BACKGROUND:Asthma-related cardiopulmonary interactions may affect right ventricular (RV) performance even when children are clinically stable. Two-dimensional speckle-tracking echocardiography (2D-STE) may detect subclinical myocardial dysfunction beyond conventional indices. This study aims to investigate the effects of childhood asthma on RV function by using 2D-STE. METHODS:In this prospective case-control study, children aged 6-18 years with physician-diagnosed asthma (n = 70) and age-matched healthy controls (n = 30) underwent standard transthoracic echocardiography, tissue Doppler imaging (TDI), and 2D-STE. Primary outcomes were RV global longitudinal strain (RV GLS) and strain rate. Conventional RV systolic indices and RV diastolic indices were also assessed. Clinical characteristics and spirometry were recorded. RESULTS:RV systolic mechanics were largely preserved in the asthma group. RV GLS, RV strain rate, and tricuspid annular plane systolic excursion (TAPSE) did not differ significantly between asthmatic children and controls. In contrast, tricuspid annular E' velocity was significantly lower in the asthma group (p = 0.007), and tricuspid E/E' ratio was significantly higher (p < 0.001). Interventricular septal diastolic thickness was also significantly increased among children with asthma (p = 0.027). Within the asthma cohort, TAPSE showed positive correlations with age (r = 0.478, p < 0.001), BMI (r = 0.398, p = 0.001), asthma duration (r = 0.431, p < 0.001), and FEV1 (r = 0.301, p = 0.011), whereas RV strain parameters were not significantly associated with demographic or respiratory variables. CONCLUSIONS:In predominantly mild-to-moderate, clinically stable pediatric asthma, RV systolic deformation by 2D-STE appears preserved, while TDI-derived indices indicate early RV diastolic involvement. Focused assessment of RV diastolic function may help to identify subclinical cardiopulmonary effects in selected children with asthma.

BackgroundThe coronavirus disease 2019 (COVID-19) has had a great impact on patients’ physical problems as well as psychological status. However, there is limited data about the impact of psychological problems on cardiac function during the COVID-19 pandemic. In this study, we aimed to investigate the relationship between mental health disorders and subclinical early myocardial systolic dysfunction by left ventricular global longitudinal strain (LVGLS) imaging in patients recovered from COVID-19.MethodsOf the 108 participants, 71 patients had recovered from COVID-19; the members of the study group were prospectively recruited to the study after COVID-19 recovery. Comparisons were made with a risk-factor matched control group (n=37). The psychological status of the subjects, namely, Depression, Anxiety and Stress Scale-21 (DASS-21), and the Impact of Events Scale (IES-R) at follow-up visits, were assessed via questionnaire forms. The relationship between the psychological parameters and LVGLS values was subsequently evaluated.ResultsOverall, 45.0% of patients with COVID-19 had some degree of anxiety after recovery. A significant negative correlation was found between LVGLS and DASS-21 total score, DASS-21 anxiety subscale score, IES-R total score, and IES-R intrusion subscale score (r= -0.251, p=0.02; r= -0.285, p=0.008; r= -0.291, p=0.007; and r= -0.367, p=0.001, respectively). Furthermore, the DASS-21 total score was identified as an independent predictor of LVGLS (β= -0.186, p=0.03).ConclusionsPatients who suffered from the COVID-19 disease may have experienced psychological distress symptoms due to COVID-19, which may be associated with silent impairment in myocardial systolic functions measured by global longitudinal strain analysis.

BACKGROUND:There is an ongoing debate on the extension of reperfusion-related microvascular damage (MVD) throughout the remote noninfarcted myocardial regions in patients with ST-elevation myocardial infarction (STEMI) that undergo primary percutaneous intervention (pPCI). The aim of this study was to elucidate the impact of reperfusion on remote microcirculatory territory by analyzing hemodynamic alterations in the nonculprit-vessel in relation to reperfusion. METHODS:A total of 20 patients with STEMI undergoing pPCI were included. Peri-reperfusion temporal changes in hemodynamic parameters were obtained in angiographically normal nonculprit vessels before and 1-h after reopening of the culprit vessel. Intracoronary pressure and flow velocity data were compared using pairwise analyses (before and 1-h after reperfusion). RESULTS:In the non-culprit vessel, compared to the pre-reperfusion state, mean resting average peak velocity (33.4 ± 9.4 to 25.0 ± 4.9 cm/s, P < 0.001) and mean hyperemic average peak velocity (53.5 ± 14.4 to 42.1 ± 10.66 cm/s, P = 0.001) significantly decreased; whereas baseline (3.2 ± 1.0 to 4.0 ± 1.0 mmHg.cm-1.s, P < 0.001) and hyperemic microvascular resistance (HMR) (1.9 ± 0.6 to 2.4 ± 0.7 mmHg.cm-1.s, P < 0.001) and mean zero flow pressure (Pzf) values (32.5 ± 6.9 to 37.6 ± 8.3 mmHg, P = 0.003) significantly increased 1-h after reperfusion. In particular, the magnitude of changes in HMR and Pzf values following reperfusion were more prominent in patients with larger infarct size and with higher extent of MVD in the culprit vessel territory. CONCLUSION:Reperfusion-related microvascular injury extends to involve remote myocardial territory in relation to the magnitude of the adjacent infarction and infarct-zone MVD. (GUARD Clinical TrialsNCT02732080).

