Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In four patients with Prinzmetal's variant form of angina, the attack was induced by the combined administration of epinephrine (0.4 to 0.5 mg, given subcutaneously at 7:30 to 8:00 A.M.) and propranolol (40 mg. given orally at 5:00 A.M.). Selective coronary cinearteriography was done before, during, and after the attack with constant monitoring of the ECG and blood pressure. Severe spasm of the right coronary artery occurred at the proximal portion in association with ST-segment elevation in Lead III during the attack and disappeared with the subsidence of the attack in all of them. These results strongly suggest that severe spasm of a large coronary artery mediated by alpha-adrenergic receptors is responsible for the attack of Prinzmetal's variant form of angina.
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PMID:Prinzmetal's variant form of angina as a manifestation of alpha-adrenergic receptor-mediated coronary artery spasm: documentation by coronary arteriography. 81 7

Only bipolar lead recording are available during ambulatory monitoring. Their sensitivity in detecting ST segment changes in relation to standard electrocardiographic leads is not known. The magnitude and direction of ST segment changes in the bipolar lead CM5 were compared with those in standard electrocardiographic leads in patients during exercise testing and percutaneous transluminal coronary angioplasty. Thirty patients with coronary artery disease were studied during exercise tests in which ST segment depression (greater than 0.5 mm) occurred in one or more standard electrocardiographic leads and 13 patients were studied during angioplasty that resulted in ST segment change in one or more leads (I, II, III, V2, V5, and CM5). Lead CM5 was the most sensitive lead (93%) during exercise testing and also showed the greatest magnitude of ST segment change below the isoelectric line in 93% of the patients. Only two patients, one with ST segment elevation in inferior leads and one with changes restricted to septal leads, had no ST segment depression in lead CM5. When ST segment shift from the baseline electrocardiogram was measured the magnitude of depression was greatest in lead CM5 in only 63% of the patients. During angioplasty of the left anterior descending coronary artery, lead CM5 showed ST segment depression in seven patients, ST segment elevation in two, and a biphasic response in one. Two of the three patients with balloon inflation in right coronary artery developed ST segment elevation in lead CM5. Thus lead CM5 is a reliable lead for detecting subendocardial ischaemia experienced during everyday activities in anginal patients. During total occlusion of coronary arteries (as in variant angina or myocardial infarction) lead CM5 commonly shows ST segment depression and changes due to right coronary artery occlusion may not be detected.
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PMID:Value of the bipolar lead CM5 in electrocardiography. 376 17

A comparison of the haemodynamic and electrocardiographic data was carried out in 180 coronary patients. All underwent catheterisation and coronary angiography for angina. They were divided into three main groups: 53 patients with coronary atheroma without significant stenosis; 43 patients with at least one coronary stenosis greater than 50%; 84 patients had myocardial infarction with ECG changes of transmural necrosis and coronary thrombosis (or greater than 80% stenosis). Parameters of left ventricular function (LVF), especially ejection fraction (EF), systolic work (LVESW), end diastolic pressure (LVEDP), end diastolic volume (LVEDV), myocardial mass calculated from angiography (LMV) and volumic compliance were analysed in all cases. Each patient had at least 5 ECG recordings analysed by a HP 6 calculator which determined the values of the principal numeric ECG parameters and the means of the 5 recordings. Particular attention was given to the sum of the R waves in the 12 leads (sigma R mV) and Macruz's index (duration of P/PR - P in Lead II). A satisfactory correlation was found overall between sigma R and EF (r = 0,45, p less than 0,001). sigma R was the only ECG variable related to LVF in patients without infarction. In this group of 96 patients, sigma R correlated with LVEDV (r = 0,46, p less than 0,001) with LVM (r = 0,46, p less than 0,001), with LVESW (r = 0,52, p less than 0,001). There was a discordance between angiographically measured LVM and the mass of electrically active myocardium in patients with infarction. sigma R was independent of LVM, LVEDV, and LVESW.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Functional content of the electrocardiogram of coronary patients]. 641 91

Anomalous origin of the left coronary artery from the pulmonary artery is a very rare congenital malformation. Re-coronary artery bypass grafting was performed in a 18-year-old man who had received coronary artery reconstruction with a homologous saphenous vein (from his mother) at 7-months old. After the first operation, clinical course was uneventful, but the patient became symptomatic because of effort angina at age 15. The electrocardiogram showed abnormal ST segments in Lead V2-5 and abnormal T waves in Lead V5-6. Coronary arteriography revealed that saphenous vein graft was occluded. The left internal thoracic artery (LITA) was anastomosed to the left anterior descending artery and a two coronary system was established. Postoperative angiography revealed that LITA was patent, and relief of angina was obtained.
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PMID:[Re-coronary artery bypass grafting for anomalous origin of left coronary artery from pulmonary artery (Bland-White-Garland syndrome) after operation in infancy: a case of 18-year follow-up]. 793 46

