Troponin levels in patients with myocardial infarction after coronary artery bypass grafting

BACKGROUND: The objective of this study was to evaluate serum cardiac troponin T and I levels in patients in whom electrocardiogram, myocardial scan, and serum CK-MB levels of the MB isoenzyme of creatine kinase indicated perioperative myocardial infarction (MI) after coronary artery bypass grafting (CABG). METHODS: We studied 590 patients who underwent CABG at the Montreal Heart Institute between 1992 and 1996. Postoperative cardiac troponin T levels (493 patients), troponin I levels (97 patients), and activity of the MB isoenzyme of creatine kinase, electrocardiograms, clinical data, and clinical events were recorded prospectively. The diagnosis of perioperative PMI was defined by a new Q wave on the electrocardiogram, by serum levels of the MB isoenzyme of creatine kinase higher than 100 IU/L within 48 hours after operation, or both. RESULTS: After CABG, 22 patients in whom troponin T levels (22/493, 4.5%) and 6 patients in whom troponin I levels (6/97, 6.2%) were measured had sustained a perioperative MI according to current diagnostic criteria. In these patients, troponin T levels higher than 3.4 microg/L 48 hours after CABG best detected the presence of perioperative MI, with an area under the receiver operating characteristic curve of 0.95, a sensitivity of 90%, a specificity of 94%, a positive predictive value of 41%, a negative predictive value of 99%, and a likelihood ratio of 15. Serum troponin I levels higher than 3.9 microg/L 24 hours after CABG confirmed the perioperative MI with an area under the receiver operating curve of 0.86, a sensitivity of 80%, a specificity of 85%, a positive predictive value of 24%, a negative predictive value of 99%, and a likelihood ratio of 5. CONCLUSIONS: Serum troponin T levels higher than 3.4 microg/L 48 hours after CABG correlated best with the diagnosis of perioperative MI. Serum troponin T levels greater than 3.9 microg/L 24 hours after CABG also correlated with the diagnosis of perioperative MI, although a larger experience is needed to confirm the validity of the chosen cutoff value.     

Biochemical markers of myocardial injury in the pericardial fluid of patients undergoing heart surgery

The purpose of this study was to compare cardiac markers in the pericardial fluid and serum in order to evaluate preoperative myocardial injury. Thirty patients were divided into three groups. The first group (AVR; n=10) received an aortic valve replacement. The second group (SA; n=10) included patients with stable angina who underwent elective coronary artery bypass grafting (CABG). The third group (ACS; n=10) included patients with acute coronary syndrome who underwent urgent CABG. Pericardial fluid and venous samples were taken after opening the pericardium and 24 h postoperatively. Serum and pericardial concentration of troponin I (cTnI), creatine kinase (CK), its MB isoenzyme (CK-MB) and myoglobin were determined. Preoperative pericardial cTnI was significantly (P<0.01) higher than in serum in all groups. Preoperative pericardial CK, CK-MB and myoglobin were significantly (P<0.01) lower than in serum in groups AVR and SA. Preoperative pericardial and serum cTnI were significantly higher in the ACS than in AVR and SA groups (P<0.01). Postoperative pericardial concentration of all markers was significantly higher (P<0.01) than in serum in all groups. We conclude that preoperative pericardial accumulation of cTnI may reflect subclinical injury which may not be demonstrated by the usual laboratory tests.     

III: Cardiac troponin T in the diagnosis of perioperative myocardial reinfarction

