Arrhythmogenic cardiomyopathy is a genetic heart muscle disease that typically affects the right ventricle. However, 2 other phenotypes affecting the left ventricle were recently discovered. Here, we report the case of an 18-year-old patient with biventricular arrhythmogenic cardiomyopathy, highlighting the challenges encountered in establishing this diagnosis. Diagnostic criteria for the left-sided phenotypic variants of arrhythmogenic cardiomyopathy were only introduced in 2020 by an international expert consensus document, known as the “Padua criteria,” they are divided in 6 categories with an emphasis on morpho-functional ventricular abnormalities and structural myocardial tissue alterations to diagnose biventricular arrhythmogenic cardiomyopathy. Arrhythmogenic cardiomyopathy (ACM) is a genetic heart muscle disease characterized by the replacement of the ventricular myocardium by fibrofatty tissue Our paper was written according to the CARE guidelines An 18-year-old male with no personal or family medical history, presented chest pain in 2021. Physical examination was unremarkable. Electrocardiogram (ECG) revealed incomplete right bundle branch block and negative T waves in the inferolateral region. Transthoracic echocardiography (TTE) showed apical akinesia of the LV with preserved ejection fraction (EF) at 55%. Late gadolinium enhancement (LGE) imaging by cardiac magnetic resonance (CMR) identified subepicardial contrast in the apex and apical segments of the anterolateral and inferior LV walls. The RV was without abnormalities . The diaACM is a genetic heart disease characterized by progressive fibro-fatty myocardial replacement and arrhythmogenic features Using Padua criteria in our case, the presence of morpho-functional and structural myocardial abnormalities in both ventricles , as well as the presence of repolarization abnormalities on ECG, enabled the diagnosis. Hence, the presence of diagnostic criteria for the RV phenotype ensured us that the concomitant abnormalities of the LV were specific to ACM. Therefore, the diagnosis of biventricular ACM could be based on phenotypic features alone, without the need for genetic testing.Adversely, an isolated LV phenotype of ACM can overlap with many differential diagnoses such as dilated cardiomyopathy, cardiac sarcoidosis, or more particularly myocarditis. Indeed, isolated LV LGE with subepicardial or mid-myocardial distribution could be mistaken for the consequence of a previous myocarditis, whereas histopathological studies are in favor of segmental ALVC. Moreover, myocarditis can induce ECG abnormalities similar to those described in ACM. Last, both myocarditis and ACM are responsible for non-ischemic myocardial scars that could generate ventricular arrythmias and SCD, especially in young people and athletes.On one hand, this explains why nonischemic LV scars should not be trivialized and considered benign; instead, they should be subject to further investigation with the search of family history of cardiomyopathy, clinical history of acute myocarditis, the presence of symptoms and the arrhythmogenicity of the myocardial fibrosis. On another hand, this justifies the necessity of genetic testing to distinguish both pathologies. Indeed, in the presence of consistent LV phenotypic features, demonstration of a pathogenic or likely-pathogenic mutation of ACM related genes is mandatory for the diagnosis of ALVC Which raises the question whether or not our patient's first presentation of myocarditis was in fact an unrecognized isolated LV phenotype of ACM, followed by biventricular involvement leading to a definitive diagnosis of ACM a year later. Unfortunately, the clinical outcome was marked by SCD before the patient could benefit from an implantable cardioverted defibrillator.ACM is a genetic heart muscle disease that typically affects the RV. However, recent studies have discovered 2 other phenotypes involving either the LV alone or both ventricles. Therefore, physicians should always evoke the diagnosis of these newly-discovered phenotypes of ACM using Padua criteria whenever needed, and request genetic testing particularly if an isolated LV phenotype is suspected to confirm this diagnosis.Hajar El Ouartassi: Study concept, Data collection, Data analysis, Writing the paper. Raid Faraj: Study concept, Data analysis,Writing the paper. Zakariae Laraichi: Study concept, Data analysis, Writing the paper. Rhita Ezzahraoui: Data collection Zaineb Bourouhou: Data collection. Nawal Doghmi: Supervision and data validation. Mohamed Cherti: Supervision and data validation.Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.N/aN/aNot commissioned, externally peer-reviewedWritten informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal on request.


Noncompaction cardiomyopathy (NCCM) and left ventricular noncompaction (LVNC), in their isolated form, are rare cardiomyopathies. They are characterized by a thickened myocardium due to the presence of deep trabeculae recesses, and to thick trabeculae. This condition is associated with a variable clinical phenotype including heart failure, thromboembolism, and sudden death. We report a case of LVNC at 26 weeks and 4 days of gestation revised on the basis of what is currently reported in the literature. A review of the literature was performed to better describe this rare condition. Left ventricular noncompaction is a rare fetal condition and it should be suspected in case of cardiomyopathy. Noncompaction cardiomyopathy (NCCM) is a rare disorder that is considered to be an unclassified cardiomyopathy according to the European Society of Cardiology (ESC) Working Group on Myocardial and Pericardial Diseases and the World Health Organization (WHO), or a genetic cardiomyopathy according to the American Heart Association (AHA).Noncompaction cardiomyopathy mainly involves the left ventricle (left ventricular noncompaction [LVNC]), and, less frequently, both ventricles (NCCM); when it involves the right ventricle, which is rare, it shows a worse prognosis. There is a high rate of intrauterine and early neonatal deaths and the prognosis is particularly serious for hydropic fetuses. Noncompaction cardiomyopathy can be diagnosed in utero, and the main diagnostic tool is echocardiography.Left ventricular noncompaction has been diagnosed and described during the fetal life in very few case reports: only one study shows the echocardiography myocardial evaluation during the antenatal diagnosis, and recently, a small case series of nine cases was published.th centile. Both ventricles appeared dilated with ventricular cavity biometry > 95th percentile, with thickened and irregular walls on the endocardial side, especially in the apical area , or a genetic cardiomyopathy according to the AHALeft ventricular non-compaction comprises the majority of the cases, but NCCM can also be seen in the right ventricle or in both ventricles.th and the 8th gestational week.th and the 8th week, the trabeculae regress following the myocardial fiber compaction. This process occurs from the basis to the cardiac apex, while the coronary system develops, supporting the growing myocardial tissue. According to the pathogenetic theory, myocardial morphogenesis interruption occurs, preventing the trabecular regression and muscle tissue compaction, although the coronary system is normally developed. This leads to a gradual myocardial fiber compaction failure, determining an excessive trabecular formation with deep ventricular wall recesses. These remarkable trabeculations, especially in the ventricular vertex, are responsible for the anomalous aspect of the ventricular cavity.Left ventricular noncompaction affects the left ventricular myocardial structure by the compaction process interruption between the 5Histopathology has shown a continuity between the endothelium of the intertrabecular recesses and that of the endocardium, distinguishing LVNC from persistent sinusoids. Other findings have included loosely organized myocytes and endocardial and subendocardial replacement fibrosis, suggestive of ischemic necrosis. Left ventricular dilatation and ischemia are frequently present, and thrombus formation in the recesses may occur, which may be associated with possible thromboembolic events. Since there is no gold standard for the diagnosis, the sensitivity and specificity of the morphologic criteria are uncertain. The Jenni et alIn conclusion, the diagnosis of LVNC is based on these morphologic and echocardiographic criteria:Thickened myocardium with a two-layered structure consisting of a thin compacted epicardial layer/band (C) and a much thicker, non-compacted endocardial layer (N) or trabecular meshwork with deep endomyocardial spaces; N/C ratio of 2:0 at end-systole in the parasternal short-axis viewHypoplasia of the papillary muscles;Noncompaction anomalies involving the lateral, inferior and apical myocardial segments;Color Doppler evidence of flow within the deep intertrabecular recesses;Trabeculae and intertrabecular recesses are covered by the endocardium, filled with blood with no communication with the coronary circulation.The clinical relevance of NCCM associated to other cardiac anomalies is still not well defined. One hypothesis, based on recent research, says that families affected by LVNC show mutations of the sarcomeric protein coding genes and myosin heavy chain in continuum with hypertrophic, restrictive cardiomyopathy and, more rarely, with dilated cardiomyopathy.Left ventricular noncompaction is almost invariably associated with other congenital cardiac malformations, including atrioventricular canal defects, double-outlet right ventricle, valvular atresia, ventricular septal defect, and transposition of the great arteries.The clinical presentation varies from no symptoms to heart failure, embolism, arrhythmia, mitral insufficiency, conduction disorders and sudden death.A retrospective study of autopsied fetuses and neonates with NCCM showed that heart failure, including heart block, is a common cause of death. NCCM is often associated with various cardiovascular malformations, but even in isolation it can be the basis for severe cardiac failure, and biventricular endocardial fibroelastosis in NCCM suggests a global pathologic process.The differential diagnosis of LVNC is based on: false tendons, remarkable trabeculae as normal variants, apical hypertrophic cardiomyopathy, dilated cardiomyopathy with no spongy myocardium, Fabry disease, right arrhythmogenic ventricular dysplasia, and endocardial fibroelastosis. Patients with LVNC should be submitted to screening for: congenital cardiac defects, genetic anomalies, and neuromuscular and metabolic diseases.Ultrasound technical improvements and the progress in the training of ultrasound operators have augmented the cardiac structure detection during fetal echocardiography. For this reason, NCCM should be considered for a differential diagnosis in cases of dilated cardiomyopathy.