Amaç: Ateroskleroz sürecinde endotelyal hücrelerde enflamatuvar tepkimeleri aktive eden sinyal yolaklarını uyaran okside LDL, kardiyovasküler hastalıkların gelişiminde önemli bir patojenik faktör olarak tanımlanmaktadır. Endotel hücrelerinde okside LDL için başlıca reseptör olan okside LDL reseptörü (LOX-1), okside LDL’leri endotel hücrelerinde özgül olarak bağlayabilme, hücre içine alabilme ve degrade edebilme özelliğine sahiptir. Bu çalışmada LOX-1’i kodlayan OLR1 geninde 3’UTR188C>T polimorfizminin koroner arter hastaları ve sağlıklı kontrollerden oluşan çalışma gruplarında serum okside LDL ve lipid düzeylerine etkisinin araştırılarak KAH hastalarında lipid parametrelerle ilişkisinin belirlenmesi amaçlanmıştır. Yöntem: Çalışmaya katılan 50 KAH hastası ve 34 sağlıklı kontrolden oluşan gruplarda OLR1 geni 3’UTR188C>T polimorfizminin tespiti için Polimeraz Zincir Reaksiyonu ve Restriksiyon Fragman Uzunluk Polimorfizmi yöntemleri kullanılmıştır. İstatistiksel analiz SPSS 20.0 ile yapılmıştır. Bulgular: KAH grubunda okside LDL (p<0,001), total-kolesterol (p=0,020), Beden Kütle İndeksi (BKİ) (p=0,015), sistolik (p<0,001) ve diastolik (p=0,002) kan basıncı değerleri ve sigara kullanım sıklığı (p=0,002) sağlıklı kontrollere kıyasla yüksek ve serum HDL-K düzeyi düşük gözlenmiştir (p<0,001). OLR1 3’UTR188C>T genotip ve allel dağılımları gruplar arasında benzer bulunmuştur (p>0,05). 188T alleli hem KAH (p<0,001) hem de kontrol (p=0,013) gruplarında yüksek okside LDL düzeyleri ile ilişkili gözlenmiştir. 188TT genotipi taşıyan hastalarda okside LDL (p<0,001), total-kolesterol, LDL-kolesterol, trigliserid ve VLDL-kolesterol düzeyleri yüksekti. Benzer şekilde sağlıklı kontrollerde de 188TT genotipi yüksek okside LDL, total ve LDL-kolesterol, trigliserid, VLDL-kolesterol, sistolik kan basıncı ve düşük serum HDL-kolesterol düzeyi ile ilişkiliydi. Sonuç: Bulgular OLR1 3’UTR 188 C>T polimorfizminin hem proaterojenik bir molekül olan serum okside LDL hem de aterojenik lipid profili lehine etkileriyle KAH gelişimiyle ilişkili olabileceğine işaret etmektedir.

