In critical patients, left ventricular ejection fraction and fractional shortening are used to reflect left ventricular systolic function. An emerging technique, two-dimensional-strain echocardiography, allows assessment of the left ventricle systolic longitudinal deformation  and the speed at which this deformation occurs (systolic strain rate). This technique is of increasing use in critical patients in intensive care units and in the peri-operative period where preload constantly varies. Our objective, in this prospective single-center observational study, was to evaluate the effect of fluid resuscitation on two-dimensional-strain echocardiography measurements in preload-dependent critically ill patients. We included 49 patients with preload dependence attested by an increase of at least 10% in the left ventricular outflow track velocity–time integral measured by echocardiography during a passive leg raising maneuver. Echocardiography was performed before fluid resuscitation (echocardiography 1) and after preload independency achievement (echocardiography 2).p < 0.01) and − 1.11 s−1 ± 0.29 to − 1.55 s−1 ± 0.55 (p < 0.001). The fluid resuscitation affects GLS and SSR in preload-dependent patients, with a shift, for GLS, from pathological to normal values.Two-dimensional-strain echocardiography was feasible in 40 (82%) among the 49 patients. With preload dependence correction, the absolute value of global longitudinal strain and systolic strain rate was significantly increased from, respectively, − 13.3 ± 3.5 to − 18.4% ± 4.5 (In critically ill patients, the assessment of the systolic function by two-dimensional-strain echocardiography needs prior evaluation of preload dependency, in order to adequately interpret this variable. Future studies should assess the ability of global longitudinal strain to guide fluid management in the critically ill patients. Systolic function assessment is crucial in the management of the critically ill patient. Using conventional echocardiography, left ventricular ejection fraction (LV EF) and fractional shortening are routinely used . HoweverStrain echocardiography (2D-strain) is a noninvasive ultrasound imaging technique that allows for an objective and quantitative evaluation of myocardial function. It measures the percentage of deformation of the left ventricle (LV) during systole (systolic strain) and the speed at which this deformation occurs (strain rate) , 5. ThisEmax) and intraventricular pressure–volume curves in a rat model. In cardiology patients undergoing routine coronary angiography, fluid resuscitation did not affect GLS and systolic strain rate (SSR) [In critically ill patients, 2D-strain allows early diagnosis of cardiac injuries that are non-detectable with conventional examinations , 11. Prete (SSR) . Other ste (SSR) , 18 in nte (SSR) , 20. Onete (SSR) . If for te (SSR) , 23. TheOur study was a prospective observational study carried out in a single 12-bed polyvalent ICU at the University Hospital La Timone in Marseille, from August to December 2016. The protocol was approved by the Ethics Committee of the French Society of Anesthesiology and Intensive Care (IRB 00010254-2016-078) on August 18, 2016. Data collection was authorized by the CNIL . Exclusion criteria were: patient under 18 years of age, absence of normal sinus rhythm, patient and/or person of trust’s refusal to participate in the study.We included all patients with preload dependence. Patients in acute circulatory failure were also included, if they were preload dependent. First, preload dependency was suspected according to at least one of the following criteria: hypotension or/and oligo-anuria or/and difficulty in weaning of catecholamine. Second, preload dependence was confirmed by an increase of at least 10% of the left ventricular outflow track velocity–time integral (Δ LVOT VTI ≥ 10%) measured by echocardiography during a passive leg raising (PLR) . If prelAcute circulatory failure was defined as mean arterial pressure < 65 mmHg, urine output < 0.5 ml/kg/h, mottled skin or arterial blood lactate > 2 mmol/L .The features , the cardiovascular comorbidities, SAPS II, SOFA and the arterial lactate levels were recorded for each patient included in the study. The arterial pressures  and heart rate were recorded before and after each fluid resuscitation. Mortality at 28 days was recorded by consulting the electronic patient files.Once the preload dependence was confirmed, two echocardiography studies were performed, the first one before fluid resuscitation (echocardiography 1) and the second one after, when the patient was no longer preload dependent (echocardiography 2). Both were performed by an expert certified physician (CN) and using a Philips CX 50 Compact Xtreme Ultrasound System  and a 3.5-Hz probe. Conventional and 2D-strain echocardiography was used in each study.M)-mode to determine the right ventricle size, interventricular septal wall thickness, left ventricle size, ratio of right ventricle/left ventricle and the diameter of the LV outflow tract. The tricuspid annular plane systolic excursion (TAPSE) was measured from an apical 4-chamber view with M-mode. We visually verified using an apical 4-chamber view that the RV/LV ratio was < 1. The LVOT VTI was measured using pulse-wave Doppler from an apical 5-chamber view. Mitral flow was assessed using an apical 4-chamber view with pulse-wave Doppler allowing measurement of the E- and A-wave velocities, the E/A ratio and the E-wave deceleration time.The conventional evaluation was performed following the American Society of Echocardiography Recommendations . The bi-E′ waves was measured , and E′median , E/E′lateral, E/E′medial and E/E′median ratios were calculated. The ejection fraction was measured using the Simpson’s biplane method in a 4- and 2-chamber view. All recorded values were averaged using three measurements.Using tissue Doppler imaging from an apical 4-chamber view, the velocity of the septal and lateral mitral annulus −1 [With regard to the 2D-strain, a 2-s loop was recorded in DICOM format for each view with a frame rate above 50/s. The analysis and measures of strain and strain rate were performed off-line using the QLAB Philips software  by a level 3  operator−1 .r2 were used to compare the distribution of variables. In univariate analysis, factors were considered significant when p < 0.05. We calculated that at least 38 patients would need to be enrolled to detect a 4% increase in GLS after fluid expansion with a 90% statistical power and a two-sided alpha value of 0.05. In order to exclude the patients in whom cardiac ultrasound was not technically feasible, we decided to include 49 patients. The correlation between the global longitudinal strain and the 4-chamber strain was performed using Spearman’s method. From all patients, intraoperator variability of GLS was determined by the intraclass correlation coefficient.All analyses were performed using R-Project for Statistical Computing 2.14 . Categorical variables were expressed as numbers and percentages (%). Continuous variables were expressed as mean ± SD or median and interquartile range (25th–75th) depending on their distribution. The Kruskal–Wallis test, the Fisher exact test and the ANOVA test Forty-nine patients were included over the period of August–December 2016.The patients’ clinical characteristics are presented in Table Data are shown in Table Crystalloid, albumin or both were administered to 25 (51%) patients, 15 (30%) patients and 9 (19%) patients, respectively. The volume of crystalloid and albumin was 960 ± 310 and 256 ± 51 mL, respectively.There was a significant increase in systolic arterial pressure (SAP), diastolic arterial pressure (DAP) and mean arterial pressure (MAP) after fluid resuscitation. There was also a nonsignificant decrease in heart rate (HR).p < 0.01). After fluid resuscitation (p < 0.01), cardiac index increased from 2.4 ± 0.9 to 3.1 ± 1.2 L/min/m2 (p < 0.01) . We did not find a significant change in the LV EF after fluid resuscitation. In our study, no patients had right heart failure.Out of the 49 preload-dependent patients, 48 patients increased their cardiac output after fluid resuscitation by at least 15%. The LVOT VTI increased from 15.6 cm ± 3.7 to 21.1 cm ± 4.5 before and after fluid resuscitation (E-wave significantly increased from 73 ± 23 to 91 ± 27 cm/s (p < 0.01). E/E′lateral, E/Emedial and E/Emedian increased from 5.4 ± 1.9 to 6.7 ± 2.4 (p < 0 0.01), 5.8 ± 2 to 7.3 ± 2.4 (p < 0.01) and 5.5 ± 1.9 to 6.9 ± 2.3 (p < 0.01).After fluid resuscitation, p < 0.01) . The GLS and the 4-chamber view strain values had good correlation  .After fluid resuscitation, the absolute value of GLS significantly changed from − 13.3% ± 3.5 to − 18.4% ± 4.5 (p < 0.001).The intraclass correlation coefficient of the intraoperator variability of GLS was 0.92 . The patients being in the preload-dependent zone are on the steep portion of the Franck–Starling curve. The preload increase then leads to an increase in the contraction force and velocity, as shown by Sonnenblick et al. in an experimental study in 1962 [Recently, Boissier et al.  showed t in 1962 . This do−1). We explain this by the fact that not only is SSR influenced by preload, but it is also influenced by the heart rate. These results are aligned with those of Fredholm et al., who found in their study that the SSR is both preload and pace dependent. We believe that the SSR staying in a physiologic zone is due to the tachycardia provoked by the hypovolemia (HR: 103 ± 20 in our study). This is, in our opinion, a physiologically adaptive mechanism to maintain a certain intrinsic contractility in hypovolemic patients. This phenomenon is known as the force–frequency relationship [More specifically for the SSR, in our study, there was a significant increase with preload correction; however, in contrast with the GLS, its value in hypovolemic patients is not pathological  which leads to an LV EF increase tending toward 100% (LV EF = LVEDV − LVESV/LVEDV × 100). Thus, in our hypovolemic patients, the LV EF is mathematically elevated. Furthermore, we had a high proportion of septic shock patients in our population (32%), and because of the vasoplegia intrinsic to this pathology, there were numerous hyperkinetic patients with a LV EF > 60%. Boissier et al. found, in their cohort of septic shock patients, 103 patients with normal or hyperkinetic LV EF out of 130 [L − Lo/Lo  refers to deformation of myocardial fibers, whereas LV EF refers to volumes and is therefore also dependent on ventriculo-arterial coupling [We did not find a significant increase in LV EF after preload correction, whereas we did find a significant increase in LVEDV and GLS. We explain this because the LV EF and GLS are not comparable. The GLS formula coupling . ConsequBased on our study, the influence of preload on the strain values measured is critical to consider. Indeed, for preload-dependent patients, a low absolute value of GLS can lead to erroneous diagnoses of systolic dysfunction. As compared with previous studies evaluating strain in septic shock, our study sheds a new light on this technology –37. PathIn line with our previous study , the sucOur study has several limitations of which we are aware. It is a single-center study. A single operator performed all of the measurements. Therefore, we could not assess the interoperator variability. Our resuscitation protocol left the choice of fluid solution to the prescribing physician. The albumin was administered over 30 min and the crystalloid over 60 min. These are indeed longer durations than recommended. Future studies should consider the association of this value and GLS.Our study showed that GLS was influenced by fluid resuscitation in preload-dependent patients. Interestingly, values shifted from pathological to normal after fluid resuscitation. In the critically ill patients, the assessment of systolic function by 2D-strain needs prior evaluation of preload dependency, in order to adequately interpret this variable. GLS variations after an increase in venous return could be a marker of the patient position in the Frank–Starling curve. Future studies evaluating the interest of GLS for guiding fluid resuscitation are required.


