Extra-Coronary Pressure Gradient Assessment: Use of the pressure wire in peripheral, valvular, and congenital heart disease
The measurement of translesional pressure gradients was an integral part of the development of coronary angioplasty. Gruentzig demonstrated a relationship between post-PTCA translesional gradient and the occurrence of both early complications and late restenosis in the 1980s.1 At that time, only fluid-filled catheter systems were used, and were limited by their bulk, lack of fidelity, and pressure damping in small catheter lumens. Intracoronary gradient assessment has been repopularized by the availability of 0.014” guidewire mounted pressure sensors. These devices have been available for a number of years, but their utility for pressure gradient measurement in a variety of extra-coronary settings is not widely appreciated. This paper will review some of the applications of gradient measurement with pressure wires for valvular, peripheral, and congenital cardiovascular diseases.
Renal Artery Stenosis
Renal artery translesional pressure gradients are used in practice for decision making about intervention for renal artery stenosis. A 20mm peak-to-peak pressure gradient between the aorta and distal renal artery is typically considered physiologically significant. There are no clear data to support this “magic number” for the determination of clinically important renal artery lesions, or to support this gradient “cut-off” as an indication intervention for renal artery stenosis. Despite the lack of evidence for a threshold value for important renal artery stenosis, pressure gradient measurement still has great utility in these cases. The absence of a gradient is useful in many cases. Monitoring changes in gradient during intervention is also useful.
Methods for Measurement: Figure 1 shows the most common method used to measure a renal artery origin lesion to obtain a translesional gradient. There is a 5 French diagnostic catheter placed into the renal orifice and then pulled back. This approach is limited by pressure damping, which may create the appearance of a gradient when none is present. It is easy to angle the catheter so it is either wedged in the lesion or damped against the wall of the vessel. A moderate lesion may appear hemodynamically severe.
Damping is only one of the artifacts to which pressure tracings are subject (Table 1). Most translesional gradient measurements are done using two fluid-filled systems. Many of the disposable pressure transducers in use today are subject to more drift than most of us realize. It is critical to zero and match both pressure systems in the aorta prior to measuring a gradient. For borderline measurements, reversing the transducers to verify a consistent gradient remains an important way to double-check the accuracy of the measurements.
Figure 2 shows the traditional method for double-pressure renal artery translesional pressure gradient assessment. A 6 Fr guide catheter is used to place a 4 Fr exchange type catheter distally in the renal artery. A distal contrast injection (lower right panel) confirms that the 4F catheter is well positioned. There is an acute angle where the guide meets the renal artery orifice, which may contribute to an unreliable distal pressure measurement.
As an alternative to two fluid-filled catheter systems, a pressure wire may be used. Figure 3 shows a case using a pressure wire to measure the translesional gradient. The stenosis is a non subtotal renal artery lesion. The patient is hypertensive, with a systemic systolic pressure that ranges between 170–200 mmHg. With the pressure wire passed through a diagnostic catheter, the peak-to-peak gradient is 15 to 20 mm Hg. The lesion is completely resolved with placement of a stent (lower panel).
Figure 4 shows a restenosis lesion in a previously placed renal origin stent. The severity of the lesion based on angiography alone is uncertain. The second angiographic panel shows a pressure wire in the distal renal artery placed via a 6F diagnostic catheter. The 0.014” pressure wire can be used with 4–6F diagnostic catheters. The simultaneous proximal and distal pressures in this case are equal. This is clearly not a hemodynamically important restenotic lesion.
