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

The diagnostic yield of endomyocardial biopsies in patients with chronic congestive heart failure of non-ischaemic aetiology remains questionable and, therefore, the use of endomyocardial biopsies under such circumstances is at stake. The present report documents the correlation between the histologic interpretation of endomyocardial biopsies and the corresponding cardiac explants in 13 patients who underwent cardiac transplantation. The biopsy diagnoses in these patients varied from 'compatible with dilated cardiomyopathy' (n = 6) to 'non-conclusive' (n = 4), 'ischaemia' (n = 2) and 'borderline myocarditis' (n = 1). Correlation with the corresponding cardiac explants revealed hypertrophy of myocytes as the leading histologic feature in the majority of cases. Because of the non-specific histopathology of dilated cardiomyopathy, the discrepancy between biopsy diagnoses and the leading explant diagnosis is mostly a matter of semantics. Ischaemia was present at high incidence, but is considered a result of imparied myocardial perfusion rather than the prime mechanism of heart failure. In four cardiac explants myocarditis was encountered, while the corresponding biopsies showed no cellular inflammation. In two, the cellular infiltrates suggested an early state of repair. One heart contained an active and extensive lymphocytic myocarditis. The fourth case showed an eosinophilic myocarditis, most likely acquired after the biopsy was taken. These discrepancies almost certainly relate to the sampling error and the time interval between biopsy and onset of symptoms. The immediate diagnostic yield of the biopsy, in this particular subset of patients, was minimal, particularly with respect to the diagnosis 'myocarditis'. Nevertheless, biopsy diagnoses such as 'compatible with' and 'non-conclusive' do contribute to the final categorization and management of these patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic non-ischaemic congestive heart disease and endomyocardial biopsies. Worth the extra? 204 56

Electrophysiologic disorders are common at all stages of heart failure due to myocardial mechanical factors, neuroendocrine disturbances, electrolyte abnormalities, or ischemia, and also because of cardiovascular drugs. The prevalence of various forms of heart block, bradycardias, and arrhythmias in heart failure is largely unknown, as is their relationship to the etiology of the syndrome. Complex and multiform ventricular premature beats and nonsustained ventricular tachycardia are common, and their frequency is broadly related to the severity of heart failure. Supraventricular arrhythmias are also common features of the syndrome. The heart failure syndrome has an ominous prognosis. Approximately half the patients die suddenly, but the causal relationship between preexisting arrhythmias and sudden death is not known. Equally vital is knowledge of the influence of drug therapy on the arrhythmias of heart failure, but at present this is scarce and needs further study.
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PMID:Arrhythmias in heart failure--therapeutic challenges. 204 70

During cardiac operations, the heart is subjected to total ischemia and reperfusion, causing serious operative and postoperative complications such as arrhythmias, heart failure, and infarctions that may be partly due to free radical generation. Thus, allopurinol was tested to see if it could reduce cardiac complications during open heart operations. Ninety patients undergoing elective coronary artery bypass grafting were studied prospectively. Fortyfive patients were treated with allopurinol and 45 patients acted as controls. Treatment requiring arrhythmias in the allopurinol group was 6.6% compared with 33.3% in the control group (p less than 0.01). The percentage of patients requiring inotropes was significantly lower in the allopurinol group than in the control group (4.4% versus 26.6%; p less than 0.01). Perioperative myocardial infarction did not occur in the allopurinol group but was seen in 8 patients (17.7%) in the control group. Intraaortic balloon pumping was used in 5 control patients (11.1%) but not in the allopurinol group. This study shows that allopurinol decreases significantly the incidence of cardiac complications in open heart operations.
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PMID:Influence of allopurinol on cardiac complications in open heart operations. 206 40

Analysis of 14 cases of stercoral ulcer showed that they tended to occur in patients over 70 years of age and associated diseases included heart failure under hemodialysis, cerebral hemorrhage, and postoperative states requiring bet rest for long duration. Constipation is always preceded the occurrence of the disease, and the initial symptoms was generally massive hematochezia of sudden onset. Massive blood transfusion was often required, however, heater probe hemostasis was effective. The most common site of involvement was the rectum, and the shape of ulcer was irregular or round. Measurement of the mucosal blood flow in the rectum revealed that blood perfusion was markedly reduced immediately after the occurrence, and that it recovered with healing of ulcer. Ischemia was considered to participate in the pathogenesis of the disease.
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PMID:[Clinical investigation of stercoral ulcer]. 207 57

