Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationship between the rate-pressure product, myocardial oxygen consumption and the production or uptake of lactate by the myocardium was studied in 45 patients under basal conditions and rapid atrial pacing (except in 3 cases with atrial fibrillation). The underlying pathology was ischemic heart disease in 25 cases, non obstructive cardiomyopathy in 9 cases, and obstructive cardiomyopathy in 11 cases. Contrary to what has been reported in normal subjects, a significant linear relationship between the rate-pressure product or indexed rate-pressure (multiplied by body surface area) and myocardial oxygen uptake. The divergence of these results may be due to the method of measuring coronary sinus blood flow, these authors having used the N 20 whereas in this study the flow was measured by thermodilution. In particular, it is possible that this divergence results from abnormalities of ventricular volume, compliance and contractility in the patients under study: these abnormalities may disturb the relationship between the rate-pressure product and myocardial oxygen consumption in normal subjects. A double linear relationship, different in each of these groups, was observed at rest between the indexed rate-pressure product and oxygen uptake, and the uptake or production of lactate: in myocardial ischemia without ischemia at rest, in non obstructive cardiomyopathy in sinus rhythm. The significance of these relations differed in each of these groups. Under atrial pacing, the increase in indexed rate-pressure product compared to basal conditions was proportional to the presence of absence of ischemia. Variations of the indexed rate-pressure product seem to be related to myocardial oxygen consumption and not to myocardial oxygen requirements. The variations of the rate-pressure product, during the administration of drugs, for example, do not reflect myocardial oxygen needs. During exercise ECG, the maximal increase in the indexed rate-pressure product reflect the functional reserve of the myocardium.
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PMID:[Rate-pressure product and myocardial oxygen requirements]. 680 46

The natural history of acute cardiogenic pulmonary edema was studied in a group of patients who did not have acute myocardial infarction, cardiomyopathy, or valvular heart disease. Most of these patients had coronary artery disease. Cardiac catheterization in selected patients showed depressed contractility in some with segmental abnormalities. In the group older than 70 years, this carried a 70 percent two-year mortality rate. It is important to approach patients with this syndrome vigorously, both diagnostically and therapeutically. Acute, reversible segmental ischemia may be responsible for this syndrome and may respond to measures designed to prevent recurrent ischemia.
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PMID:Acute pulmonary edema due to ischemic heart disease without accompanying myocardial infarction. Natural history and clinical profile. 688 Nov 86

To characterize externally detectable changes in the myocardial metabolism of free fatty acids (FFA) and glucose, which are associated with ischemia and cardiomyopathy, omega-123I-heptadecanoic acid (stearic acid analogue), 75Br-phenylpentadecanoic acid, and 3-0-11C-methyl-D-glucose were used as indicators. It could be demonstrated that in the metabolism of free fatty acids at least two different patho-physiological situations may exist. Disturbances in the mechanism of the accumulation of free fatty acids lead to a decrease of the amount of the free fatty acids which are available for energy production (these disturbances can be recognized as indicator accumulation defects). Disturbances associated with the mechanism of free fatty acid catabolism lead to a decrease of the ability of the myocardial cell to utilize the free fatty acids (these disturbances can be recognized as changes in indicator elimination rates). Whereas in ischaemic heart disease, the areas with altered FFA accumulation correlate with the areas of altered FFA-elimination, no correlation was found in the case of cardiomyopathy. The 11C-methylglucose seems to be an excellent indicator for the in-vivo assessment of the function of transport system in the myocardial cell membrane.
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PMID:[Studies of cardiac metabolism with 123I-labelled fatty acids and 11C-methylglucose (author's transl)]. 697 45

To clarify the pathogenesis of chest pain in patients with cardiomyopathies, we compared coronary blood flow and other indicators of ischemia at rest and during pacing-induced tachycardia in nine patients with cardiomyopathy (four hypertrophic and five congestive) and in five control subjects. Coronary blood flow was reduced at rest and during pacing in cardiomyopathy patients compared with controls. In patients with hypertrophic cardiomyopathy, pacing induced chest pain in all, increased ST-segment depression in three patients and increased coronary venous lactate concentration. With pacing, two of five patients with congestive cardiomyopathy had chest discomfort and three had increased ST-segment depression, but coronary venous lactate concentration did not change significantly. In both groups of cardiomyopathies, the ratio of the systolic and diastolic pressure-time indexes tended to decrease more than in controls during pacing. Thus, myocardial perfusion is decreased in patients with cardiomyopathy, both at rest and during pacing. The changes detected during pacing point to subendocardial ischemia as the likely mechanism for angina in hypertrophic and possibly also in congestive cardiomyopathy.
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PMID:Pathophysiology of chest pain in patients with cardiomyopathies and normal coronary arteries. 719 3

