OR 2.860, 95% CI 1.297–6.306, p = 0.009), SDI , and EMATc ]. The area under the receiver operating characteristic curve for EMATc was 0.89, with an optimal cutoff point of 12.2, EMATc had a sensitivity of 80% and a specificity of 83%. By contrast, an optimal cutoff point of 100 pg/ml, Serum brain natriuretic peptide had a sensitivity of 46% and a specificity of 83%. Our findings suggest the predictive value of EMATc for the occurrence of EVR in these patients was also identified; EMATc may be a simple, quick, and effective way to diagnose EVR after AMI.Acoustic cardiography is a completely new technology, it has great advantages in the rapid diagnosis of cardiovascular diseases. The purpose of this study was to investigate the clinical value of the fourth heart sound (S4), cardiac systolic dysfunction index (SDI), and the cardiac cycle time-corrected electromechanical activation time (EMATc) in the prediction of post-percutaneous coronary intervention (PCI) early ventricular remodeling (EVR) in patients with acute myocardial infarction (AMI). We recruited 161 patients with AMI of 72-h post-PCI, including 44 EVR patients with left ventricular ejection fraction (LVEF) < 50% and 117 Non-EVR patients . EMATc, S4, and SDI were independent risk factors for post-PCI early ventricular remodeling in patients with AMI [S4 ( A strong relationship has been demonstrated among disease prognosis, heart failure, and ventricular remodeling after AMI. Ventricular remodeling is an independent predictor of the development of heart failure2. Many guidelines for the management of cardiovascular diseases refer to the importance of ventricular remodeling after AMI and its treatment modalities4. Ventricular remodeling after AMI can be divided into early ventricular remodeling and late ventricular remodeling, with various clinical manifestations, such as enlarged left ventricle, reduced left ventricular ejection fraction (LVEF), and abnormal ventricular wall motion6. Asymptomatic left ventricular systolic dysfunction (LVSD) is a major manifestation of early ventricular remodeling, with an occurrence of up to 30–60% in patients after AMI7. Early detection of ventricular remodeling after AMI is key to effective treatment. Although B-type brain natriuretic peptide (BNP) and echocardiography can be utilized in the diagnosis of LVSD, they carry several disadvantages, including increased cost, need for specialized technicians, and difficulty in achieving dynamic monitoring. Therefore, acoustic cardiography is gaining attention as a simple, rapid, non-invasive, and effective diagnostic modality for LVSD.Acute myocardial infarction (AMI) is a common cardiovascular disease that poses a serious threat to human health. Percutaneous coronary intervention (PCI) and standardized drug therapy can effectively treat most patients, but many patients still develop ventricular remodeling, which can contribute to heart failure post-PCI10. However, acoustic cardiography has been rarely used in the diagnosis of coronary artery disease. Several studies have shown improved sensitivity and specificity using standard ST-T changes combined with S4 > 3.6 as diagnostic criteria for coronary artery disease11. Additionally, our previous study confirmed the clinical significance of acoustic cardiography in the diagnosis of coronary artery disease and ventricular remodeling12.Many clinical studies have confirmed the diagnostic value of acoustic cardiography in a variety of cardiovascular diseases, especially in the diagnosis of heart failure. Some studies have shown that cardiac cycle time-corrected electromechanical activation time (EMATc), left ventricular systolic time (LVST), and third heart sound (S3) are superior to serum BNP levels in the diagnosis of heart failure. EMAT is related to left ventricular systolic function. Furthermore, S3 and S4 are less affected by age, which increase their utility in evaluating cardiac systolic and diastolic functionThe present study investigated the relationship between parameters of acoustic cardiography and early ventricular remodeling and examined the predictive value of each parameter for early ventricular remodeling after PCI in patients with AMI.A total of 183 inpatients from the Departments of Cardiology of the Third Affiliated Hospital of Chongqing Medical University and Haikou People’s Hospital were enrolled in the study from March 05, 2019 to June 30, 2021 [22 patients were excluded due to poor quality electrocardiograms (ECGs)]. 161 patients with asymptomatic acute anterior wall MI after emergency PCI were included . Serum BNP, acoustic cardiography , and Color Doppler echocardiography were performed pre-operatively. Color Doppler echocardiography was also performed after 72 h, and LVEF% < 50%  72-h post-PCI was defined as early ventricular remodeling. The study subjects were divided into two groups: early ventricular remodeling group  and normal left ventricular systolic function group .https://powerandsamplesize.com/Calculators/.we calculated sample size between Non-EVR group and EVR group with regard to EMATc. With power equal to 0.9,we chose a ratio of 3:1 for the Non-EVR and EVR groups, the total sample size needed is 120.We have a sufficient number of cases. The study was approved by the Third Affiliated Hospital of Chongqing Medical University in the participating institutions (protocol number202133), and was conducted in accordance with the Declaration of Helsinki.The exclusion criteria were: (1) atrial fibrillation, pre-excitation syndrome, and intraventricular block; (2) severe liver and kidney disease; (3) patients on mechanical ventilation; (4) inferior wall MI; and (5) patients with pacemaker. Before participation, written-informed consent was obtained from each patient. We calculated the sample size through Power and Sample Size online; the website is Echocardiography  was performed in all patients. The biplane Simpson's method was used to calculate both end-diastolic and end-systolic volumes. These volumes were employed to calculate LVEF.Electromechanical activation time (EMAT), the time from Q wave onset to the mitral component of the first heart sound S1) Fourth heart sound (S4) score: measurement of the intensity of S4 based on timing, persistency, intensity, and frequency of the sound Fig. ; one valThird heart sound (S3) score: measurement of the intensity of S3 based on timing, persistency, intensity, and frequency of the sound Fig. ; one valSystolic dysfunction index (SDI): SDI = exp (S3 score/10) × QRS duration × QR interval × EMAT/RR. The SDI value undergoes a nonlinear transformation and is mapped into a scale of 0–10.Each patient underwent an acoustic cardiography examination in the supine position. For the measurement of heart sounds, acoustic cardiography raw data were analyzed by a computerized algorithm. At least 3 examinations were performed on each study subject, and the average values of each variable were used for analysis. In this study, the following acoustic cardiography parameters were evaluated:P value < 0.05 was considered statistically significant. Continuous variables with a normal distribution were expressed as mean ± standard deviation (SD). For predicting EVR, the receiver operating characteristic (ROC) curves were generated to determine the area under the curve (AUC), sensitivity, specificity, positive likelihood ratio (LR+), and negative likelihood ratio (LR−). Multivariate logistic regression analysis was used to analyze the independent risk factors of EVR. In addition, comparisons between groups were tested by using both Student’s t test for normally distributed data and Mann–Whitney U test for skewed data.SPSS, version 20, was used for statistical analyses . A two-sided A total of 161 patients were enrolled into this study. Table Compared with Non-EVR patients, those EVR patients had higher EMATc, S4 score, SDI, and BNP and lower LVEF. p < 0.001). With an optimal cutoff point of 12.2, EMATc produced a sensitivity of 80% and a specificity of 83%. The AUC for S4 was 0.7 . With an optimal cutoff point of 4.3, S4 strength produced a sensitivity of 56% and a specificity of 75%. The AUC for SDI was 0.8 . With an optimal cutoff point of 3.9, SDI strength produced a sensitivity of 91% and a specificity of 54%. The AUC for BNP was 0.8 . In addition, with an optimal cutoff point of 92.5 pg/ml, BNP produced a sensitivity of 73% and a specificity of 72%, whereas, with an optimal cutoff point of 100 pg/ml, BNP produced a sensitivity of 46% and a specificity of 83%. As can be seen in Fig. By using ROC curve analyses, the value of a variety of acoustic cardiographic parameters and BNP were determined for the prediction of EVR. As shown in Fig. OR 2.3, 95% CI 1.4–3.7, p < 0.001), SDI , and BNP , were independent risk factors for EVR. There were no statistical differences in the parameters of S3, S4, HR, sex, diabetes, and age.As shown in Table 1. It has suggested that > 15% increase in left ventricular end systolic volume, measured by echocardiography, 6 months after PCI for AMI, is evidence of ventricular remodeling13. However, a meta-analysis of data from Medline and Embase showed that the LVEF was below 50% in patients with asymptomatic LVSD after AMI14. In a prospective study of 284 patients with AMI treated with PCI, 30% had ventricular remodeling after 6 months15. Early ventricular remodeling usually occurs 24–72 h after AMI and presents clinically as asymptomatic LVSD, but is underdiagnosed7. There are a number of clinical indicators that predict LVSD;copeptin was shown to be a valid indicator16;heart rate-corrected QT interval prolongation to the Global Registry of Acute Coronary Events risk score improves the predictive value for early mortality in patients with acute coronary syndrome17; Of course, there are many other methods of prediction, such as BNP, echocardiography, and magnetic resonance imaging,, but these approaches are expensive, cumbersome and cannot be monitored systematically. Moreover, many patients refused these tests to be performed. Therefore, acoustic cardiography is gaining attention as a simple, rapid, non-invasive, and effective diagnostic modality for asymptomatic LVSD which leads to HF. The practical value of acoustic cardiography, with EMATc, as the main parameter, in the clinical diagnosis of heart failure has also been reported. Dillier et al.10 showed that in healthy subjects there was no circadian rhythm variation in EMAT, no significant change from wake-to-sleep state, and no change with age. However, prolonged EMATc in patients with HF is associated with LVSD, poor HF prognosis, and rehospitalization, independent of serum BNP levels and LVEF18. Roos et al.19 reported that in 108 patients who underwent elective diagnostic cardiac catheterization, EMAT > 110 ms had a high specificity for LVEF (~ 50%) patients with LVSD. In a study of 433 patients, Kosmicki et al.8 found that EMAT, LVST, and S3 were better than serum BNP in the diagnosis of LVSD; acoustic cardiography alone and acoustic cardiography combined with BNP had equivalent clinical value in the diagnosis of LVSD; in the "gray zone" of serum BNP (100 ng/L to ≤ 500 ng/L), acoustic cardiography was superior to BNP. Many other studies have found the clinical applications of EMATc in disease prediction. Zhang et al. reported that the elevated EMATc measured on admission was an independent risk factor for major adverse cardiovascular events in hospitalized patients with congestive heart failure. Acoustic cardiography measured on admission may provide a simple, non-invasive method for risk stratification of patients with congestive heart failure20. Chao et al. found that EMAT-guided post-discharge management was superior to traditional symptom-driven therapy in patients hospitalized for acute heart failure in terms of 1-year outcomes18. There are few clinical studies on the value of acoustic cardiography in the diagnosis of AMI. Some studies have shown that STT changes combined with S4 as the standard for the diagnosis of coronary heart disease have a sensitivity and specificity of 68% and 84% respectively; S3 or S4 combined with ECG increases the detection rate of myocardial ischemia by 32%21.Although the widespread use of PCI has improved the prognosis of patients with AMI, many patients still develop heart failure. Ventricular remodeling after AMI is an independent predictor of the development of HF and is one of the major factors affecting prognosis but without uniform and clear criteriaIn the present study, we identified three parameters, EMATc, S4, and SDI, as independent risk factors for post-PCI early ventricular remodeling in patients with AMI and their predictive value for the occurrence of early ventricular remodeling. We determined the value of various acoustic cardiographic parameters and serum BNP levels for predicting early ventricular remodeling and showed that the AUC of EMATc was 0.89, the optimal threshold was 12.2, the sensitivity of EMATc was 80%, and the specificity was 83%. By contrast, when the optimal threshold of serum BNP was set at 100 pg/ml, the sensitivity of BNP was 46% and the specificity was 83%. Therefore, our results suggested that EMATc was superior to serum BNP levels.We believe that acoustic cardiography is a simple, quick, and effective way to diagnose early ventricular remodeling after AMI. However, there are some limitations of the present study that need to be addressed. First, the sample size was small (n = 161). Therefore, more subjects are needed to determine the clinical value of acoustic cardiography in the diagnosis of AMI. Second, we selected only the patients with anterior MI. Third, echocardiography data were limited to EF% values and therefore, did not provide additional information on other echocardiography variables that may have led to the discovery of other significant correlations. A better way to determine early ventricular remodeling should be the decrease in LVEF after PCI compared with pre-PCI LVEF. However, echocardiography is often overlooked in order to complete the procedure as quickly as possible pre-PCI. Therefore, it was difficult for us to obtain complete information. Finally, we only studied the early ventricular remodeling rather than the relationship between acoustic cardiography and late ventricular remodeling, which would take a long time.We identified three parameters, EMATc, S4, and SDI, as independent risk factors for post-PCI early ventricular remodeling in patients with AMI and also identified the predictive value of these parameters for the occurrence of early ventricular remodeling in these patients. Acoustic cardiography can be a simple, quick, and effective way to diagnose early ventricular remodeling after AMI.


