局部动脉注射阿替普酶溶栓治疗急性缺血性脑卒中的临床效果

目的分析局部动脉注射阿替普酶溶栓治疗急性缺血性脑卒中的临床效果。方法本溪市中心医院从2011年1月至2013年10月期间共收治90例急性缺血性脑卒中患者,患者在入院的6 h内接受了阿替普酶溶栓的局部动脉注射治疗,观察总结患者接受治疗24 h和3个月内的疗效,并依据临床观察和NHISS评分结果来评价患者的神经功能恢复情况。结果 90例患者当中有58例前循环缺血患者和32例后循环缺血患者,在接受溶栓治疗的24 h内有64例患者神经功能得到良好恢复,占总数的71.11%,还有26例患者神经功能不良,占总数的28.89%;3个月后通过随访了解到有82例患者神经功能良好,占总数的91.11%,8例患者功能仍然处于不良状态,占总数的8.89%,治疗前后患者的神经功能恢复比较差异具有统计学意义（P〈0.05%）。结论局部动脉注射阿替普酶溶栓治疗急性缺血性脑卒中,患者能够得到有效恢复,疗效显著,值得在临床上推广使用。     

重组组织型纤溶酶原激活剂静脉溶栓治疗发病4.5小时内急性脑梗死近期疗效的回顾性研究

目的:研究发病4.5小时内的急性脑梗死患者早期应用重组组织型纤溶酶原激活剂(rt-PA)静脉溶栓治疗的临床效果。方法:回顾性分析2018年07月1日到2020年10月31日我院神经内科收治的发病在4.5小时内的652例急性脑梗死患者的临床资料,其中使用rt-PA静脉溶栓治疗的患者285例为溶栓组,未溶栓仅使用抗血小板聚集、他汀类降脂、脑保护等常规治疗的患者367例为对照组。记录两组患者治疗前及治疗后24小时、7天、14天的美国国立卫生研究院卒中量表(NIHSS)评分和治疗3个月后的改良Rankin量表(mRS)评分。对于有吞咽障碍的患者,收集洼田饮水试验结果。统计两组患者出血情况和死亡率。结果:溶栓组治疗后24小时、7天、14天的NIHSS评分以及治疗后3个月的mRS评分改善明显,与对照组相比,差异有统计学意义(P<0.05);对于有吞咽障碍的患者,溶栓组的治疗有效率高于对照组(P<0.05);溶栓组轻微出血的概率大于对照组(P<0.05);两组在症状性及致死性脑出血方面的差异无统计学意义(P>0.05);溶栓后大量及致死性脑出血部位多在梗死的中心区、出血量多大于10 mL,患者临床NIHSS评分≥24分。溶栓组死亡率较对照组下降(P<0.05)。结论:发病4.5小时内的急性脑梗死患者接受rt-PA静脉溶栓治疗的近期治疗效果良好,轻微出血风险较高,但是死亡率下降。临床神经功能缺损重、NIHSS评分≥24分、出血风险大的患者预后不良,不推荐溶栓治疗。     

In vivo microscopic assessment of cremasteric microcirculation during hindlimb allograft rejection in rats.

