Читать книгу Interventional Cardiology - Группа авторов - Страница 165

The purpose of angiography and revascularization is to improve blood flow and thereby reduce myocardial ischemia. However, angiographic assessment of coronary stenosis has limited value in determining the degree of ischemia imposed and the viability of the subtended myocardium. Angiographic parameters also have limited predictive value of clinical outcome measures, and often, even mild and moderate stenoses can be important and underappreciated [1]. Furthermore, while many patients undergo non‐invasive functional testing prior to angiography, the findings can be at odds with the coronary appearances.

International guidelines recommend coronary physiology for angiographically moderate coronary stenoses (diameter stenosis 50–90%) where non‐invasive functional information is lacking [2,3]. Additionally, in many cases, invasive physiology provides additive information over and above non‐invasive functional testing. Intracoronary pressure wires offer an established and rapid solution for assessing the significance of coronary disease, while also assessing myocardial viability and offering insights into the best treatment strategies [4]. Pressure wires provide greater spatial localization of ischemia, not only to the vessel but also to the lesion level. This is particularly pertinent in multi‐vessel disease where relative perfusion changes can be matched leading to underestimation of ischemia.

There are complex pressure‐flow relationships that determine the measurable pressure gradient across a stenosis (Figures 7.1–7.3) [5], however these can be simplified to produce pressure‐only measurements that are simple to use in the cardiac catheterization laboratory. Multiple research studies have validated these pressure‐only measures of coronary physiology against non‐invasive ischemia testing [6–10] and major international outcomes studies have demonstrated that stenoses of all severities can be managed efficiently by pressure‐only indices such as instantaneous wave‐free ratio (iFR) or Fractional Flow Reserve (FFR) (Figure 7.4) [11–18]. These are now included in international guidelines both in North America and Europe [2,19–21]. Safe deferral of lesions that are non‐ischemic will reduce stent related events. In patients with confirmed ischemia, the pressure wire can determine interventional approaches and, following PCI, can be assessed to validate the hemodynamic success of the intervention [22,23] and identify those at higher risk of later events [24–38].

Figure 7.1 Behavior of resting and hyperemic flow in relation to stenosis severity. Resting flow is remarkably preserved despite worsening stenosis severity – upto 85% diameter stenosis by formal measurement. Hyperemic flow starts falling when stenoses are 30% but falls significantly once stenoses are 50%. Adapted from Gould, Lipscomb and Hamilton 1974.

Figure 7.2 The flow of blood across a coronary stenosis. Pressure gradients across stenoses are due to both viscous and separation losses. Pressure is lost owing to viscous friction along the stenosis (Poiseuille’s law). Flow also accelerates as it passess through the narrowed segment, causing pressure loss as pressure is converted into kinetic energy (Bernoulli’s law). Flow separation and the formation of eddies prevent complete pressure recovery at the exit of the stenosis. Measurement of intracoronary haemodynamics includes proximal perfusion pressure (P_a), coronary pressure and flow velocity distal to the stenosis (P_d and V_d, respectively), and the venous pressure (P_v), which is typically assumed to be negligible. ΔP is the difference between P_d and P_a. Normal diameter (D_n), stenosis diameter (D_s), proximal velocity (V_n), and stenosis velocity (V_s) are indicated. From van de Hoef et al (2013).

Figure 7.3 The curvilinear relationship between pressure and flow is unique for each stenosis. Pressure drop across a stenosis is determined by ΔP = Fv + Sv² (where F is friction losses and S is separation losses). This produces curvilinear relationship unique to any stenosis; the steepness of the curve reflects the severity of the lesion (eg. Reference vessel, stenosis A, B, C). Increasing the flow velocity across a stenosis will alter the pressure gradient observed. In stenosis A, there is a large resting pressure gradient that is accentuated during hyperemia with little increase in flow. In stenosis B, increasing the concentration of hyperemic agent (depicted as arrows) will increase flow velocity to generate a larger gradient; since resting flow is unchanged, CFR and FFR will move in opposite directions. In even milder stenoses, such as A, large escalations of flow velocity from a relatively low resting value could create a large pressure gradient; in these situations, pressure does not reflect the change in flow. Adapted from van de Hoef et al (2013).

Figure 7.4 Results of FAME and FAME II Studies. FAME randomized patients with multi‐vessel disease to a FFR or angiographic guided approach; stenoses with FFR>0.80 were deferred. FAME II randomized patients with a stenosis found to have an FFR ≤0.80 to PCI with optimal medical therapy (OMT) or to OMT alone.

Finally, pressure wire assessment can add utility in patients who have recurrent chest pain but angiographically unobstructed coronary arteries. Assessment of the microcirculation has proven useful in managing this traditionally difficult cohort of patients.

This chapter will discuss these matters in turn with a focus upon the practical application of coronary physiology in day‐to‐day practice. The principal focus will be on pressure‐based indices FFR and non‐hyperemic pressure ratios (NHPR), which are measured under hyperemic and resting conditions, respectively. Whilst a number of flow‐based and combined pressure and flow‐based parameters exist, their traction outside of the academic setting and in mainstream clinical practice is minimal.