The aim of this study was to establish M-mode echocardiographic reference values in Pantja goats and to study the effect of gender and body weight (BW) on these parameters.A total of 18, clinically healthy, adult Pantja goats of either sex, aged 2-4 years and weighing 10-44 kg were included in the study. Echocardiographic examination was performed in the standing unsedated animal. All measurements were made from the right parasternal long-axis left ventricular outflow tract view of the heart. The following parameters were recorded: Left ventricular internal diameter at diastole and systole, interventricular septal thickness at diastole and systole, left ventricular posterior wall (LVPW) thickness at diastole and systole, end diastolic and systolic volumes, stroke volume, fractional shortening, ejection fraction, percent systolic thickening of interventricular septum, percent systolic thickening of LVPW, cardiac output, left atrial (LA) diameter at diastole and systole, aortic (AO) root diameter at diastole and systole, LA/AO, LA posterior wall thickness at diastole and systole, left ventricular ejection time, DE amplitude, EF slope, AC interval and e-point to septal separation.This study demonstrated specific reference ranges of M-mode echocardiographic parameters and indices in healthy Pantja goats. Normal echocardiographic values obtained in Pantja goats were quite different from other goat breeds. Gender had no influence on echocardiographic parameters, while high correlations were found between most echocardiographic parameters and BW.The echocardiographic values obtained in the study may serve as a reference for future studies in this breed, for cardiovascular disease diagnosis and for utilizing the goat as a model for cardiac disorders in humans. Echocardiography is a non-invasive method for assessment of cardiac structure and function. In goats, structural cardiac abnormalities are rarely diagnosed clinically because this species is relatively resistant to cardiac disease and is rarely presented for detailed medical evaluation at veterinary hospitals. Despite this, echocardiography has proved to be an interesting tool for diagnosing cardiovascular diseases in goats ,2.Unlike other animals, goats are easily manageable and have a heart size comparable with that of human beings, which makes them an ideal candidate for the developing of animal models for human cardiovascular research . HoweverPantja is the local goat of Tarai region of Uttarakhand. Studies on body weight (BW), body measurements, scrotal morphology, production traits, growth pattern, and mortality rate of Pantja goats -11 have This study was conducted in accordance with the guidelines laid down by the Institutional Animal Ethics Committee.A total of 18, clinically healthy, adult Pantja goats , aged 2-4 years and weighing 10-44 kg  were included in the study. Animals were acclimatized to approaching, handling and housing conditions for a period of 21-28 days before start of the echocardiographic examination. Animals were considered to be free of cardiovascular disease based on history, clinical examination, complete hematobiochemical examination, cardiac auscultation, normal lead II electrocardiogram, and routine echocardiography.rd to 5th right intercostal spaces starting just caudal to the triceps muscle mass, from 3 to 5 cm below right olecranon to 5-10 cm above it was prepared for echocardiographic examination. Echocardiography was performed in a standing position with the right front leg pulled slightly forward by an assistant. M-mode echocardiographic evaluation of heart was guided by simultaneous display of real time two-dimensional echocardiographic images.Echocardiographic examination was carried out with a Scintilla Color Doppler Ultrasound Scanner (Larsen and Toubro Limited) equipped with 2.5-3.5 MHz multi-frequency phased-array transducer. Region between 3Echocardiographic examination was performed using leading edge method as per the recommendations of the American Society of Echocardiography from frozen images on the screen . All meaTeicholz formula  was usedData were analyzed using statistical software SPSS 14.0. Independent sample t-test was used to study differences between male and female dogs. Mean values among different groups based on BW was compared using one-way ANOVA and Duncan’s multiple range test as per methods described by Snedecor and Cochran . Linear M-mode echocardiographic reference values in Pantja goats were determined and its subjective comparison with other goat breeds was done. In addition, the possible effect of gender and BW on echocardiographic parameters was determined. Mean±standard error of M-mode echocardiographic parameters and indices in Pantja goats is presented in LVDd and LVDs in Pantja goats was lower than adult goats, Saanen goats, and Swedish goats -7. IVSd Nonsignificant influence of gender on various echocardiographic parameters  in Pantja goats  was in aBW correlated significantly (p<0.01) with most M-mode echocardiographic parameters  in Pantja goats Tables- and 3. SFrom the results of this study, it can be concluded that echocardiographic values in Pantja goats differ from other goat breeds. Gender had no influence while most echocardiographic parameters were influenced significantly by animal’s BW. Values obtained in the study may serve as a reference for future studies in this breed as well as for cardiovascular disease diagnosis in humans.PS: Research was done by this author as the part of her M.V.Sc. thesis dissertation. NSJ: Designed the study and supervised the research. DB, MK and PS: Analysed and interpreted the data. All authors read and approved the final manuscript.


HF). The objective of the study was to create a rabbit model through multiple coronary artery ligations to investigate the postoperative structure‐function remodeling of the left ventricle (LV) and coronary arterial trees. Here, we hypothesize that the interplay of the degenerated coronary vasculature and increased ventricle wall stress relevant to cardiac fibrosis in vicinity of myocardial infarction (MI) precipitates the incidence and progression of ischemic HF. Echocardiographic measurements showed an approximately monotonic drop of fractional shortening and ejection fraction from 40% and 73% down to 28% and 58% as well as persistent enlargement of LV cavity and slight mitral regurgitation at postoperative 12 weeks. Micro‐CT and histological measurements showed that coronary vascular rarefaction and cardiac fibrosis relevant to inflammation occurred concurrently in vicinity of MI at postoperative 12 weeks albeit there was compensatory vascular growth at postoperative 6 weeks. These findings validate the proposed rabbit model and prove the hypothesis. The post‐MI rabbit model can serve as a reference to test various drugs for treatment of ischemic HF.Animal models are of importance to investigate basic mechanisms for ischemic heart failure ( Heart failure (HF) is caused by cardiovascular diseases, for example, myocardial ischemia and infarction, hypertension, valvular heart diseases, etc  images. Histological data were used for evaluation of myocardial infarction and fibrosis. The significance, implication, and limitation of the study were discussed in relation to potential improvements of cardiac performance in post‐MI patients.The objective of the study is to investigate the structure‐function remodeling of the LV and coronary arterial trees in rabbit hearts for 12 weeks after myocardial infarction through multiple coronary artery ligations. Here, we hypothesize that cardiac fibrotic remodeling relevant to inflammation impairs the myocardium and coronary vasculature in vicinity of myocardial infarction, which is a critical risk factor to precipitate the incidence and progression of ischemic HF. To verify the hypothesis, myocardial infarction was created in male New Zealand White rabbits through multiple ligations of coronary arteries. The follow‐up study was carried out for 12 weeks. Echocardiographic measurements were performed weekly. Hematological and hemodynamic parameters were measured before the termination. Morphometric data of coronary arterioles were obtained from micro‐CT  and 20 animals of MI through multiple coronary artery ligations . Experiments were performed in the two groups for 6  or 12  weeks postoperatively. All animal experiments were performed in accordance with Chinese National and Hebei University ethical guidelines regarding the use of animals in research, consistent with the NIH guidelines  on the protection of animals used for scientific purposes. The experimental protocols were approved by the Animal Care and Use Committee of Hebei University, China.In sterile environment, rabbits were first anesthetized by an intravenous (IV) injection of 25% urethane (4 mL/Kg) through an ear vein. Animals were then intubated and ventilated with room air using a Harvard ventilator (Inspira). Intravenous access was established for drug injection and ECG signals were monitored during the entire surgical operation.After the chest was shaved and sterilized, a left thoracotomy was performed between the third and fourth intercostal spaces, followed by a pericardiotomy , interventricular septum end‐systolic wall thickness (IVSs), left ventricle end‐diastolic diameter (LVDd), left ventricle end‐systolic diameter (LVDs), left ventricle end‐diastolic posterior wall thickness (LVPWd) and left ventricle end‐systolic posterior wall thickness (LVPWs) were measured according to the American Society of Echocardiography leading edge rule  and aortic outflow peak velocity (APV).Echocardiographic measurements were carried out weekly in rabbit hearts after myocardial infarction as well as age‐matched shams. Similar to a previous study  for 11 weeks after the surgery. Standard hematological parameters including white blood cells (WBC), red blood cells (RBC), monocytes percentage (MO%), eosinophils percentage (E%), basophils percentage (B%), platelet distribution width (PDW), mean platelet volume (MVP), plateletcrit (PCT), nucleated red blood cells percentage (NRBC%), hemoglobin content (HGB), mean corpuscular volume (MCV), neutrophils percentage (NE%), lymphocyte percentage (LY%), hematocrit (HCT), and red blood cell distribution width (RDW) were determined using a LH 750 analyzer (Beckman Coulter).