Experimental and clinical studies of vascular allogenic extremity transplantation have yielded disappointing results and have not been clinically useful. With recent advances in transplantation immunology, considerable interest has focused on the understanding of leukocyte-endothelial interaction at the microcirculatory level. The objective of this study was to characterize the alterations in leukocyte-endothelial interaction in the early stages of rat hindlimb allograft rejection. To study the changes at the microcirculatory level, a new microsurgical model was developed; the cremaster muscle was incorporated into the transplanted hindlimb. The purpose of this study was to report on the microcirculatory changes during rat hindlimb allograft rejection. A total of 24 transplantations were performed among the four experimental groups. In a control group, 12 rat hindlimb-cremaster grafts were transplanted between genetically identical animals, Lewis to Lewis. Microcirculatory measurements of graft survival were taken at 24 hours (group 1A, n = 6) and at 72 hours (group 1B, n = 6). In the rejection control group, 12 transplantations were performed across a major histocompatibility barrier between Lewis-Brown Norway and Lewis rats. Microcirculatory measurements were taken at 24 (group 2A, n = 6) and 72 hours (group 2A, n = 6) as above. The following parameters were evaluated to discover the leukocyte-endothelial interaction: endothelial edema index and the number of rolling, adherent, and transmigrating leukocytes and lymphocytes in the postcapillary venule. Physical signs of limb rejection, such as edema, erythema, scaling, plaque formation on the skin, hair loss, and skin surface temperature, were monitored. Microcirculatory signs of rejection included the following. There was a significant increase in the number of adherent leukocytes in allograft transplants at both 24 hours (205 percent; 2.05 +/- 0.38) and 72 hours (431 percent; 9.11 +/- 3.41) when compared with isograft controls (1.00 +/- 0.89 at 24 hours; 2.11 +/- 0.34 at 72 hours) (p < 0.05). The activation of leukocyte transmigration increased more than 7-fold in muscle allografts at 24 hours (0.55 +/- 0.25 versus 4.16 +/- 1.89) and more than 6-fold at 72 hours (0.72 +/- 0.38 versus 4.38 +/- 1.28) after transplantation (p < 0.05). Endothelial edema index, a measure of endothelial swelling and cellular deposit accumulation, increased more than 119 percent in the allograft group 72 hours after transplantation (1.23 +/- 0.07 versus 1.46 +/- 0.09) (p < 0.05). The first clinical signs of limb rejection were scaling of the skin or hair loss; they were observed between the seventh and ninth postoperative days. The composite rat hindlimb-cremaster model presented in this study introduces a new in vivo approach to monitor acute graft rejection using the intravital microscopy system. This is a valuable model for defining the timing, sequence, and correlation between immunologic events and clinical signs during the acute phase of allograft rejection.     

Coronary revascularization after thrombolytic therapy for myocardial infarction: what caseloads could Canadian centres face?

A simple model was developed to project the potential effect of intravenous thrombolytic therapy on the caseloads of revascularization early after acute myocardial infarction. Published data were used to estimate the proportion of infarct patients eligible for thrombolytic treatment and their subsequent rates of percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass surgery (CABS) within 2 weeks and up to 6 to 12 weeks after treatment. Toronto regional caseload data were obtained from registries and hospital discharge records. Our primary projections, based only on coronary angiography for evidence of spontaneous or exercise-induced ischemia, suggest a 165% increase in the post-thrombolysis use of PTCA within 2 weeks of infarction and even greater increases 6 to 12 weeks after infarction. Adding in selective use of salvage PTCA for some patients with persisting pain despite thrombolysis increases the overall PTCA caseload within 2 weeks by 242%. Data on the current caseload of post-thrombolysis CABS are unavailable. However, our projected caseload for the 30% of infarct patients treated with thrombolytic drugs equals or exceeds the current number of CABS procedures performed on all infarct patients within a month of the event. All these projections are conservative, in that they consider neither procedures 3 to 12 months after infarction nor restenosis after PTCA. This analysis illustrates that current approaches to revascularization after thrombolytic therapy could have a substantial effect on PTCA and CABS caseloads. Further studies with improved caseload data are needed to validate these preliminary projections.     

Prospective evaluation of eligibility for thrombolytic therapy in acute myocardial infarction.

OBJECTIVES--To determine the proportion of patients presenting with acute myocardial infarction who are eligible for thrombolytic therapy. DESIGN--Cohort follow up study. SETTING--The four coronary care units in Auckland, New Zealand. SUBJECTS--All 3014 patients presenting to the units with suspected myocardial infarction in 1993. MAIN OUTCOME MEASURES--Eligibility for reperfusion with thrombolytic therapy (presentation within 12 hours of the onset of ischaemic chest pain with ST elevation > or = 2 mm in leads V1-V3, ST elevation > or = 1 mm in any other two contiguous leads, or new left bundle branch block); proportions of (a) patients eligible for reperfusion and (b) patients with contraindications to thrombolysis; death (including causes); definite myocardial infarction. RESULTS--948 patients had definite myocardial infarction, 124 probable myocardial infarction, and nine ST elevation but no infarction; 1274 patients had unstable angina and 659 chest pain of other causes. Of patients with definite or probable myocardial infarction, 576 (53.3%) were eligible for reperfusion, 39 had definite contraindications to thrombolysis (risk of bleeding). Hence 49.7% of patients (537/1081) were eligible for thrombolysis and 43.5% (470) received this treatment. Hospital mortality among patients eligible for reperfusion was 11.7% (55/470 cases) among those who received thrombolysis and 17.0% (18/106) among those who did not. CONCLUSIONS--On current criteria about half of patients admitted to coronary care units with definite or probable myocardial infarction are eligible for thrombolytic therapy. Few eligible patients have definite contraindications to thrombolytic therapy. Mortality for all community admissions for myocardial infarction remains high.     