Efforts at Developing Predictive Hemodynamic Assessment Indices: There have been various conflicting results from efforts to predict which renal lesions will respond to treatment.2 Radermacher et al. used a renal artery resistive index to predict which patients might respond to revascularization. This index is based on noninvasive duplex ultrasound exams. If the renal bed is significantly diseased, there is a high resistance in the renal arterial circulation and there is a high resistive index. If these patients are revascularized, the kidney is already relatively less functional and improvement in renal function or blood pressure is unlikely. If the resistive index is low and revascularization is performed, there is a greater likelihood that creatinine or blood pressure will improve. This was validated using a sample of patients who were treated variously with medicine, plain balloon angioplasty, or surgical revascularization. Among 138 patients who had unilateral or bilateral renal-artery stenosis of more than 50 percent of the luminal diameter and who underwent renal angioplasty (without stenting) or surgery, the procedure was technically successful in 95 percent. The mean duration of follow-up was 32+/-21 months. Among the 35 patients (27 percent) who had resistive-index values of at least 80 before revascularization, the mean arterial pressure did not decrease by 10 mm Hg or more after revascularization in 34 (97 percent). Renal function declined in 80 percent; 46 percent became dependent on dialysis and 29 percent died during follow-up. Among the 96 patients (73 percent) with a resistive-index value of less than 80, the mean arterial pressure decreased by at least 10 percent in all but 6 patients (6 percent) after revascularization; renal function worsened in only 3 (3 percent), all of whom became dependent on dialysis; and 3 (3 percent) died (P
In contrast, Zeller at al. studied the outcome of stenting for renal artery stenosis and found no relation between resistive index and clinical outcome.3 One-year follow-up was completed in 191 surviving patients. In 52 percent of the patients, serum creatinine concentration decreased during 1-year follow-up. Median serum creatinine concentration dropped significantly from 1.21 mg/dL at baseline to 1.10 mg/dL at 1 year (P=0.047). On average, mean arterial blood pressure decreased from 102+/-12 mm Hg at baseline to 92+/-10 mm Hg at 1 year (P
A possible explanation for the disparity between these studies is that the Radermacher investigation used angioplasty without stenting as a method for revascularization. Plain angioplasty may be no better than medical therapy.4
van Jaarsveld et al randomly assigned 106 patients with hypertension who had atherosclerotic renal-artery stenosis (defined as a decrease in luminal diameter of 50 percent or more) and a serum creatinine concentration of 2 mg per deciliter (200 micromol per liter) or less to undergo percutaneous transluminal renal angioplasty or to receive drug therapy.4 According to intention-to-treat analysis, at 12 months, there were no significant differences between the angioplasty and drug-therapy groups in systolic and diastolic blood pressures, daily drug doses, or renal function. In the treatment of patients with hypertension and renal-artery stenosis, angioplasty has little advantage over antihypertensive-drug therapy; stent therapy may be necessary to see any therapeutic effect.
The renal circulation is more complicated than the coronary circulation. First, because of the dual control of the efferent and afferent renal arterioles, both not necessarily behaving synchronously with various physiologic, pathophysiologic or provocative stresses, provocative vasodilator agents are difficult to assess. When drugs are used to stimulate a change in renal blood flow, it’s critically important to figure out whether the change is a consequence of medulary or cortical blood flow. That is, whether it is flow affecting the nephrons or not. Future research might help develop a renal perfusion index or to validate what kind of pressure gradient is the correct “cut point” for decision making.
Valvular Heart Disease
Valvular heart disease is another area where there are many ways to make important measurement errors in the hemodynamic evaluation of a patient. Figure 5 illustrates the difference between a distal aortic sheath pressure and a central aortic pressure due to pressure amplification in the distal aorta from a combination of stiff arteries and aortic insufficiency. The appearance of a reverse gradient created by pressure measurement from the sheath is obviously artifact, and highlights the potential for pressure amplification.
Figure 6 is a more typical example of distal pressure amplification artifact in the evaluation of aortic stenosis. The figure shows femoral artery pressure recorded from a sheath versus the central aortic pressure. This is from a 6 Fr 23 cm sheath with a 5 Fr diagnostic catheter. In contrast to the aortic pressure recorded from the sheath, the recording from the central aorta versus left ventricle in Figure 6 shows a significantly different picture. Depending on the cardiac output, the difference in gradient may represent the difference between a prosthetic valve or medical therapy.
Figure 7 is from a patient with an iliac origin stenosis just distal to the bifurcation of the aorta (angiogram inset). This was difficult to image because of the hip pin. The aortic pressure just above the iliac stenosis is falsely amplified, and below the stenosis it is decreased.
Figure 8A shows two traditional “gold standards” for gradient measurement in aortic stenosis.5 The left panel utilizes a double femoral puncture, with one catheter above the aortic valve and one in the left ventricle. This requires two arterial punctures. Figure 8B shows transseptal access to the left ventricle through a Hancock mitral valve prosthesis. There is a second catheter in the aortic root, passed retrograde via femoral access. The need for two arterial punctures or the use of transseptal access is more complicated than is needed or desirable in many cases. Use of a pressure wire passed through a diagnostic or guiding catheter is a method to obtain gradient measurements with a single arterial puncture, and has the advantage of placing the sampling points directly on either side of the target. Damping and amplification artifacts are thus minimized.
A double lumen pigtail catheter is also an option from a single femoral arterial puncture. The disadvantage is the need for a large 8F sheath. Older versions of the double lumen pigtail had a small caliber second lumen, which was subject to pressure damping. Current versions are better engineered, and provide good quality pressure tracings.
