Takenori Ikoma

Background: To evaluate the efficacy and safety of outpatient exercise training in clinically stabilized patients with chronic thromboembolic pulmonary hypertension (CTEPH) after balloon pulmonary angioplasty (BPA). Methods: Twenty-four patients with CTEPH after BPA were enrolled in this prospective single-center study. Patients were assigned to the exercise and control groups. The exercise group comprised 12 patients who received 15 weeks of exercise training, with usual care. The control group received only the usual care, without exercise training. The exercise program included aerobic exercise thrice weekly and resistance exercise once or twice weekly. The assessments employed included a 6-min walk test, cardiopulmonary exercise testing, and an emPHasis-10 questionnaire. Results: In the exercise group, the 6-min walk distance was significantly longer (510.0 [467.5, 595.0] m vs. 425.0 [395.0, 465.0] m, p = 0.020), the time taken to walk 10 m was shorter (6.4 [5.9, 7.5] s vs. 8.9 [8.1, 9.1] s, p = 0.020), and the walking speed was faster (1.6 [1.3, 1.7] m/s vs. 1.1 [1.1, 1.2] m/s, p = 0.020) at 15 weeks compared with the results for the control group. The quality of life tended to improve at 15 weeks compared with that before the exercise training. However, hemodynamics did not change significantly before and after the exercise training, and no fatal arrhythmias or syncope were observed. Conclusions: Exercise training improved gait performance, without any adverse events, in patients with CTEPH after BPA. Therefore, exercise training as an adjunct to medical therapy may be a safe potential therapy for patients with CTEPH after BPA.

Background: Atrial fibrillation (AF) ablation is performed under deep sedation, which may cause inspiration-induced negative left atrial pressure (INLAP) associated with deep inspiration. INLAP could be the cause of periprocedural complications. Methods: We retrospectively enrolled 381 patients with AF (mean age, 63.9 ± 10.8 years; 76 women; 216 cases of paroxysmal AF) who underwent CA under deep sedation using an adaptive servo ventilator (ASV). Patients whose LAP was not obtained were excluded. INLAP was defined as 2DS₂-Vasc scores (2.3 ± 1.5 vs. 2.1 ± 1.6) and 3% oxygen desaturation indexes (median 18.6 (interquartile range 11.2–31.1) vs. 15.7 (8.1–25.3)), and higher prevalence of diabetes mellitus (23.3 vs. 13.3%) than patients without INLAP. Air embolism occurred in four patients with INLAP (3.0 vs. 0.0%). Conclusion: INLAP is not rare in patients undergoing CA for AF under deep sedation with ASV. Much attention should be paid to the possibility of air embolism in patients with INLAP.

Heart failure (HF) frequently coexists with conditions associated with glucose insufficiency, such as insulin resistance and type 2 diabetes mellitus (T2DM), and patients with T2DM have a significantly high incidence of HF. These two closely related diseases cannot be separated on the basis of their treatment. Some antidiabetic drugs failed to improve cardiac outcomes in T2DM patients, despite lowering glucose levels sufficiently. This may be, at least in part, due to a lack of understanding of cardiac insulin resistance. Basic investigations have revealed the significant contribution of cardiac insulin resistance to the pathogenesis and progression of HF; however, there is no clinical evidence of the definition or treatment of cardiac insulin resistance. Mitochondrial dynamics play an important role in cardiac insulin resistance and HF because they maintain cellular homeostasis through energy production, cell survival, and cell proliferation. The innovation of diagnostic tools and/or treatment targeting mitochondrial dynamics is assumed to improve not only the insulin sensitivity of the myocardium and cardiac metabolism, but also the cardiac contraction function. In this review, we summarized the current knowledge on the correlation between cardiac insulin resistance and progression of HF, and discussed the role of mitochondrial dynamics on the pathogenesis of cardiac insulin resistance and HF. We further discuss the possibility of mitochondria-targeted intervention to improve cardiac metabolism and HF.