Absolute coronary flow can be measured by intracoronary continuous thermodilution of saline through a dedicated infusion catheter (RayFlow®). A saline infusion rate at 15–20 mL/min induces an ...immediate, steady-state, maximal microvascular vasodilation. The mechanism of this hyperemic response remains unclear. We aimed to test whether local hemolysis is a potential mechanism of saline-induced coronary hyperemia.
Twelve patients undergoing left and right catheterization were included. The left coronary artery and the coronary sinus were selectively cannulated. Absolute resting and hyperemic coronary flow were measured by continuous intracoronary thermodilution. Arterial and venous samples were collected from the coronary artery and the coronary sinus in five phases: baseline (BL); resting flow measurement (Rest, saline infusion at 10 mL/min); hyperemia (Hyperemia, saline infusion at 20 mL/min); post-hyperemia (Post-Hyperemia, 2 min after the cessation of saline infusion); and control phase (Control, during infusion of saline through the guide catheter at 30 mL/min).
Hemolysis was visually detected only in the centrifugated venous blood samples collected during the Hyperemia phase. As compared to Rest, during Hyperemia both LDH (131.50 ± 21.89 U/dL Rest and 258.33 ± 57.40 U/dL Hyperemia, p < 0.001) and plasma free hemoglobin (PFHb, 4.92 ± 3.82 mg/dL Rest and 108.42 ± 46.58 mg/dL Hyperemia, p < 0.001) significantly increased in the coronary sinus. The percentage of hemolysis was significantly higher during the Hyperemia phase (0.04 ± 0.02% Rest vs 0.89 ± 0.34% Hyperemia, p < 0.001).
Saline-induced hyperemia through a dedicated intracoronary infusion catheter is associated with hemolysis. Vasodilatory compounds released locally, like ATP, are likely ultimately responsible for localized microvascular vasodilation.
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•Absolute coronary flow and resistance can be measured with continuous intracoronary thermodilution of saline through the RayFlow catheter.•The mechanisms underlying saline-induced hyperemia are still unknown. Local hemolysis might be involved.•Serum markers of hemolysis were measured from blood samples collected from the coronary artery and the coronary across different phases of the study.•There was a significant increase in LDH, plasma free Hb and % of hemolysis during hyperemia as compared to baseline and resting conditions.•Saline-induced coronary hyperemia is mediated by intravascular hemolysis, likely through the local release of vasodilatory compounds (i.e. ATP, NO).
Wall shear stress (WSS) has been associated with atherogenesis and plaque progression. The present study assessed the value of WSS analysis derived from conventional coronary angiography to detect ...lesions culprit for future myocardial infarction (MI).
Three-dimensional quantitative coronary angiography (3DQCA), was used to calculate WSS and pressure drop in 80 patients. WSS descriptors were compared between 80 lesions culprit of future MI and 108 non-culprit lesions (controls). Endothelium-blood flow interaction was assessed by computational fluid dynamics (10.8 ± 1.41 min per vessel). Median time between baseline angiography and MI was 25.9 (21.9–29.8) months. Mean patient age was 70.3 ± 12.7. Clinical presentation was STEMI in 35% and NSTEMI in 65%. Culprit lesions showed higher percent area stenosis (%AS), translesional vFFR difference (ΔvFFR), time-averaged WSS (TAWSS) and topological shear variation index (TSVI) compared to non-culprit lesions (p < 0.05 for all). TSVI was superior to TAWSS in predicting MI (AUC-TSVI = 0.77, 95%CI 0.71–0.84 vs. AUC-TAWSS = 0.61, 95%CI 0.53–0.69, p < 0.001). The addition of TSVI increased predictive and reclassification abilities compared to a model based on %AS and ΔvFFR (NRI = 1.04, p < 0.001, IDI = 0.22, p < 0.001).
A 3DQCA-based WSS analysis was feasible and can identify lesions culprit for future MI. The combination of area stenoses, pressure gradients and WSS predicted the occurrence of MI. TSVI, a novel WSS descriptor, showed strong predictive capacity to detect lesions prone to cause MI.
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•Lesions culprit of future myocardial infarction (MI) had higher area stenosis, pressure gradient, time-averaged wall shear stress (TAWSS) and topological shear variation index (TSVI).•A three-dimensional quantitative coronary angiography (3DQCA)-based software provided in few minutes reliable WSS simulations.•The WSS topological skeleton feature TSVI showed strong predictive capacity for MI.