±dpdt) were determined from the measured pressure waves  was inserted through the right carotid artery into the LV to record pressure waves in 30 cardiac cycles, which was repeated three times. The zero‐pressure baseline of the catheter was calibrated in 37°C saline. A conductance catheter (Suzhou Runxin Company) was also inserted to the LV to measure the volume  were selected for the μCT scanner (PerkinElmer). Images were collected in a wide field of view (FOV = 72 mm). The X‐ray energy power and voltage were 8 W and 90 kV, respectively. The isotropic voxel size was 9 μm. Total scan time for an entire heart was about 1 h. A region of myocardial infarction was identified as the distal region to a ligation with gray color and thin wall thickness. Some plugs (~4 × 4 mm) in normal and border zones  were transmurally sectioned from the heart, as shown in Figure The scanning for an entire heart was performed using a Quantum GX μCT images using a gray‐scale threshold method in a commercial software , as shown in Figure correct by fitting a Gaussian distribution function  to the line profiles followed by computation of the input square wave. To reduce the sampling error of finite discrete grid, coronary arterial trees with vessel diameter ≥36 μm (four times the voxel size) were used. Moreover, vessel densities (vessel number per mm3) were determined in each plug using the Living Image Software.Morphometric data of coronary arterial trees were extracted from μm thickness, deparaffinized with xylene, and rehydrated. The Hematoxylin/Eosin and Masson trichrome staining was performed according to standard procedures. Furthermore, infarct and fibrotic area ratios  were determined using the Image‐Pro‐Plus 6.0 software .Ten rabbits in each group  were selected for the histological analysis. After a midline sternotomy, rabbits were terminated with a bolus injection of saturated KCl through the jugular vein. The heart was rapidly removed and rinsed in 0.9% saline solution. Multiple plugs of myocardial tissues (~ 4 × 4 mm) were removed from the LV apex, fixed in 10% buffered formalin, and embedded in paraffin. Plugs were completely sectioned transmurally into 5 P < 0.05 was indicative of a significant difference between the two populations.Morphometric and hemodynamic data were expressed as mean ± SD (standard deviation) in sham and ligation groups. Similar to a previous study , HR and body weight (BW) between sham and ligation groups for 6 and 12 weeks after the surgery, which have no statistical difference. In contrast, myocardial infraction leads to a significant decrease in APV and MPV (P < 0.05). Figure s, LVDd, FS (%), and EF (%) postoperatively. The difference of four parameters between sham and ligation groups increases with time (P < 0.05). Hemodynamic parameters, LVSP and LVEDP, have mean±SD values of 99 ± 20 and 6 ± 3 mmHg in the sham group and 90 ± 16 and 18 ± 11 mmHg in the ligation group at postoperative 12 weeks, which show significant difference of LVEDP (P < 0.05). There is a ~40% decrease of ±dpdt values in the ligation group as compared with the sham group at postoperative 12 weeks (P < 0.05). Moreover, Figure Figures V P < 0.0. Figure μCT measurements, Figure Vessel densityVessel density in sham and a unit value in the sham group) at normal and border zones. Border zones in rabbits of myocardial infarction have a twofold increase in vessel density at postoperative 6 weeks, but a slight decrease at postoperative 12 weeks. There is no statistical difference in normal zones between sham and disease animals. Furthermore, Figure Table This study developed a post‐MI rabbit model through ligations of the LAD artery and primary branches of the LCx arterial tree. In general, rabbits had a dominant LCx arterial tree, but a thin and small LAD artery  of wall thickness at infarction and border zones, respectively, as compared with normal zones, which cannot be observed through echocardiographic exams. The structure‐function remodeling after multiple coronary artery ligations in rabbit hearts accurately mimics the progression of ischemic HF in post‐MI patients  occurred for 6 weeks after myocardial infarction and converted to the rarefaction from 6 to 12 weeks in border zones, as shown in Figure A key finding of the study was that compensatory arteriolar growth  (Hasenfuss Although experimental measurements were performed to analyze the structure‐function remodeling after multiple coronary artery ligations in rabbits, computational results of LV wall stresses (Lee et al. A post‐MI rabbit model was created through multiple ligations of coronary arteries. The in vivo and ex vivo measurements showed the clinically relevant structure‐function remodeling for 12 weeks after MI, for example, persistent enlargement of the LV, slight mitral regurgitation, monotonic drop of fractional shortening and ejection fraction, etc. Moreover, coronary vascular rarefaction and cardiac fibrosis relevant to inflammation occurred concurrently in the border zone at postoperative 12 weeks while there were compensatory vascular growth and scanty fibrosis at postoperative 6 weeks. The interplay of degenerated coronary vasculature and increased LV wall shear, associated with cardiac fibrosis at the border zone, is a risk factor for the vicious cycle of ischemia and HF. The proposed post‐MI rabbit model can serve to investigate basic mechanisms for progression of ischemic HF as well as test anti‐inflammatory agents for treatment.None.


T1 mapping in end diastole requires correct identification of the diastolic pause, and an appropriate input of the trigger delay time (TD) into acquisition parameters to ensure parametric mapping during the true diastolic pause for minimal motion-related blurring of myocardium. This diascan can be derived for individual patients from either the 4 chamber or the short axis stack. However, this additional step adds complexity and time to the scan and potentially introduces error. We investigated whether the TD could be estimated from the heart rate (HR) to simplify MOLLI acquisitions.Patients who had a clinical scan were randomly selected retrospectively and grouped by their mean heart rate  as shown in table 1. These patients had a mixture of conditions including valvular disease, coronary disease, cardiomyopathy and normal scans. Cardiac diastasis duration and TD were measured from cine images as per the formula TD=((time at beginning of diastolic stasis)+(time at end of diastolic stasis)/2) for each patient. Assuming a linear relationship a line of best fit was calculated for the 70 measurements. From the line-fit, TD could be estimated for any prospective scan on the basis of HR. The calculated values were validated against a separate cohort of retrospective patients . Then prospectively 10 volunteers  underwent native T1 mapping  using the calculated TD and the estimated TD to allow comparison. A low or high resolution version of the sequence was used if HR was < or >90 bpm. Each had basal and mid level T1 mapping repeated twice, and using the average of the two levels a total of 10 basal and 10 mid level values for the whole cohort were available for comparison.There was a strong linear relationship between each HR group and calculated TD, Estimated TD = -40.82 × HR +633, R2 = 0.82 Figure  suggestiThis work suggests that the estimated TD may provide a suitable alternative to manual calculations of TD for patients scheduled for T1 mapping using an 11HB MOLLI. Larger studies might allow a more accurate estimation of the TD particularly if more factors are modeled, rather than HR alone in multiple pathologies. However, at present pre-patient optimization of TD from their cine images remains more accurate and should be considered as the default.


Systemic sclerosis (SSc) is an autoimmune disease characterized by microvascular abnormalities, inflammation and fibrosis. We hypothesized that myocarditis may be diagnosed in asymptomatic SSc, undergoing routine cardio-vascular magnetic resonance (CMR) for fibrosis assessment, using the Lake Louise criteria: T2 ratio, early (EGE) and late gadolinium enhanced (LGE) images.Eighty-two asymptomatic SSc, diagnosed according to American College of Rheumatology criteria, aged 43 ± 5 yrs., 62 with diffuse (dSSc) and 20 with localized (lSSc) systemic sclerosis were evaluated by CMR, performed at 1.5 T scanner, according to Lake Louise criteria.CMR documented normal biventricular function in all SSc. However, 7/62 (11.2%) with dSSc and 2/20 (10%) with lSSc, had CMR signs of myocarditis according to Lake Louise criteria, without any clinical cardiac symptom. In these 9 patients, T2 ratio, EGE ratio and LGE  were 2.8 ± 0.5%, 8 ± 3% and 5 ± 3% of LV mass, respectively. No correlation between CMR and blood inflammatory indices (C-reactive protein and erythrocyte sedimentation rate), cardiac troponin T, disease characteristics or type of SSc was identified. A repeat CMR at 6 months, after treatment with prednisone and azathioprine, showed normalisation of the acute inflammation CMR indices.Silent myocarditis may be diagnosed using the Lake Louise paper criteria in SSc patients without cardiac symptoms, has no correlation with blood inflammatory indices, cardiac troponin or disease characteristics. CMR is a promising tool to diagnose silent myocarditis in SSc and monitor the response to immunosuppressive treatment. Systemic sclerosis (SSc) is an autoimmune disease characterized by microvascular abnormalities, inflammation and increased fibrosis of all organs, including the heart . AsymptoMyocarditis, fibrosis, pulmonary hypertension and blood vessel abnormalities are considered as the main etiologic factors of cardiac involvement in SSc. Myocarditis is a contributor of recent-onset cardiac disease in SSc, and if timely treated, the progression to further cardiac damage can be avoided by immunosuppression . HoweverCardiovascular Magnetic Resonance (CMR), a non-invasive, non-radiating, operator independent technique, has been successfully used for the evaluation of myocardial fibrosis in SSc , 9. The We hypothesized that the Lake Louise criteria for myocarditis  may be aEighty-two consecutive SSc without cardiac symptoms, diagnosed according to 2013 American College of Rheumatology criteria  , T1-weighted before and early after contrast media injection (EGE) and late enhanced images (LGE). The study was considered as positive for myocarditis, according to Lake Louise criteria .Cardiovascular magnetic resonance examination was performed in a 1.5 T Philips Intera system using STIR T2-weighted (T2-W), T1-weighted (T1-W) before and early after contrast media injection (EGE) and late enhanced images (LGE). ECG-triggered, STIR T2-W multislice spin-echo sequence was performed in axial orientation and the signal ratio was calculated from the left ventricular myocardium and the skeletal muscle in the same slice. ECG-triggered T1-W multislice spin-echo images were also obtained in axial orientation with identical parameters before and after an intravenous bolus of 0.1 mmol/kg Gd-DTPA. Measurements were performed after 1 min of injection of Gd-DTPA for early gadolinium enhancement (EGE) in the same area as in T2-W. Immediately after this, 0.1 mmol/kg Gd-DTPA was given again and late gadolinium-enhanced images (LGE) were taken 15 min later, using an a 3D–T1-TFE sequence, preconditioned with a 180 degrees inversion pulse . Images were analyzed according to previously described protocols .For each subject, localizing scans were obtained to define the long (2-chamber) axis of the left ventricle. A mid ventricular short axis view was prescribed, and used to plan a 4-chamber view. The short axis orientation was then defined accurately, perpendicular to both the 2- and 4-chamber views. To cover the entire left ventricle, 10 contiguous (gap = 0 mm) short axis slices were acquired in each study. The imaging sequence was a 2D, multi-phase , steady-state free-precession (SSFP) sequence  characterized by the