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Purpose: The endovascular approach for eccentric calcified lesions of the no-stenting zone is challenging. This study aimed to investigate the effect of a novel technique for these lesions.Methods: We performed EVT for severe and eccentric calcified lesions using the technique, which is presented previously and named aggressive wire recanalization in calcified atheroma and dilatation (ARCADIA). In brief, a guidewire is passed to the residual lumen firstly. Next, another guidewire is advanced into and cross through the calcified plaque and returned to the distal original lumen with intravascular ultrasound (IVUS) guided. The calcified plaque is dilated by using a scoring-balloon or non-compliant balloon.Results: Consecutive 14 peripheral artery disease patients with isolated and eccentric calcification in a no-stenting zone were treated using ARCADIA technique between January 2018 and March 2020. In IVUS data, lumen cross-section area was significantly increased from 5.2 ± 2.0 mm2 to 18.1 ± 6.9 mm2 (p < 0.01), lumen area was expanded roundly evaluating as symmetry index from 0.45 ± 0.09 to 0.81 ± 0.12 (p < 0.01). There were no distal embolization and perforation after ARCADIA technique. One-year target lesion revascularization occurred in only 2 cases. The primary patency of 1 year was 85.7%.Conclusion: ARCADIA technique is safe and appropriate, and can be 1 option to treat for eccentric calcified lesions of the no-stenting zone as an optimal wire crossing method. [ABSTRACT FROM AUTHOR]

Obesity is associated with marked increases in plasma leptin concentration, and hyperleptinemia is an independent risk factor for coronary artery disease. As a result, the purpose of this investigation was to test the following hypotheses: 1) leptin receptors are expressed in coronary endothelial cells; and 2) hyperleptinemia induces coronary endothelial dysfunction. RT-PCR analysis revealed that the leptin receptor gene is expressed in canine coronary arteries and human coronary endothelium. Furthermore, immunocytochemistry demonstrated that the long-form leptin receptor protein (ObRb) is present in human coronary endothelium. The functional effects of leptin were determined using pressurized coronary arterioles (< 130 [micro]m) isolated from Wistar rats, Zucker rats, and mongrel dogs. Leptin induced pharmacological vasodilation that was abolished by denudation and the nitric oxide synthase inhibitor [N.sup.[omega]]-nitro-L-arginine methyl ester and was absent in obese Zucker rats. Intracoronary leptin dose-response experiments were conducted in anesthetized dogs. Normal and obese concentrations of leptin (0.1-3.0 [micro]g/min ic) did not significantly change coronary blood flow or myocardial oxygen consumption; however, obese concentrations of leptin significantly attenuated the dilation to graded intracoronary doses of acetylcholine (0.3-30.0 [micro]g/min). Additional experiments were performed in canine coronary rings, and relaxation to acetylcholine (6.25 nmol/l-6.25 [micro]mol/l) was significantly attenuated by obese concentrations of leptin (625 pmol/l) but not by physiological concentrations of leptin (250 pmol/l). The major findings of this investigation were as follows: 1) the ObRb is present in coronary arteries and coupled to pharmacological, nitric oxide-dependent vasodilation; and 2) hyperleptinemia produces significant coronary endothelial dysfunction. coronary circulation; endothelium: microcirculation; metabolic syndrome; obesity