Figure 9 shows a pressure wire passed via a diagnostic catheter.6 This allows the pressure wire to sample left ventricular pressure, and the diagnostic catheter to sit in the aortic root, just above the valve, utilizing a single femoral arterial access. There is one critical trick needed to keep the wire in place in the left ventricle, which is to bend the wire into a large radius distal curve. If you only put a little coronary sized “j” on the end of the wire and place it into the ventricle through a diagnostic catheter, as soon as you pull the diagnostic catheter back out of the left ventricle over the wire, the pressure wire will be ejected. A large secondary bend in the wire will follow the basal inferior wall and stabilize the wire, as shown in the left two panels in Figure 9. I use a catheter that is made by Cook, which has an Amplatz-like shape, shown in Figure 9.7 This shape is easy to orient towards the aortic valve and has side holes to facilitate pressure measurement. The angiographic inset in Figure 9 shows how to deliver the pressure wire out of the 5 Fr catheter. The pressure tracings in Figure 10 show two left ventricular pressures from the 5 Fr fluid and the pressure wire. They are well matched. At that point, you back the diagnostic catheter out, put a little forward pressure on the pressure wire, and the wire lays along the basal inferior wall and the tip is curled backward in the left ventricular apex.
Figure 11 shows another recording from a patient with aortic stenosis. The femoral artery pressure measured from the sheath is amplified significantly. The diagnostic catheter is in the aorta right above the valve, showing central aortic pressure, and the pressure wire is in the left ventricle (LV). The difference between the gradient from sheath versus LV compared to central aorta versus LV is large enough to result in a discrepancy in valve area calculation. The difference in gradient is particularly important in the low output, low gradient setting.
Figure 12 is a case where the aortic valve measurement based on a sheath with aortic pressure amplification results in a diminished gradient, with a valve area of 0.9cm2, which might warrant watchful waiting. The heart rate is irregular, so the gradient varies beat to beat. Simultaneous recording of LV and aortic pressure is thus necessary, but not necessarily sufficient. The pressure wire gives an unadulterated, accurate measure, and a calculated valve area of 0.7cm2, which is clearly treated with surgery in a symptomatic patient (Table 2).
Figure 13 shows pressure recorded from a 23 cm, 6 Fr sheath. The sheath flushes easily and is sitting above the bifurcation of the aorta in the descending aorta. It is damped, but this would not be apparent without another independent measure of the central aortic pressure. The damping likely results from tortuosity in the iliac, or possibly from thrombus in the sheath. There is no phase delay in the foot of the central aortic pressure recorded from the pressure wire, which distinguishes it as the correct measure.
Congenital Heart Disease
Accurate measurement of gradients is important in children with valve disease and in congenital lesions, since valve area may change with patient size, and decisions to intervene are often based on gradient alone.
Coarctation of the aorta is a difficult lesion to assess hemodynamically. In some cases, even if the coarctation is not very tight, it may be eccentric. It is sometimes a struggle to cross the coarct lesion with anything but a wire. Figure 14 is a case where there is a 20 mm gradient across the coarctation segment. The patient is symptomatic, with leg fatigue with modest activity. Interpretation of the gradient is challenging in the de novo coarctation because collaterals can be so good that there may be almost no gradient across a virtually occluded aorta.
Recently, percutaneous valve replacement in pulmonary artery (Fontan) conduits has been performed in congenital heart disease patients with stenosis in their bioprosthetic valves.8 Figure 15 is a case in which it was impossible to get a catheter beyond the conduit inlet into the distal PA conduit. Properly assessing whether the prosthetic valve in these pulmonary artery conduits is or is not functioning is essential for proper management. Reoperations may be a second, sometimes a third or a fourth procedure for these patients. In Figure 15, a conventional catheter could not be passed into the distal pulmonary conduit, but a 0.014” pressure wire could be placed relatively easily. There is a large gradient, indicating severe pulmonic prosthetic stenosis, which warrants intervention.
The application of translesional pressure gradient assessment has been well studied in the coronary circulation, and fractional flow reserve measurement has become a routine part of practice largely due to the ability to place a pressure wire into the coronary circulation. Limitations on pressure gradient measurement that were common when only standard fluid-filled catheters were available have been overcome by pressure wire technology. Gradient measurement in renal artery stenosis and other peripheral lesions, and in valvular and congenital heart diseases, can solve a wide variety of both mundane and unusual clinical problems.
Address for correspondence: Ted Feldman, MD, FSCAI, FACC, Professor of Medicine, Northwestern University Medical School; Director, Cardiac Catheterization Laboratory, Evanston Hospital, Cardiology Division, Burch 300, 2650 Ridge Ave., Evanston, IL 60201. E-mail: TFeldman@enh.org