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

The clinical course and postmortem findings of an unusual case of complete transposition of the great arteries, in which the Mustard operation was not performed until the patient was 12 years of age, are documented with serial catheterizations showing adequate repair. The clinical course of the patient was uneventful for 8 years after surgery, when right (systemic) ventricular failure occurred, resulting in the patient's death at 20 years of age. Late cardiac failure, the cause of death, is not a commonly described problem after successful surgical repair of transposition of the great arteries.
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PMID:Late right ventricular failure after Mustard operation for transposition of the great arteries. 66 20

Measurements of mean left ventricular (LV) and regional myocardial blood flow rates were made at rest in 161 patients with 133Xe and a multiplecrystal scintillation camera. Myocardial perfusion rates were correlated with assessments of the degree of coronary artery disease made from the arteriograms obtained during the same studies. In patients with normal coronary arteries without heart failure, the presence of hypertension, aortic stenosis, or aortic insufficiency was not associated with changes in mean LV perfusion from the control value of 61+/-7 ml/100 g-min. However, mean LV perfusion was significantly reduced in patients with normal coronary arteries who had cariomyopathy and impaired ventricular performance. Mean LV perfusion was not significantly different from control values in patients with "mild" coronary artery disease (less than 50% obstruction) or in patients with significant isolated disease (greater than 50% obstruction) of the left anterior descending (lad) artery. Significant reductions in mean LV perfusion were found in patients with greater than 50% obstruction of two coronary arteries (LAD + right or LAD + circumflex) and in patients with triple-vessel disease. The average perfusion rate for regions distal to LAD obstructions in patients with isolated LAD disease was not lower than the LAD perfusion in control patients, but was significantly reduced in patients with LAD + right coronary artery disease (43+/-14 ml/100 g-min). In the latter group average perfusion distal to the LAD lesion was significantly lower than the average regional perfusion rate for the remainder of the LV. However, the mean blood flow rate for the remainder of the LV was also significantly lower than control values despite the lack of significant circumflex disease. The data demonstrate that the presence of radiographically "mild" or significant isolated LAD coronary disease is not associated with reductions in mean LV perfusion at rest, but that mean LV perfusion is reduced in the presence of significant disease of two or three coronary artieries. None of the patients experienced angina during the resting studies and most had clinical evidence of ventricular failure. The observation of depressed LV perfusion in this group, as in the patients with cardiomyopathy, raises the possibility that a lowered resting blood supply may be adequate for a reduced level of performance of a diseased ventricle. The lack of selective reductions of regional perfusion at rest in the majority of the patients with LAD lesions suggests that regional myocardial blood flow must be measured during an intervention which increases myocardial oxygen consumption in order to assess the physiological significance of lesions which are observed at coronary arteriography.
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PMID:The relationship between regional myocardial perfusion at rest and arteriographic lesions in patients with coronary atherosclerosis. 120 79

A 42-year-old patient with acute left-ventricular failure is described in whom pheochromocytoma was diagnosed only after prolonged and fruitless efforts. Pheochromocytoma may present without the typical features of paroxysmal or sustained hypertension, headache, increased sweating, and palpitations. Therefore, in cases of acute left-sided cardiac failure of primarily undetermined origin, pheochromocytoma should be considered in differential diagnosis.
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PMID:[Acute left heart insufficiency: possible leading symptom of a pheochromocytoma]. 157 67

Cardiac failure is the principal medium-term complication of myocardial infarction. Changes in left ventricular geometry are observed after infarction, called ventricular remodeling, which, though compensatory initially, cause ventricular failure in the long-term. Experimental and clinical studies suggest that early treatment by coronary recanalisation, trinitrin and angiotensin converting enzyme inhibitors may prevent or limit the expansion and left ventricular dilatation after infarction, so improving ventricular function, and, at least in the animal, reduce mortality. Large scale trials with converting enzyme inhibitors are currently under way to determine the effects of this new therapeutic option. It would seem possible at present, independently of any reduction in the size of the infarction, to reduce or delay left ventricular dysfunction by interfering with the natural process of dilatation and ventricular modeling after infarction.
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PMID:[Ventricular "remodeling" after myocardial infarction]. 191 Mar 27

Chronic cardiac failure with normal left ventricular systolic function is observed in conditions without ventricular failure (pericardial adiastole, obstruction to intracardiac blood flow) or with ventricular failure due to isolated abnormalities of left ventricular filling. These forms of cardiac failure are often subject to diagnostic error. However, it is essential that they be recognised because traditional therapy must be used with caution and because of the efficacy of treatment of the underlying pathology whenever this is possible.
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PMID:[Treatment of chronic cardiac insufficiency with normal left ventricular systolic function]. 212 12

Cardiac failure is defined as the inability of the heart to provide the necessary blood flow for the metabolic and functional needs of the vital organs under normal conditions. The underlying physiopathological mechanisms are multiple: cardiac failure without ventricular failure, ventricular failure with or without abnormal ventricular systolic function, prolonged tachycardias or tachyarrhythmias in normal hearts. The association of several mechanisms aggravates the prognosis. Peripheral and central compensatory mechanisms in such situations are not always beneficial. The principles of treatment depend on the type of cardiac failure encountered. The medium and long-term therapeutic objectives are not only to correct the haemodynamic abnormalities but to improve the quality of life and, if possible, the duration of survival.
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PMID:[Cardiac insufficiency. Definition, mechanisms, principles of treatment]. 214 69