We reviewed the literature related to the effects of high-dose zinc in arteriosclerosis-induced angina pectoris. Lipid peroxidation and LDL oxidation are believed to be critical for arteriosclerosis, and consequently angina pectoris. Administration of biologically available zinc was a beneficial treatment in a significant percentage of patients with severely symptomatic, inoperable atherosclerotic disease. In these patients, there was no difference in zinc concentration between patients with and without atherosclerosis in whole blood, erythocytes or hair, but there was a major difference between normal aorta and diseased aortas (40.6 ppm zinc in normal aorta vs. 23.2 ppm zinc in atherosclerotic aorta, 40.6 ppm zinc in normal aorta vs. 19.4 ppm zinc in atherosclerotic aneurysm aorta, and no difference between normal and aneurysm aorta), although copper was low in aneurysm aorta. Medication with high-dose zinc sulfate to raise zinc serum concentrations from 95 to 177 microg/dl resulted in objective improvement in 12 of 16 of these patients, including a patient that also had Raynaud's disease. Long term environmental exposure to zinc resulted in a 40% reduction in the incidence of angina of effort compared to people not exposed to environmental zinc (P<0.01) and a 40% reduction in the incidence of probable ischemia in exercise (P<0.001). Lead had no effect while cadmium exposure resulted in more than tripling the incidence of angina of effort (P<0.001). The antioxidative action of zinc prevents oxidation of LDL cholesterol and consequently stops the main mechanism of atherogenesis. Zinc blocks calcium and its several actions on atherogenesis. Increased amounts of cytotoxic cytokines such as TNF-alpha, IL-beta and IL-8, often produced in the elderly, are blocked by high-dose zinc. We hypothesize that higher serum concentrations of LDL cholesterol resulting from administration of 300 mg of zinc per day is caused by a release of low density cholesterol from cardiovascular tissues, beneficially flushing it into the serum where it is readily observed, thus decreasing arteriosclerosis, increasing circulation, terminating angina pectoris and restoring more youthful cardiac function. Although prevention of cholesterol-induced arteriosclerosis by zinc is predicted from findings related to oxidative stress and lipid peroxidation, removal of LDL might be attributable to action of ionic zinc on ICAM inhibition. In stark contrast to current practice, high-dose zinc should be considered as basic in the strategy of prophylaxis and therapy of the atherosclerosis process to terminate angina pectoris and restore youthful cardiac function.
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PMID:High-dose zinc to terminate angina pectoris: a review and hypothesis for action by ICAM inhibition. 1608 66

Changing axis deviation has been reported also during atrial fibrillation or atrial flutter. Changing axis deviation has been also reported during acute myocardial infarction associated with atrial fibrillation too or at the end of atrial fibrillation during acute myocardial infarction. Patients with unstable angina have a higher incidence of left main coronary artery (LMCA) and proximal left anterior descending (LAD) coronary artery disease compared to patients with stable angina pectoris. In 1982, Wellens and colleagues described two electrocardiographic patterns that were predictive of critical narrowing of the proximal LAD artery, and were subsequently termed Wellens' syndrome. The criteria were: a) prior history of chest pain, b) little or no cardiac enzyme elevation, c) no pathologic precordial ST segment elevation, d) no loss of precordial R waves, and e) biphasic T waves in leads V2 and V3, or asymmetric, often deeply inverted T waves in leads V2 and V3. The ECG changes are best recognized outside the episode of anginal pain. Lead aVR and lead v1 ST segment elevation, during chest pain, has been reported in patients with LMCA disease with ST segment depression in leads V3, V4 and V5 (with maximal depression in V4).We present a case of changing axis deviation in a 37-year-old Italian man with a LAD coronary artery subocclusion associated with a LMCA subocclusion. This case focuses attention on the importance of the recognition of the patterns suspected for LAD coronary artery disease or for LMCA disease.
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PMID:Wellens' syndrome and other electrocardiographic changes in a patient with a left anterior descending artery subocclusion associated with a left main coronary artery subocclusion. 1933 63

Exercise-induced ST-segment elevation in lead aVR accompanied by ST-segment elevation in lead V1 might be a specific finding of left main coronary artery (LMCA) stenosis. Lead aVR and lead v1 ST segment elevation has been reported, during an attack of chest pain, in patients with LMCA disease with ST segment depression in leads V3, V4 and V5 (with maximal depression in V4). ST-segment elevation in lead aVR in patients with angina at rest can be related to transmural ischemia of the basal part of the interventricular septum, frequently due to LMCA or multivessel coronary disease too. 3-vessel coronary artery disease (CAD) and LMCA disease show a frequent combination of leads with abnormal ST segments during chest pain with ST-segment depression in leads I II V4-V6, and ST-segment elevation in lead aVR. When ST-segment status in lead aVR combines with troponin T, ST-segment elevation in lead aVR and positive troponin T on admission are useful predictors of LMCA or 3-vessel CAD. We present a case of acute myocardial infarction with significant left main coronary artery stenosis, significant 3-vessel coronary artery disease and elevated troponin I at admission in an 83-year-old Italian woman. Also this case focuses attention on the importance of the recognition of the patterns suspected for LMCA and/or 3-vessel coronary disease.
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PMID:Acute myocardial infarction with significant left main coronary artery stenosis, significant 3-vessel coronary artery disease and elevated troponin-I at admission. 1935 9