P < .0001 and P < .001, respectively). The Q-VS in patients with Abbott devices was significantly shorter compared to that in patients with Medtronic devices at both the mid-septum and the apex in both patient groups (P < .0001). In conclusion, RV lead positioning at the mid-septum is associated with a shorter electrical delay compared to positioning at the apex in both narrow QRS and RBBB patients.Ventricular sensing relies on the analysis of a local intracardiac electrogram in reference to the QRS on the surface electrocardiogram. If both signals do not coincide in time, there is a delay in sensing intrinsic ventricular activity. We evaluated possible differences in the electrical delay between the mid-septum and apex as determined by the right ventricular (RV) lead position using a pacing system analyzer (PSA) during conventional pacemaker implantation. Patients without significant heart disease and intrinsic atrioventricular conduction underwent their first Medtronic  or Abbott  dual-chamber pacemaker implantation with the RV lead first positioned at the apex and then subsequently at the mid-septum. Real-time ventricular sensing data were obtained through PSA to determine the electrical delay Q-VS value as the time difference between the QRS and the released RV-sensed event marker “VS.” Among 212 patients, 139 had narrow QRS and 73 had complete right bundle branch block (RBBB). Overall, both narrow QRS and RBBB patients exhibited shorter Q-VS lengths at the mid-septum compared to the apex (50.4 ± 24.2 ms and 66.7 ± 32.3 ms vs. 63.9 ± 27.6 ms and 71.7 ± 32.2 ms;  With endocardial electrode catheters, early studies have demonstrated significant differences in the time of ventricular activation at the different RV anatomical locations, including early septal excitation starting at the left ventricular side and spreading to the right, activation of the RV apex before the RV outflow tract, and delayed RV activation in the presence of complete right bundle branch block (RBBB).5 Similar conclusions have been drawn more recently with 3-dimensional catheter-based mapping techniques.6 On this basis, one might speculate that differences in the timing of RV local activation at different locations correspond to different electrical delays in sensing through the RV lead. This proof may raise important issues related to the management of intrinsic ventricular activity or the occurrence of ventricular fusion/pseudofusion, a common pitfall in device follow-up, as not only pacemakers but also cardioverter-defibrillators and devices for cardiac resynchronization therapy (CRT) use the RV lead itself for sensing.8 Yet, basic knowledge regarding the relationship in time between QRS and acquired EGM from the RV lead is lacking in both narrow QRS and RBBB. One question of particular interest is the time at which RV lead sensing occurs at the mid-septum, which is nowadays considered the main alternative to the undesirable RV apical site for conventional pacemaker implantation.9Sensing in pacemaker therapy means the ability of the device to recognize the heart’s intrinsic signal through the implanted lead by analyzing the local endocardial electrogram (EGM) with specific reference to the QRS on the surface electrocardiogram (ECG).This study was performed to determine potential electrical delays in RV lead sensing at the mid-septum and the apex in patients with intrinsic narrow QRS or RBBB undergoing routine pacemaker implantation. As usual, RV sensing was intraoperatively tested by using a pacing system analyzer (PSA). The electrical delay (Q-VS) was calculated as the time between the reference QRS and the sensed EGM by the PSA (“VS”). Apical electrical delay Q-VS data were compared with those obtained by the same RV lead placed at the mid-septum in intraindividual comparisons.10The study population consisted of 212 patients with normal left ventricular ejection fraction in the absence of significant structural heart disease who underwent their first conventional transvenous dual-chamber pacemaker implantation for standard indication after giving written informed consent. Eligible patients were hemodynamically stable and asymptomatic during the operation and had preserved intrinsic atrioventricular (AV) conduction of >40 bpm due to sinus bradycardia or second-degree AV block type II, with conducted narrow QRS (<120 ms), or wide QRS (≥120 ms) of RBBB configuration. Patients did not have a history of cardiovascular or systemic disease, severe pulmonary or kidney disease, or heart failure but had normal cardiac chamber size and left ventricular systolic function as assessed by M-mode and 2-dimensional echocardiograms. Patients exhibiting left bundle branch block, other intraventricular conduction disturbances with a pattern not conforming to RBBB, or third-degree AV block were excluded from this study. Patients were excluded if they had an atrial or ventricular arrhythmia, or if they needed either sympathomimetic drugs or atropine or temporary ventricular pacing during surgery. Patients undergoing pulse generator change or lead revision were also excluded. Based on the baseline ECG before the operation, the patients were separated into 2 groups according to narrow QRS or RBBB recognized by signs of delay in RV depolarization.2 or Abbott™ model 2088 with tip electrode surface area 6.9 mm2; both 58 cm in length with a tip-to-ring spacing of 10 mm) was used. The RV lead was initially positioned near the RV apex where the first measurements were taken. It was then advanced into the pulmonary artery and, after exchanging the stylet with another bent distal with posterior angulation, it was pulled back by fluoroscopy guidance to fall below the RV outflow tract (mid-septum), at the center of a radiographic 9-square grid. The mid-septal position was verified by combined fluoroscopy views and characteristic ECG of the early transition zone in the precordial paced QRS, as demonstrated in Figure 1.11Implantation of a Medtronic  or Abbott  pacemaker generator was performed under continuous ECG monitoring through an external surface 12-lead ECG polygraph . Standard implant techniques were used with local anesthesia. Active-fixation leads were placed in the right atrium and the right ventricle. A commercially available bipolar steroid-eluting RV lead of the same brand  were configured to display simultaneous ECG lead II, markers, and RV EGM recordings on rhythm strips in real time. The standard programmer’s ECG cables and lead wires of Medtronic™ and Abbott™ manufacturers  connected the programmers to skin electrodes for ECG recording. The use of a PSA (Medtronic™ model 2290 or Abbott™ model EX3100) of the same pacemaker brand was considered for traditional sensing measurements. PSA cable connections (Medtronic™ model 5833SL measuring 3.66 m in length or Abbott model 4051L measuring 3.7 m in length) were used to acquire the EGM in bipolar mode by using crocodile clips on the terminal pins of the RV lead. and 3. Baseline ECG and rhythm strip data were analyzed manually over 3 cardiac cycles and then averaged using an electronic digitizer  by a single investigator, with an intraobserver variability of 0.89 ± 6.2 ms.For baseline ECG analysis, a 12-lead intrinsic ECG was recorded before implantation at a paper speed of 50 mm/s with 10 mV/cm gain. The QRS duration was measured as the interval from the first onset of the QRS in any lead until the latest offset in any lead. During the PSA session, real-time rhythm strips were obtained through the programmer’s internal printer at a sweep speed of 50 mm/s comprising concurrent ECG lead II, marker telemetry, and EGM for Q-VS measurement. This was defined as the time delay difference between the beginning of QRS to the onset of the released ventricular sensed event marker “VS” at the corresponding apical versus mid-septal RV lead position if both recordings did not coincide t test or Wilcoxon signed-rank test for paired data and Student’s t test or Mann–Whitney U test for unpaired data) were used for continuous variables and chi-squared tests were used for categorical variables, with a level of significance P < .05. Statistical analysis was performed using the SPSS statistical software package (version 24) .Results of patient characteristics are presented as mean ± standard deviation values or as percentages. Appropriate parametric or non-parametric statistical tests  had narrow QRS and 73 (34%) had RBBB isolated or associated with left anterior hemiblock. Both groups were comparable in terms of age, sex, and history of hypertension and diabetes. The indication for pacing was symptomatic sinus bradycardia in 72% of the patients