Ischemia and angina with non-obstructive coronary arteries (INOCA/ANOCA) have evolved into a defined clinical entity, with invasive coronary functional testing now guideline-recommended to establish the underlying endotypes. Yet diagnostic progress has outpaced pathophysiological understanding and therapeutic development. This article examines the principal unmet needs across INOCA/ANOCA: the observational nature of current registries; the unresolved molecular basis, natural history and overlap of the microvascular and vasospastic endotypes; persistent underdiagnosis and unstandardized invasive physiology; the absence of validated non-invasive tools and biomarkers; and the lack of endotype-targeted therapies proven to improve outcomes. Addressing these gaps is essential to advance mechanism-based personalized care.

Coronary dysfunction encompasses a spectrum of pathophysiologically distinct endotypes with differing therapeutic implications. The aim of this article was to provide an overview of device-based therapies targeting the various forms of coronary dysfunction. A systematic review of the available literature was performed. Multiple device-based strategies have been proposed for the treatment of angina in the absence of obstructive coronary artery disease, reflecting the heterogeneity of underlying mechanisms, and tailored approaches based on specific endotypes may improve symptom control and clinical outcomes.

Management of chronic coronary syndromes has shifted from an obstructive coronary artery disease-focused model to a phenotype-guided approach that includes angina with nonobstructive coronary arteries/ ischemia with nonobstructive coronary arteries (INOCA), vasospastic angina (VSA), and coronary microvascular dysfunction (CMD). Background therapies such as statins, angiotensin-converting enzyme inhibitors, antiplatelets, and sodium-glucose cotransporter-2 inhibitor inhibitors improve vascular health, but the WARRIOR trial highlighted the limits of intensive therapy in unselected INOCA patients. Anti-ischemic treatment should be mechanism-based: calcium channel blockers for VSA, beta-blockers and ranolazine for CMD, while nitrates may worsen microvascular disease.

Over 3 decades, invasive coronary physiology has evolved into a cornerstone of cardiovascular care. Fractional flow reserve (FFR) enabled lesion-specific assessment of epicardial stenoses, improving percutaneous coronary intervention (PCI) selection beyond angiography. Recognition of ischemia without obstructive disease expanded its role, with contemporary testing integrating adenosine-based flow assessment and acetylcholine-based evaluation of endothelial and vasomotor function, allowing identification of angina with nonobstructive coronary arteries endotypes, and tailored therapy. Physiologic pullback and post-PCI indices support procedural planning. Emerging tools, including angiography-derived indices, FFR-computed tomography, and optical coherence tomography (OCT)-based virtual flow reserve, are extending physiology-guided care toward noninvasive assessment and precision cardiovascular intervention.

Myocardial ischemia in chronic coronary syndromes extends far beyond the presence of obstructive epicardial coronary stenoses. Advanced cardiovascular imaging has emerged as a cornerstone for the identification of the diverse anatomic and functional mechanisms underlying myocardial ischemia, including atherosclerotic coronary artery disease, vasospastic angina, myocardial bridging, and coronary microvascular dysfunction. Coronary computed tomography angiography, cardiac magnetic resonance, and PET provide complementary insights. This article reviews the diagnostic performance, characteristic imaging findings, and contemporary clinical applications of these modalities, highlighting their role in refining phenotypic characterization and enabling a more precise and individualized approach to patients with chronic coronary syndromes.

Chronic coronary syndromes represent one of the principle causes of death and disability all over the world. ESC guidelines suggest the use of clinical risk scores such as the Risk Factor-Weighted Clinical Likelihood to estimate the probability of obstructive coronary artery disease, and underline the role of functional imaging tests, such as stress echocardiography. This article offers a comprehensive overview of the main applications of stress test, including indications, stress protocols, differences between stressors, and comparison with exercise stress test. This article also highlights emerging applications of traditional stress tests.