OBJECTIVE:Bicuspid aortic valve (BAV) is the most common congenital heart defect. Ascending aorta dilatation is related to BAV- and hypertension (HTN)-associated aortopathy. The aim of this study was to investigate aortic elasticity, as well as aortic deformation of the ascending aorta, using strain imaging, and to evaluate the possible relationship of biomarkers, such as endotrophin and matrix metalloproteinase-2 (MMP-2), with ascending aorta dilatation in patients with BAV- or HTN-associated aortopathy.PATIENTS AND METHODS:This prospective study included patients with ascending aorta dilatation with BAV (n = 33), or normal tricuspid aortic valve with HTN (n = 33), and 20 control subjects. The mean age of the total patients was 42.76 ± 10.4 years (67% male, 33% female). We calculated aortic elasticity parameters using the relevant formula by M-mode echocardiography and determined layer-specific longitudinal and transverse strains of the proximal aorta by speckle-tracking echocardiography. Blood samples of the participants were drawn for the analysis of endotrophin and MMP-2.RESULTS:Aortic strain and aortic distensibility were significantly decreased, whereas the aortic stiffness index was significantly increased in patient groups with BAV or HTN compared to the control group (p < 0.001). Moreover, longitudinal strain of both the anterior and posterior aortic walls of the proximal aorta were significantly impaired in BAV and HTN patients (p < 0.001). Serum endotrophin levels were significantly reduced in the patient cohort compared to the controls (p = 0.001). Endotrophin was noted to be significantly positively correlated with aortic strain and aortic distensibility (r = 0.37, p = 0.001; r = 0.45, p < 0.001, respectively), whereas inversely associated with aortic stiffness index (r = -0.402, p < 0.001). Furthermore, endotrophin was the single independent predictor of ascending aorta dilatation (OR = 0.986, p < 0.001). A cut-off value of endotrophin ≤ 82.38 ng/mL predicted ascending aorta dilatation with a sensitivity of 80.3% and specificity of 78.5% (p < 0.0001).CONCLUSIONS:The present study showed that aortic deformation parameters and elasticity are impaired in BAV and HTN patients, and strain imaging allows for a good analysis of ascending aorta deformation. Endotrophin could be a predictive biomarker of ascending aorta dilatation in BAV and HTN aortopathy.

Objective Mitral annular plane systolic excursion (MAPSE) is a simple way to evaluate-left ventricle (LV) function. Our aim was to explain the relationship of MAPSE with LV function and biochemical markers in patients with preserved ejection fraction (EF), and to determine whether it has an effect on prognosis in echocardiography (echo) practice. Methods Consecutive patients referred to the echo laboratory between November 2020 and March 2021 were included in the study. In addition to conventional parameters, MAPSE of the lateral mitral annulus was measured in all patients. Patients were divided into three groups according to lateral MAPSE: low (<12 mm), relatively preserved (12-15 mm), and high (>= 15 mm). Results A total of 512 patients with preserved EF were included in the study. MAPSE was low in 44 patients (9%), relatively preserved in 231 patients (45%), and high in 237 patients (46%). The mean age was higher in the low group compared to the other two groups (p < 0.001) and the body mass index was increased in the low group compared to the high group (p = 0.010). Atrial fibrillation and hypertension were more common in patients with low MAPSE. The rate of diastolic dysfunction (DD) and all-cause hospitalization were higher in the low and relatively preserved groups than in the high group (p < 0.001, p = 0.002; respectively). The pro-BNP level and mortality rate were higher in the low group compared to the relatively preserved and high groups (p = 0.007, p = 0.005; respectively). MAPSE was identified as independent predictor of hospitalization (OR: 0.284, 95% CI: 0.093-0.862, p = 0.026) via multivariate analysis and independent predictor of in-hospital mortality (HR: 0.002, 95% CI: 0-0.207, p = 0.008). Conclusions Analysis of LV longitudinal function by echo-derived lateral MAPSE when LV ejection fraction is normal provides important information about DD and related heart failure and may predict prognosis in echo practice.

