Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Creatine kinase (CK) release curves were analysed in 40 patients with acute myocardial infarction. Three groups could be identified. Group A (duration of CK release less than 30 hours) comprised 15 patients whose CK release was completed within 22.8 hours. In these patients chest pain was noted on the first hospital day and necropsy in three showed a homogeneous myocardial infarction. Group B (duration of CK release greater then 30 hours) comprised 16 patients who had a significantly longer CK release time of 42.2 hours (P less than or equal to 0.05). Their chest pain persisted for two to three days and pathological examination in five patients showed a heterogeneous composition of the infarcted myocardium. Group C comprised nine patients who had a second rise of serum CK. This was always associated with chest pain. It reflected an extension of the infarct which accounted on average for 24 per cent of the size of the final infarct. We concluded that a CK release of short duration indicated infarction without extension, CK release of longer duration indicated a gradual extension of infarction, and a repeated CK release resulted from a sudden extension of an infarct. According to these criteria an extension of the infarct occurred in 62 per cent of our patients.
 ...
PMID:Creatine kinase release in acute myocardial infarction: correlation with clinical, electrocardiographic, and pathological findings. 119 32

To observe the clinical course after reperfusion and recovery from myocardial stunning of the left ventricular anterior wall, we prospectively reviewed and analyzed cardiac enzymes, ECG changes, echocardiograms, and cineangiograms in 8 patients with the acute ischemic syndrome who fulfilled the following criteria: 1) no history of previous myocardial infarction, 2) repeated and/or prolonged episodes of chest pain, 3) critical stenosis of the left anterior descending artery with wall motion abnormalities, 4) successful emergency percutaneous transluminal coronary angioplasty, and 5) normal wall motion on repeat cineangiography 4 to 8 weeks later. Creatine kinase (CK) and/or its cardiac isoenzyme (CK-MB) were minimally elevated in all cases. Wall motion was normalized with the reduction of end-systolic volume (end-diastolic volume: from 139 +/- 25 to 140 +/- 37 ml, ns, end-systolic volume: from 68 +/- 16 to 39 +/- 13 ml, p < 0.001, ejection fraction: from 51 +/- 6 to 71 +/- 6%, p < 0.001). Serial echocardiograms showed normalization of wall motion within 4 to 28 days. T wave inversion in the left precordial leads developed 30 min to 5 hours after the cessation of chest pain or successful reperfusion, and prominent negative T waves (1.6 +/- 0.6 mV) with QT prolongation (0.56 +/- 0.08 sec) in V3 or V4 reached their peak values within one to 5 days. ECG abnormalities resolved after 21 to 95 days. These ECG findings may indicate reperfusion injury and the presence of myocardial stunning in the anterior wall of the left ventricle.
 ...
PMID:Prominent negative T waves with QT prolongation indicate reperfusion injury and myocardial stunning. 133 91

To determine how early myocardial infarction can be detected, serial creatine kinase MB concentrations were sampled in 313 patients during triage of acute (less than 12 hours) chest pain. Serum was sampled on hospital arrival (baseline) and hourly for 3 hours (total of four samples). Creatine kinase MB concentrations were subsequently analyzed for their ability to detect infarction. Infarction was present in 70 patients (22%) and was diagnosable from the index electrocardiograms in 27 of these (39%). Sensitivity and specificity for detection of infarction were 76% and 72%, respectively, as determined from baseline MB values only and increased with each additional sample to a maximum of 92% and 96%, respectively, in all four samples. Analysis of two serum samples taken 2 hours apart showed a sensitivity of 94% and a specificity of 91%. If these results are confirmed, improved initial diagnostic accuracy with this rapid assay technique in acute chest pain may (1) conserve resources when initial suspicion of infarction is low, (2) identify patients with infarction appropriate for early intervention, and (3) avoid premature hospital discharge of patients with infarction.
 ...
PMID:Use of rapid serial sampling of creatine kinase MB for very early detection of myocardial infarction in patients with acute chest pain. 173 70