Coronary blood flow is regulated by oxygen demand through coordinated control of vascular resistance within different domains. Endothelial cells represent an important key factor in the regulation of coronary microvascular tone throughout synthesis and releasing of different vasodilator substances. The main vasodilator factor, produced by the endothelial cells, is nitric oxide. Endothelin-1 is a potent vasoconstrictor peptide which stimulates the proliferation of smooth muscle cells. Vessels smooth muscle cells play a major role in the pathogenesis of endothelium-independent coronary regulation of the vascular tone, principally mediated by Rho-kinase activation.

Structural coronary microvascular dysfunction (CMD) is an important endotype of ischemia with nonobstructive coronary arteries (INOCA) and is characterized by adverse arteriolar remodeling and capillary rarefaction. These alterations impair coronary vasodilator capacity and increase microcirculatory resistance, all of which contribute to impaired myocardial perfusion. In this article, we aim to review the anatomic and pathophysiological basis of structural CMD, its clinical presentation and prognostic relevance, and the role of invasive physiologic indices in its identification. We also highlight new considerations about dynamic aspects of structural CMD laying the groundwork for emerging therapeutic strategies and future research directions.

Epicardial coronary disease includes dynamic disorders capable of causing myocardial ischaemia without fixed obstructive stenosis. Vasospastic angina (VSA) and myocardial bridging (MB) are paradigmatic entities characterized by transient luminal narrowing and reversible flow impairment. Although traditionally viewed as distinct, they frequently overlap, sharing mechanisms such as endothelial dysfunction, smooth muscle hyperreactivity, altered shear stress, and autonomic imbalance. VSA results from episodic coronary constriction, whereas MB involves systolic compression of an intramyocardial segment with possible diastolic flow limitation. The aim of this article is to provide a mechanistic appraisal of these conditions and their clinical implications within chronic coronary syndromes.

Epicardial structural coronary disease remains a principal mechanism of ischemia in chronic coronary syndromes. This article provides key definitions and summarizes the pathobiologic continuum from diffuse plaque burden to focal flow-limiting stenosis, highlighting why angiographic severity alone is an imperfect surrogate of ischemic potential. We then review contemporary invasive physiologic assessment of epicardial disease, including hyperemic and non-hyperemic pressure indices, pullback mapping to distinguish focal versus diffuse patterns, and the potential role of post-percutaneous coronary intervention (PCI) physiology in detecting residual flow limitation and guiding optimization. Integrating anatomy and physiology is essential for individualized management and physiologically meaningful revascularization.

The cardiovascular intensive care unit (CVICU) presents unique opportunities and challenges for integrating palliative care. A growing population of patients living longer with advanced cardiac disease, persistent symptoms, and functional limitations may benefit from early palliative involvement. With increasing use of advanced therapies such as mechanical circulatory support, many patients die in the CVICU, while survivors often experience long-term physical and psychosocial burdens. Despite evidence that early palliative care improves quality of life and reduces nonbeneficial interventions, it remains underutilized because of prognostic uncertainty and inconsistent referral guidance. This review explores therapies, palliative roles, and end-of-life practices in the CVICU.

Failure to rescue (FTR), defined as mortality after a postoperative complication, is now a central quality metric in cardiac surgery, where high-acuity patients and resource-intensive care increase vulnerability to deterioration. Although complications are common, survival depends on timely recognition, effective escalation, and coordinated multidisciplinary management. This article synthesizes current evidence on the epidemiology, mechanisms, and system-level drivers of FTR, highlighting how patient, provider, and institutional factors influence rescue success. We outline practical, evidence-based strategies to reduce FTR in cardiac surgery after prolonged ventilation, renal failure, stroke, and reoperation, by emphasizing protocolized care, staffing models, team communication, and rapid response infrastructure.

Enhanced recovery after cardiac surgery (ERAS) advocates for consistent and standardized delivery of evidenced-based perioperative care. Multidisciplinary teams deliver integrated patient care elements across all phases of care. Elements include risk-screening, prehabilitation, nutritional support, organ protection, patient blood management, early mobilization, optimal analgesia, and prevention of complications. Implementation of an ERAS program has been shown to improve patient recovery and reduce complications, length of stay, and resource utilization. However, the evidence is inconsistent and often low grade. Ongoing research, education, and institutional commitment remain essential for continued quantification of ERAS and its role in caring for cardiac surgical patients.