Transient reduction of autoantibodies against oxidized ldl in patients with acute myocardial infarction

Fifteen consecutive patients (mean age 66 ± 14, range 31–82) with an acute myocardial infarction (MI) suitable for thrombolytic therapy were included in this study. Autoantibodies against oxidized low-density lipoprotein (LDL) were determined by enzyme-linked immunosorbent assay (ELISA). Patients (n = 10) with marked elevation of the MB isoenzyme of creatinine kinase (CK-MB)-mass had significant decreases of oLDL-Ab during the acute phase, with a minimum after 8 h following the onset of thrombolytic therapy (within-group significance: p < .001; between groups: p = .01). Patients (n = 5) with CK-MB-mass values less than 70 ng/ml did not show this phenomenon. Furthermore, significant correlations existed between CK-MB-mass and oLDL-Ab after 6 and 8 h (n = 15; R = .72; P = .003) and the time of the highest CK-MB-mass values (after 12 h) and the time of the maximal decrease of oLDL-Ab (after 8 h) (r = .74; P = .003). Our observations provide further evidence for the release of free radicals and for increased lipid peroxidation during reperfusion after prolonged ischemia. The decrease of oLDL-Ab appears to be a marker for the severity of MI.     

THE ROLE OF ENDOGENOUS ACID IN THE DEVELOPMENT OF ACUTE GASTRIC ULCER INDUCED BY ISCHEMIA-REPERFUSION IN THE RAT

We investigated the role of endogenous gastric acid in the development of gastric ulcer from erosion induced by ischemia-reperfusion of the celiac artery in the rat. A half-hour clamping of the celiac artery (ischemia) caused acute gastric erosions 1 hour after reperfusion and such acute injuries progressed to ulcers 48–72 hours after reperfusion without any necrotizing agents. Gastric acid secretion decreased immediately after ischemia and didn't recover until 12 hours after reperfusion. Intraperitoneal administrations of cimetidine (100 mg/kg, every 12 hours) or omeprazole (30 mg/kg, every 24 hours) were started at 1, 6, or 12 hours after reperfusion. When administrations were started 1 hour after reperfusion, both drugs significantly decreased the total damaged area and prevented the progression of gastric erosions to ulcers. However, administrations started 6 or 12 hours after reperfusion failed to inhibit the total damaged area and to prevent ulcer formation. These results suggest that endogenous gastric acid may play an important role in the progression of gastric erosions to ulcers although ischemia itself reduces acid secretion. Furthermore, treatment with anti-acid-secretory drugs in the early stage of mucosal damage may be important for the prevention of ulcer. © 1997 Elsevier Science Inc.     

Thrombolysis and acute cerebral infarction

Thrombolytic therapy are the most important advance in the management of acute ischemic stroke and has been evaluated in several randomised trials. Thrombolysis with recombinant tissue plasminogen activator (rt-Pa) is effective within 3 h of onset of ischemic stroke and this efficacy is similar between different stroke subtypes. New trials will determine if extension of this time-window can be substantiated. Therapy beyond the 3-hour window, with intra-arterial thrombolysis, appears to improve outcome but are applicable to selected group of patients. Thrombolytic drugs can also carry an important risk (5 % to 10 %) of brain hemorrhage and edema that can prove fatal. The risk of symptomatic intracranial hemorrhage is directly proportional to stroke severity and inversely proportional to time to treatment. There is a growing interest in the use of MRI in acute ischemic stroke. It helps identify location of early cerebral ischemia and provides valuable information not only of the penumbra but also of vessel occlusion. Its use might help in selecting patients who will benefit most from treatment such as thrombolysis. In spite of these results, community use of thrombolytic therapy remains dismally low. Many physicians and medical centers are not presently equipped or willing to give thrombolytic drugs for stroke treatment. Increasing stroke awareness in the community, creating stroke unit and physicians education are necessary to extend the effective use of acute treatment in cerebral infarct to a larger group of patients.     