To investigate the association between the coaptation height of mitral valve and mitral regurgitation after mitral valve repair.From Sep 2014 to Jun 2015, 20 patients underwent mitral valve valvuloplasty for mitral regurgitation were included. Ring annuloplasty was performed in all cases. Mitral valve short-axis dimension (MVd), coaptation height (CH), Left ventricular ejection fraction (LVEF) were measured by the transesophageal echocardiography before the operation in operation room and 3 months and 12 months after the operation by the transthoracic echocardiography. A degree from 0 to 4 was used to measure the degree of mitral regurgitation.p < 0.05). MVd and LVEF were not significantly changed after mitral valve repair. Furthermore, CH after resuscitation have a statistically significant negative correlation with the degree of mitral regurgitation 12 months after operation.There were 14 patients with 0, 3 patients with 1, 3 patients with 2 of mitral regurgitation 12 months after the operation. CH (3.53 ± 1.91 mm) increased significantly at 3 months (5.05 ± 1.09 mm) and 12 months after operation (5.22 ± 1.15 mm) (The mitral valve repair with mitral valve ring induce the morphologic change of the mitral valve structure. The increase of CH after mitral valve repair may be one of the main factors in regulation of mitral regurgitation. Mitral valve repair is a surgical procedure that has continuously developed through decades. Since 1968, Carpentier has developed the concept of prosthetic ring annuloplasty which aimed to restore the shape of the deformed annulus fibrosus of the MV , 3. NowaDoppler echocardiography was used to detect the functional information of transvalvular flow velocity, which could be used to measure the pressure gradient across valve and regurgitant flow . Mitral Therefore, in this study we used above methods to investigated whether it is possible to measure the degree of mitral regurgitation by measuring the mitral coaptation height. Accordingly, the present study aimed to evaluate the correlation between the height of mitral valve coaptation and mitral regurgitation after mitral valve repair.This was a retrospective study with the prospective follow-up of mitral valve regurgitation patients who underwent mitral regurgitation using a annuloplasty strip for mitral valve repair. This study was approved by Capital medical university affiliated Beijing anzhen hospital.A total of 20 patients were treated with the MV at Capital medical university affiliated Beijing anzhen hospital between Sep 2014 and Jun 2015. Transesophageal echocardiography (TEE) assessment assessment were routinely performed before the intervention to assess LVEF, mitral valve morphology and mitral regurgitation grade, and evaluation of factors that may contraindicate the procedure. Transthoracic echocardiographic (TTE) examination was performed after the operation. This study was approved by the ethics committee of Capital medical university affiliated Beijing Anzhen hospital. The informed consent was obtained form all the included patients.All operations included in this study were performed via a median sternotomy approach. Cardiopulmonary bypass was established by ascending aortic and bicaval cannulation. The aorta was cross-clamped and cardiac asystole was achieved using intermittent antegrade and retrograde cardioplegia. Posterior leaflet prolapse was primarily repaired by leaflet resection. The resection size and shape were determined by a surgeon in charge of each case. Neochordal placement was added if necessary. Ring annuloplasty was performed in all cases. The type of ring was chosen based on surgeon’s preference. The size of ring was determined by sizing the area of anterior leaflet using prosthetic sizers made by each manufacturer.The surgical procedures with prosthetic ring annuloplasty were performed in all patients. Prosthetic ring annuloplasty was performed in 5 cases with 30-mm prosthetic ring (Edwards physio 2), 8 cases with 32-mm prosthetic ring (Edwards 5200), 5 cases with 34-mm prosthetic ring (Edwards physio 2) and 2 cases with 36-mm prosthetic ring (Edwards physio 4450).TTE was performed using commercially available ultrasound systems  equipped with an S5–1 transducer, and 2D, M-mode and Doppler data were acquired with the patient in the left lateral decubitus position. Transthoracic echocardiography was performed at 3 months and 12 months postoperatively. TEE with X7-2 t transducer was applied. The TEE view for the measurement was 3-chamber view and the middle square of mitral apparatus in short axis .The values obtained were analyzed with Student’s T test. Linear regression analysis was determined using the least squares method. A The mean age of all patients was 52.45 ± 14.26 years and 11 patients (55%) were women. In the 20 cases studied, mitral regurgitation was degree 1 in 2 patients, degree 2 in 4 cases, and degree 3 in 14 cases before the operation. All patients had a posterior middle scallop prolapse, the mean LVEF was 62.75 ± 7.94%. All patients underwent MVP with prosthetic ring. Pre-operative and operative data are shown in Table p < 0.05 r = 0.81)  Fig. .Fig. 2ThSurgical valve repair for mitral regurgitation (MR) has significant advantages over valve replacement and has acquired greater importance as a surgical treatment of MR. Some researches have already confirmed that the mitral valve repair could provided great long term results for the patients with mitral insufficiency , 12. AltThe main results of the our study showed that the LVEF and MVd were not significantly influenced after mitral valve repair. However, the coaptation height was significantly increased after the operation. Interestingly, CH after heart resuscitation showed a statistically significant negative correlation with degree of mitral regurgitation 12 months after operation, which meant CH after heart resuscitation may be an important predictive factor for the post-operative mitral regurgitation. Some other researches have also investigated the change of the mitral valve morphology after mitral annuloplasty. It was reported that the mitral annuloplasty with ring could significantly improve the stresses and the valve coaptation with annular dilatation . The recThere were also some limitations in our study. The number of the cases in our study is small. Further study with lager numbers is still needed. The differences of the surgery procedures and cardiac function were not excluded in this study, which may affect the measurement of mitral regurgitation.In conclusion, mitral valve repair could induce the morphologic change of the mitral valve structure. The increase of CH after mitral valve repair may be one of the main factors in regulation of regurgitation after mitral valve repair.


The preexcited myocardium of Wolff-Parkinson-White (WPW) syndrome would have different characteristics from normal myocardium and these findings might be related to persistent left ventricular systolic dysfunction. We evaluated myocardial tissue characteristics at the preexcited segment in adult WPW syndrome patients and their implicated findings.For this prospective study, we enrolled 22 adult WPW syndrome patients  with echocardiographic findings of regional wall motion abnormality in our electrophysiology clinic. Of these patients, 14 underwent radiofrequency ablation before cardiac magnetic resonance imaging. All patients underwent cardiac magnetic resonance imaging including cine and late gadolinium enhancement. The ventricular morphology, function and myocardial characteristics of the preexcited segment were analyzed.P = 0.011). The prevalences of regional myocardial wall thinning and regional akinesia were significantly higher (P = 0.001 for both) and left ventricular function was significantly decreased in patients with late gadolinium enhancement (P < 0.001). In addition, there were no significant relationships between radiofrequency ablation and regional akinesia (P > 0.999), regional myocardial wall thinning (P > 0.999), late gadolinium enhancement (P = 0.662) and low ejection fraction (P > 0.999).A relatively high prevalence of late gadolinium enhancement  was observed exclusively at the basal septum. The septal accessory pathway was significantly more prevalent in patients with late gadolinium enhancement (Myocardial fibrosis was observed at the preexcited myocardium of adult WPW syndrome patients with septal accessory pathway, which could accompany regional akinesia and regional myocardial wall thinning and might be related to persistent left ventricular systolic dysfunction even after radiofrequency ablation. Wolff–Parkinson–White (WPW) syndrome is defined as a congenital condition involving an abnormal conductive accessory pathway between the atrium and ventricle that bypasses the atrioventricular node ,2. This This prospective study was approved by our institutional review board and the local ethics committee. Written informed consent was obtained from all study participants. A cardiologist and a radiologist reviewed the electrical medical record database and searched for new adult WPW syndrome patients (age ≥ 20 years) who had undergone echocardiography at their first examination in our electrophysiology (EP) clinics between January 2010 and December 2014, and 327 patients were identified. Of them, 77 patients  who had abnormal echocardiographic findings of regional wall motion abnormality (RWMA), which did not correspond with vascular territory and was noted at the expected preexcited segment, were selected. A flow diagram for the study population and exclusion criteria is summarized in All available clinical data were recorded after reviewing electronic medical records and/or after interviewing