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)

In experimental hyperthyroidism, acceleration of lipid peroxidation occurs in heart and slow-oxidative muscles, suggesting the contribution of reactive oxygen species to the muscular injury caused by thyroid hormones. This article reviews various models of oxidative muscular injury and considers the relevance of the accompanying metabolic derangements to thyrotoxic myopathy and cardiomyopathy, which are the major complications of hyperthyroidism. The muscular injury models in which reactive oxygen species are supposed to play a role are ischemia/reperfusion syndrome, exercise-induced myopathy, heart and skeletal muscle diseases related to the nutritional deficiency of selenium and vitamin E and related disorders, and genetic muscular dystrophies. These models provide evidence that mitochondrial function and the glutathione-dependent antioxidant system are important for the maintenance of the structural and functional integrity of muscular tissues. Thyroid hormones have a profound effect on mitochondrial oxidative activity, synthesis and degradation of proteins and vitamin E, the sensitivity of the tissues to catecholamine, the differentiation of muscle fibers, and the levels of antioxidant enzymes. The large volume of circumstantial evidence presented here indicates that hyperthyroid muscular tissues undergo several biochemical changes that predispose them to free radical-mediated injury.
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PMID:Oxidative muscular injury and its relevance to hyperthyroidism. 218 67

Today silent myocardial ischemia (SMI) is a well-recognized phenomenon. However, in the absence of clinical signs suggesting coronary artery disease (CAD), a streamlined diagnostic approach for precise clarification has proved to be difficult. Sensitivity and specificity of ergometric results are rather poor in symptom-free patients. Thus the question arises, whether the necessity of coronary angiography can be established more precisely by 201Tl myocardial SPECT in these patients. Treadmill exercise according to the Bruce protocol, 201Tl myocardial SPECT and coronary angiography were performed in a total of 106 patients with suspected SMI. In group I (high probability of ischemia; n = 46), reversible defects detected by SPECT correlated well with significant stenoses and irreversible defects with subtotal stenoses or complete occlusions. SPECT sensitivity in the detection of ischemia was 91%, its specificity 96%. In group II (low probability of ischemia; n = 60), SPECT sensitivity was as high as in group I (94%) but due to a high number of false-positive results (e.g. cardiomyopathy) specificity was only 75%. However, SPECT was superior to exercise ECG (sensitivity 70%; specificity 56%) in the detection of SMI. In addition, beta-endorphin levels were determined in 180 healthy subjects, 37 patients with symptomatic CAD and in 34 patients with SMI before and during maximum exercise. Exercise values in patients with SMI were significantly higher than in healthy subjects or in patients with symptomatic CAD.
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PMID:201Tl myocardial SPECT and beta-endorphin levels in patients with suspected silent ischemia. 221 10

Stimulated skeletal muscle grafts have been proposed as a means to reinforce ventricular wall in the treatment of severe myocardial failure. Latissimus dorsi cardiomyoplasty was performed in 11 patients with advanced heart failure due to cardiomyopathy who were in New York Heart Association (NYHA) class III or IV despite maximal medical therapy. There were no operative deaths. Eight patients were followed for a mean of 10.8 months. Two patients remain in muscle conditioning protocol. One patient died with latissimus dorsi ischemia and congestive heart failure. Four of the eight patients in long-term follow-up are in NYHA class I, three in class II, and one in class III. At 3 months of follow-up, rest radioisotopic left ventricular ejection fraction increased from 20.5 +/- 3.6% to 26.8 +/- 8.1% (p less than 0.01). Doppler-echocardiography demonstrated that left ventricular segmental wall shortening improved from 11.3 +/- 2.5% to 16.5 +/- 3.9% (p less than 0.01) and left ventricular stroke volume from 22.9 +/- 4.6 to 33.1 +/- 10 ml (p less than 0.01). Cardiopulmonary exercise test showed that maximal oxygen consumption during treadmill test increased from 14.8 +/- 3.7 to 18.2 +/- 3.3 ml/kg.min (p less than 0.05). At 6 months of follow-up, all the above values remained essentially unchanged. Furthermore, nonsustained ventricular tachycardia was abolished without specific medical therapy in four patients. Thus, cardiomyoplasty improves left ventricular function, reverses congestive heart failure, and may improve long-term survival in severe cardiomyopathies.
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PMID:Latissimus dorsi cardiomyoplasty in the treatment of patients with dilated cardiomyopathy. 222 13

