Perioperative myocardial cell damage assessed by immunoradiometric assay of ?-myosin heavy chain serum levels in patients undergoing coronary bypass surgery (original) (raw)
Related papers
International Journal of Cardiology, 1996
In order to investigate myocardial cell damage in patients undergoing coronary bypass surgery, serum levels of cardiac myosin fragments, using monoclonal antibodies to myosin p heavy chains, were measured in serial blood samples of 85 patients, 79 male and 6 female, 43-66 years old, after a total of 86 internal mammary artery and 137 saphenous vein graft implants. Eight patients had perioperative acute myocardial infarction (MI), detected by abnormal Q waves and a rise of CK-MB levels. After surgery, j3-myosin levels increased from post-operative day 3 and reached peak values on day 5 in patients without and in day 7 in patients with perioperative MI; in these 8 patients, myosin peak levels were greater as compared to 77 patients without perioperative MI (3452 2 1596 vs. 761 ? 494; P < 0.01). There was a correlation between myosin peak levels and creatine kinase (CK) (r = 0.71; P < 0.05) and CK-MB peak levels (r = 0.74; P < 0.05) only in the patients with perioperative MI, but not in the patients without MI. There was no correlation between myosin peak levels and the times of aortic cross clamping or cardiopulmonary bypass. Peak myosin levels over 75% confidence limits of the mean were found in 23 patients; post-operative low output syndrome occurred in 10 of these 23 patients and in 7 out of 62 patients with peak myosin levels within 75% of the mean (P < 0.005). The increase in P-myosin heavy chain serum levels observed in almost all patients undergoing coronary surgery suggests lesser perioperative damage of the contractile apparatus, which could be detected by the usual enzyme and ECG criteria. The higher prevalence of low output syndrome in patients with higher increases in myosin levels suggests more pronounced damage to the contractile apparatus in these patients. The higher myosin levels clearly indicate the presence of perioperative MI.
Myocardial damage following coronary bypass surgery: assessment with antimyosin antibody uptake
British Journal of Radiology, 1992
To assess the role of '"In antimyosin antibody (AbAm) in the delineation of myocardial damage following coronary bypass surgery, we studied 51 consecutive patients who underwent coronary surgery, 27 of whom had a history of prior myocardial infarction. All patients underwent a diagnostic protocol comprising: (1) "Tc m pyrophosphate (PYP) and AbAm injection 48 h after surgery (AbAm imaging 24 and 48 h post-injection) (myocardial/background and myocardial/lung ratios were obtained respectively from the computer image); (2) Radioimmunoassay (RIA) serum CK-B levels from samples obtained immediately before surgery, and 24 and 48 h later; (3) clinical and ECG follow-up. Twenty-five patients showed positive AbAm studies, 10 had positive PYP images, and 21 had CK-B levels above normal limits at 24 h. One patient with abnormal AbAm, PYP and CK-B studies had new Q waves on the ECG after surgery. This patient was considered to have sustained a peri-operative myocardial infarction. The large number of positive AbAm studies probably reflects myocardial damage frequently associated with coronary bypass surgery.
Cardiac troponin I as an early marker of myocardial damage after coronary bypass surgery
European journal of …, 1998
Study objective: To evaluate the performance of cardiac specific markers, cardiac troponin I (cTnI) and CK-MB by mass assay (CK-MB mass), for the early diagnosis of myocardial ischemia and/or infarction after coronary bypass surgery. Methods: Prospective clinical, electrocardiograpic and biologic follow-up of 117 patients undergoing isolated coronary surgery with the use of intermittent anterograde normothermic blood cardioplegia. Blood samples for biochemical analysis were drawn before surgery (T 0) and at 2 (T 1), 6 (T 2), 10 (T 3) and 20 h (T 4) after aortic cross-clamp release. Without knowledge of the biochemical data, patients were classified according to the electrocardiographic evolution into two groups: group 1, uneventful recovery and group 2, evidence of ischemia/infarction based on continuous ST-T segment monitoring and 12-lead ECG. Results: No patients had abnormal markers at T 0. At T 1 , although both markers were elevated, no difference was noted between the two groups. At T 2, 6 h after surgery, cTnI and CK-MB mass levels were significantly higher in group 2 than in group 1 (median = 17 vg/l,
Human Ventricular Myosin Light Chain Isotype 1 as a Marker of Myocardial Injury
Cardiology, 1994
A monoclonal enzyme immunoassay for measuring human ventricular myosin light chain isotype 1 (HVMLCI) in serum has been developed. To evaluate the method in patients with suspected myocardial injury, we studied 51 patients (16 acute myocardial infarction (AMI), 19 unstable angina pectoris (UAP), 9 stable angina pectoris, 3 nonischemic heart disease, 4 hip surgery patients), and 190 controls (blood donors). Serial bloodsamples were drawn from patients; a single blood-sample from controls. The diagnostic value of the HVMLC 1 assay was compared with total creative kinase (CK), CKMB activity, CKMB mass concentration, lactate dehydrogenase isoenzyme 1 (LD 1), troponin T (TnT) and mitochondrialaspartate aminotransferase (m-ASAT). The detection limit of HVMLCI was 0.4 tg/1(linear range 0-20 µg/1). Sera from 190 reference persons did not contain detectable levels of HVMLC 1(<0.4 µg/1; 99% percentile). The coefficients of variation were 13% (1.0 µg/1) and 3.1% (17.7 µg/1). Crossreactivity with myosin from skeletal muscle was seen. Times to peak value were: CK 19.3 ± 2.0, LD1 43.4 ± 3.2, HVMLCI 72.9 ± 7.0, and m-ASAT 67.3 ± 5.6 h. Time-curves of HVMLCI and m-ASAT were similar, whereas time-curves for HVMLCI and TnT were quite different in most cases. Peak value of HVMLCI was five times higher than CK peak value and eight times that of LD1. HVMLCI appeared in the blood within hours after the onset of chest pain and in the majority remained for more than a week after AMI. Among patients with UAP 16% (3/19) had elevated HVMLCI in serum, whereas elevated TnT was seen in 26% (5/19) and elevated CKMB mass in 26% (5/19). We conclude that the new HVMLCI assay offers a sensitive diagnosis of myocardial injury. It is characterized by a wide diagnostic time window. The similarity of the HVMLCI and m-ASAT curves indicates that it may be used to estimate the extent of myocardial necrosis.
