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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systemic hemodynamic changes and noradrenaline concentrations in coronary sinus blood were studied at rest and during work before and after acute beta-receptor blockade. Patients with congestive cardiomyopathy were compared to patients with primary valvular diseases and to healthy subjects. Noradrenaline concentrations were higher in coronary sinus blood than in arterial blood and increased after beta blockade and during work. Noradrenaline concentrations were more increased in patients with more pronounced myocardial failure and did not seem to separate patients with congestive cardiomyopathy from those with valvular disease. Patients with congestive cardiomyopathy showed a good hemodynamic tolerance toward acute beta blockade.
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PMID:Effects of work and acute beta-receptor blockade on myocardial noradrenaline release in congestive cardiomyopathy. 4 91

A case of beriberi heart failure in a chronic hemodialyzed patient is described. The etiology and the diagnostical criteria are discussed. The possibility of this complication in chronic hemodialyzed patients is considered.
Nephron 1975
PMID:A possible case of beriberi heart failure in a chronic hemodialyzed patient. 12 21

Patients with cardiac disorders have defective parasympathetic control of heart rate. To evaluate the possibility of similar changes in sympathetic control of heart rate, we compared reflex chronotropic responses to 80 degree upright tilt and nitroglycerin-induced hypotension in 31 cardiac patients and 7 normal individuals before and after partial parasympathetic blockade with atropine. Tilting revealed an attenuation of the normal heart rate increase in patients; the magnitude of this defect was greatest in patients with more severe symptoms (class III) and evidence of left ventricular dysfunction (the heart rate increase averaged 25 plus or minus 3 beats/min in normal subjects, 12 plus or minus 2 beats/min in class I-II patients, and 7 plus or minus 1 beats/min in class III patients). Class III symptoms due to mechanical causes (mitral stenosis), however, were not associated with this defect. A marked reduction in heart rate rise with hypotension was seen only in those class III patients without mitral stenosis (0.4 plus or minus 0.1 beats min-minus 1 mm Hg-minus 1 vs. 3.0 plus or minus 0.5 beats min-minus 1 mm Hg-minus 1 in normal subjects). This abnormality also persisted after atropine administration, thus confirming a defect in the sympathetic as well as the parasympathetic component of baroreceptor-mediated reflex heart rate control in patients with cardiac dysfunction. Infusions of isoproterenol produced equivalent rises in heart rate in patients and normal individuals, excluding a reduction in beta-receptor responsiveness as a cause of impaired sympathetic influence. Norepinephrine depletion, however, is a well-recognized concomitant of cardiac failure. It is possible that the reduction in sympathetically mediated heart rate responses results in part from depletion of the sympathetic neurotransmitter.
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PMID:Impairment of autonomically mediated heart rate control in patients with cardiac dysfunction. 80 57

Serial measurements of vital capacity (VC) were performed on nine patients on chronic haemodialysis. In six patients the VC remained stable, they were all adequately dialysed and working full-time. Reduction of dialysis time in one of these patients brought about a gradual onset of left heart failure which was preceeded by a decline of VC. In the three remaining patients a decrease of VC preceeded the onset of heart failure, and a rise of VC values signified improvement of cardiac performance. Serial recordings of VC are recommended as a useful objective guide to evaluation and treatment of patients on haemodialysis.
Nephron 1977
PMID:Serial measurement of vital capacity in patients on chronic haemodialysis. 89 62

15 patients have been treated with dopamine (2.0--6.0 gamma/kg/min) in the initial phase of cardiogenic shock after cardiac surgery. Indication was a systolic blood pressure of less than 85 mmHg associated with oligurie and peripheral vasoconstriction. 12 patients survived the cardiocirculatory crisis and the early postoperative period. Dopamine alone increased the arterial blood pressure in 6 patients from 52.4 to 80.1 mmHg and the urine flow from 25.2 ml/hr to 181.2 ml/hr. To obtain an optimal perfusion pressure additional application of Noradrenalin was used in 8 patients. In these patients the urine flow rose from 9.1 ml/hr to 131 ml/hr. In one patient no reaction, neither to dopamine, nor in combination with Noradrenalin was seen. The effect of pulse rate, central venous pressure and arterial oxygen tension has been discussed. Dopamine seems to be a useful substance in surgical patients with temporary cardiac insufficiency.
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PMID:[Clinical experiences with dopamine after heart surgery]. 108 Oct 33

The authors report on the myocardiopathy of seven patients with end-stage renal disease, characterized by fever, in four patients; tachycardia, gallop rhythm, pericardial rub, in most of patients; signs and symptoms of cardiac failure and increased cardiac area and alterations of the EKG in all patients. Good remission of the symptoms ws achieved in two patients by hemodialysis and by successful renal transplantation in the others. The likely etiologic factors of the syndrome are discussed.
Nephron 1975
PMID:Uremic myocardiopathy. 109 61