and AV block in 28%. A similar proportion of narrow QRS and RBBB patients were taking angiotensin-converting enzyme inhibitors or calcium-channel blockers .Demographic and clinical parameters of the 212 study patients  are summarized in P < .01) than RBBB patients. Overall, more Medtronic than Abbott pacemakers were allocated in the overall population  as well as separately in the narrow QRS  and the RBBB  patient groups.Patients with narrow QRS had a higher heart rate (P = non-significant). There were no differences in R-wave amplitude or slew rate values obtained by the different PSAs when the study patients were analyzed as separate groups of narrow QRS patients versus RBBB patients .Narrow QRS and RBBB patients had similar R-wave amplitudes and slew rates at both the mid-septum and the apex . Similarly, the separate groups of narrow QRS and RBBB showed a shorter Q-VS at the mid-septum compared to the apex . In addition, the presence of RBBB contributed to a greater Q-VS at both the mid-septum and the apex . Of note, on 5 occasions in the narrow QRS group (4%) and 24 occasions in the RBBB group (33%), the Q-VS interval at the mid-septum was found to be either equal or prolonged compared to that at the apex. Overall, the average absolute Q-VS difference between the mid-septum and apex was 13.5 ms in narrow QRS patients and 5 ms in RBBB patients. In almost all cases, display of the “VS” marker by the RV lead was delayed in relation to QRS onset; only a few instances of nearly simultaneous records were seen.Data on the Q-VS results are presented in Table 2 shows the results of the electrical delay according to the PSA manufacturer. Overall, the Q-VS at the mid-septum was shorter compared to that at the apex in both patient groups with either Medtronic or Abbott devices (P < .05). Longer mid-septal than apical Q-VS periods were found in 2 of 103 Medtronic patients (2%) and 1 of 36 Abbott patients (3%) with narrow QRS and 15 of 44 Medtronic patients (34%) and 9 of 29 Abbott patients (31%) with RBBB, respectively. The average absolute difference in Q-VS between the mid-septum and apex with Medtronic or Abbott devices was 15.7 and 7.1 ms in normal QRS patients and 5.8 and 4.2 ms in RBBB patients, respectively. The Abbott device population’s Q-VS was significantly shorter compared to that of the Medtronic device population at both the mid-septum and the apex in both patient groups (P < .0001).The specific aim of this study was to compare systematically the RV lead electrical delay at the mid-septum versus the apex using a PSA during conventional pacemaker implantation. To the best of our knowledge, this report verified for the first time that placement of the RV lead at the mid-septum is associated with a shorter electrical delay compared to placement at the apex in both narrow QRS and RBBB patients.5 In prior studies, on average, the activation front appeared to arrive in normal QRS patients at the RV apex in 18 ms and at the RV outflow tract in 33–40 ms, whereas, in RBBB patients, it arrived at 51–54 ms and 78–84 ms, respectively. To date, little is known about the importance of the electrical delay at different RV lead locations of implanted devices. Previous studies have mainly focused on use of the electrical interventricular delay between the right and the left ventricular leads as an indicator of a better CRT response.13Timing differences in RV excitation have long been known about in both patients with normal QRS and RBBB.While there is no doubt that the device’s sensing function is a daunting engineering undertaking, the clinician’s intraoperative task is easy, usually involving only the measurement of amplitude and the slew rate of the endocardial EGM signal by the PSA. In this regard, following implantation, the implanted pulse generator is expected to offer sensing data similar to those obtained intraoperatively. This study questioned the accuracy of the sensing performance in the time measured by the PSA, as determined by the specific RV lead position. If the released RV-sensed event marker “VS” does not coincide in time with the reference QRS complex on the ECG, timing information for accurate sensing local ventricular activity could have become lost. Nevertheless, a time lag for ventricular sensing is certainly real for a great variety of reasons. These involve possibly different raw materials in lead and device construction as well as different QRS recognition methods and band-pass filters for processing sensing EGM.5 our results verified that placement of the RV lead at the mid-septum entailed a shorter electrical delay compared to that at the RV apical position in patients with structurally normal hearts and either narrow QRS or RBBB. Overall, we found that the absolute timing difference of the electrical delay between the mid-septum and apex averaged 13.5 ms in narrow QRS and 5 ms in RBBB patients, respectively. These differences might be considered small, particularly when using the Abbott PSA system, but they were statistically significant. Further, the substantial interpatient electrical delay variability measured by the PSA of either manufacturer suggests individualized assessment and tailored AV delay programming.In line with the theoretical background of the spread of ventricular excitation,15 This should be particularly considered when autointrinsic conduction search algorithms are not available or activated or the clinician uses manual programming and fixed long AV intervals in patients with intact, low-degree, or intermittent AV conduction. On the other hand, the electrical delay may allow fusion/pseudofusion to occur, which in turn may confound special pacemaker functions, such as wasting battery due to repetitive pacing threshold tests or falsely counting intrinsic beats as ventricular paced events.16 Thus, if a sensing delay is present, it needs to be carefully tailored to the individual AV delay. In point of fact, programming a longer AV delay, at least to the value of RV lead electrical delay, may encourage intrinsic ventricular activity. Conversely, a shorter sensed AV interval may be allowed in CRT recipients to increase true biventricular pacing.The clinical consequences of RV lead electrical delay largely relate to the concept of preventing unnecessary ventricular pacing. With increased electrical delay, the sensed AV interval becomes more prolonged and the ventricular channel waits longer to alert for potential incoming ventricular activity. A longer sensed AV interval may be beneficial by allowing more intrinsic ventricular activity in patients who are not pacemaker-dependent, supporting the concept of ventricular pacing minimization.17 This might not be needed to be prolonged far beyond the apparent P–R interval if the RV lead is positioned at the mid-septum.In RBBB, the well-known phenomenon of non-sensing by the RV lead due to the presence of ipsilateral bundle branch block or ectopic depolarization arising from the contralateral ventricle is based on the concept of delayed RV activation because the activation front spreads from the left ventricle toward the RV lead recording site. A longer programmed sensed AV interval than the baseline apparent P–R interval is generally recommended in dual-chamber pacing to avoid loss of sensing or inappropriate ventricular pacing.In the present study, selective RV lead placement at the apex and mid-septum was chosen, and the effect of RV lead placement on the electrical delay at other alternative RV sites was not assessed. Also, the sensing behavior of the pacemaker generator sensing circuit instead of the PSA may be different. In addition, the extrapolation of our results from our select population to patients with structural heart disease is precarious. Finally, we did not analyze patients with isolated RBBB and those with concomitant left anterior hemiblock separately. However, given the very modest RV sensing delay differences between the mid-septum and apex of ≤5 ms, we postulate that a separate assessment of these conduction disturbances would not lead to notable sensing delay differences.RV lead placement at the mid-septum enables shorter electrical delays than those at the apex in both narrow QRS and RBBB. This result strengthens the choice of an RV lead mid-septal position as regards the accuracy of the device’s sensing function in time. One must be aware that the individual sensed AV delay may vary among device manufacturers and ECG features. In dual-chamber pacing, by remembering about the RV lead electrical delay, the extension of the sensed AV delay to the value of electrical delay may contribute to the avoidance of unnecessary ventricular pacing.


