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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Echocardiographic septal and posterior wall thicknesses and the percent change with systole were measured in 146 patients with the following diagnoses: acute myocardial infarction (40), chronic coronary artery disease (49), congestive cardiomyopathy (8), atrial septal defect (20), and no cardiac disease (29). Mean diastolic thicknesses for the groups of patients with coronary artery disease and congestive cardiomyopathy were not significantly different from normal although there were abnormal values for individual patients within each group. Mean diastolic thickness of the septum was greater than normal for the group with atrial septal defect (P less than 0.02). Wall thinning with systole was associated with acute infarction or ischemia (P less than 0.0001); decreased thickening (less than normal) commonly occurred in patients with acute myocardial infarction, chronic coronary artery disease, and congestive cardiomyopathy. Patients with atrial septal defect had normal thickening with abnormal motion. Results of this study show that 1) systolic thinning is indicative of an acute event; 2) abnormal changes in systolic wall thickening occur commonly in patients with coronary artery disease or congestive cardiomyopathy; and 3) abnormal wall motion may occur without abnormal wall thickening, as the echoes of patients with atrial septal defect indicate.
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PMID:Systolic thickening and thinning of the septum and posterior wall in patients with coronary artery disease, congestive cardiomyopathy, and atrial septal defect. 83 Jan 97

1. The myocardial collagen matrix is an active participant in determining ventricular architecture and diastolic function, and myocardial structural integrity and mechanical properties. It consists of a network of fibrillar collagen which is intimately related with the myocyte, myofibril and muscle fiber as well as the coronary vasculature. Consisting primarily of collagen types I and III, this material exhibits a high tensile strength which, even though normally present in relatively small amounts, plays an important role in the behavior of the ventricle during diastole. 2. Removal of less than half of the normal amount of collagen results in a dilated ventricle with increased compliance. Collagen degradation of this magnitude and similar myocardial and ventricle with increased compliance. Collagen degradation of this magnitude and similar myocardial and ventricular histologic and functional alterations are evident during ischemia and in dilated cardiomyopathy. Thus, it would appear that a chronic change in the shape and size of the heart must be preceded by alterations in the interstitial collagen matrix. 3. With elevations in the circulating levels of angiotensin and/or mineralocorticoids, the hypertrophic response of the myocardium to the accompanying hypertension includes a progressive remodeling of the collagen component. Typically there is an increase in collagen concentration, thickening of existing fibrillar collagen and the addition of new collagen at all levels of the matrix. The consequences of this remodeling are an adverse alteration of the passive mechanical properties of the myocardium and LV diastolic dysfunction. This pathophysiologic aspect of the hypertrophic process is independent of the concomitant remodeling of the myocyte.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial collagen remodeling and left ventricular diastolic function. 134 31

Beta-adrenoreceptor blocking agents have been used to relieve symptoms mainly in patients with ischemic heart disease. Prophylactic use of beta blockade in patients after acute myocardial infarction has shown a reduction in total mortality and also in sudden death. The overall total mortality reduction amounts to about 30%, whereas the reduction in the sudden death rate is 50%. The mechanisms behind this reduction in sudden death are probably manifold. Antiarrhythmic effects in ischemic myocardium, prevention of new ischemia, and also perhaps other factors may play a role. Apart from the prevention effect in chronic ischemic heart disease, beta blockers have also been able to reduce the sudden death rate in the long QT syndrome and are suggested for use in congestive cardiomyopathy.
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PMID:Prevention of sudden death by beta-blockade. 198 82

