Calcified coronary lesions remain a challenge in percutaneous coronary intervention (PCI) in both situations of acute myocardial infarction (MI) and stable coronary syndrome. It significantly increases the risk of procedural complications due to difficulty in equipment delivery, balloon expansion, and stent delivery. Furthermore, stent thrombosis, dissection, perforation, and future in-stent restenosis occur more frequently in calcified coronary lesions, impacting repeat target vessel revascularization and increasing the risk of future MI. With intracoronary imaging (intravascular ultrasound and optical coherence tomography), peri-procedural success for treating calcified lesions has increased significantly. Different modalities of calcium modification techniques have since been introduced. This review will discuss the pathophysiology and phenotypes of calcium deposition in the coronary vessels, including eccentric calcified plaques and calcified nodules. We will also focus on calcium modification techniques and their mechanisms: (1) Balloon escalation technique, (2) intravascular lithotripsy, (3) orbital atherectomy, and (4) rotational atherectomy. We will focus on the strengths and limitations of each technique, based on current recommendations and expert consensus from SCAI. We will also provide contemporary evidence of each modality for treating different phenotypes of calcified lesions. In summary, this article provides a comprehensive review of current guidelines for optimizing the treatment of calcified coronary lesions in PCI.

Background: Cardiac amyloidosis (CA) is an increasingly recognized but historically underdiagnosed cause of restrictive cardiomyopathy and heart failure with preserved ejection fraction (HFpEF). It results from the extracellular deposition of misfolded protein fibrils, most commonly transthyretin (ATTR) or immunoglobulin light chains (AL), leading to progressive myocardial dysfunction and multi-organ involvement. Objective: This review provides a comprehensive, cardiology-centered overview of cardiac amyloidosis, with an emphasis on early recognition, diagnostic strategies, subtype differentiation, and the evolving therapies. Content: We summarize the epidemiology, pathophysiology, and clinical manifestations of both ATTR and AL subtypes. Key diagnostic tools, including echocardiography, cardiac magnetic resonance imaging, bone scintigraphy, monoclonal protein screening, and endomyocardial biopsy, are reviewed in the context of a stepwise diagnostic approach. Special attention is given to clinical presentation, electrocardiographic and imaging “red flags,” and to differentiating CA from mimickers such as hypertrophic cardiomyopathy, hypertension-induced left ventricular hypertrophy, and aortic stenosis. Staging systems are detailed, highlighting the prognostic role of cardiac biomarkers. Therapeutic strategies are explored, including subtype-specific regimens (e.g., daratumumab-based therapy for AL; tafamidis and gene silencers for ATTR), the judicious use of conventional heart failure medications, and emerging therapies such as CRISPR-based gene editing. Conclusions: Timely recognition and accurate diagnosis of cardiac amyloidosis are critical to improving outcomes. As diagnostic tools and disease-modifying therapies evolve rapidly, cardiologists must remain at the forefront of multidisciplinary care. A structured biomarker- and imaging-guided approach can enhance diagnostic yield, inform prognosis, and optimize patient-specific management.

Cardiac amyloidosis, once considered a rare and untreatable disorder, is now increasingly recognized as a significant cause of heart failure, particularly in older adults. The two most clinically relevant subtypes of cardiac amyloidosis—immunoglobulin light-chain amyloidosis (AL) and transthyretin-related amyloidosis (ATTR)—differ in pathogenesis, natural history, and management strategies, thereby necessitating a tailored approach to diagnosis and therapy. Advances in multimodality cardiac imaging, including echocardiography, cardiac magnetic resonance, and nuclear scintigraphy, have enabled earlier detection and improved differentiation between subtypes. Management of AL centers on rapid initiation of plasma cell-directed therapies to suppress light-chain production, with autologous stem cell transplantation and novel chemotherapeutic regimens improving survival. In contrast, ATTR management focuses on stabilizing or reducing transthyretin deposition through disease-modifying agents, such as stabilizers, gene-silencing therapies, and emerging fibril-disrupting approaches. Supportive care, including guideline-directed heart failure therapies and arrhythmia management, as well as advanced therapies such as transplantation, remains essential across both subtypes, albeit with unique considerations due to amyloid-related hemodynamics. This review synthesizes current evidence on the diagnosis and treatment of AL and ATTR, highlights recent therapeutic breakthroughs, and discusses ongoing challenges in optimizing patient outcomes, from equitable access to therapies to the integration of multidisciplinary care.

Background: Sudden cardiac death (SCD) and sudden cardiac arrest (SCA) remain leading causes of mortality in young athletes, highlighting the importance of cardiac screening prior to play. The guidelines on screening protocol are continually evolving but are often inconsistent across organizations. We explore the role of different screening modalities including electrocardiography (ECG) and various cardiac imaging testing; their effectiveness, cost considerations and clinical utility regarding sports cardiac screening, comparing European and American cardiac screening protocols. Additionally, we also discuss the divergence between the European and American guidelines and appraise the literature surrounding this topic. Methods: A comprehensive literature review was conducted using studies published between 2010–2025 on cardiac screening for young athletes. Parameters included an English filter with review of observational studies, systematic reviews, meta-analyses, and randomized controlled trials (RCTs). Manual searches of PubMed, Embase, and Google Scholar libraries were also performed to enhance the reach of our investigation. Articles were chosen based on relevance to the topic. Results: When compared to PPCS physical exam, ECG advantages include increased detection of cardiac conditions leading to SCD, improved sensitivity and specificity compared to history alone, Disadvantages are the need for trained specialists to complete testing properly, unreliability for detecting congenital coronary anomalies, cost-effectiveness concerns, and false positive risk. However, these disadvantages can be improved with improved ECG interpretation training for non-cardiologists and policies easing access to advanced cardiac care. Conclusions: ECG remains the cornerstone of cardiovascular screening due to its affordability and sensitivity in detecting electrical abnormalities, its limitations necessitate a multimodal approach. Integrating targeted ECG screening with echocardiography and advanced imaging in select cases may enhance diagnostic accuracy while balancing cost-effectiveness and accessibility. While the benefits of routine ECG are strongly supported by the literature, nationwide implementation of it remains challenging due to economic, geographical and logistical restraints. Therefore, more research needs to be conducted on the mortality benefits and cost-effectiveness of routine ECGs implementation in PPCS screening for young athletes.