Diagnosis of a perioperative myocardial infarction (PMI) on the basis of measurement of the creatine kinase MB fraction (CKMB) alone is not always easy. Surgical traumatisation of muscle fibres can lead to false-positive elevations. Newly introduced laboratory tests for cardiac troponins seem to facilitate the diagnosis of PMI. We measured serum values of cardiac troponin T in 139 patients described in detail in part I and compared them with common diagnostic tools for myocardial infarction. Methods. In all, 139 patients were enrolled (part I). Clotted serum samples were taken preoperatively and daily until day 3, centrifuged, and stored at −20° C until analysis. Our Department of Clinical Biochemistry and Haematology used a commercially available sandwich immunoassay (Troponin T ELISA, Boehringer, Mannheim, Germany). The measurements of CK and CKMB were performed with an automated analyser (CK, CK-MB, Boehringer, Mannheim, Germany). Serum values of troponin T were defined according to company recommendations: detection level: 0.04 ng/ml, threshold value for myocardial ischaemia: ≥0.2 ng/ml, value for diagnosis of non-Q-wave infarction: ≥1.0 ng/ml, and value for diagnosis of Q-wave infarction: ≥3.0 ng/ml. We therefore assumed a value of ≥1.0 ng/ml troponin T as being positive for MI, comparable with a CKMB value ≥6% of total CK (part I). Statistical analysis was the same as described in part I. Results. Six of the 139 patients had a perioperative infarction, 3 of them had CKMB levels ≥6%, 3 had an elevation of troponin T ≥1.0 ng/ml. The sensitivity was 50% for both troponin T and CKMB. Values for specificity were 98% for troponin T and 95% for CKMB. Two of 8 patients with troponin T levels ≥0.2 ng/ml preoperatively had a reinfarction (Table 5). Three of 8 patients with preoperative elevations of cardiac troponin T ≥0.2 ng/ml versus 4 of 131 others had left ventricular failure postoperatively (P<0,05). On day 3 significantly more patients with pathological levels of troponin T had left ventricular failure (5 of 12 vs. 0 of 127, P<0.05). Patients with pathological depression of the ST segment on Holter ECG more often had elevations of troponin T values on day 3 than patients without (3 of 25 vs.4 of 75, P=0.048). There was an unexplained coincidence of elevated preoperative serum creatinine levels >120 μmol/l and troponin T values (Table 6). Conclusion. Troponin T is a highly specific marker for perioperative myocardial cell necrosis. Patients with raised levels preoperatively seem to be at higher risk for postoperative reinfarction and left ventricular failure. The prognostic value of such an elevation is not clearly defined, especially in patients with chronic renal failure.      

Significance of right bundle branch block in the diagnosis of myocardial ischemia in patients undergoing coronary artery bypass grafting.

BACKGROUND: Perioperative diagnosis of myocardial ischemia following cardiac surgical procedures remains a challenging problem. Particularly, the role of new conduction disturbances as markers of postoperative ischemia is still questionable. The goal of this study was to elucidate the diagnostic significance of new postoperative right bundle branch block (RBBB) for the detection of perioperative myocardial ischemia in patients undergoing elective coronary artery bypass grafting (CABG). METHODS: In 169 consecutive patients, three-channel Holter monitoring and serial assessment of serum enzymes were performed for 48 h, and 12-lead ECG repeated for up to 5 days postoperatively. Postoperative events were classified as either myocardial infarction (MI), transient ischemic events (TIE) or various conduction disturbances. RESULTS: Transient (n=9) or permanent (n=4) RBBB occurred in 13 patients (8%); 14 patients (8%) showed signs of perioperative MI and 18 patients (11%) evidence of TIE. Peak activity of creatine-kinase (CK, 561+/-135 vs. 316+/-19, P<0.05) and CK-MB (22.7+/-3.2 vs. 13.4+/-0.8, P<0.01) were higher in patients with RBBB than in patients without perioperative ischemic events. Peak CK-MB levels were significantly higher in patients with MI as compared to those with RBBB (33.4+/-7.6 vs. 22.7+/-3.2, P<0. 05). Patients with TIE had similar perioperative enzyme levels as patients with no events. CONCLUSION: It is concluded that the combined assessment of repeated 12-lead ECG, continuous Holter monitoring and enzyme analysis allows a reliable diagnosis of perioperative myocardial ischemia and conduction disturbances. The occurrence of new RBBB following elective CABG is indicative of perioperative myocardial necrosis and thus serves as a valuable tool for the diagnosis of new, perioperative ischemic events.     

Cardiac troponin I release after open heart surgery: a marker of myocardial protection?

Background. Unlike creatine kinase MB isoenzyme, cardiac troponin I (cTnI) is a highly specific marker of myocardial injury. Its release has recently been studied after coronary artery bypass grafting operation. However, its significance after open heart surgery (OHS) remains to be determined. This protein release could be a marker of myocardial protection. We sought to study cTnI release after OHS in patients with normal coronary arteries and to compare it with cTnI release in patients after coronary artery bypass graft (CABG) surgery.

Methods. Eighty-five patients undergoing OHS and 86 patients undergoing CABG were enrolled in the study. CTnI concentrations were measured in serial venous blood samples drawn before surgery and immediately, 12 hours, 24 hours, 48 hours, and 5 days after aortic unclamping.

