Use of Fraction Flow Reserve to Predict Changes over Time in Management of Superficial Femoral Artery

Lotfi, Amir; Sivalingam, Senthil; Giugliano, Gregory R.; Ashraf, Javed; Visintainer, Paul

doi:10.1111/j.1540-8183.2011.00691.x

Cited by 24 publications

(22 citation statements)

References 30 publications

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“… 3 , 4 Various parameters have been proposed to determine hemodynamic significance, including mean pressure gradient (MPG), peak-to-peak PG, and ratio of mean pressure (also referred to as the peripheral fractional flow reserve [pFFR]) with or without vasodilators. 5 – 9 However, the validity of these parameters for treatment planning is unclear. Therefore, the purpose of this study was to verify whether trans-stenotic absolute PG and pFFR measured using a 0.014-inch pressure wire under hyperemia can be used to establish hemodynamic significance in iliofemoral angiographically intermediate stenosis.…”

Section: Introductionmentioning

confidence: 99%

Validation of pressure gradient and peripheral fractional flow reserve measured by a pressure wire for diagnosis of iliofemoral artery disease with intermediate stenosis

Murata

Aihara

Soga

et al. 2015

MDER

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ObjectiveTo examine the pressure gradient and peripheral fractional flow reserve (pFFR) measured by a pressure wire as indicators of hemodynamic significance in iliofemoral angiographic intermediate stenosis.BackgroundThe utility of pressure measurements using a pressure wire with vasodilators is unclear in cases with intermediate iliofemoral stenosis.MethodsThe mean pressure gradient (MPG) and mean pressure ratio (MPR) were measured at baseline and after injection of isosorbide dinitrate in 23 lesions with angiographically intermediate iliofemoral stenosis. Patients with complex lesions, infrapopliteal artery lesions, chronic total occlusion, and surgical bypass grafts were excluded. Hyperemic MPR was considered equivalent to pFFR. Changes in parameters in response to vasodilators were assessed and correlations of peak systolic velocity ratio (PSVR) with hyperemic MPG and pFFR were examined using duplex ultrasound.ResultsAfter injection of isosorbide dinitrate, hyperemic MPG increased significantly (from 9.0±5.7 to 16.3±6.2 mmHg; P<0.05) and hyperemic MPR (pFFR) decreased significantly (from 0.92±0.06 to 0.81±0.07; P<0.05). PSVR was significantly correlated with hyperemic MPG (R=0.52; P<0.05) and pFFR (R=−0.50; P<0.05). The optimal cut-off value of pFFR as an indicator of significant hemodynamic stenosis (PSVR >2.5) was 0.85 (area under the curve 0.72; sensitivity 94%; specificity 50%, P<0.05).ConclusionpFFR measured using a pressure wire is reliable for prediction of hemodynamic significance in iliofemoral intermediate stenosis.

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Section: Introductionmentioning

confidence: 99%

Validation of pressure gradient and peripheral fractional flow reserve measured by a pressure wire for diagnosis of iliofemoral artery disease with intermediate stenosis

Murata

Aihara

Soga

et al. 2015

MDER

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“…39 In patients with claudication, initial studies have shown that FFR measurements correlate with the lesion peak systolic velocity, a noninvasive measurement of lesion severity. 40 Further studies will be necessary to correlate the clinical use of FFR measurements to potentially guide revascularization or other treatment strategies in PAD.…”

Section: Exercise Hemodynamicsmentioning

confidence: 99%

Pathogenesis of the Limb Manifestations and Exercise Limitations in Peripheral Artery Disease

