Manual delineation of the leftventricular contour using manual biplane Simpson's rule, by many considered to be the reference method of choice, displayed a larger varia- tion in measured values than corrected AutoEF for the novices, but not for the experts (Table 2). To reduce this variation, the use of especially trained technicians in core labs has been suggested which, however, is unrealistic in clinical work . Another avenue for improvement could be the use of computer based methods using learned pattern recognition and artificial intelligence such as AutoEF. Previous authors  found encouraging results using single plane AutoEF. Objections were voiced by Rahmouni et al, who, however, did not perform man- ual corrections of obviously erroneous delineations of the left ventricle . They reported a low correlation between AutoEF and manual planimetry as well as between AutoEF and MRI, but did not show the correla- tion between planimetry and their gold standard MRI. The suboptimal performance of single plane AutoEF seems rather obvious for left ventricles with regional wallmotion abnormalities. Results should improve with a biplane approach such as in our study. In contrast to other studies, we did not exclude patients on the basis of image quality. Those with poor image quality showed a similar agreement compared to MPI as those with good image
In this case, fetal ultrasonography showed an obviously enlarged and spherical left ventricle, thin leftventricularwall, diffusely thick leftventricular endocardium, enhanced echo, and reduced ventricularwallmotion, which were in Figure 3. The blood flow in this cavity was “reciprocating” with the relaxation
Normal values for GLS and LSS have not been standard- ized yet. Inter-vendor variability, age and sex related changes in strain values are the main factors preventing the determination of cut-off value. It’s recommended to use the same software and vendor-specific normal refer- ence values for interpretation [28, 29]. Marwick et al.  used the same vendor as we did and demonstrated an average GLS of − 18.6 ± 0.1%. Takidiki et al. assessed nor- mal range of 2D LS and compared three vendors (− 21.3 ± 2.1% vs − 18.9 ± 2.5% vs − 19.9 ± 2.4, p < .001). Recently three studies, using the same vendor as we used, were published investigating the normal values of longitudinal LSS [23–25]. Nakata et al.  defined the normal values for transmural, endocardial and epicardial GLS as − 20.0 ± 2.0%, − 23.1 ± 2.3% and − 17.6 ± 1.9%, respectively, whereas the values found by Alcidi et al. for all layers were − 22.7 ± 1.8%, − 25.4 ± 2.1% and − 21.1 ± 1.8%, re- spectively. Shi et al.  also identified similar values for all layers (− 21.3 ± 2.9%, − 24.3 ± 3.1%, and − 18.9 ± 2.8%, respectively). In aggreement with these studies the cut-off values for GLS-trans, GLS-endo and GLS-epi were similar to the normal values abovementioned ( − 19.3%, − 23.4% and − 17.3%, respectively).
Meanwhile, a short axis view of the delayed gadolinium enhancement image revealed myocardial scarring extend- ing to the upper part of the ventricular septum across the aneurysm (Figure 2B). Furthermore, pace mapping from the RV side of the RV–LV hinge point matched the clinical VT, with short pacing QRS intervals (40 ms; Figure 1B). Taking these data into account, we hypothesized that the VT reentrant circuit could include the intramural upper septum and the VT exit at the RV–LV hinge point. Although we initially delivered RF energy with a unipolar system at the RV–LV hinge point from the LV side to make continuous ablation areas, the unipolar ablation was ineffective. In addition, as the voltage map from the RV was completely normal, we suspected that the VT reentrant circuit might be located partially in the depth of the ventricular septum, as was also suggested by cardiac MRI. Therefore, we subsequently chose the bipolar system. The first catheter (NAVISTAR THERMOCOOL; Biosense Webster) was placed at the anterior aneurysm in the
echocardiographic measurements of leftventricular sys- tolic function, such as ejection fraction (EF) and wall mo- tion scoring (WMS), have been considered as essential in this process [1,2] However both EF and WMS are limited by being highly user dependent with a rather long learning curve and poor reproducibility [3,4]. Subsequent studies have introduced the diastolic echocardiographic param- eter E/e' -ratio, that reflects the filling pressure of the left ventricle  as a prognostic parameter with incremental value to EF and WMS [6,7]. It has also been shown that this parameter adds complementary prognostic value to biochemical markers such as type B natriuretic peptide [8,9] after acute myocardial infarction (AMI) [10,11].