application of balanced gradients in all directions [In T2-W the signal ratio was measured from the region of interest covering the left ventricular myocardium as well as within a skeletal muscle in the same slice.xIn T1-W early enhancement (EGE), which reflects hyperaemia and capillary leak as a marker of inflammation, the early myocardial enhancement was measured from the region of interest covering the left ventricular myocardium as well as within a skeletal muscle in the same slice .To assess the contrast-enhanced images (LGE), all short-axis slices from base to apex were evaluated for areas of normal (completely nulled) myocardium , 10. MeaCine images were used for the evaluation of left and right ventricular ejection fraction (LVEF/RVEF), using the MRI-MASS  software was used and the readers were blinded to the clinical data .p < 0.05.All measurements were expressed as mean ± SD. Statistical significance of the differences was investigated using unpaired Student’s T-test. Correlation between variables was sought with Pearson’s correlation coefficient. For non-parametric data, the Mann-Whitney test and Spearman’s correlation coefficient were used respectively. Statistical significance was considered for In our study, CMR documented normal biventricular function in all SSc evaluated. However, 7/62 with dSSc and 2/20 with lSSc, although they had no cardiac symptoms/signs, were positive for myocarditis, according to Lake Louise criteria . In all There was no correlation between the CMR findings and the blood inflammatory indices (C-reactive protein/CRP and erythrocyte sedimentation rate/ESR), the cardiac troponin T (cTnT) measured at the time of CMR evaluation, the disease characteristics or type of SSc was identified. CMR findings of SSc were presented in Table Treatment with prednisone 20 mg poqd and azathioprine 100 mg poqd started after the positive CMR result for myocarditis was available. A follow up CMR was performed in all SSc patients after 6 months of immunosuppression. These follow up CMR investigations showed complete normalisation of CMR indices indicative of acute myocarditis .In our study, using the Lake Louise criteria, we documented that 10% of patients with either dSSc or lSSc presented CMR evidence of myocarditis, although they had no cardiac symptoms/signs and positive inflammatory or cardiac biomarkers. No correlation between type of SSc, disease duration, inflammatory indices or cTnT levels and CMR findings was identified. After 6 months of immunosuppression a complete normalization of CMR indices indicative of acute inflammation was identified.Although myocardial involvement in SSc was usually attributable to non-inflammatory causes, there are early reports presenting SSc patients with evidence of myocarditis and good response to the combination of either corticosteroids and azathioprine  or cortiAlthough parametric imaging was not available in these SSc patients, recent unpublished data from our group after assessment of 24 SSc patients evaluated by both Lake Louise criteria and parametric imaging in our department showed an increase of T2 mapping in 15/24 SSc with values ranging between 62 and 75 msec, STIR T2 ratio > 2 in 17/24 and native T1 values ranging between 1110 and 1235 mesc in all 22/24 SSc patients. These very preliminary data seem rather support of the use of T2 instead of T1 mapping as an index of recent inflammation in SSc.Another important issue is the lack of correlation between the blood inflammatory indices and cTnT and CMR indices. However, this is not unusual because lack of such correlation was also identified in both infective  and autoEndomyocardial biopsy (EMB), although it carries serious limitations due to its invasive nature, interobserver variability and sampling error, is considered as the diagnostic “gold standard” in clinical scenarios suggestive of myocarditis , 26. AutThe published literature in the field supports the crucial role of CMR in the diagnosis of myocarditis, as a contributor of heart disease in SSc –9, 13–18The patients’ sample was smallT1 and T2 mapping was not performed, because these sequences were not available at the time of the CMR examination at our center. However, we should mention that although these indices represent an important part of current CMR research, they are not widely available and standardization of the relevant protocols and normal values are still under evaluation .Endomyocardial biopsy (EMB) for comparison with CMR findings was not performed, because our patients were not eligible for EMB, due to lack of symptoms and normal biventricular function . FurtherThe following limitations may be discussed for this study:Silent myocarditis may be diagnosed using the Lake Louise criteria in a considerable percentage of SSc patients presenting without clinical cardiac symptoms, and has no correlation with blood inflammatory indices  or further clinical disease characteristics. CMR signs of myocarditis frequently normalize 6 months under after immunosuppressive treatment with corticosteroids and immunosuppressive treatment.


The remaining values were higher or lower than those from the long‐used Medasys system. These differences might have changed cancer patient chemotherapy clinical decisions. As a result, our institution elected not to implement either new system.Before implementing one of two new LVEF radionuclide gated ventriculogram (MUGA) systems, the results from 312 consecutive parallel patient studies were evaluated. Each gamma‐camera acquisition was simultaneously processed by semi‐automatic Medasys Pinnacle and by fully automatic and semiautomatic Philips nuclear medicine computer systems. The Philips systems yielded LVEF results within PACS: 87.57.U‐ Nuclear medicine imaging The company later became Medasys and produced the Pinnacle MUGA system. While other imaging techniques such as quantitative gated SPECT (QGS) and volumetric ultrasound have subsequently been developed for LVEF determination, planar radionuclide ventriculography remains a generally accepted standard against which other LVEF measurement techniques are evaluated.(–) In particular, at institutions with active cancer treatment centers, this study is frequently performed on patients receiving chemotherapy regimens with various cardiotoxic drugs.(–)The MUGA (multigated acquisition) study has long been used as a non‐invasive method for quantification of left ventricular ejection fraction (LVEF).–3 OnFor over 17 years, the standard planar radionuclide ventriculogram at our institution had been the Medasys Pinnacle MUGA study. However, when Medasys went out of business several years ago and stopped supporting their hardware and software, our institution sought a replacement system. No universally accepted gold standard exists for left ventricular ejection fraction.To understand why we decided to clinically test the two systems, it is important to discuss briefly how each processing algorithm works. The Medasys Pinnacle system is semiautomated: the operator positions a box defining the search limits for the algorithm to find the edges of the left ventricular (LV) chamber using standard second‐derivative search criteria. The operator employs Fourier phase data to help position this box accurately to exclude left atrial (LA) activity. The operator then visually evaluates the data to exclude right ventricular (RV) activity and non‐cardiac (e.g. splenic) activity from the area being searched. The sensitivity of the edge‐detection algorithm can be manually adjusted if necessary in the four quadrants of the LV chamber to maximize edge tracking accuracy. This system has demonstrated reproducible results at our institution for over 17 years and thus serves as a reasonable standard for testing the new algorithms.At the onset of this project, Philips Medical Systems Odyssey systems had two available planar radionuclide ventriculography software packages; we elected to test both. The first system, the Philips GBP‐Dual system (GBP‐D), was written to emulate the Medasys program on the more modern Odyssey computer platform. One notable difference is that this system is fully automatic. As a result, the operator cannot define or limit the LV search area or adjust edge‐detection sensitivity. Likewise, Fourier phase data is available but cannot be used by the technologist to define the search area for the LV. The second system is the Philips GBP‐Multi software (GBP‐M) package. This software does not directly emulate the Medasys system, but its semiautomated algorithm permits the operator to define a search area for the LV.Our goal was to determine how closely the left ventricular ejection fractions calculated by the newer systems reproduced the calculation of the Medasys system. In particular, we wanted to see how often discrepancies in the calculated LVEF might affect treatment decisions.The study group included all patients who underwent gated planar left ventriculography (MUGA) at our institution in the two‐year period from May 2004 through April 2006. Three hundred and fifteen (315) total examinations were performed, including repeat examinations on 37 patients. Of these examinations, three examinations processed only with the Medasys system  were excluded from the analysis.in vivo with intravenous stannous pyrophosphate followed by Tc‐99m sodium pertechnetate . The patients were then imaged in the best LAO projection to separate RV and LV with a Siemens Orbiter gamma camera, which had already undergone acceptance testing. The raw data from the gamma camera were sent to the Medasys and Philips hardware simultaneously and processed by all three software systems independently. This simultaneous acquisition and processing method was the same as that employed by Carpentier for the original validation of the GBP‐D system. All three systems provided LVEF data for analysis; only the Medasys results were reported to clinicians for therapy decisions.Red blood cell labeling was performed ±5 ejection fraction percentage points difference between the test systems and Medasys were selected based on our institutional standard that such a difference represents a clinically significant change in LVEF. The mean difference and 95% confidence intervals were calculated to determine whether the test systems’ results generally fell within the clinic limits with respect to the Medasys results.The data were then analyzed using a least‐squares fit comparing the Medasys LVEFs to the test systems’ LVEFs to determine degree of correlation, forcing the fit through . In all of the tests, the Medasys results were used as the basis for comparison. In addition, we performed a Bland‐Altman analysis(–) For this reason, we also collected data of LV end diastolic volume (LVEDV) to evaluate whether small volumes might contribute to different results between the Medasys and the test systems. Only Medasys and GBP‐D provided this data, not the GBP‐M system.LVEF determination by Quantitative Gated SPECT (QGS) from stress sestamibi perfusion myocardial scans is known to cause false‐high measurements in patients with very small LV volumes.