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

Ventricular dysfunction caused by ischemia is frequently a consequence of episodes of myocardial infarction which occur in the context of coronary disease, as well as of the ischemic situation in patients with severe failure in the main coronary arteries. The physiopathological mechanisms, as well as the therapeutic possibilities, are different in the case of diagnosed necrosis of myocardium or in situations of its circulatory deficiency, and, in the latter case, they depend on the period of absence of blood flow to the ischemic area, and on the occurrence of reperfusion of the area at the end of the ischemic event, the existence of an adequate collateral flow, etc. Classically, moderate degrees of ischemic ventricular dysfunction were considered as a preferential indication for revascularization surgery, together with the existence of coronary disease anatomically suitable for bypass. However, severe degrees of ventricular dysfunction were regarded as a contraindication to surgery, as they were considered irreversible due to an ischemic myocardiopathy which could not be palliated by an ulterior revascularization. These patients were referred to heart transplantation or to medical treatment when they did not fulfill the criteria to be included in transplantation programmes. In a later stage, due to a scarcity of donors for transplantation and to the disappointing results of pharmacological treatment in these patients, revascularization operations begun to be performed on patients with severe heart failure. Although initial results were not comparable to the ones obtained nowadays, work continued on this track and rapid improvement was achieved when particular clinical and diagnostic patterns were followed. Thus the concept of myocardial viability was created, presently being a central criterion in deciding which patients should go through revascularization. There are different methods to assess viability, and new ones are added to the diagnostic arsenal every day. With an adequate assessment of this concept, it is presently possible to really predict which patients may obtain clinical and functional improvement from their coronary disease in spite of severe deterioration of their cardiac function. This article analyzes the physiopathology of ventricular dysfunction, present methods to detect the viability of myocardial cells, as well as present indications and results obtained with ventricular revascularization in patients with severe depression of ventricular function as an alternative, currently well established, to heart transplantation.
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PMID:[Revascularization versus transplantation in patients with limited ejection fraction]. 971 12

There is convincing evidence that (prolonged) episodes of myocardial ischemia lead to impairment of left ventricular (LV) function and ultimately to chronic congestive heart failure (CHF), but whether the opposite is also true has not been well established. We studied this issue in two groups of CHF patients with positron emission tomography (PET) by using [13N]ammonia (13NH3) as a tracer. In the first protocol we compared 12 patients with idiopathic dilated cardiomyopathy (who have normal coronary arteries) with 12 healthy controls. In the second protocol we studied a group of 24 patients with documented coronary artery disease (CAD). In this protocol, we compared patients with normal LV function to those with LV dysfunction and CHF. In patients with cardiomyopathy, myocardial blood flow at rest was normal but flow reserve (after dipyridamole infusion) was significantly impaired (1.7 +/- 0.08) compared with normal subjects (2.7 +/- 0.04; p <0.05). Furthermore, by examining [18F]fluorodeoxyglucose (18FDG) uptake, a perfusion-metabolism mismatch was observed in 24 +/- 6% of the myocardium in patients with cardiomyopathy as opposed to 0% of normals (p <0.05). In patients with CAD, myocardial blood flow reserve (measured in non-stenotic arteries to non-infarcted area) was impaired in CHF patients (1.7 +/- 0.06) compared to those with normal LV function (2.3 +/- 0.05; p <0.05). In both groups of CHF patients, the impairment of blood flow reserve showed a significant correlation with the severity of CHF. In conclusion, myocardial blood flow reserve is impaired in patients with CHF in proportion to the degree of CHF. Metabolic studies with 18FDG further show that, in patients with idiopathic dilated cardiomyopathy and CHF, flow-metabolism mismatch is present in a substantial part of the myocardium, suggesting a pathogenetic role for ischemia.
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PMID:Ischemia and left ventricular dysfunction: a reciprocal relation? 973 95

Orotic acid (OA), a naturally occurring substance, is a key intermediate in the biosynthetic pathway of pyrimidines. Previous investigations in the heart suggest that orotate can protect recently infarcted hearts against a further ischemic stress and may be beneficial in certain types of experimental cardiomyopathy. At the Hamburg symposium on magnesium orotate, a number of studies of this form of metabolic supplementation were presented that indicate orotic acid and its magnesium salt have a modest beneficial effect on the myocardium under conditions of stress ranging from myocardial infarction to severe physical exercise. The following conclusions can be drawn: (1) Orotic acid can improve the energy status of the recently infarcted myocardium (rat hearts). (2) Orotic acid may improve myocardial purine and pyrimidine levels by stimulating hepatic release of uridine into the bloodstream, which in turn augments depleted myocardial pyrimidines and purines (rat heart). (3) Orotic acid improves the tolerance of the recently infarcted heart to global ischemia (rats). (4) Magnesium orotate may reduce the severity of chronic myocardial dysfunction and structural damage in cardiomyopathy (cardiomyopathic hamsters). (5) Magnesium orotate may improve exercise tolerance in patients with coronary artery disease and in trained athletes (humans). (6) Magnesium orotate has only a weak inotropic effect, if any, on normal hearts (rats). (7) Further clinical testing is indicated to determine if the effects described could be of significant clinical benefit in the treatment of heart disease.
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PMID:Metabolic supplementation with orotic acid and magnesium orotate. 979 88