A U-shaped contraction pattern was shown to be associated with a better Cardiac resynchronization therapy (CRT) response. The main goal of this study is to automatically recognize left ventricular contractile patterns using machine learning algorithms trained on conventional quantitative features (ConQuaFea) and radiomic features extracted from Gated single-photon emission computed tomography myocardial perfusion imaging (GSPECT MPI). Among 98 patients with standard resting GSPECT MPI included in this study, 29 received CRT therapy and 69 did not . A total of 69 non-CRT patients were employed for training, and the 29 were employed for testing. The models were built utilizing features from three distinct feature sets ), which were chosen using Recursive feature elimination (RFE) feature selection (FS), and then trained using seven different machine learning (ML) classifiers. In addition, CRT outcome prediction was assessed by different treatment inclusion criteria as the study’s final phase. The MLP classifier had the highest performance among ConQuaFea models . RF achieved the best performance in terms of AUC, SEN, and SPE with values of 0.65, 0.62, and 0.68, respectively, among radiomic models. GB and RF approaches achieved the best AUC, SEN, and SPE values of 0.78, 0.92, and 0.63 and 0.74, 0.93, and 0.56, respectively, among the combined models. A promising outcome was obtained when using radiomic and ConQuaFea from GSPECT MPI to detect left ventricular contractile patterns by machine learning.The online version contains supplementary material available at 10.1007/s10278-022-00705-9. Heart failure (HF) is a relatively common cardiovascular disorder with prominent morbidity and mortality . HF is c2 [Cardiac resynchronization therapy (CRT) demonstrated significant success in treating patients with fatal HF , 7. Pati2 . Nonethe2 –12 in sp2 . ConsequIn line with finding new and more appropriate indicators for CRT patient selection, several studies have been conducted. In a study by Bax et al. , LV dyssTwo types of left ventricular contraction patterns including U-shaped and non-U-shaped patterns have been recently proposed by different imaging modalities . A U-shaMyocardial perfusion imaging (MPI) with gated single-photon emission computed tomography (GSPECT) is a practical technique to assess perfusion and function of left ventricle (LV). Evaluation of LV dyssynchrony and LV contraction patterns can also be ascertained by applying phase analysis to GSPECT MPI. The advantage of simultaneous assessment of perfusion abnormalities, such as the extent and severity of ischemia and scar, and functional parameters including LV dyssynchrony, LVEF, and LV volumes make this modality an eligible method for evaluation and diagnosis of patients with HF and LV dysfunction. Besides, the automated nature of phase analysis results in an acceptable repeatability and reproducibility of this technique. As a result, MPI GSPECT is a relevant modality for examining the left ventricular contractile pattern , 23.Recent studies concerning quantitative radiomics analysis, through acting as biomarkers, have provided new insights into better handling of diseases, such as cancer  and coroIn this work, the purpose of automatic detection of left ventricular contractile patterns is fulfilled by radiomic and conventional quantitative features (ConQuaFea) using machine learning algorithms and MPI GSPECT images. This study aims to help clinicians to more confidently select patients who are eligible for CRT treatment and will also save them time and energy. In the last step, a comparison was made with the evaluation of response to CRT treatment using the left ventricular contraction pattern diagnosed by two experienced nuclear medicine physicians and the models presented in this study and standard criteria for prescribing CRT.Figure 3) in the reconstructed images. The photopeak was adjusted to 140 keV with 20% energy window. Image reconstruction was accomplished using filtered backprojection technique with a post-reconstruction Butterworth filter .This is a retrospective study including 98 patients encompassing 29 patients who underwent CRT treatment and 69 patients who did not (not being treated yet at the time of data collection or refused treatment) but had the same inclusion criteria: (a) EF ≤ 35% based on echocardiography and (b) QRS duration ≥ 130 ms [p values were calculated for continuous features using t-test and for categorical features using chi-square. Moreover, the way of scoring different regions of the heart is available in Table Phase analysis was also performed using quantitative gated SPECT (QGS) software Table  to extraThe myocardial uptake is divided into a limited number of raw perfusion samples after the left ventricle has been segmented, each represented by the mean or maximal wall photon counts at a specific place on the myocardial surface . The objMechanical left ventricular dyssynchrony can produce different patterns in polar map images as a result of two types of electrical activity propagation in the left ventricular myocardium, which include a U-shaped pattern and a non-U-shaped pattern. U-shaped pattern means that electrical activity propagation is blocked in a line while the other walls are almost contracted. For example, a contraction of an area starts from the anteroseptal wall and then goes to the apex, the lateral wall, and finally to the anterior wall. However, there are two types of non-U-shaped pattern. The first type is a homogeneous pattern; for example, contraction goes from the septal wall to the lateral wall. The second type is the heterogeneous pattern, in which there are multiple areas for myocardial contraction . Differe3 voxels. Intensities within the volume of interest (VOI) were separated to 32 discrete gray levels with fixed bin number technique. A total of 107 radiomic features including shape, intensity, and second-/high-order texture features from GLDM, GLCM, GLRLM, GLSZM, and NGTDM families were extracted. The name and short description of all radiomic features are presented in Supplementary Table A.2.To extract MPI SPECT radiomic features, the left ventricle was segmented by an experienced nuclear medicine technologist and edited/verified by a nuclear medicine physician. Then, feature extraction was conducted utilizing pyradiomics, a library in python compliant with image biomarker standardization initiative (IBSI) , 46. Re-As can be seen in Fig. The feature selection method used in this study was recursive feature elimination (RFE). Modeling was performed using logistic regression (LR), decision tree (DT), random forest (RF), extreme gradient boosting (XGB), multi-layer perceptron (MLP), support vector machine (SVM), and gradient boosting (GB) algorithms. As a result, a total of 21 different models  were implemented. Hyper-parameters were optimized using GridSearch with 5-fold cross-validation in training data, and best values were selected to train model followed by applying the trained model on test data by 1000 bootstrap. The best hyper-parameters for each classifier are presented in Table A.3. Area under the ROC curve (AUC), accuracy (ACC), sensitivity (SEN), and specificity (SPE) metrics were used to evaluate the models. All analysis was performed on Python 3.8.8.p values. Consequently, adjusted p values, also known as q values, were assessed. P values less than 0.05 were considered statistically meaningful.Using Delong test, comparisons between AUC of all models were performed, which was in turn followed by false discoveries rate (FDR) correction with Benjamini–Hochberg method applied on In the final step of the study, the task of differentiating between patients responding to CRT or not was assessed by different inclusion criteria for the treatment, namely, (1) conventional criteria and (2) left ventricle contractile pattern status assessed visually by two nuclear medicine physicians or alternatively by machine learning and ConQuaFea/radiomic features. These patients considered as responders to CRT, experienced an improvement of at least 5% in LVEF during six months of follow-up .Based on RFE feature selection, 9 ConQuaFea, 18 combined, and 12 radiomic features were selected. Figure Figure The models were developed using features from three different feature sets , selected by RFE feature selection method, and trained with seven different machine learning methods . Figure The best performance among ConQuaFea models was achieved by MLP classifier . Among radiomics models the best models was RF model . Among the combined models, the best ones were GB and RF machines .q values. Regarding radiomic features, the RF classifier did not have any significant q values. In terms of models with combined feature sets, GB and RF classifiers had 11 and 3 significantly higher q values, respectively.The results of the Delong test are illustrated in Fig. The primary aim of this study was to predict contractile patterns using GSPECT MPI, but the performance of the different models regarding the prediction of CRT response for 29 patients undergoing the treatment were also evaluated. Table Echocardiography, non-contact mapping (NCM), cardiac magnetic resonance (CMR), and myocardial perfusion imaging (MPI) are discovering two types of contraction patterns in the left ventricle. NCM is considered the gold standard of assessing the patterns of LV electrical activation. Yet the hazardous and invasive nature of the procedure restricts its wide clinical application . AccessiTo the best of our knowledge, our study represents the first attempt to label left ventricular contractile patterns by ConQuaFea and radiomic features using machine learning and GSPECT MPI images. While this task has been previously studied in GSPECT MPI , it has Toward the identification of most relative radiomic features, Fig. Toward the identification of the optimum automated model, different combinations of RFE feature selection and machine learning algorithms were applied on the included feature sets . ConQuaFea feature sets showed superiority over radiomic features. Nevertheless, radiomic features also showed an adequate performance. However, it was suggested that further studies should investigate the correlations between different feature sets in an independent analysis.In summary, our study highlighted the potential of MPI SPECT ConQuaFea. Radiomic features for the identification of left ventricular contractile patterns also showed an acceptable performance. Physicians may benefit from evaluating each patient’s specific condition and determine if CRT is needed. Moreover, it can reduce the workload and time spent by physicians, since the detection of U-shaped contractile patterns takes an average of 5 min per patient. In addition, excessive workloads, long working hours, sleep deprivation, expertise of the physician, and other factors can lead to misdiagnosis. Hence, this study attempts to help physicians making better and more precise decisions in short time.. [. [As mentioned earlier, despite the effectiveness and importance of CRT , 7, at l. , 47, the. [.  