Strain parameters on speckle tracking echocardiography (STE) have been proposed as effective indexes for evaluating right ventricular (RV) function. This pilot study investigated the role of STE-derived strain parameters in assessing global and regional RV myocardial mechanical changes in patients with acute pulmonary embolism (PE) before and after thrombolytic therapy. In this case–control study, a total of 73 PE patients, 34 with pulmonary hypertension (PH) and 39 without PH, who underwent thrombolytic therapy were included. Healthy volunteers were included as controls. The peak longitudinal systolic strain (PLSS) and time to PLSS (TTP) for the global and regional RV were analyzed by STE software immediately before and 14 days after thrombolytic therapy. Changes in STE-derived strain parameters and conventional ultrasound parameters were compared. PLSS and TTP decreased before treatment in PE patients compared with measurements in the control group, particularly in those with PH. Also, the strain parameters decreased more significantly for the free wall than for the septum wall (P < 0.05). Moreover, the RV diastolic diameter (RVDD) and RV/left ventricular (LV) diameter ratio increased, while RV fraction shortening (RVFS), RV fractional area change (RVFAC), tricuspid regurgitation pressure gradient (TRPG), and tricuspid annular peak systolic excursion (TAPSE) decreased (P < 0.05). The global strain parameters for the RV were positively correlated with RVDD and RV/LV diameter ratio, but negatively correlated with RVFS, RVFAC, TRPG, and TAPSE (P < 0.05). After treatment, the strain parameters differed significantly between PE patients with PH and controls but did not differ between PE patients without PH and controls. STE-derived parameters are effective for detecting changes in global and regional RV function in PE patients with or without acute PH. Despite significant improvements in diagnostic and therapeutic strategies in recent years, pulmonary embolism (PE) remains a severe pulmonary vascular disease with a high incidence and mortality. For patient with PE, subsequent right ventricular (RV) dysfunction has become an important cause of death, and early appearance of RV dysfunction after PE has been confirmed as an independent risk factor of mortality in these patients . AccordiIn this case–control study, a total of 73 patients  diagnosed with PE in People’s Hospital of Hunan Province between March 1, 2016 and March 1, 2020 were included in this study . Another 40 healthy volunteers without PE were included as controls . Diagnosis of PE was performed in accordance with the 2014 European Heart Society guidelines for PE Management , PE pati2 + average RA pressure.Echocardiography was performed using a GE Vivid E9 ultrasound system with a M5S transducer  at a frame rate of ≥ 50 frame/sec. During the examination, participants were in a calm state and kept in the left lateral position or supine position. If the condition of the patient was not satisfactory for the examination, we waited until the general condition of the patient was relatively suitable for the examination. Conventional parameters for RV function evaluation, including RV diastolic diameter (RVDD), RV fraction shortening (RVFS), RV fractional area change (RVFAC), right atrium diastolic diameter (RADD), and RV/left ventricular (LV) diameter ratio were measured and calculated in the standard apical four chamber section. Tricuspid annular peak systolic excursion (TAPSE) was measured by M-mode ultrasound. Tricuspid regurgitation pressure gradient (TRPG) was measured by continuous-wave (CW) Doppler, and the pulmonary arterial systolic pressure (PASP) was subsequent calculated according to the Bernoulli equation: PASP = 4 × (velocity of tricuspid regurgitation) All participants were instructed to hold their breath at the end of exhalation , and the apical RV focused view dynamic images were recorded for three consecutive cardiac cycles with a stable heart rhythm. Then the strain parameters were analyzed by STE software configured by the instrument. With the inner wall boundary of the RV traced by spots at the end of systolic period, the software automatically calculates the displacement of the spots in the region of interest in each frame of the whole cardiac cycle, and then the longitudinal strain curves for the six segments of the RV  are obtained. The degree of myocardial deformation and peak longitudinal strain represent the percentage of longitudinal shortening of each segment of interest in systole compared with that in diastole. The time needed to reach the peak strain is time to peak strain. The time of QRS wave initiation is taken as the reference point. Strain indexes including peak longitudinal strain (PLSS) and time to PLSS (TTP) of the global RV as well as the six segments of the RV  were obtained. The global PLSS and TTP of the RV were calculated as the average values of the above six segments. Typical images for STE measurements before and after thrombolytic therapy are shown in Figs. To determine the repeatability of RV strain parameters evaluated by STE, the analyses were repeated in a randomly selected group of 30 study subjects by two examiners with the same qualifications, and 30 cases who were randomly selected from the subjects were analyzed by the same examiner at an interval of two weeks.Intraclass correlation coefficients (ICC) were used to assess inter-observer reliability and test–retest reliability. The investigators were blinded to the results of all previous measurements. The calculated ICCs indicated excellent inter-observer reliability (0.72–0.84%) and test–retest reliability (0.78–0.89%).2 test. A P value < 0.05 was regarded as statistically significant. Pearson’s correlation analysis was performed to evaluate the correlations between the strain parameter PLSS and conventional ultrasonic parameters. All statistical analyses were performed using SPSS 13.0 software .Continuous data were presented as mean ± standard deviation (SD). The Shapiro–Wilk test was used to determine the distribution of data in the PE and control groups. The t test was used to identify differences in clinical characteristics and conventional ultrasound parameters between healthy controls and PE patients with PH and between the healthy controls and PE patients without PH before treatment. Also, the t test was used to identify differences in PLSS and TTP for the global RV and six segments of the RV between healthy controls and PE patients with PH, between healthy controls and PE patients without PH before and after treatment. Qualitative data are expressed as percentages (%) and were compared using the χA total of 73 PE patients  with an average age of 58.37 ± 8.12 years (range: 44–72 years) and 40 controls  with an average age of 55.95 ± 8.84 years (range: 40–70 years) were enrolled in this study. Among the 73 patients, 39 were without PH at the time of PE diagnosis, while the remaining 34 had PH. No significant differences in the demographic and baseline clinical characteristics were observed between the groups . The degree of strain parameter reduction in PE patients with PH was greater than that in PE patients without PH. In each segment of the RV, the strain parameters for the free wall segment decreased more significantly than those for the septum wall in the PE groups. After treatment, no significant differences in strain parameters were observed between the without PH group and the control group  and negatively correlated with RVFS, RVFAC, TRPG, and TAPSE  both before and after thrombolytic therapy (Fig. In this study, we used STE-derived strain parameters, including PLSS and TTP, to detect changes in global and regional RV function in PE patients with or without PH before and after thrombolytic therapy. We found that the global strain parameters for the RV were positively correlated with the RVDD and RV/LV diameter ratio and negatively correlated with the RVFS, RVFAC, TRPG, and TAPSE, demonstrating the good correlation between STE-derived parameters and conventional ultrasonic parameters for RV function. Taken together, the findings of the present study support the use of STE-derived strain parameters such as PLSS and TTP for the detection of changes in RV function during treatment for acute PE.It has been suggested that STE may provide new quantitative indexes for regional and global cardiac function in clinical practice due to its angle-independent characteristics, which could lead to a more accurate evaluation of LV and RV function in both the long axis and short axis . Strain Our study showed that the longitudinal strain and strain rate of the RV can be used as an index for early diagnosis of RV dysfunction in patients with PE. It has been shown that the PLSS reduction is correlated with the severity of PH in these patients . A typicThe increase in pulmonary vascular resistance in PE patients can cause pulmonary arterial hypertension and RV enlargement and dysfunction, which has been associated with a 2.29-fold mortality increase in PE patients . The myoTAPSE is the displacement amplitude of the systolic wave of the lateral tricuspid annulus measured by M-mode ultrasound from the end of diastole to the end of systole, which has been related to the degree of pulmonary artery pressure overload and the degree of RV myocardial damage. TAPSE has been proposed as a prognostic factor in PE patients, conferring stronger prognostic efficacy than the RV/LV diameter ratio . TAPSE rThrombolysis is one of the main treatments for patients with PE and may effectively reduce PE and associated right heart overload, thereby attenuating the impairment of RV function. The degree of pulmonary artery pressure control plays an important role in improving the structural changes and functional lesions of the RV, because PH has been recognized as one of the most important risk factors for RV dysfunction . SuccessThe study has some limitations. First, we excluded some cases with poor quality of ultrasound image and whether this had an impact on the results has not been determined. Second, we did not consider the scope of PE when grouping the patients. It is possible some patients with shock did not undergo cardiac ultrasound, and thus, the patients included in the study were likely to be hemodynamically stable. Also, due to the limited number of patients included, we were unable to divide PE patients into mild, moderate, and severe PH groups. Third, we did not use CMR to evaluate subjects, because this examination is expensive and time-consuming. Additionally, previous studies have shown that cardiac function parameters evaluated by STE are in good agreement with those evaluated by CMR. We also did not take into account the impact of gender, history of medication use, blood pressure, or diabetes on the results. However, gender distribution was matched between PE patients and controls in this study. The influence of other factors should be further evaluated in large-scale studies in the future. We did not consider whether anticoagulant therapy or other inotropic, vasopressor support had an impact on the research results, and further follow-up of patients will be included in the next research plan.STE-derived strain parameters, such as PLSS and TTP, can sensitively and accurately reflect the changes in RV global and regional stain functions in PE patients before and after thrombolysis. Moreover, these parameters showed good correlation with conventional ultrasound indexes, and thereby, can provide a supplementary ultrasonic index for clinical evaluation of curative effect. The strain parameters for the RV free wall changed more significantly when RV function was damaged. RV myocardial function in PE patients with PH is impaired more seriously. These findings support the use of STE-derived strain parameters such as PLSS and TTP for the detection of changes in RV function during the diagnosis and treatment of acute PE.


