With mounting data on its accuracy and prognostic value, cardiovascular magnetic resonance (CMR) is becoming an increasingly important diagnostic tool with growing utility in clinical routine. Given its versatility and wide range of quantitative parameters, however, agreement on specific standards for the interpretation and post-processing of CMR studies is required to ensure consistent quality and reproducibility of CMR reports. This document addresses this need by providing consensus recommendations developed by the Task Force for Post Processing of the Society for Cardiovascular MR (SCMR). The aim of the task force is to recommend requirements and standards for image interpretation and post processing enabling qualitative and quantitative evaluation of CMR images. Furthermore, pitfalls of CMR image analysis are discussed where appropriate. With mounting data on its accuracy and prognostic value, cardiovascular magnetic resonance (CMR) is becoming an increasingly important diagnostic tool with growing utility in clinical routine. Given its versatility and wide range of quantitative parameters, however, agreement on specific standards for the image interpretation and post processing of CMR studies is required to ensure consistent quality and reproducibility of CMR reports. This document addresses this need by providing consensus recommendations developed by the Task Force for Post Processing of the Society for Cardiovascular MR (SCMR). The aim of the task force is to recommend requirements and standards for image interpretation and post processing enabling qualitative and quantitative evaluation of CMR images. Furthermore, pitfalls of CMR image analysis are discussed where appropriate.The Task Force is aware that for many of the recommendations, the body of evidence is limited. Thus, this document represents expert consensus providing guidance based on the best available evidence at present as endorsed by the SCMR. As CMR undergoes rapid development, updated recommendations for image acquisition, interpretation and post processing are needed regularly and will be provided by online appendices when needed and updated Task Force papers in due course.The recommendations are considered for the application of CMR in clinical routine. For some applications, quantification is considered as providing added information but is not mandatory (e.g perfusion imaging), whereas for others quantification is required for all clinical reports (e.g. T2* assessment in iron overload). In general the intention of this task force is to describe, in which scenarios quantitative analysis should be performed and how it is performed.The recommendations respect societal recommendations for structured reporting of cardiovascular imaging studies in general (ACCF / ACR / AHA / ASE / ASNC / HRS / NASCI / RSNA / SAIP / SCAI / SCCT / SCMR)  and in sThe recommendations do not supersede clinical judgment regarding the contents of individual interpretation of imaging studies.The Task Force made every effort to avoid conflicts of interests and, where present, to disclose potential conflicts.Digital Imaging and Communications in Medicine) source images. Readers should have adequate training and clinical experience. The identity and responsibility of the reader should be appropriately documented in the report. Data acquisition should conform to the recommendations of SCMR .-10.8-10]ii) Outflow tract: The LV outflow tract is included as part of the LV blood volume. When aortic valve cusps are identified on the basal slice(s) the contour is drawn to include the outflow tract to the level of the aortic valve cusps.iii) Basal descent: As a result of systolic motion of the mitral valve toward the apex  care must be taken with the one or two most basal slices. A slice that contains blood volume at end-diastole may include only left atrium (LA) without LV blood volume at end-systole. The LA can be identified when less than 50% of the blood volume is surrounded by myocardium and the blood volume cavity is seen to be expanding during systole. Some software packages automatically adjust for systolic atrioventricular ring descent using cross-referencing from long-axis locations.c) LV massi) Calculation: difference between the total epicardial volume  minus the total endocardial volume , which is then multiplied by the specific density of myocardium (1.05 g/ml).ii) Papillary muscles: Papillary muscles are myocardial tissue and thus ideally should be included with the myocardium, and this is particularly relevant in diseases with LV hypertrophy. However, readers may decide to exclude trabecular tissue and papillary muscles from the myocardial mass. Reference ranges that use the same approach should be used and the inclusion / exclusion of papillary should be specifically mentioned in the report Figure  8-10].-10.8-10]iii) Basal descent and apex: When the most basal slice contains only a small crescent of basal lateral myocardium and no discernable ventricular blood pool, an epicardial contour for the visible myocardium is included for LV mass only. Similarly, when the most apical slice contains only a circle of myocardium without cavitary blood pool, an epicardial contour without an endocardial contour should be drawn for LV mass calculations.d) Rapid quantitative analysisi) A rapid quantitative analysis can also be performed using rotational long axis views (e.g. 2- and 4-chamber views). In cases without expected significant regional variation of wall motion, this technique allows for faster evaluation and is not limited by problems related to basal descent. When the area-length method is used, with either a single long-axis view or a bi-plane approach, specific mention of the analysis technique should be made in the report.ii) Calculation -13:2/ LV-length. This is typically performed using a 4-chamber view with calculations of LV volume obtained on both end-diastolic and end-systolic phases. LV-area is the planimetered area of the LV cavity from an endocardial contour with the base drawn as a straight line through the medial and lateral aspects of the mitral annulus. LV-length is the linear dimension from the midpoint of the mitral annular line to the apical tip of the endocardial contour.– Single long-axis equation: LV volume = 0.85 × (LV-area)– Bi-plane equation: LV volume = 0.85 × (LV-area1 x LV-area2)/ LV-length. Here, both 4-chamber (LV-area1) and 2-chamber [or vertical] (LV-area2) long axis views are used to calculate both end-diastolic and end-systolic volumes, similar to the single long-axis equation.e) Cavity diameter and LV wall thickness can be obtained similar to echocardiography using two CMR approaches ,14:i) Basal short axis slice: immediately basal to the tips of the papillary muscles;ii) 3-chamber view: in the LV minor axis plane at the mitral chordae level basal to the tips of the papillary muscles.iii) Both approaches have good reproducibility. The 3-chamber view is most comparable to data obtained with echocardiography.f) Research:i) Quantitative evaluation of LV dynamics  is feasible by several imaging techniques  and requires specific post-processing software. As research applications are evolving and consensus evidence is being accumulated, the Task Force chooses to refrain from making a dedicated statement at this time.a) Before analyzing the details, review all cines in cine mode, validate observations from one plane with the others, and check for artifacts and reliabilityb) Assessment of global and regional right ventricular (RV) function , where appropriate. Categorization should be noted as: hyperkinetic, normokinetic, hypokinetic, akinetic, dyskinetic.c) Assessment of both ventricular chambers for hemodynamic interaction (i.e. constrictive physiology)a) General recommendationsi) Calculated parameters: RV end-diastolic volume, RV end-systolic volume, RV ejection fraction, RV stroke volume, cardiac output, and body-surface area indexed values of all except ejection fraction. Similar to the LV, the parameters quantified may vary depending on the clinical need .ii) The contiguous stack of short axis images or transaxial cine images is evaluated with computer-aided analysis packages Figure  16,17].,17.16,17iii) Transaxial stack of cines covering the RV enable best identification of the tricuspid valve plane.iv) Endocardial borders are contoured at end-diastole and end-systole Figure .v) The RV end-diastolic image should be chosen as the image with the largest RV blood volume. For its identification, the full image stack has to be evaluated and one phase has to be identified as end-diastole for all short / transaxial locations.vi) RV end-systolic image should be chosen as the image with the smallest RV blood volume. For its identification, the full image stack has to be evaluated and one phase has to be identified as end-systole for all short / transaxial locations.vii) As for the LV, it may be necessary to review all image slices in the stack to define end-systole.viii) The pulmonary valve may be visualized, and contours are included just up to, but not superior to this level.ix) Trabeculations of the RV are ignored and a smooth endocardial border is drawn to improve reader reproducibility.b) RV volumesi) Total volumes are taken as the sum of volumes from individual 2D slices, accounting for any interslice gap and slice thickness. RV trabeculae and papillary muscles are typically included in RV volumes.c) RV massi) Usually not quantified in routine assessment.d) Confirmation of resultsi) If no intra- or extracardiac shunts are present, the RV and LV stroke volumes should be nearly equal . Since the LV stroke volume is more reliably determined than the RV stroke volume, the LV data can be used to validate RV data.a) For most clinical indications, visual analysis of myocardial perfusion CMR images is appropriateb) Work-flow:i) Display rest and stress perfusion images side-by-side. If possible also display corresponding LGE images.ii) Adjust window and level: The aim of image adjustment is to set a maximal window width without “overspilling” of the LV cavity signal into the myocardium. Ensure that myocardium before contrast arrival is nearly black and that signal in the RV and LV cavities is bright grey rather than a pure white. Correct level and window settings may require review of both pre- and peak contrast images.iii) Apply the same contrast, brightness and window settings to all images of the dynamic series.iv) Review series as cines and/or by scrolling through individual images. Some software packages allow the display of only dynamic images during the first myocardial passage.v) The key diagnostic feature is contrast arrival and first passage through the LV myocardium.vi) Visual analysis allows a comparison between regions to identify relative hypoperfusion. Comparison can be made between endocardial and epicardial regions, between segments of the same slice or between slices.c) Compare rest and stress images to identify inducible perfusion defects and artifacts. Note that unlike nuclear perfusion methods, in CMR the finding of a “fixed perfusion defect” on rest and stress perfusion images is not the preferred method to identify myocardial scar. Instead, scar should be identified from LGE images.d) Criteria for an inducible perfusion defect Figure a:i) Occurs first when contrast arrives in LV myocardiumii) Persists beyond peak myocardial enhancement and for several RR intervals iii) Is more than one pixel wideiv) Is usually most prominent in the subendocardial portion of the myocardiumv) Often manifests as a transmural gradient across the wall thickness of the segment involved: densest in the endocardium and gradually becoming less dense towards the epicardiumvi) Over time, defect regresses towards the subendocardiumvii) Is present at stress but not at restviii) Conforms to the distribution territory of one or more coronary arteries.e) Interpret location and extent of inducible perfusion defect(s) using AHA segment model ,7.i) Estimate number of segments involvedii) Comment on transmurality of perfusion defectiii) Indicate extent of perfusion defect relative to scar on LGEf) Pitfalls of visual analysisi) Dark banding artifacts Figure b: A commbefore contrast arrival in the LV myocardium, depending on applied sequence– typically occur first and are most prominent when contrast arrives in the LV blood pool, i.e. reduction in signal compared with baseline myocardial signal . These subtle differences can be hard to appreciate visually. It can therefore be helpful to draw a region of interest (ROI) around the suspected artifact and display its signal-intensity-time profile.– lead to a – persist only transiently before the peak myocardial contrast enhancement, often for less than approximately 6 RR intervals– appear predominantly in the phase-encoding direction– are approximately one pixel widenot on its own be considered diagnostic for an inducible perfusion defect.Dark banding present at stress and at rest with no corresponding scar on LGE images is also indicative of an artifact . Note hoii) Multi-vessel disease: as visual analysis is a relative assessment of perfusion within an imaged section of the heart, the presence of balanced multi-vessel disease can result in most or all of the imaged section appearing hypoperfused. This can lead to false-negative readings and needs to be considered in relevant clinical circumstances. On visual analysis, a clear endocardial to epicardial signal gradient may be seen in multi-vessel disease . Quantitiii) Microvascular disease: Diseases that affect the myocardial microvasculature  may lead to concentric reduction in perfusion -24. Thisiv) When performing a stress first-rest second perfusion protocol, caution is needed when a defect over a region of infarction may be misinterpreted as reversible. Contrasting the extent and location of reversibility by perfusion imaging with LGE is important to avoid over-calling of segmental ischemia .v) If vasodilator stress during data acquisition was inadequate, visual analysis may lead to false-negative interpretation . Quantitvi) Signal intensity may vary depending on the distance of myocardium from the surface coil and may lead to misinterpretation if not considered in the analysis. These problems are less likely if acquisition is corrected for coil sensitivity.a) Objective description of SI change in myocardial perfusion CMR studies can be performed. Several methods have been described for this purpose. In clinical practice, these are rarely required, but they may supplement visual analysis for example in suspected multi-vessel disease or suspected inadequate response to vasodilator stress. Quantitative analysis is also frequently used in research studies.b) Requirements:i) Validation and definition of a normal range with the specific pulse sequence and contrast regime used for data acquisition. If only a comparison between regions of the same study is made, establishing a normal range is less relevant.ii) Consideration of contrast dosage at time of acquisition .c) Semi-quantitative analysis:i) Analysis methods that describe characteristics of the SI profile of myocardial perfusion CMR studies without estimating myocardial blood flow are typically referred to as “semi-quantitative analysis methods”.ii) Work-flow:– Select an image from the dynamic series with good contrast between all cardiac compartments (some post-processing tools generate an average image of the series).– Outline LV endocardial and epicardial contours on this image  Figure c.– Propagate contours to all other dynamic images.– Avoid myocardial fat in the ROI– Correct contour position for through-plane motion .– Depending on the type of analysis to be performed, place a separate ROI in the LV blood pool. Preferably the basal slice is used. Exclude papillary muscles from the ROI.– Select a reference point in the LV myocardium for segmentation.– Segment LV myocardium according to AHA classification .– Generate SI / time profiles for myocardial segments +/- LV blood pool.– Consider generating division into endocardial and epicardial layers and repeat analysis.iii) Frequently used semi-quantitative analysis methods  – The upslope integral  .iv) Limitations of semi-quantitative analysis methods:– SI may vary according to distance from coil– No absolute measurement of myocardial blood flow derivedd) Quantitative analysisi) Analysis methods that process the SI profile of myocardial perfusion CMR studies to derive estimates of myocardial blood flow are typically referred to as “quantitative analysis methods”. See  for reviii) Requirements:– It is a prerequisite for reliable quantification that data acquisition used an appropriate pulse sequence and contrast regime.– An “input function” for analysis of the myocardial tissue response can be derived from the ROI in the LV blood pool. In order to reduce saturation effects in the blood pool, a “dual-bolus” myocardial perfusion regime may be used, in which the input function is derived from a pre-bolus with a small contrast agent concentration.– The contrast dose and delivery need to be chosen to minimize saturation effects also the myocardium and typically contrast doses required for reliable quantitative analysis are lower than those optimized for visual analysis in clinical routine.– A temporal resolution of 1-2 RR intervals is required.iii) Work-flow:– Typically, the same source data as for semi-quantitative analysis are used– Further post-processing may then take place on the same or a separate off-line workstation.iv) Several analysis methods have been described, including:– Model-based methods – Model-independent methods a) For most clinical indications, visual assessment of LGE images is sufficientb) Work-flow:i) Modify image window and level so that:– Noise is still detectable (nulled myocardium should not be a single image intensity)– LGE regions are not clipped (LGE regions should not be a single image intensity)ii) Note if normal myocardium has a faint “etched” appearance , this signifies an inversion time that was set too short and will lead to underestimation of the true extent of LGE Figure . In genec) Criteria for presence of LGEi) High SI area that may be as bright as the LV blood poolii) Rule out artifacts (see below)d) Assess pattern of LGEi) Coronary artery disease (CAD) type: Should involve the subendocardium and be consistent with a coronary artery perfusion territoryii) Non-CAD-type: Usually spares the subendocardium and is limited to the mid-wall or epicardium, although non-CAD-type should be considered if subendocardial involvement is global ,36.e) Interpret location and extent using AHA 17-segment model ,5352,53]– This issue is not significant when using the double inversion recovery (black blood) sequence d) Cut-off values (at 1.5 Tesla):i) Normal cardiac T2* is 40ms ii) T2* < 20 ms = cardiac iron overload iii) T2* <10ms indicates increased risk of development of heart failure e) CMR assessment of T2* at 3T for assessment of iron overload cardiomyopathy cannot be recommended at this time. T2* shortens with increasing field strength making assessment of severe iron overload more problematic, and there is a lack of clinical verification.a) Appropriately aligned acquisitions of cines and stacks of cines can give valuable information on flow in relation to adjacent structures, notably on the directions, time courses and approximate dimensions of jets resulting from valve regurgitation, stenoses or shunts. Such information can be important in assessing the credibility of measurements of flow, which may be subject to several possible sources of error. Gradient echo cines differ somewhat from SSFP in terms of degrees of signal augmentation or reduction attributable to flow effects. Of note, SSFP can provide clear delineation between the relatively bright signal from voxels aligned within the coherent core of a jet, and low signal from the shear layer that bounds such a jet core. In- or through-plane phase contrast flow velocity acquisitions can also provide visual information on the directions, dimensions and time courses of flow; it can also image morphology, which can yield a clue to the etiology of an abnormal jet  58,59],5958,59]b) Pitfalls:i) Flow appearances on both cine and phase encoded acquisitions are highly dependent on image location and orientation, especially in the case of jet flowii) If the range of velocity encoding (VENC) is set too high, visualization of the jet may not be obtained. If it is set too low, a mosaic pattern on the images will be visualized .iii) If slice thickness is too large on in-plane velocity mapping, the higher velocities will be “averaged out” with the lower velocities and stationary tissue; jets and flow may not be visualized correctly.iv) If the annulus of valves is very dynamic or the imaging plane is not set correctly, the valve morphology may not be visualized.v) If imaging in the presence of metal containing devices, signal loss may be present as artifact and interpretation must proceed with caution.vi) The TE should be as low as possible for increased accuracy, especially with high velocity turbulent jets; this should be kept to 3.5 ms or lower .a) Work-flow:i) Load phase and magnitude images into software. Window the magnitude and phase images to the appropriate brightness and contrast so that the borders of the ROI are sharp.ii) Examine the images to ensure the quality is sufficient and that the VENC was not exceeded, or there was little contrast (ie the VENC was too high).iii) Trace the borders of the vessel of interest on each phase and magnitude image so that only the cavity of the vessel is included Figure ; make suiv) Baseline-correction or comparison to a phantom for flow measurements may be considered ,63.v) Directly calculated parameters include: antegrade volume, retrograde volume, peak velocity and mean velocityvi) Derived parameters include:– Net volume [ml| = antegrade volume - retrograde volume– Regurgitant fraction [%] = ( retrograde volume / antegrade volume) * 100– Cardiac output (liters/min = (net volume [ml] x heart rate [beats/minute])/1000) and cardiac index (cardiac output/BSA) when integrating heart rate and body surface area– Regional flow to both lungs by measuring cardiac output in each branch pulmonary artery (eg percentage of flow to the right lung = (right pulmonary artery flow / right pulmonary artery flow + left pulmonary artery flow) × 100).– Regurgitant volumes of the atrioventricular valves may be obtained by either of 2 methods: A) direct measurement of diastolic flow across the valve and subtraction of systolic forward flow across the associated semilunar valve or B) measurement of stroke volume using cine CMR and subtraction of forward flow across the associated semilunar valve.b) Pitfalls:i) On the phase images, the area of flow may be slightly larger than the area of the magnitude images.ii) If the VENC is exceeded, most software packages allow for moving/changing the “dynamic range” of the images so that the VENC is not exceeded. For example, if the peak velocity in the aorta is 175 cm/s and the VENC was set at 150 cm/s, the dynamic range is between -150 cm/s and +150 cm/s (i.e. 300 cm/s). This may be moved to -100 cm/s and +200 cm/s to account for this accelerated velocity. This will be demonstrated on the graph of the velocity where the phase in which the VENC is exceeded does not “clip” (appears to go the wrong way) after correction.iii) In general, the area that exceeds the VENC in the ROI is in the center of the vessel and not at the edges; if at the edges, it is usually  outside the vessel.iv) If imaging in the presence of devices, signal loss may be present as artifact and interpretation must proceed with caution.v) When measuring peak velocity, some software packages will determine the peak velocity in one pixel in the ROI whereas others may take the peak velocity of the average of a few adjacent pixels in the ROI. By reporting the peak velocity in a single pixel, noise may make this measurement inaccurate. By reporting this as an average of a few adjacent pixels, noise is less of an issue, however, the true “peak velocity” may be higher than the reported value. These factors must be kept in mind and interpretation may need to be adapted to the measurement technique used.vi) When attempting to measure peak velocity using through plane velocity mapping along a vessel, interpretation should be tempered by the notion that this parameter may be an underestimate as the true peak velocity lies somewhere along the vena contracta; the through plane velocity map may not have been obtained at the level of the true peak velocity. If the vena contracta is itself narrow or ill defined, jet velocity mapping is unlikely to be possiblevii) Peak velocity is only minimally affected by small background phase offsets, while volume measurements can be dramatically affected by even a small background phase offset due to the cumulative aspect of integration overspace (within the ROI) and time (over the cardiac cycle). Dilatation of a great vessel tends to increase error of this type .viii) Orientation of the image plane perpendicular to flow direction can have a significant impact on peak velocity measurement, while not significantly affecting volume flow .a) 4D flow: The utility of this approach is the subject of ongoing research.b) Real time velocity mapping: The utility and post processing algorithm best applied to this approach is the subject of ongoing research.a) Maximum intensity projections (MIP) for first review of 3D data and for demonstration purposes Figure A. Volumeb) Aorta :i) Wall thickness: Review balanced steady state free precession (bSSFP) or turbo spin echo images.ii) Wall irregularities: Review 3D-MRA source images and bSSFP or turbo spin echo.c) Pulmonary arteries :i) Multiplanar double oblique and targeted MIP reconstructions for assessment of wall adherent thrombi, wall irregularities and abrupt diameter changes.d) Pulmonary veins :i) Screen for atypical insertion and small accessory veins.e) Coronary arteries:i) Coronary MRA may play a role in assessment of congenital anomalies but not usually in the context of ischemic heart disease. The course of coronary arteries is best assessed on source images, multiplanar reconstructions (MPR) or targeted MIP reconstructions.a) Aorta:i) Multilevel measurements of aortic diameters on double oblique multiplanar images perpendicular to blood flow at standardized levels Figure  66]. Me. Me66]. ii) Inner diameter (lumen width). In the presence of wall thickening  outer diameter including vessel walls should also be reported.iii) Diameters of sinuses or sinotubular junction may not be measured on ungated images since motion artifacts can lead to blurring and may result in diameter under- or overestimation. These require ECG gated acquisitions, either from 3-dimensional SSFP acquired in late diastole, or from a contiguous stack of cines aligned to transect the axis of the aortic root. Consistent methods of acquisition and measurement are essential for the evaluation of any change over time, for example by the measurement in late diastole, of all three sinus-commissure dimensions of the aortic root, which may dilate asymmetrically.iv) Standardized report including table of diameters.b) Pulmonary artery:i) The widest inner diameter is measured perpendicular to the long axis of the main pulmonary artery at the level of the pulmonary bifurcation in transaxial slicesc) Pulmonary veins:i) MPR of pulmonary veins perpendicular to blood flow for diameter measurements.bSSFP: Balanced steady state free precession; CAD: Coronary artery disease; CMR: Cardiovascular magnetic resonance; FWHM: Full width half maximum; LGE: Late Gadolinium enhancement; LV: Left ventricle; MIP: Maximum intensity projection; MPR: Multiplanar reconstruction; PSIR: Phase sensitive inversion recovery; ROI: Region of interest; RV: Right ventricle; SD: Standard deviation; SI: Signal intensity; STIR: Short-tau inversion recovery; TE: Echo time; TI: Inversion time; TR: Repetition time; TSE: Turbo spin echo; VENC: Velocity encoding; VR: Volume rendering.The authors declare that they have no competing interests.JSM wrote paragraphs, edited manuscript, corresponding author. DAB, JB, SDF, MAF, MGF, RJK, FvKB, CMK, DJP, SP and EN wrote paragraphs, edited manuscript. All authors read and approved the final manuscript.


Hypertrophic cardiomyopathy (HCM) is the most common genetic heart disease. Congestive symptoms of heart failure, such as effort dyspnea, may occur in this cardiovascular disorder. Myocardial fibrosis is a pathological feature of extracellular matrix remodeling, that may promote alterations in myocardial ventricular function. Magnetic Resonance Imaging (MRI) is now used as an non-invasive standard tool to detect focal myocardial fibrosis. The presence of scar using Delayed Enhancement technique (DE) is related to a worse prognosis in HCM. The relationship between the progression of myocardial fibrosis and the functional clinical status was not previously investigated.a) to assess the severity and speed of progression of left ventricle (LV) fibrotic tissue formation by DE MRI b) to investigate if a relation between the rate of progression of LV scar and a worst clinical status exists.In 29 patients with HCM  we repeated two cardiac magnetic resonance examinations, using a 1.5 Tesla scanner . We evaluated LV mass and volumes and LVEF by the acquisition of conventional SSFP cine short axis images. DE was detected using T1 GRE IR acquired 10 minutes following contrast injection. Quantification of DE was performed as previously described (1).At the first CMR DE was detected in 21 subjects (72%), with an average extent of 8.1 ± 8 % of LV mass. CMR was repeated after an average of 772 ± 300 days. At the second CMR exam DE was found in 28 patients (97%). Among them, 16 subjects showed a significant increase of extent of DE . During the time interval between the 2 examination, NYHA class worsened in 10 patients who presented higher increase of DE extent than those with preserved functional status .From these data we conclude that the progression of fibrosis in HCM is fast. The increase of extent of fibrosis in these patients is related to a worse clinical status. Therefore MRI can be applied as an useful safe tool, for longitudinal follow up evaluation of progression of the disease.


Subclinical myocardial involvement is common in systemic sclerosis (SSc) and associated with poor prognosis. Early detection, particularly during follow-up, is important. Two-dimensional speckle tracking echocardiography (STE) has already been shown to detect early left ventricular systolic impairment in SSc patients with advanced disease. The aim of this study was to assess the ability of STE to diagnose changes in left ventricular function in patients with SSc with preserved LV ejection fraction (LVEF) and normal pulmonary pressure over time.This single-center pilot study included nineteen SSc patients without pulmonary hypertension and preserved LVEF . We performed STE at baseline and after two years (mean 756.6 ± 8.8 days). Pulmonary hypertension was ruled out in all patients by right heart catheterization (average mean PAP 17.7 ± 3.5 mmHg).P = ns), but the global longitudinal peak systolic strain of the left ventricle was significantly lower: baseline -22.0 ± 2.3% vs. follow-up -20.8 ± 2.1% (P = 0.04). The regional analysis showed a heterogeneous distribution of segmental systolic dysfunction that did not match any particular coronary artery distribution. In contrast, the LV diastolic function remained stable during follow-up.The LVEF remained unchanged (63.3 ± 4.2% vs. 63.2 ± 5.0%, STE might be a sensititive and valuable method to detect early LV systolic impairment in patients with SSc and preserved LVEF during two years. Prospective evaluations are needed for prognostic implications of these changes. Clinical myocardial dysfunction in patients with systemic sclerosis (SSc), an entity characterized by extensive fibrosis, is recognized only in 15-25%,4. In thThe aim of this study was to assess subclinical changes in LV function by STE in SSc patients with preserved left ventricular ejection fraction (LVEF) and without pulmonary hypertension over a duration of two years.21 SSc patients without pulmonary hypertension, reduced LVEF, or known coronary heart disease who were included in the DETECT (Detection of PAH in SSc) study in our cStandard transthoracic echocardiography was performed in the left decubitus position using an ultrasound system  with a 3.4-MHz multifrequency transducer. The LVEF was obtained according to the recommendations of the ASE.Left ventricular diastolic function was assessed using pulsed-wave Doppler and pulsed-wave Doppler tissue imaging (DTI) recordings on the basis of the recommendations of the ASE. Transmitral flow was acquired to obtain peak early (E) and atrial (A) flow velocities. We used the average peak early diastolic (E’), peak late diastolic (A’) and peak systolic velocity (S’) obtained from the septal and lateral sides of the mitral annulus in the fourchamber view with proper DTI settings. The E/E’ ratio was calculated to estimate LV filling pressures.For assessment of longitudinal strain, we recorded standard 2D ultrasound images with a frame rate between 60 and 80 frames per second (fps) from the apical long axis, and two- and four-chamber views. We stored these recordings digitally for offline analysis  as previously described. In shorTwo echocardiographers, blinded to previously obtained data, separately measured global PSS from 13 random patients for interobserver variability analysis. Additionally, an experienced observer calculated strain values twice on two consecutive days for analysis of intraobserver variability. We employed inter- and intraobserver variability to determine the interclass coefficient.All results are expressed as mean ± standard deviation (SD). Statistics were calculated using SPSS 21.0 . Wilcoxon-test was used for the comparison of the paired observations. Interclass Correlation Coefficient by Kolmogorov-Smirnov was used to calculate inter- and interobserver variability. P values of < 0.05 were considered statistically significant. The echo templates for Figure three were originally created by Patrick J. Lynch and C. Carl Jaffe, MD and used with permission under the Creative Commons Attribution 2.5 License 2006.Table Conventional echocardiographic findings are presented in Table p = ns) .Table  Figure . In addip = 0.04) (Table p = 0.006) while there was only a trend for lower strain in the two-chamber view and apical long axis view.The mean global PSS value at follow-up was still in normal range, but significantly reduced compared to baseline examination  Table . Figure Regarding regional analysis we found reduced mean PSS in all segments but only the medial segments in the four-chamber view were statistically significant Table .The intraobserver variability for the LV longitudinal strain was 0.93 (CI 0.79-0.98). The interobserver variability for the LV longitudinal strain was 0.90 (CI 0.57-0.99).Cardiac involvement in patients with SSc is associated with a poor prognosis and is more frequent in SSc patients than clinically suspected. TherefoAlthough it has been shown that STE-derived strain is a sensitive marker for the detection of clinical and subclinical myocardial left heart dysfunction in a variety of pathologies, even during follow-up, to our In clinical routine, assessment of global systolic function is usually based on the LVEF. This parameter, however, is insufficient in describing the complex myocardial motion. Moreover, LVEF mainly depends on the radial and circumferential deformation caused by less sensitive mid-myocardial and epicardial fibres. In contrast, longitudinal function is predominantly influenced by subendocardial fibres which are most susceptible to evident myocardial damage with preOur regional analysis showed a heterogeneous distribution of declining systolic dysfunction that did not match any particular coronary artery distribution. Histologic studies diagnosed a patchy myocardial fibrosis in up to 80% of patients with SSc. This paNo patients had to be excluded due to poor image quality. This indicates an acceptable feasibility of echocardiographic assessment of LV function by speckle tracking in SSc patients.First, our study was designed as a retrospective, pilot single-center study with only a small number of patients and we cannot draw definite conclusions regarding the prognostic implications of these mild changes in LV function. Additional prospective studies are needed to clarify whether systematic echocardiographic surveillance should be recommended in order to improve the prognosis in this population. Second, we did not track healthy controls over time. Therefore, we cannot completely exclude other variables that might have influenced our results in patients with SSc, e.g. like ageing. Nevertheless, we do not believe in aging effects since it takes decades for longitudinal function to decrease. Third, STE detect subtle changes of systolic LV function in patients with SSc and preserved LVEF and normal pulmonary pressure after two years. Since cardiac involvement is common, our results may be explained by a progression of subclinical myocardial fibrosis. STE might be a sensititive and valuable method for follow-up of SSc patients, but prospective evaluations are needed for prognostic implications of these changes.The authors declare that they have no competing interests.SS: Study conception, echocardiographic examinations, data analysis and interpretation, drafting of the manuscript. KR: Acquisition of data and interpretation, participating in statistical analysis. GR: Data analysis, study conception, critical revision of the manuscript. ACB: Data analysis and interpretation, critical revision of the manuscript. SS: Echocardiographic examinations, critical revision of the manuscript. GRB: Data analysis, critical revision of the manuscript. BH: Performed the statistical analysis, data analysis. GB: Study conception and design, data analysis and interpretation. HD: Data analysis and interpretation, preparation of figures, critical revision of the manuscript. FK: Echocardiographic examinations, data analysis and interpretation, revision of the manuscript. All authors read and approved the final manuscript.


Late gadolinium enhancement (LGE) is identified frequently in LVNC. However, the features of this findings are limited. The purpose of the present study was to describe the frequency and distribution of LGE in patients meeting criteria for left ventricular non-compaction (LVNC), as assessed by cardiovascular magnetic resonance (CMR).Forty-seven patients  considered to meet standard CMR criteria for LVNC were studied. The LGE images were obtained 15 ± 5 min after the injection of 0.2 mmol/kg of gadolinium-DTPA using an inversion-recovery sequence, and analyzed using a 17-segment model.Mean number of non-compacted segments per patient was 7.4 ± 2.5 and the NC:C was 3.2 ± 0.7. Non-compaction was most commonly noted in the apical segments in all patients. LGE was present in 19 of the 47 patients (40%), and most often located in the ventricular septum. The distribution of LGE was subendocardial , mid-myocardial , subepicardial , and transmural  in total of 90 LGE (+) segments.In patients considered to meet criteria for LVNC, LGE distributions visible were strikingly heterogeneous with appearances potentially attributable to three or more distinct cardiomyopathic processes. This may be in keeping with previous suggestions that the criteria may be of low specificity. Further work is needed to determine whether conditions such as dilated cardiomyopathy, previous myocardidtis or ischaemic heart disease increase the apparent depth of non-compact relative to compact myocardium. Left ventricular non-compaction (LVNC) is a disorder characterized by numerous prominent ventricular trabeculations and deep intratrabecular recesses , high moThe purpose of this retrospective study is to describe the frequency and distribution of LGE in patients considered to meet CMR cine imaging criteria for LVNC.The study was conducted between April 2006 and January 2011 in our hospital. We enrolled 47 consecutive LVNC patients with first a diagnosis of LVNC. The diagnosis of LVNC was based on the presence of the following CMR and clinical criteria : (a) appAll CMR exams were performed using a 1.5-T unit  with a high-performance gradient system . Twelve-element matrix coils (6 anterior and 6 posterior) equipped with the scanner and wireless vector electrocardiograph gating triggering were activated for data acquisition. All imaging acquisitions were captured under breath control. Scout transversal and sagittal images were acquired followed by a half-Fourier acquisition single shot turbo spin echo sequence  for the exact determination of the long-axis, 4-chamber, and short-axis plane position. Retrospective electrocardiographic gating cine images were acquired in three long-axis views  and a contiguous set of short-axis sections encompassing the entire LV using true fast imaging with steady-state free precession . Fifteen ± 5 min after the injection of 0.2 mmol/kg of gadolinium-DTPA  with an inversion-recovery sequence, the LGE images were obtained in a standard short axis view covering the entire ventricle, and in long axis views .All CMR data were transferred to a workstation  for analysis. The LV end-diastolic diameter, LV end-diastolic volume, LV end-systolic volume, and LV ejection fraction were calculated from the short axis cine images. The NC:C myocardium in diastole was calculated for each of the three long-axis views, and only the maximal ratio was used for analysis.The presence or absence of LGE was qualitatively determined for each LV myocardial segment using the 17 segments model, according to the American Heart Association recommendation  by reviet-test for continuous variables and a chi-square test or Fisher exact test for non-continuous variables in two groups. A two-tailed P-value <0.05 was considered statistically significant. Statistical analysis was performed using the SPSS software package .All values are expressed as the mean ± SD or counts (percentage). Clinical and CMR characteristics were compared using a Student’s The clinical characteristics of the entire group are summarized in Table Three hundred fifty (44%) LV segments were considered to fulfil the definition of non-compaction; the mean number of LV non-compacted segments per patient was 7.4 ± 2.5 and the NC:C was 3.2 ± 0.7. Non-compaction was most commonly noted in the apical segments in all patients. Basal-septal segment involvement was not noted in any patient Figure .LGE was evident in 19 (40%) of the 47 patients. LGE was present in all 17 segments, not only involved non-compacted segments but also normal segments of the heart. Totally, 9028%) LV segments showed LGE. Seventy-two (80%) LGE (+) LV segments were located in compacted segments, most commonly in the ventricular septum , while only 18 (20%) LGE (+) LV segments were in non-compacted segments (Figure 8% LV segLVNC has a wide spectrum of clinical and pathophysiological findings . ClinicaCMR is becoming increasingly widely used in assessment of suspected LVNC. Petersen et al.  found thIn agreement with previous studies, we observed LGE in approximately 40% patients considered to meet criteria for LVNC. The possibly pathophysiological mechanisms leading to LGE in LVNC have not been determined. Jenni et al.  describeNucifora et al.  found thOur study has a number of limitations. It was conducted at a single center with a relatively small sample size, and the diagnosis was based on CMR cine appearances in relation to clinical findings. However, not all patients had coronary artery disease ruled out by invasive coronary angiography. More thorough documentation of all previous investigations and findings would have been desirable. Clinical follow-up data were not available so the relationship between LGE and prognosis in LVNC patients remains unknown.In patients considered to meet criteria for LVNC, LGE distributions visible were strikingly heterogeneous with appearances potentially attributable to three or more distinct cardiomyopathic processes. This is in keeping with previous suggestions that the criteria may be of low specificity. Further work is needed to determine whether conditions such as dilated cardiomyopathy, previous myocardidtis or ischaemic heart disease increase the apparent depth of non-compact relative to compact myocardium.The authors declare that they have no competing interests.JYW, SHZ and BCH conceived and designed the study. JYW drafted the manuscript. SHZ reviewed and edited the manuscript. MJL, GY and SLJ carried out images analyses. XJG and YJY were responsible for cases selected and analysis. All authors read and approved the final manuscript.The study was supported by grant No. 81130029 from the key projects of National Natural Science Foundation of China and by grant No. 2009–1004 from Research Foundation of Capital Medical Development.


Acute myocardial depression in septic shock is common . Myocardt test was used to compare heart rate, contraction amplitude, speeds of contraction and relaxation with TNFa and control measurements and after removal of TNFα.After profound anesthesia with pentothal, the Wistar rats were killed by exsanguination. After sternotomy, the heart was taken and connected to the Langendorf column. The apex of the heart was hooked to a strength sensor. Biopac student laboratory software was used to record and analyse heart contractions. Contractions were recorded every 5 minutes during periods of 20 minutes. Control measurements were first recorded. We measured four parameters: heart rate, contraction force, speeds of contraction and relaxation for control, during TNFα (20 ng/ml) exposure and after removal of TNFα. We express the variations of parameters as percentage of the control ± SEM. A paired Eight rat hearts Wistar (weight = 325 ± 23 g) were studied. See Table TNFα decreases significantly the heart rate, contractile force, speeds of contraction and relaxation on isolated perfused rat heart. TNFα probably plays a role in the pathophysiology of cardiomyopathy during septic shock. The partial reversibility of these effects could explain why left ventricular hypokinesia in patients with septic shock is reversible.


Robotic cardiac operations evolved from minimally invasive operations and offer similar theoretical benefits, including less pain, shorter length of stay, improved cosmesis, and quicker return to preoperative level of functional activity. The additional benefits offered by robotic surgical systems include improved dexterity and degrees of freedom, tremor-free movements, ambidexterity, and the avoidance of the fulcrum effect that is intrinsic when using long-shaft endoscopic instruments. Also, optics and operative visualization are vastly improved compared with direct vision and traditional videoscopes. Robotic systems have been utilized successfully to perform complex mitral valve repairs, coronary revascularization, atrial fibrillation ablation, intracardiac tumor resections, atrial septal defect closures, and left ventricular lead implantation. The history and evolution of these procedures, as well as the present status and future directions of robotic cardiac surgery, are presented in this review. The purported benefits of minimally invasive cardiac surgery have been well described; smaller, less invasive incisions have the theoretical benefit of less pain, shorter length of stay, improved cosmesis, and quicker return to preoperative level of functional activity. Minimally invasive approaches have become the standard of care at many institutions, and excellent results have been achieved.As minimally invasive cardiac operations gained favor, developments in tele-manipulation technology and optics fostered the evolution of robotic-assisted cardiac surgery. Currently, the da Vinci™ surgical system  is the only US Food and Drug Administration (FDA)-approved robotic system used for cardiac surgical procedures. Today, robotic heart surgeons perform complex mitral valve repairs, coronary revascularizations, atrial fibrillation ablations, intracardiac tumor resections, and congenital heart surgery procedures.Before robotic cardiac surgery became a viable technique, minimally invasive heart surgery had been developed and perfected. These alternatives to the gold standard median sternotomy incision became increasingly commonplace as advances in minimally invasive access and exposure, perfusion strategies, and myocardial protection were made. The development of these techniques enabled the application of endoscopic visualization and instrumentation to be developed. This advancing pathway led to the robotic tele-manipulation of materials and tissues that we have today. The da Vinci™ surgical system provides increased operative dexterity for surgeons. The wrist-like articulating instruments move with six degrees of freedom, compared with the four degrees of freedom that endoscopic instruments provide. Other benefits are tremor-free movements, ambidexterity, and the avoidance of the fulcrum effect that is intrinsic when using long-shaft endoscopic instruments. Moreover, the system improves operative visualization greatly through the use of three-dimensional high-definition imaging.The most commonly performed robot-assisted cardiac procedure today is a mitral valve repair or replacement. As in other less invasive cardiac operations, minimally invasive and subsequently robotic mitral valve surgery evolved from modifications of incisions performed previously under direct vision. Large series from Cohn and Cosgrove showed that mitral surgery, done via minimal access incisions and performed under direct vision, offered comparable results to the sternotomy approach .62 trapezoidal resection with an intracorporeal suture repair followed by annuloplasty band implantation.11The first robotic mitral repair was performed by Carpentier in 1998, using an early prototype of the da Vinci™ surgical system.n = 114), partial sternotomy (n = 270), and right mini-anterolateral thoracotomy (n = 114). Outcomes were compared on an intent-to-treat basis using propensity score matching. Median cardiopulmonary bypass time was 42 minutes longer for robotic than for complete sternotomy, 39 minutes longer than partial sternotomy, and 11 minutes longer than right mini-anterolateral thoracotomy (P < 0.0001). There were no in-hospital deaths in any group, and neurologic, pulmonary, and renal complications were similar among groups (P > 0.1). The robotic group had the lowest occurrences of atrial fibrillation and pleural effusion, contributing to the shortest hospital stay (median 4.2 days); 1.0, 1.6, and 0.9 days shorter than for complete sternotomy, partial sternotomy, and right mini-anterolateral thoracotomy , respectively.Mihaljevic et al. reported their results for 261 robotic mitral valve repairs done between 2006 and 2009.P = 0.04), despite longer cross-clamp and bypass times . Mean packed red blood cell transfusion was also lower among patients who underwent robotic-assisted mitral valve surgery .Similar reductions in length of stay were seen at the University of Pennsylvania in a comparison of 39 patients who underwent sternotomy and mitral valve repair, or replacement, with 26 patients who underwent robotically assisted mitral valve repair or replacement.Today, most robot-assisted mitral valve repairs are accomplished either through a 3–4-cm right anterolateral mini-thoracotomy or a 2-cm lateral working port. The articulating EndoWrist™  instruments and dynamic left atrial retractor allow console surgeons to employ Carpentier’s and others’ “toolbox” of repair techniques.Our institution has performed over 800 robotic mitral valve repairs. Results have been published for the first 540 patients.11We use topographic valve models, derived from intra-operative high-quality three-dimensional transesophageal echocardiography images to plan a successful repair. To isolate the right lung, patients are either intubated with a dual-lumen endotracheal tube or single-lumen tube with bronchial blocker. The patient’s right side then is elevated to 30 degrees. Cardiopulmonary bypass is achieved via bicaval venous cannulation  and femoral arterial cannulation. In patients with either inadequate femoral artery size or aorto-iliac atherosclerotic disease, the right axillary artery is cannulated through an 8-mm polytetrafluoroethylene (PTFE) side-arm graft. The aorta is occluded using the Chitwood transthoracic aortic cross-clamp , and antegrade crystalloid Bretschneider’s cold cardioplegia is used to arrest the heart. In reoperative cases and patients with an atherosclerotic or calcified ascending aorta, hypothermic (26°C) fibrillatory arrest is used for myocardial protection. Thereafter, robotic instrument arm trocars are inserted into the chest, and the da Vinci™ surgical cart is docked by the patient’s left side.15The da Vinci™ surgical system has been used very successfully to harvest the internal thoracic artery (ITA) for coronary artery bypass grafting (CABG). In most cases the ITA-coronary anastomosis has been hand-sewn via either a mini-thoracotomy or median sternotomy. However, several surgeons have shown good results on both beating and arrested hearts with totally endoscopic robotic coronary artery bypass grafting (TECAB).Using a first-generation da Vinci™ surgical system, the first TECAB was performed in two patients by Loulmet et al. in 1998.16Srivastava et al. reported results from 150 patients who underwent a robotic ITA harvest with off-pump CABG via a mini-thoracotomy.Argenziano reported the FDA multicenter robotic coronary bypass Investigational Device Exemption trial in 2006.n = 334), double (n = 150), triple (n = 15), or quadruple (n = 1) bypass. One-third of the cases had a hybrid procedure, i.e. CABG combined with percutaneous coronary intervention. The median operative, cardiopulmonary bypass, and cross-clamp times were 305 minutes, 98 minutes, and 73 minutes, respectively. Bilateral internal thoracic arteries were used in 22% of patients with a median harvest time of 34 minutes for the left and 32 minutes for the right. The operative mortality was 1% with 10% having conversions to a sternotomy and 5% having ITA harvest injuries. Major morbidity and mortality was 5% as defined by death, myocardial infarction, stroke, vascular complication, or long-term ventilation requiring a tracheostomy. Operative success, as defined by freedom from repeat revascularization, reoperation for bleeding, or conversion to a larger incision, was present in 80% of patients.The largest TECAB experience to date was published by Bonaros et al.P < 0.0001). In a more recent cohort, the SYNTAX trial, which compared multivessel drug-eluting stenting with multivessel CABG in patients with triple-vessel or left main coronary disease during the 2005 to 2007, reported a postoperative LOS in the CABG cohort (n = 897) of 9.5 ± 8 days.22The same group reported on their length of stay results for 541 consecutive TECAB patients in two different institutions on different continents.The operative approach, as described by Bonaros et al., was as follows.To summarize, these reports have shown some success with robot-assisted revascularization in properly selected patients. However, it is clear that TECAB is a challenging procedure, and the learning curve is significant. The limited data on this subject suggest that robotic coronary operations still have a long way to go to uniformly have the same results as traditional coronary grafting. Moreover, committed and large clinical volume robotic coronary surgeons have obtained the best results. The newest generation of the da Vinci™ SI robotic system with a fourth arm and an endostabilizer may enable more complex bypass operations to be done on both beating and arrested hearts. At several centers, and with increasing frequency, TECAB is being done in concert with a percutaneous coronary intervention as a hybrid operation. This combines the survival benefits of left internal thoracic artery (LITA) to LAD grafting with the benefits of minimally invasive access of the percutaneous coronary intervention (PCI).The excellent results using the classic Coxmaze for treating atrial fibrillation operation have been well documented.Despite a lack of level I evidence, cryoablation is gaining traction among surgeons as a safe and effective treatment option for atrial fibrillation. Several small retrospective, randomized clinical trials have shown a conversion rate to sinus rhythm at 12 months in the range of 60%–80%.25In 2012, we reported a series of 86 patients who underwent combined robotic mitral valve repair with concomitant cryomaze.Robotically assisted epicardial ablation with microwave energy has also been performed with few complications. The largest series, by Pruitt and colleagues, reported on 33 paroxysmal and 17 permanent atrial fibrillation patients who underwent thoracoscopic or robotic-assisted off-pump epicardial microwave ablation. The investigators reported no perioperative death, a mean length of stay of 4 days, and a 79.5% success rate overall, with a cure rate of 93.5% in paroxysmal disease versus 69.2% in permanent disease.27P = 0.001) and had a lower ejection fraction  than surviving patients.29Epicardial left ventricular (LV) lead insertion for cardiac resynchronization therapy offers an important rescue therapy for failed percutaneous coronary sinus LV lead placement. Robot-assisted LV lead placement is an enticing and safe alternative to more invasive epicardial lead surgery in this very-high-risk population of patients with poor ventricular function. Often the enlarged ventricle in these patients presents a technical challenge, which can be safely overcome using robotic assistance. Kamath et al. reported 78 consecutive patients, who underwent a robot-assisted epicardial lead placement, and found improvement in both pacing thresholds and lead impedance over both the short (<12 months) and long term (>12 months). At 44 ± 21 months’ follow-up there were 20 deaths (26%). These patients were older . There were no mortalities, reoperations for bleeding, strokes, or wound infections in either group. There was no significant difference in administration of blood products, incidence of pneumonia, renal failure, or atrial fibrillation. Additionally, there was no difference in length of hospital stay or intensive care unit length of stay between the robotic-assisted and traditional myxoma surgical procedure groups.Although much less common than mitral valve surgery, coronary revascularization, or atrial fibrillation ablation, several case reports exist in the literature for other cardiac procedures, such as intracardiac tumor resections and atrial septal defect (ASD) closures. Murphy et al. reported three successful atrial myxoma resections using the da Vinci™ surgical system in 2005.Torracca et al. and Wimmer-Greinecker et al. were the first to report small series of patients undergoing robotic atrial septal defect (ASD) closures.Currently, there are several successful robotic cardiac surgery centers. Whether this technology will continue to gain more widespread acceptance remains to be seen. Despite all of the above-described benefits, several limitations have hampered the acceptance of robotic heart surgery. With improved technology, many of these limitations should also diminish. For instance, many surgeons remain concerned about the lack of haptic feedback. Robotic surgeons have become familiar with “ocular tactility,” relying on visual tissue deformation to judge the amount of force being applied to tissues. In our experience the lack of haptic feedback has not been a concern. Future robotic systems will likely incorporate strain sensors to the instrument arms, allowing for haptic feedback and precise control of force. Instrument and camera sizes will decrease, and optics will improve, allowing for smaller incisions. A greater variety of robotic instruments will be developed, allowing for more operative options and improved dexterity. Advances in three-dimensional echocardiography and modeling software will continue to be made, possibly allowing a “blueprint” model to be overlaid on the operative field image at the console.It has become evident that in order to achieve success with a robotic cardiac surgery program, several key elements are required. For one, the concept of a highly specialized and trained robotic team is paramount, to include anesthesiologists, perfusionists, operating room staff, nurses, and surgeons. With limited access to and visualization of the heart, skilled echocardiographers are crucial. Achieving safe cannulation, planning for complex valve repairs, and monitoring cardiac function are all predicated on high-quality, three-dimensional transesophageal echocardiography. Finally, robotic heart surgery centers must have an adequate referral base to attain safety and efficiency. To date, several centers have achieved success in robotic cardiac surgery, performing a variety of heart operations reproducibly, reliably, effectively, and safely. We are confident that this promising technology will continue to advance and grow in utilization internationally.


Ischemia-reperfusion injury is a composite of damage accumulated during reduced perfusion of an organ or tissue and the additional insult sustained during reperfusion. Such injury occurs in a wide variety of clinically important syndromes, such as ischemic heart disease and stroke, which are responsible for a high degree of morbidity and mortality worldwide. Basic research has identified a number of interventions that stimulate innate resistance of tissues to ischemia-reperfusion injury. Here, we summarise the experimental and clinical trial data underpinning one of these “conditioning” strategies, the phenomenon of remote ischemic preconditioning. Ischemia-reperfusion injury underpins the damage of myocardial infarction, stroke, and other conditions complicated by interruption of the blood supply to tissues. Strategies to limit the duration of ischemia have achieved substantial health gains in myocardial infarction and, to a lesser degree, stroke. However door-to-needle times have probably reached the minimum that is possible in many health-care delivery systems, so further reduction in morbidity and mortality from IR injury will require strategies to increase tissue tolerance to ischemia or reduce damage that occurs on reperfusion. One such approach is ischemic preconditioning, and its variant remote ischemic preconditioning, the subject of this paper.Ischemic preconditioning (IPC) describes the phenomenon whereby transient, brief periods of ischemia confer protection against a subsequent prolonged and injurious period of ischemia. There are a number of ways in which preconditioning can be induced. Local preconditioning occurs when the preconditioning stimulus is applied to the same organ or tissue that will subsequently sustain the ischemic injury. Remote ischemic preconditioning refers to a stimulus applied to a distant organ or tissue, which then protects against index ischemia. For example, the preconditioning stimulus might be suprasystolic blood pressure inflations on an arm or leg, which then confer myocardial protection against subsequent ischemia. Postconditioning occurs when there is staged reperfusion, for example, in the setting of balloon angioplasty. Its variant perconditioning occurs when the conditioning stimulus is applied during ischemia.Ischemic preconditioning was first described in 1986, when Murry et al. demonstrated that in the dog, brief episodes of ischemia (4 cycles of 5-minute occlusion followed by reperfusion) of the circumflex artery reduced the extent of infarction induced by subsequent prolonged occlusion of that vessel –4. DespiA major breakthrough in clinical applicability of preconditioning protection came with the discovery that ischemic preconditioning also had a systemic protective phenotype. This facet, termed remote ischemic preconditioning (RIPC), resulted in protection from ischemia-reperfusion injury at sites remote from those undergoing the preconditioning stimulus. This was first described in the setting of experimental coronary artery occlusion, where preconditioning one vascular territory of the heart effected protection in adjacent tissue that had not undergone any preconditioning ischemia . InterorDuring ischemia, anaerobic metabolism predominates and ATP production decreases. There is insufficient available energy to maintain cell membrane pump activity, antioxidant defences, pH and calcium homeostasis, and mitochondrial integrity. These and other consequences of ischemia inevitably lead to cell death, unless blood flow is restored. Though reperfusion with oxygenated blood is essential for any tissue salvage, the sudden influx of oxygen leads to the formation of reactive oxygen species. A key event in cell death is mitochondrial permeability transition, a phenomenon that occurs when the mitochondrial permeability transition pore (mPTP) becomes permeable to molecules of 1500 kDa or smaller. This leads to a rapid influx of small molecules, mitochondrial swelling, and subsequent cell death .ATP) channel is activated with evidence that this leads to closure of the mPTP. IPC also initiates a complex genomic and proteomic response that underpins the late phase of protection. This includes antiapoptotic and anti-inflammatory gene transcription, likely to be responsible for the second window of protection [IPC activates three main salutatory pathways, the cyclic guanosine monophosphate/cGMP-dependent protein kinase (cGMP/PKG) pathway , the repotection , 14.κB), activator-protein-1 (AP-1), nuclear factor-like 2 (Nrf2), and hypoxia-inducible-factor-1α (HIF-1α)). Later phase protection requires synthesis of inducible nitric oxide synthase (iNOS), heat shock proteins (HSPs), or cyclooxygenase-2 (COX-2). These then act locally via the mPTP or KATP channels to induce a state of cardioprotection [Triggers in the initial cascade recruit early mediators (such as protein kinase C (PKC), tyrosine kinase, phosphatidylinositol 3-kinases (PI3K), protein kinase B (PKB or Akt) , mitogenotection .Evidence for involvement of a humoral factor in mediating systemic spread is supported by the observation that protection can be transferred by the transfusion of serum from a rabbit that has undergone ischemic preconditioning to one which has not , 18. ThiNeurogenic mechanisms have also been explored using autonomic ganglionic blockade. In a rat myocardial infarction model hexamethonium abolished protection by RIPC achieved by mesenteric artery occlusion (MAO) but had no effect on myocardial IPC. Cardioprotection was absent when MAO was sustained throughout the study, indicating that reperfusion in the small intestine was essential to activate the neurogenic pathway . The autNoradrenaline has been implicated; however, studies are conflicting about its potential role. Administration of noradrenaline has been shown to induce preconditioning in animal models ; howeverSensory nerves have also been implicated in spread of protection. Intramesenteric bradykinin has been demonstrated in animal models to stimulate local sensory nerves, resulting in RIPC-like protection that is abolished by hexamethonium . This suThe nonselective adenosine antagonist 8-(p-sulfophenyl)theophylline (8-SPT) has been shown in a rabbit , 32, 33 The humoral and neuronal pathways may work in series to spread protection systemically. In the rat, release of the dialysable humoral factor is prevented by hindlimb denervation .The mechanisms of tissue protection and systemic spread have been summarised in ATP channel blockers prevents IPC in healthy volunteers, and IPC is mimicked by KATP channel opening drugs [The development of a vascular model of human IR injury has facilitated the investigation of the mechanism of IPC and RIPC. In this model the arm is made ischemic for 20 minutes, and this safely induces a transient period of endothelial dysfunction in the conduit and resistance vessels. Endothelial assessment has been made using ultrasound of conduit vessels to measure flow-mediated dilatation or forearm plethysmography to characterize the response of resistance vessels to endothelium-dependent agonists. In this model, vascular smooth muscle function is preserved. Endothelial dysfunction is largely prevented if the ischaemic period is preceded by brief, repeated periods of ischaemia ipsilaterally (IPC)  and contng drugs , 40. A nng drugs , 42, makng drugs . Regarding drugs , 38, thoAlthough initial clinical trials in this area focussed on the application of remote ischemic preconditioning in ischemic cardiac disease, interest has broadened to other areas of potential clinical benefit, including acute kidney injury, stroke, and transplantation.A table summarising clinical trials in remote ischemic preconditioning to date is shown .The first clinical trial of remote ischemic preconditioning was in 2000, when 8 patients undergoing coronary artery bypass grafting (CABG) were randomised to receive either ischemic preconditioning (forearm cuff inflated to 300 mmHg for 2 cycles of 3 minutes) or control. The study demonstrated an increase in lactate dehydrogenase (LDH) in the preconditioned group, which was attributed to an ability to maintain anaerobic metabolism in preconditioned cells .α) in the preconditioned group. In this study, those randomised to the preconditioning group received preconditioning at 24 hours and 1 hour before surgery, to utilise both early and late phases of protection [Following this, a randomised controlled trial of RIPC in the setting of pediatric surgery (37 patients) for congenital cardiac defects demonstrated that 4 cycles of 5 minutes of lower limb ischemia prior to surgery were effective in reducing troponin levels, postoperative inotropic requirements, and airways resistance at 6 hours . A studyotection .Subsequently in 2007, Hausenloy et al. demonstrated a reduction in troponin T levels in patients randomised to receive ischemic preconditioning (3 cycles of 5-minute forearm cuff inflation to 200 mmHg after induction of anaesthesia) prior to coronary artery bypass grafting . In bothHowever, in 2010, Rahman et al. published a larger single-centre double-blind randomised controlled trial in which 162 patients undergoing CABG were randomised to receive either 3 × 5-minute cycles of upper limb cuff inflation to 200 mmHg (separated by 5-minute reperfusion) or placebo (in which the cuff was inflated on a “dummy arm”). In this study there was no difference in troponin release between the 2 groups . There wThe RICO trial  is ongoing to examine the effects of remote ischemic preconditioning, remote ischemic postconditioning, or remote ischemic pre- and postconditioning on the development of atrial fibrillation on holter monitor within 72 hours after coronary artery bypass grafting . This wiA current multicenter double-blind randomised controlled trial, “Effect of Remote Ischemic Preconditioning on Clinical Outcomes in Patients Undergoing Coronary Artery Bypass Graft Surgery” (ERICCA), is currently underway to investigate whether RIPC improves one-year cardiovascular outcomes and reduces acute kidney injury (AKI) in the setting of cold-blood cardioplegia CABG. This trial aims to recruit 1610 patients, randomised to either RIPC or sham-RIPC.In 2006, Iliodromitis et al. investigated whether RIPC by 3 cycles of 5-minute ischemia applied to both arms would attenuate the inflammatory response in elective single vessel PCI with coronary stenting. They in fact demonstrated an increase in CK-MB, troponin I, and CRP in the preconditioned group and postulated that RIPC increased the inflammatory response .Subsequently, Hoole et al., in 2009, in a study of 242 patients undergoing elective PCI demonstrated that RIPC (3 cycles of 5-minute forearm cuff inflation to 200 mmHg) prior to PCI attenuated procedure-related cardiac troponin I (cTnI) release . Diabetiperconditioning in the setting of AMI . In a trial of 333 patients, they demonstrated an improvement in myocardial salvage index (%) at 20 days after primary PCI in the group randomised to receive preconditioning [Also of note, Bøtker et al. demonstrated the potential for prehospital use of remote ischemic itioning . In a suitioning .In open abdominal aortic aneurysm (AAA) repair, 82 patients were randomised to receive either RIPC (two cycles of intermittent cross-clamping of the common iliac artery with 10-minute ischemia followed by 10-minute reperfusion) or none. RIPC reduced the absolute risk of myocardial injury, myocardial infarction, and renal injury . AnotherA UK-based trial of remote ischaemic preconditioning in the setting of elective abdominal aortic aneurysm repair is currently underway in Bristol.A pilot clinical trial of 70 patients undergoing carotid endarterectomy, randomised to remote ischemic preconditioning with 10 minutes of ischemic applied to each leg showed a numerical but not statistical reduction in saccadic latency deteriorations . There was no significant difference between cardiac endpoints .However, in a trial in 40 adult cervical spondylotic myelopathy patients undergoing elective decompression surgery there was a significant reduction in markers of ischemic neurological injury (serum S-100B and neuron-specific enolase) in the RIPC group. Patients randomized to RIPC received 3 × 5-minute arm cycles. Postsurgical recovery at 7 days, 1, and 3 months after surgery  was higher in the preconditioned group .In stroke, the “New Acute Treatment for Stroke—The Effect of Remote Perconditioning” has recently closed to recruitment and results awaited. This trial has examined the utility of remote ischemic preconditioning using arm ischemia in the ambulance prior to hospital admission and thrombolysis. The primary endpoint in this study is salvage index, measured on diffusion-weighted T2 MRI.IR injury contributes to the majority of AKI. Common causes of AKI such as sepsis, surgery, or drugs, for example, NSAIDS, ACE inhibitors, are all essentially wholly or in part due to ischemia-reperfusion injury, secondary to hypotension or reduced renal blood flow. AKI is responsible for morbidity and increased mortality in hospital admissions; however, its onset is often unpredictable and patients present when AKI is already manifest. Therefore, use of RIPC to protect against acute kidney injury has most widely been documented in the setting of surgery. In this setting, however, the acute injury is complex and multifactorial in nature.Secondary analysis from two trials in elective coronary artery bypass grafting has demonstrated a reduction in AKI in nondiabetic patients randomised to RIPC (three 5-minute cycles of forearm ischemia). However, the numbers were small, there were more concomitant aortic valve replacements in the RIPC group, the analysis was post hoc, and, although there were more episodes of AKI in the nonintervention group, this was all AKI stage 1.  In a sepTrials examining the effects of preconditioning on AKI in the setting of AAA surgery have been detailed above.The ultimate renal IR injury occurs in renal transplantation, and in the case of live donor transplantation this has a predictable time of onset. Loukogeorgakis et al. have previously demonstrated an almost 20% improvement in eGFR  formula) after 2 years in children who underwent RIPC before live donor renal transplantation. Both donor and recipient received 3 cycles of 5-minute forearm ischemia-reperfusion, 24 hours prior to transplantation. This was a small randomised controlled trial in 20 patients; however, a larger, 400-pair multicentre randomised controlled trial ) is currently underway. A trial of RIPC in the setting of cadaveric renal transplantation is being undertaken by Bøtker et al. The RIPCOT trial , which utilises lower limb remote ischemic preconditioning in the setting of deceased donor liver, kidney, or pancreas transplantation, and RIPC before abdominal surgery trial in those undergoing abdominal, large bowel, pancreatic, and hepatic surgery are also currently underway.Remote ischemic preconditioning harnesses a powerful innate protective mechanism against ischemic injury. The mechanism is as yet not fully elucidated; however, it has shown promise in clinical trials. No trial has yet been large enough to demonstrate an effect of RIPC to reduce the incidence or impact of clinically relevant consequences of IR injury. However, large adequately powered studies will report within the next 2-3 years. These trials will either endorse the clinical usefulness of ischemic preconditioning or consign it to the laboratory.


In patients (p) with acute myocardial infarction (AMI), quantitation of myocardial regional function may be useful to differentiate between stunned and necrotic myocardium and to predict ventricular function recovery during follow-up. Different parameters exist to evaluate regional myocardial function such as circunferential /radial strain and displacement. The purpose of this study is to determine the most useful parameter for prediction of contractile function recovery obtained from tagged MRI.12 p admitted to our institution with a first episode of AMI, treated with primary angioplasty and good angiographic result were included in the study . A cardiac MRI study was performed with a 1.5T unit (Philips Intera), including cine images with left ventricle full coverage, T2-STIR black blood, tagged MRI in basal, mid and apical short axis views, first pass perfusion and 3D late enhancement after administration of 0.2 mmol/kg gadolinium-derived contrast. A second MRI was performed at 6-months' follow-up. Regional ratial/circunferential displacement and strain were quantified with propietary software developed for tagged-MRI postprocessing, based on non-rigid registration algorithms. A 16-segment model was used for analysis. 188 myocardial segments, 80 dysfunctional, were analyzed. Circunferential strain and radial strain were inversely correlated with transmural extension of late enhancement.In circunferential strain, a cutoff point of 9.3 allowed prediction of ventricular function recovery with sensitivity 83% and specificity 72%.Regional myocardial circunferential strain in AMI is strongly correlated with contractile function recovery at 6 months' follow-up.


This study was designed to evaluate the left ventricular systolic synchronization in patients implanted with dual-chamber DDD mode cardiac pacemakers by real-time three-dimensional echocardiography (RT3DE). Twenty patients implanted with DDD mode cardiac pacemakers for 12 months and 20 healthy subjects underwent RT3DE. This method provided left ventricular end-diastolic volume (LEDV), left ventricular end-systolic volume (LESV), stroke volume (SV), left ventricular ejection fraction (LVEF), the mean value of the time to minimal systolic volume of the 16 left ventricular segments (Tmean), the standard deviation of Tmean (T-SD), the maximal difference of the time to minimal systolic volume of the 16 left ventricular segments (Tmax) and time-volume curves of the 16 left ventricular segments. Results showed that compared with the healthy group, LESV was significantly increased (P<0.05), SV and LVEF were significantly decreased (P<0.05) and T-SD and Tmax were significantly prolonged (P<0.05) in patients implanted with DDD mode cardiac pacemakers. The time to minimal systolic volume of the 16 left ventricular segments time-volume curves differed in patients implanted with DDD mode cardiac pacemakers. Asynchronization of the left ventricular systolic performance in patients implanted with DDD mode cardiac pacemakers was observed. The results showed that RT3DE is a quantitative method used to evaluate left ventricular systolic synchronization. An artificial cardiac pacemaker, important in treating cardiac bradycardia, is able not only to stimulate heart contraction, but also to provide a method and instrument of arrhythmia interventional diagnosis and treatment. DDD mode cardiac pacemakers have been applied in the clinic since the end of the 1970s. DDD mode cardiac pacemakers are able to pace and monitor the atria and ventricles, whereas the reactive mode of perception restrains or triggers stimulation.Real-time three-dimensional echocardiography RT3DE) is a crucial technical breakthrough in the field of ultrasonic imaging, providing investigators with full-volume data, analysis of the size, shape and function of the cardiac chambers, and a feasible and simple new technique for evaluating heart global and segmental function as well as systolic synchronism ,2. PreviDE is a cThe study population included 20 healthy subjects  and 20 patients implanted with DDD mode cardiac pacemakers . The 20 healthy subjects were confirmed by history, physical examination, electrocardiography, X-ray and echocardiography. All of the patients presented with sinus node dysfunction prior to implantation with DDD mode cardiac pacemakers and, according to the results of coronary angiography and echocardiography, were diagnosed with coronary artery disease and other heart diseases. The patients implanted with DDD mode cardiac pacemakers were in a stable haemodynamic condition when included in the study. The maximum cardiac output obtained from echocardiography was set to the optimal atrioventricular delay in DDD pacing. The programmable upper frequency was set to maximal heart rate <(220-age) x90%. According to 24 Holter analysis, ventricular pacing accounts for >80% of the effective pacing. The site of the right ventricular lead was placed at the apex in the right ventricle. Informed consent was obtained from all subjects and the study was approved by our local Ethics Committee .Healthy subjects and patients implanted with DDD mode cardiac pacemakers for 12 months underwent left ventricular measurement by RT3DE in the left lateral decubitus position.RT3DE was performed with iE33  and X3-1 matrix array transducer. Pyramidal volume, which has a relatively narrow sector width, is obtained in real time. To obtain a larger volume, it is necessary to visualize the entire left ventricle, since full-volume acquisition is used. The optimized apical four-chamber view was obtained during the full volume acquisition. Four real-time volumes may be obtained from consecutive cardiac cycles. Apical full-volume imaging of the left ventricle was obtained for all subjects. Full-volume acquisition is performed during breathhold and requires a stable R-R interval to minimize the stitch artifacts.Quantitative analysis involved regulating the sagittal and coronal sections, located in the middle of the left ventricle, and the transverse section was laid at the mitral valve loop level at the end-diastole and end-systole separately. Subsequently, five endocardium sample points of the four-chamber view mitral valve loop level’s interventricular septum and lateral wall, and two-chamber view mitral valve loop level’s inferior wall, anterior wall and cardiac apex were selected for the analysis. Q-LAB software was employed to trace out the outline of the triaxial endocardium automatically. The 16 left ventricular segments were defined by the American Heart Association . Left veRT3DE data were stored and analyzed with Q-LAB quantitative analysis software. To minimize the variability of the measurements, all ultrasonic recordings were performed by the same author. In total, 40 subjects were selected for reliability analyses between two independent observers.Data were presented as the mean ± SD. All the analyses were performed with SPSS 13.0 for Windows. For the comparison of parametric variables, the independent samples t-test was used. P<0.05 was considered to indicate a statistically significant result.RT3DE recordings were adequate for analysis in all subjects.The difference between the two groups for the clinical and left ventricular function parameters of age, HR, LEDV, LESV, SV and LVEF, are listed in No significant differences in age, HR and LEDV were found between the two groups. Compared with the healthy group, LESV was significantly increased , SV was significantly decreased  and LVEF was significantly decreased  in patients implanted with DDD mode cardiac pacemakers.Results showed that compared with the healthy group, T-SD   and TmaxThe time-volume curves of the 16 left ventricular segments appeared ordered and regular, with a homodirectional waveform. The time to minimal systolic volume of the 16 left ventricular segments was consistent in the healthy group . The timIn the present study, we explored the feasibility of using RT3DE to assess the left ventricular systolic synchronicity, which proved to be practical and reproducible. By using RT3DE, it is possible to integrate the systolic function of 16 left ventricular segments into an index that may be used to assess the left ventricular dyssynchrony. Compared with the healthy group, indices were significantly different in patients implanted with DDD mode cardiac pacemakers.Following the renewal and development of pacemakers, the importance of cardiac hemodynamics in patients implanted with pacemakers has been recognized. Cardiac pacemakers are able, not only to ameliorate the bradycardiac symptom, but also to supply an individual, optimal hemodynamics effect pacing system for patients. Therefore, the evaluation of cardiac function in patients implanted with cardiac pacemakers is the principal research subject of cardiac pacing.The evaluation of left ventricular systolic synchrony –9 includet al , SV and LVEF were significantly decreased (P<0.05) and T-SD and Tmax were significantly prolonged (P<0.05) in patients implanted with DDD mode cardiac pacemakers. The time-volume curves of the 16 left ventricular segments presented a heterodirectional waveform and the time to the minimal systolic volume point differed in patients implanted with DDD mode cardiac pacemakers. The results indicated that right ventricular pacing may decrease left ventricular coordinated motion and systolic function.Pacing from the right ventricular apex in DDD pacemakers involved first activating the right ventricular apex and propagating it within the interventricular septum. Subsequently, it was transferred to the free wall of the right and left ventricles, ending at the basilar part of the left ventricle. The sequence of ventricular activation and modality of motion was opposed to sinus rhythm, which produced an abnormal blood shunt in the chambers. Pacing at the right ventricular apex caused regional precontraction and myocardial strain of the right ventricular apex and adjacent regions. The blood in the ventricle flowed to the free wall and basilar part of the left ventricle, causing apical aneurysm, dilation, asynchronism and paradoxical motion. When activation propagated from the cardiac basilar region, the myocardial strain of the cardiac base and peripheral myocardium impulsed the blood to the apex, the left ventricular apex became swollen and bulged, similar to a ventricular aneurysm. When the interventricular septum became depolarized and contracted, the left ventricular free wall depolarized and then contracted. When the interventricular septum was at diastole, the strain originated from the contraction of the left ventricular free wall and the blood flow pressure in the ventricle reversed the direction and dilation of the interventricular septum. The incompatible systole and diastole of the regional ventricular myocardium, as well as the paradoxical motion caused abnormal blood shunt in the ventricle, while the global, prompt and synchronous left ventricular contraction changed into a torpid, incompatible segmental left ventricular contraction. Accordingly, systole was prolonged, the left ventricular ejection period was shortened, the stroke volume was reduced and the left ventricular ejection fraction decreased.This study was designed to validate RT3DE as a method of quantifying myocardial systolic synchrony of the left ventricle in patients implanted with DDD mode cardiac pacemakers and healthy subjects. The RT3DE analysis and manual tracing endocardium outline of the left ventricle are subjective and depend on imaging quality. Thus, a totally blinded analysis would be preferable. The limitation of a full-time 60x60° sector may induce volume envelope insufficiency in patients with cardiac dilation and apex bulging. The accuracy of our method for quantifying left ventricular systolic synchrony was carried out by using RT3DE, but with no comparison with a gold standard. In the absence of a gold standard, the clinical value of each technique should be compared to establish the accuracy and clinical utility of each technique.In conclusion, RT3DE is a feasible and reproducible method to quantify left ventricular function and systolic synchrony. Asynchronization of the left ventricular systolic performance was observed in patients with DDD mode cardiac pacemakers. The T-SD and Tmax of the 16 left ventricular segments measured by RT3DE may become effective indices in assessing ventricular systolic synchronism. The time-volume curves of the 16 left ventricular segments may reflect the regularity of ventricular systolic synchronism as well as show the time to minimal systolic volume point in all segments.