also sug. [. , the aut. [.  conducte. [.  stated t. [. .In our study, the QGS program was used to extract phase analysis indices, and when the features were selected by RFE, the apex standard deviation and inferior standard deviation from ConQuaFea data set and apex entropy and lateral bandwidth from combined features were selected. Since these features are related to the left ventricular contractile pattern and the left ventricular contractile pattern to the type of CRT response, the phase analysis parameters, as mentioned in the above studies, are related to the type of CRT response.. [p value < 0.02), and an increased event-free survival with concordance index = 0.61 vs. 0.56 .In a study by Feeny et al. , a machi. [. [In a study by Tao et al. , contrac. [. , LV leadThis study inherently bears a few limitations. Regarding the task of CRT outcome prediction, we set the criteria on the basis of the left ventricular contractile pattern and did not consider matters, such as the location of the CRT leads. Future studies might consider both to develop more comprehensive automated models for this important task. In addition, our dataset was obtained from one institute which undermines the robustness of the findings. Further studies might gather larger and diverse dataset obtained from multiple institutes with different image acquisition parameters and patients’ ethnicity to improve the reproducibility of the models . HoweverIn this study, machine learning models were developed to predict left ventricular contractile patterns with ConQuaFea and radiomic features from GSPECT MPI using different machine learning approaches with acceptable and promising results. ConQuaFea performed better than radiomic features in recognizing left ventricular contractile pattern. In addition, by diagnosing the patients’ left ventricular contraction pattern, it is possible to improve the patient’s selection for CRT treatment.Supplementary file1 (DOCX 24 KB)Below is the link to the electronic supplementary material.


Congenital diaphragmatic hernia (CDH) is a structural defect caused by inadequate fusion of the pleuroperitoneal membrane that forms the diaphragm, allowing peritoneal viscera to protrude into the pleural cavity. Up to 30% of newborns with CDH require extracorporeal membrane oxygenation (ECMO) support. As with all interventions, the risks and benefits of ECMO must be carefully considered in these patients. Cardiopulmonary function has been shown to worsen rather than improve after surgical CDH repair. Even after a detailed perioperative assessment, sudden cardiopulmonary failure after surgery is dangerous and requires timely and effective treatments.Three cases of cardiopulmonary failure after surgical CDH treatment in newborns have been reported. ECMO support was needed for these three patients and was successfully discontinued. We report our treatment experience.ECMO is feasible for the treatment of postoperative cardiopulmonary failure in newborns with CDH. Congenital diaphragmatic hernia (CDH) is a severe congenital structural malformation in that occurs in one of every 2000–5000 newborns . The dea+ 4 weeks, with a birth weight of 2,995 g and an Apgar scores of 9–10–10. The newborn was transferred to the CICU under nasal catheter oxygen inhalation. The pulmonary artery systolic pressure estimated by transthoracic echocardiography (TTE) was approximately 57 mmHg, the patent ductus arteriosus was 7 mm in diameter with a right to left shunt, and the left ventricular ejection fraction (EF) was 65%. The patient developed shortness of breath at 6 h after birth and was treated with tracheal intubation and mechanical ventilation . On the second day after birth, the patient underwent thoracoscopic CDH repair. After surgery, cardiac insufficiency was observed. The left ventricular EF was 31.9%, the left ventricular fractional shortening (LVFS) was 13.8%, and the pulmonary artery systolic pressure was approximately 61 mmHg. The patient received inhaled NO (INO) to reduce the pulmonary artery pressure 2 h after surgery. Positive inotropic drugs  were used to improve cardiac function. At 12 h after the operation, the radial blood pressure decreased progressively, fluctuating at 40–55/20–30 mmHg. Blood gas analysis showed that a pH of 7.527, PaO2 of 23.5 mmHg, PaCO2 of 34.5 mmHg, and Lac of 18 mmol/l. The calculated oxygenation index (OI) value was 76. Echocardiographic evaluation showed a left ventricular EF of 21.9%, an LVFS of 9.22%, and a pulmonary systolic pressure of 61 mmHg. Considering the complication of left heart failure, the patient met the indications for ECMO treatment. Venoarterial (VA) ECMO was used. The right common carotid artery and internal jugular vein were incised and intubated under direct vision. The diameter of the artery cannula was 8 Fr and the depth was 3 cm. The diameter of the vein cannula was 10 Fr with a depth of 7 cm  delivered a male newborn at 40 + 4 weeks of gestation, with a birth weight of 3,360 g and Apgar scores of 8–10–10. At the 31st week of pregnancy, a left CDH was diagnosed by pregnancy color ultrasound, and the estimated LHR was 1.92. Thoracoscopic CDH repair was performed on the second day after birth and the patient was in a clinically stable condition. The operation lasted 134 min. After surgery, respiratory support was given . Blood gas analysis was conducted two hours after surgery, showing a pH of 7.201, PaO2 of 56.5 mmHg, PaCO2 of 52.4 mmHg, and Lac of 1.8 mmol/l. On the first postoperative day, the SpO2 gradually decreased to 55%, the heart rate gradually decreased to 50 beats/min, and the blood pressure gradually decreased to 55/32 mmHg. Dopamine was used to improve circulation and maintain blood pressure. Blood gas analysis showed a pH of 6.942, PaO2 of 20.2 mmHg, PaCO2 of 59.8 mmHg, and Lac of 16 mmol/l. The pulmonary systolic pressure estimated by TTE was more than 100 mmHg, and the left ventricular EF was approximately 25%. The calculated OI value was 90, and the vasoactive inotropic score was 120. Then, sudden cardiac arrest occurred, which might have been due to pulmonary hypertension crisis. The duration of cardiac arrest was short because cardiopulmonary resuscitation performed for 5 min was successful. After INO treatment, the hypoxemia remained uncorrected, and cardiac arrest occurred intermittently and required cardiopulmonary resuscitation. Then, V-A ECMO was performed. The diameter of the artery cannula was 8 Fr and the depth was 3 cm. The diameter of the vein cannula was 10 Fr and the depth was 7 cm . Fetal color ultrasonography indicated a CDH, and the estimated LHR was 2.4. Due to the blood gas analysis suggesting respiratory acidosis, the mode was changed to HFOV . TTE showed that the patent ductus arteriosus was 5 mm in diameter with a right to left shunt, and the pulmonary artery pressure was 70 mmHg. The patient's blood pressure decreased 16 h after birth, fluctuating between 70 and 75/43–45 mmHg. Noninvasive hemodynamics showed that the CO was 0.4 L/min, and the CI was 2.8 L/min/m2. Low cardiac output was considered due to cardiac compression. Electrocardiogram indicated a first-degree atrioventricular block. Twenty-four hours after birth, the thoracic surgeon surgically repaired the diaphragm. Two hours after surgery, the patient's heart rate decreased slowly (70–85 beats/min). The arrhythmia worsened, and atrioventricular block developed, followed by intermittent ventricular fibrillation. It was not easy to restore sinus rhythm after bedside defibrillation. The patient's hemodynamics gradually became unstable. We suspected a rapid shift of the heart to the left cavity, resulting in increased arrhythmia. TTE showed that the left ventricular EF was 45% and the pulmonary artery pressure was 58 mmHg. Blood gas analysis results showed a pH of 7.423, PaO2 of 38.5 mmHg, PaCO2 of 69.2 mmHg, and Lac of 2.9 mmol/l. Considering the ECMO indication, V-A ECMO was used. The diameter of the artery cannula was 8 Fr and the depth was 3 cm. The diameter of the vein cannula was 10 Fr and the depth was 7 cm  . EpisodeTo improve the treatment of CDH, it is essential to manage PPHN and choose the optimal time for diaphragm repair . In factMany studies have reported the importance of TTE in patients with CDH. Early cardiac insufficiency and severe pulmonary hypertension are independent predictors of adverse outcomes in “low-risk” patients with CDH –17. A JaArrhythmia is rarely reported after CDH surgery, and the relationship between diaphragmatic hernia and atrioventricular conduction disorder remains unclear. Elevated intrathoracic pressure (such as pneumothorax) associated with atrioventricular conduction disorders has occurred in only a few patients . In Case2)  , 26. All2) –29. V-A ECMO is feasible for the treatment of postoperative cardiopulmonary failure in newborns with CDH. Timely implementation is of positive significance for improving the survival rate of newborns. However, only three cases were reported in this paper, and more patients need to be evaluated to obtain more experience in ECMO treatment after CDH surgery.


