Tissue Doppler Imaging and Troponin I evaluation proved useful tools to detect early affection of the left ventricle in obese patients even in the absence of left ventricular hypertrophy.

Early heart iron overload in beta thalassemia major patients can be quantified through T2* cardiovascular magnetic resonance (CMR). To clarify the value of tissue Doppler imaging (TDI) in early detection of myocardial dysfunction in iron loaded thalassemia patients diagnosed by CMR. Two groups were included in the study; Group I: 69 asymptomatic thalassemia patients (28 females, 41 males), mean age 18.1 ± 7.03 years (range 6-39 years); Group II (n = 41) healthy normal controls matched for age and sex. Serum ferritin and CMR were performed to assess the cardiac siderosis (T2* < 20 ms). Group I was subdivided into two subgroups; Group Ia (n = 26) T2* < 20 ms and Group Ib (n = 43) T2* > 20 ms. Conventional and Doppler echocardiography of LV, RV dimensions and functions and pulmonary artery pressure were evaluated. Right ventricular diastolic function assessed by tricuspid annular E'/A' was positively correlated with T2* value; lower tricuspid E'/A' ratios were correlated with lower T2* values (r = 0.366, P = 0.002). Tricuspid annular A' was significantly higher in group Ia compared to group Ib (16.7 ± 5.2 vs 12.1 ± 4.0 cm/s, P < 0.001). Tricuspid E'/A' < 1 was common in group Ia compared to group Ib (19/26 (73.0) vs 3/43 (6.97%), P < 0.001). By multivariate analysis, right ventricular diastolic dysfunction (tricuspid E'/A' < 1) was associated with serum ferritin and T2* level of the thalassemia patients. TDI is a promising tool for quantitative assessment of myocardial function and early detection of right ventricular diastolic dysfunction in iron loaded beta thalassemia major patients.

Severe angio-obliterative PAH remains a disease characterized by great morbidity and shortened survival. Unfortunately, the only currently available treatments for angio-obliterative changes are palliative in the form of pulmonary vasodilators evolving from the phosphodiesterase inhibitor sildenafil to endothelin receptor antagonist: Bosentan; while the only definitive treatment is lung transplantation which remains dependent on the availability of donors and the transplant policies which vary widely from a country to another. PPARs, especially the γ isoform, are largely expressed in pulmonary artery endothelial cells and smooth muscle cells. They are also found on endothelial progenitor cells. Several previous studies have highlighted the role of PPAR γ agonists in reversal of vascular remodeling especially in coronary, carotid and peripheral vascular disease atherosclerotic plaques. Experimental studies have also revealed that PPAR γ activation affects many different pathways; thus, the effect of PPAR γ is multifaceted, affecting almost every pathobiological pathway involved in the development of PAH simultaneously. We thereby hypothesize that PPAR γ agonists may play a key role in reversing severe pulmonary angio-obliterative changes and promote microvascular regeneration which may substitute the need for heart-lung transplantation in such patients.

Background Turner syndrome (TS) patients have increased cardiovascular risk. This cardiovascular risk is famously attributed to structural abnormalities of the left side of the heart such as aortic stenosis and aortic coarctation. However, due to insulin resistance and subsequent pathogenic mechanisms, normotensive TS patients without structural abnormalities may develop varying degrees of myocardial dysfunction. The aim of this research was to examine the role of speckle tracking echocardiography in early detection of Turner cardiomyopathy and to correlate this myocardial dysfunction with measures of insulin resistance. Methods This cross-sectional case control study included 30 children with TS and 30 age-matched healthy controls. TS patients were excluded if: hypertensive, with major structural abnormalities of the heart or other systemic diseases that may affect myocardial function. Conventional speckle tracking echocardiography and glucose-insulin ratio were performed for all study subjects. Results Routine echocardiographic parameters of left ventricular systolic function were similar in cases and controls while global longitudinal and circumferential strain (GLS and GCS) were lower in patients with TS than controls: (−13.2±1.1 vs. −18.3±2.4, p-value<0.000) and (−11.3±1.1 vs. −16.3±2.1, p-value<0.000), respectively. Fasting glucose:insulin ratio (FGIR) proved to be the best predictor of myocardial dysfunction in TS patients by multivariate analysis. Conclusions This study points towards the potential role of two-dimensional (2D) speckle tracking echocardiography in early detection of subtle systolic myocardial dysfunction in TS patients. It also points towards the implication of insulin resistance in precipitation of the observed dysfunction in TS patients.