Left bundle branch pacing (LBBP) is an emerging physiological pacing modality. Left ventricular (LV) myocardial work (MW) incorporates afterload and LV global longitudinal strain to estimate global and segmental myocardial contractility. However, the effect of LBBP on LV MW remains unknown. This study aimed to evaluate the impact of LBBP on LV MW in patients receiving pacemaker for bradyarrhythmia.n = 46) and non-selective His-bundle pacing (NS-HBP) (n = 24). For comparative analysis, patients receiving right ventricular pacing (RVP) (n = 16) and control subjects (n = 10) were enrolled. Two-dimensional speckle tracking echocardiography was performed. The LV pressure-strain loop was non-invasively constructed to assess global LV MW.We prospectively enrolled 70 bradycardia patients with normal LV systolic function receiving LBBP (P = 0.002), higher global constructive work (GCW) , lower global wasted work (GWW)  and higher global MW efficiency (GWE)  compared with RVP group, and had lower GWW  and higher GWE  compared with NS-HBP group.After 6-month follow-up, LBBP group (with >40% ventricular pacing during 6 months) had shorter peak strain dispersion (PSD) compared with RVP group, and higher LV global longitudinal strain compared with RVP group and NS-HBP group, but had no difference in left intraventricular mechanical dyssynchrony, including septal-to-posterior wall motion delay and PSD, compared with NS-HBP group. During ventricular pacing, LBBP group had higher global MW index (GWI)  high ventricular pacing burden (>40%), LBBP preserved more LV MW compared with NS-HBP and RVP. Further studies are warranted to assess the association between LV MW and long-term clinical outcomes in LBBP with high ventricular pacing burden. Right ventricular pacing (RVP) over the right ventricular (RV) apex or the RV septum has been reported to increase the risks of atrial fibrillation, heart failure (HF) hospitalization, or mortality , 2. Prev2.2.1Patients with symptomatic sinus nodal dysfunction and atrioventricular block receiving conduction system pacing were prospectively enrolled in our hospital between July, 2020 and December, 2021. For comparative analysis of case-control study, gender- and comorbidity-matched patients receiving transvenous RVP for symptomatic bradyarrhythmia and gender- and comorbidity-matched control subjects without pacemaker between July, 2020 and December, 2021 were also enrolled in this study. The exclusion criteria included patients with: (1) any history of HF with left ventricular ejection fraction (LVEF) <50% due to severe valvular heart disease or cardiomyopathy, (2) permanent atrial fibrillation, (3) left bundle branch block, (4) end-stage renal disease, and (5) malignancy with expected lifespan <1 year.2.2The detailed procedures are provided in 2.3Echocardiography was performed within 7 days and at 6-month follow-up after the pacemaker implantation. All echocardiographic measurements were obtained initially during sinus or intrinsic rhythm for patients with normal atrioventricular conduction at the time of echocardiography, and then obtained during the DDD pacing mode with an atrioventricular delay of 100–120 ms to ensure complete capture by pacing without fusion in patients with normal atrioventricular conduction, at 2-fold output of pacing threshold, and a pacing rate between 80 and 110 beats/min. Because of inconsistent pacing threshold of HBP group during follow-up, echocardiographic images were only acquired during non-selective HBP (NS-HBP). Transthoracic echocardiographic images were recorded using a Vivid E9 ultrasound system  with M5S 3.5 MHz transducers. All echocardiographic measurements were obtained for at least 3 consecutive beats for sinus and pacing rhythm, and 5 consecutive beats for atrial fibrillation rhythm, and were stored with digital loops for offline analysis with EchoPAC .Based on the recommendations for cardiac chamber quantification by echocardiography , left at2.4The intraventricular and interventricular synchronies were evaluated by pulsed-wave Doppler imaging echocardiography, tissue Doppler (Ts) imaging and STE. The regional durations of time measured for the basal segments in the LVFW, RVFW and interventricular septum (IVS) were from the start of QRS to the peak velocity of S' wave of Ts in the LVFW (Ts-LVFW), RVFW (Ts-RVFW) and septum (Ts-IVS), respectively .The LV GLS, peak strain dispersion (PSD), septal-to-posterior wall motion delay (SPWMD), and difference of Ts between LVFW and IVS (Ts-LVFW-IVS) were used as LV mechanical synchrony parameters , 17, 18.2.5Global LV MW data were quantified using non-invasive LV pressure-strain loop estimations and the area within the LV pressure–strain loop represents MW , 14. Non2.6P < 0.001) for GLS and 0.948 (P < 0.001) for GWI. Inter-observer variability was performed by a different cardiologist repeating measurements from the same images. For interobserver analysis of the LV synchrony data, 18 random measurements were analyzed. The intraclass correlation coefficients for interobserver agreement were 0.986 (P < 0.001) for GLS and 0.910 (P < 0.001) for GWI.Intra- and inter-observer variabilities were calculated by intraclass correlation coefficient and the standard error of measurement. For intra-observer analysis of the LV synchrony data, 18 random measurements were reanalyzed, with a period of 2–4 weeks between the first and second analyses. Intraclass correlation coefficients for intra-observer agreement were 0.933 , with Bonferroni correction when significant events were detected. A two-sided P-value <0.05 was considered statistically significant. All statistical analyses were performed using the SPSS software .Continuous variables are expressed as mean ± standard deviation, and categorical variables were expressed as numbers and percentages. Continuous variables were compared using unpaired Student's 3.3.1This study recruited 109 consecutive patients receiving transvenous permanent conduction system pacing. Thirty-nine patients were excluded, including 6 patients with history of HF due to severe valvular heart disease or cardiomyopathy, 7 patients with end-stage renal disease, 6 patients with permanent atrial fibrillation, 3 patients that refused to join the study and 17 patients with left ventricular septal pacing (LVSP) according to the reported criteria –22. Fina3.23.3P < 0.001)  . About p< 0.001) .3.4P = 0.031)  . The LV = 0.031) .3.5P < 0.001) at implant and  at 6-month follow-up, longer PSD compared with LBBP and NS-HBP groups  at implant and  at 6-month follow-up, lower LV GLS, especially over segments of anteroseptal and septal walls, compared with LBBP and NS-HBP groups  at 6-month follow-up, and longer Ts-LVFW-IVS compared with LBBP and NS-HBP groups  at implant and  at 6-month follow-up  compared with LBBP group at 6-month follow-up, longer IVMD compared with the LBBP group  at implant and  at 6-month follow-up, and longer Ts-LVFW-RVFW compared with the LBBP group  at implant  at implant and  at 6-month follow-up, and NS-HBP group had higher GWI compared to RVP group only at the 6-month follow-up  (P = 0.009) at 6-month follow-up (P < 0.001) at 6-month follow-up, and consequently, LBBP group had higher GWE compared with RVP and NS-HBP groups  at implant and  at 6-month follow-up  during sinus or intrinsic rhythm among the 4 groups at implant and at the 6-month follow-up . However= 0.010) . During ollow-up . During ollow-up .4.The main findings of this study were (1) LBBP group had less left intraventricular mechanical dyssynchrony during ventricular pacing compared with RVP group but had no difference in left intraventricular mechanical dyssynchrony compared to NS-HBP group at 6-month follow-up; (2) right intraventricular mechanical synchrony during ventricular pacing of LBBP group did not differ from that of NS-HBP and RVP groups; (3) LBBP group had less interventricular mechanical dyssynchrony during ventricular pacing compared with RVP group at 6-month follow-up; (4) LBBP group had better LV MW parameters  during ventricular pacing compared with RVP group and better LV MW parameters (GWW and GWE) during ventricular pacing compared with NS-HBP group at 6-month follow-up .4.1Long-term RVP can cause LV systolic dysfunction, pacing-induced cardiomyopathy and HF –4, 23. TThe left atrial size significantly increased during ventricular pacing at 6-month follow-up in the RVP group compared with the LBBP and NS-HBP groups . Consequ4.2Interventricular and intraventricular mechanical dyssynchronies play a crucial role on ventricular pump function , 17, 23.Interventricular dyssynchrony indicates a delay in activation between LV and RV, resulting in a lack of coordinated contraction between LV and RV. In HF patients, interventricular dyssynchrony was associated with higher risk of cardiac events, independent of the QRS duration and LVEF . In this4.3Global LV MW is a novel method to estimate LV systolic function, derived from computed LV pressure-strain loops incorporating both brachial cuff systolic blood pressure recordings and STE data , 14. Pre5.There are several limitations in this study. First, this was a single-center prospective study with small sample size, and STE study only at implant and 6-month follow-up. Second, although several studies reported how to differentiate between LBBP and LVSP –22, it i6.After 6-month of >40% ventricular pacing burden, LBBP resulted in less left intraventricular mechanical dyssynchrony and better LV MW parameters  compared with RVP, and had better MW parameters (GWW and GWE) compared with NS-HBP. Further studies are warranted to assess the association between GWE and long-term clinical outcomes in LBBP with high burden ventricular pacing.