Background Intramyocardial edema and hemorrhage are key pathological mechanisms in the development of reperfusion‐related microvascular damage in ST‐segment–elevation myocardial infarction. These processes may be facilitated by abrupt restoration of intracoronary pressure and flow triggered by primary percutaneous coronary intervention. We investigated whether pressure‐controlled reperfusion via gradual reopening of the infarct‐related artery may limit microvascular injury in patients undergoing primary percutaneous coronary intervention. Methods and Results A total of 83 patients with ST‐segment–elevation myocardial infarction were assessed for eligibility and 53 who did not meet inclusion criteria were excluded. The remaining 30 patients with totally occluded infarct‐related artery were randomized to the pressure‐controlled reperfusion with delayed stenting (PCRDS) group (n=15) or standard primary percutaneous coronary intervention with immediate stenting (IS) group (n=15) (intention‐to‐treat population). Data from 5 patients in each arm were unsuitable to be included in the final analysis. Finally, 20 patients undergoing primary percutaneous coronary intervention who were randomly assigned to either IS (n=10) or PCRDS (n=10) were included. In the PCRDS arm, a 1.5‐mm balloon was used to achieve initial reperfusion with thrombolysis in myocardial infarction grade 3 flow and, subsequently, to control distal intracoronary pressure over a 30‐minute monitoring period (MP) until stenting was performed. In both study groups, continuous assessment of coronary hemodynamics with intracoronary pressure and Doppler flow velocity was performed, with a final measurement of zero flow pressure (primary end point of the study) at the end of a 60‐minute MP. There were no complications associated with IS or PCRDS. PCRDS effectively led to lower distal intracoronary pressures than IS over 30 minutes after reperfusion (71.2±9.37 mm Hg versus 90.13±12.09 mm Hg, P=0.001). Significant differences were noted between study arms in the microcirculatory response over MP. Microvascular perfusion progressively deteriorated in the IS group and at the end of MP, and hyperemic microvascular resistance was significantly higher in the IS arm as compared with the PCDRS arm (2.83±0.56 mm Hg.s.cm−1 versus 1.83±0.53 mm Hg.s.cm−1, P=0.001). The primary end point (zero flow pressure) was significantly lower in the PCRDS group than in the IS group (41.46±17.85 mm Hg versus 76.87±21.34 mm Hg, P=0.001). In the whole study group (n=20), reperfusion pressures measured at predefined stages in the early reperfusion period showed robust associations with zero flow pressure values measured at the end of the 1‐hour MP (immediately after reperfusion: r=0.782, P<0.001; at the 10th minute: r=0.796, P<0.001; and at the 20th minute: r=0.702, P=0.001) and peak creatine kinase MB level (immediately after reperfusion: r=0.653, P=0.002; at the 10th minute: r=0.597, P=0.007; and at the 20th minute: r=0.538, P=0.017). Enzymatic myocardial infarction size was lower in the PCRDS group than in the IS group with peak troponin T (5395±2991 ng/mL versus 8874±1927 ng/mL, P=0.006) and creatine kinase MB (163.6±93.4 IU/L versus 542.2±227.4 IU/L, P<0.001). Conclusions In patients with ST‐segment–elevation myocardial infarction, pressure‐controlled reperfusion of the culprit vessel by means of gradual reopening of the occluded infarct‐related artery (PCRDS) led to better‐preserved coronary microvascular integrity and smaller myocardial infarction size, without an increase in procedural complications, compared with IS. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT02732080.

Objective: The aim of this cross-sectional, retrospective, descriptive study was to review and classify cardiac masses systematically and to determine their frequencies. Methods: The medical records of 64,862 consecutive patients were investigated within 12 years. Every patient with a cardiac mass imaged by transthoracic echocardiography (TTE) and confirmed with an advanced imaging modality such as transesophageal echocardiography (TEE), computed tomography (CT) and/or cardiac magnetic resonance imaging (CMR) was included. Acute coronary syndromes triggering thrombus formation, vegetations, intracardiac device and catheter related thrombi were excluded. Results: Data demonstrated 127 (0.195%) intracardiac masses consisting of 33 (0.050%) primary benign, 3 (0.004%) primary malignant, 20 (0.030%) secondary tumors, 3 (0.004%) hydatid cysts and 68 (0.104%) thrombi respectively. The majority of primary cardiac tumors were benign (91.67%), predominantly myxomas (78.79%), and the less malignant (8.33%). Secondary cardiac tumors were common than the primary malignant tumors (20:3), with male dominancy (55%), lymphoma and lung cancers were the most frequent. Intracardiac thrombi was the majority of the cardiac masses, thrombi accompanying malignancies were in the first range (n = 17, 25%), followed by autoimmune diseases (n = 13, 19.12%) and ischemic heart disease with low ejection fraction (n = 12, 17.65%). Conclusions: This retrospective analysis identified 127 patients with cardiac masses. The majority of benign tumors were myxoma, the most common tumors that metastasized to the heart were lymphoma and lung cancers, and the thrombi associated with malignancies and autoimmune diseases were the most frequent.

BACKGROUNDGalectin-3 has been shown to play a key pathophysiological role in pulmonary associated inflammatory response and lung fibrosis in COVID-19 and is a mediator for viral adhesion. However, there is limited data about its potential role in severity and prognosis of COVID-19. This study aimed to investigate the predictive role of serum galectin-3 concentrations in the severe clinical outcomes of hospitalized COVID-19 patients: the severity of pneumonia, in-hospital mortality, and the need for intensive care unit (ICU) admission.METHODSThis single-center study included 68 patients with laboratory- and radiologically-confirmed COVID-19 admitted to our emergency department. The study population was divided into patients with primary clinical out-comes (n = 32) and those without (n = 36). The need for ICU admission and/or in-hospital mortality were the primary clinical endpoints. The study group was also classified based on pneumonia severity: severe or mild/moderate. Blood samples were collected within 48 hours of admission to estimate serum galectin-3 concentrations.RESULTSMultivariate regression analysis showed that lower concentrations of galectin-3 and arterial oxygen saturation (SpO2) were independently associated with the primary clinical outcomes (OR = 0.951, p = 0.035; OR = 0.862, p = 0.017, respectively); increased concentrations of galectin-3 were an independent predictor of severe pneumonia (OR = 1.087, p = 0.016). In the receiver operating characteristics curve analysis, serum galectin-3 concentrations at hospital admission predicted pneumonia severity with 52.1% sensitivity and 90% specificity with a cutoff of 38.76 ng/mL.CONCLUSIONSCirculating galectin-3 at hospital admission could be a useful biomarker for identifying COVID-19 patients at high risk for severe pneumonia.