each patient with a standard questionnaire. Clinical presentation in terms of palpitation, chest pain and syncope was reviewed. The 12-lead electrocardiography (ECG) during sinus rhythm at the time of diagnosis was reviewed. On ECG, we reconfirmed ventricular preexcitation by Kent fibers with a short PR interval, widened QRS complex with slurred upstroke and secondary repolarization changes. An automatic computerized system recorded the longest QRS duration exhibited by the leads and the accessory pathway location was determined . All stu2, acquisition matrix 126 x 192, flip angle 35°, and slice thickness 8 mm. Short-axis images were acquired at the apical, mid and basal levels of the left ventricle. Images for T1 measurements were obtained before and 15 minutes after contrast administration.CMR was performed with a 3.0-T imaging system  and an 8-channel cardiac coil. After a localized scan, ECG-gated cardiac cine images were obtained with the following parameters: True fast imaging with steady-state free precession sequence, TR 3.31 ms, TE 1.44 ms, flip angle 50°, field of view 337 x 400 mm, matrix 216 x 216, 25 phases and slice thickness 8 mm without gap in the four-chamber, long-axis and short-axis planes encompassing the whole ventricles. LGE imaging was performed 10 minutes after injection of gadobutrol  at 2 ml/sec. Scanning parameters were as follows: segmented inversion recovery prepared turbo fast low-angle shot sequence, TR 9.9 ms, TE 4.9 ms, flip angle 20°, field of view 380 x 380 mm, matrix 320 x 320 and slice thickness 8 mm without gap in the four-chamber, long-axis and short-axis planes encompassing the whole ventricles. Data acquisition was synchronized with ECG in the mid-diastolic phase. An 11-heartbeat modified Look-Locker sequence with inversion recovery was used for T1 measurement of the myocardium . Scanninm/ΔR1b) x (1 –hematocrit) x 100, for which R1m is R1 in the myocardium, R1b is R1 in the blood, and ΔR1 is the change in relaxivity before and after gadolinium chelate administration, respectively [All CMR images were transferred to dedicated software . Two observers  who were both blinded to each patient’s clinical findings reviewed the images in consensus. From the cine images, observers evaluated the presence of regional myocardial wall thinning, which was defined as a myocardial wall thickness of 5.5mm or less on the end-diastolic image . To evalectively .P value of < 0.05 was considered to indicate statistical significance.Statistical analyses were performed using statistical software . Continuous variables were expressed as mean values with standard deviations and categorical variables were expressed as percentages. We divided the patients into two groups according to the presence of LGE, and compared clinical characteristic and other CMR findings between the two groups. Additional analyses were done in which the study population was divided into two groups according to the performance of RFA or the presence of RWMA. The Mann-Whitney U test was used to appraise the differences between the two groups for continuous variables and the chi-square contingency tables or Fisher’s exact test were used to evaluate the differences between the two groups for categorical variables. A The clinical characteristics of the study population are summarized in Median time interval from first diagnosis to CMR was 499.5  days. Median time interval from RFA to CMR was 465.5  days for the 14 patients with RFA. The CMR findings from the study population are summarized in P = 0.021). The prevalence of septal accessory pathway was significantly higher in patients with LGE compared to patients without LGE (P = 0.011). In addition, the prevalence of lateral accessory pathway was significantly lower in patients with LGE compared to patients without LGE (P = 0.046). Other findings did not show significant differences between the two groups. Among CMR findings, a significantly higher prevalence of regional myocardial wall thinning was observed in patients with LGE (P = 0.001). The prevalence of akinesia was also significantly different between the two groups (P = 0.001) with akinesia being more prevalent in patients with LGE. However, for premature contractions, there was no significant difference between the two groups (P > 0.999). The mean left ventricular end-diastolic volume was significantly larger (P = 0.003) and left ventricular ejection fraction was significantly decreased (P < 0.001) in patients with LGE. Likewise, the prevalence of low ejection fraction was significantly higher in patients with LGE  than patients without LGE  (P < 0.001). In addition, patients with LGE showed significantly decreased right ventricular ejection fraction compared to patients without LGE (P = 0.001). The mean values of myocardial native T1 and extracellular volume fraction were significantly higher in patients with LGE compared to patients without LGE , especially at the septum (P < 0.001 for both), but not for the lateral wall of the left ventricle .Among clinical findings, the QRS duration was significantly longer in patients with LGE compared to patients without LGE (P = 0.002). However, we observed no significant differences in the prevalences of regional akinesia and regional myocardial wall thinning between the two groups (P > 0.999 for both). In addition, there were no significant differences in the prevalences of LGE and low ejection fraction between the two groups .The major findings were compared according to performance of RFA and the results are summarized in P < 0.001) from the diagram. The prevalence of LGE in patients with RWMA  was also significantly higher than in patients without RWMA  (P < 0.001).A set diagram was drawn to describe logical relations between the major findings . All 9 pWe evaluated myocardial characteristics of the preexcited myocardium using CMR in adult patients with WPW syndrome. In our results, we observed a relatively high prevalence of LGE in the study participants  exclusively at the basal septum. The prevalence of septal accessory pathway was significantly higher in patients with LGE. In addition, the prevalences of regional myocardial wall thinning and regional akinesia were significantly higher in patients with LGE. Left ventricular end-diastolic volume was significantly larger and both ventricular ejection fractions were significantly decreased in patients with LGE. The native T1 value and extracellular volume fraction were significantly increased in patients with LGE, especially at the septum, which might support the presence of myocardial fibrosis. In addition, there were no significant relationships between RFA and abnormal CMR findings such as regional akinesia, regional myocardial wall thinning, LGE and low ejection fraction in the present study.Although we included patients with RWMA observed on echocardiography, only 13 patients  had RWMA on CMR. This is probably because the patients without RWMA on CMR underwent RFA before undergoing CMR. As ventricular preexcitation in the manifest WPW syndrome occurs at the myocardium close to the ventricular insertion of the accessory pathway, we thought that abnormal findings in the myocardium on CMR might be exclusively observed at the basal left ventricle . In addiRecently published literatures have reported that non-physiologic activation through the accessory pathway can directly lead to heart failure ,13,14,24The hitherto published literatures have almost all focused on echocardiographic findings in pediatric patients, whereas we focused on CMR for adult patients, who might be diagnosed later in life and who might be exposed to the accessory pathway for a long period of time. Hence, we observed different findings such as myocardial fibrosis that could be related to persistent left ventricular systolic dysfunction even after successful RFA. We thought that our research could also help explain why three pediatric patients in a previous study had irreversible heart failure in spite of RFA . ExpectaThis study has some limitations. First, we included a small number of patients in this preliminary study. Second, we selected eligible patients with grossly visible RWMA on echocardiography because non-visible RWMA can be related to very small areas of preexcited segment, and it would be difficult to characterize myocardium on CMR considering spatial resolution. In actual practice, however, not all patients with WPW syndrome would undergo echocardiography. This ultimately raises the possibility of a selection bias, and consequentially the incidence of LGE might have been higher than its actual value. Third, although we prospectively performed CMR in this study, not all patients underwent the EP study and clinical follow-up varied among the patients. To investigate clinical findings related to myocardial fibrosis and heart failure in patients with WPW syndrome, further prospective studies with larger populations are necessary.We observed a relatively high prevalence of myocardial fibrosis at the preexcited myocardium of adult WPW syndrome patients, exclusively at the basal septum with septal accessory pathway in the present study. In some cases, myocardial fibrosis accompanied regional akinesia and regional myocardial wall thinning. These abnormal findings might have occurred from continuous premature contractions by the septal accessory pathway and might be related to persistent left ventricular systolic dysfunction even after successful RFA. A further prospective study using CMR with a large population is necessary to identify myocardial characteristics at the preexcited myocardium in WPW syndrome, which might provide new perspectives for the disease and help develop management strategies in the future.


