In tandem and diffuse coronary disease, iFR pullback predicted the physiological outcome of PCI with a high degree of accuracy. Compared with angiography alone, availability of iFR pullback altered revascularization procedural planning in nearly one-third of patients.
Background As younger patients are being considered for transcatheter aortic valve implantation (TAVI), the assessment and treatment of concomitant coronary artery disease is taking on increased importance. Methods and Results Thirteen contemporary lower‐risk patients with TAVI with severe aortic stenosis (AS) and moderate‐severe coronary lesions were included. Patients underwent assessment of coronary hemodynamics in the presence of severe AS (pre‐ TAVI ), in the absence of severe AS (immediately post‐ TAVI ), and at longer‐term follow‐up (6 months post‐ TAVI ). Fractional flow reserve decreased from 0.85 (0.76–0.88) pre‐ TAVI to 0.79 (0.74–0.83) post‐ TAVI , and then to 0.71 (0.65–0.77) at 6‐month follow‐up ( P <0.001 for all comparisons). Conversely, instantaneous wave‐free ratio was not significantly different: 0.82 (0.80–0.90) pre‐ TAVI , 0.83 (0.77–0.88) post‐ TAVI , and 0.83 (0.73–0.89) at 6 months ( P =0.735). These changes are explained by the underlying coronary flow. Hyperemic whole‐cycle coronary flow (fractional flow reserve flow) increased from 26.36 cm/s (23.82–31.82 cm/s) pre‐ TAVI to 30.78 cm/s (29.70–34.68 cm/s) post‐ TAVI ( P =0.012), to 40.20 cm/s (32.14–50.00 cm/s) at 6‐month follow‐up ( P <0.001 for both comparisons). Resting flow during the wave‐free period of diastole was not significantly different: 25.48 cm/s (21.12–33.65 cm/s) pre‐ TAVI , 24.54 cm/s (20.74–27.88 cm/s) post‐ TAVI , and 25.89 cm/s (22.57–28.96 cm/s) at 6 months ( P =0.500). Conclusions TAVI acutely improves whole‐cycle hyperemic coronary flow, with ongoing sustained improvements at longer‐term follow‐up. This enhanced response to hyperemic stimuli appears to make fractional flow reserve assessment less suitable for patients with severe AS. Conversely, resting diastolic flow is not significantly influenced by the presence of severe AS. Resting indices of coronary stenosis severity, therefore, appear to be more appropriate for this patient population, although large‐scale prospective randomized trials will be required to determine the role of coronary physiology in patients with severe AS.
Background: After early revascularisation, restoration of macrocirculatory perfusion parameters is the primary objective in the management of cardiogenic shock complicated acute myocardial infarction. Nevertheless, vital organ perfusion may be compromised at the systemic microcirculatory level, even in patients with preserved macrohaemodynamics. Microvascular perfusion was shown to have independent prognostic value for early mortality. The present study aims to compare the prognostic value of microcirculatory versus macrocirculatory perfusion parameters. Methods: This substudy of the culprit lesion-only percutaneous coronary intervention versus multivessel percutaneous coronary intervention in cardiogenic shock (CULPRIT-SHOCK) trial examined the sublingual capillary network using videomicroscopy post-percutaneous coronary intervention to determine the proportion of perfused capillaries (<20 µm) and perfused capillary density. Thirty-day follow-up was performed to obtain the occurrence of a combined clinical endpoint of all-cause death and renal replacement therapy. Results: Videomicroscopy measurements were performed in 66 patients. There was a significant adjusted association between microcirculatory perfusion parameters and the combined clinical endpoint (proportion of perfused capillaries: P=0.020; perfused capillary density: P=0.035), whereas there was no significant adjusted association between macrocirculatory perfusion parameters and the combined clinical endpoint (systolic blood pressure: P=0.205). Normotensive patients with compromised microcirculatory perfusion parameters had a higher risk of the combined clinical endpoint than normotensive patients with preserved microcirculatory perfusion parameters (proportion of perfused capillaries: Breslow P=0.014; perfused capillary density: Breslow P=0.076). Conclusions: There is a significant and independent association between microcirculatory perfusion parameters perfused capillary density and proportion of perfused capillaries and the combined clinical endpoint of all-cause death and renal replacement therapy at 30 days follow-up. In patients with loss of haemodynamic coherence between microcirculatory and macrocirculatory perfusion parameters, microcirculatory perfusion parameters confer dominant prognostic value.
Introduction of the Navvus microcatheter leads to clinically relevant stenosis severity overestimation in intermediate stenosis.
