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BACKGROUND: Intravascular ultrasound (IVUS) was only rarely used in landmark trials comparing percutaneous coronary intervention (PCI) with coronary artery bypass grafting (CABG) in patients with multivessel disease. OBJECTIVES: The authors aimed to evaluate clinical outcomes after optimal IVUS-guided PCI in patients undergoing multivessel PCI. METHODS: The OPTIVUS (OPTimal IntraVascular UltraSound)-Complex PCI study multivessel cohort was a prospective multicenter single-arm study enrolling 1, 021 patients undergoing multivessel PCI, including left anterior descending coronary artery using IVUS, aiming to meet the prespecified criteria (OPTIVUS criteria: minimum stent area > distal reference lumen area [stent length≥28mm], and minimum stent area >0.8× average reference lumen area [stent length

Balloon pulmonary angioplasty (BPA) is now a treatment option for patients with inoperable chronic thromboembolic pulmonary hypertension (CTEPH). However, the incidence of restenosis and long-term changes in vessel diameters in pulmonary arteries after BPA are unknown. The present study investigated the incidence of restenosis by measuring changes in vessel diameter after BPA. We reviewed 58 patients (168 lesions) with CTEPH who underwent single dilation for the target lesion (type A/B/C lesions) during BPA procedure followed by selective pulmonary angiography more than 6 months after the final BPA procedure. The outcomes of BPA were assessed in terms of pulmonary artery diameters. In a median follow-up of 1.9 (1.2-2.7) years, restenosis occurred in only one case with a type C lesion after BPA (0.6%). In type A/B lesions, the minimal lumen diameter was significantly enlarged at follow-up after BPA [3.48 (2.59-4.34) to 4.22 (3.31-4.90) mm]. In type C lesions, the minimal lumen diameter was unchanged at follow-up after BPA [3.15 (1.96-3.64) to 3.28 (2.38-4.61) mm]. The present results revealed that restenosis after BPA rarely occurs in type A/B/C lesions. Minimal lumen diameters for type A/B lesions continually increased and those for type C lesions did not decrease. Stent implantation in type A/B/C lesions would be unnecessary after BPA.

Pulmonary injury is a major complication of balloon pulmonary angioplasty (BPA) for chronic thromboembolic pulmonary hypertension (CTEPH). Lung injury after BPA can be exacerbated by a high mean pulmonary arterial pressure (PAP). Although oxygen inhalation is expected to lower mean PAP in patients with CTEPH, no relevant investigation has been conducted.Consecutive patients with CTEPH who underwent BPA were enrolled in this study. We evaluated the hemodynamics using right heart catheterization while breathing ambient air and with administration of 5 L/min oxygen for 10 min.This study included 52 consecutive patients with CTEPH, of whom 23 (44%) were treated with specific pulmonary vasodilators. Exposure to oxygen was well tolerated. Oxygen administration significantly decreased mean PAP by 3.8 ± 3.2 mmHg (p0.001) and pulmonary vascular resistance by 0.8 ± 1.8 Wood units (p0.001). Moreover, the ratio of pulmonary vascular resistance to systemic vascular resistance was significantly reduced by 13.5% (p0.001). Multivariate regression analysis identified baseline mean PAP (β = -0.427, p = 0.006) as the only significant predictor of decreased mean PAP under oxygen administration. No significant difference in oxygen effect on mean PAP was found between patients with and without vasodilators.In patients with CTEPH, 5 L/min supplemental oxygen inhalation could decrease mean PAP significantly by selective pulmonary artery dilatation, regardless of the usage of vasodilators, and thus could be helpful to maximize the safety of BPA.UMIN Clinical Trials Registry (No.: UMIN000026882); URL: https://www.umin.ac.jp/ctr/index.htm.

A 54-year-old man was transferred to our hospital due to congestive heart failure and left ventricular thrombi. Transthoracic echocardiography (TTE) showed mobile "ball-like" not only left ventricular but also right ventricular thrombi associated with severe impaired left and right ventricular function. Contrast-enhanced computed tomography (CT) and cardiac magnetic resonance imaging (MRI) also detected biventricular apical thrombi complicated with right renal infarction. Coronary angiography showed non-significant stenosis. Due to the mobility of thrombi and complication of systemic infarction, the surgical transatrial video-assisted removal of biventricular thrombi was performed and postoperative course has been uneventful over a period of 6 months. Endomyocardial biopsy performed during an operation showed no specific findings such as endomyocarditis, indicating the diagnosis of dilated cardiomyopathy (DCM). This is a rare case of DCM complicated with biventricular apical thrombi detected clearly by multimodality imaging such as TTE, contrast-enhanced CT and cardiac MRI, and surgical removal was performed successfully. .

Background: Pulmonary arterial hypertension (PAH) has a poor prognosis despite the available therapeutic options. Normalization of hemodynamics would be needed to obtain the good prognosis. Aims and Objectives: We aimed to investigate the determinants in PAH patients for normalization of hemodynamics only with oral drugs. Methods: We retrospectively reviewed 190 patients with PAH treated at a single referral center. Hemodynamic parameters were investigated before and after treatments. All the patients were divided into a good control group with mean pulmonary arterial pressure (mPAP)＜30mmHg and a poor control group with mPAP≧30mmHg at follow-up. Results: Eighty-two patients were idiopathic/heritable, 65 patients were connective tissue disease, 22 patients congenital heart disease and 21 patients were portal hypertension. mPAP decreased significantly from baseline to follow-up (51±18.7 mmHg to 34.1±15.2 mmHg, p Conclusions: To achieve normalization of hemodynamics in PAH, parenteral prostanoid should be used in cases with baseline mPAP exceeding 40mmHg.

Peripheral pulmonary artery stenosis (PPS) presenting in adulthood is an uncommon disease and may be misdiagnosed as idiopathic pulmonary artery hypertension or chronic thromboembolic pulmonary hypertension. Standard curative treatment has not fully established because of the limited experience of