As the sensing capabilities of wearable devices improve, there is increasing interest in their application in medical settings. Capabilities such as heart rate monitoring may be useful in hospitalized patients as a means of enhancing routine monitoring or as part of an early warning system to detect clinical deterioration.To evaluate the accuracy of heart rate monitoring by a personal fitness tracker (PFT) among hospital inpatients.2.R) was also measured as a positive control.We conducted a prospective observational study of 50 stable patients in the intensive care unit who each completed 24 hours of heart rate monitoring using a wrist-worn PFT. Accuracy of heart rate recordings was compared with gold standard measurements derived from continuous electrocardiographic (cECG) monitoring. The accuracy of heart rates measured by pulse oximetry . Personal fitness tracker device performance was significantly better in patients in sinus rhythm than in those who were not .On a per-patient basis, PFT-derived heart rate values were slightly lower than those derived from cECG monitoring . By comparison, Spo2.R-derived heart rates. Performance was worse among patients who were not in sinus rhythm. Further clinical evaluation is indicated to see if PFTs can augment early warning systems in hospitals.Personal fitness tracker–derived heart rates were slightly lower than those derived from cECG monitoring in real-world testing and not as accurate as SpoClinicalTrials.gov NCT02527408; https://clinicaltrials.gov/ct2/show/NCT02527408 (Archived by WebCite at  http://www.webcitation.org/6kOFez3on) Over the last 5 years, consumer interest in self-monitoring and personal health tracking has grown considerably -4. What There has been growing enthusiasm for the potential use of wearable devices to improve health care delivery ,6. A numCurrent clinical uses for wearable devices are mostly limited to outpatient and ambulatory settings, with a focus on the management of chronic diseases -13. ApplThere is ample opportunity to leverage the sensing capabilities of wearable devices in the inpatient setting as well. Many newer wearable devices use photoplethysmography (PPG) to record heart rate by measuring differential reflection of light from the skin, based on the pulsatility of superficial blood vessels . Heart rThe ability of wearable PPG sensors to reliably measure heart rate in the outpatient population has been demonstrated in at least one study ; however2) monitoring.In order to address these and other questions, we examined the accuracy of heart rate measurements derived from PFTs. We focused on patients in the ICU as this cohort is closely monitored using continuous ECG (cECG) monitoring, which provides a gold standard measurement of heart rate. Because the degree of agreement that would be sufficient for clinical applications is not well defined, we also examined the agreement between cECG-derived heart rate measurements and a more widely accepted method of heart rate measurement, namely, pulse oximetry  PFT to monitor heart rate in 50 patients admitted to the ICU at Kingston General Hospital (KGH), a tertiary academic medical center in Ontario. The 33-bed ICU at KGH is a mixed medical, surgical, trauma, and neurosciences unit. The PFT device studied is a wrist-worn device resembling a watch, which uses PPG to detect periodic changes in blood flow beneath the sensor, thereby deriving heart rate measurements. Heart rate values are recorded every 5 minutes. The Fitbit Charge HR is a commercially available PFT and is not currently regulated by the US Food and Drug Administration.Staphylococcus aureus and Clostridium difficile infections. We further excluded patients with the potential for vascular compromise of the arm on which the device was to be placed, including those with deep venous thrombosis of the upper extremity, peripherally inserted central catheters, radial arterial lines, dialysis fistulas, and severe upper extremity trauma or fracture. Patients were monitored only once for a total duration of 24 hours.In order to study a cohort of patients that would best resemble hospital ward patients, we included only stable patients who were not receiving mechanical ventilation, continuous analgesia, or sedation. To reduce the risk of transmitting nosocomial infections, we excluded patients under contact precautions for methicillin-resistant 2 monitoring (Spo2.R), both recorded every minute. These data were acquired as XML files and processed using an automated Python script to derive minute-level heart rate data. We synchronized bedside monitor data and PFT data using a correction factor that accounted for the difference between each device’s internal clock.The study used 6 separate PFTs , each of which was assigned a unique email address and log-in credentials for the Fitbit website. An automated R script was used to download and process PFT data from the Fitbit website. Heart rate data are recorded by the PFT every 5 minutes. To provide a gold standard measurement of heart rate, we recovered data from the ICU bedside monitors using specialized software . Data included heart rate values, as well as heart rate data derived from continuous SpoWe analyzed heart rate data in aggregate across all patients, as well as on a per-patient basis. We determined the difference between cECG and PFT readings measured simultaneously, the median of differences over a 24-hour period, the interquartile range (IQR) of differences, and the Pearson correlation coefficient between cECG and PFT measurements. We used a Wilcoxon signed rank test to determine if the distribution of cECG-derived heart rates differed from that of the PFT-derived heart rates. Finally, we used Bland-Altman analysis to measure the agreement between the PFT and cECG methods of heart rate monitoring, as well as the bias of the PFT relative to cECG.2.R pairs in order to compare the accuracy of PFT measurements with that of a well-established and widely used alternative for heart rate measurement. On the basis of the mechanism of sensing used by the PFTs, we hypothesized that accuracy would differ in patients not in sinus rhythm and conducted a subgroup analysis to test this effect. Rhythm status was based on examination of cECG recording both at the time of device application and at the time of device removal, with patients designated as being in sinus rhythm only if this was present at both time points. To assess the potential for degradation in PFT performance over time, we compared the accuracy in the first 20 patients with that of the last 20 patients.We calculated all the above-mentioned metrics for cECG-SpoThe study was approved by the Health Sciences Research Ethics Board of Queen’s University (DMED-1818-15) and is registered with ClinicalTrials.gov (NCT02527408). Patients or their substitute decision makers provided informed consent. All study data were deidentified. The study did not receive funding from the device manufacturer or from any other source. All statistical analyses were done using R (v 3.2.2).Between August 2015 and January 2016, we enrolled a convenience sample of 50 patients meeting our enrollment criteria. Patients were admitted with a variety of medical and surgical conditions and were of low clinical acuity at the time of monitoring .The PFT device was removed prematurely in 2 cases; in one case a patient was discharged from the ICU early, and in another case a patient developed a diffuse drug rash. In 4 cases cardiorespiratory monitoring was discontinued early, resulting in incomplete comparison data. Personal fitness tracker devices in these cases continued to collect data for the full 24-hour period. Excluding the 2 patients whose devices were removed early, PFTs showed a high degree of data capture (mean 98% of eligible data).2.R heart rate pairs. Most of the 24-hour heart rate recordings conformed to a skewed or bimodal distribution (P<.001). By comparison, Spo2.R-derived heart rates more closely approximated cECG, with a median difference of 0 bpm, correlation coefficient of .91, and 89% of readings within 5 bpm of the cECG value. The Spo2.R and cECG heart rate distributions were similar (P=.18). Visual inspection of the Bland-Altman plots revealed a tendency for the PFT to underestimate heart rate values in the range of approximately 75 to 120 bpm . The limits of agreement were wider with the PFT method compared with the Spo2.R method: −31 (95% CI −31.22 to −30.40 bpm) to 21 bpm (95% CI 21.06-21.87 bpm) versus −17 (95% CI −17.01 to 16.77 bpm) to 16 bpm . On average, PFT recordings yielded a higher IQR, lower Pearson correlation coefficient, larger bias, and wider limits of agreement than Spo2.R recordings .Scatterplots for individual patients are provided in P<.05 for all comparisons, P=.61). Individual PFT devices were used between 5 and 13 times (mean 9 times).Our subgroup analyses compared 8 patients who were not in sinus rhythm with 40 patients in sinus rhythm. Median heart rate difference, IQR, Pearson correlation coefficient, bias, and limits of agreement were all significantly worse in patients with rhythms other than sinus  have been shown to accurately predict cardiac arrest and hospital mortality, with some studies suggesting a reduction in these events following EWS implementation . Heart rThere are a number of potential advantages to augmenting hospital monitoring practices using wrist-worn PPG-based heart rate sensors such as the one we studied. A cost advantage may be achievable given that the device we tested retails for approximately US $170 and that we were able to reuse devices on average 9 times without seeing a decrement in performance. By comparison, conventional heart rate monitoring on inpatient wards  has been estimated to incur expenses of just under US $40 per patient per day in direct costs and as much as an additional US $170 in opportunity costs . AlthougThe use of wrist-worn devices for heart rate monitoring in hospitals also has potential disadvantages. Consumer-grade PFTs do not provide information regarding respiratory rate or blood pressure, both of which have been shown to add value in EWS . Wrist-wOur study has a number of strengths. We examined the use of PFTs in a sizeable cohort of hospitalized patients under real-world conditions. Devices were adjusted only once at the time of application and were not reassessed for the duration of the 24-hour recording period by either study personnel or clinical staff. We used high-frequency data captured from continuous bedside monitoring to provide an accurate gold standard assessment of heart rate and analyzed PFT performance on both a pooled and per-patient level.One of the potential limitations of our study arises from the fact that the PFT-derived and cECG-derived heart rate values were obtained from different devices, with separate internal clocks. Although correction factors were used to synchronize the time stamps from the 2 heart rate sources, it is possible that in some cases the heart rate values that were treated as simultaneous were in fact separated by a short time interval. As the PFT device only recorded heart rate measurements every 5 minutes—an interval longer than the maximal device time discrepancy observed—the impact of any potential asynchrony was likely minimal.Our study was conducted in the ICU, where cECG monitoring provides a gold standard comparator for heart rate. The extent to which our results can be generalized to hospitalized patients on the wards is therefore not certain; however, all patients enrolled were stable and were receiving ward-level care at the time of monitoring. Finally, our subgroup analysis included a relatively small number of patients not in sinus rhythm, thereby limiting the statistical power of the results.Our study used one particular type of PFT, namely, the Fitbit Charge HR. Although many consumer-grade PFTs have similar intended functionality and use similar heart rate sensing technology, our results cannot necessarily be generalized to other wearable devices. Given that the different performance characteristics of various PFTs are not known, a study in which a mix of devices is used would be vulnerable to unwarranted mixing of effects or would require an increase in sample size proportional to the number of different devices tested.Our study is the first to report on the accuracy of heart rate recordings from wearable devices among hospital inpatients. Previous work has focused on the technical and engineering aspects of PPG-based wearable heart rate sensors, as well as discussion of their potential uses in health care settings ,8,11. StThe health care sector is expected to drive a large proportion of sales of wearable devices in the coming years . Optimal


There are often false‐positive alerts of thoracic impedance monitoring; however, the “false‐positive alerts” might indicate any clinical problem of patient. In the present case, an alert for a drop in intrathoracic impedance, which generally indicates exacerbation of heart failure, enabled early detection of twiddler syndrome. In the era of remote monitoring (RM), it is possible to obtain much information about patients using cardiac implantable electronic devices (CIEDs). RM systems have the potential for early detection of arrhythmia, heart failure, and device failure. This report describes a rare case of twiddler syndrome after implantation of a CIED, which was detected as an alert for intrathoracic impedance as an indicator of heart failure.An 84‐year‐old woman was diagnosed as having New York Heart Association (NYHA) class 3 chronic heart failure based on the dilated phase of hypertrophic cardiomyopathy and received a defibrillator capable of cardiac resynchronization therapy (CRT‐D)  for low ejection fraction (EF) , complete left bundle branch block evident by electrocardiography (QRS duration was 162 msec), and documented nonsustained ventricular tachycardia in May 2012. The generator was implanted in the pocket fashioned in her pectoral subcutaneous space. She also had dementia and had been treated with medication. Her CIED was monitored remotely by the Merlin™.net Patient Care Network (St. JUDE MEDICAL).In May 2013, a CorVue™ congestion monitoring alert, associated with a drop in intrathoracic impedance, suggested exacerbation of heart failure. We requested the patient to immediately visit our hospital to check the CIED because of suspected exacerbation of heart failure. The device data indicated that the intrathoracic impedance had dropped in late April 2013 and that the left ventricular (LV) lead threshold had also increased at the same time  lead and right ventricular (RV) lead were not changed but the threshold of the LV leads was increased to 3.25 V/0.5 msec. Because it was difficult to replace the LV leads, we decided to use the original ones. After the LV lead was inserted as possible into the vein, the threshold was improved to 1.75 V/0.5 msec. The generator was replaced under the greater pectoral muscle and fixed at the periosteum of the clavicle by nylon thread. After the generator replacement, the thoracic impedance had increased by about 50 ohm and recovered to the baseline. The patient was discharged 1 week after, and no generator dislodgement occurred thereafter.The major findings in this case are that a remote monitoring system enables early detection of twiddler syndrome and the changes in device's parameters were recorded during the occurrence of twiddler syndrome.Twiddler syndrome, in which twisting or rotating of the device in its pocket results in lead dislodgement and device malfunction, can occur in patients with implanted devices such as a pacemaker, an implantable cardioverter–defibrillator (ICD), cardiac resynchronization therapy (CRT), or a defibrillator allowing cardiac resynchronization therapy (CRT‐D) In the IN‐TIME trial, in which there was a reduction in all‐cause death by automatic multiparameter RM, there were no effects on heart failure‐specific end points including hospital admissions, length of hospital stay, worsening of NYHA class, or worsening of self‐assessed condition The cause of twiddler syndrome is an increased pocket size and movement of the generator in the pocket. In this case, the generator was replaced under the greater pectoral muscle and fixed at the periosteum of the clavicle using nylon thread. The implanted limb was strictly fixed by bandaging after reoperation. Thereafter, the generator was well fixed and the twiddler syndrome did not recur.No conflict of interests declared.SS: wrote the initial draft of the manuscript. MW and AM: contributed to analysis and interpretation of data. TY and TS: contributed to critical revision of the article for important intellectual content. YM: involved in final approval of the article.


