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)

The chest X-ray films of 251 patients with cardiovascular lesions, collected in the major hospitals of Papua New Guinea, were reviewed. Cor pulmonale (18%) and rheumatic heart disease (16%) were the predominant cardiac disorders, and cor pulmonale was the most common cause of cardiac failure (58%). Cardiomegaly or cardiac failure of unknown cause, possibly due to cardiomyopathy or myocarditis, made up 9% of the group and may be more important than has been thought previously. Aortic-arch calcification typical of atheroma was present in 21% of the patients, and is thus quite common, even though ischaemic heart disease remains very rare (1%). More than half of the patients with aortic atheroma had chronic lung disease, and though this could be explained by the coincidental frequency of both conditions, the possibility of an association or link in pathogenesis between them deserves further consideration. Anaemia was a common cause of cardiac enlargement (14%), and sometimes led to cardiac failure. Only 16 patients had hypertension (essential in 10 patients and renal in six), and this may indicate a change from the previously reported predominance of renal hypertension in Papua New Guinea towards a more equal incidence of the two conditions. Aneurysms of unknown cause were encountered in three fairly young patients. They had some resemblance to the aneurysms in arteritis of obscure origin described in Africa. There were also two dissecting aneurysms and one syphilitic aneurysm of the aorta. Congenital lesions (8%), pericarditis due to various causes (including tuberculosis), bacterial endocarditis (in four patients with rheumatic heart disease), and miscellaneous conditions made up the remainder of the series.
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PMID:Cardiovascular disease in Papua New Guinea. 644 34

Chronic renal failure is found in different stages, from the fully compensated stage until the terminal form of uremia. Complications like metabolic acidosis and hyperkalemia as well as renal hypertension with following cardiac insufficiency are influencing the prognosis. If conservative therapy is of no avail any more renal grafting is besides dialysis an additional treatment not sufficiently used in our country.
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PMID:[Problems in chronic renal insufficiency]. 701

Therapy of chronic renal failure requires individual management in diet and vigorous treatment of disorders of fluid and electrolyte metabolism and renal acidosis. Concomitant diseases such as renal hypertension, arrhythmia, cardiac insufficiency, pulmonary complications, gastrointestinal disorders, renal anaemia, affection of central nervous system, disturbance in glucose, uric acid and lipid metabolism and infections, demand careful medication Selection of drugs and doses related to impaired renal functions, is indicated.
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PMID:[Therapy in chronic renal insufficiency (author's transl)]. 724 18

M-mode echocardiography was performed 18 to 22 hours after a haemodialysis session in 16 patients under chronic dialysis. The patients (12 men and 4 women, mean age 21 years, haematocrit 24 +/- 5%) were normotensive and had no clinical or radiological sign of heart failure. Patients with renal hypertension, diabetes or amyloidosis had been excluded from the study. Eight healthy subjects of similar age, heart rate and blood pressure were used as controls. In all 24 individuals the following parameters were calculated: end diastolic time diameter index (DTDI), end systolic time diameter index (STDI), ejection time (ET), mean velocity of circumferential fiber shortening (VCF) and ejection fraction (EF). DTDI was greater in haemodialyzed patients (31 +/- 2 mm/m2) than in controls, but STDI and ET were the same in both groups. This would explain the increase of VCF (1.68 +/- 0.1 c/sec) and EF (0.78 +/- 0.05) observed in dialyzed patients. After compression of the fistula for 3 min the differences disappeared. These results suggest that the echocardiographic measurements listed above give a better idea of the true contractile state of the left ventricle in haemodialyzed patients, disregarding load changes due to the fistula, to anaemia and to intermittent volume expansion.
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PMID:[Echocardiographic measurement of true left ventricular inotropism in patients under haemodialysis (author's transl)]. 731 3