Early results of acute non-traumatic ischemia of the limbs]

The results of therapy of 726 patients with the acute non-traumatic ischemia of the limbs are discussed. These patients were treated in the 11 centres of vascular surgery in Poland between 1986 and 1988. Out of causes of the acute non-traumatic ischemia of the limbs arterial embolism was diagnosed in 450 patients, thrombosis in 229 cases, and dissecting aneurysm in 8 patients as well as phlegmasia coerulea dolens in 1 patient Surgical treatment included 665 patients, and the remaining 383 patients were treated conservatively. The results of the conservative and surgical treatment were scored with a 5-point scale. Excellent results with the return of complete functioning of the affected limb and presence of peripheral pulse were achieved in 291 patients, positive result, i.e. lack of the peripheral pulse, in 197 cases, moderate result in 80 patients in whom complete functioning of the limb has not been restored. In case of 64 patients an amputaion proved necessary. Nine four patients died.     

Reduction of skeletal muscle injury in composite tissue allotransplantation by heat stress preconditioning

Ischemia-reperfusion injury is a dominant factor limiting tissue survival in any microsurgical tissue transplantation, a fact that also applies to allogeneic hand transplantation. The clinical experience of the 12 human hand transplantations indicates that shorter ischemia times result in reduced tissue damage and, ultimately, in better hand function. Heat stress preconditioning and the accompanying up-regulation of the heat shock protein 72 have been shown to reduce the ischemia-reperfusion injury following ischemia of various organs, including organ transplantation. The aim of this study was to reduce the ischemia-reperfusion injury in a model of composite tissue allotransplantation. Allogeneic hind limb transplantations were performed from Lewis (donor) to Brown-Norway rats. Donor rats in group A (n = 10) received a prior heat shock whereas rats in group B (n = 10) did not receive any prior heat shock. Group C served as a control group without transplantation. The transplantations were performed 24 hours after the heat shock, at which time the heat shock protein 72 was shown to be up-regulated. The outcome was evaluated 24 hours after transplantation by nitroblue tetrazolium staining and wet-to-dry weight ratio of muscle slices (anterior tibial muscle). The nitroblue tetrazolium staining showed a significant reduction of necrotic muscle in group A (prior heat shock) (p = 0.005). The wet-to-dry ratio was significantly reduced in group A (prior heat shock), indicating less muscle edema and less tissue damage (p = 0.05). Heat shock preconditioning 24 hours before an ischemic event leads to an up-regulation of heat shock protein 72 in muscle and to a tissue protection reducing ischemia-reperfusion injury in composite tissue transplantation.     

Debate: Should the elderly receive thrombolytic therapy or primary angioplasty?

Thrombolysis and primary angioplasty are both recommended reperfusion strategies for elderly patients presenting with myocardial infarction (MI). Primary angioplasty is most beneficial in high-risk patients. While the elderly have a high absolute risk of dying or developing complications after MI, they also have an increased risk of intracranial haemorrhage if they are given thrombolytic therapy. It could therefore be reasonably argued that primary angioplasty is the reperfusion strategy of choice in the elderly. However, primary angioplasty has not been shown to have a greater relative benefit than thrombolytic therapy in the elderly. Recent data from the Fibrinolytic Therapy Trialists' (FTT) Collaborative Group show that thrombolytic therapy significantly reduces mortality compared with control treatment in patients over 75 years of age presenting within 12 h of symptom onset, with ST-segment elevation or bundle branch block. Future advances in adjunctive therapies may improve myocyte perfusion and hence the outcomes achieved by both invasive and noninvasive reperfusion strategies. Better thrombolytic regimens incorporating adjunctive agents such as bivalirudin may reduce the risk of intracranial haemorrhage. Few hospitals can provide a 24-h primary angioplasty service with door-to-balloon times consistently less than 90 min, and thrombolytic therapy is therefore a far more practical option in most instances.     

Debate: Should the elderly receive thrombolytic therapy, or primary angioplasty, for acute myocardial infarction? The case for primary angioplasty

As the population ages the number of elderly patients presenting with acute myocardial infarction (AMI) will continue to increase. There has been no head-to-head trial of thrombolytic therapy versus primary percutaneous coronary intervention (PCI) in this patient cohort, but there is evidence that favors primary PCI. Most elderly patients are candidates for primary PCI, but many have contraindications to thrombolytic therapy. Hemorrhagic complications are more common in the elderly, and many of these patients present with conditions in which thrombolytic agents have decreased efficacy, such as heart failure or prior bypass surgery. PCI can also obviate the need for further risk stratification in most patients.     