Pulmonary hypertension (PH) is associated with a poor outcome in chronic obstructive pulmonary disease (COPD) and is diagnosed invasively. We aimed to assess the diagnostic accuracy and prognostic value of non-invasive cardiovascular magnetic resonance (CMR) models.Patients with COPD and suspected PH, who underwent CMR and right heart catheter (RHC) were identified. Three candidate models were assessed: 1, CMR-RV model, based on right ventricular (RV) mass and interventricular septal angle; 2, CMR PA/RV includes RV mass, septal angle and pulmonary artery (PA) measurements; 3, the Alpha index, based on RV ejection fraction and PA size.p<0.0001). Splitting RHC-mPAP, CMR-RV and CMR-PA/RV models by 35mmHg gave a significant difference in survival, with log-rank chi-squared 5.03, 5.47 and 7.10. RV mass and PA relative area change were the independent predictors of mortality at multivariate Cox regression (p=0.002 and 0.030).Of 102 COPD patients, 87 had PH. The CMR-PA/RV model had the strongest diagnostic accuracy (sensitivity 92%, specificity 80%, positive predictive value 96% and negative predictive value 63%, AUC 0.93, CMR provides diagnostic and prognostic information in PH-COPD. The CMR-PA/RV model is useful for diagnosis, the RV mass index and PA relative area change are useful to assess prognosis.Pulmonary hypertension is a marker of poor outcome in COPD.• MRI can predict invasively measured mean pulmonary artery pressure.• Cardiac MRI allows for estimation of survival in COPD.• Cardiac MRI may be useful for follow up or future trials.• MRI is potentially useful to assess pulmonary hypertension in patients with COPD.•  Pulmonary hypertension is a predictor of death and hospitalisation –5 in patThe gold standard for diagnosis of pulmonary hypertension is right heart catheter (RHC), however, this is an invasive test . As suchSeveral predictive cardiac magnetic resonance (CMR) imaging models have been proposed for estimation of pulmonary artery pressure –17. The All consecutive patients who underwent MRI at a pulmonary hypertension referral centre  from AprCardiac MRI was performed in a pulmonary hypertension tertiary referral centre , on a GEMR images were manually analysed by DC (a cardiac MRI radiographer of 9 years cardiac MRI experience) on a GE Advantage Workstation 4.4 and GE Advantage Workstation ReportCard software, with the observer blinded to all clinical information and other investigations. Left and right ventricular end-diastolic volume, end-systolic volume, right and left ventricular stroke volume and mass were calculated , right and left ventricular ejection fraction, ventricular mass index (RV mass divided by LV mass)  and inteThe CMR-RV model is based on ventricular mass index and interventricular septal angle: mPAP = –4.6 +  + (ventricular mass index x 16.3), see Fig. The PA/RV model is similar to the CMR-RV model (above), with the addition of basic function metrics of the pulmonary artery: CMR-PA/RV = -21.806 +  + (ventricular mass index x 11.5) + (diastolic pulmonary artery area x 0.01) – (PA relative area change x 0.22), see Fig. The alpha index comprises both functional and structural information, utilising right ventricular function along with pulmonary artery size: Alpha index = minimum PA area/RV ejection fraction. This model was assessed in a cohort of 185 patients, with an area under ROC curve of 0.95 .Previously published parametric models, developed for diagnostic and prognostic assessment in PH, were derived from cardiac MRI metrics:The diagnostic cut-off for pulmonary hypertension for CMR-RV was ≥32 and alpha index ≥7.2, as published in the literature –17. CMR-Right heart catheterisation was performed using a balloon tipped 7.5 Fr thermodilution catheter . Pulmonary hypertension was defined as a resting mPAP ≥25 mmHg and severe pulmonary hypertension as a resting mPAP ≥35 mmHg. Cardiac output was calculated using thermodilution.Pearson’s correlation between CMR models and RHC-mPAP were calculated. The relative accuracy of the models was assessed using Bland-Altman plots. Diagnostic accuracy was calculated from the 2x2 contingency table to calculate sensitivity, specificity, negative predictive value and positive predictive value. Receiver operating characteristic (ROC) curves were constructed and the area under the ROC curve (AUC) recorded.The interval from CMR until all cause death or census was regarded as the follow-up period. The census was performed on 25/02/2016. Log-log plots were visually inspected to ensure linearity with outcome data. Survival analysis was performed using univariate and multivariate Cox proportional hazards regression. In order to allow for comparison between each metric, this was performed with each variable standardised as the z score for the population studied. Multivariate analysis was performed in a forward direction, for all variables with a statistically significant association with mortality on univariate analysis.p-value of <0.05 was considered statistically significant.Kaplan-Meier plots were generated for each model and RHC measured mPAP, dichotomised by a value of 35, and Chi square values were calculated using the Log rank test, as this is the threshold value for severe pulmonary hypertension . StatistA total of 1864 patients were referred to the pulmonary hypertension centre during the period studied and underwent right heart catheterisation: of these 145 had a documented diagnosis of COPD from a respiratory specialist. One hundred and two had MRI and RHC within 90 days so were included in the study. There were 87 patients with pulmonary hypertension (69 of these had severe pulmonary hypertension) and 15 patients without pulmonary hypertension  than in the patients with mPAP ≥35 mmHg .Table Bland-Altman plots were also created to assess the accuracy of the models against RHC-mPAP Fig. , this wap=0.009, p<0.001, p=0.002 and p=0.023, respectively). RHC measured mPAP was a strong predictor of mortality (p=0.004), as were the CMR-RV and CMR-PA/RV models . There was a statistically significant difference in survival when the population was split by a threshold of 35 mmHg for RHC-mPAP, CMR-RV and CMR-PA/RV models, with a log rank chi squared of 5.03, 5.47 and 7.10, respectively  and 0.561 , respectively.During a mean follow up period of 1.5 years (standard deviation 0.9) there were 33 deaths. Table This study demonstrates that CMR models can be used to assess for the presence of pulmonary hypertension in COPD with good diagnostic accuracy, whilst also providing prognostic information similar to right heart catheterisation. This data supports the potential use of CMR in the non-invasive assessment of suspected pulmonary hypertension in patients with COPD. We have shown that single measurements from cardiac MRI  correlate strongly with right heart catheter measured mPAP. A model which includes measurements from the right ventricle, the diagnostic accuracy is slightly reduced, but inclusion of basic measurements of pulmonary arterial structure and function increases the accuracy of predicted mPAP and, therefore, the presence of pulmonary hypertension. Therefore, we recommend the use of CMR-PA/RV model in the diagnosis of pulmonary hypertension in patients with COPD. In the presence of COPD, right ventricular mass index and PA relative area change are the strongest predictors of outcome, but further work to develop prognostic thresholds is required.Studies performed primarily in patients with pulmonary arterial hypertension have shown that structural and functional indices of the right ventricle  and pulmonary artery  correlate with RHC measured mPAP. Inter- and intra-observer reproducibility data for these cardiac MRI metrics for DC and AJS have been previously published. RV end-diastolic and systolic measurements had excellent inter-observer reproducibility (ICC 0.959 and 0.991) and pulmonary artery relative area change had high inter-observer reproducibility (ICC 0.891). Right ventricular ejection fraction also had high inter-observer reproducibility (ICC 0.957) . We and The alpha model showed good correlation with mPAP, but had a low diagnostic accuracy: this model suffered from a diagnostic threshold that was too low for this cohort, significantly reducing its specificity. Changing the threshold of the alpha index to 16 increased the diagnostic accuracy of this model to 77% sensitivity and 80% specificity. This inaccuracy may be related to the measurement of right ventricular ejection fraction, particularly the reproducibility between different centres. In the original paper, it was not described how the right ventricular endocardial contours were measured, specifically, whether the papillary muscles and RV trabeculations were included, which may potentially add a bias into the calculation.2 0.95) [Pulmonary hypertension, confirmed by right heart catheter, has been recognised for many years as a marker of disease severity in COPD. In this study we have shown that cardiac MRI measured right ventricular mass and therefore ventricular mass index, along with pulmonary artery relative area change are significant predictors of mortality on univariate analysis. However, by using CMR derived parametric models, particularly the CMR-RV model which combine these CMRI derived measures, we can improve the prediction of outcome in COPD patients on multivariate analysis. These models may be further improved with novel imaging biomarkers in pulmonary hypertension assessment. One such marker is the 4D flow assessment of the life of vortices within the pulmonary artery, which has been shown to have a very high correlation with mPAP (r2 0.95) .A potential source of error arises from the use of MR models, which were developed for use in a cohort of all causes of pulmonary hypertension and not validated in specific sub-groups, such as PH-COPD in this case. We feel that it is likely that the findings of a raised interventricular septal angle and ventricular mass index are likely to occur most subgroups of pulmonary hypertension (with the exception of left heart disease) as they are related to the pressure differential between the left and right ventricles. The measures of pulmonary arterial structure and function (size and relative area change) are likely to be transferable across subgroups, as they are markers of pulmonary vascular compliance and remodelling. We, therefore, feel that it reasonable to use these models in specific sub-groups of pulmonary hypertension, although validation, such as in this paper, would be useful. The models that are used in this paper use parameters that are stated with a degree of precision (for example an offset of 21.806 for CMR-PA/RV), likely more than is required for this purpose. We have maintained the equations in the published form to reduce any bias in the calculations, but it is likely that fewer decimal places could be used for these parameters for the prediction of outcome and the presence of pulmonary hypertension in COPD.Currently, RHC is the gold standard test for the assessment of pulmonary hypertension and is used to assess prognosis in suspected COPD-PH cases. The ability to use non-invasive CMR models in this patient group may avoid the need for RHC, as we have shown CMR to be as good in the assessment of prognosis. The strong correlation of CMR imaging models with RHC mPAP suggest it may also have a role in follow-up, and also in assessment of treatment response in possible future trials assessing vasodilator response in COPD-PH. The role of cardiac MRI in COPD is further strengthened as this is a cohort of patients in which echocardiography is challenging. In the presence of COPD echocardiography has a relatively high rate of non-diagnostic quality studies. It has a good negative predictive value, but a poorer positive predictive value . In patiThe non-invasive estimation of mPAP has multiple other potential uses, beyond prognosis in COPD, although these have not been addressed in this paper. In advanced COPD patients considered for lung volume reduction surgery (LVRS), severe pulmonary hypertension is considered a contraindication , so the This study is limited by its single centre, retrospective design, at a tertiary pulmonary hypertension referral centre where the severity of pulmonary hypertension is more severe. The results, therefore, represent a biased population, as the patients have been screened by echocardiography and excessive symptoms for the presence of pulmonary hypertension before referral (the vast majority of patients with COPD are managed in primary care). This has resulted in a smaller proportion of non-pulmonary hypertension patients than would be present in a general population of COPD; however, in the absence of a prospective trial, this is difficult to overcome. Furthermore, the assessment of the presence of COPD in the population relied upon the accurate documentation of a clinical diagnosis of COPD. This likely resulted in a lower proportion of patients being identified, but is likely to be more robust than using either spirometry or CT defined emphysema alone. Despite this, we feel that these tools are valid for the assessment of patients who are referred to a pulmonary hypertension centre regarding the presence of pulmonary hypertension and prognosis, as this is the population that was studied. It may be that more specific diagnostic thresholds would be suitable for use in the general COPD population.The use of the CMR-PA/RV model, derived from cardiovascular magnetic resonance imaging in the assessment of COPD allows for accurate, non-invasive estimation of pulmonary artery pressure and the presence of pulmonary hypertension. Right ventricular mass index and pulmonary artery relative area change are most predictive of outcome.


