The role of vascular resistance on coronary perfusion: differences between healthy and anomalous coronary origin under rest and exercise conditions

Figures

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  Figure 1. Diagram showing myocardial oxygen supply and demand interactions under exercise conditions.

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  Figure 2. (A) Schematic of the in-vitro coronary model showing the sinuses of Valsalva (SV), left coronary artery (LCA), right coronary artery (RCA), ascending aorta (AAo), aortic valve flange (AVF), inflow conduit (IN), and pressure ports (pLV−pAo). (B) Normal configuration, where the LCA and RCA originate from the left (LS) and right (RS) sinuses, respectively. (C) Anomalous configuration, in which both coronaries arise from the RS and the LCA follows an intramural course within the aortic wall. Adapted from “FIG. 3. (a) Schematic of the laboratory model including the aortic sinuses of Valsalva (SV), LCA and RCA, ascending aorta (Asc), aortic valve flange module (AVF), inflow tube (IN), and pressure sensors T-junctions (P1–P2); (b) cross section of the Valsalva sinuses (black) with normal origin of the LCA from the left sinuses of Valsalva (LS) and RCA from the right sinuses of Valsalva (RS); and (c) anomalous LCA origin from the right sinuses of Valsalva (RS) with an intramural segment coursing within the aortic wall” by Seyyed Mahmoud Mousavi, Gianluca Zitti, Marco Pozzi and Maurizio Brocchini, with the permission of AIP Publishing.

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  Figure 3. Diagram of the experimental setup. A pulsatile pump provides the driving flow to the coronary model. Flow distribution and pressure conditions are controlled via resistance valves (R1–R3, RLCA, and RRCA) and compliance chambers (C1, C2, CB). Hemodynamic signals are recorded using four pressure transducers (pLCA, pRCA, pAo, pLV) and a flow sensor (FS). Adapted from “FIG. 4. Schematic of the laboratory setup. A computer-controlled pulsatile pump drives the flow inside the laboratory model, where six resistance valves (R1–R6) and three compliance chambers (C1, C2, and CB) regulate the system's fluid dynamics. Additionally, four pressure transducers (P1–P4) and one flowmeter sensor (FS) are used to measure pressure and flow rate values; T1 and T2 are water tanks regulating the reference pressure of the systemic circulation” by Seyyed Mahmoud Mousavi, Gianluca Zitti, Marco Pozzi and Maurizio Brocchini, with the permission of AIP Publishing.

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  Figure 4. Effects of varying mean LCA resistance (R¯LCA) under rest conditions. Panels (A) and (B) show results for the normal model: (A) time-averaged pressures (p¯LV,p¯Ao,p¯LCA, and p¯RCA) vs. mean LCA resistance, and (B) mean RCA flow rate (q¯RCA) vs. mean LCA resistance. Panels (C) and (D) show the corresponding results for the anomalous model: (C) time-averaged pressures vs. mean LCA resistance, and (D) mean RCA flow rate vs. mean LCA resistance.

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  Figure 5. Effects of mean aortic pressure on coronary perfusion. Panels (A) and (B) show the relationship between mean aortic pressure and measured mean LCA and RCA flow rates during rest in the normal and anomalous models, respectively. Panels (C) and (D) present the corresponding results during exercise for the normal and anomalous models.

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  Figure 6. Schematic summary of the experimental observations and their relation to the anomalous coronary configuration. Solid arrows show relations measured in the present resistance- and pressure-variation tests. Altered wave dynamics in the anomalous LCA were demonstrated in our previous study (25). Dashed arrows indicate the proposed interaction of these mechanisms during exercise.