Detection of ventricular arrhythmias and left ventricular (LV) dimensional and kinetic abnormalities in a young patients raises the issue of a correct diagnostic workup. This situation becomes more complicated if we are dealing with a pregnant woman, considering that safety for the fetus of some fundamental diagnostic tools, such as cardiac magnetic resonance (CMR) with contrast agent, has not been established yet. Here we describe the diagnostic process and the clinical management of this patient.A 34-year-old primiparous woman at sixth week of pregnancy, previously asymptomatic, complained of palpitations at rest. Family history reported a diagnosis of dilated cardiomyopathy (DCM) in the mother with Implantable cardioverter-defibrillator (ICD) implant for recurrent episodes of sustained ventricular tachycardia. The mother died later because of a neoplastic disease. Despite the family history of DCM, the patient did not have a previous cardiac evaluation. Moreover, the family was of a small size and no other family members were available for clinical study or were reported to be affected by an arrhythmic cardiac disease.2) with ejection fraction at lower normal limits (50%) and presence of kinetic alterations localized in the posterior wall. The right ventricle (RV) was mildly dilated with normal systolic function.At first evaluation, 12-lead ECG showed sinus rhythm, low QRS voltages in limb leads, repolarization abnormalities in precordial leads and presence of premature ventricular beats (PVBs)  with superior axis deviation. Routine blood biomarkers, including Troponin I and BNP, were within limits and a mild hypokalemia was the only altered parameter. She was treated with beta-blocker therapy (metoprolol 50 mg twice daily) and hypokalemia correction and was followed up in cooperation with the Obstetrics Department.2) while systolic function was mildly reduced (ejection fraction = 46%). RV dimension and function were unchanged. During the following weeks, the patient was asymptomatic and instrumental findings remained stable with recording of isolated PVBs.At the 11th week of pregnancy, she was admitted to our Cardiologic department because of detection at 24-h Holter monitoring of numerous polymorphic PVBs and a few runs of non-sustained ventricular tachycardia (NSVT)  with RBBB and superior axis deviation  and an ACE inhibitor (Ramipril 2.5 mg) was added to beta-blocker therapy. Finally, a complete diagnostic cardiological workup was carried out. CMR showed a moderate LV dilation with mild systolic dysfunction and segmental abnormalities on inferior and lateral walls. The RV was mildly dilated with normal systolic function. Moreover, a LV epicardial fibrofatty substitution involving inferior and mid lateral walls was present Fig. b–d. Card3 It is noteworthy that also myocarditis may show a phenotypic overlap with both forms of cardiomyopathies, even if family history of cardiomyopathy is less in keeping with this diagnosis.4Identification of an inherited arrhythmic disease characterized by a dilated LV with impaired systolic function leads to the need to make a differential diagnosis mainly between DCM and AC with left dominant phenotype.In our patient, arrhythmic symptoms occurred in the first weeks of pregnancy and a significant degree of electrical instability characterized the clinical onset of the disease.6 Echocardiographic evaluation documented the presence of moderate LV dilation with a mildly reduced systolic function with kinetic abnormalities and a mild dilatation of RV with normal function. These findings could be in keeping with both DCM, AC with left dominant phenotype and myocarditis diagnosis, even if the presence of regional kinetic abnormalities is less common in DCM.5 Moreover, in our patient, the pregnancy condition had important implications in the diagnostic assessment as CMR with contrast agent should be usually avoided during pregnancy for possible fetal effects.6 In our subject, the detection of subepicardial fibrofatty substitution in inferior and mid lateral walls was in keeping with both the diagnosis of AC and myocarditis. Augusto et al. found a specific CMR LGE pattern, characterized by circumferential subepicardial involvement  in 57% of the FLNC population. Moreover, in 87% of DSP/FLNC mutation carriers, LGE was localized on subepicardial basal lateral segments.7 According to these findings, in our patient, we found a nonischemic subepicardial LGE distribution in inferior and mid lateral walls  was excluded because of the onset of symptoms and detection of ventricular abnormalities in the first trimester of pregnancy. The current definition of PPC includes the development of heart failure toward the last trimester of pregnancy and the first 6 months postpartum, in the absence of other identifiable causes, in the presence of an EF LV less than 45%.10 As our patient showed an AC with left dominant phenotype, we could speculate that the behavior during pregnancy could be similar to that of DCM patients. It is well known that pregnancy could be poorly tolerated in some women with DCM, with the potential for significant deterioration in LV function and that predictors of maternal mortality are NYHA class III/IV and ejection fraction less than 40%.6 None of these negative-predictive factors was present in our case.Family screening plays an essential role in the diagnosis of cardiomyopathy. Also in our case, family history of cardiomyopathy was helpful in differential diagnosis with an acquired cardiac disease. It is noteworthy that our patient, despite a family history of DCM, did not undergo previous cardiac evaluation that could have allowed an early diagnosis. Even if she had a stable hemodynamic condition, the abrupt onset of arrhythmic symptoms with detection of frequent NSVT episodes induced us to rule out the presence of a chronic myocarditis through an endomyocardial biopsy. In addition to diagnosis, the management of a newly diagnosed AC during pregnancy is also challenging, as data are limited to the ‘classical’ AC form in which RV is predominantly involved. In this AC phenotype, the majority of pregnancies have a positive outcome, without significant differences in incidence of sustained ventricular arrhythmias and in heart failure onset compared with a control group of nulliparous affected women.FLNC gene mutations have been identified in patients with ‘classical’ right dominant AC, in left dominant AC forms and in a DCM phenotype characterized by extensive nonischemic LV fibrosis and occurrence of life-threatening ventricular arrhythmias (VAs) and sudden cardiac death.14 Currently, no data on pregnancy tolerance in patients carrying FLNC gene mutations are available. Thus, even if existing studies seem to indicate that pregnancy is well tolerated in AC and DCM patients with NYHA I class and a mildly reduced ejection fraction, strict cardiac monitoring and accurate management in close cooperation with obstetricians are mandatory.As far as the genetic test result is concerned, 6Regarding medical therapy, beta-adrenergic blocking agents are generally well tolerated in pregnancy, even if they can be associated with increased rates of fetal growth restriction and hypoglycemia. Beta-1-selective drugs, such as metoprolol, are preferred as they are less likely to affect uterine contraction and peripheral vasodilation, and they have shown lower rates of fetal growth retardation. On the contrary, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are contraindicated.FLNC gene is not related to LV systolic function. Following the 2019 Heart Rhythm Society (HRS) consensus in this type of patient, an ICD implantation is recommended (class IIa) as primary prevention in those with a mild reduction in LV ejection fraction (<45%).16 In our case, the presence of a presyncopal episode and frequent NSVT induced us to implant an ICD. Subsequently, results of genetic analysis supported our decision. Nonetheless, the correct timing of ICD implantation in our patient could be debatable, as it is known that it can be implanted safely, especially in the first 8 weeks of gestation.6As far as ICD indication is concerned, current guidelines mainly refer to classical right or biventricular forms of AC, although data on arrhythmic stratification in patients with AC with left dominant phenotype are still lacking. Recent studies reported that the risk of sudden arrhythmic death in carriers of truncated mutations in the This case emphasizes the role of pregnancy in revealing a previously concealed cardiomyopathy and raises the issue of diagnostic and therapeutic strategies in pregnant women affected by newly diagnosed cardiac disease. Moreover, this report underlies the need for close cooperation between cardiologists and gynecologists in the clinical management of this kind of patient. Finally, it confirmed the central role of family history, CMR and genetic study both in diagnosis and treatment planning in patients with arrhythmic cardiomyopathy.There are no conflicts of interest.


