However, relatively weak, but significant, correlation was observed between the duration of heavy drinking and DT, A and E/A (r = 0.27, p < 0.05; r = 0.47, p < 0.0001; r = 0.39, p < 0.0005, respectively).
No significant relation was found between the duration of detoxification (abstinence) and echocardiographic parameters, except for a weak relation with LV end-diastolic volume index (r = 0.25, p = 0.016). Duration of abstinence did not relate to the duration of alcoholism.
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Discussion
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This study demonstrated that chronic alcoholics without symptoms and signs of heart disease had LV dilation with preserved EF and abnormal Doppler transmitral flow pattern indicating impaired LV relaxation. Left ventricular diastolic filling abnormalities were more remarkable in patients with longer drinking histories. We found that changes in LV volume occurred before the changes in LV mass and impairment of LV diastolic filling, and may be a sensitive marker of the detrimental effect of alcohol on the heart. However, once alcoholism occurred, the duration of heavy drinking related to diastolic filling parameters but not to systolic indexes.
LV systolic function and mass in asymptomatic alcoholics.
It has been shown that symptomatic alcoholic patients may have systolic dysfunction of various degrees, known as alcoholic cardiomyopathy (18). However, data on systolic function in asymptomatic alcoholics are conflicting (4,19,20). Previous studies, using systolic time intervals, have shown abnormal LV systolic function (2,21), which can persist during prolonged abstinence (22). Urbano-Marquez et al. (8) reported significantly lower EF in alcoholics compared with control subjects. In contrast, Kupari et al. (9) and Reeves et al. (23) found no significant abnormalities in LV systolic function assessed by echocardiography in chronic alcoholics. In this study, we found that asymptomatic alcoholics had slightly dilated ventricles with normal EF.
Several echocardiographic studies have demonstrated increased LV mass and wall thickness in chronic alcoholics with different incidences of these abnormalities (4,5,24). We also found that the LV mass was larger and the posterior wall was thicker in alcoholics than it was in control subjects. This is in accordance with the previously reported necropsy study from Schenk and Cohen (25). No additional increase in LV wall thickness was found in patients with a longer drinking history compared with those with a shorter drinking history, which is consistent with other reports (4,6,7,10,23).
Possible reasons for these discrepancies may include differences in the severity of alcoholism. We grouped patients into three groups according to the duration of heavy drinking, which should be useful to assess effects of alcohol intake on LV structure and function. Another reason could be inaccurate information on alcohol consumption (26). The exact information on the quantities of alcohol consumed was a major problem in most studies because many alcoholics tend to underestimate their daily alcohol consumption. We believe that our data on alcohol consumption was reliable because we got information from their families and friends as well as from patients.
LV diastolic function in asymptomatic alcoholics.
Conflicting results have also been reported regarding diastolic function of asymptomatic alcoholics. Dancy et al. (11), using M-mode echocardiography, found increased LV diastolic diameter in chronic alcoholics, but no signs of impaired LV diastolic filling. Cerqueira et al. (7) found no differences in LV diastolic function at rest between asymptomatic alcoholics and controls, as assessed by radionuclide ventriculography. The opposite was reported by Kupari et al. (9) and Silberbauer et al. (10) who found impaired relaxation as an early sign of alcoholic cardiomyopathy using Doppler echocardiography. We also found that asymptomatic alcoholics had impaired LV relaxation. In addition to the abovementioned possible reasons, these discrepancies may be due to the different method used to assess diastolic function (12). M-mode filling indexes describe segmental ventricular function only. However, Doppler indexes of transmitral flow assesses global LV diastolic performance (27).
It has been shown that chronic alcohol intake may impair the transport of calcium ions from the sarcoplasma into the sarcoplasmic reticulum (28). This abnormality may lead to the delay of the inactivation of the actomyosin interaction and could be responsible for delayed myocardial relaxation (9). Our results may reflect altered biochemistry of the myocardium in chronic alcoholics. In addition, associated ventricular dilation or myocardial hypertrophy may also be responsible for delayed relaxation (29).
Duration of alcoholism and the progression of LV systolic and diastolic abnormalities.
Data are scarce on the impact of the duration of alcoholism on LV systolic and diastolic function. Askanas et al. (4) reported that the LV systolic function and mass were not affected by the duration of heavy drinking. In other studies (9,10), no relation was found between the duration of heavy drinking or quantity of ethanol exposure and LV diastolic filling. In contrast to those studies, Urbano-Marquez et al. (8) reported that total lifetime consumption of ethanol showed a significant positive correlation with LV mass and a significant negative correlation with EF. Kupari et al. (21) showed that the LV mass index and systolic time interval ratio had a curvilinear, rather than a simple linear, relation to the total duration of heavy alcohol consumption. However, to our knowledge, no comparable data regarding diastolic function have been reported to date.