Negative U waves on the surface electrocardiogram are reported to be a specific marker of myocardial disease. In the setting of ischemia, they correlate with stenosis of the left main and left anterior descending coronary arteries. To determine whether U wave changes are unique for anterior ischemia, the development of new U waves on the intracoronary electrogram was correlated with the location and magnitude of ischemia during coronary balloon angioplasty. Recordings were obtained during dilation of 43 vessels in 37 patients. New negative U waves developed during dilation of 12 vessels (7 of the left anterior descending, 4 of the left circumflex and 1 of the right coronary artery). New positive U waves developed during dilation of 18 vessels (12 of the left anterior descending, 3 of the left circumflex and 3 of the right coronary artery). The magnitude of ST segment change was 10.9 +/- 6.7 mm in the presence of a new U wave but only 3.4 +/- 2.8 mm in the absence of a new U wave (p less than 0.001). It is concluded that 1) negative U waves on the intracoronary electrogram are not specific for anterior ischemia; 2) new positive U waves on the intracoronary electrogram are as sensitive as new negative U waves for acute ischemia; 3) the development of a new positive or negative U wave is associated with the magnitude of myocardial ischemia; and 4) the recording of U waves may be related to the proximity of the recording leads to the location of ischemia.
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PMID:Lack of specificity of new negative U waves for anterior myocardial ischemia as evidenced by intracoronary electrogram during balloon angioplasty. 231 53

From 1982 to 1986, 1230 sudden death cases were autopsied in Osaka Medical Examiner's Office. Among them, 810 cases were sudden cardiac deaths (SCD) including coronary heart disease (77%), cardiomyopathy (7%), valvular disease (3%). All SCD cases were dead within 24 hours of the appearance of the fatal symptoms, and most of them (72%) were considered instantaneous death. Many of the fatal symptoms began in bed (31%), at bath (17%), at toilet (8%), or at work (8%). Thirty-four percent of them were thought by themselves or by their families to be healthy before the death. Hypertension (38%), coronary heart disease (13%) and diabetes mellitus (11%) were the major past history recorded. Microscopic observation of the hearts of 200 cases autopsied in 1986 showed various cardiac lesions: hypertrophy, atrophy, degenerations of myocytes, cellular and fatty infiltrations of the interstitium. According to their cardiac lesions and degrees of severity of coronary sclerosis, patients who died suddenly were divided into 8 groups as follows: 1. myocardial infarction (41) 2. myocarditis (6) 3. hypertrophic cardiomyopathy (19) 4. chronic ischemia with severe coronary sclerosis (65) 5. chronic ischemia with moderate coronary sclerosis (27) 6. small vessel disease (18) 7. amyloidosis (1) 8. unknown (23). These results suggest that coronary heart disease and hypertension play an important role in SCD.
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PMID:An epidemiologic and histopathological study of sudden cardiac death in Osaka Medical Examiner's Office. 263 29

Electrocardiographic manifestation mimicking the hyperacute phase of myocardial infarction and the electrical alternans of the elevated ST-segment in association with subarachnoid hemorrhage were reported in two patients with no evidence of heart disease. In both cases the ST-segment changes were transient and there were no persistent changes suggestive of underlying myocardial damage or ischemia. These findings suggested that the electrocardiographic changes were probably secondary to subarachnoid hemorrhage and not an expression of primary myocardial disease. The electrocardiographic abnormalities could be explained by altered autonomic activity to coronary arteries or directly to the myocardium.
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PMID:Transient ST-segment elevation in subarachnoid hemorrhage. 270 30

