Coronary autoregulation is the intrinsic ability of the coronary circulation to maintain stable blood flow despite fluctuations in myocardial perfusion pressure, provided that metabolic demands remain constant. Central to this process is the dynamic modulation of microvascular resistance within the coronary microcirculation, which acts as the main determinant of coronary blood flow. This regulatory mechanism enables the coronary vasculature to adapt to variations in aortic pressure and epicardial resistance, preserving myocardial perfusion. Historically, the study of coronary autoregulation relied on animal models using implanted flow probes. In humans, modalities such as nuclear imaging and intracoronary Doppler have been employed. Most recently, continuous intracoronary thermodilution has emerged as a robust technique, allowing simultaneous and accurate assessment of absolute coronary blood flow, epicardial resistance, and microvascular resistance. Yet, despite its fundamental role in the understanding of coronary physiology, coronary autoregulation remains complex, often overlooked, and poorly understood. This review focuses on the pivotal role of the coronary microcirculation, specifically microvascular resistance, in maintaining stable resting flow in the context of epicardial coronary artery disease. It provides a theoretical framework, summarizes key animal and human data, and presents an integrative model illustrating the haemodynamic transition from rest to maximal hyperaemia from the perspective of coronary resistance. Finally, it highlights the importance of understanding coronary autoregulation and the interplay between epicardial and microvascular resistance when interpreting not only the clinical presentation of patients with epicardial disease but also the results of the coronary physiological assessment.

Background: Left main coronary artery (LMCA) compression by a dilated pulmonary artery (PA) is one of the lesser known but severe complications in the setting of severe pulmonary hypertension (PH). This phenomenon can lead to critical myocardial ischaemia and poses unique diagnostic and therapeutic challenges. Case Summary: A 36-year-old female with PH due to peripheral pulmonary arterial stenoses presented with significant dyspnoea and exercise intolerance. Echocardiography revealed mild biventricular systolic dysfunction. Right heart catheterization confirmed severe pre-capillary PH, while coronary computed tomography angiography demonstrated a dilated PA compressing the proximal LMCA. Invasive coronary angiography confirmed a subocclusive LMCA stenosis, but during the procedure the patient developed refractory cardiogenic shock with biventricular failure. LMCA percutaneous coronary intervention (PCI) with a single drug-eluting stent was performed with the assistance of mechanical circulatory support (MCS). After the procedure, the ventricular function gradually improved, the patient was weaned from MCS by day 2 and discharged after 10 days. Discussion: LMCA compression in PH is often underdiagnosed due to its non-specific symptoms. However, early recognition is crucial as it significantly impacts outcomes by preventing the progression to biventricular dysfunction and reducing the risk of sudden death. Management typically requires a multi-disciplinary approach, with PCI often being the treatment of choice due to the high surgical risk in PH patients and the peculiar aetiology of the stenosis secondary to extrinsic compression instead of luminal atherosclerosis. In this case, the use of MCS was essential in stabilizing the patient and enabling successful PCI.

Aims: Transcatheter aortic valve implantation (TAVI) has become a standard treatment for severe aortic stenosis, yet clinical outcomes vary significantly. Epicardial adipose tissue (EAT), visceral adipose tissue (VAT), and circulating adiponectin may contribute to this heterogeneity. This study aimed to determine how adipose tissue characteristics, in combination with adiponectin levels, affect clinical outcomes following TAVI. Methods and results: This single-centre retrospective study included 243 patients with severe aortic stenosis who underwent TAVI. Pre-procedural computed tomography scans were processed using artificial intelligence to quantify EAT density (EATHU) and VAT area at the level of the L3 vertebra (VATL3A). Patients were stratified into groups based on median adiponectin (6.54 µg/mL), VATL3A (135 mm), EATHU (−82.0 HU), and EATVOL (31 mL). The primary endpoint was 1-year major adverse cardiac and cerebrovascular events (MACCE), defined as all-cause mortality, heart failure hospitalization, or stroke. Over a mean follow-up of 344 ± 77 days, there were 25 deaths (10%), 12 heart failure hospitalizations (5%), and 7 strokes (3%). Circulating adiponectin (adjusted HR 1.34 per 5 μg/mL, 95% CI 1.05–1.70; P = 0.017) and VATL3A (adjusted HR 0.63 per 100 mm2, 95% CI 0.44–0.91; P = 0.014) independently associated with MACCE, EATHU, and EATVOL did not. All three combined adipose–adiponectin phenotypes demonstrated significant graded risk (P-for-trend 0.003–0.048), with the high EATVOL/high adiponectin phenotype showing the strongest association (adjusted HR 4.25, 95% CI 1.80–10.07). Conclusion: Circulating adiponectin and VATL3A independently predict 1-year MACCE after TAVI. EAT parameters become prognostically informative only when combined with adiponectin.

Stent underexpansion remains a major contributor to restenosis and stent thrombosis following percutaneous coronary intervention (PCI), yet intravascular imaging is not used routinely in many settings. Digital stent enhancement (DSE) offers an angiography-based approach to improve visualization of metallic stents through real-time image processing, enabling rapid assessment of stent expansion and deployment abnormalities. In this review, we describe the underlying principles and commercially available DSE systems, summarize diagnostic performance data with emphasis on detection of stent underexpansion, and highlight where DSE may complement IVUS and OCT. Finally, we review emerging innovations, including three-dimensional stent reconstruction, and propose future research priorities to define clinical impact.