Advances in fetal cardiac magnetic resonance imaging (CMR) have expanded its role as an adjunct to expert fetal echocardiography in the prenatal evaluation of complex cardiopulmonary anomalies. This review outlines an evidence-based framework for integrating fetal CMR when it provides diagnostic or prognostic information that can informs counseling, delivery planning, or postnatal management. Fetal CMR offers high-resolution, multiplanar imaging with superior soft-tissue contrast and wide field of view, enabling improved assessment of cardiopulmonary structures where echocardiography is limited by technical or physiologic factors, or when expert echocardiography raises clinically relevant questions. MRI enables improved delineation of aortic arch and pulmonary venous anatomy, characterization of pulmonary parenchymal changes, and quantify lung and ventricular volumetry without relying on geometric assumptions. Emerging flow-based techniques allow evaluation of fetal hemodynamics and cardiovascular physiology beyond static imaging. These technologies provide diagnostic and prognostic information in select, often critical, congenital heart diseases. Fetal cardiac CMR serves as a complementary modality to expert echocardiography when applied selectively to address clinically meaningful diagnostic or prognostic questions. However, limited availability, technical complexity, and the need for specialized expertise currently constrain widespread adoption. Continued technical refinement and outcome-based validation are required before fetal CMR can be routinely integrated into clinical practice.

Cardiovascular disease is a leading cause of morbidity and mortality among patients with cancer, yet individual risk is highly heterogeneous. This review examines cardiometabolic vulnerability as a unifying framework linking baseline cardiometabolic risk factors with cancer therapy-related cardiovascular injury and discusses emerging pharmacologic and lifestyle interventions for cardiovascular risk mitigation. Epidemiologic and mechanistic studies demonstrate that obesity, insulin resistance, dyslipidemia, and hypertension, often exacerbated by cancer therapies, amplify systemic inflammation, neurohormonal activation, endothelial dysfunction, and metabolic inflexibility. These disturbances interact with specific anticancer treatments, including anthracyclines, HER2-targeted agents, VEGF pathway inhibitors, endocrine therapies, and immune checkpoint inhibitors, increasing susceptibility to diverse cardiovascular toxicities. Emerging evidence supports multimodal preventive strategies integrating pharmacologic interventions targeting neurohormonal, metabolic, and inflammatory pathways with lifestyle modifications, though optimal approaches require further validation in cancer populations. Cardiometabolic vulnerability provides a framework to understand heterogeneous cardiovascular risk in cancer patients. Integrating cardiometabolic profiling with therapy-specific risk assessment may improve prevention strategies in cardio-oncology. Continued research is needed to refine risk stratification and inform personalized approaches for this growing population.

Hypertension is the most common chronic disease in developed countries, with a prevalence exceeding 25-30% of adults. The updated hypertension guidelines define evidence-based blood pressure targets and provide clinicians with a framework for achieving them. Examining the underlying hypertension phenotypes provides a complementary approach to the management of hypertension. Rather than a one-size fits all approach, a more directed hypertension management involves tailoring therapy toward the predominant pathophysiologic mechanism or "Phenotype" responsible for blood pressure elevation, rather than adhering to a uniform, stepwise treatment algorithm. Such an approach allows clinicians to tailor therapy to the key biological drivers of hypertension in the individual patient. It is important to note that these pathways overlap and are not isolated, while oftentimes, one single phenotype is the predominant over the others. This article examines these distinct phenotypes, outlining their key characteristics and the best therapeutic approaches for each. Our ability to delineate hypertension phenotypes through biomedical, genetic and clinical testing is advancing rapidly, and precision medicine innovations are reshaping hypertension care with a level of specific and clinical insights that were not previously attainable, paving the way for the refinement of future hypertension guidelines.

To synthesize current evidence supporting intentional weight reduction as a cardiometabolic strategy for treating and preventing heart failure (HF) across the ejection-fraction spectrum, examine the influence of baseline obesity on treatment effects of established HF therapies, and highlight key knowledge gaps and future research directions. Visceral adipose tissue, central obesity, and dysfunctional adipose mass are linked to the development and progression of HF with preserved ejection fraction (HFpEF). Recent trials show that incretin-based therapies (semaglutide, tirzepatide) improve exercise capacity, symptoms, and quality of life in HFpEF, and potentially reduce HF events. Patients with higher degrees of obesity may derive greater benefit from incretin-based therapies and other guideline-directed therapies, including mineralocorticoid receptor antagonists (MRA), sodium-glucose transport 2 (SGLT2) inhibitors, and angiotensin receptor-neprilysin inhibitor (ARNI). While observational studies suggest intentional weight loss may lower HF risk, randomized trials of antiobesity medications have yet to further clarify this potential benefit. Weight loss is currently recommended as an optimal strategy for individuals with obesity and HFpEF, given consistent benefits for exercise capacity, functional status, and quality of life, with a potential for reducing clinical events. Intentional weight loss impact in HFrEF and its role in primary HF prevention remains uncertain. Large, well designed cardiovascular outcome trials of intentional weight-loss interventions in populations with obesity and HF, or obesity and elevated HF risk, are needed to establish clinical efficacy and better define individuals who benefit from those interventions across the spectrum of ejection fraction.