Myocardial injury is common in patients without acute coronary syndrome, and international guidelines recommend patients with myocardial infarction are classified by aetiology. The universal definition differentiates patients with myocardial infarction due to plaque rupture (type 1) from those due to myocardial oxygen supply-demand imbalance (type 2) secondary to other acute illnesses. Patients with myocardial necrosis, but no symptoms or signs of myocardial ischaemia, are classified as acute or chronic myocardial injury. This classification has not been widely adopted in practice, because the diagnostic criteria for type 2 myocardial infarction encompass a wide range of presentations, and the implications of the diagnosis are uncertain. However, both myocardial injury and type 2 myocardial infarction are common, occurring in more than one-third of all hospitalised patients. These patients have poor short-term and long-term outcomes with two-thirds dead in 5 years. The classification of patients with myocardial infarction continues to evolve, and future guidelines are likely to recognise the importance of identifying coronary artery disease in type 2 myocardial infarction. Clinicians should consider whether coronary artery disease has contributed to myocardial injury, as selected patients are likely to benefit from further investigation and in these patients targeted secondary prevention has the potential to improve outcomes. The definition of acute myocardial infarction has evolved to accommodate increasingly sensitive markers of myocardial necrosis and imaging methods that allow greater understanding of the pathogenic mechanisms of acute coronary syndrome. As such, the universal definition of myocardial infarction proposes that we classify patients with myocardial infarction based on aetiology.We now recognise a spectrum of acute and chronic myocardial injury due to a variety of cardiac and non-cardiac causes in clinical practice. The most contentious diagnosis is that of type 2 myocardial infarction, which is defined as myocardial necrosis with evidence of ischaemia due to myocardial oxygen supply-demand imbalance in the context of another acute illness. Differentiating between patients with type 2 myocardial infarction and those patients with myocardial necrosis in the absence of ischaemia, in whom the recommended classification is myocardial injury, is challenging, as there is considerable overlap between these two clinical entities.Here, we summarise the available literature on the prevalence and outcomes of subtypes of myocardial injury and infarction, and aim to provide practical guidance for the clinician to aid the assessment and investigation of patients with undifferentiated myocardial injury.Cardiac troponin is the only recommended biomarker for the detection of myocardial necrosis, and it is integral to the diagnostic criteria for myocardial infarction.8There is now widespread adoption of cardiac troponin assays in clinical practice across Europe, with >95% of laboratories using cardiac troponin as the preferred marker for the diagnosis of myocardial infarction.Recent studies have demonstrated that cardiac troponin concentrations below the 99th centile can help in the risk stratification of patients with suspected acute coronary syndrome.16The introduction of more sensitive cardiac troponin assays and lower diagnostic thresholds led to a major revision of the guidelines introducing a classification by aetiology to acknowledge that myocardial injury occurs in a wide range of clinical presentations . The thiThe classification distinguishes between type 1 myocardial infarction due to thrombosis of an atherosclerotic plaque and type 2 myocardial infarction due to myocardial oxygen supply-demand imbalance in the context of another acute illness.This classification is contentious and was based on expert consensus rather than evidence from prospective clinical trials. While it has been adopted in research studies, implementation in clinical practice has been less consistent. The most contentious diagnosis is that of type 2 myocardial infarction; a concept based on clinical hypothesis and observation without prospective mechanistic evaluation. Patients classified with type 2 myocardial infarction are heterogeneous and have myocardial ischaemia secondary to a variety of acute medical or surgical conditions. Based on the current criteria, a diagnosis of type 2 myocardial infarction could be applied to patients without coronary artery disease. At present, there is no guidance or consensus on the optimal cardiac investigation, management or treatment strategy for patients with type 2 myocardial infarction.The global task force is reviewing the universal definition of myocardial infarction and recognises the need to provide clearer diagnostic criteria and guidance.The majority of cardiac troponin is intracellular, with >90% of troponin isoforms located within the sarcomere, and the remainder unbound within the cytoplasmic pool.21It is now recognised that cardiac troponin may be released out with the context of myocardial ischaemia and necrosis, with several purported mechanisms. Cardiomyocytes undergo mechanical stretch in response to pressure or volume overload, and this may trigger activation of intracellular proteases associated with intracellular degradation of troponin.24The universal definition makes a distinction between type 2 myocardial infarction and myocardial injury based on the presence or absence of symptoms and signs of myocardial ischaemia; however, there remains considerable overlap and to date there have been no prospective mechanistic studies to evaluate the range of underlying pathophysiology in these patients. Acute myocardial injury may occur in a variety of cardiac and non-cardiac illnesses  as a conChronic myocardial injury may occur in structural heart disease  or secondary to other non-cardiac illnesses such as chronic renal failure. As an example, the detection of chronic myocardial injury may be clinically useful in valvular heart disease, with serum cardiac troponin I concentrations associated with cardiac mass, replacement fibrosis and prognosis in patients with aortic stenosis.26The introduction of high-sensitivity cardiac troponin assays and lower diagnostic thresholds into clinical practice is likely to result in a disproportionate increase in the number of patients with type 2 myocardial infarction or myocardial injury compared with type 1 myocardial infarction,27–29et al,31–40The majority of studies have not used high-sensitivity cardiac troponin assays and therefore may underrecognise the incidence of myocardial injury and type 2 myocardial infarction. The largest reported registry to date was published by Baron Differences in the reported incidence may in part be explained by the inconsistent approach to distinguishing type 2 myocardial infarction from acute and chronic myocardial injury across studies. It is perhaps unsurprising that the diagnosis of type 2 myocardial infarction is less frequent in selected populations with acute coronary syndrome.A previous study at our centre evaluated all patients with elevated plasma cardiac troponin concentrations irrespective of presenting complaint n=2165), admitted during the validation and implementation of a contemporary sensitive cardiac troponin I assay.5, admitt6Whether adoption of high-sensitivity troponin assays and the 99th centile for diagnosis of myocardial infarction translates into improvements in clinical outcomes for patients with suspected acute coronary syndrome is being evaluated in a stepped wedge cluster randomised trial across Scotland . If increased sensitivity does not impinge on specificity for the diagnosis of type 1 myocardial infarction, then these assays will improve patient outcomes through better targeting of therapies for coronary artery disease. However, if increased sensitivity leads to poor specificity, then patients may be misdiagnosed and given inappropriate cardiac medications with potentially detrimental outcomes. This trial will establish whether the introduction of high-sensitivity assays into routine clinical practice is detrimental or beneficial to patient management and outcomes; a fundamental and critical assessment for the modern definition of acute myocardial infarction.et al found an increased risk of death in those with an adjudicated diagnosis of type 2 versus type 1 myocardial infarction at 30 days  and at 1 year .32Patients with type 2 myocardial infarction or myocardial injury have poor clinical outcomes, worse than those patients with type 1 myocardial infarction, with one in three patients dead at 1 year.et al reviewed 3762 patients who underwent cardiac troponin testing on clinical indication. Patients with acute myocardial injury were at significantly greater risk of all-cause mortality than those with myocardial infarction at a median follow-up of 3.2 years . In a subgroup analysis, they demonstrate no difference in risk for all-cause mortality between patients with type 2 myocardial infarction or myocardial injury (adjusted hazard ratio (HR) 1.28, 95% CI 0.97 to 1.65).Sarkisian The distinction between type 2 myocardial infarction and myocardial injury may, however, be clinically important, as it has been demonstrated that patients classified as having a type 2 myocardial infarction are twice as likely as those with myocardial injury to be readmitted with a type 1 myocardial infarction in 1 year.