Misael Estepa

Aims The number of patients with cardiac implantable electronic devices (CIEDs) is increasing. However, there is limited experience regarding vasodilator-stress cardiovascular magnetic resonance (CMR) and resulting device artifacts on perfusion images. The aim of this study was to determine CMR image quality in patients with different CIED types for CMR-based perfusion stress testing. Methods and results A total of 156 patients with active CIEDs underwent CMR on a 1.5-Tesla scanner. Both conventional steady-state-free-precession (SSFP) and modified spoiled gradient-echo (sGE) protocols under stress and resting conditions were used to evaluate image artifacts in a 16-segment segment model of the heart. The study group comprised 39% conventional pacemaker (PM), 4% cardiac resynchronization therapy-pacemaker (CRT-P), 38% conventional implantable cardioverter-defibrillator (ICD), 6% cardiac resynchronization therapy-ICD (CRT-D), and 13% subcutaneous ICD (S-ICD) patients. PM-carriers showed only minor image artifacts in both perfusion protocols. Artifacts caused by ICDs were predominantly located in the left-ventricular (LV) inferolateral and anterior segments. S-ICDs showed the highest extent of artifacts with an anterolateral accentuation. The artifact extent was significantly reduced when sGE-based perfusion was used compared to SSFP-based sequences. 69% of the patients received a stress-perfusion protocol, and elective coronary angiography confirmed the presence of coronary stenosis in three cases. No major safety-relevant issues occurred. Conclusion Myocardial perfusion imaging by CMR is safe and feasible with moderate-to-high image quality in patients with all types of CIEDs, including non-conditional devices, ICDs, and S-ICDs. A sGE-based perfusion protocol should be preferred in patients with left-sided ICDs, CRT-Ds, or S-ICDs. Graphical abstract Central illustration: Artefact extent in CMR first-pass perfusion imaging in different CIED patients. PM pacemaker, ICD implantable cardioverter defibrillator, S-ICD subcutaneous ICD. The color scale reflects the mean artifact extent in percentage; dark blue = high artifact extent, light blue = low artifact extent

Background: While left-bundle-branch-block-related contraction patterns as well as echocardiography-derived strain are variably associated with the volumetric response to cardiac resynchronization therapy (CRT), the role of CMR-derived strain parameters is unexplored. Methods: A total of 50 patients receiving CRT implantation were retrospectively analyzed, all of whom had undergone CMR imaging within one year before, and echocardiography within 6 months before and 6–12 months after CRT implantation. We assessed CMR-derived morphological and functional parameters with regard to the echocardiographic response, defined as a reduction in the left ventricular end-systolic volume of ≥15%. Results: Among the standard CMR parameters, the indexed right ventricular volumes in end-diastole (RVEDVi) (74.5 ± 19.5 vs. 94.8 ± 30.2 mL/m², p = 0.006) and end-systole (RVESVi) (43.2 ± 13.3 vs. 61.6 ± 28.8 mL/m², p = 0.003), as well as the left atrial (LA) area (24.8 ± 3.5 vs. 30.4 ± 9.5 cm², p = 0.020), differed significantly between CRT responders and non-responders. In strain analysis, CRT responders showed a significantly better LA global longitudinal strain (GLS) (25.1 ± 10.4 vs. 15.3 ± 10.5, p = 0.002), LA global circumferential strain (GCS) (27.9 ± 14.7 vs. 17.1 ± 13.1%, p = 0.012), RV GLS (−25.0 ± 6.5 vs. −18.9 ± 7.6%, p = 0.004) and RV free wall strain (−31.1 ± 7.9 vs. −24.9 ± 9.5, p = 0.017). Conclusions: CMR-derived peak septal circumferential strain and RVEDVi correlated with the echocardiographic volumetric response to CRT at 6–12 months.

Background: While left-bundle-branch-block-related contraction patterns as well as echocardiography derived strain are variably associated with volumetric response to cardiac resynchronization therapy (CRT), the role of CMR-derived strain parameters is unexplored. Methods: 50 patients receiving CRT implantation were retrospectively analysed, all of which had undergone CMR imaging within one year before, and echocardiography within 6 months before and 6-12 months after CRT implantation. We assessed CMR-derived morphological and functional parameters with regard to echocardiographic response, defined as reduction of left ventricular end-systolic volume ≥15%. Results: Among standard CMR parameters, indexed right ventricular volumes in end-diastole (RVEDVi) (74.5 ±19.5 vs. 94.8 ±30.2 ml/m², P=.006) and end-systole (RVESVi) (43.2 ±13.3 vs. 61.6 ±28.8 ml/m², P=.003) as well as left atrial (LA) area (24.8 ±3.5 vs. 30.4 ±9.5 cm², P=.020) differed significantly between CRT responders and non-responders. In strain analysis, CRT responders showed significantly better LA global longitudinal strain (GLS) (25.1 ±10.4 vs. 15.3 ±10.5, P=.002), LA global circumferential strain (GCS) (27.9 ±14.7 vs. 17.1 ±13.1%, P=.012), RV GLS (-25.0 ±6.5 vs. -18.9 ±7.6%, P=.004) and RV free wall strain (-31.1 ±7.9 vs. -24.9 ±9.5, P=.017). Conclusions: CMR-derived peak septal circumferential strain and RVEDVi correlated with echocardiographic volumetric response to CRT at 6-12 months.

Myocarditis is an inflammatory disease that may lead to dilated cardiomyopathy. Viral infection of the myocardium triggers immune responses, which involve, among others, macrophage infiltration, oxidative stress, expression of pro-inflammatory cytokines, and microRNAs (miRNAs). The cardioprotective role of estrogen in myocarditis is well documented; however, sex differences in the miRNA expression in chronic myocarditis are still poorly understood, and studying them further was the aim of the present study. Male and female ABY/SnJ mice were infected with CVB3. Twenty-eight days later, cardiac tissue from both infected and control mice was used for real-time PCR and Western blot analysis. NFκB, IL-6, iNOS, TNF-α, IL-1β, MCP-1, c-fos, and osteopontin (OPN) were used to examine the inflammatory state in the heart. Furthermore, the expression of several inflammation- and remodeling-related miRNAs was analyzed. NFκB, IL-6, TNF-α, IL-1β, iNOS, and MCP-1 were significantly upregulated in male mice with CVB3-induced chronic myocarditis, whereas OPN mRNA expression was increased only in females. Further analysis revealed downregulation of some anti-inflammatory miRNA in male hearts (let7a), with upregulation in female hearts (let7b). In addition, dysregulation of remodeling-related miRNAs (miR27b and mir199a) in a sex-dependent manner was observed. Taken together, the results of the present study suggest a sex-specific expression of pro-inflammatory markers as well as inflammation- and remodeling-related miRNAs, with a higher pro-inflammatory response in male CVB3 myocarditis mice.