Creatine kinase-MB Isoenzyme Release Research Articles

Intermittent Antegrade Tepid Versus Cold Blood Cardioplegia in Elective Myocardial Revascularization

Background. The ideal temperature for blood cardioplegia administration remains controversial. Methods. Fifty-two patients who required elective myocardial revascularization were prospectively randomized to receive intermittent antegrade tepid (29°C; group T, 25 patients) or cold (4°C; group C, 27 patients) blood cardioplegia. Results. The two cohorts were similar with respect to all preoperative and intraoperative variables. The mean septal temperature was higher in group T (T, 29.6° ± 1.1°C versus 17.5° ± 3.0°C; p < 0.0001). After reperfusion, group T exhibited significantly greater lactate and acid release despite similar levels of oxygen extraction ( p < 0.05). The creatine kinase-MB isoenzyme release was significantly lower in group T (764 ± 89 versus 1,120 ± 141 U · h/L; p < 0.04). Hearts protected with tepid cardioplegia demonstrated significantly increased ejection fraction with volume loading, improvement in left ventricular function at 12 hours, and decreased need for postoperative inotropic support ( p < 0.05). The frequency of ventricular defibrillation after cross-clamp removal was lower in this cohort ( p < 0.05). There were no hospital deaths, and both groups had similar postoperative courses. Conclusions. Intermittent antegrade tepid blood cardioplegia is a safe and efficacious method of myocardial protection and demonstrates advantages when compared with cold blood cardioplegia in elective myocardial revascularization.

Free-Radical Activity after Reperfusion in Diabetic and non-diabetic Patients with Acute Myocardial Infarction

1. Oxygen-derived free radicals have been implicated in reperfusion injury after thrombolytic therapy in acute myocardial infarction. To test the hypothesis that diabetic patients may have increased oxidative stress which may lead to increased reperfusion damage and thereby contribute to a poorer outcome in these patients, we measured two indices of free-radical activity, diene conjugate molar ratios as an index of lipid isomerization and thiobarbituric acid-reactive material as an index of lipid peroxidation, in 66 non-diabetic and 26 diabetic patients admitted with acute myocardial infarction who received thrombolytic therapy and in whom reperfusion was assessed using early time to peak creatine kinase-MB isoenzyme release. 2. Baseline diene conjugate molar ratios or thiobarbituric acid-reactivity did not differ significantly between diabetic and non-diabetic patients (1.97 +/- 0.98 versus 2.16 +/- 1.34; not significant and 2.10 +/- 0.60 versus 1.99 +/- 0.73 mumol/l; not significant). In patients with enzymic evidence of reperfusion (i.e. time to peak enzyme release < or = 12 h) diene conjugate molar ratios peaked at 6 h compared with 12h in those with unsuccessful reperfusion (i.e. time to peak enzyme release > 12 h). In patients with unstable angina the maximum increase in the diene conjugate molar ratios was significantly less than in patients with acute myocardial infarction (6.80 +/- 12.3 versus 15.82 +/- 22.55%; P = 0.035). There was a significant fall in thiobarbituric acid-reactivity at 24 h in patients with enzymic evidence of reperfusion (P = 0.017). There were no major differences in these rises and falls between diabetic and non-diabetic patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventricular function after normothermic versus hypothermic cardioplegia

Warm cardioplegia produced by essentially continuous infusion has been used as an alternative to traditional cold intermittent infusion techniques during cardiac surgery, but its effects on postoperative left ventricular function have not been defined. We performed a randomized clinical trial to assess the effects of warm and cold blood cardioplegia on load-independent indices of ventricular function. Fifty-three patients were randomized to warm (n = 27) or cold (n = 26) cardioplegia. Myocardial oxygen consumption, lactate production, adenine nucleotides, and adenine nucleotide degradation products were measured during cardioplegia and reperfusion. In 13 patients per group, pressure-volume loops were constructed and ventricular function was assessed 3 hours after the operation. Warm cardioplegia resulted in greater myocardial lactate production but improved recovery of oxygen consumption during reperfusion. Depletion of adenosine triphosphate was similar between groups, but total adenine nucleotides (adenosine triphosphate + adenosine diphosphate + adenosine monophosphate) fell further during warm cardioplegia. Cold cardioplegia was associated with an accumulation of adenosine diphosphate and adenosine monophosphate. Creatine kinase MB isoenzyme release was reduced in the warm group. Three hours after the operation, end-systolic elastance and preload-recruitable stroke work index were increased after warm cardioplegia, and early diastolic relaxation was also increased. Increased systolic function after warm cardioplegia may have been related to improved myocardial protection, elevated arterial lactate concentrations, or increased circulating catecholamine levels. Altered diastolic compliance in the warm group may reflect greater active relaxation during early diastolic filling.

Catheter ablation of the atrioventricular junction with radiofrequency energy.

Catheter ablation of the atrioventricular junction using direct-current defibrillator discharges requires general anesthesia and may have serious side effects. Sixteen patients with drug-refractory supraventricular tachycardia underwent catheter ablation of the atrioventricular junction using radiofrequency energy. A standard 7F quadripolar electrode catheter was positioned to record the largest unipolar His potential (580 +/- 640 microV) from the distal electrode. An electrocoagulator (Microvasive Bicap 4005) supplied continuous, unmodulated energy at 550 kHz. One to 14 applications of radiofrequency current were delivered between the distal electrode and a large-diameter chest wall electrode. Transient, mild chest discomfort was reported by seven of 16 patients. None had significant arrhythmias or blood pressure changes during radiofrequency ablation. Complete atrioventricular block was produced in nine of 16 patients and high-grade second-degree atrioventricular block was produced in one patient with radiofrequency current. Attenuated His bundle electrograms could still be recorded in the remaining six patients, four of whom underwent successful atrioventricular junctional ablation using direct-current shock during the same session. Atrioventricular block persisted in all 10 patients successfully treated with radiofrequency ablation during a mean follow-up of 4.2 months. Compared with a group of historic control subjects treated with direct-current shock ablation, the 10 patients successfully treated with radiofrequency current had significantly less creatine kinase-MB isoenzyme release (5.7 +/- 5.1 vs. 22 +/- 13 IU, p = 0.006). A junctional escape rhythm was present in all patients after radiofrequency-induced atrioventricular block. In contrast, three of 10 control patients had an idioventricular escape after direct current shock ablation, and four patients had no escape rhythm at all.(ABSTRACT TRUNCATED AT 250 WORDS)

Significance of technetium-99m/thallium-201 overlap on simultaneous dual emission computed tomography in acute myocardial infarction

To examine the significance of technetium-99m pyrophosphate/thallium-201 scintigraphic overlap as an indicator of identifying early coronary reperfusion (≤3 hours), 32 patients, in whom coronary recanalization was attempted for acute myocardial infarction (AMI), underwent myocardial imaging 3 days after the onset of AMI. The imaging was performed by simultaneous dual emission computed tomography, which allows simultaneous recording of technetium-99m pyrophosphate and thallium-201 images and comparison between both images in the same slice. The patients were separated into 3 groups: 9 patients in whom reperfusion was successful and showed scintigraphic overlap (group A), 12 with successful recanalization but no overlap (group B) and 11 with neither coronary reflow nor overlap (group C). No patient in whom reperfusion failed showed scintigraphic overlap (p < 0.05). Groups A and B were comparable in age, infarct vessel, collateral circulation, residual coronary stenosis and cumulative release of creatine kinase-MB isoenzyme. However, compared with group B, group A had a shorter interval between onset of AMI and reflow (2.5 ± 0.8 vs 4.8 ± 1.3 hours, p < 0.001). The presence of scintigraphic overlap identified early coronary reflow with a sensitivity of 80%, specificity of 91%, positive predictive accuracy of 89% and negative predictive accuracy of 83%. Thus, technetium-99m/thallium-201 overlap on dual emission computed tomography can be used as an index of documenting early recanalization and might reflect the presence of salvaged myocardium adjacent to the necrotic tissue.

Estimation of infarct size by myocardial emission computed tomography with thallium-201 and its relation to creatine kinase-MB release after myocardial infarction in man.

We evaluated emission computed tomography (ECT) for thallium-201 (201TI) myocardial imaging in estimating infarct size (IS). In 18 patients in whom IS was estimated enzymatically at the time of the acute episode, planar 201TI perfusion scintigraphy and ECT with a rotating gamma camera were performed 4 weeks after the first myocardial infarction. From the size of 201TI perfusion defects, the infarct area in planar images and the infarct volume in reconstructed ECT images were measured by computerized planimetry. When scintigraphic IS was compared with the accumulated creatine kinase-MB isoenzyme release (CK-MBr), infarct volume determined from ECT correlated closely with CK-MBr (r = 0.89), whereas infarct area measured from planar images correlated less satisfactorily with the enzymatic IS (for an average infarct area from three views, r = 0.69; for the largest infarct area, r = 0.73). Although conventional scintigraphic evaluation is useful for detecting and localizing infarction, quantification of ischemic injury with this two-dimensional technique has a significant inherent limitation. The ECT approach can provide a more accurate three-dimensional quantitative estimate of infarction, and can corroborate the enzymatic estimate of IS.

EFFECTS OF EARLY ADMINISTRATION OF A HIGHLY PURIFIED HYALURONIDASE PREPARATION (GL ENZYME) ON MYOCARDIAL INFARCT SIZE

79 patients with suspected myocardial infarction entered a randomised trial to establish the safety of early intravenous administration of a highly purified hyaluronidase preparation (GL enzyme) and to assess its effects on eventual infarct size as measured by electrocardiographic, enzymatic, and scintigraphic criteria. Of the 71 patients with infarction, 35 received GL enzyme and 36 placebo within 6 h of the onset of chest pain. GL enzyme injected into a peripheral vein produced no adverse changes in the clinical, haemodynamic, biochemical, or haematological variables studied. GL enzyme reduced precordial electrocardiographic indices of infarct size as reflected by a diminution (p<0·02) in the degree of both R wave loss and Q wave development. In addition, the number of leads developing pathological Q waves (NΔQ≥2), a sign of progression from ischaemia to necrosis, was reduced (p<0·05) after GL nzyme treatment. However, there were no significant differences in infarct size as measured by cumulative creatine kinase MB isoenzyme release or technietium-99m pyrophosphate scintigraphic infarct area, or in clinical outcome during the hospital stay. Interpretation of the enzymatic and scintigraphic data was complicated by chance bias in pre-treatment randomisation which resulted in more (p<0·05) patients with severe haemodynamic impairment (and hence probably larger infarct sizes) entering the GL enzyme group. Nonetheless, a favourable effect of GL enzyme on infarct size was demonstrated by precordial electrocardiographic QRS mapping, where each patient acts as his or her own control.

Digitalis and myocardial infarction in man.

The use of digitalis after acute myocardial infarction is controversial. The effect of digoxin on computer-quantitated thallium-201 perfusion scintigrams (Tl-201), left ventricular (LV) ejection fraction (EF), and percentage of abnormally contracting LV regions (% ACR) was determined in 23 patients. A correlation was established between creatine kinase MB isoenzyme release and initial radionuclide-gated blood pool wall motion estimates of EF (r = -0.73) and % ACR (r = 0.71). After radionuclide assessments, 14 patients received digoxin 18 +/- 23 hours (mean +/- SD) after the rise in CK-MB from baseline, while the remaining nine patients served as controls. In the control group, the mean EF was 0.33 +/- 0.12 on the first study and 0.30 +/- 0.08 on the second study (p = NS). In the digoxin group, the EF after digoxin administration (mean 0.33 +/- 0.11) was significantly different from the initial EF (mean 0.29 +/- 0.09, p less than 0.03); however, digoxin had no apparent effect on infarct size as assessed by sequential % ACR and Tl-201 perfusion data. These data indicate that digoxin resulted in a minimal but significant improvement in EF that did not occur at the expense of LV perfusion or regional wall motion.

Correlation of angiographic estimates of myocardial infarct size and accumulated release of creatine kinase MB isoenzyme in man.

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 additional two patients with first (inferior) infarct secondary to stenosis of the right coronary artery proximal to the origin of the right ventricular arterial blood supply had disproportionately large sigma CK-MB, suggesting a combination of LV and RV necrosis. In the 15 patients with prior infarct, there was no significant correlation between sigma CK-MB and %ACS or EF. However, in the subgroup of patients with anterior MI, %ACS correlated with sigma CK-MB, both in patients with no prior MI (r = 0.88, N = 12) and in patients with prior MI (r = 0.69, N = 9). These independent angiographic and enzymatic data suggest that enzymatic infarct size estimates utilizing accumulated CK-MB release may be a valid and reliable clinical measure for assessing the extent of LV necrosis in the setting of acute anterior myocardial infarction. However, limitations may exists in certain cases of inferior MI, probably because of concomitant right and left ventricle necrosis.