Murai et al. devised a novel physiology-based method of estimating the amount of myocardium subtended by coronary stenosis, which is feasible and can be performed in the catheterization laboratory with a Doppler sensor-equipped guidewire. The study was published in the recent issue of Circulation: Cardiovascular Interventions.
In the setting of stable coronary artery disease (CAD), the amount of ischemic myocardium has been identified as a key predictor for adverse outcomes. Current practice guidelines recommend revascularization in patients with signs of reversible myocardial ischemia. However, functional assessment by fractional flow reserve (FFR) before percutaneous coronary intervention (PCI) is not routinely performed in clinical practice. Furthermore, in the FAME 2 trial, approximately 73% of medically managed patients with hemodynamically significant stenosis (FFR <0.80) did not experience a major adverse cardiac event in five years, indicating that the cardiovascular outcome may be determined by the ischemic burden rather than the presence of functional stenosis. Therefore, the study by Murai et al. aimed to design a method to quantify myocardial mass subtended by a stenotic coronary lesion on an ad hoc basis, using currently available tools of intracoronary physiology.
The study enrolled patients who underwent both invasive coronary physiological assessment and coronary computed tomography angiography (CCTA) for suspected stable angina or non-ST segment elevation acute coronary syndrome. Patients with a history of coronary artery bypass surgery, prior myocardial infarction in the perfusion territory of the target artery, unstable heart failure, significant valvular disease, persistent arrhythmia, chronic renal failure requiring hemodialysis, extremely tortuous vessels, vessels with severe stenosis, non-ST-segment elevation myocardial infarction (NSTEMI) culprit vessels, vessels with visible collaterals, and patients with ejection fraction <50% were excluded.
The proposed method was premised on the flow continuity principle (i.e., coronary blood flow volume equals total myocardial blood flow volume required for the metabolic demand of the subtended myocardial bed; Qinflow = Qmyocardium). Qinflow or coronary blood flow is the multiplication of average blood flow velocity by the cross-sectional area of the coronary artery. The former was approximated by 0.5 x average peak coronary blood flow velocity (directly measured by a Doppler sensor guidewire), and the latter was estimated from the vessel diameter. On the other hand, Qmyocardium is the multiplication of the amount of perfused myocardial mass or partial myocardial mass (PMM) by average myocardial blood flow, which can be estimated from resting heart rate and systolic blood pressure. Consequently, PMM can be calculated from a simple formula consisting of average peak coronary blood flow velocity, vessel diameter, heart rate, and systolic blood pressure. The physiology-based PMM values were measured by two independent analysts and compared with PPM values estimated from CCTA, which was currently the most accurate method to assess the absolute myocardial mass.
A total of 43 myocardial regions from 32 patients were analyzed. Median PMM was 15.8 g (IQR: 11.7 to 28.4 g) for physiology-based PMM, and 17.0 g (IQR: 12.5 to 25.9 g) for CCTA–based PMM (P=0.84). There was a strong correlation between the two methods (Spearman rank correlation coefficient=0.916; P<0.001) without constant or proportional differences. The Bland-Altman analysis showed a mean bias of 0.5 g, with a limit of agreement between −9.1 to 10.2 g. These results suggest that the novel method can accurately quantify the ischemic burden and is feasible in clinical practice without the need for additional drugs, devices, or techniques.
“Physiology-based calculation of subtended myocardial mass (PMM) in the catheterization laboratory is feasible and can be accurately performed as part of functional stenosis assessment with intracoronary pressure and Doppler guidewires.” – Murai et al. concluded.
Several limitations need to be considered. First, the study only included patients with stable CAD and preserved left ventricular function, thus limiting the external validity of the findings. Second, the calculation requires information about coronary flow velocity, which may be technically challenging for operators with limited experience. Last, the analysis did not include culprit vessels in NSTEMI patients, and the results may not be generalized to the full spectrum of NSTE-ACS patients.
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