Noradrenaline and adrenalin levels in different sections of the heart of persons deceased of myocardial infarction were measured, this being paralleled by determining the content of the said amines in the adrenal glands. It is shown that the noradrenaline level in the myocardium was down by comparison with controls during all periods of myocardial infarction studied. The most marked fall of the noradrenaline level in the heart muscle was noted to have occurred in persons who died in consequence of a progressive circulatory insufficiency. The authors believe that depletion of the noradrenaline reserves in the myocardium can be one of the causative factors in the development of cardiac insufficiency. An elevated concentration of adrenalin was found in the perinfarction region of the myocardium during acute period of infarction, especially 1-2 days following the onset of the latter. The highest rise in the adrenalin level was detected in individuals with repeated myocardial infarction evolving in a recurrent manner and complicated by well-marked arrhythmias. It cannot be ruled out that the amassment of adrenalin in the perinfraction zone may be causative of arrhythmias and recurrent lesions of the myocardium. In cases of myocardial infarction the catecholamines level in the adrenal glands is down, especially 1 more month following the development of infarction.
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PMID:[Noradrenaline and adrenaline content in different areas of the heart in patients dying of myocardial infarct]. 123 6

As soon as there is evidence of left ventricular dysfunction, even before clinical signs of chronic cardiac failure (CCF) have developed, intrinsic and extrinsic compensatory mechanisms are brought into play by the body. The majority of these mechanisms are under the influence of neurohumoral systems. When neurohormonal responses persist, as in CCF, they take on a beneficial nature since they participate in adaptation of the cardiovascular system as a whole, but they are also harmful since they worsen the working conditions of the myocardium by their cardiac and peripheral effects. Hyperactivity of the noradrenergic sympathetic nervous system is seen in CCF with levels 2 to 3 times higher as compared with subjects with normal left ventricular function. The circadian rhythm of catecholamines is modified. The increase in circulatory catecholamines is all the greater when cardiac failure is advanced. This release of noradrenaline (NA) is under the control of arterial baroreceptors which normally send to the central nervous system inhibitory inflow from the sympathetic nervous system. Inhibitory tone is released in case of a fall in blood pressure. Noradrenaline acts on beta-predominant myocardial receptors (inotropic and tachycardic) and alpha-predominant vascular receptors, resulting in arteriolar vasoconstriction. There is rapid onset of down regulation of myocardial beta-receptors. This fall essentially concerns beta 1, but beta 2 also, since they may be affected according to the etiology of CCF (ischemia). The Renin Angiotensin System (RAS) is also activated by the fall in systemic blood pressure. This consists of a cascade of reactions leading to the synthesis of angiotensin II responsible for powerful vasoconstriction of all arterial areas, including the coronary vessels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Metabolic changes in cardiac failure]. 130 Sep 20

Patients with acute heart failure or cardiogenic shock following myocardial infarction have a high mortality. The first priority is to salvage any remaining viable myocardium, either by thrombolytic agents or, if necessary, by coronary angioplasty. A mechanical cause for the heart failure or shock needs to be excluded. Thereafter, the optimal therapeutic regimen needs to be chosen on the basis of each patient's hemodynamic profile. Patients can be broadly classified into three groups: (1) patients with a high left ventricular filling pressure (> 18 mm Hg) and a cardiac index < 2.2 L/min/m2 but systolic arterial pressure > 100 mm Hg; (2) patients with a systolic arterial pressure < 90 mm Hg, left ventricular filling pressure > 18 mm Hg, and cardiac index < 2.2 L/min/m2; and (3) patients with an elevated right ventricular filling pressure (> 10 mm Hg) and cardiac index < 2.2 L/min/m2 and a systolic arterial pressure < 100 mm Hg. Patients in the first subset usually require the use of vasodilator therapy and/or dobutamine. The choice of inotropic agent in patients in the second hemodynamic subset depends on the degree of systemic hypotension; dopamine is usually preferred initially because it increases arterial pressure in addition to improving cardiac output. Once the systemic blood pressure has been stabilized, dobutamine can be substituted for superior augmentation of cardiac output and its additional beneficial effects on the left ventricular filling pressure. Norepinephrine may be indicated in cases of severe systemic hypotension. Patients in hemodynamic subset 3, ie, right ventricular infarction, are treated with volume expansion and dobutamine. Use of nonpharmacologic means of circulatory support, eg, intra-aortic balloon pump or left ventricular assist device may also be required in any of these subsets.
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PMID:Pathogenesis and management of acute heart failure and cardiogenic shock: role of inotropic therapy. 142 38

A 60-year-old uremic patient treated with hemodialysis for 13 years developed acute hypotension during hemodialysis and overt heart failure subsequently in a period of relatively mild hypocalcemia after parathyroidectomy. Blood pressure during hemodialysis was maintained by continuous calcium infusion alone. Cardiomegaly was improved by normalization of serum calcium. The cardiac complication is considered to be exacerbation of the underlying myocardial dysfunction by the acute decline of serum calcium which might be a feature of the 'hungry bone' syndrome. Latent myocardial dysfunction might be exacerbated by only mild hypocalcemia after parathyroidectomy in long-term hemodialysis patients.
Nephron 1992
PMID:Exacerbation of latent heart failure by mild hypocalcemia after parathyroidectomy in a long-term hemodialysis patient. 158 26


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