Stress perfusion cardiac magnetic resonance imaging (CMR) has gained increasing adoption across North America and Europe for the evaluation of symptomatic suspected or established ischemic heart disease (IHD). Over the past decade, stress perfusion CMR has demonstrated excellent diagnostic and prognostic performance, particularly in patients at intermediate or high risk of IHD or with established coronary artery disease (CAD). After the landmark ISCHEMIA trial, stress CMR may play an important role in selecting patients for invasive management strategies and determination of revascularization technique. Artificial intelligence has streamlined CMR scanning techniques and in-line automation of quantitative pixelated perfusion maps. Quantitative stress CMR can evaluate absolute myocardial blood flow and perfusion reserve that improves risk stratification and detection of coronary microvascular disease (CMD). CMD detection may assist clinicians with diagnosis of chest pain in patients without obstructive CAD and improve prognostication and detection of pathophysiological mechanisms in a variety of cardiomyopathies. Quantitative stress perfusion CMR will play an important clinical role in evaluating patients at risk of IHD and cardiomyopathy with iterative cost and time efficiency owing to continued integration of artificial intelligence techniques. More widespread adoption will likely improve cost effective cardiac care and reduce adverse clinical outcomes.

Purpose of reviewComplete revascularization (CR) by percutaneous coronary intervention (PCI) in acute coronary syndromes with multivessel coronary artery disease (CAD) was previously contraindicated in the absence of cardiogenic shock or high-risk ischemia. Over the last decade, CR has been a focus of recent clinical investigation and practice evolution due to high-quality evidence supporting hard cardiovascular outcome benefit, contributing to a reversal in international guidelines. This review provides concise syntheses of contemporary and emerging randomized evidence underpinning current strategies and unresolved questions regarding patient selection, timing of CR and guidance modalities for the identification and treatment of nonculprit lesions.Recent findingsThe randomized evidence base supporting CR with PCI for acute coronary syndromes (ACS) and multivessel CAD has increased recently with large-scale trials comparing immediate versus staged CR and physiology-guided versus angiography-guided CR, including reports of longer-term comparative outcomes. Enough events have recently accrued to enable demonstration of all-cause mortality benefits with CR.SummaryContemporary randomized data increasingly support CR with PCI in haemodynamically stable patients. However, ACS type, timing of intervention and method of evaluation still necessitate individualized shared clinical decision-making, and further trials are required to validate the optimal PCI strategies by which to achieve CR in the correct populations.

Early (<10 days) recovery of the left ventricular ejection fraction (LVEF) in Takotsubo syndrome (TTS) has been associated with better short- and long-term clinical outcomes compared to delayed recovery (>10 days). This review aims to comprehensively address the literature regarding its clinical implications, the pathological basis underlying a chronic inflammatory heart failure phenotype; as well as the potential pharmacological and nonpharmacological therapies that might aid in LVEF recovery and improve clinical outcomes in TTS. We describe the clinical findings of the two large studies addressing this topic, derived from ongoing prospective registries (RETAKO and InterTAK) in which inflammatory biomarkers are the strongest independently associated factor with late left ventricular (LV) recovery (>10 days). This is in line with the previous studies suggesting a chronic inflammatory phenotype with elevated inflammatory biomarkers (e.g. interleukin-6) that persists even 5 months after the index event and long-lasting myocardial energetic impairment >1 year after the TTS episode. Late LV recovery in TTS is linked to a worse short- and long-term prognosis, identifying these patients for closer monitoring might be clinically relevant for the early detection of complications. Mechanistical research needs to be undertaken to elucidate the cellular and molecular pathways implicated in late LV recovery, this could aid in the selection of pharmacological and nonpharmacological therapies to aid LV recovery.

Purpose of reviewThis paper reviews the current understanding of coronary vascular dysfunction (CVDys) in patients with angina and no obstructive coronary artery disease (ANOCA), based on recent findings from a comprehensive, large-scale study. It also discusses potential future directions for research and clinical practice.Recent findingsCVDys involves enhanced vasoconstriction or impaired vasodilation caused by endothelium-dependent and/or -independent dysfunction in the epicardial or microvascular coronary arteries. It is classified into four subtypes based on anatomical location and underlying mechanisms, and can be assessed using coronary reactivity testing (CRT). Previous studies have evaluated their prognostic implications separately or in limited populations.A recent study assessed all subtypes within a single ANOCA cohort and confirmed that endothelium-dependent epicardial dysfunction and both types of microvascular dysfunction are associated with worse prognosis. Moreover, it demonstrated that microvascular function – both endothelium-dependent and -independent – serves as an independent prognostic factor for major adverse cardiovascular events. These findings emphasize the value of CRT-based comprehensive evaluation for risk stratification.SummaryWhile evidence regarding the prognostic impact of CVDys has become increasingly robust, effective treatment strategies remain undefined. Future efforts should focus on developing CRT-guided interventions targeting coronary dysfunction, with the goal of improving clinical outcomes.

Cardiomyopathy caused by pathogenic variants in the desmoplakin gene has recently emerged as an entity distinct from other genetic cardiomyopathies. This review summarizes recent literature, including the first large cohort studies of this disease, that have begun to characterize its natural history and specific management challenges. Desmoplakin cardiomyopathy may be characterized by episodic "hot phases", cutaneous findings, and a high risk of sudden cardiac death. Gene-specific risk factors for sudden cardiac death have begun to be elucidated. Genetic testing in arrhythmogenic cardiomyopathy and recurrent myocarditis can identify patients with desmoplakin variants who may have a unique phenotype that requires gene-specific management. More research is needed in this population to further guide treatment, counseling, and risk stratification.