d) One field of application, which in itself would guaran- tee the survival of TDI is the study of ventricular contrac- tile dyssynchrony. The development of ultrasound platforms capable of imaging at high frame rates leads to temporal resolution high enough as to allow for a metic- ulous analysis of the different phases of the cardiac cycle. The measurement of TDI-derived time intervals has been more easily accepted, firstly because they were related to parameters cardiologists are already confident with, sec- ondly because they were validated in hemodynamic labo- ratories and thus have been confronted to a "gold standard" . The application of these methods has brought upon the definition and the calculation of delays in global (interventricular) and regional (intraventricular) mechanical contraction . All this has had the merit of drawing attention to the impact of dyssynchrony on car- diac performance and has shed light on the presence of significant ventricular asynchronicity even in the absence of left bundle branch block in patients with normal or near normal duration of QRS, as well as in patients with heart failure and without severely reduced LVEF . The deciding driving force was a fortunate historical coinci- dence: the concurrent interest of the scientific community in cardiac resynchronization therapy in patients with severe heart failure despite optimal medical therapy and enlargement of the QRS complex in the electrocardiogram . Evidence emerged in literature emphasizing the pos- sible superiority of TDI in respect to ECG and traditional echocardiography in the identification of a significant number of cases of mechanical ventricular dyssynchrony which is fundamental to identify those candidate patients for implantation of a biventricular pace-maker who will be "responders" and benefit from this procedure [38,40- 48]. Further, it is possible to map the delays, knowing which of the walls are being activated with greater delay and among those more capable of recovery, and thus pro- viding important information to the electrophysiologist to plan the modality and the site of stimulation . Even in this field, where it performed with great success, TDI remained a prisoner of excessive differences in methodol- ogies in use and modalities of measurement of ventricular delays. Some authors use spectral pulsed Doppler ,
In accordance with the American Heart Association Scientific Statement , the 10 middle and apical LV myocardial segments were assessed for LV first pass PDs, LGE, and inducible WMA. Participants in this study were characterized into one of 3 groups including those: 1) without a PD or WMA (Group I), 2) with a PD but with- out a WMA (Group II), and 3) with both a PD and a WMA indicative of ischemia (Group III). The differences in demographic, hemodynamic, CMR volumetric parame- ters, and indices of myocardial oxygen demand between the 3 Groups were assessed by an analysis of variance test of equality (ANOVA). In Tables 1 and 2, the p-values are displayed for the overall equality of the three groups. In the Figures, the comparisons between specific groups were accomplished using pairwise comparisons. A p-value of <0.05 was considered significant for either forms of testing. The differences in the LV myocardial SW and the PVA were adjusted for preload (resting and peak dose LV end-diastolic volume index or LVEDVi), afterload (peak dose PWV), contractility (LV ejection fraction or LVEF), and LV concentricity using analysis of covariance. Multiple regression models adjusting for SBP, LVEDV baseline and LVEDV peak dose were selected and reported by stepwise regression. The sensitivity and specificity of dobutamine related wallmotion abnormalities for detecting obstruct- ive CAD was assessed with the results of the perfusion component of the DCMR protocol serving as the refer- ence standard. Results were expressed as means ± stand- ard error of the estimate unless stated otherwise.
These changes may be caused by several reasons. During a normal pregnancy, there is a physiologic remodeling by fetal syncytial trophoblasts which penetrate and remodel maternal arteries, causing them to dilate into large, flaccid vessels. This remodeling accommodates the increased maternal circulation needed for adequate placental perfusion during pregnancy. However in preeclampsia patients this remodeling is somehow prevented, which causes increased left ventricle (LV) wall thickness and mass more pronounced than in normal pregnancy, but less pronounced LV widening. 12 This concentric
Pharmacological measures like phenylepherine or rapid fluid challenge may be used to assess the ischaemic MR.83 Parameters like grossly dilated left ventricle, multiple regurgitant jets , systolic sphericity index, wallmotion score index, ESV( end-systolic volume), severe MR, >2.5 cm2 systolic tenting area, , large angle (≥45°) of the posterior leaflet, >1 cm distance between coaptation point and mitral annulus are recognized as predictors of bad outcome of procedures like mitral valve repair by annuloplasty .84-86 Several adjunctive techniques have been proposed like chordal cutting, internal direct repositioning or external repositioning of the displaced papillary muscle. 8, 87 However, they are not yet clinically approved for routine management of ischaemic mitral regurgitation. PERCUTANEOUS REAPIR Percutaneous edge- to-edge Alfieri procedure has been used for the treatment of MR due to either ischaemic or organic cause. In it, the central parts of both mitral leaflets are apposed producing a double orifice. 8, 88 Many
Whilst echocardiography demonstrated a LVWT is 14 mm at the septum, it is well established that a minority of Caucasian athletes (< 2%) also demonstrate physiolo- gical LVH between 13-16 mm [7,8,18]. However, physio- logical LVH is typically associated with LV cavity dilatation of 55-65 mm. Hence, the LV cavity size of 44 mm in this case is unexpectedly reduced and typical of the disparity seen in individuals with HCM. Given the diagnostic uncertainty in this athlete, this case study also highlights the important role of including CMR in the workup of individuals presenting “ grey zone ” LVH (12-15 mm). There was a major discrepancy between maximal LV wall thickness derived by echocardiography (14 mm) and that of CMR (17 mm). Indeed, a wall thickness of 17 mm is not routinely observed within athletes regardless of body surface area [7,8] and points ominously towards pathology. CMR provides a compre- hensive assessment of both ischemic and non-ischemic cardiomyopathies providing detailed precise information on cardiac anatomy, function, tissue characterisation, epicardial and microvascular perfusion, valvular flows, and coronary and peripheral angiography. Measure- ments of maximal wall thickness are highly accurate, as is the pattern definition of LV wall thickening (focal vs. mild concentric) and unlike echocardiography, no geo- metrical assumptions need to be made about the ventri- cle [19,20]. Indeed, in some regions of the LV chamber, the extent of hypertrophy can be underestimated by echocardiography compared to CMR [21,22], which is not diagnostically helpful in “grey zone” athletes. Finally, LGE provides a sensitive tool for the detection of myo- cardial fibrosis, abnormalities not typically seen in phy- siological LVH, thus highlighting pathology [23-25].
4. Bruch C, Stypmann J, Grude M, Gradaus R, Breithardt G, Wichter T. Tissue doppler imaging in patients with moderate to severe aortic valve stenosis: clinical usefulness and diagnostic accuracy. Am Heart J. 2004;148:696 – 702. 5. Lafitte S, Perlant M, Reant P, Serri K, Douard H, DeMaria A, et al. Impact of impaired myocardial deformations on exercise tolerance and prognosis in patients with asymptomatic aortic stenosis. Eur J Echocardiogr. 2009;10:414 – 9. 6. Dumesnil JG, Pibarot P, Carabello B. Paradoxical low flow and/or low gradient severe aortic stenosis despite preserved leftventricular ejection fraction: implications for diagnosis and treatment. Eur Heart J. 2010;31:281 – 9.
In concurrence with previous studies [2,15-20] we ob- served that all peak velocities during the cardiac cycle were higher in the right ventricular free wall compared to septum and the leftventricular free wall - consistent with right ventricular dominance. As can be seen in Figure 4, the right ventricle also showed a greater stroke length compared to the left. We could also confirm the gestational increase in fetal myocardial velocities despite a maturational fall in fetal heart rate , and the in- crease of the e’/a’ ratio, corresponding to a redistribution from A-wave towards E-wave dominance with gesta- tional age. The higher ventricular filling velocities con- firming the active Frank-Starling mechanism in the fetal heart , which is particularly apparent during fetal ar- rhythmias . The maturational rate of s’ and e’ was higher in the right ventricular free wall compared to the leftventricular free wall and septum, implying that the differential loading of the ventricles does influence the measures of myocardial maturation, unlike Gardiner et al. previously suggested . Sex was not decisive for any of the measured variables even though HR was ob- served to be significantly higher for the female fetus up until 30 weeks of gestation. Unlike Bilardo et al ., we did not observe a relationship between sex and e’ , however, multiple regression analysis showed that a combination of HR and gestational age enhanced the correlation for the rapid filling phase. This would imply that an increased HR might affect the ability to measure e’ accurately.
In our study, multivariate logistic regression analysis identified the TG level as an indepen- dent factor, significantly associated with myo- cardial injury caused by T2DM, supporting the concept that lipid metabolism disorders may promote the occurrence of diabetic myocardial injury in patients with T2DM. Lipid oxidation increases with increasing energy supply in the myocardium when insulin is deficient or insulin sensitivity decreases; consequently, TGs and free fatty acids accumulate in myocardial cells [21, 22]. Previous studies demonstrated that fatty acid oxidation affects the distribution of calcium ion, and then inhibits the activity of the enzymatic system of myocardial cells [17-20, 23]. Meanwhile, intramyocardial lipid accumu- lation could cause myocardial injury such as cell hypertrophy and apoptosis, interstitial fib- rosis, leftventricular hypertrophy, and LVFS re- duction [19, 24]. Our result that elevated TG levels in patients with T2DM may be associated with myocardial injury induced by T2DM, is con- sistent with those of previous studies [19, 20]. In conclusion, our study indicates that the dura- tion of diabetes is a significant indicator of sys- tolic dysfunction. Diastolic dysfunction preced- es systolic dysfunction, and every patient with T2DM may have diastolic dysfunction to some degree, suggesting that such patients, with a prolonged duration of diabetes, should under- go regular ultrasonic cardiographic examina- tions to detect abnormal diastolic function and diabetic myocardial injury, as early as possible. Monitoring of the IVS thickness will help assessing leftventricular hypertrophy, and the IVS thickness is possibly a more significant indicator of systolic dysfunction and prognosis in patients with DCM. Elevated TG levels in patients with T2DM might promote the occur- rence of diabetic myocardial injury, suggesting
III, and aVF (Figure 1). The troponin I level was 92 ng/L (normal value < 14 ng/L). The patient underwent acute coronary angiography, which demonstrated no significant stenosis in the LAD (Figure 2(a)). The dominant left circumflex coronary artery (LCX) was mildly diseased (Figure 2(b)). In contrast to the ST-segment elevations in the left precordial leads V 2 through V 4 , a complete oc-
with systemic arterial involvement and accentuated wave reflections in most patients with stenotic coronary arteries. The findings are similar to those recorded in our 69-year-old patient with ischemic heart disease and associated peripheral vascular disease (Figure 7). In the patient with a massive leftventricular scar, it seems the reflected wave freely propagated along the scar tissue without being absorbed. Moreover, the wave was apparently amplified as it travelled toward the apex, like in a rigid tube (arrows in Figures 7A, 7B, and 7C). The findings can serve as a distinct example of the effects of reflected waves on ventricularmotion patterns and their clinical relevance. However, these represent individual cases, and further studies involving larger groups of patients with different cardiac and vascular pathology are required to vali- date our data. Furthermore, quantifying the reflected wave may provide important information in disease states. Methods which enable reflected wave quantification are important considerations. 30 Consequently, the effects of reflected waves
This was a retrospective study and, as such, has some inherent limitations. More advanced echocardiographic parameters, such as tissue Doppler imaging and dias- tolic function evaluation, were not systematically assessed in our population of cats. These might have helped distinguishing TMT from HCM cats, although the echocardiographic variables assessed in our study are the ones most commonly used in routine clinical practice. Another limitation is that echocardiography was performed at diﬀerent time points after presenta- tion, and some cats received diuretics before the initial echocardiographic assessment. These were cats in criti- cal condition presented in acute left-sided CHF that hindered detailed echocardiographic assessment. Myocardial thickening could have therefore been caused by pseudohypertrophy due to hypovolemia secondary to diuretic treatment or as a result of some of the reported antecedent events. However, we believe it is unlikely that the increased LVWT in the cats with TMT was pseudohypertrophy, as left atrial enlargement was one of the inclusion criteria, and all cats showed com- plete resolution of clinical signs with diuretic treatment.
lead implantation in the operating room. The patient was placed in the supine position and the left chest was elevated. An incision of about 5cm in length was made at the left anterolateral chest (Figure 1). Access to the chest was obtained through the fifth intercostal space. A longitudinal incision was made in the anterior pericardium to expose the heart. Two 6-0 prolene sutures were preset in the epicardium beneath the first diagonal branch of the left anterior descending artery to fix the epicardial lead in the avascular zone (Figure 2). The pacing parameters were measured. The leftventricular impedance was 783Ω, the threshold was 2.0mV, and the R-wave amplitude was 2.5mV. Then, a small incision was made in the corresponding part of the pericardium to allow removal of the epicardial lead line, which was then pulled through the upper intercostal space to the subcutaneous tunnel and brought into the pocket of the pacemaker. A fistula was made in the pericardium posterior to the left phrenic nerve for drainage. Intermittent suture of the pericardial incision was carried out. The pacing parameters were measured again. The leftventricular impedance was 783Ω, the threshold was 1.0V, and the R-wave amplitude was 2.5mV. Phrenic nerve irritation matching the higher threshold was observed once during the adjustment process. A drainage tube was placed through the left chest wall and the chest wound was closed.