In our study, duration of heavy drinking did not influence ventricular volume and EF. In addition, although the age-associated impairment in LV systolic function has been reported (30), our data revealed no apparent influence of age on EF in the alcoholics, even in those with long duration of heavy drinking. Interestingly, we found that alcoholics with longer drinking history showed longer DT and higher A than alcoholics with shorter duration of alcoholism, despite no differences in LV volumes and mass between the two groups. This is in accordance with a previous study, which showed LV diastolic impairment without associated increase in LV volume or mass in a canine chronic alcoholism model (31). These results suggest that prolongation of LV relaxation may be a sensitive sign that can be used for the assessment of progression of cardiac dysfunction in asymptomatic alcoholics. Our study is the first one that showed a direct relationship between the progression of relaxation abnormalities and the duration of alcoholism.
Clinical implications.
In this study, the earliest manifestation of cardiac abnormalities in asymptomatic alcoholics was found to be LV volume changes followed by LV mass increase and impairment of diastolic function. The mechanisms of the volume changes remained unexplained.
Diastolic dysfunction has been known to precede systolic dysfunction in some forms of heart failure. Since EF was preserved, even in patients with a long drinking history, it appears that in chronic alcoholism, diastolic dysfunction precedes systolic dysfunction. Therefore, serial evaluation of LV relaxation may be helpful in the assessment of progression of cardiac dysfunction in asymptomatic alcoholics.
It would be going too far to state that our findings represent the onset of alcoholic cardiomyopathy. Alcoholic dilated cardiomyopathy clinically occurs in a small minority of patients with chronic alcohol intake, and it is possible that our findings may show a prelude to this condition in select patients. However, this conclusion cannot be blindly accepted without careful longitudinal observations.
Study limitations.
Although transmitral flow velocity pattern provides a measure of diastolic filling, almost all of the indexes derived from the pattern are load dependent (27). Since the alcoholics were asymptomatic, there was nothing to suggest that any of them had extremely high or low preload in this study. Thus, when significant changes in loading conditions are not expected, as it was in this study, transmitral flow velocity pattern is useful to assess global LV diastolic performance (27).
This study was performed in a cross-sectional fashion. Therefore, strictly speaking, we could not tell whether or not an alcoholic patient would develop diastolic dysfunction if he or she continued to drink. To clarify the time-related changes in diastolic function in alcoholics, a large prospective study should be conducted.
Conclusions.
Chronic asymptomatic alcoholics showed LV dilation, which preceded increase in LV mass and impairment of LV relaxation. It appeared that the progression of LV diastolic filling abnormalities related to the duration of alcoholism. It is likely that, in select patients, combination of LV dilation with preserved EF and impaired LV relaxation may indicate a prelude to alcoholic cardiomyopathy.
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Acknowledgments
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We would like to thank the nursing staff of the Cardiology Division, Banja Luka Medical Center. We are grateful for the assistance of Du anka Teanovi , MD, Tatjana Nin i, MD and Petar Nastasi, MD, who took part in the recruitment of patients for this study. We also wish to thank Zoran Popovi, MD for his thoughtful discussion.
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Footnotes
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Dr. Aleksandar M. Lazarevi was supported by a scholarship from the Ministry of Education, Science and Culture of Japan, Tokyo, Japan. Dr. Aleksandar D. Popovi died in December 1998.
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References
|
|---|
1. Regan TJ. Alcohol and the cardiovascular system. JAMA. 1990;264:377–381[Abstract/Free Full Text]
2. Spodick DH, Pigott VM, Chirife R. Preclinical cardiac malfunction in chronic alcoholism. N Engl J Med. 1972;287:677–681[Medline]
3. Arroyo LH, Regan TJ. Ethanol and the heart. Topol EJ. Textbook of Cardiovascular Medicine. 1st ed. Philadelphia: Lippincott-Raven; 1998. p. 219–229
4. Askanas A, Udoshi M, Sadjadi SA. The heart in chronic alcoholism: a noninvasive study. Am Heart J. 1980;99:9–16[CrossRef][Medline]
5. Kino K, Imamitchi H, Morigutchi M, Kawamura K, Takatsu T. Cardiovascular status in asymptomatic alcoholics, with reference to the level of ethanol consumption. Br Heart J. 1981;46:545–551[Abstract/Free Full Text]
6. Friedman HS, Vasavada BC, Malec AM, Hassan KH, Shah A, Siddiqui S. Cardiac function in alcohol-associated systemic hypertension. Am J Cardiol. 1986;57:227–231[CrossRef][Medline]
7. Cerqueira MD, Harp GD, Ritchie JL, Stratton J, Walker D. Rarity of preclinical alcoholic cardiomyopathy in chronic alcoholics <40 years of age. Am J Cardiol. 1991;67:183–187[Medline]
8. Urbano-Marquez A, Estruch R, Navarro-Lopez F, Grau JM, Mont L, Rubin E. The effects of alcoholism on skeletal and cardiac muscle. N Engl J Med. 1989;320:409–415[Abstract]
9. Kupari M, Koskinen P, Suokas A, Ventila M. Left ventricular filling impairment in asymptomatic chronic alcoholics. Am J Cardiol. 1990;66:1473–1477[CrossRef][Medline]
10. Silberbauer K, Juhasz M, Ohrenberger G, Hess C. Noninvasive assessment of left ventricular diastolic function by pulsed Doppler echocardiography in young alcoholics. Cardiology. 1988;75:431–439[Medline]
11. Dancy M, Leech G, Bland JM, Gaitonde MK, Maxwell JD. Preclinical left ventricular abnormalities in alcoholics are independent of nutritional status, cirrhosis and cigarette smoking. Lancet. 1985;1:1122–1125[Medline]
12. Spirito P, Maron BJ, Bellotti P, Chiarella F, Vechhio C. Noninvasive assessment of left ventricular diastolic function: comparative analysis of pulsed Doppler ultrasound and digitized M-mode echocardiography. Am J Cardiol. 1986;58:837–843[CrossRef][Medline]
13. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). 4th ed. Washington, DC: American Psychiatric Association; 1994.