Patients with chest pain lasting greater than 6 hours and suggesting acute myocardial infarction (AMI) are often excluded from thrombolytic therapy, because myocardial necrosis is believed to be largely irreversible beyond that time. To evaluate the relation between time of onset of chest pain and enzymatic evidence of myocardial necrosis, enzymes on admission were analyzed in 221 consecutive patients with greater than or equal to 2 mm ST-segment elevation by electrocardiography on admission and no contraindications to thrombolytic therapy. Patients with symptoms within 6 hours (n = 170, early) received thrombolytic therapy, but those with symptoms after 6 hours did not (n = 51, late). Eventually, 219 (168 early, 51 late) patients had enzymatically proven AMI within 24 hours. Creatine kinase levels on admission less than twice the upper normal limit were found in 155 (91%) early patients, but surprisingly, also in 30 (59%) late patients. By electrocardiography on admission, ST-segment elevation per lead was 2.1 +/- 1.1 mm in late patients with low initial enzymes versus 1.1 +/- 0.3 mm in those with elevated initial enzymes (p less than 0.0001). Concomitantly, Q waves in leads with ST-segment elevation were present in 17 (57%) late patients with low enzymes on admission versus 17 (81%) with elevated enzymes on admission (p = 0.06). Eventually, maximal creatine kinase levels were similar in all late patients irrespective of enzyme levels on admission. Therefore, many patients with symptoms of AMI after 6 hours have low enzymes on admission and may still be eligible for thrombolytic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Usefulness of electrocardiographic findings and creatine kinase levels on admission in predicting the accuracy of the interval between onset of chest pain of acute myocardial infarction and initiation of thrombolytic therapy. 195 Nov 13

Seventy patients hospitalized with chest pain after cocaine use were retrospectively evaluated to define the risk and clinical course of acute myocardial infarction (AMI). AMI developed in 22 patients (31%) and transient myocardial ischemia was seen in an additional 9 patients (13%). Coronary risk factors did not distinguish those who developed AMI from those who did not. The presenting electrocardiogram was abnormal in 20 of 22 patients who evolved AMI and in 19 of 48 of those who did not. Creatine kinase levels were elevated in 75% of the patients, including 65% of those who did not develop AMI, but creatine kinase-MB elevations were only observed in the AMI group. The route of cocaine administration did not predict AMI and there was no predilection for a particular coronary vascular bed. The length of time between drug use and onset of AMI pain was often quite prolonged (median interval, 18 vs 1 hour in the non-AMI group). Eight of the patients with AMI underwent cardiac catheterization and 4 had significant coronary narrowing.
 ...
PMID:Acute myocardial infarction and chest pain syndromes after cocaine use. 189 9

Serum samples from patients admitted to a coronary care unit with a history of acute chest pain suggestive of myocardial infarction in the previous 12 h were obtained on admission and at 6 and 12 h, thereafter. Creatine kinase (CK), CK-MB isoenzyme, CK-MM sub-bands, myoglobin, and lactate dehydrogenase (LD) isoenzymes were examined. Changes were evaluated in relation to the diagnosis obtained from clinical examination, serial electrocardiography and 'routine' cardiac enzymes (CK, aspartate transaminase and alpha-hydroxy butyrate dehydrogenase daily for 3 days following admission). The slope of the logarithms of CK, CK-MB activity and CK-MB concentration in the early post infarct period fully distinguished between infarct and non-infarct patients. Measurement of myoglobin and lactate dehydrogenase isoenzymes was less sensitive. Serial estimation of CK-MM sub-band patterns allowed the time from infarction to be estimated. Serial estimation of CK in the 12 h following admission can be substituted for conventional daily enzyme estimations for the diagnosis of acute myocardial infarction in patients with onset of chest pain within the previous 12 h. This could reduce laboratory and in-patient costs.
 ...
PMID:Early diagnosis of myocardial infarction by timed sequential enzyme measurements. 321 18

Subforms of creatine kinase MM isoenzyme (isoforms, pI: MMA = 7.95, MMB = 7.76, MMC = 7.54) in human myocardium and serum were quantified by chromatofocusing. Creatine kinase MMA was a dominant isoform (greater than 94% of MM) in normal (n = 3) and in both infarcted and non-infarcted myocardium (n = 2). To investigate isoform conversion in vitro partially purified MMA was incubated with human plasma at 37 degrees C for 24 h (n = 5). Creatine kinase MMB (0%, 47%, 44% of MM at 0, 12, 24 h respectively) and MMC (0%, 22%, 42%) sequentially appeared in incubation media whereas MMA (100%, 31%, 14%) disappeared rapidly with a mean disappearance rate of -0.00169(0.00021)(SD) min-1. Individual differences in conversion velocity were small (SD less than 5%). To investigate isoform conversion in vivo serum isoforms were analysed in patients with acute myocardial infarction (n = 7). MMA was first dominant (A:B:C = 54:34:12%) in the early stage (6-9 h after the onset of chest pain) followed by MMB dominant (19:42:39%) in the middle stage (24-35 h), and MMC dominant (6:22:72%) in the late stage (54-60 h). Changes in isoform proportion were time dependent regardless of serum creatine kinase activity. These findings are consistent with canine isoform conversion reported previously except that in man the velocity of conversion was slower than in the dog. Thus analysis of serum creatine kinase MM isoforms may allow the onset of acute myocardial infarction to be precisely dated. Moreover, determination of MMA, the isoform native to myocardium with a short serum half life, may be useful in the prompt diagnosis of myocardial infarction.
 ...
PMID:Time dependent conversion of creatine kinase MM isoforms in man. 365 11