Tanaka, Mitsuaki, Hiroshi Kanatsuka, Boon-Hooi Ong, Toshinori Tanikawa, Akira Uruno, Tatsuya Komaru, Ryoji Koshida, and Kunio Shirato. Cytochrome P-450 metabolites but not NO, PG[I.sub.2], and [H.sub.2][0.sub.2] contribute to ACh-induced hyperpolarization of pressurized canine coronary microvessels. Am J Physiol Heart Circ Physiol 285: H1939-H1948, 2003. First published July 24, 2003; 10.1152/ajpheart.00190.2003.--The endothelium-dependent hyperpolarization of cells has a crucial role in regulating vascular tone, especially in microvessels. Nitric oxide (NO) and prostacyclin (PG[I.sub.2]), in addition to endothelium-derived hyperpolarizing factor (EDHF), have been reported to hyperpolarize vascular smooth muscle in several organs. Studies have reported the hyperpolarizing effects of these factors are increased by a stretch in large coronary arteries. EDHF has not yet been identified and cytochrome P-450 metabolites and [H.sub.2][0.sub.2] are candidates for EDHF. With the use of the membrane potential-sensitive fluorescent dye bis-(1,3-dibutylbarbituric acid)trimethione oxonol [DiBA[C.sub.4](3)], we examined whether NO, PG[I.sub.2], cytochrome P-450 metabolites, and [H.sub.2][0.sub.2] contribute to ACh-induced hyperpolarization in pressurized coronary microvessels. Canine coronary arterial microvessels (60-356 [micro]m internal diameter) were cannulated and pressurized at 60 cm[H.sub.2]0 in a vessel chamber perfused with physiological salt solution containing DiBA[C.sub.4](3). Fluorescence intensity and diameter were measured on a computer. There was a linear correlation between changes in the fluorescence intensity and membrane potential. ACh significantly decreased the fluorescence intensity (hyperpolarization) of the microvessels without any inhibitors. Endothelial damage caused by air perfusion abolished the ACh-induced decrease in fluorescence intensity. The inhibitors of NO synthase and cyclooxygenase did not affect the ACh-induced decreases in the fluorescence intensity. The addition of 17-octadecynoic acid, a cytochrome P-450 monooxygenase inhibitor, to those inhibitors significantly attenuated the ACh-induced decreases in fluorescence intensity, whereas catalase, an enzyme that dismutates [H.sub.2][0.sub.2] to form water and oxygen, did not. Furthermore, catalase did not affect the vasodilation produced by ACh. These results indicate that NO and PG[I.sub.2] do not contribute to the ACh-induced hyperpolarization and that the cytochrome P-450 metabolites but not [H.sub.2][0.sub.2] are involved in EDHF-mediated hyperpolarization in canine coronary arterial microvessels. microcirculation; endothelium-derived hyperpolarizing factor; endothelium

The case of an 80-year-old male with claudication of his left foot who was referred to our hospital for evaluation and treatment. Computed tomography (CT) angiography revealed occlusion of left common and external iliac (EIA) arteries. Recanalization of the EIA lesion under intravascular ultrasound (IVUS) guidance and placement of 2 stent grafts was completed successfully. Nine months later, 27 × 29 mm pseudoaneurysm of the left EIA was identified that appeared to have developed secondary to migration of the original stent graft. A new stent graft was placed. [ABSTRACT FROM AUTHOR]

The Crosser catheter is a unique device that facilitates antegrade intraluminal recanalization by high-frequency vibration energy and cavitation. We used this device not only as a chronic total occlusion (CTO) crossing device, but also as a flossing device in stenotic lesions and we also evaluated the efficacy of this device when used with both the 'Crosser preceding' and the 'Guidewire preceding' in CTOs. Complications related to this device were investigated, too. We retrospectively analyzed a total of 90 consecutive patients with peripheral artery disease in the femoropopliteal artery and below-the-knee artery (BTA). Primary technical success was defined as the successful delivery of this device into the distal true lumen. Secondary technical success was defined as successful revascularization. The safety endpoints were events of angiographic complications, including the occurrence of detachment of the metal tip from the shaft, slow flow, dissections, and perforations. Overall primary technical success rate was 93.3% and the secondary technical success rate was 96.7%. Detachment and slow flow occurred 14.4 and 4.4%, respectively, with no occurrences of either dissection or perforation. A predictor of detachment was Proposed Peripheral Arterial Calcium Scoring System (PACSS) grade 4 (OR 14.6; CI 1.26-168.5; P = 0.032). The Crosser catheter is useful not only as a CTO crossing device used with both the 'Crosser preceding' and the 'Guidewire preceding', but also as a flossing device in stenotic lesions. But we have to pay attention to complications related to the Crosser. [ABSTRACT FROM AUTHOR]