Abnormalities of the microvasculature are centrally involved in the pathogenesis of some forms of heart disease, but in others are consequences of it. Microvascular abnormalities may contribute to the progression of viral myocarditis and Chagas' disease. Focal abnormalities may occur early in some cardiomyopathies and do occur later in most types of myocarditis. The thickening of arteriolar walls in chronic hypertension is likely to contribute significantly to the impairment of coronary haemodynamics associated with adaptive ventricular hypertrophy and the consequent diminution of coronary reserve, increasing diffusion distances and failure of angiogenesis to compensate. However, the resulting myocyte necrosis stimulates inflammatory angiogenesis. When ischemic myocyte injury becomes irreversible there is a concomitant loss of capacity for reperfusion, the no-reflow phenomenon. Less severe temporary ischemia reduces the proportion of functional capillaries. Multiple mechanisms are involved in this microvascular stunning, including: reperfusion injury; leukocyte activation; adhesion and accumulation; and impaired endothelium-dependent vasodilation. Many of the microvascular changes are those of the inflammatory response to cell death and form part of a final common pathway in myocarditis, cardiomyopathy, cardiac hypertrophy and failure, and ischemic heart disease. Stimulation of angiogenesis prior to myocyte necrosis in hypertrophy and control of leukocyte activity in ischemic heart disease could minimize myocyte loss.
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PMID:Microvascular involvement in cardiac pathology. 999 May 24

Myocardial viability assessment is useful in patients with severe coronary artery disease and severe left ventricular dysfunction. Whereas most studies have focused on recovery of regional function, there are emerging data on patient outcome. Review of these data suggests that patients with chronic ischemia, cardiomyopathy, and viable myocardium who are treated medically have a worse, outcome than those treated with coronary revascularization. However, there are no prospective randomized trials. We present perspectives for future studies.
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PMID:Prognostic utility of myocardial viability assessment. 1008 Apr 21

The value of magnetic resonance (MR) imaging and 31P spectroscopy is reported for evaluating the anatomy, function, and high-energy phosphate metabolism of the heart in patients with cardiovascular disease. Recent developments include the evaluation of myocardial contraction under pharmacologic stress and direct tracking of wall motion with myocardial tagging, assessment of first-pass myocardial perfusion with ultrafast MR in conjunction with MR contrast agents, and MR velocity mapping to determine flow velocity and volume in medium-sized vascular structures. The clinical significance of 31P spectroscopy is expanding, as shown in several studies in patients with ischemic heart disease and cardiomyopathy. The phosphocreatine to ATP ratio proved to be a sensitive marker for regional ischemia in patients with critical coronary artery stenoses. Changes in high-energy phosphate metabolism may be detected in patients with dilated cardiomyopathy, which may be useful to differentiate primary and secondary cardiomyopathies. MR imaging and 31P spectroscopy may be combined for a complete evaluation of patients with cardiovascular disease.
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PMID:Magnetic resonance imaging and spectroscopy of the heart. 1014 2

Cell death can be induced by 2 different mechanisms: necrosis and apoptosis. Necrosis, on the one hand, is usually caused by unphysiological stress factors such as hyperthermia or hypoxia, apoptosis, on the other hand, is part of the normal organ development and controls for example immune responses. Morphologically, necrosis is characterized by swelling of cells and their organelles leading to the disruption of the cell membrane, which in turn causes an inflammatory reaction in the surrounding tissue. Morphological and biochemical criteria (Figure 1, Table 1) of apoptosis are the condensation of chromatin leading to the development of apoptotic bodies or membrane-enclosed vesicles containing oligonucleosomal DNA fragments. Important diagnostic tools of cell death (Table 2), such as the TUNEL test (Figure 2) or gel electrophoresis of extracted DNA (Figure 3) are based on the above mentioned biochemical characteristics, but a reliable differentiation of apoptotic versus necrotic processes is not always possible. Experimental studies in animals and studies in various diseases of the cardiovascular system were able to show that apoptosis in myocytes can be induced, an issue that has long been discussed controversially. Ischemia, reperfusion, and myocardial infarction were also shown to lead to apoptosis in cardiomyocytes, whereas cell destruction was caused mainly by necrosis. Several authors (Table 3) demonstrated apoptotic indices in cardiomyocytes of patients with dilatated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy and patients with acute infarction from 0.25 to 35% by the use of the TUNEL test. Others were able to demonstrate an elevated expression of Fas-receptor in cells of atheroslerotic plaques in patients with atherosclerosis and high indices of apoptotic cardiomyocytes in patients with chronic heart failure. We investigated endomyocardial biopsies of patients with inflammatory cardiomyopathy, DCM without inflammatory reaction but the presence of adenoviral or cytomegaloviral genome and idiopathic DCM using the TUNEL test. The percentage of apoptotic cardiomyocytes in biopsies of patients with DCMi was 1.03 and in biopsies of patients with adenoviral genome 0.25, whereas in all other groups no apoptosis was found. If apoptosis plays a major role in myocardial diseases such as heart failure, arrhythmia and others, blocking this mechanism will have to be considered as a therapeutical strategy. Therefore, studies on the extent of apoptotic processes in diseased versus healthy cardiac tissue are of great importance.
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PMID:[Cell death in inflammatory heart muscle diseases--apoptosis or necrosis?]. 1041 44