Creatine kinase (CK)-MM and -MB isoforms were evaluated for the early diagnosis of myocardial infarction in patients aged over 65 years admitted to a district general hospital with acute chest pain. Samples were collected for standard cardiac enzymes, timed CK slope analysis, and CKMM and CKMB isoform analysis from 48 patients admitted with acute chest pain. CKMM and CKMB isoform analyses were conducted using a Helena Rep electrophoresis system under standard conditions supplied by the company. In addition to the results of the biochemical tests the discharge diagnosis of the patients were also recorded. CKMM isoform analysis resulted in three false-negative classifications of patients and one false-positive. The predictive value of this test was 100% for a positive result and 94% for a negative result. CKMB isoform analysis was less accurate and there were six false-negative results and five false-positive results. The predictive value of a positive result was 75% and 85% for a negative result. CK isoform analysis became unreliable when mean total CK levels in serum were 210 IU/l (+/- 171). CK isoform analysis may be of use in the investigation of patients whose samples have a total CK concentration greater than the reference range but was no better than timed CK slope analysis for the detection of myocardial infarction in patients aged more than 65 years.
 ...
PMID:Creatine kinase isoform electrophoresis for the early confirmation of myocardial infarction detected by timed sequential CK slope analysis. 782 14

The time-related frequency of elevated results for the mass concentrations of the MB isoenzyme of creatine kinase and of troponin T were compared with that of creatine kinase and creatine kinase-MB activity in patients with acute myocardial infarction. Patients (322; 175 with and 147 without myocardial infarction) consecutively admitted for evaluation of possible acute myocardial infarction were investigated. Reference limits for troponin T (0.1 microgram/l) and creatine kinase-MB mass concentration (5.0 micrograms/l) were exceeded frequently in patients with unstable angina pectoris (troponin T 43%, creatine kinase-MB mass concentration 24%) in contrast to patients with no acute ischaemic heart disease (both < 5%). Within 4 and between 4-8 hours after onset of chest pain, the frequency of elevated results for creatine kinase-MB mass concentration and troponin T in patients with acute myocardial infarction was considerably higher (20-30%) than for creatine kinase and creatine kinase-MB activity. Creatine kinase-MB mass concentration and troponin T both allowed earlier diagnosis of acute myocardial infarction than creatine kinase and creatine kinase-MB activity, but troponin T was not elevated before the creatine kinase-MB mass concentration.
 ...
PMID:The mass concentrations of serum troponin T and creatine kinase-MB are elevated before creatine kinase and creatine kinase-MB activities in acute myocardial infarction. 830 15

Creatine kinase (CK) and its isoenzyme CK-MB are important tools for the diagnosis of acute myocardial infarction. The content of CK-MB relative to total CK in myocardial cells is variable; it is low in normal myocardium and increased several-fold in hypoxic myocardium. We tested the hypothesis that CK-MB mass (CK-MBm) could be related to cardiovascular history, preinfarctional medication and clinical course during myocardial infarction. In a prospective study CK and CK-MBm were measured 0, 6, 12, 18, 24, 36, 48 and 72 h after the admission to the coronary care unit. Peak values and areas under the curve (AUC) were determined and normalized for total CK activity (CK-MBm/CK). Of 185 patients with acute chest pain, 70 patients had 71 acute myocardial infarctions and were enrolled in the study. A history of chronic angina pectoris or hypertension had no influence on CK-MBm/CK levels. In contrast, treatment with beta-blockers before infarction resulted in a lower relative CK-MBm peak value (CK-MBm/CK 6.0 (median value), range 3.1-15.3, versus 7.0, range 0.5-17.3: p < 0.05). Other drugs had no influence. Patients with persistent pain on admission tended to have higher relative CK-MBm values (peak CK-MBm/CK: 6.8, range 0.5-17.3, versus 5.3, range 1.4-7.9, p = 0.08; AUC CK-MBm/CK: 0.05, range 0.01-0.10, versus 0.03, range 0.01-0.06, p < 0.05). Three vessel disease on coronary angiography was associated with higher peak CK-MBm/CK values during the acute phase of myocardial infarction than those with 1-2 vessel disease (Peak CK-MBm/CK: 7.9, range 5.5-17.3, versus 6.4, range 3.1-10.2, p < 0.05; AUC CK-MBm/CK: 0.06, range 0.02-0.11, versus 0.04, range 0.02-0.07, p < 0.05). We conclude that relative CK-MBm/CK levels reflect to a certain degree the extent of the coronary disease and that preinfarctional beta-blockade may result in lower CK-MBm levels.
 ...
PMID:Creatine kinase MB during myocardial infarction: relationship to preexisting coronary heart disease and medication. 942 40


1 2 3 Next >>