Mitral valve stenosis can be a highly symptomatic condition with significant complications if left untreated. In such cases, mitral valve replacement with a bioprosthetic or mechanical valve may be a viable solution to prevent progressive disease. Current guidelines do not recommend continued anticoagulation beyond 6 months for patients who have undergone bioprosthetic valve replacement without a separate indication for anticoagulation. With this case discussion we aim to 1) Review the current indications for anticoagulation for bioprosthetic mitral valves in patients without atrial fibrillation and 2) Discuss the constellation of comorbidities that may affect the decision to begin anticoagulation therapy.We present a case describing a 55-year-old male with end-stage renal disease, coronary artery disease with coronary artery bypass graft surgery, and bioprosthetic mitral valve replacement 2 years prior with rapid degeneration of the replaced valve and on warfarin without a clear indication for anticoagulation. The patient was admitted for symptomatic, severe mitral stenosis and consideration of transcatheter mitral valve-in-valve replacement. During hospital admission, warfarin was discontinued and replaced with prophylactic anticoagulation. However, 8 days after warfarin cessation an intraoperative transesophageal echocardiography revealed a newly developed large left atrial thrombus leading to cancellation of the planned operation.This patient developed a left atrial thrombus after discontinuing warfarin in the setting of rapidly deteriorating bioprosthetic valve stenosis and vascular comorbidities. The decision to discontinue warfarin was made in concordance with current guidelines, which do not indicate systemic anticoagulation post 3–6 months after bioprosthetic valve replacement without separate indication for anticoagulation. This case identifies the need to investigate rebound hypercoagulability and further risk stratify comorbidities which may independently increase the risk of clot formation in the setting of severe mitral valve stenosis. According to current valvular heart disease guidelines, mitral stenosis is not an indication for therapeutic anticoagulation in the absence of atrial fibrillation or additional indications. Moreover, without further indications for anticoagulation a short course of aspirin with warfarin is typically recommended for three to 6 months following bioprosthetic mitral replacement . Further2 , and left atrial appendage ligation repair in Sept 2020 Fig. . Post-op2 Table . He expe2), without evidence of thrombus  with goal of 2.5 to 3.5 per standard of care. In January of 2023, Transesophageal echocardiography (TEE) revealed progressive worsening of severe bioprosthetic valve stenosis with immobilization of two fused leaflets and mean MV gradient that increased to 21 mmHg  bioprosthetic valves explanted due to structural failure were found to have deterioration attributed to valvular thrombosis. Of those cases, 65% were detected after the first-year post-procedure, and 15% were found 5 years post-procedure with the majority occurring between 13 to 24 months . The ratAccording to the 2020 American College of Cardiology (ACC)/American Heart Association (AHA) guidelines for management of patients with surgical bioprosthetic valve replacement, monotherapy with aspirin 75 mg to 100 mg daily is adequate after completing 3 to 6 months of anticoagulation without additional indications for continued anticoagulation [It is known that a hypercoagulable state may transiently exist shortly after beginning warfarin which necessitates bridging therapy with heparin. Like novel oral anticoagulants (NOACs), prior studies have also described a potential rebound hypercoagulable period following discontinuing warfarin –13. Howe2DS2VASc score above 5 for bridging to heparin infusion, as elevated scores have been shown to be associated with higher rates of prosthetic valvular thrombus formation [The patient’s highest risks for thrombus were existing prosthetic valve with concomitant stenosis, severe left atrial dilation, presence of left atrial SEC, atherosclerosis, ESRD, and peripheral artery disease , 19. Strormation , 21. How2DS2VASc for prosthetic valve thrombus in patients with bioprosthetic cardiac valve replacements.We encourage additional investigation into the need for further risk stratification to guide anticoagulation recommendations in patients with severe bioprosthetic valve dysfunction with concomitant risk factors for thrombogenesis. Identification of hemodynamic parameters including mean gradients or pressure half-times in MS that increase the risk of prosthetic thrombosis that could be particularly helpful in certain cases is not addressed in current valvular heart disease guidelines. Additionally, the removal of anticoagulation should be carefully considered in patients with such risk factors. Risk stratification could potentially be based on factors such as duration of prior warfarin therapy, severity of trans-mitral gradient, duration of hemodialysis, age of onset of renal failure, and overall risk of thrombus formation accounting for prior history of vasculopathy. Further studies should examine the predictive value of CHAThe etiology of our patient’s progression of bioprosthetic mitral valve disease eventually resulting in thrombus was likely multifactorial in the setting of several comorbidities conferring a prothrombotic state in addition to rebound hypercoagulability following anticoagulation cessation. Patients with dysfunctional mitral valve prostheses may represent a unique population that deserves further consideration for empiric therapeutic anticoagulation, and whose risk of de novo thrombosis may be underappreciated. We suggest nuanced clinical decision-making be applied when considering anticoagulation in patients with bioprosthetic mitral valves who have additional comorbidities present even though they may not meet current guideline criteria. Further investigation into risk stratification of comorbidities may be beneficial to help prevent thrombosis for patients at higher risk.