Results. In the OHS group and in the CABG group without acute myocardial infarction (AMI), cTnI peaked at 12 hours postoperatively (6.35 ± 6.5 and 5.38 ± 8.55 ng/mL, respectively) and normalized on day 5 postoperatively (0.57 ± 2 and 0.72 ± 1.62 ng/mL, respectively). CTnI concentration did not differ significantly between the OHS group and the CABG group in the absence of AMI for any samples considered. In the CABG group, 2 patients had AMI. In the OHS group, cTnI levels at 12 hours postoperatively were found to correlate closely with CPB and aortic cross-clamping (ACC) times, contrary to the CABG group, which correlated only with occurrence of AMI. CTnI release was independent of age and ejection fraction in either group.

Conclusions. cTnI release in patients after OHS with normal coronary arteries has the same profile as cTnI release in patients after CABG in the absence of AMI. However, its peak at 12 hours postoperatively is only correlated to ACC and CPB times, which is contrary to cTnI release after CABG surgery. This observation suggests that cTnI could be a marker of myocardial ischemia after OHS.     

Perioperative myocardial injury after elective open abdominal aortic aneurysm repair predicts outcome.

OBJECTIVE: Myocardial injury, detected by rises in cardiac troponin I (TnI), is common and associated with decreased survival following open AAA surgery. We examined the relationship between perioperative myocardial injury and postoperative outcome. DESIGN: Observational Cohort Study. METHODS: Forty-three consecutive patients who underwent elective open AAA repair were screened for perioperative myocardial injury or infarction using serial TnI measurements (taken on days 1, 3, and 7), ECG and clinical assessment. The primary outcome was survival free of cardiac failure, or myocardial infarction (MI) at follow-up. RESULTS: Twenty (47%) of the 43 patients had a TnI elevation. Of these, 11 (26%) patients met the criteria for MI. At a mean (+/-SD) follow-up of 1.5+/-0.8 years, 12 (28%) subjects had experienced at least one endpoint event. Survival free of cardiac failure or MI was 55% in patients who had TnI rises compared to 87% in those without (P=0.02). Logistic regression revealed that TnI elevation was an independent predictor of outcome with an odds ratio of 5.4 (95% CI 1.2-2.4, P=0.03). CONCLUSION: Perioperative myocardial injury after elective open AAA repair predicts outcome after surgery. Routine TnI measurement should be considered in all patients, especially in those with high cardiovascular risk.     

Strict thermoregulation attenuates myocardial injury during coronary artery bypass graft surgery as reflected by reduced levels of cardiac-specific troponin I

We assessed the cardioprotective effects of perioperative maintenance of normothermia by determining the perioperative profile of troponin I, a highly cardiac-specific protein important in risk stratification of patients with acute ischemic events. Candidates for their primary coronary artery bypass grafting (CABG) were randomized into a new thermoregulation system group, Allon( thermoregulation (AT; n = 30), and a routine thermal care (RTC; n = 30) group. Anesthetic and operative techniques were similar in both groups. Intraoperative warming was applied before and after cardiopulmonary bypass (CPB) and up to 4 h after surgery. Perioperative temperature and hemodynamic data were recorded. Blood samples for creatine kinase (CK) and its isoform, MB (CK-MB), and for cardiac-specific troponin I (cTnI) were obtained at predetermined intervals throughout the entire operation. Core and skin temperatures were higher in the AT group at all time points. The systemic vascular resistance was lower and the cardiac index higher in the AT group at all intra- and postoperative time points. Increases in CK, CK-MB, and cTnI levels indicated intraoperative ischemic insult in all patients. The respective CK levels for the AT and RTC groups were 53.3 +/- 22.7 IU/L and 47.9 +/- 17.86 IU/L at the time of anesthesia and 64.7 +/- 45.6 IU/L and 47.8 +/- 19.4 IU/L 30 min after the onset of surgery, demonstrating thereafter a steep increase before the discontinuation of CPB. CK-MB mass concentrations in both groups behaved almost identically. Pre-CPB cTnI levels at anesthesia induction were 0.3 +/- 0 ng/mL in both groups, followed by a distinctive profile observed after separation from CPB: 28.1 +/- 11.4 ng/mL, 26.05 +/- 9.20 ng/mL, and 22.3 +/- 8.9 ng/mL at discontinuation from CPB, chest closure, and 2 h after surgery, respectively, in the RTC group, versus 0.6 +/- 4.6 ng/mL, 6.6 +/- 5.5 ng/mL, and 7.9 +/- 4.76 ng/mL at these three time points, respectively, in the AT group (P < 0.01 between groups at the specified time points). Contrary to conventional thinking about the benefits of hypothermia, maintenance of normothermia throughout the non-CPB phases during CABG was demonstrated to be important in attenuating myocardial ischemic injury. Insofar as troponin I was more sensitive than other tested markers, it may provide important data on possible protection from myocardial insult and on other cardioprotective measures.     