Usefulness of myosin in the postmortem diagnosis of myocardial damage
International Journal of Legal Medicine, 1995
In some situations the postmortem diagnosis of myocardial infarction is made difficult by the brief course of the fatal episode or by interferences caused by autolysis. In such cases, biochemical indices may provide a useful adjunct to morphological studies. Myosin is the main component of the contractile apparatus of muscle cells, so its determination may well be useful to evaluate myocardial injury. The purpose of the present study was to establish the diagnostic efficacy of postmortem myosin heavy chain determinations using monoclonal antibodies and to compare this data with structural findings used to diagnose acute myocardial ischaemia. We studied 105 cadavers with a mean age of 61.63 + 2.21 years. Cases were allocated to 1 of 7 diagnostic groups depending on the probable intensity of myocardial damage and cause of death. The highest serum and pericardial fluid values of myosin heavy chains were seen in subjects who showed morphological evidence of myocardial ischaemia. Mean pericardial fluid/serum ratios differed significantly between subjects with and without observable signs of heart damage.
Determinants and Prognosis of Myocardial Damage After Coronary Artery Bypass Grafting
The Annals of Thoracic Surgery, 2005
Background. Myocardial infarction remains a devastating complication after coronary revascularization. Although electrocardiography (ECG) and echocardiography suggest transmural infarction, myocardial damage and the quality of myocardial protection are not recognized unless troponin I (TnI) is assessed. Determinants and prognosis of TnI elevation after coronary artery bypass grafting (CABG) were evaluated.
Cardiac Troponin: a New Biochemical Marker for Peri-operative Myocardial Injury
European Journal of Vascular and Endovascular Surgery, 2001
who have objective evidence of MI. 6 The ECG is difficult to interpret in the post-operative setting and often Peri-operative myocardial infarction (MI) occurs in does not display the classical ST segment elevation of acute myocardial infarction. 7 Lastly, even if there is a 5-10% of patients undergoing major vascular surgery, is fatal in 50% of these cases and in total will account significant rise in creatine kinase leaked from dying myocardial cells (CK-MB) this may be masked by for more than 50% of all post-operative deaths. 1 An even larger proportion of operated patients will suffer large quantities of creatine kinase (CK) released from skeletal muscle as the result of direct surgical trauma cardiac complications, which may be fatal or non-fatal, that are not demonstrably related to peri-operative or ischaemia/reperfusion injury. 8 This makes the CK/ CK-MB ratio difficult to interpret. MI. 2 These complications may have metabolic causes, but are perhaps more likely to be due to myocardial infarction that cannot be detected by the standard diagnostic tests for peri-operative MI. 3,4 This injury Micro-infarction and the acute coronary may be referred to as minor myocardial injury or syndromes micro-infarction.
Clinica Chimica Acta, 1988
Myocardial injury after aorto-coronary bypass surgery was estimated in 72 patients from total release into plasma of cardiac creatine kinase (CK-MB) and alpha-hydroxybutyrate dehydrogenase (HBD). Actrvrtres of CK-MB were determined both by immuno-inhibition of CK-M units and by ion-exchange chromatography. After correction for per-operative hemolysis, the estimates based on HBD were in agreement with the estimates based on CK-MB as determined by the ion-exchange method. Both enzymes indicated a mean loss of only about 2 gramequivalents of myocardium. Such minimal injury was also found in metabolic and ultrastructural studies of myocardial biopsies in the same patients, as reported earlier [1,2].
Transfusion and Apheresis Science, 2001
In a prospective study we evaluated the concentration of cardiac troponin I (cTnI) and creatine kinase activities (CK) in shed mediastinal blood in the early postoperative period after coronary artery bypass grafting (CABG). Forty seven patients who underwent ®rst time elective CABG were studied. CTnI levels and CK activities in arterial blood and shed mediastinal blood were measured after admission to the intensive care unit (ICU) and 6 h after unclamping the aorta. Mediastinal shed blood samples were drawn from 23 patients (group A) before the ®lter of the cardiotomy reservoir and from 24 patients (group B) behind. Additionally, both markers were measured in blood samples collected from the cellsaver. There were no signi®cant dierences between both groups (A and B) with regard to perioperative parameters. Mean loss of mediastinal shed blood in all patients was 207 AE 127 ml within the ®rst 6 h after operation. There was a positive correlation between CK activities and cTnI concentrations in serum and mediastinal shed blood, but shed blood contained signi®cantly higher concentrations of cTnI as well as CK activities than the circulating blood after admission to the ICU and 6 h after unclamping the aorta. At both time points the cTnI-concentrations and CK activities in shed blood in group B were lower than those in group A but much higher than in serum. The eects of the use of a blood ®lter diminishes with time. Mediastinal shed blood contains extremely high cTnI concentrations and CK activities. Retransfusion of higher quantities of shed blood might lead to false-positive diagnosis of perioperative myocardial infarction. Ó