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 patients with chest pain somatic pain (thoracic wall pain) has to be differentiated from visceral pain (organ pain). History and careful physical examination are diagnostic in most cases. Presented are rare and not well-known diseases like valvular aortic stenosis, idiopathic hypertrophic subaortic stenosis and the mitral valve prolapse syndrome. Not seldom they are masked by angina pectoris-like symptoms, although in general the coronary arteries are normal. In acute chest pain differential diagnostic considerations have to include lung embolism, acute pericarditis, spontaneous pneumothorax, acute dissecting aneurysm of the aorta and diseases of the gastrointestinal tract as well. Only after exclusion of any organic cause the diagnosis of "effort syndrome" may be made.
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PMID:[Chest pain: differential diagnosis in general practice]. 49 63

A woman with Prinzmetal's variant angina had spontaneous attacks of myocardial ischemia characterized by severe chest pain, hypotension, inferior ST-segment elevation, transient complete heart block and selective right ventricular dysfunction. Despite initial improvement following intravenous administration of atropine and sublingual administration of nitroglycerin she died of cardiogenic shock. Autopsy showed normal coronary arteries and acute pericarditis, more pronounced over the right side of the heart. It is postulated that the pericardial inflammation elicited severe spasm of the subjacent right coronary artery.
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PMID:Prinzmetal's angina, normal coronary arteries and pericarditis. 67 98

A young Coloured man with a history of acute transmural anteroseptal and anterolateral myocardial infarction presented with angina pectoris. Skeletal muscle biopsy showed unequivocal evidence of polyarteritis nodosa. Complete cardiac catheterization, left ventricular cine angiography, and selective coronary arteriography demonstrated a large aneurysm involving the apex and the left ventricular free wall. Diffuse aneurysmal dilatation of the right coronary artery was noted, as well as very severe obstructive lesions of the proximal left anterior descending and left circumflex coronary arteries. Five days after cardiac catheterization the patient suffered an acute transmural inferior myocardial infarction, complicated by acute pericarditis and complete heart block, which necessitated insertion of a pacemaker. This was soon followed by acute perforation of a peptic ulcer (documented at laparotomy), after which the patient died. As far as the author can ascertain, this is the first adult with polyarteritis nodosa (PAN) who underwent cardiac catheterization and selective coronary arteriography. The literature on cardiac involvement in the adult with PAN is reviewed.
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PMID:Polyarteritis nodosa in the adult. Report of a case with repeated myocardial infarction and a review of cardiac involvement. 611 90

The diagnostic and prognostic significance of plasma inactive creatine kinase B protein (CK-Bi) levels measured by radioimmunoassay was determined in various ischemic myocardial syndromes. In 120 stable angina patients free of pain at time of blood sampling, mean CK-Bi level was 114 +/- 42 (SD) micrograms-equiv/ml; 195 micrograms-equiv/ml (95% confidence interval) represented upper limit of normal. In seven coronary artery disease (CAD) patients atrial pacing induced ischemia was not associated with increased coronary sinus CK-Bi. Of 201 consecutive patients with suspected acute infarction (AMI), 45 developed ECG criteria of transmural AMI with concomitant increased plasma CK-Bi levels (498 +/- 133, range 372-718 micrograms-equiv/ml). Elevated CK-Bi levels in evolving transmural AMI were detected before raised CK enzyme activity. Elevated plasma CK-Bi levels also occurred in acute pericarditis and in unstable angina. In the 84 patients not developing ECG changes or elevated plasma CK activity, their plasma CK-Bi levels were also normal and no coronary events occurred in the next 6 months. The remaining 55 patients had nontransmural AMI, with 15 also having elevated plasma CK and CK-Bi levels, of whom six developed re-AMI in the next 3 months. In the other 40 nontransmural AMI patients, plasma CK-Bi levels (350 +/- 65 micrograms/equiv/ml, range 228 to 445) increased significantly without associated CK activity rise, and 24 developed re-AMI (three fatal) in the next 6 months. These data suggest that: (1) plasma CK-Bi protein radioimmunoassay measurement provides a sensitive means for detecting myocardial necrosis or inflammation and (2) elevated plasma CK-Bi levels in coronary disease patients during myocardial ischemic pain may afford identification of a CAD clinical subset at high risk of subsequent AMI.
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PMID:Detection of coronary disease patients at high risk for recurrent myocardial infarction by elevated plasma inactive creatine kinase B protein levels. 722 96