Troponin I sensitivity and specificity for the diagnosis of acute myocardial infarction

This article describes the sensitivity and specificity of troponin I when compared to creatine kinase-MB (CK-MB) and electrocardiography (ECG) for diagnosing acute myocardial infarction (AMI). Two different lower levels for defining positive results with troponin I were evaluated. A retrospective study of 153 patients who presented to the emergency department of a community hospital supplied the pool of patients for this study. Patients included in this study were those for whom a CK-MB was ordered. The majority of these patients were evaluated for chest pain or symptoms suggesting an acute cardiac event. Of the 153 patients studied, CK-MB results were positive in 91 (59%) patients; ECG revealed AMI in 72 (47%) patients. There were 103 (67%) patients who had either positive CK-MB or ECG results. Ninety (59%) patients had a troponin I level greater than 2.0 ng/mL, and 18 (12%) patients had a troponin I level between 0.6 and 2.0 ng/mL. Seven patients whose troponin I level was between 0.6 and 2.0 ng/mL had negative CK-MB and ECG results. Therefore, 11 patients with troponin I between 0.6 and 2.0 ng/mL had AMI. Five patients with positive troponin I results (> 2.0 ng/mL) had negative CK-MB and ECG results. When a troponin I level greater than 0.6 ng/mL was used as a positive value, compared to CK-MB and ECG using either time zero or time 6 hours, the sensitivity was 94% and specificity was 81%. When troponin I greater than 2.0 ng/mL was used to define a positive test, the sensitivity was 85% and specificity was 91% when compared to CK-MB and ECG.     

Cardiac troponins have no prognostic value for acute and chronic cardiac events in asymptomatic patients with end-stage renal failure

BACKGROUND: Cardiovascular diseases determine overall mortality in patients with end-stage renal failure. Therefore, testing for myocardial ischemia is important. Elevation of cardio-specific troponins have been frequently measured in patients with end-stage renal failure. Thus, we studied systematically whether patients on chronic intermittent hemodialysis without overt coronary heart disease have increased serum levels of cardiac troponin T and cardiac troponin I. After 2 years, the patients were screened again for cardiac events. METHODS AND RESULTS: The patients had no history of angina during the previous 3 months or myocardial infarction (MI) within the previous 2 years. For analysis we used two cardio-specific assays for troponin T as well as for troponin I and compared the results with the CK-MB concentration. In a number of patients serum concentrations were elevated above the reference range as follows: troponin T rapid bedside assay: 41 of 100 patients, troponin I rapid bedside assay: 27 of 100 patients, quantitative measurement oftroponin T: 22 of 100 patients, quantitative measurement oftroponin I: 7 of 100 patients, CK-MB: 2 of 100 patients. The increased serum levels of cardiac troponins were neither the result of uremic perimyocarditis (pericardial effusion), changes in the hemodialysis regimen, pulmonary congestion nor were they consistent with the etiology of renal failure. None of the patients with an elevated troponin level in either of the test suffered from any acute cardiac event initially. Within 2 years 18 of 100 patients died, 13 out of them because of cardiac events. Fourteen patients had a myocardial infarction and 19 patients developed angina pectoris. Sensitivity and specificity (0.75 and 0.67) of troponin T rapid bedside assay for MACE (angina pectoris, MI, cardiac death) was lower compared to studies in patients with normal renal function. Correlation between troponin elevation and late outcome was low or absent. CONCLUSION: Patients on chronic intermittent hemodialysis frequently present with elevated TnT and TnI levels which cannot be used as predictors of acute and chronic cardiac events. Rapid bedside assays have a lower specificity than quantitative assays.     

Influence of normothermic systemic perfusion temperature on cold myocardial protection during coronary artery bypass surgery.