Prompt interventions prevent adverse events (AE) in hypertrophic cardiomyopathy (HCM). We evaluated the pattern and the predictive role of feature tracking (FT)-cardiac magnetic resonance (CMR) imaging parameters in an HCM population with a normal left ventricular ejection fraction (LVEF) and a low fibrosis burden.P-value below 0.05 was considered significant.The CMR and clinical data of 170 patients, consisting of 142 HCM  and 28 healthy  subjects, who were enrolled from 2015 to 2020, were evaluated. HCM patients had a normal LVEF with a late gadolinium enhancement (LGE) percentage below 15%. Between-group differences were described, and the potent predictors of AE were determined. A Ps < 0.05). Strains were significantly impaired in the HCM patients with a normal MMI. A progressive decrease in LVGLS and a distinct fall in LVGCS were noted with a rise in MMI. AE were predicted by LVGLS, LVGCS, and the LGE percentage, and LVGCS was the single robust predictor . An LVGCS below 16.2% predicted AE with 77% specificity and 58% sensitivity.LV global longitudinal, circumferential, and radial strains  and the LV myocardial mass index (MMI) were different between the healthy and HCM cases (all LV strains were impaired in HCM patients with a normal EF and a low fibrosis burden, even in the presence of a normal MMI. CMR parameters, especially FT-CMR values, predicted AE in our HCM patients. Hypertrophic cardiomyopathy (HCM) is an inherited disorder characterized by left ventricular (LV) hypertrophy and is unexplainable by other causes –3. HCM iin vivo fibrosis , although cardiac magnetic resonance imaging (CMR) provides better identification and risk stratification by detecting fibrosis .Several studies have examined imaging features that could better elucidate myocardial abnormalities and patient outcomes –12. One In the present study, utilizing the feasible cardiac magnetic resonance feature-tracking (CMR-FT) method, we aimed to define the myocardial strain pattern in HCM patients. Moreover, we investigated the role of CMR parameters in the prognostication of HCM patients with a normal LVEF and a low fibrosis burden.The institutional research committee approved this study and waived the need for informed consent due to the retrospective design of this study.The current investigation retrospectively enrolled 241 patients with HCM who underwent CMR between 2015 and 2020 in our institution. Additionally, the CMR findings of 28 healthy volunteers were retrieved from the center's normal CMR examination archives. Healthy subjects had a normal physical examination, no personal or family history of cardiac disease, and no cardiovascular risk factors, composed of hypertension, diabetes mellitus, and dyslipidemia.All patients with a definite diagnosis of HCM, according to the American heart association/American college of cardiology guidelines for diagnosing and treating patients with hypertrophic cardiomyopathy, were enrolled .The exclusion criteria were an LVEF below 55%, a late gadolinium enhancement (LGE) percentage of more than 15%, hypertension, aortic valve disease, infiltrative heart diseases , athlete's heart, ischemic heart disease, significant cardiac arrhythmias during CMR acquisition, and renal impairment (defined as an estimated glomerular filtration rate <30 ml/min precluding gadolinium injection). Also, other types of HCM, such as apical HCM, are excluded from the study. Furthermore, CMR studies that yielded equivocal findings due to suboptimal quality were excluded from the study .The medical records of the patients were reviewed. Then, based on their transthoracic echocardiography (TTE)-measured LVOT gradient, the patients were classified into 2 groups: an LVOT gradient of less than 50 mm Hg and an LVOT gradient of 50 mm Hg or higher. TTE examinations with a maximum interval of 6 months from the CMR examination were selected for analysis. The former group was regarded as a no or mild LVOT obstruction group and the latter as a severe LVOT obstruction group , 17.2 for females and 85 g/m2 for males was regarded as increased  into normal and increased MMI categories. An MMI exceeding 81 g/mncreased .CMR images were acquired using a 1.5-T MRI equipment  with an 8-element phased-array receiver surface coil. A semi-automatic post-processing program  was applied for the measurements.Electrocardiography-gated cine steady-state free precession in the 2-, 3-, and 4-chamber views, the right ventricular and LV outflow tracts planes, and a stack of short-axis slices covering LV during breath-hold at end-expiration  were acquired. Parallel imaging was utilized. The endocardial and epicardial borders were manually drawn in short-axis end-diastolic and end-systolic images and propagated throughout all ventricular slices. Functional parameters, composed of the EF, end-diastolic and end-systolic volumes, the LV mass index, the maximal septal thickness, the presence of the systolic anterior motion of the mitral valve, and the ratio of the asymmetric septal hypertrophy, were registered.LV end-diastolic and end-systolic frames of 2-, 3- and 4-chamber views and the short-axis plane were selected. Optimal brightness adjustment was done to ensure the best contrast to make accurate discrimination between the endocardium and the blood pool. The endocardial and epicardial contours were defined manually and propagated throughout the slices, and 3D LV strains, consisting of global longitudinal (GLS), global circumferential (GCS), and global radial (GRS) strains, were calculated utilizing the CMR-FT method . The absLGE images were obtained 15 min after the injection of the gadolinium contrast agent, gadotetrate meglumine (Dotarem), applying the phase-sensitive inversion recovery sequence. Breath-held segmented single-shot protocol  with selecting the inversion time to null the normal myocardium  was applied. Considering a 5-standard deviation from the mean myocardial signal intensity, the LGE percentage was measured. The results were assessed visually and modified if needed.Based on echocardiographic findings obtained from patients' medical records, the patients' LVOT gradients were collected. Gradient measurement was performed based on the modified Bernoulli equation.On CMR, cine LVOT images in at least 5 consecutive slices were acquired. The presence of the systolic anterior motion of the mitral valve and LVOT turbulence were registered.For each patient, we considered at least one follow-up. If a patient had several follow-ups, we considered the last one. A composite of adverse events, consisting of sudden cardiac death, aborted sudden cardiac death (unsuccessful cardiopulmonary resuscitation), implantable cardioverter defibrillator insertion, and deteriorated systolic function (an EF decline to <40%), was considered and registered.CMR measures were registered by two experts with more than five years of expertise (a cardiologist and a radiologist) in cardiovascular imaging. Readers were blind to the study population's data. Interobserver variability was reported, and both examiners' consensus resolved any conflicts.Echocardiographic, clinical, and follow-up data, including physician visits, lab data, and imaging examinations, were collected by reviewing patients' medical records and/or telephone calls whenever needed.t, Mann–Whitney U, analysis of variances (ANOVA), and χ2 tests, whichever was appropriate. The post hoc test of the least significant difference described the pattern of the intergroup changes. Univariate and multivariate Cox regression analyses were applied to evaluate the role of CMR parameters in revealing undesirable outcomes. For the definition of the cutoff point, specificity, and sensitivity of the predictor variables, the receiver operating characteristic (ROC) curve was utilized. Moreover, P-values below 0.1 for the univariate Cox regression analysis and 0.05 for the rest of the tests were considered statistically significant.SPSS version 22 (IBM incorporation) was utilized for statistical analysis. Categorical and continuous variables were reported as frequencies (percentages) and mean ± standard deviation (SD), respectively. The Kolmogorov–Smirnov test was utilized to assess the normality of distribution. Between-group comparisons were performed using the CMR examinations of 170 patients, consisting of 142 subjects with HCM  and 28 healthy subjects , were included. Interobserver variability was estimated to be 6.3% and the examiners’ consensus-resolved conflicts.2 ± 0.14, and the mean ± SD of MMI was 59.57 g/m2 ± 8.56 for the healthy subjects. No significant differences were observed in LVEF and end-diastolic and end-systolic volumes between the healthy population and the patients with HCM, whereas significant differences were noted between the 2 groups in LV MMI, LVGLS, LVGCS, and LVGRS .The mean ± SD of the body surface area was 1.87 mP > 0.05).The difference in mean strain values was significant between the healthy controls and the HCM group. However, the mean strain values were not different between the 2 LVOT gradient groups (Ps < 0.05). Between-group changes were evaluated by applying the post hoc least significant difference test, and the results are depicted in The 1-way ANOVA revealed a significant difference in all 3 strain parameters between the healthy controls and the HCM cases with normal and increased myocardial mass . Scatter plots are demonstrated in The Pearson correlation test revealed a moderate inverse linear correlation between MMI and LVGLS and LVGCS (The median (interquartile range) follow-up time was 25 months (23). Twenty-three patients developed adverse events. The results of the independent t-test analysis are depicted in P-values below 0.1, consisting of LVGLS, LVGCS, and the LGE percentage, were entered into the multivariate Cox regression. The results revealed that LVGCS was the single predictor of adverse events .The results of the Cox regression analyses are depicted in P = 0.001)  .A.The HCM and control groups were not statistically meaningfully different concerning LVEF and end-diastolic and end-systolic volumes, whereas the difference between them in all 3 global strain values and MMI constituted statistical significance.B.In the HCM group, the severity of LVOT obstruction did not influence strain measurements.C.LVGLS and LVGRS were impaired in the HCM group even if there was no increase in the myocardial mass. Along with an increase in the myocardial mass, a further decline in the LVGLS and LVGCS was detected.D.Two of the strain values, LVGLS and LVGCS, and the LV myocardial LGE percentage predicted adverse events, with LVGCS being the single robust predictor.E.An LVGCS value of 16.2% or less predicted adverse events with 77% sensitivity and 58% specificity.Our results supported the notion that despite an unimpaired systolic function, abnormal myocardial deformation is present even without significant myocardial fibrosis. A previous study proved that CMR-FT parameters were impaired even in the carriers of HCM without the overt disease (HCM is one of the prevalent causes of sudden cardiac death in young adults, hence the vital significance of its timely diagnosis and appropriate management strategy. In the present study, we investigated the CMR findings of 142 HCM patients with normal LV systolic function and a low myocardial fibrosis burden. Furthermore, we meticulously registered the follow-up data of the study population to determine whether CMR data could predict adverse events. Our principal findings are as follows: disease . TherefoMultiple factors may affect the measurement of strain values –22. AccoOur study is one of the first investigations to address the mechanical changes secondary to an abnormal MMI. Our selection of HCM patients without systolic dysfunction and with a low fibrosis burden enabled us to evaluate the net effect of the LV myocardial mass to a great extent. We found a decreased LVGLS and an increased LVGRS in our selected HCM patients with normal myocardial mass. On the other hand, when the myocardial mass increases, LVGCS decreases distinctly. We suppose that it could be due to increased myocyte disarrangement in enlarged myocardial mass, which especially results in LVGCS decline. These findings are in agreement with previous studies suggesting that myocardial disarray in patients with HCM is a limiting factor of myocardial compliance and contractile function . NeverthRemarkably, our results revealed a moderate inverse linear correlation between the net values of LVGLS and LVGCS and MMI. Strain values indicate function, especially in our selected population, who exhibited no decline in EF values. In a previous study, Dohy et al. showed that while there is no linear correlation between LVEF and MMI, LVGLS, as a functional parameter, correlated with MMI . TherefoPrevious studies have investigated the role of CMR parameters in indicating the outcome of patients with HCM –27. ParaIn the present study, we observed that patients with a positive family history were more likely to show an increased LVOT gradient. It is noteworthy that 60% of HCM patients with a positive family history have at least one of the eleven known sarcomere protein-encoding genes mutations. However, only 30% of HCM patients without positive family history have them . These gDespite its remarkable findings, the present investigation has some limitations. Firstly, the retrospective design of this study limited the data to available medical records and CMR images. Prospective studies with precise predefined clinical variables and CMR protocols may provide more reliable findings. For example, although the gold standard for LVOT gradient measurement is cardiac catheterization, we could not find the catheterization data in the medical records. Doppler echocardiography at rest and with provocative maneuvers were employed to estimate the highest LVOT gradient in our cases. However, previous studies' report of a good correlation between Doppler echocardiography estimations and cardiac catheterization results, convinced us to a great extent . AdditioCardiac MRI-derived strain measures are valuable in revealing subclinical functional alterations in HCM patients with unimpaired EF values and low fibrosis burdens. Furthermore, CMR-FT measures, distinctly LVGCS, are powerful predictors of the outcome in this patient population. It is noteworthy that the CMR-FT method can explain alterations in LV mechanics in different myocardial mass measures.