–17 F±5 ejection fraction percentage points. Overall, only 168 calculations (54%) of the GBP‐D system and 116 calculations (37%) of GBP‐M system agreed with Medasys to within ±5LVEF percentage points. Nineteen (7%) of the GBP‐D system and 4 (1%) of the GBP‐M system data were more than 5 percentage points lower, while 125 (40%) of the GBP‐D system and 192 (62%) of the GBP‐M system were more than 5 percentage points higher.Figure These figures also demonstrate a number of cases with markedly different values of LVEF obtained by the test systems than by the Medasys system. We assessed these differences by visually inspecting the left ventricular contour determined by each algorithm. The cases with the worst correlation typically showed that the search algorithm had extended the boundaries well outside the visualized LV boundary. In particular, for the fully automated GBP‐D system, the search algorithm sometimes included one or more extraneous structures in addition to the LV, or entirely excluded the LV from the calculation. Figure Unlike the QGS system of LVEF measurement, the LVEDV value for the GBP‐D system has no significant influence on LVEF measurements. As illustrated in Fig. Our data indicate that the LVEFs calculated by the Medasys and GBP‐D methods lie within 5 LVEF percentage points in approximately half of the cases, with less agreement between the Medasys and GBP‐M systems. The remaining cases were significantly disparate, both higher and lower, with some GBP‐D and GBP‐M results markedly diverging from the Medasys calculation. These data show both a systematic trend – the test systems’ LVEFs were on average higher than those from the Medasys system – as well individual failures of the test systems in certain cases.(–) In practice, however, many software programs are not extensively tested prior to clinical use. One of the most comprehensive and recent studies by De Bondt et al.,With regard to the systematic differences between the test systems and Medasys, it is difficult to determine which system correctly calculates the LVEF. First, there is no true gold standard for clinical determination of left ventricular ejection fraction, and therefore no definite reference technique.–20 IWithout detailed access to manufacturers’ processing algorithms, it is not possible to determine precisely which features of the algorithm contribute to the discrepancies. One likely source of systematic difference observed in our study may be differences in background subtraction: relative oversubtraction of background counts elevates the calculated LVEF, while undersubtraction decreases it.Such systematic differences could be identified by testing all new LVEF algorithms with a validated left ventricular phantom; however, such phantoms are not widely or commercially available. In the particular case of planar radionuclide ventriculography (MUGA), phantom studies present a challenge because a dynamic phantom  is not commercially available. Individual centers may not have access to such a phantom to do this testing. This type of testing may be best accomplished by manufacturers working with institutions with access to such a phantom.in vivo RBC labeling may influence determination of LVEF in real patients compared to mechanical phantoms. In particular, such variability in real patients may overwhelm the capabilities of the left ventricular edge‐detection algorithms. Importantly, the phantom designed by De Bondt, modeled only the left ventricle. The marked variability observed in our study was in some cases attributable to inclusion of erroneous structures in the test systems’ left ventricular volume calculation, which cannot happen in this phantom.More troubling than the overall systematic differences were the marked differences between some of the LVEFs calculated by the test programs and those calculated in the Medasys system. The observed variability may stem in part from significant patient variables in this patient population. Body habitus, difficulties in patient positioning, and medicines that interfere with To identify errors that arise in live patients, pre‐market validation of new algorithms should include testing in an adequate number of live patients, in addition to testing in phantoms. Our study in over 300 patients suggests that the initial clinical testing on 30 patients may not have adequately sampled the variabilities that live patients present. Additionally, smaller centers may not have adequate case volumes, experience, trained nuclear medicine specialists, or medical physicists necessary to do clinical testing on large numbers of patients. This effectively puts the onus of doing such testing on the manufacturers, likely in conjunction with a large institution.As a result of this study, our institution decided not to implement these new software programs. The manufacturer was informed of our findings and pulled the product from the market. They further used our test data for validation of a new product now being sold.This study illustrates the importance of a large‐scale clinical evaluation of any new medical imaging tool that generates quantitative clinical values important to patient care. In this particular case, one of the newer software packages introduced fully automated functions to generate these values. Before purchasing a new system, we recommend seeking out all previous clinical evaluations of the equipment. If no such study has been performed, then the purchasing institution should strongly consider conducting such a study, particularly in comparison with a clinically tested system.More generally, our results suggest that adequate testing of new software packages should include phantom studies, when possible, and clinical testing on a reasonable number of patients.


C and peak troponin I were the only independent predictors for late gadolium enhancement while ΔQTc and left ventricular ejection fraction were independent predictors of myocardial salvage index <60%. The receiver operative curve of ΔQTc showed an area under the curve of 0.77 to predict a myocardial salvage index <0.6. In conclusion, in a subset of patients with a first occurrence of early revascularized anterior STEMI, ΔQTc is inversely correlated with CMR-derived myocardial salvage index and may represent a useful parameter for assessing efficacy of reperfusion therapy.Assessing the efficacy of revascularization therapy in patients with ST-segment elevation myocardial infarction (STEMI) is extremely important in order to guide subsequent management and assess prognosis. We aimed to determine the relationship between corrected QT-interval (QTc) changes on standard sequential ECG and myocardial salvage index in anterior STEMI patients after successful primary percutaneous coronary intervention. Fifty anterior STEMI patients treated by primary percutaneous coronary intervention underwent quantitative ECG analysis and cardiac magnetic resonance. For each patient the difference (ΔQTc) between the QTc of ischemic myocardium (maximum QTc in anterior leads) versus remote myocardium (minimum QTc in inferior leads) during the first six days after STEMI was measured. The QTc in anterior leads was significantly longer than QTc in inferior leads (p<0.0001). At multivariate analysis, ΔQT Assessing the efficacy of revascularization therapy in patients with anterior ST-segment elevation myocardial infarction (STEMI) is extremely important in order to guide subsequent management and assess prognosis. Estimation of infarct size with late gadolinium enhancement (LGE) technique and assessment of myocardial salvage index (MSI) measured by cardiac magnetic resonance (CMR) within the first week after primary percutaneous coronary intervention (pPCI) are independently related to early ST-segment resolution, adverse LV remodelling ,2, majorTypically, significant changes of ventricular repolarization are detected early by standard 12-lead-ECG in patients with STEMI ,6. WhethThus, we sought to determine the relationship between QTc changes on standard sequential ECG and MSI in anterior-STEMI patients after successful pPCI.From a cohort of 208 consecutive patients with STEMI referred to the Centro Cardiologico Monzino in Milan between January 2011 and June 2015, we identified 86 patients with anterior-STEMI. The diagnosis was based on symptoms, ECG findings (ST-segment elevation) and proximal or middle left anterior descending artery (LAD) lesions were included. Exclusion criteria were: a) previous MI (8 patients); b) atrial fibrillation or use of antiarrhythmic drugs (6 patients); c) catecholamine administration (2 patients) d) PCI performed >12h after chest pain onset (4 patients); e) bundle branch block (3 patients); f) incomplete reperfusion (2 patients); g) electrolyte imbalance (2 patients); h) conduction disorders such as atrio-ventricular-block (1 patient) and intermittent pre-excitation (1 patient); i) technical difficulties in QT measurement (4 patients); j) pericardial effusion (1 patient); and k) enrolment in STEMAMI Study (active treatment) (2 patients). Therefore, 50 patients with a first anterior-STEMI were finally included in the study. The study was approved by the university ethics review board (Comitato Etico degli IRCCS Istituto Europeo di Oncologia e Centro Cardiologico Monzino). All patients signed informed consent and the study conformed to the ethical guidelines of the 1975 Declaration of HelsinkiFor each patient, standard 12-lead-ECGs  were recorded at admission, within the first hour after pPCI, and every 24h for the first six hospital days. For each ECG, the QT was measured in all leads from the onset of the QRS to the end of the T-wave on the isoelectric baseline . The isoFor each patient, the ΔQTc-AI-MA defined as the maximum dispersion between anterior and inferior leads (maximum anterior QTc—minimum inferior QTc) and the ΔQTc-AI-ME defined as the difference between the mean QTc values in anterior and inferior leads were calculated. Electrocardiographic data were evaluated twice by an expert reader  blinded to patient clinical history and data. Another expert reader repeated ECG data assessment. Kappa values were calculated for inter-observer and intra-observer variability.All patients were studied with a 1.5T scanner  after pPCI. After acquiring localizer images of the heart, breath-hold steady-state-free-precession cine sequences were obtained using the following parameters: echo time 1.57msec, 15 segments, repetition time 46msec without view sharing, slice thickness 8mm, field of view 350mmx263 mm, and pixel size 1.4mmx2.2 mm. A cine short axis stack, 2-, 3-, and 4-chamber long axis views of the left ventricle (LV) were acquired . Breath-CMR data were transferred to a dedicated workstation and analysed with a commercially available cardiac software . Using T2-weighted short-axis images, infarct-related edema was considered present when the signal intensity (SI) of the myocardium was >2SD the mean SI of the contralateral remote region of normal myocardium . MicrovaContinuous variables are expressed as mean±SD or median [27–75 percentile], whereas categorical variables are expressed as percentages. During hospital stay, QTc changes were evaluated with paired Student T-test. Spearman’s