The endothelium-dependent hyperpolarization of cells has a crucial role in regulating vascular tone, especially in microvessels. Nitric oxide (NO) and prostacyclin (PGI[sub 2]), in addition to endothelium-derived hyperpolarizing factor (EDHF), have been reported to hyperpolarize vascular smooth muscle in several organs. Studies have reported the hyperpolarizing effects of these factors are increased by a stretch in large coronary arteries. EDHF has not yet been identified and cytochrome P-450 metabolites and H[sub 2]O[sub 2] are candidates for EDHF. With the use of the membrane potential-sensitive fluorescent dye bis-(1,3-dibutylbarbituric acid)trimethione oxonol [DiBAC[sub 4](3)], we examined whether NO, PGI[sub 2], cytochrome P-450 metabolites, and H[sub 2]O[sub 2] contribute to AChinduced hyperpolarization in pressurized coronary microvessels. Canine coronary arterial microvessels (60-356 µm internal diameter) were cannulated and pressurized at 60 cmH[sub 2]O in a vessel chamber perfused with physiological salt solution containing DiBAC[sub 4](3). Fluorescence intensity and diameter were measured on a computer. There was a linear correlation between changes in the fluorescence intensity and membrane potential. ACh significantly decreased the fluorescence intensity (hyperpolarization) of the microvessels without any inhibitors. Endothelial damage caused by air perfusion abolished the ACh-induced decrease in fluorescence intensity. The inhibitors of NO synthase and cyclooxygenase did not affect the ACh-induced decreases in the fluorescence intensity. The addition of 17-octadecynoic acid, a cytochrome P-450 monooxygenase inhibitor, to those inhibitors significantly attenuated the ACh-induced decreases in fluorescence intensity, whereas catalase, an enzyme that dismutates H[sub 2]O[sub 2] to form water and oxygen, did not. Furthermore, catalase did not affect the vasodilation produced by ACh. These results indicate that NO and PGI[sub 2] do not contribute to the AChinduced hyperpolarization and that the cytochrome P-450 metabolites but not H[sub 2]O[sub 2] are involved in EDHF-mediated hyperpolarization in canine coronary arterial microvessels. [ABSTRACT FROM AUTHOR]

Background: Selective use of distal filter protection during percutaneous coronary intervention (PCI) for acute coronary syndromes (ACS) decreased the incidence of no-reflow phenomena and in-hospital serious adverse cardiac events compared with conventional PCI in patients with attenuated plaque ≥5 mm; however, its long-term clinical outcome remains unknown.Methods and Results:Patients who had ACS with attenuated plaque ≥5 mm were assigned to receive distal protection (DP) (n=98) or conventional treatment (CT) (n=96). The rate of major adverse cardiovascular events (MACE), a composite of death from any cause, non-fatal myocardial infarction, or target vessel revascularization (TVR) at 1 year, was the pre-specified secondary endpoint of the trial. MACE at 1 year occurred in 12 patients (12.2%) in the DP group and 3 patients (3.1%) in the CT group (P=0.029), which was driven by a higher risk of TVR (11 [11.2%] vs. 2 [2.1%], P=0.018). In patients treated with bare-metal stents (n=42), MACE occurred in 25.0% of the patients in the DP group and in none of the patients in the CT group (P=0.029), whereas in patients treated with drug-eluting stents (n=151), rates of MACE were similar in the groups (8.1% vs. 3.9%, P=0.32)., Conclusions: In ACS patients with attenuated plaque ≥5 mm, the 1-year rates of MACE were higher in the DP group than in the CT group. This effect might be mitigated by the use of drug-eluting stents.

Background: The results of previous clinical trials on the effects of ezetimibe-statin combination therapy on atherosclerosis are inconsistent, and the anti-atherosclerotic effect of ezetimibe remains controversial.Methods and Results:We conducted a prospective, randomized open-label study at 10 centers. One hundred and twenty-eight statin-naïve patients with acute coronary syndrome (ACS) undergoing intravascular ultrasound (IVUS)-guided percutaneous coronary intervention were randomized to receive either 2 mg/day pitavastatin plus 10 mg/day ezetimibe, or 2 mg/day pitavastatin. One hundred and 3 patients had evaluable IVUS of non-culprit coronary lesions at baseline and at follow-up. The primary endpoint was the percentage change in non-culprit coronary plaque volume (PV) and lipid PV on integrated backscatter IVUS. Mean low-density lipoprotein cholesterol was reduced from 123 mg/dL to 64 mg/dL in the combination therapy group (n=50) and 126 mg/dL to 87 mg/dL in the statin alone group (n=53; between-group difference, 16.9%, P<0.0001). The percent change in PV was -5.1% in the combination therapy group and -6.2% in the statin alone group (P=0.66), although both groups had reduction of PV compared with baseline (both P<0.01). The percent change in lipid PV did not differ between the groups (4.3 vs. -3.0%, P=0.37)., Conclusions: In statin-naïve patients with ACS, combined therapy with ezetimibe and statin did not result in a significant change in coronary plaque regression or tissue component compared with statin alone. [Clinical Trial Registration: www.clinicaltrials.gov (NCT00549926)].