The right ventricle (RV) has a complex geometry and physiology which is distinct from the left. RV dysfunction and failure can be the aftermath of volume- and/or pressure-loading conditions, as well as myocardial and pericardial diseases.Echocardiography, magnetic resonance imaging and right heart catheterisation can assess RV function by using several qualitative and quantitative parameters. In pulmonary hypertension (PH) in particular, RV function can be impaired and is related to survival.An accurate assessment of RV function is crucial for the early diagnosis and management of these patients. This review focuses on the different modalities and indices used for the evaluation of RV function with an emphasis on PH. RV myocardial fibres are arranged circumferentially in the superficial and longitudinally in the deep layers leading to a contraction from inlet to outlet and from the free wall to the septum. RV contraction relies more on longitudinal shortening than twisting and rotational movements as in the LV [The right ventricle (RV) has a very distinct anatomy compared to the left (LV). It consists of 3 segments as follows: the inlet which includes the tricuspid valve (TV), the outlet or infundibulum with the pulmonary valve and a trabeculated apex . The RV n the LV , 5. Hencn the LV . This fen the LV .RV function should be examined along with pulmonary arterial (PA) function •. RV andPA load consists of two elements as follows: a steady and a pulsatile load. PVR is an expression of the steady load and pulmonary artery compliance (PAC) of the pulsatile load. PVR and PAC are inversely related . PAC is This review will focus on the assessment of RV function in pulmonary arterial hypertension (PAH) which is the archetypical example of a pressure-loaded RV. In PAH, the proliferative changes in the small pulmonary arteries may lead to a decrease in PAC and a subsequent increase in PVR. The RV adapts to the increased afterload by concentric hypertrophy which can raise its contractility 4 to 5-fold, and thus ‘RV-PA coupling’ will be maintained . HoweverRight heart failure (HF) is a syndrome characterised by alteration in structure and/or function of the RV-PA unit leading to suboptimal blood flow to the pulmonary circulation , 19. ItsEchocardiography is an established tool for the evaluation of cardiac structure and function and can be used for diagnosis, monitoring and treatment guidance. Its widespread availability, versatility and relative ease of use makes it a fundamental investigation. Its limitations include incomplete visualisation of all aspects of the RV, poor echogenicity in some subjects and a lower repeatability than cardiac MRI. In addition, loading conditions (e.g. high cardiac output status and significant TR), ventilatory failure and the use of inotropes or invasive ventilation may influence RV function and should be considered during its evaluation. Echocardiography can provide qualitative and quantitative assessment of RV function. 2D imaging, M-mode, Doppler, Tissue Doppler Imaging (TDI) and colour flow mapping are standard approaches, whilst strain and 3D echocardiography have garnered a significant evidence base for diagnosis and prognostication. Often no single parameter is sufficient, and a holistic approach  is requiThe complex geometry of the RV and its retrosternal position make its imaging challenging. In standard 2D imaging, the RV focused apical 4-chamber view (RVf4C) rather than the conventional 4-chamber view should be used as the standard tomographic plane to measure linear metrics of RV size and function , 24–26. 27Tricuspid annular systolic plane excursion (TAPSE) is defined as the displacement  of the lateral TV annulus during systole with M-mode echocardiography Fig. . It is sS′ is the peak systolic velocity of the lateral TV annulus Fig. . It is mRV FAC is evaluated in the RVf4C view. It requires manual tracings of RV endocardial area at end-systole and end-diastole Fig. . It shouas < 35% •, whereaas < 35% •.Strain is a dimensionless measure of myocardial deformation. RV longitudinal strain (RVLS) is the longitudinal shortening of fibres between the base and apex of the RV in systole and is expressed as a negative percentage . It is mOver the past decade improvements in 3D echocardiography (3DE) have led to its incorporation in the assessment of the left heart . This haThe myocardial performance index (MPI) has generally fallen out of favour for TAPSE, S′ and FAC but is still used in some institutions. It should be measured with PW-TDI on the lateral TV annulus. It is defined as the ratio of isovolumic time (contraction and relaxation) to ejection time and an abnormal value is > 0.55. It is load-dependent and invalid in high RA pressures , 23. Ass.TAPSE:PASP ratio has also been tested in pre-capillary PH where it correlated with haemodynamics and was an independent predictor of survival [This ratio was first proposed and evaluated as a surrogate of RV-PA coupling in a series of patients with HF and showed a prognostic role independent of the severity of LV dysfunction –79. .TAPsurvival , 81. TAPsurvival . Consequsurvival • and hassurvival . Its limA recent study has highlighted an independent prognostic role for the baseline RV free wall longitudinal strain RVFWLS:PASP ratio in treatment-naive patients with precapillary PH . A preliAll of the metrics described above can be evaluated at rest and after peak stress (exercise or with dobutamine). Most of the data so far have been derived from healthy volunteers, but there are several small to medium-sized studies which have evaluated the prognostic role of RV contractile reserve in patients with PH, valve disease and HF .In PH, RV failure is the main determinant of death , 88. MRIFour-dimensional flow (4D) flow is an MRI technology that overcomes limitations of traditional 2D flow imaging in the evaluation of PH. Unlike conventional imaging, 4D flow provides a 3D visualisation of vascular flow and enables accurate assessment of vessel, transvalvular or intra-cavity flow, providing a more comprehensive description of complex flow changes in the pulmonary circulation. In the context of PH, 4D flow has been utilised to identify abnormal flow patterns in the main PA , 111, whThe quantification of myocardial deformation strain is an established MRI technique . One metLate gadolinium enhancement (LGE) is an MRI technique that uses gadolinium’s paramagnetic properties to identify areas of myocardial fibrosis . LGE is Native myocardial T1 mapping is a pixel-by-pixel representation of the longitudinal relaxation times within a tissue, providing surrogate tissue characterisation data that are measured on a standardized scale –129. T1 A major strength of MRI is its high repeatability with a great value in the assessment of cardiac changes in response to PAH therapy . The 202Direct measurement of four pulmonary haemodynamic parameters — RA pressure (RAP), PAP, PA wedge pressure (PAWP) and cardiac output (CO) — via right heart catheterisation (RHC) allows assessment of RV preload, afterload, function and PAC Table . RHC witRAP reflects central venous pressure but can also be increased in severe TR and impaired RV and RA compliance . In the 2 = oxygen consumption; Ca = arterial oxygen content = systemic oxygen saturation  × haemoglobin (g/dL) × 1.34/100 and Cv = mixed venous oxygen content = mixed venous saturation  × haemoglobin (g/dL) × 1.34/100. The DF method is recognised as the gold-standard method but relies on direct measurement of VO2 which requires specialised equipment in the catheter suite which is not widely available. The TD method has been shown to be a reliable method of measuring CO when compared with DF, even in patients with TR or low outputs [CO may be assessed via RHC by thermodilution (TD), the direct Fick (DF) or indirect Fick (IF) technique •. TD inv outputs , 159. Th outputs •.HR). SV indexed for body surface area (RVSWI = 0.0136 × SVi × (mPAP-RAP)), which aims to reflect effective work performed by the RV in every cardiac cycle but has limited supportive data in PAH [PADP is PA diastolic pressure, relates the ability of the RV to produce SV to its filling pressure and has been shown to be strongly predictive of survival in patients with advanced HF, but its role in PAH is less clear [RV SV can simply be calculated by dividing CO by heart rate  can therefore be described as the ratio between  failure . Interes failure .PVR, which accounts for ≈75% of RV afterload, is calculated using the equation uivalent •. Large uivalent •.PP is pulse pressure i.e. PASP-PADP [PAC leads to greater pulse wave reflection during systole which results in higher PASP requirements and hence higher RV energy requirements to create the same ejection.PAC may be calculated using the 2-element Windkessel model; however, the simplest way of estimating it is by using the equation ASP-PADP , 170. InPVR and PAC (the resistance-compliance or RC time) represents the diastolic decay constant of PAP and in most conditions is constant, suggesting that most of both resistance and compliance occurs in the more distal vasculature [The relationship between culature .A systematic evaluation of RV size and function requires the use of several parameters derived from different invasive and non-invasive modalities. 2DE and 3DE as well as speckle tracking can provide a quantitative assessment of RV systolic performance. MRI-derived RVEF remains the gold-standard metric of RV global function and can be used in a serial manner to assess response to treatment and disease progression in PH. RHC is not only the gold-standard method for the diagnosis of PH, but it can also estimate CO, RV contractility and RV-PA coupling. It is imperative for the clinician to know the strengths and weaknesses of its test and use them in a complementary fashion accordingly (Fig.