高压氧对局灶性脑缺血后细胞凋亡的影响及其机制

目的：观察不同时间点高压氧（HBO）治疗对短暂性脑缺血的作用,并探讨其对细胞凋亡的影响。方法：在客观监测局部脑血流的条件下,大鼠经历短暂脑缺血后3h,6h,12h应用HBO治疗,24h后行神经功能评分和梗死体积测定,免疫组化染色各组Bcl-2、Bax、活性Caspase-3、活性Caspase-9以及TUNEL法检测细胞凋亡。结果：缺血后3h HBO治疗减少70％梗死体积,缺血后6hHBO治疗则减少梗死体积约44％,早期应用HBO治疗增加半暗带区细胞内Bcl-2的表达,减少活性Caspase-9和活性Caspase-3以及TUNEL阳性细胞数;缺血后12h应用HBO治疗却恶化神经功能,扩大梗死范围,而对上述凋亡各指标无影响。结论：HBO治疗短暂性局灶脑缺血具有时间窗,应争取在缺血后6h内应用HB0治疗,其早期治疗的神经保护作用与抑制细胞凋亡有关。     

尿激酶静脉溶栓治疗急性心肌梗死的疗效观察--附35例报告

目的 观察尿激酶静脉溶栓治疗急性心肌梗死的疗效.方法将66例急性心肌梗塞住院患者随机分成两组,溶栓组35例在常规治疗的同时,用尿激酶静脉溶栓治疗,非溶栓组仅用常规治疗,两组进行比较分析.结果 溶栓组血管再通率74.3%,非溶栓组为25.81%,两组间有明显差异(P<0.05),住院4周的病死率,溶栓组为2.86%,非溶栓组为16.16%,两组间有显著差异(P<0.01).结论 尿激酶静脉溶栓能明显提高急性心肌梗死患者的血管再通率和抢救成功率,降低近期病死率.     

Acute,Delayed and Chronic Remote Ischemic Conditioning Is Associated with Downregulation of mTOR and Enhanced Autophagy Signaling

Background

Remote ischemic conditioning (RIC), induced by brief periods of limb ischemia has been shown to decrease acute myocardial injury and chronic responses after acute coronary syndromes. While several signaling pathways have been implicated, our understanding of the cardioprotection and its underlying mediators and mechanisms remains incomplete. In this study we examine the effect of RIC on pro-autophagy signaling as a possible mechanism of benefit.

Methods and Results

We examined the role of autophagy in the acute/first window (15 minutes after RIC), delayed/second window (24 hours after RIC) and chronic (24 hours after 9 days of repeated RIC) phases of cardioprotection. C57BL/6 mice (N = 69) were allocated to each treatment phase and further stratified to receive RIC, induced by four cycles of 5 minutes of limb ischemia followed by 5 minutes of reperfusion, or control treatment consisting solely of handling without transient ischemia. The groups included, group 1 (1W control), group 2 (1W RIC), group 3 (2W control), group 4 (2W RIC), group 5 (3W control) and group 6 (3W RIC). Hearts were isolated for assessment of cardiac function and infarct size after global ischemia using a Langendorff preparation. Infarct size was reduced in all three phases of cardioprotection, in association with improvements in post-ischemic left ventricular end diastolic pressure (LVEDP) and developed pressure (LVDP) (P<0.05). The pattern of autophagy signaling varied; 1W RIC increased AMPK levels and decreased the activation of mammalian target of rapamycin (mTOR), whereas chronic RIC was associated with persistent mTOR suppression and increased levels of autophagosome proteins, LC3II/I and Atg5.

Conclusions

Cardioprotection following transient ischemia exists in both the acute and delayed/chronic phases of conditioning. RIC induces pro-autophagy signaling but the pattern of responses varies depending on the phase, with the most complete portfolio of responses observed when RIC is administered chronically.     

Tuesday morning rounds

Survival in the acute phase of myocardial infarction and the subsequent prognosis are critically dependent on the time between onset of symptoms and medical intervention. Studies have shown that the time that patients take to decide to seek help accounts for most of the delay. We documented the length of time from onset of symptoms to arrival in hospital for 201 patients consecutively admitted to one of four hospitals in the Regional Municipality of Ottawa-Carleton between October 1986 and February 1987 for suspected acute myocardial infarction. Of the 160 survivors 42% waited more than 4 hours (a critical time for effective thrombolytic therapy) before coming to hospital, and nearly a third did not arrive within 6 hours. On the basis of interviews conducted with 42 patients, sociodemographic factors, education, past experience with an acute myocardial infarction, a previous diagnosis of angina and a coronary-prone behaviour pattern did not explain the delay. How patients perceived the seriousness of their symptoms and how they used other illness-related coping strategies explained 46% of the variance in the delay. Interventions aimed at reducing the delay between onset of symptoms and treatment must focus on patients'' preadmission behaviour.     