BackgroundHemodynamically significant (HS) patent ductus arteriosus (PDA) is a significant cause of mortality in preterm neonates. Early detection of HS PDA and pre-symptomatic closure may help in avoiding complications. For this to happen, easily performed predictors must be available; the aim of this paper is to test the reliability and repeatability of tissue Doppler-derived parameters for prediction of HS PDA.MethodsPreterm neonates <32 weeks were screened with echocardiography at Day 3 of life; 80 neonates with PDA were classified into HS group and hemodynamically insignificant (HIS) group based on benchmark parameter namely left ventricular outflow to superior vena caval flow ratio (LVO/SVC), and a ratio ≥4 was considered predictive of HS PDA. Tissue Doppler-derived left ventricular myocardial systolic and diastolic velocities were also performed.ResultsIn total, 105 neonates (55 among HS and 60 among HIS groups) were included in the study. Septal systolic velocity (S′) proved of high sensitivity (100%) in the prediction of HS PDA; nevertheless, it proved to be more repeatable than the initially discriminating parameter (LVO/SVC) with a Kappa of 0.92.ConclusionThis study concludes that septal S′ can be reliably used even by neonatologists for pre-symptomatic detection of HS PDA. This may also indicate the need of adding tissue Doppler parameters to the standard protocol of targeted neonatal echocardiography.

Background Several reports of unheeded complications secondary to the current mass international rollout of SARS-COV-2 vaccines, one of which is myocarditis occurring with the FDA fully approved vaccine, Pfizer, and others. Main body of the abstract Certain miRNAs (non-coding RNA sequences) are involved in the pathogenesis in viral myocarditis, and those miRNAs are interestingly upregulated in severe COVID-19. We hypothesize that the use of mRNA-based vaccines may be triggering the release of host miRNAs or that trigger the occurrence of myocarditis. This is based on the finding of altered host miRNA expression promoting virus-induced myocarditis. Short conclusion In conclusion, miRNAs are likely implicated in myocarditis associated with mRNA vaccines. Our hypothesis suggests the use of miRNA as a biomarker for the diagnosis of mRNA vaccine-induced myocarditis. Additionally, the interplay between viral miRNA and the host immune system could alter inflammatory profiles, hence suggesting the use of therapeutic inhibition to prevent such complications.

The relationship between myocardial iron load and eccentric myocardial remodeling remains an under-investigated area; it was thought that remodeling is rather linked to fibrosis. This study aims to determine whether or not measures of remodeling can be used as predictors of myocardial iron. For this purpose, 60 patients with thalassemia were studied with 3D echocardiography and myocardial relaxometry (T2*) by Cardiac MRI. 3D derived sphericity index was significantly higher in patients with myocardial iron load. It was correlated with T2* with a 100% sensitivity and specificity (cut-off value of 0.34) to discriminate between patients with and without myocardial iron overload.

Background: Fontan procedure is the final stage of a three-stage palliation process in patients born with a univentricular heart as part of Hypoplastic Left Heart Syndrome (HLHS) or other types of Univentricular Heart. As essential as this procedure has proven to be for such cases, the Fontan physiology diminishes the cardiac output and expands systemic venous pressure which leads to venous congestion that can be complicated by Protein Losing Enteropathy (PLE). The aim of this retrospective research was to study the predictors of such complications in all patients who underwent completion of Fontan in our center in the past eight years. It involved the examination of medical records of patients who underwent completion of Fontan repair in our center since the inauguration of its cardiac surgery program. Exclusion criteria included the absence of any of the required predictors in a medical report. Included patients were divided into two groups: those who developed PLE and those who did not. For each group, the following data were collected: The degree of AV valve regurge, the ventricular functions, the invasive SVC, and pulmonary pressures before Fontan completion and the original cardiac diagnosis. Results: 48 patients were included: only 13 developed PLE, accounting for 25% of the total patients. A multivariate regression analysis of the best predictors of the occurrence of PLE was the degree of AV valve regurge (P = 0.008), SVC mean pressure (P value = 0.01), and Ventricular functions (P value = 0.02). A ROC analysis was performed for each of the best predictors and showed that SVC pressure > 11 was 100% sensitive, moderate and severe regurge were 69% sensitive, and moderate to severe impairment of ventricular functions was 53% sensitive in predicting subsequent PLE. Conclusion: The unleashed findings might be game-changing in the decision-making of whether to complete the Fontan pathway or not in our growing cardiac surgery center, which is one of the largest in its respective region. The presence of moderate to severe AV valve regurge, moderate to severe ventricular dysfunction, and a Superior Vena caval pressure above 11 before Fontan completion should be regarded as contraindications to completion of the procedure.