14. Sherlock S. Alcoholic liver disease. Lancet. 1995;345:227–229[CrossRef][Medline]
15. Schiller NB, Shah PM, Crawford M, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr. 1989;2:358–368[Medline]
16. Devereux RB, Alonso DR, Lutas EM, et al. Echocardiographic assessment of left ventricular hypertrophy: comparison with necropsy findings. Am J Cardiol. 1986;57:450–458[CrossRef][Medline]
17. Sahn DJ, DeMaria AN, Kisslo J, Weyman A. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation. 1978;58:1072–1083[Abstract/Free Full Text]
18. Regan TJ. Alcoholic cardiomyopathy. Prog Cardiovasc Dis. 1984;27:141–152[CrossRef][Medline]
19. Wu CF, Sudhaker M, Ghazanfar G, Ahmed SS, Regan TJ. Preclinical cardiomiopathy in chronic alcoholics: a sex difference. Am Heart J. 1976;91:281–286[CrossRef][Medline]
20. Levi GF, Quadri A, Ratti S, Basagni M. Preclinical abnormality of left ventricular function in chronic alcoholics. Br Heart J. 1977;39:35–37[Abstract/Free Full Text]
21. Kupari M, Koskinen P, Suokas A. Left ventricular size, mass and function in relation to the duration and quantity of heavy drinking in alcoholics. Am J Cardiol. 1991;67:274–279[CrossRef][Medline]
22. Sanchez-Zambrano S, Ment MR, Spodick DH. Myocardial malfunction in chronic alcoholism during controlled abstinence. Cardiology. 1974;59:198–200[Medline]
23. Reeves WC, Nanda NC, Gramiak R. Echocardiography in chronic alcoholics following prolonged period of abstinence. Am Heart J. 1978;95:578–582[Medline]
24. Mathews E Jr, Gardin JM, Henry WL, et al. Echocardiographic abnormalities in chronic alcoholics with and without overt congestive heart failure. Am J Cardiol. 1981;47:570–578[CrossRef][Medline]
25. Schenk EA, Cohen J. The heart in chronic alcoholism. Pathol Microbiol. 1970;35:96–104
26. McCall D. Alcohol and the cardiovascular system. Curr Probl Cardiol. 1987;12:349–414
27. Thomas JD, Weyman AE. Echo-Doppler evaluation of left ventricular diastolic function: physics and physiology. Circulation. 1991;84:977–990[Free Full Text]
28. Noren GR, Staley NA, Einzig S, Mikell FL, Asinger RW. Alcohol-induced congestive cardiomyopathy: an animal model. Cardiovasc Res. 1983;17:81–87[Medline]
29. Brutsaert DL, Sys SU, Gillebert TC. Diastolic failure: pathophysiology and therapeutic implications. J Am Coll Cardiol. 1993;22:318–325[Abstract]
30. Turner MJ, Mier CM, Spina RJ, Ehsani AA. Effects of age and gender on cardiovascular responses to phenylephrine. J Gerontol A Biol Sci Med Sci. 1999;54:17–24
31. Thomas G, Haider B, Oldewurtel HA, et al. Progression of myocardial abnormalities in experimental alcoholism. Am J Cardiol. 1980;46:233–241[CrossRef][Medline]
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D. Aguilar, H. Skali, L. A. Moye, E. F. Lewis, J. M. Gaziano, J. D. Rutherford, L. H. Hartley, O. S. Randall, E. M. Geltman, G. A. Lamas, et al.
Alcohol consumption and prognosis in patients with left ventricular systolic dysfunction after a myocardial infarction
J. Am. Coll. Cardiol.,
June 2, 2004;
43(11):
2015 - 2021.
[Abstract]
[Full Text]
[PDF]
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|
|
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|
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M. R. Piano
Alcoholic Cardiomyopathy* : Incidence, Clinical Characteristics, and Pathophysiology
Chest,
May 1, 2002;
121(5):
1638 - 1650.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Wynne
Stirred, Not Shaken
Ann Intern Med,
February 5, 2002;
136(3):
247 - 249.
[Full Text]
[PDF]
|
|
|
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Abstract
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