Between 50 and 70% of patients with heart failure die suddenly and unexpectedly before they have deteriorated to New York Heart Association class IV symptoms. It has long been known that ventricular ectopy predicts sudden cardiac death in coronary heart disease, and this has also been shown in dilated cardiomyopathy. It is less certain whether antiarrhythmic drugs reduce this risk and improve prognosis. Supraventricular arrhythmias frequently develop in heart failure of all causes. They nearly always cause symptoms, and the establishment of atrial fibrillation may mark a permanent deterioration. Except for sustained ventricular tachycardia, ventricular arrhythmias are often occult. Hypokalemia and digitalis toxicity may have been precipitated by diuretics or interaction with antiarrhythmic drugs. In coronary heart failure, arrhythmias may be related to scar tissue or ischemia, which may also be responsible in dilated cardiomyopathy. Use of inotropes and inodilators may precipitate arrhythmias, whereas drugs that conserve energy or potassium, such as beta blockers and angiotensin-converting enzyme inhibitors, may prevent them. Since suppression of ventricular arrhythmias has not been shown to prevent sudden death or prolong life in patients with heart failure, it may be that such arrhythmias do not directly presage ventricular fibrillation except in so far as they are markers of a poor prognosis with a risk of sudden death. If so, such arrhythmias are most likely to be suppressed by agents that result in improvement of left ventricular function and, through that, prolongation of life.
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PMID:Genesis of arrhythmias in the failing heart and therapeutic implications. 202 Nov 15

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

We have shown previously that the physical properties of myocardium in dogs can be characterized with quantitative ultrasonic integrated backscatter and that interrogation of the tissue with ultrasound can delineate cardiac cycle-dependent changes in ultrasonic backscatter in normal tissue that disappear with ischemia and reappear with reperfusion if functional integrity is restorable. To determine whether this approach can be applied to man, we implemented an automatic gain compensation and continuous data acquisition system to characterize myocardium with quantitative ultrasonic backscatter and to detect cardiac cycle-dependent changes in real time. We developed a two-dimensional echocardiographic system with quantitative integrated backscatter imaging capabilities for use in human subjects that can automatically differentiate ultrasonic signals from blood as opposed to those obtained from tissue and adjust the slope of the gain compensation appropriately. Real-time images were formed from a continuous signal proportional to the logarithm of the integrated backscatter along each A-line. In our initial investigation, 15 normal volunteers (ages 17 to 40 years, heart rates 44 to 88 beats/min) and five patients with dilated cardiomyopathy (ages 22 to 52, heart rates 82 to 120 beats/min) were studied with conventional parasternal long-axis echocardiographic views. Diastolic-to-systolic variation of integrated backscatter in the interventricular septum and left ventricular posterior wall was seen in each of the normal subjects averaging 4.6 +/- 1.4 dB (SD) and 5.3 +/- 1.5 dB (n = 127 sites), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quantitative ultrasonic tissue characterization with real-time integrated backscatter imaging in normal human subjects and in patients with dilated cardiomyopathy. 331 50

In addition to radionuclide ventriculography and thallium scintigraphy, already well established in nuclear medicine, assessment of myocardial metabolism is also of interest for diagnosis and follow-up observations in heart disease. Under aerobic conditions and in the fasting state, the heart muscle primarily oxidizes fatty acids; during ischemia, in contrast, there is slowing of fatty acid turnover and increased anaerobic glycolysis. With 11C-palmitic acid, in humans, reduced fatty acid uptake has been documented in infarcted myocardial regions. The analysis of 11C-palmitic acid in dogs showed a three-phased elimination curve in normal myocardium. In ischemic myocardium, there was diminished utilization of free fatty acids and the glucose utilization was concomitantly increased. After insulin-glucose infusion, as well, there was increased glucose utilization and a reduction in fatty acid utilization. Studies with 11C-palmitic acid require the equipment for positron emission tomography (PET); because of the short half-life of 20.3 minutes, the nuclide must be generated by a cyclotron in the immediate vicinity. In the search for well-suited isotopes for use in planar scintigraphy employing a gamma camera, the uptake and elimination of a variety of isotopically-marked fatty acids were measured and compared with the characteristics of 14C-palmitic acid. For 17-123I-heptadecanic acid (IHA) the elimination curve was similar to that of 14C-palmitate: disadvantage, however, was the relatively high percentage of water soluble marked catabolites which required dual parameter analysis by means of 99-m-technetium pertechnetate or 123I sodium iodide to quantify the amount of myocardial fatty acid utilization through subtraction of the externally measured water soluble catabolite from the externally measured total activity. In studies with the gamma camera in fasting patients in whom 2 to 3 mCi IHA was injected intravenously after symptom limited bicycle ergometry, in healthy subjects the elimination halftime for the first rapid phase was 24.4 +/- 4.7 minutes. Patients with angiographically-documented coronary artery disease, in the afflicted myocardial segments, had diminished fatty acid uptake and prolonged elimination halftime as compared with normally perfused segments. In patients with dilated cardiomyopathy there was an inhomogeneous distribution of activity in the myocardium and, in contrast to coronary artery disease, a discordance between local fatty acid uptake and turnover rate. After chronic and acute alcohol consumption there were comparable findings which were shown to be reversible after several weeks of abstinence.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Planar scintigraphy versus PET in measuring fatty acid metabolism of the heart]. 349 62

