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DESCRIPTIONPeripheral arterial disease (PAD) is a common atherosclerotic syndrome that is associated with significant morbidity and mortality. A less-common cause of PAD is Buerger disease, also called thromboangitis obliterans, which is a nonatherosclerotic segmental inflammatory disease that occurs in younger patients and is associated with tobacco use. Development of PAD is characterized by narrowing and occlusion of arterial vessels and eventual reduction in distal perfusion. Critical limb ischemia is the endstage of lower extremity PAD in which severe obstruction of blood flow results in ischemic pain at rest, ulcers, and a significant risk for limb loss. The standard therapy for severe, limb-threatening ischemia is revascularization aiming to improve blood flow to the affected extremity. If revascularization has failed or is not possible, amputation is often necessary.
Two endogenous compensating mechanisms may occur with occlusion of arterial vessels, capillary growth (angiogenesis) and development of collateral arterial vessels (arteriogenesis). Capillary growth is mediated by hypoxia-induced release of chemo- and cytokines such as vascular endothelial growth factor (VEGF), and occurs by sprouting of small endothelial tubes from pre-existing capillary beds. The resulting capillaries are small and cannot sufficiently compensate for a large occluded artery. Arteriogeneis with collateral growth is, in contrast, initiated by increasing shear forces against vessel walls when blood flow is redirected from the occluded transport artery to the small collateral branches, leading to an increase in the diameter of pre-existing collateral arterioles.
The mechanism underlying arteriogenesis includes the migration of bone marrow-derived monocytes to the perivascular space. The bone marrow-derived monocytes adhere to and invade the collateral vessel wall. It is not known if the expansion of the collateral arteriole is due to the incorporation of stem cells into the wall of the vessel or to cytokines released by monocytic bone marrow cells that induce the proliferation of resident endothelial cells. It has been proposed that bone marrow-derived monocytic cells may be the putative circulating endothelial progenitor cells. Notably, the same risk factors for advanced ischemia (diabetes, smoking, hyperlipidemia and advanced age) are also risk factors for a lower number of circulating progenitor cells.
The rationale of hematopoietic stem-cell/bone marrow-cell therapy in PAD is to induce arteriogenesis by boosting the physiological repair processes. This requires large numbers of functionally active autologous precursor cells, and subsequently a large quantity of bone marrow (e.g., 240-500 mL). The SmartPReP2® Bone marrow Aspirate Concentrate System (Harvest Technologies) has been developed as a single-step point-of-care, bedside centrifugation system for the concentration of stem cells from bone marrow. The system is composed of a portable centrifuge and an accessory pack that contains processing kits including a functionally closed dual-chamber sterile processing disposable. The SmartPReP2® system is designed to concentrate a buffy coat of 20 mL from whole bone marrow aspirate of 120 mL. The concentrate of bone marrow aspirate contains a mix of cell types, including lymphocytoid cells, erythroblasts, monocytoid cells, and granulocytes. Following isolation and concentration, the hematopoietic stem-cell/bone marrow concentrate is administered either intra-arterially or through multiple injections (20 to 60) into the muscle, typically in the gastrocnemius.
Standard outcomes for critical limb ischemia include the Rutherford criteria for limb status, healing of ulcers, the ankle-brachial index (ABI), transcutaneous oxygen pressure (TcO2), and pain-free walking. The Rutherford criteria include ankle and toe pressure, the level of claudication, ischemic rest pain, tissue loss, nonhealing ulcer, and gangrene. The ABI measures arterial segmental pressures on the ankle and brachium, and indexes ankle systolic pressure against brachial systolic pressure (normal range 0.95 – 1.2). An increase > 0.1 is considered to be clinically significant. TcO2 is measured with an oxymonitor; the normal value is 70-90 mmHg. Pain free walking may be measured by time on a treadmill, or more frequently by distance in a 400 meter walk.
The SmartPReP2® Bone Marrow Aspirate Concentrate System is a microprocessor-controlled dedicated centrifuge with decanting capability and an accessory BMAC IDE PAD Pack for processing a patient’s bone marrow aspirate. The system is in a Phase III trial; expected completion of the trial is in 2014.
Related medical policies are as follows:
POLICYTreatment of peripheral arterial disease, including critical limb ischemia, with injection or infusion of cells concentrated from bone marrow aspirate is considered investigational.
POLICY GUIDELINESInvestigative service is defined as the use of any treatment procedure, facility, equipment, drug, device, or supply not yet recognized by certifying boards and/or approving or licensing agencies or published peer review criteria as standard, effective medical practice for the treatment of the condition being treated and as such therefore is not considered medically necessary.
The coverage guidelines outlined in the Medical Policy Manual should not be used in lieu of the Member's specific benefit plan language.
POLICY HISTORY07/21/2011: Approved by Medical Policy Advisory Committee
07/17/2012: Policy reviewed; no changes.
08/14/2013: Policy reviewed; no changes.
SOURCE(S)Blue Cross Blue Shield Association policy # 8.01.55
CODE REFERENCEThis may not be a comprehensive list of procedure codes applicable to this policy.