There is a complex network of collagen throughout the heart. It is composed of a hierarchy of fibrils and fibers ranging from 10 nm to 2-3 microns in diameter. This network can be broken down by ischemia, adriamycin administration, or disulfide administration in laboratory animals. Following loss due to coronary artery ligation, the ischemic area begins bulging within 3 h. General loss of portions of the collagen matrix is induced by intravenous oxidizing glutathione, and results in marked diffuse ventricular dilatation. Generalized collagen loss in the ventricles, as induced by disulfide administration or adriamycin infusion, persists for 6 months at which time evidence of some replacement is visible, and evidence of diffuse fibrosis is present. In humans, cardiac dilatation occurs in a variety of disease states without overstretch of sarcomeres. This presumes rearrangement of the muscle bundles, which can only occur with marked alterations of the collagen matrix. Ventricular dilatation, associated with viral myocarditis or puerperal cardiomyopathy, may persist for months, suggesting the collagen loss, as with the experimental animals, takes many months to repair. The cardiac dilatation may ameliorate, or, in some patients, deteriorate into heart failure. The animal experiments with loss of the collagen matrix, ventricular dilatation, and failure to replace the matrix for many months provide an explanation for persistent cardiac dilatation in various human diseases.
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PMID:Myocardial connective tissue alterations. 209 Dec 28

Over 30 per cent of coronary patients die of cardiac failure excluding the acute phase of myocardial infarction. With the exception of preexisting hypertension, there is no compensatory hypertrophy in ischemic heart disease. However, hypertrophy is a costly adaptation in terms of myocardial oxygen demand and, therefore, coronary flow. Fibrous zones are unresponsive to inotropic drugs and so the treatment of cardiac failure due to ischemic heart disease consists in limiting or preventing episodes of ischemia. Each mechanism of ischemia has an appropriate treatment: the preload is reduced by trinitrin and its derivatives and by molsidomine; the after-load by calcium antagonists and angiotensin converting enzyme inhibitors; tachycardia and hypercontractile states by betablockers. The risk of arrhythmia, aggravated by many inotropic therapies, constitutes the major danger to ischemic heart failure; amiodarone, betablockers and preventive nitrate therapy are the most effective and least dangerous antiarrhythmics. Revascularisation is effective for permanently ischemic segments or for ischemia on effort but does not improve large plaques of fibrosis which sometimes require surgical ablation or plastic procedures. But these measures are incomplete if all aspects of the disease are not taken in consideration: loss of excessive body weight, exercise rehabilitation by modern techniques, limitation of bed rest at the ultimate stage of the disease allowing patients with ischemic cardiac failure a better quality of life without aggravating the prognosis.
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PMID:[Treatment of cardiac insufficiency in ischemic heart disease]. 212 13

Diastolic heart failure is characterized by increased resistance to diastolic filling of one or both cardiac ventricles. Although some degree of diastolic failure exists in most patients presenting clinically with heart failure, a substantial subset of patients have relatively pure diastolic heart failure with normal systolic function. Diastolic heart failure can be due to structural abnormalities that increase resistance to ventricular inflow, and these structural abnormalities can be extramyocardial (e.g., constrictive pericarditis and mitral stenosis) or intramyocardial (e.g., fibrosis and amyloidosis). In addition to structural abnormalities, physiological derangement of myocardial inactivation and relaxation can contribute importantly to diastolic dysfunction in patients with heart failure. There is mounting evidence that advanced myocardial hypertrophy is associated with increased resistance to ventricular diastolic inflow due to both structural alteration (increased wall thickness and altered collagen matrix) and impaired diastolic relaxation of the hypertrophied myocardium. Physiological mechanisms for impaired relaxation in advanced hypertrophy remain controversial but can include disordered function of myocardial sarcoplasmic reticulum, subendocardial ischemia, and altered adenylate cyclase function. Diastolic dysfunction can play an important role in the genesis of flash pulmonary edema seen in patients with ischemic heart disease because myocardial ischemia is associated with a decline in relaxation rate, increased resistance to early diastolic filling, and in some cases, a striking upward shift in the left ventricular diastolic pressure-volume relation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diastolic dysfunction and congestive heart failure. 213 51