It is known that a blood transfusion is necessary for survival in patients with thalassemia, but it may cause myocardial dysfunction due to myocardial siderosis as in other organs. The aim of this study was to evaluate myocardial perfusion by means of stress thallium scanning (MPS) and left ventricular functions by rest radionuclide ventriculography (RNV). Twenty-one patients at ages 9-16 (mean 12.1 +/- 3.2) who have been diagnosed with thalassemia for 4-15 years (mean 12.7 +/- 4.8) were included in the study. They had blood transfusions 78-318 times (mean 162.1 +/- 71). MPS and RNV was performed within two days after the any transfusion. MPS showed ischemia in 3 patients and normal perfusion in 18 patients. RNV revealed normal systolic parameters (wall motion, EF, PER, TPE) but diminished diastolic parameters (TPF, PFR) compared with normal values (p < 0.05). We conclude that ischemia or fixed defects may be seen in stress MPS as a result of cardiac involvement in patients with thalassemia. But, RNV is an important and preferable test for the early detection of subclinic cardiomyopathy. RNV may therefore show diastolic abnormalities before the systolic abnormalities show up.
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PMID:Evaluation of cardiac functions in patients with thalassemia major. 1043 78

Iodinated fatty acid compounds have an important role in early detection of myocardial abnormalities and provide insights into pathological states in the heart. Among them, 15-(p-iodophenyl)-3R,S-methyl pentadecanoic acid (BMIPP) has been most widely used providing excellent images of the left ventricular myocardium due to high myocardial uptake and long retention. The previous chapters have focused on the basic characters and clinical applications of this compound. However, the precise mechanisms of myocardial kinetics should be further investigated under various conditions. Most of the studies showed reduced BMIPP uptake relative to perfusion in a variety of myocardial disorders, whereas an increase in BMIPP uptake relative to perfusion is often reported. The potential mechanisms of such conflicting results are discussed, but basic studies should be performed to clarify such results in detail. There are a number of clinical values of this compound. Since alteration of fatty acid is observed in the repetitive ischemia, BMIPP can be used for detecting severe ischemic episodes. The concept of 'ischemic memory' imaging can be applied for patients with unstable or vasospastic angina at rest and for those with acute myocardial infarction with successful revascularization to identify the risk area. The discordant decrease in BMIPP uptake relative to perfusion is often seen in ischemic but viable myocardium, and therefore, the combined imaging of BMIPP and perfusion can be used for assessment of tissue viability. Furthermore, abnormal BMIPP uptake is most often observed in hypertrophic cardiomyopathy, and thus, this compound can be used for an early detection and differential diagnosis of the cardiomyopathy. Although BMIPP imaging seems to be quite promising in many fields, the number of patient data remain limited. In this respect, a multicenter study with a vast majority of patients is warranted to confirm these important values of BMIPP. In addition, this attractive tracer should be available all over the world to confirm its clinical value in the near future.
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PMID:Future aspects of BMIPP. 1045 6

After cardiac injury, there are changes in the cardiac myocyte morphology, function, matrix, and molecular gene expression. These all play an important role in remodeling of the injured heart, contributing to the progression toward heart failure. The role of the microvasculature in the progression toward heart failure is less well characterized. However, laboratory studies have established that there are important interactions between the microvascular endothelium and the myocyte. Furthermore, in a multitude of animal models of heart failure and cardiomyopathy, there is always an association with microvascular abnormalities. Reversal of these abnormalities is also associated with improvement in the cardiomyopathy. Major mediators that likely play an important role in the microvasculature include endothelin and nitric oxide. These are elaborated by both endothelium and myocyte compartments of the myocardium. Preliminary clinical studies already demonstrate that microvascular ischemia may have prognostic power in patients with nonischemic dilated cardiomyopathy. Results from these studies showed a reduction in mortality from treatment with amlodipine, suggesting a possible benefit based on changes in the microvasculature.
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PMID:Potential role of the microvasculature in progression of heart failure. 1048 Apr 42


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