|
|
||||||||
Eur J Cardiothorac Surg 2004;25:1001-1005
© 2004 Elsevier Science NL
a Department of Cardiovascular Anesthesia, IRCCS San Raffaele Hospital of Milan, Via Olgettina, 60, 20132 Milan, Italy
b Department of Cardiac Surgery, IRCCS San Raffaele Hospital of Milan, Milan, Italy
c Department of Mathematics, University of Milan, Milan, Italy
Received 18 November 2003; received in revised form 24 February 2004; accepted 25 February 2004.
* Corresponding author. Tel.: +39-02-2643-7154/7164/4524; fax: +39-02-2643-7178/7155
e-mail: landoni.giovanni{at}hsr.it
| Abstract |
|---|
|
|
|---|
Key Words: Myocardial infarction Cardiac surgery Electrocardiogram Q wave Troponin Creatinekinase
| 1. Introduction |
|---|
|
|
|---|
We investigated the clinical significance and the prognostic value of new Q-waves and the elevation of cardiac biomarkers after cardiac surgery.
| 2. Materials and methods |
|---|
|
|
|---|
|
40 ms in at least two adjacent leads; the loss of R wave amplitude in precordial leads was considered a Q wave equivalent when greater than 50%. Blood samples were drawn at the same time as ECG recording to assay levels of cardiac Troponin I (cTnI) and Creatine Kinase subfraction MB (CK-MB). CTnI and mass CK-MB were analyzed with Dimension X Pand (Dade-Bohering diagnostics). Biochemical markers cut-off values were based on the routine criteria currently employed at our Institute (CK-MB>40 ng/ml and cTpI>11 ng/ml). Peak biomarker release was considered for analysis.
We defined a cardiac event as the occurrence of low output syndrome (CI<2 l/min/m2) secondary to ventricular dysfunction requiring high doses inotropes (>0.05 ug/kg/min) or intra-aortic balloon pumping for more than 24 h.
2.1. Statistical analysis
Data are expressed as percentages, as mean ±1 standard deviations or as median (25th75th percentiles). A logistic regression analysis with two independent variables (Q waves+one biomarker) was performed among patients who developed cardiac events or had a benign cardiac course to evidence the capability of cardiac biomarkers and new Q waves to predict adverse cardiac events. For each marker studied, ROC curves were constructed by plotting sensitivity against (1-specificity) for cardiac events [5]. ROC curves were repeated for the combined (Q wave+one biomarker) rules. The capacity of the cardiac biomarker of predicting cardiac events (in presence or absence of a new Q wave) was calculated. All analysis were repeated for both cardiac biomarkers (cTnI, CK-MB). Data were analyzed by use of SAS software, version 8 (SAS Institute).
| 3. Results |
|---|
|
|
|---|
Peak enzyme levels were above our predefined cut-off values in 72 patients for cTnI and in 92 patients for CK-MB. Cardiac biomarker release is shown in Table 2 and patients outcome in Table 3.
|
|
The study population was divided therefore into four groups according to the presence or absence of new Q-waves and peak cardiac marker elevations. Each group (Figs. 1 and 2) was analyzed for postoperative cardiac events. The total number of cardiac events was 25. The concomitant presence of the study criteria defined an incidence of postoperative cardiac events of 75% with CK-MB, and of 85.7% with cTnI.
|
|
In two cases (both valvular patients) the ECG changes disappeared on the first postoperative day (transient Q-wave) and the remaining isolated new Q-waves (all 5 patients underwent CABG) were associated with an anamnestic non-Q infarction and chronic occlusion of the posterior descending artery.
The logistic regression analysis with two independent variables (Q waves+one biomarker) was performed. In the Q wave+MB model: MB (OR 1.01 C.I. 1.0051.024 per unit P=0.003); new Q wave (OR 5.7 95% CI, 1.719.4 P=0.005). In the Q wave+cTnI model: cTnI (OR 1.07 95% CI, 1.031.12 P=0.001); new Q wave (OR 6.5 95% CI, 2.021.3 P=0.002).
For each biochemical marker, we performed ROC curve analyses for the prediction of cardiac events. These curves were constructed for the whole cohort of patients. For each marker, a cut-off value above which cardiac event was likely, was determined from the ROC curves (Figs. 3 and 4) through an attempt to identify the best compromise between sensitivity and specificity (MB 44 mg/ml: Sensitivity 0.77, 1-Specificity 0.34) (cTnI 10.3 mg/ml: Sensitivity 0.77, 1-Specificity 0.32). These results were very close to our prespecified cut-off level and in accordance to literature [6]. The ROC curves were repeated for the combined (Q wave+one biomarker) rules without significant increases of specificity and sensitivity: MB Sensitivity 0.76, 1-Specificity 0.32; cTnI Sensitivity 0.77, 1-Specificity 0.31. MB>44 mg/ml predicted 35% of cardiac events when in combination with a new Q wave and 8% of cardiac events when no Q wave appeared. CTnI>10.3 mg/dl predicted 38% of cardiac events in combination with a new Q wave and 9% of cardiac events when no Q wave appeared.
|
|
| 4. Discussion |
|---|
|
|
|---|
The European Society of Cardiology and the American College of Cardiology suggested troponin as the preferred indicator of cardiac injury, but its elevation does not define the mechanism of cardiac injury in the specific context of cardiac surgery [7]. In fact, cardiac surgery can cause myocardial cellular damage with mechanisms different from infarction: focal trauma by heart manipulation, diffuse ischemia for inadequate myocardial protection, air embolism in the coronary arteries or vein grafts, atriotomy, pericardiectomy, direct electrical cardioversion, myocardial stunning.