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.

OBJECTIVE:In this study, we aimed to compare the functional adaptations of the left ventricle in variant forms of left ventricular hypertrophy (LVH) and to evaluate the use of two-dimensional speckle tracking echocardiography (2D-STE) in differential diagnosis and prognosis.METHODS:This was a prospective cohort study of 68 patients with LVH, including 20 patients with non-obstructive hypertrophic cardiomyopathy (HCM), 23 competitive top-level athletes free of cardiovascular disease, and 25 patients with hypertensive heart disease (HHD). All the subjects underwent 2D transthoracic echocardiography (TTE) and 2D-STE. The primary endpoint was all-cause mortality. Global longitudinal strain (GLS) below -12.5% was defined as severely reduced strain, -12.5% to -17.9% as mildly reduced strain, and above -18% as normal strain.RESULTS:The mean LV-GLS value was higher in athletes than in patients with HCM and HHD with the lowest value being in the HCM group (HCM: -11.4±2.2%; HHD: -13.6±2.6%; and athletes: -15.5±2.1%; p<0.001 among groups). LV-GLS below -12.5% distinguished HCM from others with 65% sensitivity and 77% specificity [area under curve (AUC)=0.808, 95% confidence interval (CI): 0.699-0.917, p<0.001]. The median follow-up duration was 6.4±1.1 years. Overall, 11 patients (16%) died. Seven of these were in the HHD group, and four were in the HCM group. The mean GLS value in patients who died was -11.8±1.5%. LV-GLS was significantly associated with mortality after adjusting age and sex via multiple analysis (RR=0.723, 95% CI: 0.537-0.974, p=0.033). Patients with GLS below -12.5% had a higher risk of all-cause mortality compared with that of patients with GLS above -12.5% according to Kaplan-Meier survival analysis for 7 years (29% vs. 9%; p=0.032). The LV-GLS value predicts mortality with 64% sensitivity and 70% specificity with a cut-off value of -12.5 (AUC=0.740, 95% CI: 0.617-0.863, p=0.012).CONCLUSION:The 2D-STE provides important information about the longitudinal systolic function of the myocardium. It may enable differentiation variable forms of LVH and predict prognosis.

Mitral regurgitation may develop due to left ventricular (LV) remodeling within 3 months following acute myocardial infarction (AMI) and is called ischemic mitral regurgitation (IMR). Ischemic preconditioning (IPC) has been reported as the most important mechanism of the association between prior angina and the favorable outcome. The aim of this study was to investigate the effect of prior angina on the development and severity of IMR at 3rd month in patients with ST elevation MI (STEMI). Fourty five (45) patients admitted with STEMI and at least mild IMR, revascularized by PCI were enrolled. According to presence of prior angina within 72 h before STEMI, patients were then divided into two groups as angina (+) (n:26; 58%) and angina (-) (n:19; 42%). All patients underwent 2D transthoracic echocardiography at 1st, 3rd days and 3rd month. IMR was evaluated by proximal isovelocity surface area (PISA) method: PISA radius (PISA-r), effective regurgitant orifice area (EROA), regurgitant volume (Rvol). LV ejection fraction (EF %) was calculated by Simpson's method. High sensitive troponin T (hs-TnT), creatine phosphokinase myocardial band (CK-MB) and N-terminal pro-brain natriuretic peptid (NTpro-BNP) levels were compared between two groups. Although PISA-r, EROA and Rvol were similar in both groups at 1st and 3rd days, all were significantly decreased (p = 0.012, p = 0.007, p = 0.011, respectively) and EF was significantly increased (p< 0 .001) in angina (+) group at 3rd month. NTpro-BNP and hs-TnT levels at 1st day and 3rd month were similar, however CK-MB level at 3rd month was found to be significantly lower in the angina (+) group (p = 0.034). At the end of the 3rd month, it was observed that the severity of IMR evaluated by PISA method was decreased and EF increased significantly in patients who defined angina within 72 h prior to STEMI, suggesting a relation with IPC.

