Alcoholic cardiac beriberi.

Carson, Philip

doi:10.1136/bmj.284.6332.1817

Cited by 10 publications

(5 citation statements)

References 5 publications

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“…The two most important criteria in diagnosing cardiovascular beriberi are a high cardiac output with predominantly right sided heart failure and recovery after treatment with thiamine.4 The syndrome is easily recognisable in the oriental type of beriberi in which the thiamine deficiency results from the patient eating polished rice.56 In the occidental type of beriberi, which is found almost exclusively in alcoholics eating a thiamine deficient diet, however, a high cardiac output may be absent 1 7and left sided heart failure may often be found in the early clinical stages.78 Thiamine treatment sometimes results in a paradoxical lowering of the cardiac output.9 10 It has been suggested that the differences between the two types of beriberi may be attributable to alcoholic cardiomyopathy.6 7 11 Blacket and Palmer have shown that the high cardiac output results from dilatation of the arterioles of the skeletal musculature, which induces a compensatory vasoconstriction in other areas such as the hands and the kidneys.3 In cases of Shoshin beriberi, in which peripheral resistance may be extremely low,' 2 this may lead to peripheral cyanosis and severe disturbances of renal function.…”

Section: Discussionmentioning

confidence: 99%

Shoshin beriberi: a rare diagnostic problem.

Engbers¹,

Molhoek²,

Arntzenius³

1984

Heart

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A chest radiograph showed an enlarged heart with mild pulmonary venous congestion, and the electrocardiogram sinus rhythm with non-specific ST segment changes. The patient was given symptomatic treatment to correct the acidosis and hyperkalaemia. Dopamine (up to a dose of 10 ,ug/kg/min) was given intravenously, which resulted in an increase in pulse rate to 120/min but a fall in blood pressure to 70/40 mm Hg. In view of the known alcohol abuse 100 mg thiamine was injected intravenously. A few hours later his blood pressure had risen to 95/40 mm Hg, and a high cardiac output state developed with bounding pulses and pistol shot sounds as well as Duroziez's sign over the femoral arteries. The cyanosis disappeared. At cardiac catheterisation using a SwanGanz thermodilution catheter the high cardiac output was confirmed and the peripheral vascular resistance was found to be low (Table). The patient was treated with thiamine and a sodium restricted diet. The cardiac output and peripheral resistance gradually returned to normal values, but right atrial and pulmonary wedge pressures were still raised on the third day (Table) when the Swan-Ganz catheter had to be removed because of a temperature rise to 39°C.Within a week of admission the electrocardiogram and renal and liver function tests returned to normal.The chest radiograph showed no pulmonary congestion after two weeks, and the heart size returned to normal a few weeks later. Erythrocyte transketolase activity before treatment was 43 U/mmol (normal 8-8-12 5 U/mmol) of haemoglobin and the thiamine pyrophosphate effect was 22% (normal 5-25%). On retesting four weeks later the transketolase activity was 9.8 U/mmol of haemoglobin and the thiamine pyrophosphate effect 3%.

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Section: Discussionmentioning

confidence: 99%

Shoshin beriberi: a rare diagnostic problem.

Engbers¹,

Molhoek²,

Arntzenius³

1984

Heart

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“…1,2 In the present case, the diagnosis of beriberi heart was suspected on the basis of the high-output heart failure, low systemic vascular resistance, lactic acidosis, and a history of alcoholism. Beriberi heart was diagnosed with certainty because of the patient's decreased blood thiamin concentration and by his marked improvement after thiamin administration.…”

Section: Discussionmentioning

confidence: 99%

“…Shoshin beriberi is a fulminant form of beriberi heart and is characterized by hypotension, tachycardia, and lactic acidosis. [1][2][3][4][5][6][7] Initially, mid-ventricular obstruction had been reported as a special form of hypertrophic cardiomyopathy, but it can be found in other conditions such as myocardial infarction, hypertensive heart disease, and even in normal subjects with alternation of loading conditions. [8][9][10][11][12][13] We report a case of shoshin beriberi and mid-ventricular obstruction of the left ventricle with an apical aneurysm.…”

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confidence: 99%

Shoshin Beriberi With Vasospastic Angina Pectoris. Possible Mechanism of Mid-Ventricular Obstruction.