Aortic regurgitation (AR) is grouped into acute or chronic AR. Acute AR, unlike chronic AR, can manifest with significant hemodynamic compromise. Acute AR is typically due to endocarditis or aortic dissection, and less commonly due to blunt trauma or iatrogenic causes. We present a patient with cardiogenic shock due to severe acute AR from anterior leaflet perforation without an identifiable rheumatologic or infectious etiology. Aortic regurgitation (AR) refers to the incomplete closure of the aortic valve leaflets resulting in regurgitant flow, which can be appreciated through the use of transthoracic echocardiogram in the parasternal long axis view with or without continuous flow doppler . MeasureA 44-year-old female with no past medical history presented to an outside hospital for 3 days of fever and arthralgias. She was started on ceftriaxone for treatment of a suspected urinary tract infection (UTI). However, despite the initiation of IV antibiotics, the patient continued to have persistent fevers and developed a new-onset headache. A computed tomography (CT) scan of the patient’s head was performed and was negative for acute pathology. Over the course of the next few days, the patient developed hemodynamic compromise including respiratory distress requiring intubation, and hypotension requiring the initiation of vasoactive medications. Streptococcus agalactiae with 50,000-100,00 colony-forming units per mL (CFU/mL). Given the unclear source of infection, the antimicrobial regimen was broadened to vancomycin, ceftriaxone, acyclovir, and doxycycline for empiric coverage of possible meningitis and tick-borne diseases. A lumbar puncture and tick panel performed on the day of admission were unrevealing for acute infectious processes. The patient was subsequently transferred to our facility with septic shock secondary to a UTI complicated by acute hypoxic respiratory failure. On arrival at our facility, the patient was intubated, mechanically ventilated, and afebrile with a temperature of 36.4 °C. She had a blood pressure of 104/59mmHg on 4mcg/min of norepinephrine, and a heart rate of 95 beats per minute. The patient was saturating 100% with a ventilator on pressure control mode with a positive end-expiratory pressure of 10, a fraction of inspired oxygen at 40%, and respiratory rates of 14 breaths per minute amounting to tidal volumes 400-500mL. Laboratory findings on admission are listed in Table On the second day of admission, a transthoracic echocardiogram (TTE) was completed for evaluation of other etiologies of shock, including cardiogenic shock. The TTE demonstrated normal left ventricular systolic function with an estimated ejection fraction of 65% with moderate aortic regurgitation, moderate to severe mitral regurgitation, and severely elevated pulmonary artery systolic pressures estimated at 60mmHg Figures , 2. DiurThe etiology of acute aortic regurgitation as determined from histologic analysis of surgically excised valves recorded in one retrospective study revealed that infective endocarditis accounted for 17% of cases, followed by aortic dissection at 10%. However, 34% of patients remained without a clear etiology of isolated AR based on histopathology [Chronic AR progresses over months to years, allowing for the LV to remodel and dilate. These LV structural changes allow for the heart to accommodate an increased volume without any reflective increase in LV diastolic pressures, while simultaneously allowing for the heart to maintain adequate cardiac output. In the settings of acute AR, however, there is no time for the LV size to dilate or remodel, which results in elevated LV diastolic pressures, and a subsequent decrease in stroke volume and cardiac output. In acute AR, the heart attempts to compensate for the drop in stroke volume by increasing the heart rate, but in most cases, the overall cardiac output still decreases despite the reflexive increase in heart rate. This acute drop in cardiac output results in cardiogenic shock. Furthermore, pulmonary edema can develop because of an increase in diastolic volume in a normal-sized LV secondary to the regurgitant flow from the perforate aortic valve. The rapid increase in LV diastolic pressure results in both increased left atrial and pulmonary venous pressures, resulting in pulmonary edema . While direct visualization of the aortic valve through TEE aided in the identification of spontaneous leaflet perforation, the patient’s presentation and hemodynamics suggested the timeline of development. The progression of chronic AR over months to years allows time for the left ventricle (LV) to remodel and dilate. This allows accommodation for increased volume without a reflective increase in LV diastolic pressures, while also maintaining adequate cardiac output. In acute AR, the LV is not given time to remodel or dilate, thus a decline in forward stroke volume occurs. Despite a reflexive increase in heart rate, the heart cannot meet the demands, and the cardiac output decreases. This acute decrease in cardiac output is known as cardiogenic shock, and on a physical exam, this can be seen as hypotension and tachycardia. Furthermore, pulmonary edema can develop because the increased volume from the regurgitant flow within a normal-sized LV causes a rapid increase in LV diastolic pressure that propagates to both increased left atrial and pulmonary venous pressures . Although the hemodynamic findings of cardiogenic shock with rapid clinic decline are consistent with acute AR, the echocardiogram findings in this case demonstrated an LVEDV (Left Ventricle End Diastolic Volume) of 172 mL and LVESV (Left Ventricle End Systolic Volume) of 86.6mL. Both values are suggestive of chronic AR, as with chronic changes the LV has had time for remodeling. However, the right ventricular systolic pressures, a surrogate to LV diastolic and pulmonary venous pressure, were significantly elevated at 60 mmHg which is suggestive that the regurgitant flow from the perforated aortic valve led to elevated LV pressures, eventually resulting in pulmonary edema. These findings suggest that the patient had chronic AR, with an acute heart failure exacerbation resulting in cardiogenic shock. However, the exact timeline of the AV perforation remains unclear, thus not entirely eliminating a component of acute AR in this case. Surgery is imperative in the treatment of acute AR due to aortic dissection or infective endocarditis. However, medical therapy to reduce the LV afterload can assist with temporary stabilization . Per theThis case demonstrates a rare presentation of aortic valve perforation resulting in cardiogenic shock. Although rare, acute AR may result in catastrophic shock and pulmonary edema which can be masked in its discovery, leading to potentially fatal outcomes if not intervened upon early. Swift management with the use of bedside ultrasound in unstable patients is key to optimizing outcomes. Further workup for unclear etiology is also important, of which the differential diagnosis should remain broad. Treatment remains limited, but valve replacement therapy in the non-acute infectious periods may be reasonable and should be considered.


Sodium-glucose cotransporter type 2 (SGLT2) inhibitors have demonstrated to reduce cardiovascular risk in patients with type 2 diabetes mellitus (T2DM) in large trials independent of glycemic control. The mechanisms of this cardioprotective property remain uncertain. Evidence suggests positive hemodynamic changes and favorable cardiac remodeling contributing to the clinical outcomes but results were conflicting. We aim to investigate the potential impact on hemodynamic parameters, cardiac structure and functions. This prospective observational study included T2DM patients receiving canagliflozin 100 mg per day in addition to their antidiabetic treatment. We analyzed hemodynamic parameters assessed by echocardiographic measurements and impedance cardiography (ICG) to evaluate systolic and diastolic functions from baseline to 24 weeks after treatment. A total of 47 patients  averaging 64.6 ± 10.9 years had a significant reduction in HbA1c, body weight, and systolic blood pressure. Hematocrit increased significantly, while NT-proBNP remained unchanged. E/e′, left atrium (LA) volume, and LA stiffness were reduced, while left ventricle (LV) global longitudinal strain (GLS) and LA strain rates increased at 24 weeks by conventional and speckle tracking echocardiography. LV mass and ejection fraction showed no differences. ICG suggested significant improvement in hemodynamic parameters with increased stroke volume index and cardiac output index and decreased systemic vascular resistance index at 12 and 24 weeks. Canagliflozin improved hemodynamic parameters and had a favorable impact on LA and LV reverse remodeling. These changes may explain the beneficial effect on cardiovascular outcomes in large clinical trials. Additionally, they reduce body weight, blood pressure, and uric acid level, independent of their hypoglycemic effects. Several SGLT2 inhibitors, such as empagliflozin, dapagliflozin, and canagliflozin, have been found to have cardiovascular benefits in large placebo-controlled clinical trials and are the first oral diabetes drugs that can reduce cardiovascular risk3. In contrast, other hypoglycemic drugs like dipeptidyl peptidase-4 inhibitors (DDP4i) and thiazolidinediones are ineffective in cardiovascular risk reduction and are even associated with increased heart failure in