Non-Invasive Modalities in the Assessment of Vulnerable Coronary Atherosclerotic Plaques.

Coronary atherosclerosis is a complex, multistep process that may lead to critical complications upon progression, revolving around plaque disruption through either rupture or erosion. Several high-risk features are associated with plaque vulnerability and may add incremental prognostic information. Although invasive imaging modalities such as optical coherence tomography or intravascular ultrasound are considered to be the gold standard in the assessment of vulnerable coronary atherosclerotic plaques (VCAPs), contemporary evidence suggests a potential role for non-invasive methods in this context. Biomarkers associated with deleterious pathophysiologic pathways, including inflammation and extracellular matrix degradation, have been correlated with VCAP characteristics and adverse prognosis. However, coronary computed tomography (CT) angiography has been the most extensively investigated technique, significantly correlating with invasive method-derived VCAP features. The estimation of perivascular fat attenuation as well as radiomic-based approaches represent additional concepts that may add incremental information. Cardiac magnetic resonance imaging (MRI) has also been evaluated in clinical studies, with promising results through the various image sequences that have been tested. As far as nuclear cardiology is concerned, the implementation of positron emission tomography in the VCAP assessment currently faces several limitations with the myocardial uptake of the radiotracer in cases of fluorodeoxyglucose use, as well as with motion correction. Moreover, the search for the ideal radiotracer and the most adequate combination (CT or MRI) is still ongoing. With a look to the future, the possible combination of imaging and circulating inflammatory and extracellular matrix degradation biomarkers in diagnostic and prognostic algorithms may represent the essential next step for the assessment of high-risk individuals.

Eosinophilic heart disease: diagnostic and prognostic assessment by cardiac magnetic resonance.

AIMS: Eosinophilic heart disease (EHD) is a rare cardiac condition with a wide spectrum of phenotypes. The diagnostic and prognostic value of cardiac magnetic resonance (CMR) in EHD remains unknown. METHODS AND RESULTS: This was a retrospective analysis of 250 patients with eosinophilia referred for a CMR scan (period 2000-2020). CMR data sets and clinical/laboratory data were collected. Patients were followed up for a mean of 24 months (range 1-224) for the composite endpoint of death, acute coronary syndrome, hospitalization for acute heart failure, malignant ventricular arrhythmias, or the need for implantable cardiac defibrillator/pacemaker. The main objectives were to explore the diagnostic value of CMR in EHD; relationships between cardiac function, late gadolinium enhancement (LGE), and EHD phenotypes; and the prognostic value of fibrosis and oedema by CMR. The prevalence of findings compatible with EHD was 39% (patients with cardiac symptoms: 57% vs. screening: 20%, P < 0.001). EHD phenotypes included subendocardial LGE (n = 58), mid-wall/subepicardial LGE (n = 26), pericarditis (n = 5) or dilated cardiomyopathy (n = 8). Myocardial oedema was present in 10% of patients. Intracardiac thrombi (7%) were associated with EHD phenotype (χ2=47.3, P = 1.3×10-8). LGE extent correlated with LVEDVi (rho = 0.268, P = 5.3×10-5) and LVEF (rho=-0.415, P = 8.6×10-11). A CMR scan positive for EHD [hazard ratio (HR) = 5.61, 95% confidence interval (CI): 1.82-17.89, P = 0.0026] or a subendocardial LGE pattern (HR = 5.13, 95% CI: 1.29-20.38, P = 0.020) were independently associated with the composite clinical endpoint. CONCLUSION: The diagnostic yield of CMR screening in patients with persistent eosinophilia, even if asymptomatic, is high. The extent of subendocardial fibrosis correlates with LV remodelling and independently predicts clinical outcomes in patients with eosinophilia.

Atrial Fibrillation: Pathogenesis, Predisposing Factors, and Genetics.

Atrial fibrillation (AF) is the most frequent arrhythmia managed in clinical practice, and it is linked to an increased risk of death, stroke, and peripheral embolism. The Global Burden of Disease shows that the estimated prevalence of AF is up to 33.5 million patients. So far, successful therapeutic techniques have been implemented, with a high health-care cost burden. As a result, identifying modifiable risk factors for AF and suitable preventive measures may play a significant role in enhancing community health and lowering health-care system expenditures. Several mechanisms, including electrical and structural remodeling of atrial tissue, have been proposed to contribute to the development of AF. This review article discusses the predisposing factors in AF including the different pathogenic mechanisms, sedentary lifestyle, and dietary habits, as well as the potential genetic burden.