Background: Lipoprotein(a) [Lp(a)] is associated with increased cardiovascular risk, but its influence on plaque characteristics at optical coherence tomography (OCT) evaluation is not fully understood. Aims: This study seeks to explore the impact of Lp(a) levels on plaque morphology as assessed by OCT in a very high‐risk subset of patients. Methods: Consecutive patients admitted for acute coronary syndrome (ACS) and undergoing OCT‐guided percutaneous coronary intervention (PCI) at a large tertiary care center between 2019 and 2022 were deemed eligible for the current analysis. The overall population was categorized into two subgroups according to baseline Lp(a) levels: (1) lower Lp(a) (Lp(a) ≤ 300 mg/L) and (2) elevated Lp(a) (Lp(a) 300 mg/L). Predictors of lipid‐rich plaques were identified using multivariable logistic regression with stepwise selection of candidate covariates. Results: A total of 202 patients were included in this study. OCT findings revealed that patients with elevated Lp(a) had a higher prevalence of lipid‐rich plaques, a significantly greater mean lipid arc, along with increased macrophage infiltration and thin‐cap fibroatheroma (TCFA). In contrast, calcific plaque prevalence was higher in the lower Lp(a) group. Multivariable regression analysis identified low‐density lipoprotein cholesterol ≥ 70 mg/dL, and elevated Lp(a) as strong predictors of lipid‐rich plaques at OCT. Conclusion: In this observational study including ACS patients undergoing OCT‐guided PCI, those with elevated Lp(a) levels exhibited a higher prevalence of lipid‐rich plaques, increased macrophage infiltration, and TCFA, thereby indicating a more vulnerable plaque phenotype. Additionally, elevated Lp(a) levels and LDL‐C levels ≥ 70 mg/dL were each independently associated with lipid enrichment of coronary plaques. These findings suggest Lp(a), beyond other well‐known risk factors, as a key marker for risk stratification, potentially informing optimal medical management strategies.

The authors describe a transcatheter mitral valve-in-valve-in-valve (VIVIV) for the correction of a degenerated transcatheter in a surgical bioprosthesis, a challenging interventional scenario that will be increasingly frequent in the near future. The key steps taken were as follows: preprocedural planning integrating data from transesophageal echocardiogram, cardiac computed tomography, and 3mensio reconstruction (Pie Medical Imaging); transfemoral transseptal VIVIV performed with EchoNavigator system (Philips) guidance; Sapien Ultra 3 26-mm valve (Edwards Lifesciences) delivered with buddy balloon maneuvers to uncage the valve from the atrial struts of the previously implanted valve; and atrial septal defect occlusion with the Amplatzer ASO 24 mm (Abbott Cardiovascular). The inability to advance the prosthesis into the ventricle, irreversible hemodynamic collapse, residual high transmitral mean gradient because of impingment of the 3 valves, residual paravalvular leaks, and left ventricular outflow tract obstruction. Mitral VIVIV procedures represent a viable option for patients with prohibitive surgical risk and a degenerated transcatheter in surgical bioprostheses. Success hinges on adequate preprocedural planning and a thorough understanding of bailout techniques to minimize failure and prevent major complications.

Nonobstructive coronary artery disease is diagnostically challenging, especially in patients with recurrent chest pain and inconclusive imaging. Coronary functional abnormalities, such as vasospasm, microvascular dysfunction, and myocardial bridging, are key contributors to ischemia. A 57-year-old man with cardiovascular risk factors and a 10-year history of chest pain, empirically treated with vasodilators, presented with ST-segment elevation and ventricular fibrillation. Coronary angiography showed normal arteries. Invasive assessment with optical coherence tomography and coronary physiology revealed diffuse, nonobstructive lipid-rich atherosclerosis and a myocardial bridge in the mid left anterior descending artery. Ischemia was confirmed by resting full-cycle ratio. Coronary function testing showed microvascular dysfunction. Beta-blockers normalized indices, with symptom resolution at 6 months. This case illustrates the diagnostic value of invasive imaging and physiology in patients with myocardial infarction/myocardial ischemia with no obstructive coronary artery disease (INOCA/MINOCA). Invasive physiology and imaging are crucial for diagnosing ischemia mechanisms in nonobstructive coronary artery disease. Empirical therapy without functional assessment may delay effective, personalized treatment.

Myocardial infarction with non-obstructive coronary arteries (MINOCA) represents a heterogeneous clinical entity encompassing multiple ischemic mechanisms, including atherosclerotic plaque disruption, coronary artery spasm, coronary microvascular dysfunction, coronary embolism, and spontaneous coronary artery dissection. Despite the absence of obstructive coronary disease, patients with MINOCA remain at substantial risk of adverse cardiovascular outcomes, underscoring the need for accurate early diagnosis and effective risk stratification. In this context, accumulating evidence indicates that circulating serum biomarkers may provide additional pathophysiological and prognostic insights in patients with a working diagnosis of MINOCA. Moreover, distinct biomarker profiles may help support the differential diagnostic evaluation between MINOCA and other causes of acute myocardial injury, such as myocardial infarction with obstructive coronary arteries, myocarditis, and Takotsubo syndrome. This narrative review summarizes current evidence on serum biomarkers in MINOCA, highlights their potential role in guiding tailored diagnostic strategies, and discusses future perspectives toward biomarker-driven precision medicine in patients presenting with acute myocardial injury.

A 79‐year‐old man presented with cardiogenic shock due to severe degeneration of a prior transcatheter aortic valve. Temporary mechanical circulatory support with a transvalvular microaxial flow pump was initiated, resulting in rapid stabilization. A staged transaxillary TAVI‐in‐TAVI procedure was subsequently performed with a favorable outcome.