Acute coronary syndrome (ACS) and stroke are interconnected conditions that often share risk factors such as atherosclerosis, thrombosis, and systemic inflammation. When these events occur simultaneously, they present unique diagnostic and therapeutic challenges. This review explores the pathophysiological mechanisms linking ACS and stroke, including common pathways like plaque instability, cardioembolism, and endothelial dysfunction, while highlighting the distinct features of ischemic and hemorrhagic strokes. The manuscript provides an overview of diagnostic strategies, emphasizing the role of biomarkers, advanced neuroimaging, and risk stratification tools in guiding acute management. Furthermore, the review delves into treatment approach, emphasizing the need to balance reperfusion therapies for ACS with thrombolysis or thrombectomy for ischemic stroke while carefully managing the challenges posed by anticoagulation in cases complicated by bleeding. Long-term strategies for secondary prevention are examined, including antithrombotic regimens tailored to the dual risk of thrombosis and bleeding, as well as lipid-lowering and blood pressure management. Future perspectives highlight the potential of novel pharmacological agents, neuroprotective therapies, and AI-driven tools to enhance patient outcomes. This review underscores the importance of integrated, multidisciplinary care and identifies key areas for future research to optimize the management of these high-risk patients.

Apical hypertrophic cardiomyopathy is a distinctive and often under-recognized variant of hypertrophic cardiomyopathy, characterized by predominant thickening of the apical segments of the left ventricle. Echocardiography and cardiac magnetic resonance imaging represent the two principal modalities for diagnosis and morphological assessment. While transthoracic echocardiography remains the first-line imaging technique, it may underestimate apical involvement, particularly when image foreshortening or poor endocardial/epicardial delineation occurs. Cardiac magnetic resonance has become the reference standard for defining apical morphology, quantifying hypertrophy, and characterizing myocardial tissue and perfusion. Beyond its diagnostic role, magnetic resonance serves as a research platform for the identification of new apical-centric criteria which, after appropriate validation, may be translated into echocardiographic practice. Echocardiography, however, retains unique strengths through its real-time evaluation of cardiac dynamics, ready-to-use approach to diastolic function assessment, and its ability to identify subtle apical or para-apical obstructive gradients that may raise the initial diagnostic suspicion. This review underscores the complementary roles of the two modalities and the multiple domains in which transthoracic echocardiography can derive substantial methodological and conceptual benefit from cardiac magnetic resonance imaging, both in imaging methodology and in the refinement of diagnostic evaluation.

Non-dilated left ventricular cardiomyopathy has recently emerged as a distinct morpho-functional phenotype defined by non-ischemic left ventricular scarring or fatty replacement or by isolated global left ventricular hypokinesia without scarring in the absence of ventricular dilatation. Whether it represents a distinct biological entity or a shared phenotypic expression across cardiomyopathies remains unresolved. This narrative review examines evidence from genetics, multimodality imaging, natural history, and outcomes. Overlap with dilated and arrhythmogenic cardiomyopathies is extensive: no currently validated genetic, imaging, histological, or circulating marker uniquely identifies the phenotype, and longitudinal studies describe heterogeneous trajectories from reverse remodeling to dilated or predominantly arrhythmogenic evolution. Genetics argues in both directions, as the genes involved are shared yet their distribution differs, pro-arrhythmogenic variants being more frequent than in dilated cardiomyopathy. We propose a hypothesis-generating framework of three probable trajectories, evolving dilated cardiomyopathy, evolving arrhythmogenic cardiomyopathy, or stable non-dilated disease, integrating genotype, multiparametric cardiac magnetic resonance, longitudinal remodeling, and arrhythmic phenotype.

Mitral valve prolapse represents the most common cause of primary mitral regurgitation in Western countries and has traditionally been viewed as a disorder driven by valvular incompetence and chronic volume overload. Within this paradigm, left ventricular enlargement was expected to correlate with regurgitant severity. However, patients with myxomatous bileaflet prolapse often exhibit left ventricular dilatation disproportionate to the degree of regurgitation, leading to the hypothesis of an intrinsic myocardial disease process. Cardiovascular magnetic resonance imaging has challenged this concept through the identification of doming volume, a previously unrecognized systolic blood compartment located between the mitral annular plane and the ventricular surface of prolapsing leaflets. This volume is mechanically coupled to ventricular contraction and contributes to total ventricular volume load independently of transvalvular regurgitation. Recognition of doming volume provides a physiological explanation for excessive ventricular remodeling observed in bileaflet prolapse and Barlow disease. Doming volume has important implications for imaging assessment. Its common exclusion from echocardiographic volumetric measurements may result in underestimation of left ventricular end-systolic volume, overestimation of ejection fraction, and underestimation of regurgitant burden, contributing to discordance between echocardiographic and cardiovascular magnetic resonance-derived measurements. Cardiovascular magnetic resonance enables comprehensive assessment, allowing accurate quantification of ventricular volumes, mitral regurgitation severity, doming volume, and myocardial tissue characteristics. Integration of doming volume into the evaluation of mitral valve prolapse improves physiological consistency between imaging findings and ventricular remodeling. However, further evidence is required before doming volume assessment can be incorporated into operative clinical indications or decision-making thresholds.