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The SYNTAX score has been shown to be an independent predictor of MACE in patients treated with PCI but not with CABG [ 4 ]. Therefore it has a role in aiding the selection of optimal treatment by identifying those patients at highest risk of adverse events following PCI.

The National Cardiovascular Database Registry (NCDR CathPCI risk score) has been validated in PCI patients and should only be used in this context [ 5 ].

The Society of Thoracic Surgeons (STS) score, and the age, creatinine, and ejection fraction (ACEF) score have been validated in surgical patients, and therefore should only be used to determine surgical risk.

It is important to acknowledge that no risk score can accurately predict events in an individual patient. Moreover, limitations exist with all databases used to build risk models, and differences in definitions and variable content can affect the performance of risk scores when they are applied across different populations. Ultimately risk stratification should be used as a guide, while clinical judgement and multidisciplinary dialogue (Heart Team) remain essential.

Patient information needs to be objective and unbiased, patient oriented, evidence based, up-to-date, reliable, understandable, accessible, relevant, and consistent with legal requirements. Informed consent requires transparency, especially if there is controversy about the indication for a particular treatment (PCI vs. CABG vs. OMT). Collaborative care requires the preconditions of communication, comprehension, and trust. It is essential to realize that health care decisions can no longer be based solely on research results and our appraisal of the patient’s circumstances. Patients taking an active role throughout the decision making process have better outcomes. However, most patients undergoing CABG or PCI have limited understanding of their disease and sometimes unreasonable expectations with regard to the proposed intervention, its complications, or the need for late reintervention, especially after PCI.

Informing patients about treatment choices allows them to reflect on the advantages and disadvantages associated with either strategy. Patients can only weigh this information properly in the light of their personal values and must have the time to reflect on the trade-offs imposed by the estimates. The patient deserves to fully understand the risks, benefits, and uncertainties associated with the condition and its treatment. Avoiding incomprehensible jargon, and consistent use of terminology that the patient understands, are mandatory. Informed medical decision making should consider short-term procedure-related benefits and risks as well as expected long-term risks and benefits in terms of survival, relief of angina, quality of life, and the potential need for late reintervention. It is equally important that any bias of stakeholders towards various treatment options for CAD is made known to the patient. Specialty bias and self-referral should not interfere with the decision process. With the exception of unstable patients or candidates for ad hoc PCI ( Table 4 ), the patient should be offered enough time, up to several days as required, between diagnostic catheterization and intervention to reflect on the results of the diagnostic angiogram, to seek a second opinion as desirable, or to discuss the findings and consequences with his or her referring cardiologist and/or primary care physician. An example of a suitable and balanced patient information document is provided in the Appendix of the online document.

Table1

Capability, merits, disadvantages, and utility of methods used for assessment of myocardial salvage

SPECT, single-photon emission computerized tomography; PET, positron emission tomography; CMR, cardiac magnetic resonance; CT, computerized tomography; AAR, area at risk; FIS, final infarct size.

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Table1

Capability, merits, disadvantages, and utility of methods used for assessment of myocardial salvage

SPECT, single-photon emission computerized tomography; PET, positron emission tomography; CMR, cardiac magnetic resonance; CT, computerized tomography; AAR, area at risk; FIS, final infarct size.


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Myocardial ischaemia-reperfusion injury is caused by a dynamic sequence of processes initiated by abrupt cessation of blood flow. A detailed description of the cellular and subcellular pathophysiological mechanisms has recently been reviewed. 9 Imaging techniques use specific events in the cascade following ischaemia reperfusion for delineation of the affected structure, including impaired flow (perfusion imaging), impaired motion (strain), oedema (T2-Imaging), reversible and irreversible mitochondrial damage ( 99 Tc-Sestamibi SPECT), cell membrane break-down (T1-Imaging with contrast agents), and finally necrosis (T1-Imaging with necrosis specific contrast agents).

Myocardial salvage is quantified by the difference between AAR and FIS, and myocardial salvage index can be calculated as the proportion of salvaged AAR (AAR-FIS/AAR). The salvage index is a measure of treatment efficacy, which allows comparisons among infarcts of different sizes. A salvage index of 1.0 indicates maximum treatment success, whereas a salvage index of 0 means no benefit of treatment. The ratio is sensitive to measurement errors when AAR is small, since the diagnostic precision of measuring perfusion defects of <3% of the left ventricle is reduced due to the limited resolution of the technique. 10

We have measured AAR, FIS, salvage, and salvage index by SPECT in a large cohort of patients undergoing successful primary percutaneous coronary intervention (PCI) for STEMI (90% obtained TIMI 3 flow). 11 The study was undertaken to compare post-infarction salvage and LV function in early (<12 h) and late presenters (12–72 h). Like others, 5 we were unable to justify a specific limit of 12 h delay for offering STEMI patients primary PCI treatment. Scintigraphic measures of tissue damage and LV function were associated with the presentation delay, but with remarkably weak correlations ( r 2 < 0.05 for all). LV ejection fraction correlated positively with salvage index ( r 2 = 0.27) and inversely to FIS ( r 2 = 0.46). AAR was a strong predictor of FIS. We found no significant dependency of salvage index on AAR. 11 Importantly, post-infarction shrinkage of AAR during the 30 days until imaging of FIS does not seem to affect the measured salvage.

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