OBJECTIVE: To determine the effect of normothermic systemic perfusion on myocardial injury when using cold cardioplegic techniques in patients undergoing coronary artery bypass surgery. METHOD: Sixty six patients with stable angina pectoris were prospectively randomized into three groups according to cardiopulmonary bypass temperature: hypothermia (28 degrees C, n = 22), moderate hypothermia (32 degrees C, n = 22) and normothermia (37 degrees C, n = 22). All patients received cold antegrade crystalloid cardioplegia and topical cooling with saline at 4 degrees C. Serum samples were collected for troponin T and I estimation preoperatively, 4 hours after removal of the aortic cross clamp, and 12, 24, 36 and 48 hours postoperatively. In addition, serial electrocardiographic studies were undertaken on days 1, 3 and 5. RESULTS: Patients were similar with regard to preoperative and intraoperative characteristics Four patients showed ECG changes typical of perioperative myocardial infarction but remained clinically well (28 degrees C, one; 32 degrees C, one; 37 degrees C, two). In the remaining 62 patients, serum troponin T increased significantly from a mean baseline value of 0.02 ng/ml to 1.5+/-0.9 ng/ml 4 hours after removal of the aortic cross-clamp (P<0.0001). Similarly, troponin I increased from 0.06 ng/ml to 0.63+/-0.47 ng/ml 12 hours after reperfusion (P<0.0001). Serum concentrations of both markers subsequently declined with time but remained higher than preoperative values at 48 hours. There were no differences between the three groups with respect to peak and cumulative serum troponin release. Normothermic cardiopulmonary bypass did not compromise the efficacy of cold myocardial protection when assessed by serum troponin concentrations in low risk patients undergoing coronary revascularization.     

How silent is perioperative myocardial ischemia? A hemodynamic, electrocardiographic, and biochemical study in patients undergoing coronary artery bypass graft surgery

OBJECTIVE: To analyze the relationship among Holter electrocardiogram (ECG) recordings, hemodynamic measurements indicative of global myocardial oxygen balance, and serum cardiac troponin I concentrations (cTnI) in the early postoperative period after coronary artery bypass graft (CABG) surgery. DESIGN: Prospective observational study. SETTING: University teaching hospital. PARTICIPANTS: Thirty patients undergoing CABG surgery. INTERVENTIONS: ECG measurements consisted of Holter and standard ECG recordings. Hemodynamic measurements included heart rate, systolic and diastolic blood pressure (SBP, DBP), pulmonary capillary wedge pressure, and cardiac index (CI). Derived indices included tension time index (TTI), rate-pressure product, pressure work index (PWI), and endocardial viability ratio (EVR). Serial measurements of cTnI concentrations were measured postoperatively; the area under the cTnI concentration time curve was calculated for each patient (AUC cTnI). MEASUREMENTS AND MAIN RESULTS: Episodes of myocardial ischemia were associated with small but significant rises in SBP (p = 0.01), DBP (p = 0.001), and TTI (p = 0.005) compared with periods without ischemia in the same patients. Serum cTnI concentrations 24 hours after cardiopulmonary bypass (p = 0.03) and AUCcTnI (p = 0.01) values were greater in patients who developed ECG myocardial ischemia compared with patients who did not. CONCLUSIONS: The small changes in hemodynamics seen, although statistically significant, are unlikely to be the primary cause of the ischemia. They more likely reflect an independent process that causes or occurs as a result of ischemic episodes. Ischemic episodes detected by the Holter monitor are associated with significant release of cardiac troponin from the myocardium.     

Do we still need CK-MB in coronary artery bypass grafting surgery?

AIM: The aim of this study was to evaluate the role of cardiac Troponin I (cTnI) and CK-MB for early prediction of outcome of patients undergoing coronary artery bypass grafting (CABG) surgery. METHODS: In 134 consecutive patients undergoing CABG-surgery blood samples were analyzed for cTnI concentration and CK-MB activity. ECG, hemodynamic parameters and the need for inotropic support, were continuously registered. Patients were divided into group A (uneventful course), group B (ischemia by ECG, hemodynamic stability) and group C (ischemia by ECG and IABP). RESULTS: After removal of X-clamp an increase cTnI and CK-MB was observed in all patients. Five hrs after stop of CPB group A (8.3+/-4.2 microg/L) had lower cTnI values compared to group B (14.8+/-5.3 microg/L) (p=0.035) and C (54+/-22.8 microg/L) (p=0.023). The cut off value was 14.8 microg/L. Sensitivity and specificity (99%/97%) was higher for cTnI than for CK-MB (90%/30%). The positive predictive value of outcome was better for cTnI (86%) than for CK-MB (33%). CONCLUSION: CTnI is a specific and sensitive marker for evaluation of perioperative myocardial ischemia (PMI). Additional determination of CK-MB activity does not provide further clinical information. CTnI should be the marker of first choice in CABG surgery.     

