Reply to: Predictors of coronary artery disease in cardiac arrest survivors: coronary angiography for everyone? A single-center retrospective analysis

We thank doctors Barriuso, Irigaray, Rivera and Fernández-Rodríguez for their interest in our paper entitled “Predictors of coronary artery disease in cardiac arrest survivors: coronary angiography for everyone? A single-center retrospective analysis”, which aimed to identify predictors of coronary artery disease in survivors of cardiac arrest (CA), to define the best timing for coronary angiography, and to establish the relationship between coronary artery disease (CAD) and mortality.(1) The authors of this letter raised three important questions regarding our paper. First, regarding the definition of significant CAD being based solely on angiographic assessments. In our paper, the cutoffs for significant CAD were a lumen reduction of at least 50% in the left main artery and of at least 70% in the remaining vessels, as recommended in the recently published American Heart Association (AHA) guidelines.(2) In our center, we routinely perform multiple angiographic views to reduce the error of visual estimation of the degree of coronary stenosis. However, we understand the authors’ point, and herein, it is important to differentiate the concept of intermediate stenosis that might not cause ischemia and unstable plaque that might be the culprit for the event. Intermediate stenosis is classically defined by a lumen reduction of 40 69%(2) in non-left main vessels, although a higher range can be found in some studies. To evaluate whether such lesions cause ischemia, a noninvasive stress test or invasive evaluation with fractional flow reserve (FFR) or instantaneous wave-free ratio (iFR) is recommended. However, recent CA is usually a contraindication for noninvasive stress tests. With regard to coronary physiology, there is very limited evidence for FFR, iFR or other indices in this clinical context, mainly because unstable patients (such as patients after CA) have been excluded from the main trials assessing these techniques, while most studies have focused on chronic coronary syndrome or non-culprit lesions of acute coronary syndrome (ACS), such as in the iFR-Swedeheart trial.(3) In addition, there are no strong data to suggest that FFR guidance improves clinical outcomes in ACS. In fact, there is some evidence suggesting that microvascular dysfunction during ACS might compromise the achievement of maximal hyperemia, increasing the number of false negatives with FFR.(4) Additionally, the recent FLOWER-MI study,(5) the only trial directly comparing FFR versus angiography for non-culprit lesions in the ACS setting, did not show superiority of an FFR-based strategy. Thus, there is no evidence that supports invasive physiology to identify the culprit lesion in ACS or after CA. Joana Rigueira1 , Inês Aguiar-Ricardo1 , Pedro Carrilho-Ferreira1 , Miguel Nobre Menezes1 , Sara Pereira1, Pedro S. Morais1, Pedro Canas da Silva1 , Fausto J. Pinto1