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)

Repetitive ischaemic episodes may have a cumulative effect leading to irreversible myocardial cell damage with enzyme release. Using plasma creatine kinase (CK) and creatine kinase B-subunit (CK-B) concentrations this theory has been tested in forty-eight patients admitted with acute chest pain, but without ECG signs of acute myocardial infarction (AMI). The patients were classified into four groups: Fourteen patients with non-ischaemic heart disease (non-IHD), seventeen with stable angina pectoris (SAP), ten with unstable angina pectoris (UAP), and seven patients who developed AMI during the study period. The enzyme variation in non-IHD delineates the background noise, and the increased variability in AMI indicates the full scale of the enzyme signals in cases of irreversible cell damage. Patients with SAP have the same enzyme signal as the background noise in respect of both CK and CK-B. However, in UAP the signal of CK-B equals the background noise, whereas the CK signal is separated from the latter. The reason may be that the signal to noise ratio of CK-B is poor and the analytical sensitivity low. Therefore, the behaviour of CK-B in this study does not support the above theory although our findings for CK indicate that the consequence of repeated ischaemic attacks is slight enzyme release.
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PMID:Creatine kinase and creatine kinase B-subunit in stable and unstable angina pectoris. 308 65

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