The risk of cardiac injury during laparoscopic fundoplication: cardiac troponin I and ECG study

BACKGROUND: Myocardial trauma has been described during gastroesophageal reflux laparoscopic surgery, in association with the proximity of cardiac structures. In addition, specific haemodynamic changes induced by CO2 pneumoperitoneum could exacerbate perioperative cardiac complication even in patients without cardiac risk factors. The aim of this study was to evaluate the influence of gastroesophageal reflux laparoscopic surgery on the perioperative ECG, cardiac troponin I and myocardial enzyme changes. METHODS: Forty-two ASA I-II patients without ischaemic heart disease or combined double-risk factors were studied. Automated ST segment analysis was used intraoperatively. ECG, plasma myocardial enzyme and cardiac troponin I concentrations were reported on arrival in the recovery room (HO), 4 h (H4) and 24 h (H24) postoperatively. RESULTS: Intraoperative ST segment changes occurred in two patients: the first during a hypotensive episode (MAP<55 mmHg; 3/42 patients) and the second during a hypertensive episode (MAP >110 mmHg; 3/42 patients). One case of intraoperative subcutaneous emphysema occurred without ST disturbance. One case of pneumothorax was observed at H0-H4 in another patient without clinical symptoms. Cardiac troponin I and CK-MB were not increased postoperatively. Transaminase concentrations increased (2-fold normal values) in 26/42 patients. In these 26 patients, 7 experienced 5-fold isolated transaminase increase, associated with left hepatic artery section. CONCLUSION: According to perioperative ECG changes and/or specific cardiac troponin I measurements, we did not identify specific myocardial damage following gastroesophageal reflux laparoscopic surgery. Unexpectedly, the incidence of hepatic cytolysis was frequent (62%) and has not previously been reported in the literature.     

Intermittent cardiac troponin-I screening is an effective means of surveillance for a perioperative myocardial infarction

OBJECTIVE: Several studies suggest that cardiac troponin-I (cTn-I) is a more sensitive indicator of cardiac injury compared with other biochemical markers of injury, but the strategy with the highest diagnostic yield (true positive and true negative) for perioperative surveillance is unknown. The authors undertook a prospective evaluation of the perioperative incidence of myocardial infarction (MI) and evaluated surveillance strategies for the diagnosis of MI. DESIGN: Prospective, cohort study. SETTING: Two university hospitals. PARTICIPANTS: Four hundred sixty-seven high-risk patients requiring noncardiac surgery. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The diagnosis of myocardial injury was determined by cardiac protein markers combined with either postoperative changes on 12-lead electrocardiography or 1 of 3 clinical symptoms consistent with MI (chest pain, dyspnea, requirement for hemodynamic support). A receiver operating characteristic curve evaluating troponin in the diagnosis of MI revealed a value of 2.6 ng/mL as having the highest sensitivity and specificity. The sensitivity and specificity of cTn-I value > or =2.6 ng/mL, troponin > or =1.5 ng/mL, total creatine kinase (CK) > or =170 IU/L with MB > or =5%, and CK-MB > or =8 ng/mL were compared. Surveillance strategies were determined on a subset of patients (n = 257). The incidence of MI was 9.0% by cTn-I > or =2.6 ng/mL criteria, 19% by cTn-I > or =1.5 ng/mL, 13% by CK-MB mass, and 2.8% by CK-MB%. The specificity of cTn-I > or =2.6 ng/mL as an indicator of MI was 98%, and its positive predictive value (PPV) was 85%. Cardiac troponin-I > or =2.6 ng/mL had equal specificity but greater PPV than the cTn-I > or =1.5 ng/mL (specificity 98% and PPV 79%). If surveillance of cTn-I > or =2.6 ng/mL was used to detect MI, then the strategy with the highest diagnostic yield was surveillance on postoperative days 1, 2, and 3. CONCLUSIONS: Perioperative cardiac injury continues to occur frequently after noncardiac surgery, as detected by cTn-I. Serial monitoring of cardiac troponin-I on postoperative days 1, 2, and 3 provides the strategy with the highest diagnostic yield for surveillance of MI.     