A congestive cardiomyopathy (CCM) model occurs in inbred broad-breasted turkeys and is manifested by reduced hatchability and a high mortality within a week of hatching. In the survivors, cardiac dilation begins by 3-4 weeks of age and further mortality occurs from chronic congestive heart failure. The mechanisms behind these changes is unknown, and, therefore, we investigated what role, if any, myocardial energy metabolism might play in these events. Ventricular myocardial samples were obtained for analysis of adenine nucleotides (ATP, ADP, AMP) and creatine phosphate (CP) in control and CCM turkeys, 1-31 days old. The adenine nucleotide energy charge (EC) was calculated using the formula EC = ATP + 1/2ADP/(ATP + ADP + AMP). We found the myocardial ATP levels and EC in CCM hearts at 1-2 days were reduced. In control turkeys, no significant age-related differences were found in myocardial high-energy phosphate compounds or in the EC. This depression in the energy metabolism of CCM turkeys may also be reflected in their poor hatchability. By 6-10 days, however, ATP levels had recovered and remained normal despite the onset of cardiac dilation and failure at 3-4 weeks of age in CCM turkeys. Because CP levels in control and CCM turkey hearts were similar in all age groups, significant ischemia did not appear to be present after hatching in CCM turkeys. Our results suggest, therefore, that an insult probably prior to hatching produced depressed myocardial energy levels in CCM turkeys and led to reduced hatchability. This early insult appears to be significant, in that late cardiac dysfunction resulted despite the recovery of myocardial ATP levels.
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PMID:Myocardial high-energy phosphate levels in cardiomyopathic turkeys. 376 30

The term "ischemic cardiomyopathy" was used initially to describe a clinical syndrome that was indistinguishable from primary congestive cardiomyopathy but due to severe, diffuse coronary artery disease. The term has been expanded to include the larger category of myocardial disease secondary to coronary artery disease. Using this expanded definition, we have discussed the varied clinical presentations of congestive ischemic cardiomyopathy and restrictive ischemic cardiomyopathy (stiff heart syndrome and right ventricular infarction), and how the effects of ischemia on left ventricular systolic and diastolic performance may cause these varied presentations. The prognosis of any ischemic cardiomyopathy is related primarily to the degree of ventricular dysfunction and the extent of coronary artery disease. Therapy is aimed at preventing or ameliorating myocardial ischemia and halting the progression of, or even reversing, the deterioration in myocardial function.
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PMID:Ischemic cardiomyopathy. 614 79

Alterations in ventricular diastolic properties are commonly seen in the diseased heart, and have been extensively studied in coronary artery disease, congestive cardiomyopathy, and left ventricular hypertrophy due to pressure or volume overload. Acute increases in left ventricular (LV) diastolic pressure relative to volume occur regularly during the transient ischemia of angina pectoris and may contribute to the dyspnea and pulmonary congestion that commonly accompany this condition. Although the mechanism of this altered disastolic distensibility is debated, a substantial body of evidence favors a role for residual diastolic interaction between contractile elements in the ischemic heart. Congestive cardiomyopathy also appears to be associated with increased LV diastolic stiffness. While this may in part be related to fibrosis of the LV wall, shifts of the abnormal diastolic pressure-volume relation toward normal have been reported with sodium nitroprusside infusion or the beta-adrenergic agonist salbutamol, suggesting important contribution of physiologic factors to the increased resting LV stiffness in this condition. LV hypertrophy (LVH) is associated with increased effective diastolic chamber stiffness, but normalized LV diastolic stiffness is increased only in LVH due to chronic pressure overload. Possible explanations for these findings are discussed.
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PMID:Diastolic pressure-volume relations in the diseased heart. 644 88


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