Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty Nigerian hypertensives with heart failure and 30 without heart failure, matched for age and sex, were studied. Diastolic blood pressures were similar in the two groups (118 +/- 15 and 118.5 +/- 13.6 mmHg, respectively) (P greater than 0.5), while systolic blood pressures were higher in the non-heart failure group (176.7 +/- 29.7 and 198.8 +/- 29.8 mmHg, respectively) (P less than 0.01). The mean durations of initial detection of high blood pressure in the previously known hypertensives in the two groups were 4.9 +/- 3.8 and 4.4 +/- 3.3 years, respectively (P greater than 0.05), and their drug compliance prior to this study was similarly poor (P greater than 0.1). In the two groups, 33.3% and 10% were thiamine deficient, respectively (P less than 0.001), with TPP greater than 15%; 23.3% and 0% had hypoalbuminaemia (P less than 0.02), with a mean serum albumin of 35 +/- 7 and 42 +/- 3 g/l, respectively (P less than 0.001); while 36.7% and 13.3% were anaemic, respectively (P less than 0.05). Heart failure was more severe in those with more than one of these adverse factors (P less than 0.05). The results suggest that these factors, more prevalent in the heart failure group, would have hastened and worsened their heart failure. It is suggested that an active nutritional approach be incorporated into the management of hypertensives, particularly in the developing world.
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PMID:Nutritional factors and heart failure in Nigerians with hypertensive heart disease. 156 82

Thiamine and vitamin B6 status was evaluated in 73 consecutive black patients with cardiac failure at Baragwanath Hospital. They consumed moderate to large amounts of traditional as well as Western-type beer and liquor. Thirty per cent had erythrocyte thiamine concentrations below the reference range. The transketolase response to thiamine pyrophosphate (TPP effect) suggested thiamine deficiency in 32.4%, of whom 13.2% were classified as severely deficient. Vitamin B6 deficiency was present in 21.4%, with a further 42.9% in the very low normal range. Only one patient had beriberi heart disease. Idiopathic dilated cardiomyopathy was the main cause of cardiac failure. It is suggested that excessive alcohol consumption is an important factor contributing to cardiac morbidity in urban blacks.
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PMID:Alcohol intakes and deficiencies in thiamine and vitamin B6 in black patients with cardiac failure. 279 73

Mitochondrial Ca(2+) plays important roles in the regulation of energy metabolism and cellular Ca(2+) homeostasis. In this study, we characterized mitochondrial Ca(2+) accumulation in Syrian hamster hearts with hereditary cardiomyopathy (strain BIO 14.6). Exposure of isolated mitochondria from 70 nM to 30 microM Ca(2+) ([Ca(2+)](o)) caused a concentration-dependent increase in intramitochondrial Ca(2+) concentrations ([Ca(2+)](m)). The [Ca(2+)](m) was significantly lower in cardiomyopathic (CMP) hamsters than in healthy hamsters when [Ca(2+)](o) was higher than 1 microM and a decrease of about 52% was detected at [Ca(2+)](o) of 30 microM (916 +/- 67 nM vs 1,932 +/- 132 nM in control). A possible mechanism responsible for the decreased mitochondrial Ca(2+) uptake in CMP hamsters is the depolarization of mitochondrial membrane potential (Delta psi (m)). Using a tetraphenylphosphonium (TPP(+)) electrode, the measured Delta psi (m) in failing heart mitochondria was -136 +/- 1.5 mV compared with -159 +/- 1.3 mV in controls. Analyses of mitochondrial respiratory chain demonstrated a significant impairment of complex I and complex IV activities in failing heart mitochondria. In summary, a less negative Delta psi (m) resulting from defects in the respiratory chain may lead to attenuated mitochondrial Ca(2+) accumulation, which in turn may contribute to the depressed energy production and myocardial contractility in this model of heart failure. In addition to other known impairments of ion transport in sarcoplasmic reticulum and plasma membrane, results from this paper on mitochondrial dysfunctions expand our understanding of the molecular mechanisms leading to heart failure.
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PMID:Mechanisms of reduced mitochondrial Ca2+ accumulation in failing hamster heart. 1738 8