Perioperative myocardial cell injury: the role of troponins

Early recognition of minor myocardial cell injury and appropriate treatment may prevent development of myocardial infarction as one of the most severe postoperative cardiac complications. Troponins have been shown to be sensitive biochemical markers for the assessment of myocardial cell injury. We investigated prospectively 67 cardiac risk patients undergoing elective non-cardiac surgery. Troponin T (TNT) concentrations were measured during the perioperative period, and in those patients with increased TNT (cut-off 0.2 ng ml-1), troponin I (TNI) concentrations were measured additionally (cut-off 0.6 ng ml-1). Patients were allocated to one of three groups: group I, all patients with normal TNT concentrations had a good cardiac outcome (80.5%). In those patients with increased TNT concentrations (19.5%) TNI was also positive; group II, patients (8.8%) with only slightly increased TNT concentrations (0.32-0.99 ng ml-1) also had a good outcome, indicating minor myocardial cell injury, whereas patients with cardiac complications (11.9%) had higher TNT concentrations (0.47-9.8 ng ml-1) (P < 0.05) (group III). With a TNT cut-off at 0.2 ng ml-1, the positive predictive value for adverse outcome was 61.5%; the negative predictive value was 100%. With a TNT cut-off at 0.6 ng ml-1, the positive predictive value for adverse outcome increased to 87.5%, but the negative predictive value was still high (98%). Most of the patients showed an increase in TNT content from the day of surgery until the third postoperative day. We conclude that serial troponin measurements during the perioperative period identify pre-, intra- and postoperative myocardial cell injury. The concentration of troponin T may reflect the degree of injury and help categorize the subsequent risk.      

The Concordance of Intraoperative Left Ventricular Wall-motion Abnormalities and Electrocardiographic S-T Segment Changes: Association with Outcome after Coronary Revascularization

Background: Transesophageal echocardiography (TEE) and Holter electrocardiography (ECG) are used to detect intraoperative ischemia during coronary artery bypass graft surgery (CABG). Concordance of these modalities and sensitivity as indicators of adverse perioperative cardiac outcomes are poorly defined. The authors tried to determine whether routine use of Holter ECG and TEE in patients with CABGs has clinical value in identifying those patients in whom myocardial infarction (MI) is likely to develop.

Methods: A total of 351 patients with CABG and both ECG-and TEE-evaluable data were examined for the occurrence of ischemia and infarction. The TEE and five-lead Holter ECGs were performed continuously during cardiac surgery. The incidence of MI (creatine kinase-MB >or= to 100 ng/ml) within 12 h of arrival in the intensive care [ICU] unit, new ECG Q wave on ICU admission or on the morning of postoperative day 1, or both, were recorded.

Results: Electrocardiographic or TEE evidence of intraoperative ischemia was present in 126 (36%) patients. The concordance between modalities was poor (positive concordance = 17%; Kappa statistic = 0.13). Myocardial infarction occurred in 62 (17%) patients, and 32 (52%) of them had previous intraoperative ischemia. Of these, 28 (88%) were identified by TEE, whereas 13 (41%) were identified by ECG. Prediction of MI was greater for TEE compared with ECG.     

Cardiac troponin I versus creatine kinase-MB in the detection of postoperative cardiac events after coronary artery bypass grafting surgery

AIM: Several studies suggest that postoperarive concentrations of cardiac troponin-I (cTnI) may increase in patients undergoing aorto-coronary bypass grafting (CABG). The degree and pattern of release appears to be associated with perioperative myocardial damage. METHODS: This was a prospective observational study with serial sampling conducted at the Departments of Cardiothoracic Surgery and Anesthesiology, University Hospital of Ioannina, Ioannina, Greece. The levels of cTnI and creatine kinase-MB (CK-MB) preoperatively, upon admission to the intensive care unit and at 12, 24, 36 and 48 hours after surgery, as well as daily from postoperative days 3-7 were determined in 41 consecutive patients (33 males and 8 females, aged 64.8+/-6.1 years) who underwent CABG with cardiopulmonary bypass. The Authors compared the patterns and variation of cTnI and creatine kinase (CK)-MB after CABG in patients with or without postoperative cardiac events (PCEs). RESULTS: Eleven patients experienced a PCE (postoperative ventricular and supraventricular arrhythmia, need for intra-aortic balloon pump (IABP) for >12 hours, or postoperative myocardial infarction, [MI]). In patients without PCE the elevation of cTnI peaked at 24 hours after surgery, while in patients with PCE maximal values of cTnI occurred after 36 hours. CTnI levels correlated with CK-MB after the procedure. Receiver-operating characteristic (ROC) curve analysis indicated that cTnI is superior to CK-MB with regard to PCE diagnosis following CABG (area under the ROC curve, 0.73, 95% CI (0.53-0.93) versus 0.54, 95% CI, (0.25-0.83). CONCLUSION: CTnI seems to be more valuable compared to CK-MB in the detection of PCEs in patients undergoing coronary surgery.     