rank correlation coefficient (r) was used to evaluate correlation between ΔQTc-AI-MA at different time points and CMR findings. Linear regression was used to study the relationship between log-transformed LGE and ΔQTc, considering demographic and clinical variables as potential confounders. Multivariable models were developed including variables with p<0.1 at univariate analysis. The association between MSI and ΔQTc was similarly analysed with logistic regression analysis. A receiver-operator characteristic (ROC) curve was performed to evaluate the ability of ΔQTc to discriminate patients with MSI <0.6 vs. those with MSI >0.6. The Youden method was used to find the best cut-off. Statistical analysis was performed with STATA version 12.1  and R version 3.0.2. A p value <0.05 was considered statistically significant.The baseline clinical, echocardiographic and laboratory data of the fifty patients  with a first anterior STEMI enrolled in the study are listed in rd day after STEMI (p = 0.004) and subsequently decreased through the 6th day. The peak ΔQTc-AI-MA was reached on the 3rd day and was significantly higher compared to that measured at admission and on the 6th day (p<0.05) (Panel C).The inter-observer agreement for QTc evaluation was 0.90 with a kappa value of 0.82 . Similarly, intra-observer agreement for the evaluation of QTc interval was 0.92 with a kappa value of 0.80 (95% CI 0.42–1.0) and 0.93 with a kappa value of 0.82 (95% CI 0.60–1.0), respectively.th day were independent predictors of LGE expressed as absolute mass or as %LV mass on multivariate analysis (Tables C-AI-MA on 6th day (p = 0.013) remained independent predictors of MSI<0.6. The ROC curve of ΔQTC-AI-MA on the 6thday exhibited an AUC of 0.77 to predict MSI<0.6  and MSI r = -0.42, p<0.05) . After ps Tables  and 4. M2, p<0.05s Tables , only pe MSI<0.6  with theThe present study found a direct relation between QT prolongation and myocardial salvage as assessed by CMR in patients with a first reperfused anterior-STEMI. In particular, we found that a significant differential value between anterior (injured myocardium) and inferior (remote myocardium) QT detected six days after pPCI correlated to and was an independent predictor of adverse MSI (<0.6) after accounting for other clinical variables. For the first time, our data provide clinical meaning of ventricular repolarization changes in reperfused anterior-STEMI applying a fast and easy tool able to stratify the prognosis of this patient subset.CMR represents the gold standard technique for the evaluation of cardiac structure and function –14. ReceThe most readily available test for STEMI patients at the time of presentation is the 12-lead-ECG. The ECG not only provides rationale for triage of patients with STEMI to coronary revascularization, but can also offer information on the presence and location of at-risk myocardium and MI. It is known that in the course of ischemia, lengthening of the QT is frequently observed, especially in the case of early transmural ischemia. When compared with clinically accepted indices of transmural ischemia  QT prolongation is the earliest ECG abnormality . In the C-interval prolongation at the site of injured myocardium (anterior leads) versus remote myocardium (inferior leads) and the extent of myocardial involvement assessed with CMR in patients undergoing successful pPCI for anterior STEMI. ΔQTC-AI-MA at 6th day was inversely related to MSI and directly related to LGE extent , in order to select who could benefit from a closer follow-up despite having a major myocardial tissue impairment. Third, the study does not include a comprehensive ECG correlation evaluating just QT measurements with MSI. Notably, although ST abnormalities are the best electrocardiographic parameters in acute coronary syndrome, the study design included only patients with prompt ST-elevation resolution post-PCI. Therefore, QT-interval was the only ECG parameter included in multivariate analysis. Fourth, QT interval was measured manually. However, the clinical experience of well-trained and blinded operators may be better than automated programs of calculation to measure QT interval accurately. Fifth, in the current era of pPCI for STEMI, hospital length of stay may not reach 7 days. Therefore, it would have been useful to provide a straightforward value at 3-day follow-up (peak) but the relative analysis of ΔQTC-AI-MA did not show a significant correlation with MSI. Attempting to explain this phenomenon, we postulate that during the first few days after STEMI all patients have myocardial alteration and consequently a long QT interval. Perhaps this is why 3-day follow-up may represent too short of a time interval.C changes at ECG as a gatekeeper for CMR in anterior-STEMI patients.In a specific subset of patients with a first occurrence of anterior STEMI, early and effectively revascularized, ΔQTc is inversely correlated with CMR-derived MSI. Additional studies are needed to further validate the use and cost-effectiveness of QTS1 TableΔQTc AI MA: delta QT corrected antero-inferior max; LGE: late gadolinium enhancement; MSI: myocardial salvage index; Post-PCI: post-percutaneous coronary intervention *P-value<0.05.(DOCX)Click here for additional data file.S2 TableACE: angiotensin converting enzyme; AWM: abnormal wall motion; CAD: coronary artery disease; CMR: cardiac magnetic resonance; GFR: glomerular filtration rate; LAD: left anterior descending artery; LVEDV: left ventricle end diastolic volume; LVEF: left ventricle ejection fraction; LVESV: left ventricle and systolic volume; PAP: pulmonary artery pressure; PCI: percutaneous coronary intervention; TTE: transthoracic echocardiography; TIMI: thrombolysis in myocardial infarction; ΔQTc AI MA = delta QT corrected antero-inferior max; ΔQTc AI ME = delta QT corrected antero-inferior mean.(DOCX)Click here for additional data file.S3 TableACE: angiotensin converting enzyme; AWM: abnormal wall motion; CAD: coronary artery disease; CMR: cardiac magnetic resonance; GFR: glomerular filtration rate; LAD: left anterior descending artery; LVEDVi: indexed left ventricle end diastolic volume; LVEF: left ventricle ejection fraction; LVESVi: indexed left ventricle and systolic volume; PAP: pulmonary artery pressure; PCI: percutaneous coronary intervention; TTE: transthoracic echocardiography; TIMI: thrombolysis in myocardial infarction; ΔQTc AI MA = delta QT corrected antero-inferior max; ΔQTc AI ME = delta QT corrected antero-inferior mean.(DOCX)Click here for additional data file.


Type 2 diabetes mellitus (DM2) may induce epicardial coronary artery diseases and left ventricular myocardial damaging as well. Left ventricular dysfunction was found in DM2. In this research, we compared the left ventricular dysfunction of coronary artery disease (CAD) patients with and without type 2 diabetes mellitus as well as normal controls using the volume-time curve of cardiac magnetic resonance (CMR).Sixty-one CAD patients (28 with DM2 and 33 without DM2) and 18 normal individuals were enrolled in this study. Left ventricular function parameters, including the end-diastolic and end-systolic volumes , stroke volume (SV) and ejection fraction (EF), and morphologic dimension parameters (end diastolic and systolic diameter (EDD and ESD), were measured and compared. Volume-time curve parameters, including the peak ejection rate (PER), peak ejection time (PET), peak filling rate (PFR), peak filling time from ES (PFT), peak ejection rate normalized to EDV (PER/EDV), and peak filling rate normalized to EDV (PFR/EDV), were derived automatically and compared.p < 0.05). LVEDD of the diabetic CAD group was significantly enlarged compared to the normal and non-diabetic CAD groups . More importantly, the lowest parameters of the left ventricle volume time curve  were obtained in diabetic CAD patients . In diabetic CAD patients, logistic regression analysis indicated that PET, PFT and PFR/EDV were independent predictors of left ventricular dysfunction . The sensitivity and specificity of PET were 81.2 and 90%, respectively, when the threshold value was greater than 164.4 msec; for PFT, the sensitivity and specificity were 87.5 and 95.0%, respectively (criterion >166.0 msec). Higher sensitivity (87.5%) and specificity (100.0%) were obtained for PFR/EDV (criterion ≤3.7EDV/s).LVEF in the diabetic CAD group was markedly reduced when compared to the normal and CAD without DM2 groups (all Parameters that are derived from the volume-time curve on CMR, including PET, PFT and PFR/EDV, allow clinicians to predict left ventricular dysfunction in diabetic CAD subjects with a high degree of sensitivity and specificity. Recently, there has been an increase in the number of DM patients worldwide. World Health Organization (WHO) predicts that number of DM patients will reach 552 million by 2030 [cardiovascular diseases, such as coronary artery disease (CAD), is approximately double compared to non-diabetics [Diabetes mellitus (DM) is a chronic  by 2030 . In patiiabetics . Furtheriabetics . Left veiabetics , 8. A beCardiac magnetic resonance (CMR) is considered to be the gold standard modality for estimating global left ventricular function because it is noninvasive and yields high soft-tissue contrast and temporal resolution , 10. CurDuring December 2014 and August 2015, 28 CAD with DM2  and 33 CAD patients without DM2  who had CMR examination were retrospectively enrolled in the study. The inclusion of CAD patient is according to the guideline of 2013 ESC guidelines on the management of stable coronary artery disease as the CAD is defined as an established pattern of angina pectoris, a history of myocardial infarction (MI), or the presence of plaque documented by catheterization . In addiCardiac magnetic resonance (CMR) was performed using a 3.0-T whole-body scanner  in the supine position using ECG-triggering and the breath-hold technique. The dedicated cardiac phased array coil was utilized in all scanning procedures. Data acquisition was obtained during end-inspiratory breath holding. Localizing imaging, including coronal, sagittal and horizontal planes, were acquired by using the TrueFISP sequence . The short axis cine sequence was performed by using the Turboflash sequence . A total of 8–12 slices of short axis cine sequences were acquired in every subject from the level of the mitral valve to the level of the left ventricle apex. Left ventricular function and volume-time curve were measured on the short axis cine sequence. A four-chamber cine sequence  was obtained in one cardiac cycle. During the entire examination period, each subject’s condition was stable.An experienced radiologist analyzed the CMR data on the offline workstation . Global left ventricular function and the volume-time curve were analyzed on the short-axis cine images using offline post-processing software . Endocardial and epicardial borders were delineated manually from the image slices between the mitral valve and the apex at the end of diastole and at the end systole within the serial short-axis imaging; additionally, papillary muscle and moderator bands were carefully assigned to the cardiac