Ito

Tanabe

Suzuki

et al. 2002

Circ J

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eriberi heart is a very rare disease today and is caused by thiamin deficiency. 1 Beriberi heart is hemodynamically characterized by high cardiac output failure associated with arteriolar vasodilatation. Shoshin beriberi is a fulminant form of beriberi heart and is characterized by hypotension, tachycardia, and lactic acidosis. [1][2][3][4][5][6][7] Initially, mid-ventricular obstruction had been reported as a special form of hypertrophic cardiomyopathy, but it can be found in other conditions such as myocardial infarction, hypertensive heart disease, and even in normal subjects with alternation of loading conditions. [8][9][10][11][12][13] We report a case of shoshin beriberi and mid-ventricular obstruction of the left ventricle with an apical aneurysm. The patient's left ventricular wall thickness was not hypertrophic, and the aneurysmal site was perfused by the left anterior descending artery, in which spasm was provoked using acetylcholine. Case ReportA 73-year-old man was admitted to hospital suffering from chest pain and adynamia of the limbs. He had a history of inferior myocardial infarction, which was followed by conventional therapy when he was aged 65 years. Thereafter, he frequently experienced angina at rest, especially at night. He was a heavy drinker from his young days and he drank to overcome his anginal chest pain instead of taking medication. His alcohol intake had increased gradually, and he had stopped eating completely and been drinking all day for 1 month prior to admission. His blood pressure on admission was 68/30 mmHg and he was in a state of shock. His first and second heart sounds were normal and, although hepatomegaly was present, bilateral pitting edema was not. The power of his inferior limbs was very weak and his deep tendon reflex had disappeared.An electrocardiogram showed sinus tachycardia with a heart rate of 120 beats/min, and ST depression in leads I, II, III, aVF, and V1-V6, as well as negative T waves in leads II, III, and V1-V3. Echocardiography demonstrated hyperkinesis of the left ventricle and mid-ventricular obstruction with a peak intraventricular pressure gradient of 30 mmHg, but his left ventricular wall thickness was not hypertrophic. Laboratory data were normal except for a slight increase in creatine kinase (CK) (223 IU/L). After administering 3 L/min of oxygen, arterial blood gases revealed a pH of 7.27, pO2 105 mmHg, and pCO2 17 mmHg.Despite massive intravenous administration of catecholamine (dopamine 20 g·min -1 ·kg -1 , dobutamine 20 g·min -1 · kg -1 , and noradrenaline 0.2 g·min -1 ·kg -1 ), his blood pressure did not increase. Despite his state of shock, cardiac output was increased markedly and systemic vascular resistance was extraordinarily low. From his hemodynamic data (Table 1), shoshin beriberi was suspected and 100 mg of thiamin was administered intravenously, resulting in the patient's condition improving quickly (Table 1); however, peripheral blood concentration of vitamin B1, which was obtained after intravenous administration of 10 mg of thiam...

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“…Vol 46 No 4 histopathological changes that occur in cardiovascular beriberi have been performed. 1, 5-7, 10, 11) Here, we present the histopathological features of biopsied myocardial tissue from a patient with nonalcoholic Shoshin beriberi, and a patient with alcoholic Shoshin beriberi.…”

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confidence: 99%

“…[1][2][3] In Western countries, cardiovascular beriberi is often associated with chronic alcoholism. [4][5][6] Cardiovascular beriberi can also be divided into a fulminant form (Shoshin beriberi) and a chronic form. 3,7,8) Shoshin beriberi is characterized by hypotension, tachycardia, and lactic acidosis and is mainly encountered in nonalcoholic patients in Asian countries, although it has also been seen in alcoholics in Western countries.…”

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Histopathological Changes of Biopsied Myocardium in Shoshin Beriberi

Kawano¹,

Hayashi

Koide³

et al. 2005

Int. Heart J.

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SUMMARYCardiovascular beriberi is caused by thiamine deficiency and usually arises for one of two reasons: alcoholism or diet. Shoshin beriberi is a fulminant form of cardiac beriberi. We investigated the histopathological features of biopsied myocardial tissue samples from two patients with Shoshin beriberi (one patient with nonalcoholic beriberi and another patient with alcoholic beriberi). Interstitial fibrosis and a variation in size of the myocardial fibers were the main findings in the sample from these patients after thiamine treatment. These findings are persistent histopathological features in the myocardium of patients with Shoshin beriberi after thiamine treatment. (Int Heart J 2005; 46: 751-759)

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Alcoholic cardiac beriberi.

Cited by 10 publications

References 5 publications

Shoshin beriberi: a rare diagnostic problem.

Shoshin beriberi: a rare diagnostic problem.

Shoshin Beriberi With Vasospastic Angina Pectoris. Possible Mechanism of Mid-Ventricular Obstruction.

Histopathological Changes of Biopsied Myocardium in Shoshin Beriberi

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