Coronary microvascular disease (CMD) comprises a spectrum of conditions characterized by the functional and structural abnormalities of coronary microcirculation, affecting vessels typically smaller than 500 μm. Despite its clinical significance as a contributor to myocardial ischemia, CMD frequently remains underdiagnosed due to the limitations of current diagnostic approaches. Invasive testing, including coronary reactivity assessment, is considered the gold standard, but it is resource-intensive and not always accessible. Non-invasive methods, such as positron emission tomography (PET) and transthoracic Doppler echocardiography (TTDE), offer alternatives but are limited by varying accuracy and accessibility. Amid these diagnostic challenges, there is increasing interest in circulating biomarkers as adjuncts in CMD evaluation. Biomarkers associated with endothelial dysfunction, inflammation, and oxidative stress, detectable through routine blood tests, may assist in CMD diagnosis, risk stratification, and therapeutic monitoring. These biomarkers can offer insights into CMD pathogenesis and enable early, non-invasive screening to identify patients who may benefit from more invasive investigations. This narrative review examines studies assessing biomarkers in CMD patients with diagnoses confirmed through invasive techniques. Our objective is to focus on circulating biomarkers linked to the invasive evaluation of coronary microcirculation, aiming to advance the understanding of the underlying mechanisms of this prevalent condition and enhance diagnostic accuracy and the clinical management of affected patients.

Background: In patients with ST-segment elevation myocardial infarction (STEMI) and multivessel disease (MVD), complete revascularization (CR) is recommended over culprit-only PCI to reduce adverse cardiovascular outcomes. However, the optimal strategy for CR, whether angiography (Angio)-guided or physiology-guided, remains uncertain. Methods: This network meta-analysis included 14 randomized controlled trials (RCTs) with 11,568 patients to compare the efficacy of angio-guided CR, physiology-guided CR, and culprit-only PCI in reducing major adverse cardiovascular events (MACE), all-cause mortality, recurrent myocardial infarction (MI), cardiovascular (CV) death, and unplanned revascularization. The frequentist and Bayesian approaches were applied to assess the effectiveness of each strategy. Results: The pairwise meta-analysis showed that angio-guided CR showed superior efficacy, significantly reducing MACE (OR = 0.44; 95% CI: 0.37–0.52), recurrent myocardial infarction, and unplanned revascularization compared to culprit-only PCI. Physiology-guided CR also reduced MACE (OR = 0.64, 95% CI: 0.45–0.91) and unplanned revascularization. The network metanalysis showed that CV death was lower in the physiology-guided CR group (OR 0.56; 95% CI 0.25–1.05), suggesting a protective effect, but the difference did not reach statistical significance. Furthermore, physiology-guided CR was not significantly better than angio-guided CR in most outcomes. Conclusions: Angio-guided CR appears to provide the best overall outcomes for patients with STEMI and MVD, outperforming physiology-guided CR in most endpoints. Further large-scale trials are needed to clarify the relative efficacy of angio-guided CR and physiology-guided CR in this patient population.

Myocarditis is an underdiagnosed inflammatory condition of the myocardium that may lead to significant complications, including life-threatening ventricular arrhythmias and sudden cardiac death, particularly in young individuals. The arrhythmogenic substrate evolves dynamically across the disease course, driven by acute inflammation, ion channel alterations, immune-mediated cytotoxicity and negative structural remodelling. Persistent myocardial inflammation and fibrosis promote conduction abnormalities, triggered activity and re-entrant circuits, creating a pro-arrhythmic milieu. Despite increasing recognition of its clinical relevance, arrhythmias management in myocarditis remains challenging due to the variability in patient presentation and disease trajectory. This review examines arrhythmogenic mechanisms associated with myocarditis, exploring differential contribution of the above-reported triggers to concurrent electrical instability. Updated therapeutic approaches to managing arrhythmias in myocarditis are discussed, with emphasis on the importance of individualised treatment plans. A deeper understanding of the complex interplay between inflammation and arrhythmias may improve clinical decision-making, and help tailor individualised management strategies for affected patients.

Background: Myocardial bridge (MB) is the most common inborn coronary artery variant, in which a portion of myocardium overlies a major epicardial coronary artery segment. Myocardial bridge has been for long considered a benign condition, although it has been shown to cause effort-related ischaemia. Case summary : We present the case of a 17-year-old female patient experiencing chest pain during physical activity. Since her symptoms became unbearable, electrocardiogram and echocardiography were performed together with a coronary computed tomography scan, revealing an MB on proximal-mid left anterior descending artery. In order to unequivocally unmask the ischaemic burden lent by MB, the patient underwent coronary angiography and physiological invasive test: instantaneous wave-free ratio (iFR) and fractional flow reserve (FFR) were calculated, both at baseline and after dobutamine infusion (5 µg/kg/min). At baseline, iFR value was borderline (= 0.89), whereas after dobutamine infusion and increase in the heart rate, the patient suffered chest pain. This symptom was associated with a decrease in the iFR value up to 0.77. Consistently, when FFR was performed, a value of 0.92 was observed at baseline, while after inotrope infusion the FFR reached the haemodynamic significance (= 0.79). Therefore, a medical treatment with bisoprolol was started. Discussion : Our clinical case shows the importance of a comprehensive non-invasive and invasive assessment of MB in young patients experiencing chest pain, with significant limitation in the daily life. The coronary functional indexes allow to detect the presence of MB-derived ischaemia, thus guiding the decision to undertake a medical/surgical therapy.

Cardiac devices have transformed the management of heart failure, ventricular arrhythmias, ischemic cardiomyopathy, and valvular heart disease. Technologies such as cardiac resynchronization therapy (CRT), conduction system pacing, left ventricular assist devices (LVADs), and implantable cardioverter-defibrillators have contributed to abated global cardiovascular risk through action onto pathophysiological processes such as mechanical unloading, electrical resynchronization, or hemodynamic optimization, respectively. While their clinical benefits are well established, their long-term molecular and structural effects on the myocardium remain under investigation. Cardiac devices dynamically interact with myocardial and vascular biology, inducing molecular and extracellular matrix adaptations that vary by pathology. CRT enhances calcium cycling and reduces fibrosis, but chronic pacing may lead to pacing-induced cardiomyopathy. LVADs and Impella relieve ventricular workload yet alter sarcomeric integrity and mitochondrial function. Transcatheter valve therapies influence ventricular remodeling, conduction, and coronary flow. Understanding these remodeling processes is crucial for optimizing patient selection, device programming, and therapeutic strategies. This narrative review integrates the current knowledge on the molecular and structural effects of cardiac devices, highlighting their impact across different disease settings.