Article: The influence of pectus excavatum on biventricular mechanics: a systematic review and meta-analysis - Minerva Cardiology and Angiology 2024 Sep 24 - Minerva Medica - Journals

The pathological remodeling of myocardial tissue is the main cause of heart diseases. Several processes are involved in the onset of heart failure, and the comprehension of the mechanisms underlying the pathological phenotype deserves special attention to find novel procedures to identify the site of injury and develop novel strategies, as well as molecular druggable pathways, to counteract the high degree of morbidity associated with it. Myocardial fibrosis (MF) is recognized as a critical trigger for disruption of heart functionality due to the excessive accumulation of extracellular matrix proteins, in response to an injury. Its diagnosis remains focalized on invasive techniques, such as endomyocardial biopsy (EMB), or may be noninvasively detected by cardiac magnetic resonance imaging (CMRI). The detection of MF by non-canonical markers remains a challenge in clinical practice. During the last two decades, two-dimensional (2D) speckle tracking echocardiography (STE) has emerged as a new non-invasive imaging modality, able to detect myocardial tissue abnormalities without specifying the causes of the underlying histopathological changes. In this review, we highlighted the clinical utility of 2D-STE deformation imaging for tissue characterization, and its main technical limitations and criticisms. Moreover, we focalized on the importance of coupling 2D-STE examination with the molecular approaches in the clinical decision-making processes, in particular when the 2D-STE does not reflect myocardial dysfunction directly. We also attempted to examine the roles of epigenetic markers of MF and hypothesized microRNA-based mechanisms aiming to understand how they match with the clinical utility of echocardiographic deformation imaging for tissue characterization and MF assessment.

Pulsed wave tissue Doppler imaging (PW-TDI) easily detects motion of cardiac structures. Hence, PW-TDI could be of value for assessing potentially cardioembolic masses. We sought to evaluate the prognostic value of left ventricular (LV) thrombus mobility assessed by PW-TDI. In 83 consecutive patients with echocardiographically detected LV thrombi, PW-TDI echocardiographic study was performed. At 1-year follow-up, the composite of major adverse cardiovascular events (MACE) defined as all-cause mortality plus hospitalizations for stroke/systemic embolism was evaluated. Seventy-two patients (77.1 ± 13.1 year/old, 32 males) were studied. All thrombi were located at the LV apex. At 1-year follow-up, 17 cardioembolic events occurred. By univariable Cox analysis, variables associated with MACE were heart rate (hazard ratio: 1.02, 95% CI: 1.00-1.05; P = .03), thrombi with mobile free edge (hazard ratio: 3.25, 95% CI: 1.25-8.44; P = .01), hypoechoic thrombi (hazard ratio: 2.86, 95% CI: 1.10-7.42; P = .03), and mass peak antegrade velocity (Va) ≥10 cm/s (hazard ratio: 8.79, 95% CI: 2.00-38.5; P = .004). By multivariable analysis, thrombi with mobile free edge (hazard ratio: 3.54, 95% CI: 1.23-10.2; P = .02), and mass peak Va ≥10 cm/s (hazard ratio: 7.97, 95% CI: 1.60-39.6; P = .01) retained statistical significance. Mass peak Va ≥10 cm/s predicted the composite end point with 94% sensitivity and 85% specificity (area under the curve = 0.86). In conclusion, PW-TDI allows objective prognostication of LV thrombi embolic risk.