Background: Patients with severe aortic stenosis (AS) often have coronary artery disease. Both the aortic valve and the coronary disease influence the blood flow to the myocardium and its ability to respond to stress; leading to exertional symptoms. In this study, we aim to quantify the effect of severe AS on the coronary microcirculation and determine if this is influenced by any concomitant coronary disease. We then compare this to the effect of coronary stenoses on the coronary microcirculation. Methods: Group 1: 55 patients with severe AS and intermediate coronary stenoses treated with transcatheter aortic valve implantation (TAVI) were included. Group 2: 85 patients with intermediate coronary stenoses and no AS treated with percutaneous coronary intervention were included. Coronary pressure and flow were measured at rest and during hyperemia in both groups, before and after TAVI (group 1) and before and after percutaneous coronary intervention (group 2). Results: Microvascular resistance over the wave-free period of diastole increased significantly post-TAVI (pre-TAVI, 2.71±1.4 mm Hg·cm·s −1 versus post-TAVI 3.04±1.6 mm Hg·cm·s −1 [ P =0.03]). Microvascular reserve over the wave-free period of diastole significantly improved post-TAVI (pre-TAVI 1.88±1.0 versus post-TAVI 2.09±0.8 [ P =0.003]); this was independent of the severity of the underlying coronary stenosis. The change in microvascular resistance post-TAVI was equivalent to that produced by stenting a coronary lesion with an instantaneous wave-free ratio of ≤0.74. Conclusions: TAVI improves microcirculatory function regardless of the severity of underlying coronary disease. TAVI for severe AS produces a coronary hemodynamic improvement equivalent to the hemodynamic benefit of stenting coronary stenoses with instantaneous wave-free ratio values <0.74. Future trials of physiology-guided revascularization in severe AS may consider using this value to guide treatment of concomitant coronary artery disease.
Background: In patients with stable coronary artery disease, the amount of myocardium subtended by coronary stenoses constitutes a major determinant of prognosis, as well as of the benefit of coronary revascularization. We devised a novel method to estimate partial myocardial mass (PMM; ie, the amount of myocardium subtended by a stenosis) during physiological stenosis interrogation. Subsequently, we validated the index against equivalent PMM values derived from applying the Voronoi algorithm on coronary computed tomography angiography. Methods: Based on the myocardial metabolic demand and blood supply, PMM was calculated as follows: PMM (g)=APV×D 2 ×π/(1.24×10 − 3 ×HR×sBP+1.6), where APV indicates average peak blood flow velocity; D, vessel diameter; HR, heart rate; and sBP, systolic blood pressure. We calculated PMM to 43 coronary vessels (32 patients) interrogated with pressure and Doppler guidewires, and compared it with computed tomography–based PMM. Results: Median PMM was 15.8 g (Q1, Q3: 11.7, 28.4 g) for physiology-based PMM, and 17.0 g (Q1, Q3: 12.5, 25.9 g) for computed tomography–based PMM ( P =0.84). Spearman rank correlation coefficient was 0.916 ( P <0.001), and Passing-Bablok analysis revealed absence of both constant and proportional differences (coefficient A: −0.9; 95% CI, −4.5 to 0.9; and coefficient B, 1.00; 95% CI, 0.91 to 1.25]. Bland-Altman analysis documented a mean bias of 0.5 g (limit of agreement: −9.1 to 10.2 g). Conclusions: Physiology-based calculation of PMM in the catheterization laboratory is feasible and can be accurately performed as part of functional stenosis assessment.
Purpose of ReviewAccumulating evidence exists for the value of coronary physiology for clinical decision-making in ischemic heart disease (IHD). The most frequently used pressure-derived index to assess stenosis severity, the fractional flow reserve (FFR), has long been considered the gold standard for this purpose, despite the fact that the FFR assesses solely epicardial stenosis severity and aims to estimate coronary flow impairment in the coronary circulation. The coronary flow reserve (CFR) directly assesses coronary blood flow in the coronary circulation, including both the epicardial coronary artery and the coronary microvasculature, but is nowadays less established than FFR. It is now recognized that both tools may provide insight into the pathophysiological substrate of ischemic heart disease, and that particularly combined FFR and CFR measurements provide a comprehensive insight into the multilevel involvement of IHD. This review discusses the diagnostic and prognostic characteristics, as well as future implications of combined assessment of FFR and CFR pressure and flow measurements as parameters for inducible ischemia.Recent FindingsFFR and CFR disagree in up to 40% of all cases, giving rise to fundamental questions regarding the role of FFR in contemporary ischemic heart disease management, and implying a renewed approach in clinical management of these patients using combined coronary pressure and flow measurement to allow appropriate identification of patients at risk for cardiovascular events.SummaryThis review emphasizes the value of comprehensive coronary physiology measurements in assessing the pathophysiological substrate of IHD, and the importance of acknowledging the broad spectrum of epicardial and microcirculatory involvement in IHD. Increasing interest and large clinical trials are expected to further strengthen the potential of advanced coronary physiology in interventional cardiology, consequently inducing reconsideration of current clinical guidelines.
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