The authors had 213 patients under observation with systemic lupus erythematosus. Changes in the heart were revealed in 171 patients, all had affection of the myocardium: myocarditis was found in 66 and myocardial dystrophy in 122. Appraisal of leucocyte migration inhibition with the myocardial antigen (in 23 patients) and detection of antibodies against the myocardium by immunofluorescence (in 33) suggest that disorders in cellular immunity play an important part in the development of lupus myocardial affection. Involvement of the heart in patients with systemic lupus erythematosus was partly associated with renal hypertension, which was conducive, first and foremost, to the development of myocardial hypertrophy and could be attended with increased cardiac ejection and peripheral resistance. A decrease in the cardiac output with a gradual growth in the activity of systemic lupus erythematosus was noted. Steroid myocardial affection was found in 1/4 of patients, which sometimes occurred with cardiac insufficiency and signs of inflammation. Besides mitral valve sclerosis (7%), mitral stenosis was revealed in 3 patients and aortic insufficiency in one. Echocardiography helped to make an early diagnosis of hypertrophy of the heart and pericardial effusion in patients with systemic lupus erythematosus.
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PMID:[Cardiovascular aspects of systemic lupus erythematosus pathology]. 739 79

Modifications to cell relaxation and handling of intracellular Ca have been demonstrated in animals with cardiac cell hypertrophy leading to decompensated heart failure. A previously described model of renal hypertension leading to cardiac cell hypertrophy in the guinea pig, produced using the Goldblatt 2-kidney, 1-clip technique, was used to investigate which of the main mechanisms causing cell relaxation (the sarcoplasmic reticulum Ca-adenosinetriphosphatase and Na/Ca exchanger) are altered in hypertrophy. Relaxation upon rewarming from a rapid cooling contracture was slowed in hypertrophied (H) compared with control (C) cells. Relaxation was further slowed in H compared with C cells when Na/Ca exchange was inhibited by rewarming in a Na-free, Ca-free solution and slowed most markedly in H cells in the presence of 10 mM caffeine. Hypertrophy led to greater modification of cell length relaxation in comparison with the decline in the indo-1 transient, but the force-pCa relationship in skinned muscles showed that myofilament sensitivity was unchanged. Such results indicate that cell relaxation and Ca handling are affected in hypertrophy, possibly involving modifications of Na/Ca exchange activity.
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PMID:Effect of hypertrophy on mechanisms of relaxation in isolated cardiac myocytes from guinea pig. 797 15

In an attempt to elucidate the effects of two major risk factors of heart failure in humans, high blood pressure and coronary artery disease, renal hypertension and coronary artery constriction were induced singularly and in combination in rats, and the functional, structural, and biochemical alterations of the myocardium were examined 12-13 wk later. Renal hypertension (RH), coronary narrowing (CN), and their association (NH) resulted in left ventricular failure demonstrated by a significant increase in left ventricular end-diastolic pressure, a decrease in +dP/dt and -dP/dt, and a reduction in stroke volume and cardiac output. Measurements of ventricular loading documented that RH was characterized by elevations in systolic and diastolic wall stress of 42 and 160%, respectively. Corresponding changes with NH were 80 and 315%. CN was accompanied by an augmentation of diastolic wall stress only (280%). The abnormalities in mural stress were coupled with reductions in systolic and diastolic wall thickness-to-chamber radius ratios of 39 and 29% after CN. These anatomic parameters were preserved with RH, whereas the systolic wall thickness-to-chamber radius ratio was reduced 31% with NH. Structurally, multiple foci of replacement fibrosis were found with each intervention. The sites of tissue injury and their volume percent in the myocardium were comparable with CN and RH but were significantly more numerous and occupied a larger fraction of the ventricular wall in the presence of NH. Biochemically, the calcium dose-response curve of myofibrillar Mg2+ adenosinetriphosphatase (ATPase) activity did not vary with CN, RH, and NH. In contrast, a marked decrease in Ca2+ myosin ATPase activity was found in NH rats in association with a shift in myosin isoenzymes from V1 to V3. In conclusion, multiple physiological, morphological, and biochemical factors may participate in the generation of the abnormalities in ventricular loading with hypertension and/or coronary artery stenosis.
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PMID:Effects of hypertension and coronary constriction on cardiac function, morphology, and contractile proteins in rats. 836 72