The value of phase analysis of multiple gated acquisition blood pool images for identifying wall motion abnormalities due to stress-induced ischemia was examined. Myocardial segments with an abnormal phase, i.e., delayed onset of wall motion, were localized on a phase distribution image of the LV and the synchrony of LV systolic wall motion was assessed from histograms of the LV phase distribution, i.e., the standard deviation (SD) from the mean of this peak, which was defined as SDP, its upper limits of normal at rest and exercise were established in seven normals as the mean +2 SD and were 12 degrees at rest and 10 degrees at maximum exercise. Of the 56 patients, 37 had coronary artery disease (CAD), 11 had valvular disease but normal coronary arteries, and eight had normal coronary arteries, no valvular disease, but had either cardiomyopathy or typical angina. In the CAD patients, SDP was abnormal in 95% during exercise while only 86% had an abnormal ejection fraction (EF) response and/Or exercise-induced wall motion abnormalities by visual interpretation. By contrast, in the 11 valvular heart disease patients, SDP was abnormal in only two despite exercise-induced wall motion abnormalities in five and an abnormal EF response in all 11. Thus, although an abnormal EF response to exercise is a sensitive indicator of cardiac disease, it is, however, like exercise-induced wall motion abnormalities, not specific for CAD. By contrast, phase analysis not only permitted separation of wall motion abnormalities induced by ischemia from those associated with valvular disease, but was also an objective, highly sensitive, and specific indicator of regional myocardial ischemia.
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PMID:Phase analysis of radionuclide ventriculograms for the detection of coronary artery disease. 720 Dec 32

Chemotherapy drugs have been reported to cause cardiac side effects including cardiomyopathy, ischemia, arrhythmias, and myocardial necrosis. Most important in terms of daily practice is anthracycline-induced cardiomyopathy. The bisdioxopiperazine compound, dexrazoxane (ICRF-187, ADR-529), has been shown to prevent this cumulative side effect of the anthracyclines. Recent randomized trials performed in breast cancer and in pediatric sarcoma patients have demonstrated the efficacy of this approach, which permits the administration of anthracyclines to greater cumulative doses and thus leads to a substantial reduction in the incidence of decreased left-ventricular ejection fraction or congestive heart failure. Response rates were not significantly different with the use of dexrazoxane in these trials. The risk ratio for a cardiac event was decreased by two to threefold in randomized breast studies involving more than 700 women. Paclitaxel also has been reported to cause arrhythmias and possibly ischemia. In a large data base, National Cancer Institute investigators found a 0.29% incidence of grade 4 or 5 cardiac toxicities, including heart block, ventricular tachycardia, and ischemic events. Other important chemotherapy-related cardiac toxicities discussed include fluorouracil-induced angina and arrhythmias, interleukin-4 induced-cardiomyopathy, and cardiotoxicity associated with autologous bone marrow transplantation procedures.
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PMID:Cardiotoxicity and cardioprotection during chemotherapy. 757 76

Cardiac complications of cocaine abuse and a rational approach to evaluating and managing them are described. Cardiac abnormalities reported among asymptomatic cocaine abusers include echocardiographic left ventricular hypertrophy and segmental wall motion abnormalities. Electrocardiogram may reveal increased QRS voltage, ST-T changes, and pathologic Q waves. Episodes of ST elevation may be seen during Holter monitoring. The management of cocaine-abusing patients who present to an emergency room with acute chest pain is controversial because the two reported studies yielded conflicting results regarding the incidence of myocardial infarction (MI). Even in the absence of infarction, electrocardiographic abnormalities are common among these patients, which complicates the decision-making regarding hospitalization. Pathophysiology of cocaine-related MI is discussed. Distinct clinical features of cocaine-related MI make it clear that the association between the two is not just temporal. However, considering the number of persons abusing cocaine, it is a rarity. Beta-adrenergic blockers should be avoided in the treatment of cocaine-induced myocardial ischemia which is best treated with nitrates and calcium-channel blockers. Reports of cocaine-induced myocarditis and cardiomyopathy are reviewed. Experimental studies and clinical case reports suggest that cocaine may cause lethal arrhythmias. Cocaine prolongs repolarization by a depressant effect on potassium current and may generate early afterdepolarizations. It is possible that cocaine-associated arrhythmias are secondary to vasospasm-related ischemia and reperfusion as well.
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PMID:Cardiac complications of cocaine abuse. 772 Feb 92

