The release of creatine phosphokinase enzymes (CPK), CK-MB isoenzyme (CK-MB), cardiac troponin, or both, in the absence of ECG waves indicating necrosis during percutaneous or surgical procedures has occurred in 10 to 35 % of cardiac patients. These indices are considered diagnostic for acute myocardial infarction (AMI) [1, 2]. Such results are important, because they are similar to those found during spontaneous cardiac events in the population of patients with coronary artery disease (CAD) [3]. The release of enzyme markers of myocardial cells allows the diagnosis of AMI, when the levels of CK-MB or troponin are elevated up to 3 times above the established standard for percutaneous interventions (PCI) and up to 5 times for surgical revascularization (CABG) even in the absence of electrocardiographic changes or clinical symptoms [4, 5]. On the other hand, these indices, considered indicative of AMI, have prognostic value according to the severity of the patient and the procedure performed. In this scenario, the prognosis for this event can be associated with the degree of elevation of biomarkers released and with the type of intervention applied. Also included in the prognosis of the condition are the number of arteries involved, the degree of arterial and ventricular impairment, and the type of intervention performed.

However, both invasive and noninvasive investigations during the period after the intervention have limitations related to the poor the sensitivity and specificity of the ECG and biomarkers. Although cardiac-specific biomarkers potentially have the greatest role in simple detection of myocyte necrosis, their independent utility in this setting remains inaccurate.

To increase the diagnosis, the accuracy of delayed enhancement CMR imaging (DE-CMR) can quantify reversible and irreversible myocyte necrosis.

In fact in recent studies, Pegg et al. [6] reported increased cardiomyocyte necrosis associated with the hybrid technique of on-pump beating-heart CABG both detected by DE-CMR and biomarkers. In this study, the authors had as an end point the effectiveness of biomarkers troponin I (TnI) and creatine kinase-MB isoform (CK-MB) and compared these with CMR to diagnose AMI.

Moreover, these authors evaluated the efficacy of cardiac enzymes for determination of cardiomyocyte necrosis after CABG and compared this with the efficacy of CMR [7].

In the MASS-V study, we will prospectively examine the incidence and extent of new DE-CMR-defined irreversible injury in patients undergoing PCI or CABG and correlate it with postprocedural changes in TnI and CK-MB. Our hypothesis is that the releasing of biomarkers does not necessarily leads to myocardial fibrosis or left ventricular dysfunction; and the cut-off levels to define periprocedural AMI would be different from the ones established in current guidelines.

The MASS-V Trial is an institutional project that the Heart Institute (InCor), Hospital das Clinicas, University of São Paulo designed to prospectively investigate 150 patients with multivessel coronary artery disease (CAD) with normal left ventricle ejection fraction (LVEF) and with a formal indication for CABG or PCI. Fifty patients will be operated on with cardiopulmonary bypass (CPB) and another 50 patients with the same arterial and ventricular conditions and also with a proper indication for myocardial revascularization will be operated on without the help of the CPB circuit. Another 50 patients with CAD and preserved ventricular function with a formal indication for percutaneous coronary intervention (PCI) with the use of intracoronary "stents” will be analyzed.

The inclusion criteria will determine which patients are eligible for which of the three procedures. Anginal symptoms must be stable and the LVEF preserved. The main steps of the procedures are shown in Figure 1. Exclusion criteria include the following: recent myocardial infarction (≤6 months); signs of manifest or suspected infections or rheumatologic disease activity; chronic renal failure (creatinine level >2.0 mg/dL); recent (≤ 6 months) pulmonary embolism or venous thromboembolism; not signing the consent form; contraindication for the use of glycoprotein IIb/IIIa inhibitors or CMR examination, for example, a person with a pacemaker or severe claustrophobia.

All patients will undergo CMR before and after surgical or percutaneous interventions to determine the presence or absence of myocardial necrosis complications after the procedure.

In addition, we will be evaluating the release of cardiac necrosis markers immediately before and after each procedure. The measurement of necrosis markers in the series will be conducted 6, 12, 24, and 36 hours after the percutaneous intervention. For the surgical procedures, dosage series will expand from 48 to 72 hours.

The release of biomarkers of myocardial necrosis occurs in most patients who undergo mechanical interventions of the heart, both CABG and PCI. Among the causes of this release are the trauma caused by the handling organ, contact of blood with the bypass circuit, aortic cross clamping, and reperfusion injury. On the other hand, periprocedural myocardial injury during PCI can result from procedural complications, such as distal embolization, side-branch occlusion, coronary dissection, and disruption of collateral flow.

The clinical significance and long-term prognosis of this condition continues to be debated. Initial short-term follow-up found no increase in the incidence of cardiac events; however, further large prospective trials have suggested that elevation of biomarkers of myocardial necrosis after PCI or CABG is clinically relevant. In addition, outcomes after CABG or PCI with very high procedural TnI or CK-MB levels have prognostic implications considered similar to those of spontaneous acute myocardial infarction.

Delayed enhancement CMR imaging can quantify irreversible myocyte necrosis for the identification of subedocardial infarction.

However, uncertainties remain about the mechanisms and functional significance of the release of cardiac biomarkers and the direct relationship between procedure-related troponin and CK-MB increase and the degree of myocardial tissue loss.

Steering Committee Members, Whady Hueb, Bernard J Gersh, Eduardo Gomes Lima, Cibele Larrosa Garzillo, Rosa Maria Rhami Garcia, Paulo Cury Rezende, Pedro Lemos, Expedito Ribeiro, Célia Cassaro Strunz, Fabio B Jatene, Noedir A G Stolf, José A F Ramires, Roberto Kalil Filho. Cardiology Committee, Whady Hueb, Eduardo Gomes Lima, Cibele Larrosa Garzillo, Paulo Cury Rezende, Fernando Teiichi Costa Oikawa, Rodrigo Morel Vieira de Melo, Leandro Menezes Alves da Costa, José A F Ramires, Roberto Kalil Filho. Hematologic Disorders Committee, Dalton A F Chamone, Roberto Abi-Rached, Alexandre Costa Pereira. Endocrinologist Committee, Rosa Maria Rhami Garcia, Raul Maranhão, Célia Cassaro Strunz. Cardiac Imaging Techniques Committee, Cesar Nomura, José Rodrigues Parga Filho, Luiz Francisco Rodrigues de Ávila, Alexandre Volney Villa. Electrocardiography and exercise stress testing Committee, Willian Chalela, Augusto H Uchida. Interventional Committee, Expedito Ribeiro, Pedro Lemos, Marco A Perin Alexandre Ciappina Hueb. Cost-effectiveness and Quality of Life Committee, Myrthes E Takiuti, Priscyla Girardi, Marcela F Silva, Ana Luiza Oliveira Carvalho, Teryo Nakano. Ancillary Studies Committee, Cesar Nomura, Alexandre Costa Pereira, Célia Cassaro Strunz, Expedito Ribeiro, Noedir A G Stolf, Fabio B Jatene. Data and Safety Monitoring Board, Eliana Lima, Laura Caringe, Marcela F Silva. Source Information, The members of the writing group, Whady Hueb, Célia Cassaro Strunz, Alexandre Costa Pereira, Expedito Ribeiro, Pedro Lemos, Cesar Nomura, Fabio B Jatene, José A F Ramires, and Roberto Kalil Filho assume all responsibility for the overall content and integrity of this article.