Sulfoconjugated catecholamines have been regarded simply as metabolites of free catecholamines. However, a conjugated form of the catecholamine, dopamine has recently attracted much attention because it is present at high levels in the plasma of humans and experimental animals. We carried out experimental and clinical studies to determine the physiological significance of this large amount of dopamine conjugate in the plasma. Clinical studies showed that the plasma level of dopamine sulfate decreased significantly during the acute phase of heart failure, whereas that of free dopamine increased. Moreover, the plasma level of conjugated dopamine in patients with essential hypertension was higher than that in control subjects, and being highest in patients with renal hypertension. In experimental studies, we examined the activity for deconjugating DA sulfate in homogenates of organs from dogs. The kidney and liver exhibited the highest activities, and in the heart, the activity was higher in the atrium than the ventricle. We also examined the effect of dopamine sulfate on isolated perfused rat heart. Dopamine sulfate was found to be converted to free dopamine, which was responsible for the positive inotropic action, in atrial tissue. Moreover, deconjugation of DA sulfate to the free form was accelerated by a high work lord on the heart. From these results, we conclude that the formation of dopamine sulfate plays a role in regulating the level of plasma free dopamine and that plasma dopamine sulfate may be a storage or reserve form of dopamine. Free (or active) dopamine may be formed through a deconjugation reaction when necessary.
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PMID:Physiological significance of plasma sulfoconjugated dopamine: experimental and clinical studies. 852 36

A 36-year-old man known as chronic alcohol abuser presently suffered from arthralgia and showed bilateral petriefied kidneys by sonography and computed tomography. Because of an unclear renal failure a kidney biopsy was performed and presented typical chronic renal oxalosis with massive oxalate crystal deposits, tubular atrophy and interstitital fibrosis. Since the man had never shown signs of hyperoxaluria in his life before, a secondary oxalosis was supposed. The subsequently prompted exploration established a three to four times abuse of rocket fuel with cola lemonade 12 years before during the patient's army time as a marine soldier. Such fuels contain ethylene glycol (glysantin) as antifreeze commonly known to cause in toxic doses acute renal tubular necrosis with hyperoxaluria. The presented case, however, suggests a rare sublethal ethylene glycol poisoning with initial renal tubular damage, oxalate crystal deposition and subsequent chronic interstitial oxalate nephritis with tubular atrophy, interstitial fibrosis and chronic renal failure. Undergoing chronic hemodialysis, the patient died 5 months after the kidney biopsy diagnosis by acute heart failure. At autopsy, progressed chronic renal oxalosis could be confirmed. Decompensated oxalate cardiomyopathy with disseminated myocardial oxalate crystal deposits caused acute heart failure promoted by myocardial hypertrophy in renal hypertension.
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PMID:[Fatal chronic oxalosis after sublethal ethylene glycol poisoning]. 938 Jun 7

The endothelins are a family of endothelium-derived peptides that possess characteristically sustained vasoconstrictor properties. Endothelin-1 appears to be the predominant member of the family generated by vascular endothelial cells. In addition to its direct vascular effects, endothelin-1 has inotropic and mitogenic properties, influences homeostasis of salt and water, alters central and peripheral sympathetic activity and stimulates the renin-angiotensin-aldosterone system. Studies with endothelin receptor antagonists have indicated that endothelin-1 probably has complex opposing vascular effects mediated through vascular smooth muscle and endothelial ET(A) and ET(B)receptors. Endogenous generation of endothelin-1 appears to contribute to maintenance of basal vascular tone and blood pressure through activation of vascular smooth muscle ET(A)receptors. At the same time, endogenous endothelin-1 acts through endothelial ET(B) receptors to stimulate formation of nitric oxide tonically and to oppose vasoconstriction. In view of the multiple cardiovascular actions of endothelin-1, there has been much interest in its contribution to the pathophysiology of hypertension. Results of most studies suggest that generation of, or sensitivity to, endothelin-1 is no greater in hypertensive than it is in normotensive subjects. Nonetheless, the deleterious vascular effects of endogenous endothelin-1 may be accentuated by reduced generation of nitric oxide caused by hypertensive endothelial dysfunction. It also appears likely that endothelin participates in the adverse cardiac and vascular remodelling of hypertension, as well as in hypertensive renal damage. Irrespective of whether vascular endothelin activity is increased in hypertension, anti-endothelin agents do produce vasodilatation and lower blood pressure in hypertensive humans. There is more persuasive evidence for increased endothelin-1 activity in secondary forms of hypertension, including pre-eclampsia and renal hypertension. Endothelin-1 also appears to play an important role in pulmonary hypertension, both primary and secondary to diseases such as chronic heart failure. The hypotensive effects of endothelin converting enzyme inhibitors and endothelin receptor antagonists should be useful in the treatment of hypertension and related diseases. Development of such agents will increase knowledge of the physiological and pathological roles of the endothelins, and should generate drugs with novel benefits.
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PMID:Endothelin as a regulator of cardiovascular function in health and disease. 979 9


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