The differential diagnosis of VTs with LBBB morphology includes several well-defined syndromes. Although the majority of cases are attributable to acquired structural heart disease, including ischemia, prior infarction, or dilated cardiomyopathy, consideration of specific right ventricular processes is essential to proper evaluation and treatment. The approach to older patients or those with evidence for heart disease should begin with an evaluation for coronary artery disease and an assessment of biventricular function. Careful evaluation for bundle branch reentry should be performed during electrophysiological study, especially when there is underlying conduction system disease. Younger patients, those without overt heart disease, or those with isolated right ventricular disease, should receive a complete noninvasive evaluation of right and left ventricular size and function. An abnormal SAECG or identification of intracardiac late potentials suggest right ventricular dysplasia or cardiomyopathy, whereas responsiveness to adenosine and absence of detectable heart disease support the diagnosis of idiopathic right VT. Newer techniques, including MRI, show promise in identifying subtle right ventricular disease not otherwise detectable even in the setting of presumed idiopathic right VT. Following surgical repair of selected congenital heart defects, particularly tetralogy of Fallot, symptoms of recurrent palpitations, near syncope, syncope, or aborted sudden death may be attributable to recurrent VT, and diagnostic electrophysiological study should be considered for these patients. Finally, SVTs with LBBB morphology, particularly cases associated with right-sided or septal accessory pathways, should always be considered in this differential diagnosis.
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PMID:Ventricular tachycardias with left bundle branch block morphology. 773 82

The use of 123I-labeled fatty acids is witnessing a resurgence of interest, primarily because of data from recent clinical protocols comparing regional myocardial uptake of 123I-labeled 15-(p-iodophenyl)-3-(R,S)-methylpentandecanoic acid (BMIPP) with flow tracers. Comparison of mismatches in BMIPP and flow tracer distribution (BMIPP < flow tracer) has demonstrated the usefulness of evaluating myocardial viability with BMIPP. BMIPP was introduced in 1993 as "Cardiodine" as an approved radiopharmaceutical in Japan by Nihon Medi-Physics, Inc. This article reviews the clinical use of BMIPP in the assessment of cardiomyopathy, myocardial infarction, ischemic heart disease and for the evaluation of myocardial viability in comparison with PET tracers. The results of two specific protocols demonstrating the utility of using BMIPP to detect viable myocardium are described in detail. The first study compares BMIPP and sestamibi uptake to wall motion and inotropic reserve after acute myocardial infarction in conjunction with two-dimensional echocardiography and low-dose dobutamine stimulation. The second example describes results of a triple SPECT technique using BMIPP reinjection for the assessment of ischemia.
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PMID:Cardiac SPECT with iodine-123-labeled fatty acids: evaluation of myocardial viability with BMIPP. 776 21

Percutaneous transluminal coronary angioplasty (PTCA) is currently performed in many patients seeking care because of severe manifestations of multivessel coronary artery disease. Previously, the majority of such patients would have undergone coronary artery bypass grafting (CABG). No definitive evidence is available as to which initial revascularization strategy has the best long-term clinical and economic outcomes. The Bypass Angioplasty Revascularization Investigation (BARI) is the largest of several recent clinical trials that were designed to test the hypothesis that an initial strategy of PTCA in selected patients with multivessel coronary artery disease does not compromise long-term clinical outcome compared with an initial strategy of CABG. This report describes how patients were screened, selected, and recruited in BARI and how this process may influence the results and the interpretation of the trial. During the enrollment period, 25,200 patients undergoing diagnostic coronary angiography at the participating institutions or with off-site angiograms referred to BARI investigators were screened for BARI eligibility. Excluded from screening were patients without coronary artery disease, those with single-vessel disease, prior revascularization, primary congenital, valvular, or myocardial disease, and age > 80 years. Slightly more than half of the patients screened (12,670) were not clinically eligible for BARI because of left main disease, insufficient symptoms, emergency revascularization, or other logistic reasons. Thus, 12,530 patients had severe angina and/or ischemia and were clinically eligible for BARI. Nearly 33% of them (4,110) had multivessel disease, which was suitable for both PTCA and CABG.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bypass Angioplasty Revascularization Investigation: patient screening, selection, and recruitment. 789 20


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