Electrocardiographic Evidence Of Acute Myocardial Infarction Research Articles

The use of myoglobin/carbonic anhydrase III ratio as a marker for myocardial damage in patients with renal failure

To evaluate the clinical significance of myoglobin and myoglobin/CA III ratio as a biochemical marker for acute myocardial infarction (AMI) in patients with renal failure, we studied 300 patients admitted to the hospital with a history of symptoms characteristic of AMI, and 33 renal failure patients who were undergoing chronic maintenance dialysis treatment and who did not have clinical or electrocardiographic evidence of AMI. Fifteen of 300 patients admitted to the hospital had AMI based on the WHO criteria, and a concomitant value of serum creatinine concentration (S-Crea) over 140 μmol/l indicating renal failure. Fourteen of these 15 patients (93%) had serum myoglobin concentration over 70 μg/l and myoglobin/CA III ratio over 2,20 as measured by time-resolved fluoroimmunoassay (TR-FIA); these values were cutoff values for AMI diagnosis. Twenty-two of 300 patients admitted to the hospital had S-Crea over 140 μmol/l in the absence of myocardial injury. Sixteen of these 22 (73%) patients had increased serum myoglobin concentration, but only four of 22 (18%) had myoglobin/CA III ratio over 2,20. A positive correlation between serum myoglobin and CA III concentrations ( r s = 0.933, P < 0.001) was observed in hemodialyzed patients with chronic renal failure. The values for serum myoglobin/CA III ratio observed in this group were similar to those measured in the 22 non-AMI patients with S-Crea over 140 μmol/l admitted to the hospital and differed statistically from that for patients with AMI ( P < 0.001). We conclude that serum myoglobin, as well as CA III values, are elevated in patients with renal failure, and therefore S-myoglobin can not be used as a marker for AMI in these patients. Our results suggest that the serum myoglobin/CA III ratio is a reliable AMI marker even in renal failure patients, and therefore provides a tool for AMI diagnosis in this patient group.

Creatine kinase and creatine kinase-MB release after nontraumatic cardiac arrest

The aim of the study was to describe the course of serum creatine kinase (CK) and its MB fraction (CK-MB) in patients surviving cardiac arrest, and to identify factors influencing CK and CK-MB release. The study was set in the community of Vienna, Austria. Data concerning cardiopulmonary resuscitation, collected within a period of 33 months, were evaluated retrospectively and compared with laboratory blood investigations collected prospectively (on admission and after 6, 12, and 24 hours) in 107 adult patients surviving a witnessed cardiac arrest for 24 hours. CK and CK-MB were elevated in >75% of the patients within 24 hours. Release of CK and CK-MB was mainly associated with electrocardiographic evidence of acute myocardial infarction (AMI), cumulative energy administered during defibrillarion, and duration of chest trauma by compression. The solCKMB CK ratio was elevated in 32% of the patients. Of patients with electrocardiographic evidence of AMI, only 49% had an elevated CK-MB CK ratio. In conclusion, the elevation in serum CK and CK-MB fraction in patients after nontraumatic cardiac arrest is a frequent finding, and is associated with ischemic myocardial injury, as well as physical trauma to the chest. This should be considered when interpreting the course of CK and CK-MB fraction for the diagnosis of AMI.

923-6 Intravenous Adenosine and Lidocaine to Limit Reperfusion Injury During Acute Myocardial Infarction: Preliminary Data

Adenosine (ADO) and lidocaine (LDO) given prior to restoration of blood flow reduces reperfusion injury in animals. We conducted a pilot study of intravenous ADO and LDO in pts undergoing direct angioplasty for acute myocardial infarction (AMI). Pts with ≤ 12 hours of chest pain and electrocardiographic evidence of AMI were given LDO 1 mg/kg iv bolus and 2 mg/min iv infusion beginning at the time of recruitment, and ADO 70 mcg/kg iv infusion beginning when coronary occlusion (TIMI grade 0 – 1 blood flow) was confirmed angiographically. Pts with bronchospasm, blood pressure &lt; 100 mmHg, or &lt; 1° heart block were excluded. ADO and LDO were given for 1 hour after vessel patency was restored. Myocardial area at risk and final infarction area were measured with serial Tc-99m-sestamibi perfusion studies (prior to angioplasty, before hospital discharge and 6 weeks after discharge). A salvage index (S1) was constructed by correcting the change in sestamibi perfusion defect for the mass of myocardium at risk. Analysis of 25 patients completing the protocol revealed a mean ( ± SD) salvage of 20 ± 17% and S1 = 0.55. Salvage and S1 were 25 ± 18% and 0.54 for anterior infarctions, 13 ± 5% and 0.57 for inferior infarctions, respectively. These data were compared to an historical control group consisting of 50 patients undergoing direct angioplasty for AMI without adjunctive ADO/LDO. After adjustment for time to treatment and perfusion nadir, analysis of covariance revealed a similar degree of early salvage in the study and control groups (p = 0.3). However, at 6 weeks, the median infarct size for study pts was 0. Using logistic regression analysis, significantly more study pts had no final measureable infarction at 6 weeks than control pts at hospital discharge (p = 0.007). After adjusting for infarct size, location and time to treatment, this difference persisted (p = 0.04). Adjunctive ADO and LDO during angioplasty for AMI may favorably affect late final infarction size. Randomized studies assessing 6 week final infarction size are needed.