DESCRIPTIONPlaque erosion within the coronary artery accounts for up to 20% of all sudden deaths and up to 40% of sudden deaths as a result of coronary thrombi in patients with coronary artery atherosclerosis.1 2We present a case of drug-resistant vasospastic angina pectoris (VSA) with erosion in the focal spastic lesion confirmed with coronary angioscopy (figure 1). A 78-year-old man presented to the coronary care unit with sudden chest pain accompanied by ECG ST segment elevation on V1-V3 and elevation of serum troponin-T level. A coronary angiography (CAG) revealed 90% stenosis in segment 2 of the right coronary artery, and this was removed by an intra-arterial injection of nitroglycerin. The left coronary artery was normal. Based on the above findings, acute coronary syndrome (ACS) associated with VSA was diagnosed. One month later, the patient was readmitted for ACS. CAG showed no stenosis, and an acetylcholine provocation test was performed in conjunction with adequate medication therapy (videos 1 and 2). As a result, focal vasospasm was induced, with the patient experiencing chest pain and an ECG change at segment 2 (figure 2). Coronary angioscopy showed yellow plaque with erosion at segment 2, similar to that of ACS (video 3 and figure 3). Percutaneous coronary intervention (PCI) was performed in this segment using a bare metal stent in conjunction with drug therapy. The PCI was successful, and the patient no longer experienced chest pain or ACS recurrence. This is the first case in which intimal injury of a focal spastic lesion has been confirmed by coronary angioscopy in a case of ACS. Pathological intimal injury has been previously observed in VSA, 1 and a causal relationship has been reported between intimal injuries (such as haemorrhage, flap, thrombusor ulcer) and VSA. These factors have not been previously reported in the context of ACS. PCI is a controversial method of treatment for VSA. While some case reports have shown the therapeutic validity of stent placement for drug-resistant focal VSA, 3 other reports have described provocation of vasospasm at the stent edge following this procedure. The influence of the stent in these cases-particularly the drug-eluting stent-was unclear. In this case, while the coronary artery stenosis was treated, we chose to supplement this treatment with PCI with a bare metal stent. As a result of this treatment, the VSA did not recur and was not provoked by follow-up acetylcholine stress testing after PCI.In conclusion, the case presented here elucidates the mechanism underlying intractable focal drugresistant VSA and provides evidence of a possible therapy for this condition.

Background: Various optimal medical therapies have been established to treat heart failure (HF) with reduced ejection fraction (HFrEF). Both HFrEF and HF with preserved ejection fraction (HFpEF) are associated with poor outcomes. We investigated the effect of topiroxostat, an oral xanthine oxidoreductase inhibitor, for HFpEF patients with hyperuricemia or gout. Methods:In this nonrandomized, open-label, single-arm trial, we administered topiroxostat 40-160 mg/ day to HFpEF patients with hyperuricemia or gout to achieve a target uric acid level of 6.0 mg/dL. The primary outcome was rate of change in log-transformed brain natriuretic peptide (BNP) level from baseline to 24 weeks after topiroxostat treatment. The secondary outcomes included amount of change in BNP level, uric acid evaluation values, and oxidative stress marker levels after 24 weeks of topiroxostat treatment. Thirty-six patients were enrolled; three were excluded before study initiation.Results: Change in log-transformed BNP level was −3.4 ± 8.9% (p = 0.043) after 24 weeks of topiroxostat treatment. The rate of change for the decrease in BNP level was −18.0 (−57.7, 4.0 pg/mL; p = 0.041). Levels of uric acid and 8-hydroxy-2'-deoxyguanosine/creatinine, an oxidative stress marker, also significantly decreased (−2.8 ± 1.6 mg/dL, p < 0.001, and −2.3 ± 3.7 ng/mgCr, p = 0.009, respectively).Conclusions: BNP level was significantly lower in HFpEF patients with hyperuricemia or gout after topiroxostat administration; however, the rate of decrease was low. Further trials are needed to confirm our findings.

This retrospective observational study aimed to examine the relationships of maximum walking speed (MWS) with peak oxygen uptake (peak VO2) and anaerobic threshold (AT) obtained by cardiopulmonary exercise testing (CPX) in patients with heart failure. The study participants were 104 consecutive men aged ≥ 20 years who had been hospitalized or had undergone outpatient care at our hospital for heart failure between February 2019 and January 2023. MWS was measured in a 5-m section with a 1-m run-up before and after the course. Multivariable analysis was used to examine the association between MWS and peak VO2 and AT by CPX. The Pearson correlation coefficient showed that MWS was positively correlated with percent-predicted peak VO2 and percent-predicted AT (r = 0.463, p < 0.001; and r = 0.485, p < 0.001, respectively). In the multiple linear regression analysis employing percent-predicted peak VO2 and percent-predicted AT as the objective variables, only MWS demonstrated a significant positive correlation (standardized β: 0.471, p < 0.001 and 0.362, p < 0.001, respectively). Multiple logistic regression analyses, using an 80% cutoff in percent-predicted peak VO2 and AT, revealed that only MWS was identified as a significant factor in both cases (odds ratio [OR]: 1.239, 95% confidence interval [CI]: 1.071–1.432, p = 0.004 and OR: 1.469, 95% CI: 1.194–1.807, p < 0.001, respectively). MWS was correlated with peak VO2 and AT in male patients with heart failure. The MWS measurement as a screening test for exercise tolerance may provide a simple means of estimating peak VO2 and AT in heart failure patients.