Hiatt¹,

Armstrong²,

Larson³

et al. 2015

Circulation Research

137

118

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P eripheral artery disease (PAD) is initiated by atherogenic mechanisms common to all major vascular territories but encompasses several distinctly important clinical sequelae.1 The global burden of PAD is large and rising, with substantial morbidity and mortality found in high-, middle-, and low-income countries. 2 The atherosclerotic occlusive disease underlying PAD is associated with an exercise limitation in the majority of patients, whereas the classic symptoms of intermittent claudication, ischemic rest pain, and ischemic ulceration are less common manifestations. 3 Patients with PAD are also at increased risk of myocardial infarction, ischemic stroke, heart failure, renovascular hypertension, and vascular death reflecting the systemic atherosclerotic burden. [4][5][6] The epidemiology of Peripheral Artery Disease Compendium© 2015 American Heart Association, Inc. The diagnosis of PAD can be ascertained by simple hemodynamic measurements, in particular, the ankle-brachial index (ABI), a test performed by measuring the systolic blood pressure in each arm and the dorsalis pedis and posterior tibial arteries of each ankle. The highest of the dorsalis pedis or posterior tibial artery pressures is the numerator of the ABI specific to each leg, whereas the highest arm pressure on either side is the denominator. A ratio of <0.90 in either leg is considered hemodynamic evidence of PAD. 16 When imaged, PAD can be characterized as one or more arterial stenoses or occlusions involving the distal aorta, iliac, femoral, popliteal, or tibial arteries. 17The underlying mechanisms responsible for the functional limitations in PAD are hemodynamic in origin, which affects the supply of oxygen and substrates to metabolically active tissue: skeletal muscle in the case of intermittent claudication and skin and subcutaneous tissues in the case of critical leg ischemia. However, additional pathophysiologic mechanisms contribute to the limb manifestations, where a reduction in blood flow alone does not fully account for the exercise limitation. Recent research into the pathophysiology of this exercise limitation has identified several important sequelae resultant from the chronic hemodynamic deficit. These changes affecting the vasculature and skeletal muscle distal to the primary hemodynamic lesions likely contribute to the mechanisms of exercise limitation in PAD. These advances are reviewed here with an additional focus on identifying possible future therapeutic strategies. Symptomatic Manifestations and Exercise Limitations in PADIn the coronary circulation, plaque rupture leading to acute ischemic events is a common clinical presentation; in PAD, progressive atherosclerosis leading to chronic stenosis and occlusion, often in series, in the arteries supplying the lower extremities dominates the symptomatic manifestations.6 Limb SymptomsPatients with PAD may present with a range of limb symptoms. Most patients are either asymptomatic or have atypical limb symptoms during exercise, whereas only a third have typical symptoms of c...

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“…3 A). Fractional flow reserve (FFR), which measures the pressure gradient across stenotic arteries, was increased in arteries with larger cross-sectional lumen areas 16 , 17 . The FFR value in the SDT group (Fig.…”

Section: Resultsmentioning

confidence: 99%

Early modulation of macrophage ROS-PPARγ-NF-κB signalling by sonodynamic therapy attenuates neointimal hyperplasia in rabbits

Yao

Zhao

Tan

et al. 2020

Sci Rep

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Disruption of re-endothelialization and haemodynamic balance remains a critical side effect of drugeluting stents (DES) for preventing intimal hyperplasia. Previously, we found that 5-aminolevulinic acid-mediated sonodynamic therapy (ALA-SDT) suppressed macrophage-mediated inflammation in atherosclerotic plaques. However, the effects on intimal hyperplasia and re-endothelialization remain unknown. In this study, 56 rabbits were randomly assigned to control, ultrasound, ALA and ALA-SDT groups, and each group was divided into two subgroups (n = 7) on day 3 after right femoral artery balloon denudation combined with a hypercholesterolemic diet. Histopathological analysis revealed that ALA-SDT enhanced macrophage apoptosis and ameliorated inflammation from day 1. ALA-SDT inhibited neointima formation without affecting re-endothelialization, increased blood perfusion, decreased the content of macrophages, proliferating smooth muscle cells (SMCs) and collagen but increased elastin by day 28. In vitro, ALA-SDT induced macrophage apoptosis and reduced TNFα, IL-6 and IL-1β via the ROS-PPARγ-NF-κB signalling pathway, which indirectly inhibited human umbilical artery smooth muscle cell (HUASMC) proliferation, migration and IL-6 production. ALA-SDT effectively inhibits intimal hyperplasia without affecting re-endothelialization. Hence, its clinical application combined with bare-metal stent (BMS) implantation presents a potential strategy to decrease bleeding risk caused by prolonged dual-antiplatelet regimen after DES deployment. For the past few decades, percutaneous coronary intervention (PCI) has been developed as a routine treatment modality for coronary atherosclerotic disease. In the era of balloon angioplasty and bare-metal stents (BMS), the major problem of PCI is intimal hyperplasia resulting in restenosis of the treated vessel, which leads to renewed symptoms and the need for repeated intervention. The antiproliferative drugs released from drug-eluting stents (DES) inhibit intimal hyperplasia but delay re-endothelialization at the expense of an increase in late stent thrombosis. Prolonged dual-antiplatelet therapy diminishes the rate of stent thrombosis at the cost of increased

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Use of Fraction Flow Reserve to Predict Changes over Time in Management of Superficial Femoral Artery

Cited by 24 publications

References 30 publications

Validation of pressure gradient and peripheral fractional flow reserve measured by a pressure wire for diagnosis of iliofemoral artery disease with intermediate stenosis

Validation of pressure gradient and peripheral fractional flow reserve measured by a pressure wire for diagnosis of iliofemoral artery disease with intermediate stenosis

Pathogenesis of the Limb Manifestations and Exercise Limitations in Peripheral Artery Disease

Early modulation of macrophage ROS-PPARγ-NF-κB signalling by sonodynamic therapy attenuates neointimal hyperplasia in rabbits

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