Purpose Asians often face the problems of clopidogrel resistance and East Asian paradox. This study aimed to evaluate the effects of P2Y₁₂ inhibitors, including low-dose prasugrel 2.5 mg, on the P2Y₁₂ reaction unit (PRU) in the chronic phase after percutaneous coronary intervention (PCI). Methods A total of 348 patients were studied. PRU was measured 6–12 months after PCI and subsequently, 6 months later using a P2Y₁₂ assay, respectively. This study evaluated the proportion of bleeding risk (PRU ≤ 85) and ischemic risk (PRU ≥ 239) as primary endpoints, and the prediction of bleeding risk and ischemic risk using multivariable logistic regression analysis. Results At baseline, 136 patients (39%) received prasugrel 3.75 mg, 48 patients (14%) received prasugrel 2.5 mg, and 164 patients (47%) received clopidogrel 75 mg. Clopidogrel 75 mg had a significantly higher proportion of ischemic risk within one year after PCI than the other groups, and was an independent predictor for ischemic risk with reference of prasugrel 3.75 mg. In addition, switching from clopidogrel 75 mg to prasugrel 2.5 mg significantly lowered and aggregated the PRU value. Whereas, dose reduction of prasugrel had a significantly lower proportion of bleeding risk over one year after PCI than the continuation of prasugrel 3.75 mg, and was an independent predictor for bleeding risk with reference of continuation of prasugrel 3.75 mg. Conclusions Prasugrel 2.5 mg has a lower ischemic risk and a more stable PRU value compared with clopidogrel treatment. Prasugrel also contributes to a decline in bleeding risk with concomitant dose reduction. Trial Registration University Hospital Medical Information Network (UMIN), ID: UMIN000029541, Date: October 16, 2017 (https://center6.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000033395).

Pulmonary hypertension (PH) is a common complication of aortic stenosis (AS). Despite the established association between PH and poor outcomes in patients with AS, the prognostic implication of a change in PH after transcatheter aortic valve implantation (TAVI) has been rarely evaluated. This study analyzed a prospective multi-center TAVI registry database involving six Japanese centers and used the transtricuspid pressure gradient (TRPG) obtained by echocardiography to estimate pulmonary artery systolic pressure. The participants (n = 2056) were first divided into two groups by TRPG before TAVI, a PH (−) group (TRPG < 30 mmHg) (n = 1407, 61.9%) and a PH (+) group (TRPG ≥ 30 mmHg) (n = 649, 28.6%). Next, by TRPG after (4.1 ± 5.3 days) TAVI, the PH (+) group was further subdivided into two groups, Recovered PH (TRPG < 30 mmHg, n = 253) and Persistent PH (TRPG after TAVI ≥ 30 mmHg, n = 396). The median follow-up duration was 1.8 years. The primary and secondary endpoints were the composite and each of cardiovascular (CV) death and heart failure hospitalization, respectively. Unadjusted Kaplan-Meier estimates with log-rank comparisons showed significantly higher cumulative incidences of primary and secondary endpoints in the Persistent PH group compared to other groups. Moreover, adjusted multivariate Cox-proportional hazard analyses showed that a decreased (−10 mmHg) TRPG after TAVI was linearly associated with a reduced risk of the primary endpoint (hazard ratio (HR): 0.76, 95% confidence interval (CI): 0.64–0.90, p = 0.0020). The findings in the present study indicate that the recovery of PH may partly contributes to the prognostic benefit of TAVI procedure in patients with AS and elevated pulmonary artery systolic pressure.

Acute coronary syndrome (ACS) remains one of the leading causes of cardiovascular morbidity and mortality. Recent advances in high-sensitivity cardiac troponin assays, multimodal imaging, and antithrombotic therapies have introduced more individualized risk assessment and management. This review highlights a precision-oriented diagnostic pathway, which integrates the 0/1-hour algorithm with imaging modalities for the comprehensive evaluation of culprit and non-culprit lesions. Revascularization strategies are advancing, with imaging-guided percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG), enabling more tailored approaches for complex diseases. Meanwhile, mechanical circulatory support offers potential benefits for cardiogenic shock; nevertheless, there are uncertainties regarding optimal timing and patient selection. Long-term antithrombotic therapy is becoming increasingly optimized. Recent strategies have focused on reducing the duration of dual antiplatelet therapy (DAPT) and exploring de-escalation approaches such as P2Y12 inhibitor monotherapy. Secondary prevention extends beyond lipid-lowering therapies and includes metabolic and anti-inflammatory interventions. Collectively, these advancements indicate a shift toward truly personalized care for ACS, aiming to improve outcomes by transitioning away from a one-size-fits-all approach.

A 35-year-old woman taking a low-dose combined oral contraceptive (COC) for uterine fibroids presented by ambulance to a referring hospital with nausea. During the initial evaluation, she suddenly became unresponsive and developed cardiac arrest, prompting immediate cardiopulmonary resuscitation. Electrocardiography (ECG) documented ventricular fibrillation (VF), and external defibrillation restored spontaneous circulation. After return of spontaneous circulation, ECG showed ST-segment elevation in leads II, III, and aVF. She was transferred to our hospital. Emergency coronary angiography demonstrated 90% stenosis of the proximal right coronary artery (RCA) and total occlusion of the mid RCA. During percutaneous coronary intervention, VF storm occurred, necessitating initiation of veno-arterial extracorporeal membrane oxygenation. Intravascular ultrasound (IVUS) revealed a plaque-containing culprit lesion, and drug-coated balloon angioplasty was performed. Subsequent thrombophilia testing disclosed anti-β2-glycoprotein I IgG positivity, establishing antiphospholipid syndrome (APS). Notably, despite the absence of conventional risk factors (e.g. dyslipidemia, diabetes), IVUS demonstrated an atherosclerotic-appearing lesion in the prothrombotic milieu of COC use and APS. In young women, it is important to consider non-atherosclerotic causes such as antiphospholipid syndrome (APS) and combined oral contraceptive use as differential diagnoses for acute coronary syndrome. Although embolic mechanisms are often implicated in such settings, the present case demonstrated an atherosclerotic-appearing lesion on intravascular ultrasound despite the absence of conventional coronary risk factors, suggesting the possibility of APS-related vascular injury contributing to plaque formation.