Nonetheless, irrespectively of the cause, a high postoperative peak of cTnI is associated with increased risk of death, death from cardiac causes, and nonfatal cardiac events within 2 years after coronary artery bypass grafting [8]; in addition cTnI concentration measured 20 h after the end of surgery is an independent predictor of in-hospital death after cardiac surgery and elevated concentrations of cTnI are associated with a cardiac cause of death and with major postoperative complications [9].
For decades the appearance of a new Q wave identified the occurrence of a new postoperative myocardial infarction [1]. Chaitman et al. analyzing data of 1340 patients included in the Coronary Artery Surgery Study, noticed a worsening of medium and long term outcome with the appearance of new Q waves [2]. These initial experiences make the clinicians identify PMI with new Q-waves.
More recent trials showed no correlation between Q-waves and poor cardiac prognosis [3,4,10,11].
Hodakowski et al. demonstrated that a postoperative Q-wave is not frequently associated to angiographic, ecocardiographic, enzymatic and clinical data of myocardial infarction [12].
In our study, patients with isolated ECG findings had an uneventful postoperative course; on the contrary, when these ECG changes were coupled with elevated peak myocardial necrosis biomarker release, patients had an impaired postoperative course requiring prolonged inotropic and/or mechanical circulatory support.
In accordance with Svedjeholm, nearly half Q-waves after cardiac surgery in our population were not related to tissue damage; in 50% of cases they were not associated to an increase of CK-MB or cTpI [6].
New Q wave was transient in two valvular cases, suggesting an etiologic role for coronary air embolism after aortic cross clamp release: their disappearance may be explained by the resolution of stunned myocardium [1317].
The remaining cases of isolated Q-wave appeared after CABG surgery; and all these patients had an anamnestic non-Q myocardial infarction and chronic occlusion of the posterior descending artery. In these cases, according to literature, we speculate that the decreased anteroapical electrical forces before operation (secondary to ischemia) cancelled the loss of opposing forces of the infarcted inferior wall; after operation, with relief of anterior ischemia by left internal mammary artery to left anterior descending artery bypass grafting, anterior electrical forces were augmented and preexisting inferior infarction unmasked [18].
Limitation of the study: the study population is rather low with only 15 Q waves studied in a selected population of patients with EF
35%; furthermore no transesophageal or coronary findings are reported.
In conclusion, our study confirms that nearly half new Q-waves appearing after cardiac surgery are not associated with major myocardial tissue damage and have little influence on short term outcome in a population with EF
35%; therefore, the use of Q wave criteria alone as the gold standard for the diagnosis of postoperative myocardial infarction is questionable as myocardial stunning and Q-wave unmasking could have a predominant role in this setting. In contrast, the association of electrocardiographic alterations and augmentation of enzymatic biomarkers is strongly associated to postoperative cardiac events.
| Acknowledgments |
|---|
All the Acknowledged RN are from the Cardiovascular Intensive Care Unit, IRCCS San Raffaele Hospital of Milan. Via Olgettina 60, 20132 Milan, Italy.
| References |
|---|
|
|
|---|
This article has been cited by other articles:
![]() |
A. Espinoza, P. S. Halvorsen, L. Hoff, H. Skulstad, E. Fosse, H. Ihlen, and T. Edvardsen Detecting myocardial ischaemia using miniature ultrasonic transducers -- a feasibility study in a porcine model Eur. J. Cardiothorac. Surg., January 1, 2010; 37(1): 119 - 126. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. A. Lurati Buse, M. T. Koller, M. Grapow, C. M. Bruni, J. Kasper, M. D. Seeberger, and M. Filipovic 12-month outcome after cardiac surgery: prediction by troponin T in combination with the European system for cardiac operative risk evaluation. Ann. Thorac. Surg., December 1, 2009; 88(6): 1806 - 1812. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. S. Halvorsen, L. A. Fleischer, A. Espinoza, O. J. Elle, L. Hoff, H. Skulstad, T. Edvardsen, and E. Fosse Detection of myocardial ischaemia by epicardial accelerometers in the pig Br. J. Anaesth., January 1, 2009; 102(1): 29 - 37. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Simon, F. Capuano, A. Roscitano, U. Benedetto, C. Comito, and R. Sinatra Cardiac Troponin I vs EuroSCORE: Myocardial Infarction and Hospital Mortality Asian Cardiovasc Thorac Ann, April 1, 2008; 16(2): 97 - 102. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. Paparella, G. Cappabianca, P. Malvindi, A. Paramythiotis, A. Galeone, N. Veneziani, C. Fondacone, and L. de Luca Tupputi Schinosa Myocardial injury after off-pump coronary artery bypass grafting operation Eur. J. Cardiothorac. Surg., September 1, 2007; 32(3): 481 - 487. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Chieffo, N. Morici, F. Maisano, E. Bonizzoni, J. Cosgrave, M. Montorfano, F. Airoldi, M. Carlino, I. Michev, G. Melzi, et al. Percutaneous Treatment With Drug-Eluting Stent Implantation Versus Bypass Surgery for Unprotected Left Main Stenosis: A Single-Center Experience Circulation, May 30, 2006; 113(21): 2542 - 2547. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. Paparella, G. Cappabianca, G. Visicchio, A. Galeone, A. Marzovillo, N. Gallo, C. Memmola, and L. d. L. T. Schinosa Cardiac Troponin I Release After Coronary Artery Bypass Grafting Operation: Effects on Operative and Midterm Survival Ann. Thorac. Surg., November 1, 2005; 80(5): 1758 - 1764. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |