Normovolemic hemodilution was used in 81 patients as preparation to reconstructive operation for the occlusion of main arteries of extremities. Regional hemodynamics was studied in 18 of them. It was established that acute hemodilution substantially increased the volume and tissue blood flow, regional systolic arterial pressure distal to the occlusion of the main vessel and reestablished the vessel tone. The oxygen transport became normal in the zones with preserved main blood flow and considerably increased in the places distal to the occlusion of the main artery.

Chronic obstructive pulmonary disease (COPD) is associated with atherosclerosis. Previous studies including limited sample sizes have shown the prevalence of peripheral arterial occlusive disease (PAOD) among COPD patients. We sought to investigate the incidence of PAOD among COPD patients in Taiwan using a national database.

The efficacy and safety of endovascular treatment (EVT) for moyamoya disease (MMD) have rarely been investigated. The objective of this study was to summarize the clinical outcomes of EVT for MMD and determine the potential role of EVT in treating symptomatic steno-occlusive lesions in MMD. Reports from January 2000 to December 2021 describing EVT in MMD were collected through a literature search. The search terms included "moyamoya", "stent", "angioplasty", and "endovascular". Data regarding baseline demographics, previous medical history, treated vessel, periprocedural complications, and angiographical recurrence were retrieved. This review included 10 studies with details of 19 patients undergoing a total of 31 EVT procedures. Twenty-one EVTs were performed as initial treatments for MMD, and 10 were performed as additional treatments for angiographical recurrence. The mean follow-up period of the initial EVTs was 9.0±11.9 months, with angiographical recurrence in 11 (68.8%) cases. The mean follow-up period of additional EVTs was 4.3±3.9 months, and seven (70.0%) EVTs showed restenosis of the re-treated vessel. Across all initial and additional EVTs, there were no differences in characteristics between the recurrence and non-recurrence groups. Overall, two periprocedural complications (9.5%) occurred, one vessel rupture and one massive intracerebral hemorrhage with subarachnoid hemorrhage. EVT plays a limited role in the management of symptomatic intracranial arterial steno-occlusive lesions of MMD. Recent advances in understanding the pathomechanism of MMD may urge neuro-interventionists to find a new endovascular approach with better balloon angioplasty or stenting mechanisms.

Background: Observational studies support an association between periodontitis (PD) and atherosclerotic vascular disease, but little is known specifically about peripheral arterial occlusive disease (PAOD).

Peripheral arterial occlusive disease (PAOD) results from atherosclerosis of large and medium peripheral arteries, as well as the aorta, and has many risk factors, including smoking, diabetes, hypertension, and hyperlipidemia. PAOD often coexists with coronary artery disease and cerebrovascular disease. Cross-matching a population-based list of Icelandic patients with PAOD who had undergone angiography and/or revascularization procedures with a genealogy database of the entire Icelandic nation defined 116 extended families containing 272 patients. A genomewide scan with microsatellite markers revealed significant linkage to chromosome 1p31 with an allele-sharing LOD score of 3.93 (P=1.04 x 10(-5)). We designate this locus as "PAOD1." Subtracting 35 patients with a history of stroke increased the LOD score to 4.93. This suggests that, although PAOD and other vascular diseases share risk factors, genetic factors specific to subtypes of vascular disease may exist.

Arterial occlusive diseases are major causes of morbidity and mortality. Blood flow to the affected tissue must be restored quickly if viability and function are to be preserved. We report that disruption of the mixed-lineage protein kinase (MLK) - cJun NH2-terminal kinase (JNK) signaling pathway in endothelial cells causes severe blockade of blood flow and failure to recover in the murine femoral artery ligation model of hindlimb ischemia. We show that the MLK-JNK pathway is required for the formation of native collateral arteries that can restore circulation following arterial occlusion. Disruption of the MLK-JNK pathway causes decreased Dll4/Notch signaling, excessive sprouting angiogenesis, and defects in developmental vascular morphogenesis. Our analysis demonstrates that the MLK-JNK signaling pathway is a key regulatory mechanism that protects against ischemia in arterial occlusive disease.

One of the most severe complications of atherosclerosis is arterial occlusive disease (AOD) and with diabetic angiopathy (DA), is a common chronic problem in clinical practice worldwide. Hyperbaric oxygen (HBO) therapy is a therapeutic modality for solving all forms of hypoxia.

Background An increasing number of patients with a peripheral arterial occlusive disease were put on statins during the past years. This study assessed whether statin therapy was effective and safe for these new users. Methods and Results Using health insurance claims data from Germany's second-largest insurance fund, BARMER, we identified patients with peripheral arterial occlusive disease who had index revascularization between 2008 and 2018 without prior statin therapy. We compared patients with and without statin therapy in addition to antithrombotics during the first quarter after discharge (new users versus nonusers). Outcomes were all-cause mortality, cardiovascular events, and incident major amputation for effectiveness and incident diabetes mellitus and incident myopathy for safety. Propensity score matching was used to balance the study groups. All analyses were stratified into patients with chronic limb-threatening ischemia and intermittent claudication. A total of 22 208 patients (mean age 71.1 years and 50.3% women) were included in the study. In 10 922 matched patients, statin initiation was associated with lower all-cause mortality (chronic limb-threatening ischemia: hazard ratio [HR], 0.75 [95% CI, 0.68-0.84]; intermittent claudication: HR, 0.80 [95% CI, 0.70-0.92]), lower risk of major amputation in patients with chronic limb-threatening ischemia (HR, 0.73; 95% CI, 0.58-0.93) and lower risk of cardiovascular events (hazard ratio, 0.80; 95% CI, 0.70-0.92) in patients with intermittent claudication during 5 years of follow-up. Safety outcomes did not differ among the study groups. Conclusions Initiating statin therapy in patients with peripheral arterial occlusive disease after index revascularization is efficient and safe with an effect size comparable to earlier studies. Awareness campaigns for evidence-based optimal pharmacological treatment among patients are recommended.

This quantitative meta-analysis was conducted to evaluate the efficacy and safety of drug-eluting balloon (DEB) vs. uncoated balloon (UCB) in patients with femoropopliteal arterial occlusive disease.

Patients with type 2 diabetes are at increased risk for cardiovascular diseases. Sodium-glucose transport 2 inhibitors (SGLT2i) have been shown to enhance cardiovascular health since their debut as a second-line therapy for diabetes. Acute coronary syndrome (ACS), peripheral arterial occlusive disease (PAOD), and ischemic stroke (IS) are types of atherosclerotic cardiovascular disease (ASCVD), although the benefits of treating these disorders have not been shown consistently.

Due to endothelial impairment, high-dose lithium may produce an occlusive-like syndrome, comparable to permanent occlusion of major vessel-induced syndromes in rats; intracranial, portal, and caval hypertension, and aortal hypotension; multi-organ dysfunction syndrome; brain, heart, lung, liver, kidney, and gastrointestinal lesions; arterial and venous thrombosis; and tissue oxidative stress. Stable gastric pentadecapeptide BPC 157 may be a means of therapy via activating loops (bypassing vessel occlusion) and counteracting major occlusion syndromes. Recently, BPC 157 counteracted the lithium sulfate regimen in rats (500 mg/kg/day, ip, for 3 days, with assessment at 210 min after each administration of lithium) and its severe syndrome (muscular weakness and prostration, reduced muscle fibers, myocardial infarction, and edema of various brain areas). Subsequently, BPC 157 also counteracted the lithium-induced occlusive-like syndrome; rapidly counteracted brain swelling and intracranial (superior sagittal sinus) hypertension, portal hypertension, and aortal hypotension, which otherwise would persist; counteracted vessel failure; abrogated congestion of the inferior caval and superior mesenteric veins; reversed azygos vein failure; and mitigated thrombosis (superior mesenteric vein and artery), congestion of the stomach, and major hemorrhagic lesions. Both regimens of BPC 157 administration also counteracted the previously described muscular weakness and prostration (as shown in microscopic and ECG recordings), myocardial congestion and infarction, in addition to edema and lesions in various brain areas; marked dilatation and central venous congestion in the liver; large areas of congestion and hemorrhage in the lung; and degeneration of proximal and distal tubules with cytoplasmic vacuolization in the kidney, attenuating oxidative stress. Thus, BPC 157 therapy overwhelmed high-dose lithium intoxication in rats.