The long-term course of angina and the electrocardiographic signs of ischemia were assessed in 13 patients (10 women and 3 men, mean age 49 +/- 6 years) with typical angina pectoris, positive exercise tests, no evidence of coronary spasm and angiographically normal coronary arteries (syndrome X). Clinical and electrocardiographic parameters as well as results of exercise testing and 24-hour electrocardiographic monitoring were assessed at presentation and after a mean follow-up of 6.3 years (range 3 to 9). Mean number of anginal episodes and nitroglycerin consumption per week were similar at presentation and at the last follow-up. Furthermore, no significant difference was noted in heart rate-systolic blood pressure product at 0.1 mV of ST-segment depression (20,363 +/- 5,747 vs 21,649 +/- 5,687 beats/min x mm Hg), at angina (19,223 +/- 5,680 vs 20,126 +/- 6,023 beats/min x mm Hg) and at peak exercise (22,057 +/- 5,669 vs 22,868 +/- 6,122 beats/min x mm Hg). Time to 0.1 mV of ST-segment depression, to angina and to peak exercise was also similar (595 +/- 163 vs 631 +/- 184 s, 524 +/- 156 vs 571 +/- 168 s and 671 +/- 168 vs 718 +/- 186 s, respectively). The number of episodes of ST-segment depression greater than or equal to 0.1 mV during electrocardiographic monitoring was similar at presentation and follow-up (31 vs 25) as was the proportion of painful episodes (39 vs 36%). None of the patients developed major coronary events or cardiomyopathy during follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term variability of angina pectoris and electrocardiographic signs of ischemia in syndrome X. 274 23

Evidence suggests that endogenous opioids, particularly the beta-endorphins and met-enkephalins, are closely involved in stress-induced analgesia and nociceptive pain control. Numerous investigations have been conducted to evaluate the role of opioids in silent vs symptomatic myocardial disease. There is good evidence to suggest that patients with asymptomatic ischemia have defective pain perception compared with those with angina; however, the precise role of the endorphin and enkephalin systems in this phenomenon remains to be elucidated. Possible sources for disparate study results include variation in patient populations, insensitive or improperly timed assay techniques, and differences in amount of ischemia.
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PMID:Endorphins and pain perception in silent myocardial ischemia. 296 55

One a tribute of a Tc 99m labeled myocardial agent is the possibility to measure both ventricular function and myocardial perfusion with a single injection. To assess this, normal volunteers, 14 patients with coronary artery disease (CAD) and two suffering from cardiomyopathy with normal coronaries, were injected with 8-10 mci carbomethoxy-isopropyl-isonitrile or 20 mci Rp-30 Tc 99m at peak semi-recumbent bicycle exercise and again at rest. Thirty msec per frame first pass data, and 5 min static anterior, 40(0-) and 70(0-) left anterior oblique images were obtained. Standard Thallium 201 stress test were also done, within one month, and were at the same level of exercise. The left ventricular ejection fraction (EF) increased with exercise (69%-76%) in normal patients. All studies showed normal myocardial perfusion on exercise. In CAD patients the EF increased in some patients who had ischemia. Perfusion images with Tc 99m during exercise and at rest had an identical correlation with Thallium 201. The results support the concept of dual ventricular function and perfusion studies using a single Tc 99m labelled myocardial agent, and suggest that this could become the standard radionuclide stress tests in the future.
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PMID:[Simultaneous test of ventricular function and myocardial perfusion, during exercise, using a new agent labeled with Tc99m]. 296 61

Standard methods of echocardiographic analysis permit accurate categorization of cardiomyopathies into dilated, hypertrophic, and restrictive types. However, ascertainment of the cause of a particular cardiomyopathy (e.g., ischemia versus inflammation as the cause of a dilated myopathy) with ultrasound would be greatly facilitated by analysis of myocardial composition with ultrasound tissue characterization techniques. Qualitative observations have identified unusual echocardiographic image texture in hypertrophic cardiomyopathy and in amyloidosis. Quantitative observations have verified these findings and have identified increased ultrasound backscatter in regions of myocardial fibrosis, calcification, and anthracycline-induced cardiomyopathy. Although several technical problems remain unsolved and further research is needed in the mechanisms of normal and abnormal ultrasound/tissue interactions, tissue characterization with ultrasound has the potential to contribute independent information on myocardial composition in patients with cardiomyopathy.
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PMID:Clinical potential of ultrasound tissue characterization in cardiomyopathies. 307 43


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