Accurate determination of intravascular volume status is challenging in acutely ill patients. Favorable patient outcome is vital to correctly identify intravascular volume depletion and avoid systemic venous congestion. Most of the conventional means of hemodynamic monitoring in the acute healthcare setting are geared toward addressing the cardiac output and maintaining an optimum mean arterial pressure. While assessing and maintaining cardiac output in an acutely ill patient is very important, a venous congestion cascade is often overlooked, which can negatively affect the intraabdominal end organs. The prospect of using point-of-care ultrasound (POCUS) to determine systemic venous congestion could be a potentially handy tool for clinicians. Venous excess ultrasound score (VExUS) has also been utilized by clinicians as a semi-quantitative assessment tool to assess fluid status. This review aims to discuss the potential role of POCUS and VExUS scores in determining systemic venous congestion through a narrative review of recently published literature. The current focus in managing critically ill patients relies on maintaining mean arterial pressure, thereby addressing cardiac output and systemic vascular resistance. Clinicians have challenges in accurately assessing and managing systemic venous congestion to avoid its deleterious effects on vital organ perfusion. Optimal fluid management is vital for acutely ill patients to avoid the negative effects of both insufficient and aggressive fluid therapy Figure  1]..1].Some of the current tools that help measure the intravascular volume include laboratory parameters such as brain natriuretic peptide (BNP), chest imaging, pre-load assessment with inferior vena cava (IVC) diameter, and central venous pressure (CVP), among others. However, several clinical factors might influence these measures and lead to inaccurate assessment of systemic venous congestion.With rapidly growing interest in point-of-care ultrasound (POCUS), acute care providers have been leaning towards bedside parameters of hemodynamic assessment and fluid responsiveness. Venous excess ultrasound score (VExUS) has also been utilized by clinicians as a semi-quantitative assessment tool to assess the fluid status and mainly predict acute kidney injury (AKI) in acutely ill patients due to cardiac causes. Current literature regarding POCUS parameters and systemic venous congestion assessment is still a relatively new field. We aim to revisit the concept of systemic venous congestion, mention conventionally used parameters for intravascular volume assessment, and discuss the potential role of POCUS and VExUS scores in determining systemic venous congestion.Systemic venous congestionMaintaining a stable cardiac output is essential for organ perfusion, achieved through the interplay of mean arterial pressure and peripheral venous resistance. The venous structure is a reservoir accommodating approximately two-thirds of blood volume at rest . The cliImportance of understanding venous congestionVenous congestion decreases arteriovenous gradient, ultimately affecting organ perfusion ,7. A dysCurrently available indices for volume assessment and their limitationsClinicians have traditionally depended on physiological parameters such as heart rate and blood pressure for volume assessment, but these parameters have been proven to be unreliable for guiding fluid replacement therapy ..34].Literature reviewTo find the appropriate article on the use of POCUS for detecting systemic venous congestion, we conducted a thorough search on PubMed, Google Scholar, and the Cochrane database. Our keyword search terms were "(systemic venous congestion) AND (point of care ultrasound OR venous excess ultrasound)." Table Beaubien-Souligny et al.  conducteA case study by Singh et al.  describeTorres-Arrese et al.  conducteUpon admission, during discharge, and for 90 days of follow-up, ultrasounds were conducted to assess multiple organs, including the lungs, IVC, and various veins such as hepatic, portal, intra-renal, and femoral, using pulsed-wave Doppler technology. The experts used the VExUS to determine a score for systemic congestion based on the dilatation of the IVC and the pulsed-wave Doppler morphology of the hepatic, portal, and intra-renal veins. The results of specific tests, such as the intra-renal monophasic pattern, as well as a portal pulsatility greater than 50% and a VExUS score of 3 indicating severe congestion, can predict the likelihood of death during hospitalization. During a follow-up visit, it was found that an IVC measurement above 2 cm and a monophasic pattern in the kidney were strong indicators of potential re-admission related to AHF. Based on the information provided, it can be concluded that having a VExUS score of 3 upon admission may indicate a higher likelihood of death during admission, death related to heart failure, and early re-admission. However, this finding is similar to other ultrasound evaluations that are easier to perform. As this is a pilot study, it is imperative to note that only four expert sonographers were chosen to conduct the examination, which may limit the reproducibility of the findings. Nevertheless, it is clear that ultrasound imaging is an essential tool for predicting mortality and hospital re-admission in AHF patients by detecting systemic venous congestion.Bhardwaj et al.  conducteTwelve patients with ADHF were included in a case series by Argaiz et al. . EligiblA group of patients who underwent outpatient and inpatient right heart catheterization were examined with VExUS right before the catheterization procedure . InternaFuture research directionsStudies have shown that POCUS may be useful in assessing systemic venous congestion, but further research is needed to fully explore its potential. To improve early recognition and intervention, we recommend investigating the sensitivity and specificity of POCUS in detecting subtle changes that indicate early systemic venous congestion. These changes include variations in CVP, hepatic vein flow patterns, and renal venous Doppler indices. By conducting such research, we can potentially prevent disease progression and reduce morbidity and mortality. Incorporating POCUS with artificial intelligence algorithms could potentially enhance diagnostic precision, simplify workflow, and facilitate remote monitoring of patients suffering from systemic venous congestion, particularly in areas with limited resources. One way to track the progression or resolution of systemic venous congestion over time is through serial POCUS examinations. Conducting longitudinal studies can provide valuable information about the natural history of the condition, as well as how patients respond to treatment and potential indicators of clinical deterioration.Identifying the volume status of critically ill patients through systemic venous congestion is crucial, yet this approach is unfortunately underutilized. POCUS is a useful and versatile tool for evaluating systemic venous congestion. It provides non-invasive, real-time imaging that helps clinicians make prompt and accurate decisions. The evidence presented in this review supports the use of POCUS in the early detection of systemic venous congestion. Clinicians can use POCUS to identify signs of venous congestion before they become clinically apparent by evaluating parameters such as CVP, hepatic vein flow patterns, and renal venous Doppler indices. Early recognition of conditions is crucial to prevent disease progression and complications. POCUS has shown promise in evaluating systemic venous congestion, but additional research is imperative. Prospective studies must investigate the impact of POCUS on patient outcomes, and there must be an effort to standardize POCUS training and establish best practices.


To investigate whether left atrial (LA) volume and left ventricular filling pressure (LVFP) assessed by cardiovascular magnetic resonance (CMR) change during adenosine delivered myocardial hyperaemia as part of a first-pass stress perfusion study.P = 0.0002), in males only  and females only . The right atrial end ventricular systolic volume increased less significantly from baseline . CMR-derived LVFP  increased significantly at the peak hyperaemic state in all , females only  and males only  cohorts.We enrolled 33 patients who had stress CMR. These patients had a baseline four-chamber cine and stress four-chamber cine, which was done at peak myocardial hyperaemic state after administering adenosine. The left and right atria were segmented in the end ventricular diastolic and systolic phases. Short-axis cine stack was segmented for ventricular functional assessment. At peak hyperaemic state, left atrial end ventricular systolic volume just before mitral valve opening increased significantly from baseline in all (91 ± 35ml vs. 81 ± 33ml, Left atrial volume assessment by CMR can measure acute and dynamic changes in preloading conditions on the left ventricle. During adenosine administered first-pass perfusion CMR, left atrial volume and LVFP rise significantly. Left atrial (LA) assessment has an established role in assessing left ventricular diastolic function. The LA modulates left ventricular filling and cardiac performance through its role as a reservoir, conduit and booster pump . CardiovHowever, it remains unclear whether LA volumes change acutely due to variations in pre- and after-loading conditions on the ventricle. It is crucial to evaluate the temporal dynamicity of LA adaptability and how it can influence the left ventricular filling pressure. For example, if the pre-loading conditions increased acutely, would the LA volume respond accordingly and vice versa.Adenosine is a naturally occurring nucleoside that can affect the left ventricular diastolic function. This effect of adenosine on left ventricular diastolic function has been investigated in several studies –12. In sWe hypothesise that LA volume changes acutely in response to dynamic changes in loading conditions on the ventricle. Hence, the main objective of this study was to understand better how LA volume changes acutely and what impact it has on left ventricular filling pressure during adenosine-administered first-pass perfusion. For this study, we used CMR data previously described .2 and any contraindication to CMR. We also excluded any patient who did not have a proper four-chamber acquisition which could limit LA assessment. Because of this, 11 patients were excluded from the analysis.The study population has been previously described . This waAll patients had CMR imaging on a 1.5T MRI system  equipped with dStream technology. A dedicated 28-channel cardiac phased array receiver coil was used. CMR imaging was performed using standard protocols , 15.1 min − 1 for at least 4 min and finally, late gadolinium enhancement imaging for scar assessment. First-pass perfusion imaging was immediately followed by the acquisition of a repeat 4-chamber cine for which all parameters were similar to the resting pre-stress 4-chamber view while adenosine was still being infused. The CMR protocol is described in more detail in Fig. The CMR protocol included balanced steady-state free precession (bSSFP) baseline cines  with 30 phases throughout the cardiac cycle, first-past perfusion post adenosine intravenous infusion administration at a dose of 140 µg kg − All CMR analysis was performed using commercially available software Circle CVI42 version 5.1 . Left ventricular volumes and ejection fraction (EF) were analysed from short-axis cine images using standard methods. The presence of any scar or a significant perfusion defect (> 10% coverage of the left ventricle) was recorded by an expert with > 10 years of experience in CMR. These variables were treated as dichotomous variables.For the four-chamber atrial volume analysis, the artificial intelligence module of CVI42 was used. Where necessary, further manual corrections were made. Figure Recently, a model to estimate LVFP using CMR-obtained left ventricular mass (LVM) and left atrial volume (LAV) has been developed . This moCMR-derived LVFP = 6.1352 + (0.07204 x LAV) + (0.02256 x LVM).Where LVFP is left ventricular filling pressure, LAV is left atrial volume in end-ventricular systole, and LVM is left ventricular mass in end-diastole.max) and minimal volume (Vmin) as follows:Both atrial ejection fractions were defined from the maximal volume (Vmax − LAVmin)/LAVmax × 100.left atrial ejection fraction (LAEF) = (LAVmax – RAVmin)/RAVmax × 100.right atrial ejection fraction (RAEF) = . Continuous variables are presented as mean ± standard deviation or median with interquartile range, as appropriate. Comparisons between rest and stress volumes were performed using paired t-test for normally