Blood samples obtained from 97 consecutive patients admitted to the hospital for chest pain were analyzed for taurine concentrations. The mean value of the maximum taurine concentration in whole blood from AMI patients were greater than the mean value of the maximum taurine concentration in patients without AMI. There was no difference in plasma taurine levels between AMI and non-AMI patients, indicating that a cellular component(s) of whole blood was sequestering taurine. The increased blood taurine concentrations in the AMI patients evolved over the course of 70 hr and paralleled the increase in total CK levels. Blood taurine concentrations, in general, did not rise in patients who had chest pain of unknown etiology, skeletal muscle trauma, pleuritic pain, SVT/VT plus CV, acute pericarditis, acute cholecystitis, or angina pectoris. It is concluded that blood but not plasma taurine concentrations rise after acute myocardial injury and tend to be higher the more extensive the infarction. The mechanism of the blood taurine rise is unknown, but a myocardial source is probable. Also, there is evidence that the myocardium selectively leaks taurine, and not other amino acids. Monitoring blood taurine concentration in AMI may provide useful diagnostic and prognostic information.
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PMID:Elevated blood taurine levels in acute and evolving myocardial infarction. 731 Feb 26

Hypertrophic cardiomyopathy is a primary disease of myocardium resulting in myocardial hypertrophy without any inciting pressure or volume overload. The typical triad of symptoms includes exertional angina, syncope, and shortness of breath. Sudden cardiac death, the most dreadful complication of this disorder, can be the first manifestation of the disease and is more common in young patients. Elderly patients, on the other hand, may have a relatively benign course with normal or near-normal life span. The electrocardiogram (ECG) and echocardiography are the two most useful measures to diagnose hypertrophic cardiomyopathy. The electrocardiographic features of hypertrophic cardiomyopathy are numerous, including ST segment elevation that may simulate other ST segment elevation syndromes, including acute myocardial infarction, variant angina pectoria, acute pericarditis, bundle branch blocks, ventricular paced rhythm, dyskinetic ventricular segment, ventricular aneurysm, left ventricular hypertrophy, Wolff-Parkinson-White syndrome, and early repolarization syndrome. This report describes a case of an asymptomatic patient who presented with ST segment elevation of acute injury type and, therefore, was admitted to rule out silent myocardial infarction. Myocardial infarction was ruled out by cardiac enzyme levels, but ST segment elevation remained persistent in all of the subsequent ECGs. Echocardiography was performed, which clearly showed hypertrophic cardiomyopathy with left ventricular outflow tract obstruction and a high intracavity pressure gradient. Subsequently, retrieval of old ECGs showed a similar type of ST segment elevation in the patient's previous ECGs.
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PMID:Persistent ST segment elevation: a new ECG finding in hypertrophic cardiomyopathy. 1033 93

A9 years boy diagnosed with nasopharyngeal carcinoma was started on chemotherapy protocol including 5-fluorouracil. After 90 hours of 5-fluorouracil infusion, he developed severe retrosternal chest pain. Electrocardiography showed signs of acute pericarditis and was managed with ibuprofen and 5-fluorouracil was discontinued. The 5-fluorouracil rarely causes cardiac complications such as angina pectoris and pericarditis in adult patients. We report acute myopericarditis in a child caused by 5-fluorouracil, which is a very rare complication of 5-fluorouracil in pediatric age group.
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PMID:Chemotherapy Induced Acute Pericarditis in a Child. 2652 11