lumen. Left ventricular function parameters  were automatically obtained by Argus using Simpson’s method. The endocardial boundary of left ventricle was traced on every slice of the short-axis images Fig.  and parap values of all data were greater than 0.05, which meant that all the data satisfied the hemogenetiy of variance. An independent t-test and non-parametric approaches (Chi-square test and Mann–Whitney U test) were utilized if appropriate to compare the basic characters between CAD with and without diabetes group. A one-way analysis (ANOVA) of variance with post hoc Bonferroni correction and Kruskal-Wallis were used to do the multiple comparisons  of the left ventricular functional, morphologic and volume-time curve parameters, ANOVA were used when the data conform to the homogeneity of variance and normal distribution and Kruskal-Wallis were used when the data is skewed distributions. Tukey’s range test has been used to conduct post-hoc analyses (after ANOVA) to verify the differences among the groups. Logistic regression was performed to screen out independent predictors of left ventricular dysfunction in CAD patients with diabetes. A receiver operating characteristic (ROC) was used to analyze the sensitivity and specificity of these predictors. A p-value <0.05 was considered significant for all statistical tests.Statistical analyses were performed with IBM SPSS  and MedCalc (version 9.2.00). The data are presented as the mean ± standard deviation (SD). All data were checked for normality using the Kolmogorov-Smirnov test. All comparisons (Levene’s test) were assessed for and satisfied the homogeneity of variance assumption of the analysis of variance. The Levene’s test showed that P > 0.05). The duration of DM2 in diabetic CAD patients ranged from 2 days to 14 years. The average HBA1c in CAD patients with diabetes was 9.38 ± 2.38%. Compared to non-diabetic CAD group, the plasma glucose of diabetic CAD patients was significantly increased . Electrocardiography revealed differences between diabetic and non-diabetic CAD groups with regard to pathological Q waves  and ST-T changes . Using catheter-based X-ray coronary angiography, 8 patients (28.57%) from the CAD with DM2 group and 13 patients (39.39%) from the CAD without DM2 group were found to have one-vessel coronary occlusion; two-vessel occlusion was found in 6 (21.43%) diabetic CAD patients and 4 (12.12%) non-diabetic CAD patients; and three-vessel occlusion was detected in 14 (50.00%) diabetic CAD patients and 16 (48.49%) non-diabetic CAD patients. All CAD patients, either with or without diabetes, had left ascending artery stenosis. 10 (35.71%) of the diabetic CAD and 17 (51.52%) of the non-diabetic CAD patients had left circumflex artery stenosis; 17 (60.71%) diabetic and 18 (54.55%) non-diabetic CAD patients were found to have right coronary artery stenosis. Percutaneous coronary intervention was performed in 21 (75.00%) diabetic CAD patients and 28 (84.84%) non-diabetic CAD patients.A comparison of basic characteristics between the normal, CAD with DM2 and CAD without DM2 groups are presented in Table p < 0.05). The LVEDV of diabetic CAD patients was larger than the both the normal and non-diabetic CAD patients . LVEDD in the diabetic CAD group was significantly enlarged compared to both the normal and non-diabetic patients . LVESD of both diabetic CAD and non-diabetic CAD patients were larger than normal controls (both p < 0.05).Left ventricular function and size parameters are shown in Table p < 0.05). PET was significantly different in all of the three groups, with the diabetic CAD group having the longest PET (p = 0.0008). PFT of diabetic CAD group was longer than both the normal group and non-diabetic CAD group . In comparing the PER/EDV and PFR/EDV values among the three groups, both the PER/EDV and PFR/EDV values were the lowest in the CAD with diabetes group, followed by the non-diabetic CADs, with the normal control group having the largest values; all comparisons were statistically significant .Volume-time curve parameters were calculated and presented in Table p = 0.0454; and PFT: OR 1.0161, 95% CI 1.0001 to 1.0326, p = 0.0412). In addition, the PFR/EDV value was another independent predictor .All statistically significant left ventricular function, morphologic and volume-time index analyses were performed using logistic regression Table . The oddRegarding these independent predictors, the ROC curve of PET, PFT and PFR/EDV for CAD patients with diabetes was calculated and is shown in Fig. Several modalities can be used to evaluate left ventricular function, such as the SPECT and echocardiography . HoweverWe acknowledge a few limitations to this research study. First, a larger sample of diabetic CAD patients is needed to further investigate cardiac dysfunction, especially for assessing the diagnostic ability of the CMR volume time curve. Second, long-term follow up is necessary to determine the outcome and mortality differences between diabetic and non-diabetic patients; longitudinal data will help to illustrate the prognostic role of volume-time curve parameters with regard to heart failure and cardiac events in both study groups.In summary, our research has indicated that CAD patients with type 2 diabetes mellitus have more severe LV dysfunction, including diastolic filling and systolic ejection, compared with non-diabetic CAD patients. PET, PFT and PFR/EDV derived from the volume-time curve on cardiac MR can be used to predict left ventricular dysfunction in diabetic CAD patients with relatively high sensitivity and specificity.


Data on left ventricular (LV) function in patients with neurocardiogenic syncope (NS) is conflicting in adults and lacking in children. The aim of this study was to analyze LV myocardial performance in children with NS at rest and during head-up tilt-table (HUTT) testing.This is the first study to combine HUTT and speckle-tracking echocardiography (STE) in children with NS. 43 consecutive normotensive pediatric patients with NS  and 41 sex- and age-matched healthy controls were included in the study. The study groups consisted of 21 patients with a positive HUTT reaction (HUTT+) and 22 with a negative HUTT reaction (HUTT-). STE was used to analyze peak systolic LV myocardial strain and strain rate.p = 0.032) and significantly depressed longitudinal strain rate (p <  0.001) at rest. Interestingly, during HUTT testing LV global strain and strain rate were similar in both groups. LV strain rate was lowest in HUTT+ followed by HUTT- and control subjects both at rest and during HUTT.Conventional echocardiographic parameters were similar in all analyzed groups. When compared to healthy controls, children with NS had depressed levels of circumferential strain rate (Resting LV longitudinal strain rate is attenuated in children with NS, especially in those with a positive HUTT response. This is further evidence that NS patients feature altered cardiac mechanics rendering them prone to vasovagal perturbations that can ultimately result in collapse.Witten/Herdecke University ethics committee clinical study number: UWH-73-2014. Syncope is a sudden, brief loss of postural tone and consciousness followed by spontaneous recovery . Up to 1Advanced echocardiography techniques – including tissue-Doppler echocardiography (TDI) and speckle-tracking echocardiography (STE) – are promising modalities for the real-time quantitative evaluation of myocardial performance without the disadvantages of adverse effects or high costs. Based on TDI studies, cardiac mechanics such as left atrial and LV filling and contractility are postulated to be altered in neurocardiogenic syncope in adults , 10. STEclinical study number: 73/2014).In this prospective study, we altogether enrolled 84 children – 43 consecutive normotensive pediatric patients aged 13.9 ± 2.6 years  with a history of vasovagal syncope and 41 healthy sex- and age-matched controls  without medical problems and with a normal transthoracic echocardiogram. A priori, the study group was further sub-categorized according to their HUTT exam reaction. Inclusion criteria for the study group were a typical history of NS, age < 18 years and a written informed consent signed by the patient and their legal guardian. Moreover, the presence of any acute or chronic condition that might affect the cardiovascular system , ECG abnormalities, chronic medication use and the lack of cooperation to participate in this voluntary HUTT study were strict exclusion criteria. 60 patients were excluded from the study due to various reasons: 53 were incompliant regarding the HUTT challenge, 2 patients were obese (BMI > 30), 2 had insufficient image quality at baseline and in 3 patients the continuous ECG signal was corrupted due to technical difficulties which made consecutive speckle tracking post-processing impossible. The study was carried out in accordance with the declaration of Helsinki’s ethical principles for medical research involving human subjects and approved by the Witten/Herdecke University ethics committee  were utilized for all statistical tests.Demographic data, baseline clinical parameters, hemodynamics and echocardiographic aspects are presented as mean and standard deviation. Analysis of variance (ANOVA) testing was used to compare clinical, hemodynamic and echocardiographic data of the analyzed groups. Strain and strain rate are displayed as box-whisker-plots. Bonferroni correction was applied to exclude multiple testing bias. Hence, p = 0.318). Height (p = 0.375), body weight (p = 0.101), body mass index (p = 0.1) and body surface area (p = 0.165) were not statistically different between the three groups. All these values were within normal limits as evaluated by Z-scores. HUTT response was positive in 21 of the 43 patients with NS and 2 of the 41 healthy controls (p <  0.001). Hemodynamic parameters, e.g. heart rate and arterial blood pressure did not differ between the three groups neither at rest nor at the moment of STE assessment during HUTT testing (0.2 < p < 0.964).Baseline clinical characteristics are outlined in Table p = 0.480), fractional shortening (p = 0.760), LV dimensions (p ≥ 0.15) and LV mass (p = 0.578). LV stroke volume was lowest in the HUTT+ group (46.7 ± 17.3 vs. 53.5 ± 21.3 vs. 53.8 ± 17.6 ml) when compared to HUTT- and healthy control subjects. However, this difference was not statistically different (p = 0.796). Moreover, LV ejection fraction (EF) was 54.3 ± 2.9% in syncope HUTT+ patients, 54.7 ± 6.6% in HUTT- and 56.7 ± 4.4% in healthy controls (p = 0.263). Furthermore, diastolic function as reflected by E/A ratio and E/E’ did not differ significantly between the analyzed groups (p ≥ 0.352). Mitral deceleration time was longer in the HUTT- group  but similar in HUTT+ patients with NS and healthy controls (0.17 ± 0.07 vs. 0.16 ± 0.06 s). However, these values were still within normal limits as evaluated by population-based age-specific reference values [Standard 2D derived conventional echocardiographic parameters were similar in all groups  and median peak systolic longitudinal strain rate  were lowest in children with NS and a positive HUTT exam (HUTT+) as compared to the HUTT- group and healthy controls  than in the control group, but the difference was not statistically different (n = 4) or longitudinal strain rate values  at rest . Interestingly, all of these patients were in the HUTT- group. One of the four patients was female and one had a history of more than one syncopal episode. The average blood pressure of this subgroup was 121 ± 9 mmHg systolic and 68 ± 2 mmHg diastolic and the average heart rate was 74 ± 10 bpm at. None of the patients with NS and a positive tilt-table response had resting LV longitudinal or circumferential strain rate values ≥ the top quartile of the healthy control group.While the overall comparison to healthy controls revealed LV myocardial strain rate at rest to be significantly lower in patients with neurocardiogenic syncope, we also observed a heterogeneous distribution of LV deformation in those patients. Interestingly, a subset of patients with NS had high LV circumferential (This is the first study to simultaneously perform speckle-tracking echocardiography (STE) and head-up tilt-table (HUTT) testing in children with NS. Interestingly, we found LV resting longitudinal strain rate to be significantly lower in NS patients than in healthy controls with a more pronounced decrease in the HUTT+ group. During HUTT challenge we found a similar but not statistically significant tendency of lower longitudinal strain rate in patients with NS. This is in line with findings from Kojo et al., who utilized a Doppler flow meter during HUTT testing and found reduced carotid artery blood flow in pediatric patients with NS . Our finOn the other hand, our findings are counterintuitive in the light of the “ventricular theory” in that we did not measure an increase but a decrease in LV contractility in patients with NS and a positive HUTT response. This, however, apart from the fact that the ventricular hypothesis is far from being established conclusively, is in agreement with a similarly performed study by Goel et al., who report attenuated resting LV strain in HUTT+ patients and conclude that – other than previously believed – increased resting LV contractility is not a prerequisite for the development of NS . NotablyThe cardiac autonomic response pattern of patients with NS during HUTT challenge has been distinguished between HUTT+ and HUTT- patients in previous studies . In lineAnother unresolved issue regarding the enigmatic pathogenesis of NS is the factor age. Even though younger and older patients react differently on the HUTT, especially in the early phase , the rolInterestingly, based on the evidence of fear and threat bradycardia in animals and the beneficial vasovagal reflex during hemorrhagic shock in humans and animals, some researchers suggest NS not to be a recently evolved human-only disease but rather the remnant of an ancient defense mechanism that has once reduced myocardial oxygen consumption and supported hemostasis before the development of larger blood losses –44. UndeDespite the incremental value of these findings, this study design bares important limitations. Firstly, while STE has been implemented in specific clinical practice of pediatric cardiology, i.e. to monitor cardiotoxicity in chemotherapy patients , it is sThis study provides further evidence that decreased LV resting performance may be a relevant factor in the etiology of neurocardiogenic syncope in children. Further experimental animal and human studies should be designed to investigate LV contractility in children and adults with NS under different cardiac loading conditions at baseline and in the context of HUTT challenge.


In April 1948, the thoracic surgeon, Russell Brock, convened a meeting at Guy’s Hospital, London of “those concerned in the management of congenital disease of the heart” .The evidence of the prior position is there in the medical texts, and in the teaching at the time that Brock convened his club. Guy’s senior physician, Sir John Conybeare, wrote in the 1946 edition of his book “cyanosis is the first sign and is so characteristic that “blue baby” and congenital heart disease are practically synonymous” . TeachinAn important lever for change came with the systemic to pulmonary artery shunt operation. This was the brain child of Helen Taussig, worked out in the laboratory by Vivien Thomas, and brought into clinical practice by Alfred Blalock. Thanks to a bond forged in wartime medical services, an exchange programme was created between Guy’s and Johns Hopkins and in 1947 Blalock came to London and performed 10 shunt operations. The operation was tactically a knight’s move, brilliant but somewhat serendipitous. The surgery was not within, but adjacent to the heart. It altered the physiology, permitting more unsaturated blood to reach the heart, and got around the obstacle of the heart being a declared no-go area for surgeons. Blalock’s operation was adopted and the clinical work of the Club became established and legitimised. It was then possible for Brock to achieve his objective of getting to the root of the problem: intracardiac surgery was achieved. He soon wrote up his intracardiac operations to relieve the cyanosis of Fallot’s tetralogy, publishing alongside the Guy’s cases the results of seven operations performed while he was on a return visit to Johns Hopkins  Figure .As a result of the work of “The Cardiac Club” and others who came after, congenital heart disease was reframed as a surgical disease. Attention was focused once more on the exact anatomy so that surgical correction could be undertaken precisely and reproducibly. Achieving survival for formerly fatal malformations created another diagnostic frame with the coining of the phrase “grown up congenital heart disease”. “GUCH” is now more prosaically rebranded as adult congenital heart diseases. In the book of “The Heart Club”, three patients of that era who are still alive and well, tell their life stories. The book is a testimony to team work, resourcefulness and perseverance.


Objective evaluation of the physical activity (PA) in patients with chronic obstructive pulmonary disease (COPD) is important. We validated a triaxial accelerometer, Active Style Pro HJA-750C® (HJA), and evaluated the necessary conditions for obtaining reproducible data.  The PA measured by HJA was compared with that measured by two already validated accelerometers in 11 patients with COPD . Then, the influence of weather and holidays on the PA and the required number of days to obtain repeatability were examined in 21 patients with COPD . p=0.024 at ≥4.0 METs by DMM and p < 0.0001 at the rest) except at ≥4.0 METs by AM, though the values measured by HJA were higher than those by AM which was reported to underestimate PA. The durations of PA on rainy days were significantly shorter than those on nonrainy days, but those on holidays were not different from those on weekdays. The values of ICC for 3, 4, or 5 days were higher than 0.8 at all intensities. The PA measured by HJA was correlated with the dyspnea scale FVC and age and tended to correlate with FEV1.  The PA values measured by HJA and those by DynaPort Move Monitor® (DMM) or Actimarker® (AM) were significantly correlated at all intensities (UMIN000016363. The HJA was validated for evaluating the PA in patients with COPD. This trial is registered with  Physical activity (PA) in patients with chronic obstructive pulmonary disease (COPD) is an important issue because it is related to the decline of lung function , hospitaThe reports of PA in patients with COPD measured by accelerometers have rapidly increased –7. RecenThe main hypothesis in this study was that the HJA is valid for evaluating the PA in patients with COPD. To prove this hypothesis, we tested the reproducibility of HJA compared to that of DMM or AM, which had been validated for patients with COPD. Then, in order to obtain repeatable data, we investigated the influence of weather or holidays on the duration of PA and also the minimal number of days required for analysis. Furthermore, we evaluated the relationships between PA and several demographic factors.For study 1, patients with stable COPD aged 40 or older were recruited from the National Hospital Organization Wakayama Hospital from April to September 2015. For studies 2 and 3, outpatients with stable COPD without any other diseases that might obviously interfere with walking were recruited from the same institute from May 2015 to January 2016 and from November 2016 to October 2017. COPD was defined as postbronchodilator forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) < 0.7. The participants had not been diagnosed with asthma or bronchiectasis . This stIn order to evaluate the validity of the device, HJA compared to DMM or AM, patients attached three devices at the same time in the daytime except while bathing for 7 days . When thTo investigate the influence of the weather or holiday on the duration of PA and determine the minimal required number of days for analysis, the HJA was attached throughout the day except while bathing for 2 weeks. The description of a diary in relation to weather and the kinds of activities was required during the measurement of PA. During the 2 weeks, the data of the first and last days were excluded , 29. WheTo evaluate the influenced factor for PA, the values of pulmonary function tests and other demographic factors were compared with the values of PA among the patients of study 2. The values of PA were calculated as mean values from the data of the first three nonrainy days except the first and last days .HJA, AM, and DMM are all triaxial accelerometers that are compact and worn only at the waist. HJA and AM can record the duration of PA according to the intensity, and DMM can record the time spent in inactive (lying and sitting), static (standing and shuffling), moving , and not worn.HJA is a small (40 mm × 52 mm × 12 mm) and lightweight (23.0 g) accelerometer that can continuously monitor the PA for 45 days. The HJA collects the data of triaxial acceleration at a rate of 32 Hz to 12-bit accuracy. The range of the acceleration data of each axis is ±6 G, resulting in a resolution of 3 mG. The acceleration signals, calculated as the average of the absolute values of the accelerometer output of each axis from 10-second epochs at the middle of each activity, were processed for various acceleration output variables. The MET value is calculated from three different linear regression formulas  produced by the relationship between the value of acceleration and the MET value measured by indirect calorimetry , 25.Statistical analysis was performed using GraphPad Prism 5  and IBM SPSS Statistics . The relationships between the PA evaluated by HJA and DMM or AM were assessed by Spearman's rank correlation, and those between HJA and AM were assessed by Bland–Altman plots. The influences of rainy days and holidays were assessed by the Wilcoxon signed-rank test. The repeatability of the data among measured days was assessed by ICC, in which ICC ≥ 0.8 is a generally accepted value for multiple ICCs in accelerometer studies –34. The r=0.808, p < 0.0001), ≥3.0 METs and locomotion , and ≥4.0 METs and locomotion   and ≥3.0 METs  but not at ≥4.0 METs  (Eleven outpatients with COPD aged 76.6 ± 6.9 were recruited . Correlap=0.024) . Correlap=0.795) . The durp < 0.001) and ≥3.0 METs (p < 0.01) but not at ≥4.0 METs (P=0.062)  (Twenty-one outpatients with COPD aged 73.0 ± 8.0 were recruited . In one P=0.062) . The durp=0.096) . The valp=0.096) .The durations of PA were positively correlated with FVC% predicted and negatively with modified Medical Research Council (mMRC) dyspnea scale score and age and tended to be positively correlated with FEV1% predicted .The correlations of PA at ≥2.0, ≥3.0, and ≥4.0 METs measured by HJA were confirmed with those measured by DMM or AM except at ≥4.0 METs by AM. However, most of the values of the duration of PA by HJA were higher than those measured by AM. When the PA of COPD was evaluated by HJA, the duration of PA was significantly shorter on rainy days than that on nonrainy days at ≥2.0 and ≥3.0 METs. In order to obtain reproducibility in the duration of PA measured by HJA, the data of at least 3 nonrainy days were necessary at all intensities. An available new triaxial accelerometer, the HJA, was validated, and the method for selecting the repeatable data was demonstrated in the current study. These results could provide Japanese physicians with the available method for evaluating the PA in patients with COPD.HJA is a more compact triaxial accelerometer than AM, and the two accelerometers can evaluate the same parameters. DMM is distributed widely mainly in Europe  and is oFor the PA at ≥4.0 METs, AM could detect only 28% of cases (10 out of 36), but HJA could detect 74% of cases (28 out of 36). This might be the reason why no correlation was observed between AM and HJA. Furthermore, most of the values of PA measured by AM were also lower than those by HJA at ≥2.0 and ≥3.0 METs, and fixed biases between HJA and AM were observed with Bland–Altman plots. The AM underestimated METs for all nonlocomotive activities except for hanging clothes and for all locomotive activities except for climbing down the stairs compared to the energy expenditure evaluated by the expired gas using the Douglas bag method . The HJAAs the composition of day-to-day variations in PA is important for evaluating the PA, factors that could affect the values of PA should be minimized. First, inclement weather might be one of the factors that could suppress PA. The PA on rainy days was significantly lower than that on nonrainy days at all intensities. These results were compatible with those of previous reports , 36. SecIn order to obtain repeatability for the PA results at all intensities (ICC ≥ 0.8), the data of 3 days were required. In most of the previous reports that evaluated the PA in COPD with an accelerometer, the data of 3 to 5 days were required , 31. TheThe durations of PA were negatively correlated with the mMRC grade. PA in COPD was reported to be correlated with mMRC , 12, 37,There are several limitations that need to be addressed: first, the numbers of recruited subjects in both studies were small. The small number might have influence on the effects of holidays in study 2 and on the correlation with pulmonary function especially FEV1 in study 3. Second, though the effects of weather and holidays were evaluated, seasonal effects were not evaluated. Since the weather or temperature might influence the PA in COPD , 41, furA new triaxial accelerometer, the HJA, was validated by comparing it with DMM and AM, which had already been validated for measuring the PA in patients with COPD. When the PA in COPD was measured with HJA, the data of 3 nonrainy days were necessary for obtaining reproducible data. The PA was associated with the dyspnea grade and pulmonary function.


In the daily practice of pacemaker insertion, the occurrence of atrial and ventricular lead switch at the pacemaker box header is a rare and unintentional phenomenon, with less than five cases reported in the literature. The lead switch may have dire consequences, depending on the indication for the pacemaker. One of these consequences is pacemaker syndrome, in which the normal sequence of atrial and ventricular activation is impaired, leading to sub-optimal ventricular filling and cardiac output. It is important for the attending physician to recognise any worsening of symptoms in a patient who has recently had a permanent pacemaker inserted. In the case of a dual-chamber pacemaker, switching of the atrial and ventricular leads at the pacemaker box header should be strongly suspected. We present an unusual case of pacemaker syndrome and right ventricular-only pacinginduced left ventricular systolic dysfunction in a patient with a dual-chamber pacemaker. In the daily practice of pacemaker insertion, the occurrence of atrial and ventricular lead switch at the pacemaker box header is a rare and unintentional phenomenon, with less than five cases reported in the literature.Patients may present with a variety of symptoms, depending on the underlying rhythm, pacing rate and percentage of the paced beats. The symptoms of pacemaker syndrome are usually non-specific but often include dizzy spells, shortness of breath, fatigue, near-syncope, syncope or frank heart failure. The occurrence of right ventricular-only pacing-induced left ventricular systolic dysfunction has been well documented.4A 40-year-old man presented with symptoms of undue fatigue and shortness of breath with minimal exertion. His resting heart rate was noted to reach 28 beats per minute (bpm) during waking hours. He was diagnosed with sick sinus syndrome and had a dual-chamber permanent pacemaker inserted. Subsequently, he reported feeling more ill and complained of dizziness, nearsyncope and syncope, worsening of shortness of breath, more fatigue, and what he described as a ‘strange heartbeat with fluttering’. Prior to the dual-chamber pacemaker insertion, he had undergone coronary angiography and left ventriculography, which showed normal epicardial coronary arteries and a left ventricular ejection fraction (LVEF) of 74%.On physical examination post pacemaker insertion, his blood pressure was 106/76 mmHg, with a heart rate (HR) of 76 bpm. The jugular venous pressure was elevated up to the angle of the jaw and cannon waves were present. His heart sounds were otherwise normal with no murmurs elicited, and there were no signs of heart failure. His chest was clear. The electrocardiogram (ECG) showed paced QRS with P wave at the end of the QRS complex, indicative of atrioventricular dyssynchrony . These cPacemaker interrogation showed that his pacemaker was programmed to AAIR–DDDR mode with a base rate of 70 bpm; the battery power was fine. The ECG showed typical right ventricular pacing compatible with VVIR mode despite AAIR– DDDR programming. Moreover, an atrial electrogram (EGM) showed ventricular pacing and a ventricular EGM showed sensed atrial depolarisation . These fThe patient subsequently underwent a corrective procedure (lead repositioning) without temporary pacing cover. During the procedure, it was confirmed that the leads were switched, with the ventricular lead connected to the atrial port, and the atrial lead connected to the ventricular port. Both the atrial and ventricular leads were disconnected and tested, after which they were reconnected to the appropriate ports at the pacemaker header. Atrial pace and ventricular sense were achieved through the AAIR–DDDR pacing mode .It was noteworthy that prior to correction, the blood pressure was 108/62 mmHg, with a HR of 45 bpm. Post correction, the blood pressure immediately rose to 141/77 mmHg, with a HR of 72 bpm (AP–VS).An echocardiogram done later the same day showed that the LVEF had dropped from 74 to 49% post pacemaker insertion. This high LVEF was thought to have been due to right ventricular-only pacing-induced left ventricular systolic dysfunction.The differential diagnosis for pacemaker syndrome includes: acute coronary syndromes, hyperthyroidism, hypothyroidism, pacemaker failure, pacemaker-mediated tachycardia and cardiogenic pulmonary oedema, among others.5 In our case, the rise in systolic blood pressure of > 20 mmHg post correction of the leads confirmed the diagnosis of pacemaker syndrome.The above differential diagnoses were ruled out as follows: the cardiac biomarkers were negative with no ST changes on the ECG, which ruled out an acute coronary syndrome. The patient was biochemically euthyroid with no clinical features of hyper- or hypothyroidism. The pacemaker was functional, ruling out the possibility of pacemaker failure. The resting heart rate was less than 100 bpm and this excluded the possibility of pacemaker syndrome in this case being due to pacemakermedicated tachycardia. The patient was clinically not in left ventricular failure, with clear lung fields on chest radiography and on auscultation, and therefore cardiogenic pulmonary oedema was an unlikely cause of his symptoms. Pulmonary embolism was also ruled out based on a negative D-dimer laboratory result.Pacemaker syndrome is defined as intolerance to ventricularbased (VVIR) pacing due to loss of atrioventricular (AV) synchrony.The overall incidence of pacemaker syndrome is unclear, with different studies reporting different results. In the Mode Selection Trial (MOST), pacemaker syndrome incidence was approximately 18%.7Low intrinsic rate and high ventricular pacing rate, as noted in our patient, results in high percentage of ventricular pacing, therefore more AV dyssynchrony, and this may also explain the development of left ventricular systolic dysfunction.Intact ventricular–atrial (VA) conduction poses a greater risk for the development of pacemaker syndrome.Patients with non-compliant ventricles, such as in diastolic dysfunction, heart failure, hypertrophic cardiomyopathy, among others, are particularly sensitive to loss of atrial contribution to ventricular filling.8Ventricular pacing leads to decreased cardiac output, with the resultant increase in left atrial pressure and left ventricular filling pressure.5The aetiology of pacemaker syndrome is poorly understood, but several risk factors are associated with its development:A major cause of AV dyssynchrony is VA conduction. Retrograde conduction leads to non-physiological timing of atrial contraction in relation to ventricular contraction. It should, however, be noted that many conditions other than VA conduction promote AV dyssynchrony.Conventional non-physiological right ventricular pacing has deleterious effects on left ventricular systolic function.3From the MOST and DAVID trials,This case demonstrated that switching of atrial and ventricular leads at the pacemaker header resulted in pacemaker syndrome in a patient with a dual-chamber permanent pacemaker. The syndrome was due to incorrectly connected leads, resulting in ventricular paced atrial sensed (VP-AS), essentially producing the VVI pacing with retrograde conduction and loss of AV synchrony. This case also illustrates the possibility of right ventricular pacing-induced left ventricular dysfunction and highlights the need to maintain a high level of concentration during device implantation.