To determine if aging engenders alterations in the functional properties of the myocardium and ventricular remodeling, the hemodynamic performance and structural characteristics of the left ventricle of male Fischer 344 rats at 4, 12, 20, and 29 mo of age were studied by quantitative physiology and morphology. In vivo assessment of cardiac pump function showed no change up to 20 mo, whereas left ventricular end-diastolic pressure was increased at 29 mo. Moreover, peak rates of pressure rise and decay, stroke volume, ejection fraction, and cardiac output were depressed at the later age interval, demonstrating the presence of ventricular failure at this time. The measurements of chamber size and wall thickness showed that ventricular end-diastolic and end-systolic volumes progressively increased with age with the greatest change occurring at 20-29 mo. Aging was also accompanied by a marked augmentation in the volume fraction of fibrotic areas in the ventricular myocardium that was due to an increase in their number and cross-sectional area with time. These architectural rearrangements, in combination with the abnormalities in ventricular function, resulted in an elevation in the volume of wall stress throughout the cardiac cycle. Wall stress increased by 64, 44, and 50% from 4 to 12, 12 to 20, and 20 to 29 mo of age. In conclusion, aging leads to a continuous rise in wall stress that is not normalized by ventricular remodeling. These two independent processes appear to be responsible for the onset of heart failure in the senescent rat.
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PMID:Severe myocardial dysfunction induced by ventricular remodeling in aging rat hearts. 222 Nov 16

The author presents a retrospective and complex pathomorphological analysis in 152 autopsy cases. Death was caused by different forms of cardiomyopathies. Aim of the study to reveal the frequency of pathology, causes and mechanisms of death. The prevailing frequency of dilated cardiomyopathy was established--106 cases, 0.88%. Hypertrophic and restrictive forms--32 (0.27%) and 14 (0.12%) of cases. the dominating cause of death (42.7%) was chronic cardiac failure. Other death causes were as follows: thrombosis and embolism--17.8%; arrhythmic collapse--13.2%; ventricular fibrillation--9.9%; acute left-ventricular failure--8.6%; real cardiogenic shock--7.8% of all cases of cardiomyopathies.
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PMID:[The causes and mechanisms of death in cardiomyopathies]. 228 61

The incidence of late systemic ventricular failure (SVF) was determined in 220 early survivors of atrial correction for transposition of great arteries (TGA), operated upon between 1964 and 1985. SVF was defined as either severe heart failure (NYHA class III or IV) or death due to the same cause, in the absence of other haemodynamic disturbances. The actuarial survival rate was 96% after 1, 94% after 5 and 87% after 10 years. SVF occurred in 16/220 patients (7.2%). SVF was more common in complex TGA (TGA + VSD or PS or both) with 11/99 patients (11%) than in simple TGA with 5/121 patients (4.1%), P less than 0.01. Actuarial freedom from SVF was 97% at 5, and 92.5% at 10 years. SVF caused 10/25 (40%) late deaths. SVF occurred from the 1st postoperative year up to 20 years after correction (average interval 6.3 years). In 1 of 2 patients a systemic atrioventricular (AV) valve annuloplasty did not improve SVF. Heart transplantation was performed in 2 patients and 1 is on the waiting list. SVF is a rare late complication of atrial correction for TGA with a constant incidence in the late course. SVF is more common in complex TGA.
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PMID:Late failure of systemic ventricle after atrial correction for transposition of great arteries. 262 61

This study was designed to determine: (1) the myocardial adenosine triphosphatase (ATPase) activities of normal humans and patients with dilated cardiomyopathy and (2) whether ATPase activity is related to age, cause and severity of heart failure, and digitalis therapy. Endomyocardial biopsies were performed in 32 subjects. Results from six were normal. Ventricular failure in the other 26 was idiopathic (n = 15), familial (n = 3), alcohol induced (n = 5), or related to doxorubicin therapy (n = 3). The biopsies were analyzed for total, mitochondrial, Na+-K+, Ca++, and Mg++ ATPase activities. Total and mitochondrial ATPase activities correlated with left ventricular ejection fraction (r = 0.65 and 0.67, respectively; both p = 0.0001). Residual Mg++ ATPase activity correlated weakly with ventricular function as measured by echocardiography (p = 0.05). Na+-K+ ATPase activity was depressed in patients receiving digitalis (p = 0.01). These results suggest that progressive ventricular dysfunction may be associated with a progressive loss of total ATPase, mitochondrial ATPase and, to a lesser extent, Mg++ ATPase activity. Although depressed mitochondrial ATPase activity is not likely to be the primary cause of ventricular dysfunction, it could perpetuate failure by leading to inadequate production of adenosine triphosphate. Further study of ATPase activities may provide additional insight into the pathogenesis of cardiac failure.
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PMID:Human myocardial adenosine triphosphatase activities in health and heart failure. 282 53


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