distributed data or a Wilcoxon signed-rank test for non-parametric data. Categorical variables are summarised by frequency (percentage). Association between continuous variables was quantified using Pearson’s correlation. The two-sided significance level was set at 5%.Statistical analysis was performed using MedCalc® Statistical Software version 20.110  had a history of myocardial infarction. The demographic data for all 33 patients are detailed in Table The average left ventricular ejection fraction was 63 ± 13%, and 14 patients (42%) had significant perfusion defects suggestive of myocardial ischaemia. In addition, 19 patients (58%) had a ventricular scar due to ischaemic aetiology. The CMR characteristics are summarised in Table P = 0.21), hypertension (P = 0.21), diabetes mellitus (P = 0.29), dyslipidaemia (P = 0.29), previous myocardial infarction (P = 0.07), previous coronary artery bypass graft procedure (P = 0.92) and having an abnormal electrocardiogram (P = 0.93).Age (62.6 ± 12 years vs. 64 ± 15 years) differed non-significantly between males and females. No statistical differences were observed between males and females in comorbidities including current smokers , LVM , global longitudinal strain (GLS)  and a significantly lower LV end-systolic volume (ESV)  and myocardial early diastolic velocity (E’)  than females. However, no significant changes were observed between the two groups in presence of infarction (P = 0.09), perfusion defects (P = 0.16), LV stroke volume (SV) (P = 0.11), LV ejection fraction (EF) (P = 0.22), myocardial late diastolic velocity (A’) (P = 0.11) and absolute change in left atrial volume pre and post stress perfusion (LAC) (P = 0.69).Males had a significantly higher LV end-diastolic volume (EDV) (151 ± 37ml/mP = 0.0002), in males only  and females only .Moreover, left atrial ejection fraction was higher at peak hyperaemic state in all (57 ± 12%) than at rest state (53 ± 11%) (P = 0.02). However, there were no significant differences between peak hyperemic and rest states in males only  and females only  groups. No significant differences were found between left atrial end ventricular diastolic volume at rest and peak hyperaemic state . Similar findings were seen in males only (P = 0.80) and females only (P = 0.29) cohorts. .At peak hyperaemic state, left atrial end ventricular systolic volume just before mitral valve opening increased significantly from baseline in all  and females only group . However, no significant changes were observed in males only group (P = 0.14). There were no significant changes observed between peak hyperaemic and rest states when measuring right atrial end ventricular diastolic volume and right atrial ejection fraction  and  respectively .The right atrial end ventricular systolic volume increased significantly from baseline in all , females only  and males only  .CMR-derived LVFP  increased significantly at peak hyperemic state in all  and left ventricular mass are associated with PCWP measured invasively on the same day , 8. UsinIt is well established that continuous intravenous infusion of adenosine results in sinus tachycardia and coronary-/peripheral- vasodilatation . ImportaMoreover, Nussbacher et al.  also notOur study has some limitations. Firstly, left atrial volume assessment was predominantly done in patients with possible ischaemic heart disease. Hence, our results cannot be applied entirely to patients with heart failure. Importantly, in advanced heart failure, where the left atrium has significantly adversely remodelled, it remains uncertain if LA volume changes at all due to changes in loading conditions on the ventricle. Secondly, this study did not recruit hemodynamically unstable patients, further introducing selection bias. Moreover, we did not have echocardiographic findings recorded in the study to demonstrate clinical translation between CMR and echocardiography. Finally, this study was not powered to evaluate changes in LA volume in patients with or without perfusion defect or even the presence of an ischemic scar on late gadolinium enhancement imaging.Left atrial volume assessment by CMR can measure acute and dynamic changes in preloading conditions on the left ventricle. During adenosine administered first-pass perfusion CMR, left atrial volume and LVFP rise significantly. Further studies are required to assess whether this can be incremental for diagnosis and prognosis.


P < 0.001) and GWI  were lower in upright posture. Longitudinal strain was most frequently reduced in upright posture in the mid-basal inferior, and/or posterolateral segments. Upright posture has a significant impact on LV deformation with lower GLS, GWI and regional LV strain in upright position. These findings need to be considered when performing echocardiography in athletes.Besides LV ejection fraction (LVEF), global longitudinal strain (GLS) and global myocardial work index (GWI) are increasingly important for the echocardiographic assessment of left ventricular (LV) function in athletes. Since exercise testing is frequently performed on a treadmill, we investigated the impact of upright posture on GLS and GWI. In 50 male athletes (mean age 25.7 ± 7.3 years) transthoracic echocardiography (TTE) and simultaneous blood pressure measurements were performed in upright and left lateral position. LVEF  was not affected by athletes’ position, whereas GLS (− 11.9 ± 2.3% vs. − 18.1 ± 2.1%;  To prevent life-threatening events (e.g. sudden cardiac death) in competitive athletes with unknown cardiovascular disease, transthoracic echocardiography (TTE) is recommended by major sport associations .Although left ventricular (LV) ejection fraction (LVEF) is mainly used to characterize LV systolic function, LV global longitudinal strain (GLS) has shown to be more sensitive in the detection of subclinical LV dysfunction than LVEF , , , –5. FurthWhile GLS is dependent on pre- and afterload conditions , global TTE at rest is usually performed in left lateral position. In competitive athletes it is not uncommon that exercise testing is performed in upright posture—especially when testing on a treadmill . While tThe objective of this study was to analyze the impact of upright posture on echocardiographic parameters of LV deformation in healthy athletes. We hypothesized that upright posture has no significant impact on LV deformation.073/18-ek).In this study 50 male athletes who underwent TTE during pre-participation screening at the University Hospital Leipzig between March 2018 and August 2021, were included. All athletes were practicing sports at a competitive level with more than 20 h of training per week. They were examined in upright posture and left lateral position and provided informed consent after full explanation of the purpose and order of all procedures . All examinations were documented by a board certified cardiologist. Data sets were analyzed by post-processing analyses using the EchoPac software . Systolic and diastolic blood pressure was measured in all patients after five minutes resting in upright position and in left lateral position.LVOT) was determined in the parasternal long axis view in the left lateral position. Relative wall thickness (RWT) was calculated by twice of the LV posterior wall diameter (LVPWD) divided by LV end-diastolic diameter (LVEDD) measured by anatomical M-Mode in parasternal short axis views verified by biplane scanning. LV longitudinal axis diameter (LVLD) was assessed in the apical long axis view by measuring the distance from the apex to the center of the closed mitral valve at end-diastole. LV mass (LVM) was calculated by the Deveraux formula and was indexed to the body surface area (LVMi). Normal ranges of LVMi were defined < 115 g/m2  [The left ventricular outflow tract diameter (DLVOT) was measured by pulsed waved (PW-) Doppler in the apical long axis view with the sample volume exactly at DLVOT measurement position. LV stroke volume (SVDoppler) was calculated by the cross-sectional area of the LVOT multiplicated by VTILVOT. The LVEF, LV end-diastolic (LVEDV) and end-systolic (LVESV) volumes and LVSVbiplane were assessed by LV biplane planimetry by the modified Simpson’s rule in the apical 2- and 4-chamber view [The LVOT velocity time integral  according to current recommendations . The begP value < 0.05 was considered statistically significant.All statistical analyses were performed using SPSS Statistics version 28.0 . Normal distribution was tested using Kolmogorov–Smirnov. Continuous variables were expressed as mean value ± standard deviation (SD) and were compared between groups using Student’s t-test. All categorical variables were expressed as numbers with their percentages (%) and compared using chi-squared or Fisher exact test, as appropriate. Linear regression and Pearson’s r were applied to evaluate association between two linear variables. Data comparisons between more than two groups were performed by one-way Analysis of Variance (ANOVA). A Kappa coefficient (κ) was used to assess intra- and interobserver variabilities in 20 patients under the same conditions. The second investigator was unaware of the results of the first examination.P = 0.104) and diastolic blood pressure values  did not differ in upright posture compared to left lateral position. The heart rate was higher in upright posture compared to left lateral position . Further demographic data are presented in Table In 50 male athletes (25.7 ± 7.3 years) systolic , RWT was higher in upright posture compared to left lateral position . LVLD, LVEDD and LVESD were lower in upright posture compared to left lateral position  and LVSVbiplane  decreased in upright compared to left lateral position.Whereas LVMi was not affected by position changing  as well as in left lateral position . Interobserver variability between two investigators showed equally good agreement for GLS in upright posture  as well as in left lateral position . Intra- and interobserver variabilities for the remaining conventional echocardiographic measurements consistently showed good agreement as well.Intraobserver variability showed high agreement for GLS in upright posture  smaller LV volumes and shorter longitudinal LV axis, (2) significantly reduced GLS—mainly due to regional deformation differences in the basal inferior and posterolateral LV segments, and (3) lower GWI in upright position.Changes of LV volumes in relation to body position have been reported by Nixon et al. observing a decrease of 30–45% of LVSV as well as an increase of 25–45% in heart rate in healthy young men after mobilization from supine to upright position . UprightLVOT increased according in this group. The longitudinal strain increased by 19%, but the increase in GLS was also shown in the group with negative PLR [The dependence of LV function - intrinsic contractility and relaxation - on pre- and afterload is an accepted physiological concept . Nafati tive PLR . This untive PLR . Moreovetive PLR . Meanwhitive PLR . At restChanges of LV wall motion in the mid-basal inferior and/or posterolateral segments in upright posture, have already been described by Sasaki et al. in a cohort of healthy volunteers . The autLongitudinal strain and work index have been advocated as more reliable methods in the assessment of LV function and are able to detect subtle abnormalities. GWI is derived and incorporates afterload information adjusting the strain results to a noninvasive measurement of LV pressure. From the physiological point of view, the pressure–volume–area predicts myocardial oxygen consumption and provides a tool to describe coupling of LV mechanical performance to energy use . More reIn conclusion both GLS and GWI are significantly preload dependent. When considering using those parameters in the assessment of LV function, the body position of the patient needs to be taking into consideration. Unfortunately, probably the most reports on normal values are derived in left lateral position. Therefore, there is an urgent need for normal values depending on the body position.In this study, only young and healthy athletes were included. Only TTE examinations of athletes with optimal imaging quality were included, athletes with poor imaging were excluded. Thus, the results are not directly transferable on patients with cardiovascular diseases.Upright posture has a significant impact on LV deformation. The reduction of regional longitudinal strain in the inferior and/or posterolateral LV segments are presumably explained by different LV filling conditions based on orthostasis and cardiac interaction with the diaphragm. A reduction of regional strain at rest in upright posture is not necessarily pathological but has a significant impact on investigating athletes, especially in case of treadmill testing.