坂倉 建一

Calcified nodule (CN) is a unique calcified plaque morphology that is pathologically characterized by fibrous-cap disruption and luminal thrombus associated with eruptive, dense calcific nodules. Although CNs account for a small proportion of acute coronary syndrome, they remain challenging substrates for percutaneous coronary intervention (PCI) due to high risks of underexpansion and in-stent restenosis. To understand their unpredictable mechanical behavior, it is crucial to recognize their origin: CNs typically arise from the fragmentation of mechanically vulnerable necrotic core calcification under mechanical stress, often exacerbated by adjacent rigid sheet calcium. Crucially, while intravascular imaging typically classifies CNs into "eruptive" or "non-eruptive" forms, this binary classification alone is sometimes insufficient to predict lesion compliance or "softness." A deeper understanding of the underlying pathological evolution-from fresh, thrombus-covered nodules to mature, ossified masses-is essential to distinguish deformable lesions from rigid ones. This review bridges this gap by proposing a pathology-imaging continuum that links histological maturity to mechanical behavior, enabling more precise phenotyping beyond surface appearance. We finally discuss how this integrated approach informs contemporary PCI strategies, including atherectomy, intravascular lithotripsy, and lifetime management, to optimize clinical outcomes.

BACKGROUND: The mortality rate for acute myocardial infarction (AMI) complicated with cardiogenic shock (CS) remains high despite advances in mechanical circulatory support (MCS). The Society for Cardiovascular Angiography and Interventions (SCAI) has proposed a 5-stage classification of CS, and in this study we compared the clinical outcomes of AMI patients with SCAI shock stage A with those in stage B. METHODS AND RESULTS: We retrospectively analyzed 257 AMI patients, classified into modified stage A (n=180) and modified stage B (n=77) groups. The primary endpoint was in-hospital adverse events, defined as a composite of in-hospital death, initiation of MCS, and mechanical complications. The secondary endpoint was long-term major adverse cardiovascular events (MACE), including all-cause death, re-admission for heart failure, or non-fatal myocardial infarction. The median follow-up duration was 786 days. Compared with modified stage A, modified stage B group had a significantly lower left ventricular ejection fraction (44.6% vs. 54.4%, P<0.001). In-hospital adverse events were comparable between the groups (P=0.128). Kaplan-Meier analysis showed a higher incidence of MACE in modified stage B (P=0.029); however, multivariate analyses revealed no significant association between modified stage B and either in-hospital adverse events or long-term MACE. CONCLUSIONS: As compared to SCAI shock modified stage A, modified stage B was not independently associated with in-hospital and long-term clinical outcomes after controlling confounding factors.