Effects of dichloroacetate in spinal stroke in the rabbit

High levels of brain lactate may contribute to cellular death and dysfunction in acute cerebral ischemia. Although sodium dichloroacetate (DCA) has been shown to lower brain lactate in incomplete cerebral ischemia, functional outcome has not been assessed with DCA. We examined the effects of DCA treatment on functional neurologic outcome using a previously developed model for "spinal stroke" in the rabbit. Thirty male New Zealand white rabbits weighing 1.3-2.8 kg were studied. After anesthesia with 15-40 mg/kg pentobarbital IV, a laparotomy was performed and the aorta exposed. A metal clamp was placed on the aorta just distal to the left renal artery for 20 minutes and then removed. The abdominal wound was closed in two layers. Animals then received either 2cc normal saline (n = 15) or 300 mg/kg DCA in 2cc normal saline (n = 15) over 10 minutes. The animals were returned to their cages when awake and were examined at 24 hours, 48 hours, and 72 hours for neurologic assessment. The exams were performed by a blinded examiner who was unaware of the treatment given. A three point ambulatory score (0 = can't walk, 1 = walk but not hop, 2 = hopping) and a two point activity score (0 = inactive, 1 = active) were used. At 24 hours, 67% of the DCA-treated animals were actively moving about compared to only 27% of the controls (P = 0.03; Fisher Exact Test). Ten of fifteen control animals were unable to walk, while only five of fifteen DCA-treated animals were unable to walk (P = 0.07). Sixty percent of the DCA animals were able to hop compared to 27% of controls (P = 0.06). These results suggest that DCA can reduce morbidity from spinal cord ischemia in the rabbit.     

静脉溶栓时机对急性ST段抬高型心肌梗死患者溶栓效果及主要不良心脏事件发生率的影响

目的:探讨静脉溶栓时机对急性ST段抬高型心肌梗死患者溶栓效果及主要不良心脏事件发生率的影响。方法:将2016年1月至2017年12月我院接诊的314例急性ST段抬高型心肌梗死患者纳入本研究,按照溶栓治疗时间不同分为A组(发病至溶栓时间6 h)172例、B组(发病至溶栓时间为6～12 h)102例和C组(发病至溶栓时间12 h)40例,比较三组患者溶栓效果、溶栓后ST段回落情况以及住院期间主要不良心脏事件发生情况。结果:A组患者梗死冠脉溶通率、溶栓后ST段回落幅度高于B组和C组,且B组高于C组,差异均有统计学意义(P0.05)。A组患者治疗后ST段回落最大幅度所需时间、住院期间主要不良心脏事件总发生率低于B组和C组,且B组低于C组,差异均有统计学意义(P0.05)。结论:急性ST段抬高型心肌梗死患者发病后6 h内静脉溶栓治疗梗死冠脉溶通率更高、ST段回落效果更好,可降低住院期间主要不良心脏事件发生风险。     

Autologous transplantation of CD34+ bone marrow derived mononuclear cells in management of non-reconstructable critical lower limb ischemia

Patients with a decrease in limb perfusion with a potential threat to limb viability manifested by ischemic rest pain, ischemic ulcers, and/or gangrene are considered to have critical limb ischemia (CLI). Because of this generally poor outcome, there is a strong need for attempting any procedure to save the affected limb. The aim of this work is to evaluate the possibility to use stem cell therapy as a treatment option for patients with chronic critical lower limb ischemia with no distal run off. This study includes 20 patients with chronic critical lower limb ischemia with no distal run off who are unsuitable for vascular or endovascular option. These patients underwent stem cell therapy (SCT) by autologous transplantation of bone marrow derived mononuclear cells. 55 % of patients treated with SCT showed improvement of the rest pain after the first month, 60 % continued improvement of the rest pain after 6 months, 75 % after 1 year and 80 % after 2 years and continued without any deterioration till the third year. Limb salvage rate after STC was 80 % after the first year till the end of the second and third years. SCT can result in angiogenesis in patients with no-option CLI, providing a foundation for the application of this therapy to leg ischemia.