Background: The patency and complications in aorto-iliac (AI) stenting remain poorly understood. The aim of this paper was to investigate the safety and efficacy after AI stenting., Methods and Results: This study was performed as a large-scale multicenter, retrospective registry. A total of 2,147 consecutive patients with AI disease were enrolled. The safety endpoints were procedure success, complications and 30-day mortality. The efficacy endpoints were primary, assisted primary and secondary patency, overall survival, freedom from major adverse cardiovascular events (MACE; all-cause death, myocardial infarction and stroke), and major adverse cardiovascular and limb events (MACLE; any repeat revascularization for limb and leg amputation in addition to MACE). Procedure success, complication rate and 30-day mortality were 97.6%, 6.4% and 0.7%. Primary patency was 92.5%, 82.6% and 77.5% at 1, 3 and 5 years, assisted primary patency was 97.0%, 92.7% and 91.9% at 1, 3 and 5 years and secondary patency was 99.0%, 98.7% and 98.5% at 1, 3 and 5 years. The overall survival rate was 95.0%, 87.6%, and 79.3% at 1, 3 and 5 years. The cause of death was cardiovascular in 44.1%. Freedom from MACE (MACLE) was 93.3% (89.9%), 84.4% (76.7%), and 74.9% (66.8%) at 1, 3 and 5 years. Female gender, diabetes, renal failure, absence of aspirin, reference vessel diameter <8.0mm and outflow lesion were found to be independent predictors of primary patency., Conclusions: The safety and efficacy after AI stenting are feasible compared to surgical reconstruction.

Peripheral arterial disease (PAD) becomes a significant health problem in Japan, mostly because the rapid increase of aging and diabetic population. Intermittent claudication, rest pain, intractable foot ulcer and gangrene are the manifestations of PAD patients. Diagnosis of PAD is obtained by ankle brachial index. Several imaging modalities, such as duplex echo, multi-detector CT, are quite useful tools not only for the diagnosis but also for the planning of endovascular therapy. In this chapter, basic diagnosis, different treatment modalities in patients with PAD are described.

Insulin resistance may enhance the neointima formation via increased oxidative stress. However, clinical trials investigating the benefit of antioxidant therapy with alpha-tocopherol showed negative results. Recent studies showed that chemical characteristics of gamma-tocopherol are distinct from those of alpha-tocopherol. We hypothesized that gamma-tocopherol is superior to alpha-tocopherol in preventing the neointima growth after arterial injury in insulin resistance. Male rats were fed with standard chow or a high fructose diet for induction of insulin resistance. Thereafter, the left carotid artery was injured with a balloon catheter. After 2 weeks, the carotid arteries were harvested and histomorphometrically analyzed. The neointima-media ratio of the injured artery was significantly greater in insulin resistance group (n=8, 1.33+/-0.12) than in normal group (n=10, 0.76+/-0.11, p<0.01). gamma-Tocopherol (100 mg/kg/day) reduced the ratio (n=5, 0.55+/-0.21, p<0.01 vs. insulin resistance group), while alpha-tocopherol was without effect (n=7, 1.08+/-0.14). The quantification of plasma phosphatidylcholine hydroperoxide, an indicator of systemic oxidative stress, and dihydroethidium fluorescence staining of the carotid artery, an indicator of the local superoxide production, showed that oxidative stress in the systemic circulation and local arterial tissue was increased in insulin resistance. Both tocopherols decreased plasma phosphatidylcholine hydroperoxide, but failed to suppress the superoxide production in the carotid arteries. Increased 3-nitrotyrosine in neointima by insulin resistance was greatly reduced only by gamma-tocopherol. In conclusion, gamma-tocopherol, but not alpha-tocopherol, reduces the neointima proliferation in insulin resistance, independently of its effects on superoxide production. The beneficial effect may be related with its inhibitory effects on nitrosative stress.