IJCS | Volume 32, Nº4, July/August 2019

327 Clinical case study A 49-year-oldmale marathon runner withmany years with consistent sub-three hour finish times presents with progressive exertional dyspnea and consequent reductions in his running pace over a 6-month period. He also noted a significant increase in race time in the last marathon three months ago. The atherosclerotic risk factor profilewasmarkedby the presence of dyslipidemia, treated with low-dose statin, and a family history of premature CAD (his father and uncle). He underwent a maximal symptom-limited exercise test with metabolic gas exchange on the treadmill that demonstrated a functional capacity well above the predicted peak value for age/sex (VO 2peak = 53.0 ml/kg.min) but experienced the described symptoms. In conjunction with dyspnea, there were 1 to 2-mmhorizontal ST-segment depressions across the precordial leads of the exercise ECG, that emerged near peak exercise and resolved completely by 3 minutes of recovery. Transthoracic echocardiography demonstrated mild 4-chamber dilatation, preserved systolic and diastolic left ventricular function, and no significant valvular disease. He underwent a conventional coronary angiography, which revealed a focal 60-70% stenosis by visual assessment in the proximal left anterior descending artery. The lesion was further characterized by FFR, which yielded a value of 0.82. Based on data from the FAME trials, 4,5 fromwhich an FFR revascularization cut- point of 0.80 was established, intervention was deferred. Despite presenting with angina syndrome and objective evidence of ischemia on functional testing, the patient was advised that his CAD was not “severe enough” to justify an intervention and then clinical treatment with beta-blocker, long-acting nitrate preparation, statin, and aspirin was initiated. As often observed in athletic patients, significant undesirable side effects were caused by the beta-blocker (further reduction in exercise capacity with no improvement of angina), nitrate (post-exertional orthostatic intolerance), and statin (myalgia), leading to treatment noncompliance and discontinuation. He presented again eight months later after being successfully resuscitated from cardiac arrest that occurred 100 meters before the finish line of a large city marathon. Repeat coronary angiography showed no evidence of plaque rupture or new lesions, and stable left anterior descending coronary artery disease both by visual angiography and repeat FFR. After a discussion with the patient about management options, the proximal left anterior descending artery was treated with a drug eluting stent. Discussion This case study highlights several areas of clinical uncertainty regarding the use of invasive coronary flow assessment in competitive athletes with atherosclerotic coronary disease. The central uncertainty relates to whether the guideline-supported decision to forgo revascularization based on the FFR data initially obtained from the patient was the appropriatemanagement option. This question cannot be answered by the available clinical trial data and underscores the challenges of applying invasive coronary physiological assessment in patients who were unrepresented in the literature. Clinical cases such as this illustrate the need for future investigations designed to assess the utility of FFR and iFR in athletes. FFR is a ratio that quantifies the difference between the proximal and distal blood pressure surrounding a focal coronary stenosis during adenosine-induced hyperemia and provides a quantitative assessment of stenosis severity. 9 For example, an FFR of 0.82 obtained across a focal stenosis of the left anterior descending artery indicates an 18 % reduction in blood flow distal to the stenosis under pharmacologically-induced maximal hyperemia. Although the catheter actually measures coronary pressure, the hyperemic conditions are thought to eliminate the effect of the resistance vessels such that the coronary pressure is essentially equivalent to coronary blood flow. 9 The iFR is an increasingly popular alternative as it obviates the need for adenosine-induced hyperemia by assessing the flow gradient during a quiescent period in diastole, when microvasculature resistance is stable, which allows uniformmeasurements during the resting state. 10 Accordingly, FFR and iFR provide insight into the supply component of the myocardial ischemia supply/demand relationship. Measurement of FFR or iFR is typically performed when the severity of angiographic lesion cannot be visually determined and the decision to proceed with or to defer revascularization must be made. The use of FFR/iFR in this context relies on clinical cut-points or binary “lines in the sand” which differentiate adequate versus inadequate blood supply. Current recommendations for FFR/iFR cut-points have emerged from careful analysis of clinical trial and registry data, 4–7 with emphasis on hard outcomes including mortality and the need for future revascularization. Specifically, FFR and iFR cut-points have been chosen to represent a lesion severity at which the risk-benefit balance of percutaneous intervention favored intervention rather Issa et al. Coronary physiologic in endurance athletes Int J Cardiovasc Sci. 2019;32(4):326-330 Viewpoint