Abstract:Accumulated creatine kinase MB isoenzyme release (sigma CK-MB) during acute myocardial infarction was correlated with biplane left ventricular (LV) angiographic estimates of percent abnormally contracting segment (%ACS) and ejection fraction (EF) in 35 patients who underwent diagnostic angiography at a mean of 33 +/- 4 days post myocardial infarction (MI). Of the 35 patients, 18 had no evidence of prior MI and their sigma CK-MB showed good correlation with %ACS (r = 0.84) and with EF (r = - 0.78). An additiona… Show more
“…The maximum concentration of CK-MB is related to the grade of myocardial damage, [23][24][25][26] and the present study showed a close relationship between the maximum concentrations of M and CK-MB. The study data suggested that the maximum concentration of M, which was obtained at 6-12 h after onset, could be related to the grade of myocardial damage.…”
Section: Relationship Between Maximum Concentrations Of Serum Myoglobsupporting
“…The maximum concentration of CK-MB is related to the grade of myocardial damage, [23][24][25][26] and the present study showed a close relationship between the maximum concentrations of M and CK-MB. The study data suggested that the maximum concentration of M, which was obtained at 6-12 h after onset, could be related to the grade of myocardial damage.…”
Section: Relationship Between Maximum Concentrations Of Serum Myoglobsupporting
“…Although the accumulated release of CK and CK-MB is more accurate for estimating infarct size than peak CK and CK-MB levels, 35 we were restrained from using the former because of the lack of some measurement data after 24 h. Although large epidemiological studies have extensively used M-mode echocardiography, technical limitations exist when calculating LVM in patients with myocardial infarction, particularly in those who have a regional wall motion abnormality. However, several studies have demonstrated a strong relationship between LV hypertrophy detected by echocardiography and necropsy.…”
Background: Several animal experiments on acute myocardial infarction (AMI) have shown that the cardioprotective effects of ischemic preconditioning are more significant in hypertensive subjects. However, because there are no clinical data on the impact of hypertension on ischemic preconditioning in patients with AMI, whether clinical ischemic preconditioning of prodromal angina was beneficial in AMI patients with hypertension was investigated in the present study.
Methods and Results:125 patients with a first anterior AMI who had undergone successful reperfusion therapy were divided into 2 groups, with or without hypertension, and into 2 further subgroups based on the presence or absence of prodromal angina. Dual-isotope (thallium-201(TL)/Tc-99 m pyrophosphate) single-photon emission computed tomography (SPECT) was performed within 1 week of reperfusion therapy. Left ventricular (LV) function and LV mass index (LVMI) were measured by left ventriculography and echocardiography, respectively. In patients without hypertension, prodromal angina resulted in significantly less myocardial damage on TL-SPECT, better LV ejection fraction and a greater myocardial blush grade compared to patients without prodromal angina. However, these cardioprotective effects of prodromal angina were significantly diminished in hypertensive patients. Importantly, the myocardial salvage effects of prodromal angina showed a significant negative correlation with LVMI, which was significantly greater in hypertensive patients.
Conclusions:The cardioprotective effects of prodromal angina were attenuated in patients with hypertension. Hypertensive LV hypertrophy may crucially limit the effects of ischemic preconditioning in AMI. (Circ J 2011; 75: 1192 - 1199
“…The SEE is about 25%, which, on average, gives a 95% confidence limit of ± 50% for the individual IS. Studies in man concerning the accuracy of estimating IS by serum CK and CK-MB measurements have shown a good correlation between accumulated serum CK and CK-MB and different indirect expressions of IS.10, [16][17][18] Whether the kinetics of CK-MB should be described as a one-or multicompartment model has been discussed. The onecompartment theory is supported by a monoexponential elimination of labeled CK in experimental dog studies,9' 29 but this is probably a simplification of a complex biologic system.…”
Section: Content Of Ck-mb In Normal Myocardiummentioning
confidence: 99%
“…Recent studies comparing IS estimated from serum CK-MB with indirect indicators indicate that this is the case. [16][17][18] We demonstrated that the IS can be calculated just as well with only few blood samples as with serial samples,"' allowing us to examine the reliability of en-…”
SUMMARY This study was performed to determine the relationship between myocardial infarct size estimated by serum CK-MB methods and the extent of irreversible injury in acute myocardial infarction. In 321 consecutive patients, infarct size was estimated by different mathematical models, and in 22 patients who died in hospital, the extent of myocardial necrosis was determined by autopsy. We also investigated the depletion of CK-MB in infarcted tissue, the recovery of CK-MB in the plasma volume, and the elimination of CK-MB from plasma.Myocardial CK-MB depletion was relatively greater in the larger infarcts, whereas the recovery of enzyme in plasma was independent of the infarct size. Correction of serum CK-MB for changes in plasma volume improved the estimate significantly (p < 0.05). The correlation between the measured infarct size (g) and the estimated infarct size (units per liter and gram-equivalents) was highly significant (r = 0.85-0.89, SEE = 23-27%, p < 0.001). Thus, a semiquantitative expression of the extent of myocardial necrosis can be determined in vivo. AMI. Of these, 72 were excluded: 48 because the symptoms of AMI had lasted more than 15 hours before admission or because the second blood sample did not show higher CK-MB activity than the first and 24 because not enough blood samples had been obtained because patients died or were transferred to another department. The remaining 321 patients form the study group. Forty-three of these patients died within 18 days and were divided into group A, which included 22 patients in whom a detailed heart autopsy was performed, and group B, which included 21 patients in whom no detailed heart autopsy was performed. All patients autopsied had survived for at least 48 hours from the appearance of CK-MB activity in serum and there were no signs of reinfarction before death. Furthermore, all plasma curves showed a pure elimination phase (first-order kinetics).The 22 patients in group A included 12 women and 10 men who died at a mean age of 69.7 years (range 49-88 years). The median time from onset of symptoms until death was 6.4 days (range 2-14 days). Cardiogenic shock was the main cause of death in 12 patients and recurrent ventricular fibrillation in six patients. Two died from asystole and two from noncardiac causes.Heart biopsies were taken postmortem every 6 hours for 30 hours in eight patients from group B. The total enzyme depletion in whole heart homogenates was measured in 10 other patients.In 10 patients who died without signs of heart disease, myocardial biopsies were made to estimate CK and CK-MB activity. Tissue extracts were made from about 0.3 g tissue (wet weight) in a mixture of 10 ml 0.25 mol/ 1 sucrose, 3 ml 0.01 mol/l TRIS buffer (pH 7.4), 3 ml 1 mmol/l EGTA (pH 7.4) and 3 ml 1 mmol/ I mercaptoethanol, and homogenized on ice in an Ultra Turax blender for 1 minute. The homogenate was centrifuged (3500 g) and the supernatant was used to determine isoenzyme activity. The samples were diluted with heat-inactivated serum or TRIS buffer to the line...
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.