‘Acute myocardial injury’ is a term that clinicians are likely to accept, analogous to ‘acute kidney injury’ or ‘acute liver injury’, and does not predicate the mechanism of injury. This term should embrace all patients with acute myocardial injury identified in the context of an alternative acute illness, including those patients with chest pain or evidence of myocardial ischemia. The mechanism of myocardial injury will determine whether any cardiac or coronary investigations or therapies are indicated.We believe there remains scope for clarification of the diagnostic criteria for type 2 myocardial infarction and myocardial injury and that this is necessary to encourage clinicians to adopt the classification proposed in the universal definition. This clinical classification acknowledges the central role of coronary artery disease in the pathogenesis of myocardial infarction.For example, while a patient with a submassive pulmonary embolism and an elevation in cardiac troponin may have both chest pain and an abnormal electrocardiogram, a diagnosis of type 2 myocardial infarction is unhelpful. The diagnosis is pulmonary embolism and acute myocardial injury due to hypoxia or right ventricular strain; coronary investigations and secondary prevention are not indicated.The term type 2 myocardial infarction should, in our opinion, be used exclusively in patients with acute myocardial injury where coronary artery disease has contributed and where there may be opportunities to improve outcomes through coronary revascularisation or medical therapy. Selection of patients with acute myocardial injury for further investigation will depend on the nature of primary illness and the patient's probability of having coronary artery disease.For example, a patient with chronic kidney disease who presents with a community-acquired pneumonia may have persistently elevated cardiac troponin concentrations. The subsequent development of chest pain and ischaemic changes on the electrocardiogram with a temporal rise in serum cardiac troponin concentrations may be due to hypoxia, tachycardia or hypotension, with the acute illness representing a ‘physiological stress test’ identifying otherwise quiescent stable coronary artery disease. The initial diagnosis is ‘acute myocardial injury’, and the need for further investigation for coronary artery disease should be guided by an assessment of cardiovascular risk. In patients with a low probability of coronary artery disease, further cardiac investigations may not be necessary. In patients with an intermediate or high probability, imaging to identify those with coronary artery disease should be considered. Should these investigations confirm the presence of coronary artery disease without evidence of plaque rupture, the diagnosis of type 2 myocardial infarction would be appropriate and secondary prevention should be considered.Until prospective studies have been performed that define the mechanism of myocardial injury in consecutive patients presenting with an alternative acute illness, clinicians will need to rely on clinical judgement to evaluate the likelihood of coronary artery disease.We propose a simple decision framework for the initial investigation strategy to determine the aetiology of myocardial injury and identify those with coronary artery disease who may benefit from secondary prevention .Patients presenting with isolated symptoms or signs of myocardial ischaemia should be assessed using established pathways for patients with suspected acute coronary syndrome . ApproprThose who develop symptoms and signs of myocardial ischaemia in the context of another acute illness should undergo serial high-sensitivity cardiac troponin testing. Patients should be classified with either acute or chronic myocardial injury based on a change in cardiac troponin concentration, ideally using assay-specific absolute delta criteria. In the absence of these criteria, those with troponin concentrations ≤99th centile at presentation with an increase of >50% of the 99th centile upper reference limit on serial testing  are considered to have acute myocardial injury. Where troponin concentrations are >99th centile at presentation, a relative change of >20% is consistent with acute injury.Those patients known to have coronary artery disease may not require further investigation if the mechanism of acute myocardial injury is secondary to oxygen supply-demand mismatch. This may occur in a wide range of conditions where there has been a sustained period of hypotension, tachycardia or hypoxaemia. However, where there is no evidence of oxygen supply-demand mismatch, invasive coronary angiography should be considered to determine whether acute myocardial injury is a consequence of plaque rupture or thrombosis. Where type 1 myocardial infarction is confirmed, application of the GRACE score confers important prognostic information.Patients with persistently elevated cardiac troponin concentrations without a rise and/or fall on serial sampling are likely to have chronic myocardial injury, which may be due to both cardiac and non-cardiac pathologies. In patients not known to have structural heart disease or a condition known to cause myocardial injury, clinical review should consider whether structural heart disease is likely and guide the need for further cardiac imaging such as echocardiography or cardiac magnetic resonance imaging.The implementation of more sensitive troponin assays in clinical practice has increased our awareness of the spectrum of both acute and chronic myocardial injury. While the universal definition classifies myocardial infarction by aetiology, inconsistency in the interpretation and application of these guidelines may be impacting on patient care and outcomes. Identifying patients with acute or chronic myocardial injury, and defining the mechanism of injury is a necessary first step. Careful clinical assessment is necessary to guide the need for further investigations and to identify those patients with coronary artery disease and type 2 myocardial infarction who may benefit from preventative therapies.


Juvenile idiopathic arthritis (JIA) is a systemic chronic inflammatory disease. Studies using tissue Doppler imaging (TDI) for the evaluation of cardiac functions of children with JIA are limited. Thus, this study was conducted to evaluate Left ventricular function, left atrial mechanical functions and atrial electromechanical delay in JIA.This study was carried out as a across sectional study. A total of 34 patients with active JIA and 34 controls were included. Atrial electromechanical delay and left atrial (LA) mechanical functions in addition to systolic and diastolic left ventricular (LV) functions were measured by using conventional echocardiography and TDI. Assessment of disease activity was done using Juvenile arthritis disease activity score (JADAS-27).vs. 1.48 ± 0.16, p = 0.01). E/Em was significantly higher in patients with JIA  denoting impaired diastolic function. Left atrial mechanical functions assessment showed significantly decreased LA passive emptying fraction, increased LA active emptying fraction and LA total emptying volume in JIA patients .JIA patients had abnormal atrial electromechanical coupling as established from prolonged lateral mitral annulus , septal mitral annulus (PA septum), inter-atrial and intra-atrial electromechanical delays compared with healthy controls. Left ventricular filling abnormalities were found characterized by a reduced E/A ratio (1.07 ± 0.56 Atrial electromechanical coupling intervals, and LA mechanical functions were impaired which can be considered as an early form of subclinical cardiac involvement in JIA patients. Significant diastolic functional abnormalities exist in JIA. Juvenile idiopathic arthritis (JIA) is defined as ‘persistent arthritis of unknown etiology that begins earlier than 16 years and persists for at least 6 weeks’ . It reprNowadays, it has been recognized that inflammation plays a significant role in the pathogenesis of atrial fibrillation (AF) . The risElectrophysiological and electromechanical abnormalities originating from conduction disturbances in the atria are associated with an increased risk of AF , 10. TheTissue Doppler imaging (TDI) has been proved to provide atrial conduction times, measurements of local systolic and diastolic myocardial velocities as well as detection of abnormalities of left ventricular diastolic function , 13. An To the extent of our knowledge, the published studies assessed left ventricular diastolic dysfunction by TDI without assessing atrial electromechanical delay and LA mechanical functions in JIA patients . TherefoThis study was carried out as a cross sectional study. Thirty-four active JIA patients with a mean age of 13.97 ± 4.77 years, fulfilling the revised criteria of the International League of Associations for Rheumatology (ILAR)  were enrAll study Children older than 16 years; children with rheumatic or congenital heart disease, history of any clinical evidence of coexisting cardiac disease, diabetes mellitus, arrhythmia, valvular heart diseases or ischemic heart diseases were excluded by history, physical examination, chest radiography, Echocardiography and standard 12-lead electrocardiography (ECG).Prior to subject recruitment, the study protocol was reviewed and approved by the research ethics committee of the Faculty of Medicine, Suez Canal University, written informed consents were obtained from all the Parents or care givers. All procedures performed in studies involving human participants were in accordance with the ethical standards of the research ethics committee of the Faculty of Medicine Suez Canal University and with the 1964 Helsinki declaration and its later amendments.2 [We gathered information regarding patient characteristics such as age, gender and disease duration. Growth parameters measured were height (to nearest 0.5 cm via Harpenden stadiometer), weight (to nearest 0.1 kg), and body mass index (BMI) was calculated as weight (kg)/height (m)2 . All sub2 .The JADAS-27 is calculated by summing the scores of four core-set criteria : 1) physTransthoracic echocardiographic measurements were performed with General Electric system VIVED 7 machine ultrasound phased array system using a 3.0-mHz transducer for two-dimensional M-mode measurements of the left ventricular structure and systolic function according to the recommendations of the American Society of Echocardiography .Measurements were recorded as average of three cardiac cycles. Left atrium (LA) dimension, left ventricular end-systolic (LVESD) and end-diastolic dimensions (LVEDD), diastolic ventricular septal thickness and diastolic LV posterior wall thickness were measured in the parasternal long-axis view. Left ventricular EF was estimated using the Simpson’s rule. Left ventricular mass was calculated with the Devereux equation  and was Left ventricular diastolic function was assessed by measuring the mitral flow velocity recorded in the apical four-chamber view. The pulse Doppler sample volume was placed in the left ventricular inflow tract at the level of mitral leaflet tips and three consecutive measurements were averaged. The various variables of diastolic function that were measured included: peak early  and peak atrial filling velocity , ratio of E to A (E/A), E acceleration time, E deceleration time , isovolumic relaxation time (IVRT) was measured in the apical five chamber view with the sample volume placed between the aorta and mitral valve where the recordings of both valves were taken simultaneously.Tissue Doppler echocardiography was performed with a concurrent Electrocardiography (ECG) recording using Fukuda Denshi FCP-7101 Interpretive ECG Machine. The frequency of the transducer was of 3.5–4.0 MHz, adjusting the spectral pulsed Doppler signal filters to obtain the Nyquist limit of 15–20 cm/sec, and using the minimal optimal gain setting. The monitor sweep speed was set at 50–100 mm/sec to optimize the spectral display of myocardial velocities. A sample volume (2 mm) was placed within mitral annulus septal myocardial wall, analyzing wall motion parallel to cursor orientation. Septal annulus now is the preferred site for tissue Doppler imaging, because this location is less influenced by the pericardium. Systolic (Sm), early diastolic (Em) and