Determinants of myocardial infarction following emergency coronary artery bypass for failed percutaneous coronary angioplasty

Acute myocardial ischemia during percutaneous transluminal coronary angioplasty (PTCA) often necessitates emergency coronary artery bypass grafting (CABG) and can result in myocardial infarction (MI). This study was undertaken to determine what factors might predispose to MI following emergency CABG for failed PTCA. Since 1980, 24 patients at Boston University Medical Center have undergone emergency CABG following failed PTCA. In 15 patients (63%), there was postoperative evidence of an MI shown by either ECG or enzyme criteria. Variables that predisposed to a perioperative MI (p less than 0.05) included multivessel PTCA, the presence of multiple vessels with 50% stenosis or more, multivessel CABG, and the presence of new ECG changes immediately following failed PTCA. Variables that did not discriminate between the two groups included age, sex, the specific vessel involved during PTCA, or a previous history of MI. The presence of coronary collaterals did not decrease the incidence of MI. This study suggests that patients with multiple major coronary stenoses in whom acute ECG changes develop following failed PTCA are more likely to sustain a perioperative MI following emergency CABG.     

Warm and tepid cardioplegia: do they provide equal myocardial protection?

BACKGROUND: Cardiac troponin I (CTnI) has been shown to be a marker of myocardial injury. The aim of this prospective, randomized study was to compare intermittent antegrade warm cardioplegia with tepid blood cardioplegia in patients undergoing first elective coronary artery bypass graft, using CTnI release as the criterion for evaluating the adequacy of myocardial protection. METHODS: Seventy patients were randomly assigned to one of two cardioplegia groups. CTnI concentrations were measured in serial venous blood samples drawn immediately before cardiopulmonary bypass and after aortic unclamping at 6, 9, 12, and 24 hours. Analysis of covariance with repeated measures was performed to test the effect of the type of cardioplegia and time on CTnI concentration. RESULTS: The total amount of CTnI released (8.23 +/- 20.5 microg in the warm group and 3.19 +/- 2.4 microg in the tepid group) was not statistically different (p = 0.23). The CTnI concentration did not differ for any sample in either of the two groups when adjusted on ejection fraction and the number of preoperative myocardial infarctions (p = 0.06). No patient in the tepid group versus 4 patients in the warm group showed CTnI evidence of perioperative myocardial infarction (p = 0.12). CONCLUSIONS: Our study showed no preference for warm or tepid cardioplegia in terms of myocardial protection, either for clinical or biological data.     

Determination of troponin I release after CABG surgery

BACKGROUND: Troponin I is used to diagnose myocardial infarction (MI). Its use and pattern of elevation is not well defined in coronary artery bypass graft (CABG) surgery. This study assessed the timing of troponin I elevation in patients undergoing urgent CABG. METHOD: Patients undergoing urgent isolated-CABG with cardiopulmonary bypass were studied prospectively. Blood samples were taken to measure CK, CK-MB, and troponin I: preoperatively, 7 hours postoperatively, 14 to 18 hours postoperatively, 30 to 48 hours postoperatively, and on postoperative day 4. Electrocardiograms and in-hospital course were recorded. Perioperative MI (PMI) was defined by either (i) ECG criteria of new Q-waves in the presence of CK-MB elevation >50 microg/L or (ii) CK-MB > 100 microg/L. RESULTS: Of the 50 patients studied, 6 met the criteria for PMI (12%); 2 by criteria (i) and 4 by criteria (ii). In patients not meeting the criteria for MI the troponin I level peaked at 7 hour post-op with a mean of 20.97 microg/L (95% CI, 17.11 to 24.83). At this time, patients who met the criteria for MI had a mean troponin I level of 46.85 microg/L (95% CI, 36.40 to 57.30). Of variables investigated for the 44 patients who did not meet MI criteria, only preoperative troponin I level impacted peak postoperative troponin I. CONCLUSIONS: CABG elevates troponin I far beyond current diagnostic benchmarks without the clinical occurrence of a MI and appears to peak during the second postoperative day. An elevated preoperative troponin I may predict an elevated peak postoperative troponin I in patients who do not have a PMI.