Background: Knowledge on endothelial dysfunction and its relation to atherosclerosis in mastocytosis is limited. Aim: To investigate the endothelial function in mastocytosis by flow mediated dilatation (FMD) and biomarkers related to vascular endothelia, the presence of subclinical atherosclerosis by carotid intima media thickness (CIMT). Method: Forty-nine patients with mastocytosis and 25 healthy controls (HCs) were included. FMD and CIMT during transthoracic echocardiography, biomarkers including endocan, endothelin-1 (ET-1), vascular endothelial growth factor (VEGF) were measured in sera of participants. Tumor necrosis factor-alpha (TNF-α), interleukine-6 (IL-6) and high sensitive c-reactive protein (hsCRP) were determined as inflammatory biomarkers. Result: The mean FMD% was lower in the patients than HCs (11.26±5.85% vs 17.84±5.27% p<0.001) and was the lowest in the advSM and SSM group among the patients (p=0.03). The median value of VEGF was significantly higher in patients than HCs. [73.30 pg/mL; min-max (32.46-295.29) pg/mL vs (46.64 pg/mL; min-max 11.09-99.86 pg/mL; p:0.001] and it was the highest in the advSM and SSM group (p:0.01). FMD was inversely correlated with endocan (r:-.390, p:0.006), ET-1 (r:-.363, p:0.01) and VEGF (r:-.402, p:0.004) but there were no correlations between FMD and TNF-α, IL-6, and hsCRP. No differences in CIMT values between patients and HCs and no correlation between CIMT and the biomarkers were observed. Conclusion: Endothelial dysfunction in mastocytosis becomes evident with decreased FMD and elevated serum VEGF, in the absence of atherosclerosis or systemic inflammation and is related to disease severity. Keywords: CIMT, Endocan, Endothelial function, Endothelin-1, FMD, VEGF

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.

