Cardiac Hemodynamics in Alcoholic Heart Disease

Gould, Lawrence; Zahir, Md. Hasan; Shariff, Mahmood; M, Dilieto

doi:10.7326/0003-4819-71-3-543

Cited by 28 publications

(3 citation statements)

References 15 publications

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“…Chronic alcoholics without cardiac symptoms have been shown to have slightly depressed myocardial function as shown especially well by systolic time intervals and by the rise in pulmonary artery pressure and end-diastolic pressure with exercise [9, 10, 11]. Acute or chronic alcohol ingestion is frequently associated with conduction abnormalities and abnormal T waves, e.g.…”

Section: Genuine Alcoholic Cardiomyopathy: Asymptomatic Typementioning

confidence: 99%

The Alcoholic Cardiomyopathies – Genuine and Pseudo

Constant

1999

Cardiology

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Two types of genuine alcoholic cardiomyopathies can produce congestive heart failure, an acute fulminate hyperkinetic type with high cardiac output and a hypokinetic type with a low cardiac output, both of which respond to thiamine. When the chronic alcoholic develops a dilated cardiomyopathy with congestive heart failure without a history of significant malnutrition, then they do not respond to thiamine. This may be explained by a study in which mice given a myotropic virus plus alcohol developed more frequent and severe viral cardiomyopathies than those not fed alcohol. This suggests that a chronic dilated cardiomyopathy in an alcoholic may not be the direct result of the alcohol but secondary to a viral myocarditis. This suggests that the preferred terminology for a dilated cardiomyopathy in an alcoholic who does not respond to thiamine and good nutrition should simply be a dilated cardiomyopathy in an alcoholic. We should assume that the cardiomyopathy is possibly of viral etiology.

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Section: Genuine Alcoholic Cardiomyopathy: Asymptomatic Typementioning

confidence: 99%

The Alcoholic Cardiomyopathies – Genuine and Pseudo

Constant

1999

Cardiology

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“…Normally, angiotensin, an afterload enhancer and potent vasoconstrictor, provokes an increase in stroke work and stroke output as a result of increase in left ventricular contractility. Gould et al [13], then Limas et al [14] demonstrated a significant reduction in stroke volume and cardiac output with a concomitant increase in left ventricular end diastolic pressures during both physiologic and pharmacologic stress test, the latter being produced by ouabine, a potent inotrope. This apparent contradiction in exercise response between the Gould's/Limas' and Murray's groups may be attributed to a more severe form of exercise and measurement of left sided filling pressures in the former compared with the latter.…”

Section: Introductionmentioning

confidence: 98%

Cirrhosis-Associated Cardiomyopathy

Zaky

Lang

2012

J Anesthe Clinic Res

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“…Alcohol is cardiotoxic. Clinical cardiomyopathy occurs in some 1-2% of chronic alcoholics, but haemodynamic abnormalities suggestive of subclinical heart disease have been demonstrated by systolic time interval (STI) measurement in some 30 % of asymptomatic alcoholics (Gould et al, 1969). We therefore investigated the value of serum enzyme and isoenzyme measurements for the detection of myocardial damage in alcoholics, using clinical or STI abnormality as evidence of clinical or subclinical cardiomyopathy respectively.…”

Section: Methodsmentioning

confidence: 99%

Detection of Alcoholic Cardiomyopathy by Serum Enzyme and Isoenzyme Determination

1979

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SUMMARY Serum creatine kinase and lactate dehydrogenase isoenzymes were studied in 73 patients with alcoholism, including two patients with clinical alcoholic cardiomyopathy and 28 patients with haemodynamic evidence (systolic time interval abnormality) of disordered myocardial function. No isoenzyme abnormalities suggestive of myocardial injury were observed. We conclude that isoenzyme examination is unsuitable for the early detection of myocardial damage from alcohol.Two patients showed clinical alcoholic cardiomyopathy. A further 28 patients showed increased PEPjLVET ratios without blood ethanol elevation. These patients were diagnosed as having subclinical cardiomyopathy.Serum total CK activity was increased in eight of these 30 subjects and HBD was elevated in three. Total CK was also raised in six and HBD in five of the remaining 43 patients without evidence of cardiac abnormality.Serum CK isoenzyme examination in all subjects showed only the 'muscle' (MM) isoenzyme. LD isoenzyme determination showed either a normal or isomorphic pattern (LD2, LDa increase) or a 'liver'j'muscle' pattern (increased LDs). NQ patient showed increase of the 'cardiac-specific' Ck-MB or LDI isoenzymes. et al., 1977). The upper reference limit (mean plus 2SD) for the PEPjLVET ratio determined in 49 healthy controls matched for age and sex was 0·350. ResultsSince STI values are known to alter during alcohol intoxication, blood ethanol levels were also measured for all subjects by gas-liquid chromatography (courtesy Dr J. Spencer-Peer). Patients and methodsSeventy-three documented alcoholic patients, 60 men (mean age 29 years) and 13 women (mean age 35 years), all previously consuming in excess of 80g ethanol per day, were studied immediately after admission to the Alcohol Unit at St Bernard's Hospital, Southall. A full clinical examination was carried out, blood samples were taken, and STI values measured.The following serum enzyme activities and isoenzymepatterns were determined, using methodology and normal values described previously (Krafft et al., 1977); creatine kinase (CK), hydroxybutyrate Discussion dehydrogenase (HBD); CK and lactate dehydrogenase(LD) isoenzymes.Determination of total CK and LD or HBD activity For STI measurement the electrocardiogram, in serum followed by CK and LD isoenzyme phonocardiogram, and carotid pulse pressure waves examination is widely used for the identification of were simultaneously recorded, and the pre-ejection myocardial injury. Total enzyme determination period relative to the left ventricular ejection time lacks cardiospecificity, and this is especially dis-(PEPjLVET ratio) was calculated. This value reflects advantageous when evidence of heart damage is the contractile efficiency of heart muscle (Lewis sought in alcoholics, in whom accompanying liver 165Measurement of enzymes and isoenzymes of cardiac origin in serum is of established value for the identification of myocardial damage. Alcohol is cardiotoxic. Clinical cardiomyopathy occurs in some 1-2% of chronic alcoholics, but haemody...

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Cardiac Hemodynamics in Alcoholic Heart Disease

Cited by 28 publications

References 15 publications

The Alcoholic Cardiomyopathies – Genuine and Pseudo

The Alcoholic Cardiomyopathies – Genuine and Pseudo

Cirrhosis-Associated Cardiomyopathy

Detection of Alcoholic Cardiomyopathy by Serum Enzyme and Isoenzyme Determination

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