INTRODUCTION

The limitations of coronary angiography to assess the functional significance of coronary stenoses have been recognised for more than 20 years.¹ Large intra- and inter-observer variability occurs when coronary angiograms are interpreted which accounts for the frequent dissociation between clinical and angiographic findings. Morphological assessment of a coronary lesion does not necessarily reflect the impairment of flow by the stenosis. This dichotomy may occur as the resistance of a coronary stenosis will vary in relation to the fourth power of the luminal radius. Thus a relatively small change in vessel radius, beyond angiographic resolution, may result in a significant alteration in flow. The resistance of a lesion to flow will also be influenced by the length of the stenosis. Furthermore, whether ischaemia is induced by any epicardial stenosis will be determined to a significant extent by the size of the perfused territory that lies beyond the stenosis.

As a result, measurements of coronary flow and pressure have been introduced to improve the functional evaluation of coronary stenoses and interventions.² Technical progress has permitted intra-coronary measurements to be made using wires with the same dimensions as those of conventional angioplasty guidewires (0.014 inches in diameter) increasing their ease of application in the catheter laboratory.

This chapter will review the physiological background of both coronary flow and pressure measurement, and will focus on the application of these techniques for diagnostic and therapeutic catheterisation.

PRESSURE MEASUREMENT

Blood flow within the coronary vessels is greatly dependent on the haemodynamic status of the patient and may demonstrate significant variations between individual recordings. To overcome this problem the concept of coronary pressure derived myocardial fractional flow reserve (FFR) has been developed. FFR is defined as the maximum myocardial blood flow in the presence of a stenosis expressed as a proportion of the theoretical maximum flow in the absence of any stenosis (Fig. 10.1). The FFR represents the summation of the severity of the epicardial stenosis, the extent of the perfused territory and the contribution of distal collateral blood flow.

Figure 10.1 Schematic representation of a coronary artery and vascular bed. Myocardial blood flow is equal to the perfusion pressure across the myocardium divided by its resistance. At maximum hyperaemia, resistance to flow (R_min) is minimal and constant. Maximum flow in the diseased vessel may, therefore, be expressed as a ratio to that of a normal vessel, i.e. one without a pressure drop, by the equation:

AO, aorta: P_a, P_d and P_v mean aortic, distal coronary and central venous pressure; Qmax, normal, theoretical maximum achievable myocardial flow if the artery were normal; Qmax, stenosis, maximal achievable flow in the presence of a stenosis.

Adapted from Pijls and De Bruyne.²²

For accurate calculation of the FFR, a steady state of maximal hyperaemia is required to maintain myocardial microvascular resistance at a constant minimal level. In submaximal hyperaemia the FFR will be artificially elevated and the severity of the stenosis underestimated. During maximal hyperaemia, any changes in the measured coronary pressure that are recorded equate to alterations in blood flow within the vessel.

The standard means for inducing hyperaemia is by the administration of adenosine. This is typically infused intravenously for 1–2 minutes (140 mg/kg/min infused via the femoral vein), though it may be used as an intra-coronary bolus dose.³ Intra-coronary injection of papaverine may also be used.³ This provides a hyperaemic plateau which lasts for 30–60 seconds though is associated with prolongation of the QT-interval and occasionally ventricular arrhythmia. The distal coronary, aortic and right atrial (RA) pressures are then measured simultaneously via the pressure wire, guide catheter and RA catheter respectively, and the FFR calculated (Fig. 10.1). For simplicity of use, the right atrial pressure is now not often recorded and is taken to have a value of 0 mmHg when calculating the FFR. This practice has been demonstrated to reduce the sensitivity of FFR for detecting significant coronary lesions.⁴ To compensate for this it is usual to accept values of FFR in the ‘grey zone’ of 0.75 to 0.80 as potentially indicative of ischaemia.

As measurement of FFR is expressed as a ratio of the proximal to distal coronary pressure within the same vessel, the possible confounding effects of microvascular disease and the contribution of distal collateral vessels are eliminated. Likewise, it is independent of changes in patient haemodynamics, such as heart rate, blood pressure and myocardial contractility.⁵ As a normal reference vessel is not required, FFR measurements may be made in multivessel disease. It may also be used to assess the cumulative effect on coronary flow of sequential lesions within a single vessel.

Application of pressure measurement

The primary indication for the use of coronary pressure measurement is to determine whether a coronary stenosis is flow limiting and as a result is responsible for myocardial ischaemia. It is now well established that an FFR below 0.75 is functionally significant and has been found to correlate well with the presence of ischaemia on perfusion scintigraphy, stress echocardiography and exercise testing in a broad spectrum of clinical settings.^5,7,8 However, it may be unreliable in acute ischaemic syndromes due to microvascular injury. Both retrospective and prospective work have demonstrated that lesions with a distal FFR greater than 0.75 may be left untreated without any increase in subsequent adverse events on follow-up.^9,10,11

A further use of pressure measurement is to determine the precise location of the lesion under assessment by defining the point at which the measured pressure ‘steps-up’ during pull-back of the wire (Fig. 10.2A and B). A particular area where this has been applied is in the assessment of ostial coronary lesions which may be missed by conventional angiography.

Figure 10.2 A This patient had significant symptoms of angina. Angiography had demonstrated a moderate stenosis in the distal left main stem. There was a suggestion of disease at the ostium of the LAD though this could not be clearly delineated angiographically. When maximal hyperaemia was induced with an intravenous infusion of adenosine there was a significant reduction in distal pressure in the mid-LAD (FFR 0.49). B During wire advancement (1) and withdrawal (2) the ‘step’ in the phasic pressure was found to be in the distal LMS/ostium of LAD indicating the presence of a haemodynamically important stenosis in this area.

Measurement of the FFR may provide important prognostic information following coronary intervention. An FFR of less than 0.75 implies that the results of the intervention are physiologically unacceptable and would be associated with myocardial ischaemia. An FFR of greater than 0.9 following balloon angioplasty without stenting, has been found to be associated with repeat intervention rates at 6, 12 and 24 months of 12%, 12% and 15% respectively.¹² Where the FFR following angioplasty was less than 0.9 the rates of re-intervention at these time points were 24%, 28% and 30%.¹²

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