BackgroundDemonstration of deposits by non-invasive methods is important especially for organs difficult to sample in amyloidosis. Transient elastography (fibroscan) is a diagnostic method being used to measure liver stiffness (LS) in different chronic liver diseases.ObjectivesWe herein aimed to test the place of fibroscan method for detecting increased LS associated with amyloid deposition in patients (pts) with amyloidosis.MethodsSix categories of pts enrolled into this cross-sectional study; AA amyloidosis (AA-a), AL amyloidosis (AL-a), Familial Mediterranean Fever (FMF) pts without amyloidosis, cirrhotic chronic liver disease, non-cirrhotic chronic hepatitis B infection (CHB) and healthy controls (HC). LS assessment by fibroscan were categorized as normal for kPa<7, significant stiffness for kPa≥7, advanced stiffness for kPa≥9.5 and kPa≥F4 stiffness. FIB-4 and APRI scores were calculated for each patient when they indicated chronic liver disease. Pts with known chronic liver disease and viral hepatitis excluded from amyloidosis and FMF groups.ResultsA total of 165 pts (AA-a, n=65; AL-a, n=15; FMF, n=20; cirrhotic pts, n=16; CHB, n=22; HC, n=27) constituted the study group. Average age was higher in the AL-a group compared to others. Median LS was highest in cirrhotic pts, and it was also higher in AA-a and AL-a pts compared to FMF and HC. Median LS was numerically higher in AL-a compared to AA-a, but it did not reach statistical significance. Median LS was also higher in FMF pts compared to HC. FIB-4 and APRI scores were lower compared to cirrhotic patients in AA-a and AL-a. ALP levels were higher in AA-a and AL-a groups compared to FMF, CHB and HC. FIB-4 and APRI scores, ALP and GGT levels were correlated with LS both in AA-a (r=0.534***,r=0.485***,r=0.437***, r=0.506***) and, AL-a (r=0.536*, 0.579*, r=0.645*, r=0.752**) and FMF-AA (r=0.584***, r=0.566***,r=0.322*, r=0.306*; *p<0.001, **p<0.01, *p<0.5) groups.Higher patient age, age at diagnosis of amylodosis, FIB-4 and LS scores, ALP levels, non-FMF causes of AA were associated with hepatic AA amyloid involvement in biopsy-proven pts. A cut-off value 12.05 kPa of LS provided 100% sensitivity and 85.5% specificity (LR=6.9, AUC=0.901, 95% CI 0.81-0.99) for pts with AA-a.ConclusionIn our single center cohort, we showed a higher median LS by fibroscan in both AL-a and AA-a pts compared to CHB, FMF and HC. It was thought to be that fibroscan may be useful in detecting hepatic amyloid involvement.Table 1.AA-a (n=65)FMF (n=20)AL-a (n=15)Cirrhosis (n=16)Chronic Hepatitis B (non-cirrhotic) (n=22)HC (n=27)p1p2p3p4p5p6Age (years)*46 (19)42.5(13)58 (16)49 (15)45 (21)45 (23)0.40.30.80.50.80.002Gender (n, %)Male38 (59)10 (50)6 (40)10 (62.5)13 (59)17 (55)0.50.810.70.70.2Female27 (41.5)10 (50)9 (60)6 (37.5)9 (40.9)14 (45.2)Diabetes Mellitus (n, %)5 (8)2 (11)2 (13)3 (15)2 (13)3 (10)0.70.60.40.80.90.6Body Mass Index (kg/m2) *25.7 (1.4)25.6 (5.4)24.8 (3.6)26.7 (6.7)25.5 (7)26 (5.7)0.90.410.70.70.3Liver stiffness (kPa)*6.7 (5.6)6.45 (2.7)9.8 (12)26.7 (22)5.7 (5)4.9 (1.6)<0.001<0.0010.03<0.001<0.0010.16Significant stiffness (kPa≥7)31 (48)11 (55)8 (58)16 (100)4 (18)2 (6.5)0.4<0.0010.012<0.001<0.0010.6Advanced stiffness (kPa≥9.5)17 (26)4 (20)7 (50)16 (100)3 (14)00.4<0.0010.20.0010.020.1S4 stiffness (kPa≥12.5)10 (15)05 (36)16 (100)2 (9)00.057<0.0010.40.020.1FIB-4 score0.97 (0.9)0.76 (0.56)1.3 (0.95)2.5 (3.4)0.85 (0.8)0.7 (0.5)<0.001<0.0010.40.0050.60.1APRI score*0.25 (0.2)0.26 (0.2)0.24 (0.2)0.77 (1.3)0.22 (0.2)0.16 (0.08)<0.001<0.0010.30.0020.020.4ALP (U/L)*97 (65)79 (55)103 (54)79 (126)76 (39)67 (22)<0.0010.50.002<0.0010.0020.7GGT (U/L)*18 (18)17 (26)24 (61)24 (51)16 (14)14 (14)0.070.20.20.070.20.08p1: AA-a and FMFp2: AA-a and cirrhosisp3: AA-a and chronic liver diseasep4: AA-a and HCp5: FMF and HCp6: AA-a and AL-a*Median, interquartile of rangeDisclosure of InterestsNone declared

OBJECTIVE:The scavenger receptor class B type 1 (SR-BI, SCARB1), which is a high-density lipoprotein (HDL) receptor that mediates selective cholesteryl ester uptake, plays an important role in reverse cholesterol transport. This study investigated the distribution of polymorphic variants of the SR-BI gene in patients with coronary heart disease (CHD) with a history of early myocardial infarction (MI) at an early age and their effects on their serum lipid levels.METHODS:SR-BI rs5888(T>C), rs4238001(C>T), and rs10846744(G>C) were analyzed in 100 male patients with CHD with a history of MI (MI+) who were younger than 50 years and 89 male control subjects without MI history (MI-) using real-time polymerase chain reaction (PCR) and mutant-allele-specific PCR techniques.RESULTS:SR-BI rs4238001 common-CC genotype was found to be more frequent in patients with MI+ than in control subjects (MI-; odds ratio 4.046, p<0.001). The rs10846744 rare-C allele showed a significant association with increased total cholesterol (p=0.014) and triglyceride (p=0.009) levels in the MI+ CHD group. Logistic regression analysis confirmed that there may be an association between the rs4238001-CC genotype (p=0.002), smoking (p=0.026), and MI+ CHD in the presence of other risk factors associated with CHD, whereas haplotype analysis confirmed that patients with MI+ CHD (rs5888-C, rs10846744-G, and rs4238001-C alleles) and CCC (rs5888-C, rs10846744-C, and rs4238001-C alleles) haplotypes were highly frequent (p<0.01 and p=0.027, respectively).CONCLUSION:These results indicated that SR-BI gene variants show different distribution in patients with MI+ CHD compared with that in MI- control subjects, and these variants may have effects in favor of dyslipidemia.

