Myocardial injury caused by COVID-19 was reported in hospitalized patients previously. But the information about cardiac consequences of COVID-19 after recovery is limited. The aim of the study was comprehensive echocardiography assessment of right ventricular (RV) in patients recovered from COVID-19. This is a prospective, single-center study. After recovery from COVID-19, echocardiography was performed in consecutive 79 patients that attended follow-up visits from July 15 to November 30, 2020. According to the recovery at home vs hospital, patients were divided into two groups: home recovery (n = 43) and hospital recovery (n = 36). Comparisons were made with age, sex and risk factor-matched control group (n = 41). In addition to conventional echocardiography parameters, RV global longitudinal strain (RV-GLS) and RV free wall strain (RV-FWS) were determined using 2D speckle-tracking echocardiography (2D STE). Of the 79 patients recovered from COVID-19, 43 (55%) recovered at home, while 36 (45%) required hospitalization. The median follow-up duration was 133  ±  35 (87–184) days. In patients recovered from hospital, RV-GLS and RV-FWS were impaired compared to control group (RV-GLS: −17.3  ±  6.8 vs. −20.4  ±  4.9, respectively [p = 0.042]; RV-FWS: −19.0  ±  8.2 vs. −23.4  ±  6.2, respectively [p = 0.022]). In subgroup analysis, RV-FWS was impaired in patients severe pneumonia (n = 11) compared to mild-moderate pneumonia (n = 28), without pneumonia (n = 40) and control groups (−15.8  ±  7.6 vs. −21.6  ±  7.6 vs. −20.8  ±  7.7 vs. −23.4  ±  6.2, respectively, [p = 0.001 for each]) and RV-GLS was impaired compared to control group (−15.2  ±  6.9 vs. −20.4  ±  4; respectively, [p = 0.013]). A significant correlation was detected between serum CRP level at hospital admission and both RV-GLS and RV-FWS (r = 0.285, p = 0.006; r = 0.294, p = 0.004, respectively). Age (OR 0.948, p = 0.010), male gender (OR 0.289, p = 0.009), pneumonia on CT (OR 0.019, p = 0.004), and need of steroid in treatment (OR 17.424, p = 0.038) were identifed as independent predictors of impaired RV-FWS (> −18) via multivariate analysis. We demonstrated subclinic dysfunction of RV by 2D-STE in hospitalized patients in relation to the severity of pneumonia after recovery from COVID-19. 2D-STE supplies additional information above standard measures of RV in this cohort and can be used in the follow-up of these patients.

Background : The novel coronavirus infection (COVID-19) disease has spread rapidly and posed a great threat to global public health. The laboratory parameters and clinical outcomes of the disease in discharged patients remain unknown. In this study, we aimed to investigate the laboratory and echocardiographic findings of patients with COVID-19 after discharge and the relation between left ventricular global longitudinal strain (LVGLS) and inflammatory parameters in discharged patients. Methods : A total of 75 patients recovering from COVID-19 as the study group were prospectively recruited from the COVID-19 outpatient clinic for their follow-up visits at a median 6 months after discharge. Patients were classified into groups according to pneumonia severity and impairment in LVGLS. Laboratory findings of patients both at admission and after discharge were evaluated and the relation with pneumonia severity at admission and LVGLS after discharge were analyzed. Results : Serum ferritin, lactate dehydrogenase (LDH) and prohormone B-type natriuretic peptide (pro-BNP) levels after discharge were significantly higher in the study group than the control group ( n = 44). Ferritin was found to be related to pneumonia severity. Serum ferritin and LDH values after discharge were significantly higher in patients with impaired LVGLS than those with preserved. There was a significant correlation between LVGLS, serum ferritin and LDH values after discharge (r = −0.252, p = 0.012; r = −0.268, p = 0.005, respectively). Conclusions : Clinicians should pay close attention to the serum ferritin and LDH levels in discharged patients for predicting the severity of COVID-19 disease and early identification of subclinical left ventricular myocardial dysfunction.

Introduction Vitamin D (VD) deficiency is a common disease that occurs in all stages of life. A growing number of studies call attention to the relationship between VD deficiency and cardiovascular disease. The aim of this study was to investigate the effect of VD on subclinical left ventricular (LV) function in diabetic and non-diabetic patients with no significant coronary artery disease. Material and methods We recruited 140 patients (80 diabetics and 60 non-diabetics) with symptoms of stable ischemic heart disease who underwent coronary angiography and who had no significant coronary artery disease in our clinic. The 25(OH)D 3 levels were measured and patients who had 25-(OH)D 3 levels below 20 ng/dl were defined as the VD deficient group. In addition to conventional echocardiographic parameters, tissue Doppler echocardiography was used for LV diastolic functions and 2D speckle tracking strain echocardiography (2D STE) for evaluating the longitudinal deformation indices of the LV myocardium. Results In all groups, LV global longitudinal strain (GLS) was significantly impaired in patients with VD deficiency ( p < 0.001) compared to patients without VD deficiency. LV global longitudinal strain rate (GLSR) was significantly impaired in patients with VD deficiency ( p = 0.003). The GLS was negatively associated with 25-(OH)D 3 in the VD deficiency group ( r = –0.52623, p < 0.001). Conversely, GLS was positively associated with 25-(OH)D 3 levels in the normal VD group ( r = 0.28, p = 0.048). Conclusions VD deficiency is associated with impaired myocardial GLS. The present study demonstrated that VD deficiency may be the cause of subclinical myocardial dysfunction in patients with or without diabetes mellitus and no history of significant coronary artery disease.

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Mutations in LTBP3 are associated with Dental Anomalies and Short Stature syndrome (DASS; MIM 601216), which is characterized by hypoplastic type amelogenesis imperfecta, hypodontia, underdeveloped maxilla, short stature, brachyolmia, aneurysm and dissection of the thoracic aorta. Here we report a novel (p.Arg545ProfsTer22) and a recurrent (c.3107‐2A > G) LTBP3 variants, in a Turkish family affected with DASS. The proband, who carried compound heterozygous variant c.3107‐2A > G, p.Arg545ProfsTer22, was most severely affected with DASS. The proband's father, who carried the heterozygous variant c.3107‐2A > G had short stature and prognathic mandible. The mother and brother of the proband carried the heterozygous variant p.Arg545ProfsTer22, but only the mother showed any DASS characteristics. The c.3107‐2A > G and the p.Arg545ProfsTer22 variants are expected to result in abnormal LTPB3 protein, failure of TGFβ‐LAP‐LTBP3 complex formation, and subsequent disruption of TGFβ secretion and activation. This is the first report of heterozygous carriers of LTBP3 variants showing phenotypes. The new findings of DASS found in this family include taurodontism, single‐rooted molars, abnormal dentin, calcified dental pulp blood vessels, prognathic mandible, failure of mandibular tooth eruption, interatrial septal aneurysm, secundum atrial septal defect, tricuspid valve prolapse, and a recurrent glenohumeral joint dislocation.