late diastolic (Am) TD velocities were measured, and the Em/Am ratio and the dimensionless parameter E/Em were computed. E/Em was found in previous studies to be directly correlated with impaired diastolic function –25.In apical four-chamber view, the pulsed Doppler sample volume was placed at the level of the LV lateral mitral annulus, and subsequently at the septal mitral annulus and right ventricular tricuspid annulus. The sampling window was positioned as parallel as possible with the myocardial segment of interest to obtain the optimal angle of imaging. Atrial electromechanical coupling was defined as the time interval from the onset of P wave on the surface electrocardiogram to the beginning of the late diastolic wave (Am wave), i.e. PA interval and was measured from the lateral mitral annulus , septal mitral annulus (PA septum), and right ventricular tricuspid annulus (PA tricuspid) . All PA Left atrial volumes were measured by the method of discs in the apical four-chamber view at end-systole , end-diastole  and at the onset of atrial systole . All volumes were indexed to BSA and expressed in ml/m2. Then, the following LA emptying function parameters were calculated :\documenP values were adjusted using false discovery rate (FDR) algorithm. Multivariate linear regression analysis was used to identify significant determinants of interatrial and intra-atrial electromechanical delay. A p value of less than 0.05 was considered significant.All statistical analyses were performed using the IBM SPSS for Windows version 22.0 . Data were expressed as mean and standard deviation. Student’s t test (two-tailed) was used for inter-group comparisons. To analyze categorical data, chi-square test was used. Nonparametric data were analyzed using Mann Whitney U test. Pearson correlation coefficient test was used to assess the degree of association between different variables. Pearson correlation was used to correlate continuous variables. p > 0.05).Clinical and laboratory characteristics of the two groups are shown in Table Patients with JIA exhibited significantly higher levels of ESR and C reactive protein (CRP). All patients exhibited active disease, the mean JADAS-27 score was 23.51 ± 9.53 and the mean disease duration was 50.24 ± 15.98 months. Methotrexate was the mostly used disease modifying anti-rheumatic drugs (DMARDs) (91.2%) in treating JIA patients.P = 0.01). Peak trans-mitral E velocity was lower among patients with JIA. This was also echoed by the E/A velocity ratio, which was significantly lower among patients compared to the healthy population. E/Em was significantly higher in patients with JIA than in the control group (p = 0.02).The main echocardiographic and Doppler findings in this series of patients with JIA without clinical evidence of cardiovascular disease were summarized in Table p > 0.05). However, LA passive emptying fraction was significantly decreased and LA active emptying fraction and LA total emptying volume were significantly increased in JIA patients .Left atrial volume measurements Table . The twop = 0.03), PA septum (p = 0.02), inter-atrial (p = 0.04) and intra-atrial (p = 0.02) electromechanical delays compared with healthy controls.Atrial electromechanical coupling intervals were measured from different areas by TDI Table . JIA patp = 0.025), JADAS-27 (p = 0.045) and Systolic Blood pressure (p = 0.013) (adjusted R2 = 0.16). Intra-atrial electromechanical delay was related to disease duration (p = 0.003) and JADAS-27 (p = 0.01) (adjusted R2 = 0.39). No association was found between Intra-atrial electromechanical delay and LA mechanical functions and to LV functions in these patients.Multivariate linear regression analysis showed that Inter-atrial electromechanical delay was significantly related with disease duration , are evident in patients with rheumatic disorders compared to healthy population as reported from literature . In our On the contrary, one research studied atrial conduction abnormalities through measuring P wave dispersion (PWD) and P wave duration and found that PWD value was similar in JIA patients and healthy children . They suOur results revealed significant increase in LVESD. Systolic function parameters (EF and FS) were lower compared to controls but within normal limits. Several studies were in harmony with our results, where they reported significant higher LVESD and LVEDD  or higheBy analyzing the measurements of the Pulsed Wave-Tissue Doppler, they revealed abnormalities in diastolic function. Peak trans-mitral E velocity and E/A velocity ratio was significantly lower among JIA patients compared to the healthy group which supports diastolic dysfunction. Our data are consistent with the data of many studies , 29, 33.Concerning TDI, our results showed that E/Em, was significantly higher and Em/Am ratio was significantly lower in JIA patients than in control group. Alkady et al.  have obsDiastolic dysfunction is associated with long disease duration, but its etiology is still unclear . Some reIn our work, we found that, LA mechanical functions were significantly impaired as LA passive emptying fraction was significantly decreased while LA active emptying fraction and LA total emptying volume were significantly increased in JIA patients.To our knowledge, LA mechanical functions was not assessed in JIA. However, other studies have reported LA impaired mechanical functions measured with TDI in other rheumatic disease, as in patients with asymptomatic scleroderma .R2 = 0.16). Intra-atrial electromechanical delay showed significant correlation to disease duration and JADAS-27 and this correlation showed strong linear relationship (adjusted R2 = 0.39). These results indicated that cardiac damage is most probably caused by long-term chronic inflammation and high disease activity. Similarly, results of a study carried out on adult RA patients, suggested that intra- and interatrial electromechanical delays are prolonged in RA patients, and that LA active emptying fraction and serum CRP level are independent factors of the inter-atrial electromechanical delay [Furthermore, in order to achieve our aim, atrial electromechanical delay (AEMD) was correlated to LA mechanical functions, LV functions and disease activity in JIA patients. Multivariate linear regression analysis showed that Inter-atrial electromechanical delay was significantly correlated with disease duration, JADAS-27 and Systolic Blood pressure but this correlation showed weak linear relationship  would be reasonable to assess the long-term effect of the disease on the heart which is essential in summing up a final conclusion. Third, there are some unmeasured confounders as socioeconomic status and adherence to treatment.


EPs diagnosed DD based on Six LBEs were deemed indeterminate by the cardiologist and excluded from the analysis. Agreement was reached in 41 out of 48 cases (85.4%). The unweighted kappa coefficient was 0.74 (95% CI 0.57–0.92). EPs identified 18 out of 20 LBEs diagnosed with diastolic dysfunction by the cardiologist.eʹA) by EP and cardiologist interpretation of LBEs. Future studies should investigate this simplified approach as a one-step method of screening for LV diastolic dysfunction in the ED.There is a good agreement between ( Diastolic dysfunction (DD) is an alteration of relaxation, filling, and/or distensibility of the left ventricle . DD can eʹ) using tissue Doppler imaging (TDI) at the septum (eʹS) and lateral wall (eʹL); and (4) left atrial (LA) volumes /2) has been described as an acceptable single-step method for assessing LV relaxation, using eʹA < 9 cm/s as a threshold [Average peak mitral annulus velocity by TDI  of patients presenting to the emergency department (ED) with asymptomatic elevated blood pressure , 13.LBEs were performed based on research staff availability by EPs (two emergency ultrasound fellowship-trained faculties and one emergency ultrasound fellow) who had performed at least 100 LBEs through routine clinical care and who underwent training and demonstrated proficiency in diastology with a board-certified cardiologist. A sonosite M-Turbo ultrasound system equipped with a harmonic 4.0-MHz variable-frequency phased-array transducer was used to obtain images and measurements. Studies were digitally archived for cardiologist review.eʹA by averaging eʹS and eʹL measurements. EPs considered an eʹA < 9 cm/s as evidence of DD without adjustment for age or other risk factors. A board-certified cardiologist with an ASE level III echocardiography certification independently reviewed LBE images while blinded to EP interpretation. The cardiologist rated the images in accordance to the 2009 ASE guidelines [E and A measurements, eʹS and eʹL, E/eʹ ratios to assess LA pressure, estimation of LA size, and the EKG rhythm strip (see Table EPs utilized electrocardiogram (EKG) rhythm strips to time diastole. EPs determined idelines  and uponEPs and cardiologist indicated DD present, DD absent, or indeterminate for each LBE study. A 3 × 3 contingency table provided a summary of agreement. Inter-rater reliability between EPs and the cardiologist was determined using an unweighted kappa with 95% confidence interval (CI) coefficient using Stata Release 15, StataCorp.Forty-eight studies were submitted to the cardiologist for review. Cardiologist and EP agreement are summarized in Table eʹA alone, EPs can identify DD with high level of agreement compared to a cardiologist following the ASE guidelines.Diastolic dysfunction is prevalent and delays in diagnosis can lead to increased morbidity and mortality. EPs with focused training in diastology may identify diastolic dysfunction with high sensitivity compared to a cardiologist trained in echocardiography. Previous studies have demonstrated that EPs can identify DD with high sensitivity, but either did not include TDI as part of their assessment  or reporeʹA and DD. EPs did not screen for regional wall motion abnormalities. Because wall motion abnormalities of the left ventricular basal segments can influence mitral annulus TDI diastolic velocities, this may have led to an overestimation of DD prevalence. Moreover, comparison was limited to cardiologist interpretation of LBE images, which may not be representative of typical exams obtained by a technician or specialist. A larger, multi-center study comparing EP assessment of eʹA against performance of a comprehensive echocardiogram can help establish external validity.Our sample size and convenience sampling may have introduced selection bias thus preventing a definitive correlation between eʹA alone achieved good agreement for determination of DD compared to LBE interpretation by cardiologist. Future studies should further investigate this simplified approach as a one-step method of screening for LV DD in the emergency department.This study highlights a promising simplified approach for identifying DD by EPs. Relying on