A 65-year-old man with an occluded popliteal artery aneurysm and calf claudication underwent PET/CT imaging with F-NaF to assess the status of active microcalcification in the aneurysm site and additional lower extremity arteries. CT imaging revealed macrocalcification of the aneurysm that colocalized with elevated retention of F-NaF on PET images. PET/CT detected additional distal arterial sites with focal uptake of F-NaF that did not coincide with CT-detectable macrocalcification. This report highlights a case of active microcalcification in an occlusive peripheral aneurysm using PET/CT. PET/CT may provide molecular insight into the remodeling of lower extremity aneurysms and atherosclerotic lesions.

Perivascular adipose tissue (PVAT) helps regulate arterial homeostasis and plays a role in the pathogenesis of large vessel diseases. In this study, we investigated whether the PVAT of aortic occlusive lesions shows specific gene-expression patterns related to pathophysiology. By a genome-wide approach, we investigated the PVAT transcriptome in patients with aortoiliac occlusive disease. We compared the adipose layer surrounding the distal aorta (atherosclerotic lesion) with the proximal aorta (plaque-free segment), both within and between patients with complete aortoiliac occlusion (Oc) and low-grade aortic stenosis (St). We found that PVAT of the distal versus proximal aorta within both Oc- and St-patients lacks specific, locally restricted gene-expression patterns. Conversely, singular gene-expression profiles distinguished the PVAT between Oc- and St-patients. Functional enrichment analysis revealed that these signatures were associated with pathways related to metabolism of cholesterol, vessel tone regulation, and remodeling, including TGF-β and SMAD signaling. We finally observed that gene-expression profiles in omental-visceral or subcutaneous fat differentiated between Oc- and St-patients, suggesting that the overall adipose component associates with a different atherosclerosis burden. Our work points out the role of PVAT and, likely, other adipose tissues play in the pathophysiological mechanisms underlying atherosclerotic disease, including the abdominal aortic occlusive forms.

Mutations in the eukaryotic translation initiation factor 2α kinase 4 (EIF2AK4) gene have recently been identified in recessively inherited veno-occlusive disease. In this study we assessed if EIF2AK4 mutations occur also in a family with autosomal dominantly inherited pulmonary arterial hypertension (HPAH) and incomplete penetrance of bone morphogenic protein receptor 2 (BMPR2) mutations.

Pulmonary arterial hypertension (PAH) is characterized by elevated pulmonary arterial pressure and right heart failure. Selective pulmonary vasodilators have improved the prognosis of PAH; however, they are not able to reverse pulmonary vascular remodeling. Therefore, a search for new treatment agents is required. H-1337 is an isoquinoline-sulfonamide compound that inhibits multiple serine/threonine kinases, including Rho-associated protein kinase (ROCK) and mammalian target of rapamycin (mTOR). Here, we investigated the effects of H-1337 on pulmonary hypertension and remodeling in the pulmonary vasculature and right ventricle in experimental PAH induced by SU5416 and hypoxia exposure. H-1337 and H-1337M1 exerted inhibitory effects on ROCK and Akt. H-1337 inhibited the phosphorylation of myosin light chain and mTOR and suppressed the proliferation of smooth muscle cells in vitro. H-1337 treatment also suppressed the phosphorylation of myosin light chain and mTOR in the pulmonary vasculature and decreased right ventricular systolic pressure and the extent of occlusive pulmonary vascular lesions. Furthermore, H-1337 suppressed aggravation of right ventricle hypertrophy. In conclusion, our data demonstrated that inhibition of ROCK and mTOR pathways with H-1337 suppressed the progression of pulmonary vascular remodeling, pulmonary hypertension, and right ventricular remodeling.