BACKGROUND:The presence of the left ventricle (LV) apical thrombus is one of the most critical complications of anterior myocardial infarction (MI). Due to the high risk of systemic embolization, the determination of LV apical thrombus (LVAT) is essential. We aimed to compare the two-dimensional echocardiography (2DE), contrast-2DE and real-time three-dimensional echocardiography (RT-3DE) in the diagnosis of LVAT and determine which imaging modality is superior. METHODS:The study was designed as a prospective cohort study, and 161 patients were included. Patients with low ejection fraction (< 40%) and LV apical wall motion abnormality (severe hypokinetic, akinetic or dyskinetic) were included. 2DE, contrast-2DE, RT-3DE, and magnetic resonance imaging (MRI) were performed on all patients within one month after anterior MI. RESULTS:Transthoracic 2DE detected thrombi in 29 patients, contrast-2DE detected thrombi in 33 patients, RT-3DE detected thrombi in 32 patients, and MRI detected thrombi in 28 patients. While MRI is accepted as the gold standard for non-invasive imaging, the specificity of detecting thrombus with 2DE is 90%, and the sensitivity is 57%, contrast-2DE had 82% sensitivity and 92% specificity for the detection of LVAT. The specificity for detecting thrombus with RT-3DE is 93%, and the sensitivity is 85%. Accuracy was 84%, 90% and 92% with 2DE, contrast-2DE and RT-3DE, respectively. CONCLUSIONS:We found that RT-3DE was more sensitive and more specific than 2DE and contrast-2DE in the diagnosis of LVAT. The diagnostic accuracy of RT-3DE was higher than 2DE and contrast-2DE for LVAT.

Background The extent of pressure‐related damage might be related to acceleration rate of the applied pressure (peak dP/dt) in the vascular system. In this study, we sought to determine whether dP/dt applied to the aortic wall (aortic dP/dt) and in turn vascular extracellular matrix degradation can be mitigated via modulation of left ventricular (LV) contractility (LV dP/dt) by pacemaker‐mediated desynchronization. Methods and Results First, in 34 patients, changes in aortic dP/dt values in 3 aortic segments in response to pacemaker‐mediated stepwise QRS widening leading to gradual desynchronization of the LV contraction by means of steadily changed atrioventricular delay (AVD) with temporary dual‐chamber pacing was examined before and after beta‐blocker (15 mg IV metoprolol) administration. Second, serum matrix metalloproteinase‐9 levels were measured in the 20 patients with permanent pacemaker while they were on sinus rhythm with normal QRS width and 3 weeks after wide QRS rhythm ensured by dual pacing, dual sensing, and dual response to sensing with short AVD. LV dP/dt substantially correlated with dP/dt measured in ascending (r=0.83), descending (r=0.89), and abdominal aorta (r=0.96). QRS width strongly correlated with dP/dt measured in ascending (r=−0.95), descending (r=−0.92), and abdominal (r=−0.96) aortic segments as well. In patients with permanent pacemaker, wide QRS rhythm led to a significant reduction in serum matrix metalloproteinase‐9 levels (from 142.5±32.9 pg/mL to 87.5±32.4 pg/mL [P<0.001]) at the end of 3 weeks follow‐up. Conclusions QRS prolongation by short AVD dual pacing, dual sensing, and dual response to sensing results in concomitant decreases in peak dP/dt values in the LV and in all aortic segments with or without background beta‐blocker administration, which in turn led to a significant reduction in circulating matrix metalloproteinase‐9 levels. Registration URL: https://www.clini​caltr​ials.gov; Unique identifier: NCT03665558.

Objective: The aim of this study was to investigate the effects of the CETP gene rs289714 polymorphism on the serum lipid profile and other metabolic parameters in Turkish patients with coronary artery disease (CAD). Methods: The CETP rs289714 variant was examined in 104 patients with CAD and 77 controls using the polymerase chain reaction-restriction fragment length polymorphism method. Results: The CETP rs289714 genotype and allele distribution was not statistically different between the groups (p>0.05). The body mass index (BMI) values in men with CAD were higher in patients with the G allele compared with those carrying the AA genotype (p=0.05). Logistic regression analysis showed that the G allele in male CAD patients was a risk factor for a BMI of >= 27 kg/m(2) (odds ratio: 0.269, 95% confidence interval: 0.075-0.966; p=0.044). The G allele in female patients was associated with lower HDL-C levels than the AA genotype (p=0.049). Conclusion: The results suggest that the CETP rs289714 polymorphism may cause risk for the development of CAD due to its effects on high-density lipoprotein cholesterol values in female patients and BMI in male patients.