The present study establishes a link between blood flow energy transformations in coronary atherosclerotic lesions and clinical outcomes. The predictive capacity for future myocardial infarction (MI) ...was compared with that of established quantitative coronary angiography (QCA)-derived predictors. Angiography-based computational fluid dynamics (CFD) simulations were performed on 80 human coronary lesions culprit of MI within 5 years and 108 non-culprit lesions for future MI. Blood flow energy transformations were assessed in the converging flow segment of the lesion as ratios of kinetic and rotational energy values (KER and RER, respectively) at the QCA-identified minimum lumen area and proximal lesion sections. The anatomical and functional lesion severity were evaluated with QCA to derive percentage area stenosis (%AS), vessel fractional flow reserve (vFFR), and translesional vFFR (ΔvFFR). Wall shear stress profiles were investigated in terms of topological shear variation index (TSVI). KER and RER predicted MI at 5 years (AUC = 0.73, 95% CI 0.65–0.80, and AUC = 0.76, 95% CI 0.70–0.83, respectively;
p
< 0.0001 for both). The predictive capacity for future MI of KER and RER was significantly stronger than vFFR (
p
= 0.0391 and
p
= 0.0045, respectively). RER predictive capacity was significantly stronger than %AS and ΔvFFR (
p
= 0.0041 and
p
= 0.0059, respectively). The predictive capacity for future MI of KER and RER did not differ significantly from TSVI. Blood flow kinetic and rotational energy transformations were significant predictors for MI at 5 years (
p
< 0.0001). The findings of this study support the hypothesis of a biomechanical contribution to the process of plaque destabilization/rupture leading to MI.
Coronary microvascular dysfunction is a highly prevalent condition in both obstructive and nonobstructive coronary artery disease. Intracoronary thermodilution is a promising technique to investigate ...coronary microvascular (dys)function in vivo and to assess its most important metric: microvascular resistance. Here, the authors provide a practical review of bolus and continuous thermodilution for the measurement of coronary flow and microvascular resistance. The authors describe the basic principles of indicator-dilution theory and of coronary thermodilution and detail the practicalities of their application in the catheterization laboratory. Finally, the authors discuss contemporary clinical applications of coronary thermodilution-based microvascular assessment in humans and future perspectives.
Fractional flow reserve (FFR) pullbacks assess the location and magnitude of pressure drops along the coronary artery. The pullback pressure gradient (PPG) quantifies the FFR pullback curve and ...provides a numeric expression of focal versus diffuse coronary artery disease. This study aims (1) to validate the PPG using manual FFR pullbacks compared with motorized FFR pullbacks as a reference; and (2) to determine the intra‐ and interoperator reproducibility of the PPG derived from manual FFR pullbacks. Patients with stable coronary artery disease and an FFR ≤ 0.80 were included. All patients underwent FFR pullback evaluation either with a motorized device or manually, depending on the study cohort. The agreement of the PPG between repeated pullbacks was assessed using the Bland–Altman method. Overall, 116 FFR pullback maneuvers (96 manual and 20 motorized) were analyzed. There was excellent agreement between the PPG derived from manual and motorized pullbacks (mean difference −0.01 ± 0.07, 95% limits of agreement LOA −0.14 to 0.12). The intra‐ and interoperator reproducibility of PPG derived from manual pullbacks were excellent (mean difference <0.01, 95% LOA −0.11 to 0.12, and mean difference <0.01, 95% LOA −0.12 to 0.11, respectively). The duration of the pullback maneuver did not impact the reproducibility of the PPG (r = 0.12, 95% CI: −0.29 to 0.49, p = 0.567). Manual pullbacks allow for an accurate PPG calculation. The inter‐ and intraoperator reproducibility of PPG derived from manual pullbacks were excellent.
ESC Core Curriculum for the Cardiologist Tanner, Felix C; Brooks, Nicolas; Fox, Kevin F ...
European heart journal,
10/2020, Letnik:
41, Številka:
38
Journal Article
Quantification of microvascular function requires the measurement of flow and resistance at rest and during hyperaemia. Continuous intracoronary thermodilution accurately measures coronary flow ...during hyperaemia.
The aim of this study was to investigate whether continuous coronary thermodilution using lower infusion rates also enables volumetric coronary blood flow measurements (in mL/min) at rest.
In 59 patients (88 arteries), the ratio of distal to proximal coronary pressure (Pd/Pa), as well as absolute blood flow (in mL/min) by continuous thermodilution, was recorded using a pressure/temperature guidewire. Saline was infused at rates of 10 and 20 mL/min. In 27 arteries, Doppler average peak velocity (APV) was measured simultaneously. Pd/Pa, APV, thermodilution-derived coronary flow reserve (CFRthermo) and coronary flow velocity reserve (CFVR) were assessed. In 10 arteries, simultaneous recordings were obtained at saline infusion rates of 6, 8, 10 and 20 mL/min.
Compared to baseline, saline infusion at 10 mL/min did not change Pd/Pa (0.95±0.05 versus 0.94±0.05, p=0.49) or APV (22±8 versus 23±8 cm/s, p=0.60); conversely, an infusion rate of 20 mL/min induced a decrease in Pd/Pa and an increase in APV. Stable thermodilution tracings were obtained during saline infusion at 8 and 10 mL/min, but not at 6 mL/min. Mean values of CFRthermo and CFVR were similar (2.78±0.91 versus 2.76±1.06, p=0.935) and their individual values correlated closely (r=0.89, 95% CI: 0.78-0.95, p<0.001).
In addition to hyperaemic flow, continuous thermodilution can quantify absolute resting coronary blood flow; therefore, it can be used to calculate coronary flow reserve and microvascular resistance reserve.
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