Pulmonary Arterial Hypertension (PAH) is a progressive condition with no cure. Even with pharmacologic advances, survival remains poor. Lung pathology on PAH therapies still shows impressive occlusive arteriolar remodelling and plexiform lesions. Cardiosphere-derived cells (CDCs) are heart-derived progenitor cells exhibiting anti-inflammatory and immunomodulatory effects, are anti -fibrotic, anti-oxidative and anti-apoptotic to potentially impact several aspects of PAH pathobiology. In preclinical trials CDCs reduced right ventricular (RV) systolic pressure, RV hypertrophy, pulmonary arteriolar wall thickness and inflammation.

Variants in the gene encoding bone morphogenetic protein receptor type II (BMPR2) are the most common genetic cause of pulmonary arterial hypertension (PAH), whereas biallelic variants in the eukaryotic translation initiation factor 2 alpha kinase 4 gene (EIF2AK4) are described in pulmonary veno-occlusive disease/pulmonary capillary haemangiomatosis (PVOD/PCH). Racial background may influence the clinical characteristics of patients diagnosed with PAH or PVOD/PCH. Here, we compared the clinical characteristics and survival between patients with BMPR2 variants or EIF2AK4 variants in a Chinese population.

An inadequate selenium level is supposed to be a risk factor for cardiovascular diseases. However little is known about variation of the genes encoding selenium-containing proteins that would confirm the causality in these diseases. The aim of this study was to analyze the relationships between two functional variants of selenoprotein P gene (SEPP1 rs3877899G>A, rs7579G>A) and the occurrence of abdominal aortic aneurysm (AAA) and aortoiliac occlusive disease (AIOD), as well as their metabolic risk factors. In AAA, the rs3877899A allele was associated with higher systolic blood (P < .003) and pulse pressure (P < .003) values (recessive model), and with coexistence of peripheral arterial disease (PAD; carriers: P = .033). The other SEPP1 variants were associated with BMI values and influenced the risk of aortic diseases, depending on body weight. The strongest associations in the case-control analysis was found between the presence of the rs3877899G-rs7579G haplotype and development of AAA in overweight and obese subjects (OR = 1.80, 95%CI = 1.16-2.79, P = .008). The higher BMI values were correlated with lower age of AAA patients and larger size of aneurysm. Our results suggests the potential role of the selenoprotein P in pathogenesis of AAA. Future studies should consider the role of the rs3877899G-rs7579G haplotype as a risk factor for aggressive-growing AAAs.

The self-expandable COMPLETE™ stent (Medtronic) has greater elasticity, allowing it to regain its shape after the compression force reduces, and has higher trackability, thus is easier to maneuver through tortuous vessels, whereas the balloon-expandable SCUBA™ stent (Medtronic) has higher radial stiffness and can afford more accurate placement without geographic miss, which is important in aortoiliac bifurcation lesions. To date, there have been no randomized control trials comparing efficacy and safety between the self-expanding stent and balloon-expandable stent in advanced atherosclerotic iliac artery disease.

Abdominal aortic calcification (AAC) is associated with low bone mass and increased fracture risk. Two previous meta-analyses have investigated the association between AAC and fracture. However, these meta-analyses only identified articles until December 2016, undertook limited searches and did not explore potential sources of between-study heterogeneity. We aim to undertake a sensitive and comprehensive assessment of the relationship between AAC, bone mineral density (BMD) as well as prevalent and incident fractures.