Use of fractional flow reserve in the assessment of chronic mesenteric ischemia

In this issue of Vascular Medicine, Sadiq et al. use a case illustration to discuss the use of fractional flow reserve to evaluate chronic mesenteric ischemia. ¹ The case presentation encompasses a number of interesting aspects about chronic mesenteric ischemia and the complexity of assessment. The anatomical findings and development of clinical symptoms following iatrogenic occlusion of the inferior mesenteric artery (IMA) underscores the importance of understanding splanchnic collateralization and its role in intestinal perfusion.

The patient manifested symptoms of small bowel ischemia rather than ischemic colitis. The authors indicate that flow from the superior mesenteric artery (SMA) via the Arc of Riolan (Marginal Artery) to the IMA compromised flow reserve to the small intestine resulting in the patient’s clinical symptoms. This collateral pathway also is commonly observed in the setting of SMA stenosis or occlusion with retrograde flow from the IMA to the SMA via the middle colic artery. Angiographic images prior to the aortic intervention would be useful to assess the possibility that the IMA was providing augmented flow to the small intestine and that its occlusion resulted in the development of symptoms, as this would have provided indirect evidence that antegrade flow in the SMA was compromised. The internal iliac arteries also are an important perfusion source for the large intestine and their patency could be a determinant of IMA flow and the degree of collateralization observed.

The authors correctly assert that assessing physiologic flow in the mesenteric vessels is difficult. The anatomical findings by both computerized tomography (CT) and conventional angiography did not suggest severe stenosis of either the celiac artery or the SMA. The use of the pressure wire provided important physiologic information that helped guide therapy. The intravascular ultrasound evaluation also confirmed a more complex and severe stenosis than what was observed with more conventional imaging. Finally the patient’s clinical improvement further supported the decision to intervene.

The more difficult questions about the value of the pressure wire measurements are what is the threshold for clinically significant gradient across the visceral vessels, and what is the response to pharmacologic induced hyperemia in both normal and diseased arteries? The authors of a previous report of using the flow wire to assess SMA stenosis reported a resting gradient of 60mmHg and did not attempt to induce splanchnic hyperemia. ² Following intervention their patient’s symptoms also improved.

The circulatory control of splanchnic perfusion is poorly understood. In addition, pressure-flow auto regulation is likely different in the celiac (hepatic arterial bed) compared to SMA flow into the small intestine.

While the pressure wire gradient did appear to help in the assessment, we must be very cautious about its wholesale clinical application. While these anecdotal case reports are helpful in identifying novel applications of available technology, they do not provide compelling evidence that we should accept their routine use in clinical practice. Prior to advocating the routine use of the pressure wire to assess mesenteric artery stenosis additional fundamental evaluation is required. Validation of the threshold for clinically significant gradient or flow reserve is the first step and of paramount importance. This can only be accomplished by well-designed pressure wire and pharmacologic induced hyperemic flow studies in both normal and diseased mesenteric arteries. Once this is accomplished, validated criteria can be established to help guide the appropriate evaluation of patients with suspected chronic mesenteric ischemia and determine who will likely benefit from revascularization.