Early reports have attributed cardiac failure during acute and chronic models of shock to peripheral vascular dysfunction and decreased venous return. More recently interest has focused on the heart as a primary target responsible for cardiovascular changes associated with acute endotoxin or hemorrhagic shock. At present, it remains controversial whether the heart fails early following the induction of experimental hypodynamic shock. Data from our laboratory have shown that myocardial contractility was increased early following acute endotoxin and splanchnic artery occlusion shock, and it was not until the agonal or terminal phase that contractility was depressed. We have used the slope of the left ventricular pressure-dimension relationship (Ees) as our index of contractile function. This technique is preferential since it is not affected by changes in the loading conditions on the heart. Unlike most reports that have used LV dP/dt as an index of contractility in the intact animal, we have shown that Ees and LV dP/dt do not uniformly reflect changes in contractility. LV dP/dt and related measures do, however, reflect the overall global changes in myocardial performance, which are affected by changes in preload, afterload, heart rate, and contractility. The reductions in LV dP/dt therefore mainly reflect the changes in arterial blood pressure associated with acute hypodynamic shock. The increase in contractility reported during endotoxin shock were shown to be induced by stimulation of beta-adrenergic receptors--when the beta-blocking drug, propranolol, was given to animals during shock, contractility decreased. The mechanism(s) responsible for the failure of the heart during the late or agonal periods of shock is (are) unknown. We have shown in dogs who die as a result of endotoxin shock that the hearts exhibit a progressive energy deficit, whereas animals surviving the experimental protocol maintained levels of ATP and creatine phosphate. It is unclear if the changes in high-energy phosphates during endotoxin shock cause irreversibility. Other potential mediators of cardiac failure have included ischemia/hypoxia, toxic myocardial depressant factors, deterioration of sympathetic influences on the heart, electrophysiologic and ionic disturbances, etc. The relationship between these factors and failure of the heart in vivo during various shock paradigms remains to be elucidated.
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PMID:When does the heart fail during shock? 213 82

Calcium ions are important in many aspects of normal cardiac function as well as in the response to certain pathologic states. The contribution that myocardial calcium influx makes to the cardiac action potential and the pharmacologic efficacy of compounds designated as calcium channel blockers is examined with respect to current knowledge regarding the structure and characteristics of cardiac sarcolemmal calcium channels. Once intracellular, calcium provides the link between cardiac electrical activity and actual mechanical shortening of cardiomyocytes through a complex interaction of regulatory and structural contractile proteins. This is followed by calcium clearance from the cytosol; the mechanisms by which this occurs are manipulated by drugs such as the digitalis glycosides to enhance myocardial contractility. The importance of intracellular 'second messengers' (eg, cyclic AMP) in constituting a final common pathway for the effects of certain cardiotonic agents is defined. The significance of abnormal calcium homeostasis under conditions of heart failure, myocardial infarction, ventricular fibrillation and cardiomyopathy is examined. The role of calcium in the mediation of myocardial damage under conditions of ischemia and secondary to a phenomenon known as 'the calcium paradox' is discussed. The finding that neonatal hearts are more vulnerable to ischemic contracture than adult hearts may be partially explained by differences between neonatal and adult myocardial calcium handling. Understanding of the interactions that exist between the calcium ion and the cardiomyocyte requires a sound knowledge of this essential partnership by both the physiologist and the practising physician.
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PMID:Calcium and the heart: an essential partnership. 217 38

From the foregoing discussion, it becomes apparent that although noninvasive risk stratification is a reasonable approach to assessment of patients following an uncomplicated myocardial infarction, the performance of early cardiac catheterization and angiography on nearly all such patients is not unreasonable and may in fact be the most practical approach. The basis for this rationalization may be summarized as follows: 1. Many subgroups will need early catheterization anyway a. Myocardial infarction complicated by recurrent ischemia, heart failure, or complex ventricular arrhythmias b. Patients receiving thrombolytic treatment c. "Young" patients (less than 50 years old?) d. "Older" patients (over ages 65 to 70?) in otherwise good medical condition e. Patients unable to exercise f. Patients with abnormal or inconclusive noninvasive test results (approximately 70 percent of patients) 2. Cardiac catheterization and angiography as a single test provides the two most powerful prognostic variables following myocardial infarction, namely, the extent of coronary artery disease and residual left ventricular function. This knowledge is reassuring to both physician and patient and allows for planning of optimal long-term management. 3. Certain limitations exist in noninvasive risk assessment strategies. 4. This approach need not be significantly more costly, if all tests are used wisely. The major risk inherent in the definition of the extent of coronary artery disease in all survivors of acute myocardial infarction might be the performance of unnecessary revascularization procedures (percutaneous transluminal coronary angioplasty or coronary bypass surgery). The burden rests with the individual clinician to (1) collect all useful and necessary data; (2) assess reliability and accuracy of various tests available at one's own institution; (3) avoid performing unnecessary and repetitive tests; (4) interpret the data in the proper context; and (5) counsel patients appropriately, correctly, and judiciously about their prognosis and therapeutic options. In this manner, all patients who might benefit appropriately from revascularization can be discovered early and offered this therapeutic option. Other patients can also be managed more appropriately; for example, those who are truly at very low risk (normal left ventricular function and either normal coronary arteries or "mild" coronary artery disease). However, it is most important to avoid unnecessary revascularization procedures. Although this discussion has focused on noninvasive and invasive testing following myocardial infarction, it is necessary to emphasize that comprehensive management of coronary artery disease and its complications should not be neglected in these patients; for example, control or amelioration of risk factors for coronary artery disease is mandatory in all these patients, and in their families as well.
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PMID:Is noninvasive risk stratification sufficient, or should all patients undergo cardiac catheterization and angiography after a myocardial infarction? 219 55


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