patients with type 2 diabetes mellitus (T2DM).Sodium-glucose cotransporter type 2 (SGLT2) inhibitors are a novel class of oral diabetes drugs that block the reabsorption of glucose via SGLT2 in the proximal tubules of the kidneys, allowing glucose to be excreted in the urine, and achieve the therapeutic effect of lowering blood sugar5. EMPEROR-Preserved further demonstrates the benefits in patients with heart failure and a preserved ejection fraction (HFpEF) with a 29% lower risk of HHF with empagliflozin6. Moreover, SGLT2 inhibitors have impressive renal outcomes with improvement in albuminuria, declining kidney function, and renal death independent of glycemic control and the presence of diabetes8.The most significant and consistent cardiovascular outcome from SGLT2 inhibitors is the reduction of hospitalization for heart failure (HHF). Recent meta-analyses of cardiovascular outcome trials show a 32–33% reduction of HHF without heterogeneity, and this effect extends to patients without type 2 diabetes10.Despite the cardiovascular benefits of SGLT2 inhibitors, the underlying mechanisms of action remain unclear and are to be elucidated. Several hypotheses have been postulated to explain these cardiorenal benefits, including diuresis effect, hemodynamic improvement, or augmented cardiac metabolism11. It utilizes skin sensors placed on the neck and chest to measure changes in electrical conductivity within the thorax to calculate cardiac output, stroke volume, systemic vascular resistance (SVR), thoracic fluid status, and other contractility indexes12. Previous studies have demonstrated that ICG improved and predicted clinical outcomes in patients with acute and chronic heart failure14. Several parameters measured by ICG also predicted mortality in the general population, even after adjustment for multiple confounders and blood pressure15.Impedance cardiography (ICG) is a convenient, non-invasive method to approximate valuable hemodynamic parameters and is often used in surgical and intensive care units to guide therapyOur observational study aims to assess the effect of canagliflozin on hemodynamic parameters measured by ICG and left ventricular functions evaluated by echocardiography in patients with T2DM. The results of this study will provide valuable insights into the mechanisms of action of SGLT2 inhibitors and their effects on cardiovascular and renal outcomes in patients with T2DM.This prospective, single-center observational study was conducted at Hsinchu MacKay Memorial Hospital, a regional hospital in Northern Taiwan, to investigate the effect of canagliflozin on patients with T2DM. The study was approved by the Institutional Review Board of MacKay Memorial Hospital (Registration Number: 18MMHIS162e) and followed the principles of the Declaration of Helsinki. Each study participant provided informed consent. The enrolled patients with T2DM who were SGLT2 inhibitor-naive received canagliflozin 100 mg once daily in addition to previously prescribed antidiabetic agents. Physical examinations and hemodynamic monitoring were performed at baseline and in the 4th, 12th, and 24th weeks after administration of canagliflozin. Body weight and fat mass were measured using a commercially available scale with a bioelectrical impedance-based (BIA) body composition monitor . Blood tests were conducted at baseline and in the 12th and 24th weeks, except for hs-CRP, aldosterone, and renin, which were measured at baseline and in the 24th week only. Echocardiography was performed at baseline and in the 24th week.2, and (3) patients taking metformin alone or taking metformin and other antidiabetic drugs. The key exclusion criteria included: (1) patients with type 1 diabetes, (2) pregnant or breastfeeding patients, (3) New York Heart Association (NYHA) Class III and IV, (4) acute or chronic inflammatory disease, (5) patients who are allergic to canagliflozin and its excipients, and (6) severe obesity (BMI ≥ 40 kg/m2).The target patient population was T2DM patients who had not taken any SGLT2 inhibitor prior to the study. These patients were recruited from outpatients at Hsinchu Mackay Memorial Hospital, Taiwan, and received standard care for T2DM during the study period. Other inclusion criteria were: (1) age ≥ 20 years old, (2) eGFR ≥ 30 mL/minute/1.73 mEchocardiography was performed by a single trained sonographer blinded to clinical information using a commercially available ultrasound system . Standardized echocardiographic measurements were obtained according to the American Society of Echocardiography (ASE) recommendations. Left atrium (LA) and left ventricle (LV) volumes were obtained via the modified biplane Simpson method from the apical two- and four-chamber views. Diastolic function was assessed from early mitral inflow velocity (E), late mitral inflow velocity (A), deceleration time (DT), and tissue Doppler imaging (TDI)-derived mitral annular early diastolic velocity (E′) from LV septal and lateral segments. The mean values of septal and lateral E′ were reported in our tables.LV and LA strains were assessed by speckle tracking analysis. Baseline 2D images were analyzed offline by manually tracing the endocardial border using proprietary software . Based on automated speckle-tracking algorithms, LV global longitudinal strain (LV GLS) curves were obtained from the three standard apical views . Peak atrial longitudinal strain (PALS) and strain rate (SR) curves  were generated for each atrial segment from apical 2- and 4-chamber views. The ratio of E/e′ to peak LA strain was used to estimate LA stiffness. Minor manual adjustment was used as necessary to ensure the best tracking quality. The absolute values of longitudinal strain  were reported in this manuscript, and the corresponding tables and figures to avoid confusion regarding the directionality of the strain changes.The non-invasive cardiac hemodynamic measuring instrument, AESCULON , was used to provide the hemodynamic parameters. The device sends a low-amplitude, high-frequency electrical current through the thorax, and two sensors attached to the neck and another two to the left side of the thorax measure the changes in conductivity created by the circulatory system. The hemodynamic parameters were available after three minutes, and the report was printed for analysis. Table p < 0.05.Data were expressed as mean ± stand deviation for continuous variables and numbers (%) for categorical variables. The comparison of each parameter before and after treatment with canagliflozin was calculated by paired sample t-test. All statistics were two-sided and statistically significant at Statistical analyses were performed using IBM SPSS Statistics for Windows, version 24.0 .The study was approved by the Institutional Review Board of MacKay Memorial Hospital (Registration Number: 18MMHIS162e).From November 2019 to February 2021, 52 T2DM patients were included in the study, and five patients did not complete the study. Three stopped the medication because of adverse drug effects , one could not have the examinations due to Covid travel restrictions, and one withdrew consent. Table 2 and 23.3 kg, respectively, indicating that the patients were overweight on average and some had a high body fat percentage. The majority of patients had a history of cardiovascular disease (95.7%), and most were taking antihypertensive medications and statins. The patient’s medications, including antihypertensives, diuretics, and antidiabetic agents, remained similar during the study period.The mean age of the participants was 64.6 ± 10.9 years. There were 25 (53%) males and 22 (47%) females. The mean body mass index (BMI) and fat content were 28.2 kg/m2, both statistically significant. However, the fat mass and ratio measured by BIA showed no difference 6 months after the administration of canagliflozin. Both fasting blood glucose level  and HbA1c  showed a considerable drop. The mean hemoglobin  and hematocrit  increased at 6 months. The above changes were observed and statistically significant at 12 weeks and continued until the end of the study. There was a trend for reduction of microalbuminuria/creatine ratio, albeit statistically insignificant. No difference was seen in lipid profiles, renal functions, electrolytes, uric acid, levels of NT-proBNP, hs-CRP, renin, and aldosterone. Clinical changes are shown in Table The mean weight changed from 74.1 ± 13.4 to 72.6 ± 13.8 kg, and the mean body mass index (BMI) 28.2 ± 4.3 to 27.6 ± 4.3 kg/mp < 0.001). LV global longitudinal strain (GLS), LV systolic and early strain rate (LVSRs and LVSRe) also significantly increased from 16.6 ± 2.8 to 18.0 ± 3.4 (p < 0.001), 1.08 ± 0.31 to 1.15 ± 0.35 (p = 0.013), and 0.90 ± 0.25 to 1.09 ± 0.31 (p < 0.001), respectively. Moreover, LA volume and LA stiffness decreased while LA systolic function assessed by PALS and LA strain rates increased with canagliflozin treatment at 24 weeks. Data are shown in Table There were no significant differences in the LV mass, LV volume, LV ejection fraction, and cardiac output derived from echocardiography 24 weeks after the administration of canagliflozin Table . Neverthp = 0.019). The average heart rate also dropped at 24 weeks from 75.0 ± 11.3 bpm to 71.5 ± 12.4 bpm (p = 0.003).The hemodynamic parameters by ICG at baseline, 4 weeks, 12 weeks, and 24 weeks of canagliflozin are summarized in Table p < 0.001).ICG parameters of blood flow and vascular system, including cardiac output, cardiac index, stroke volume, stroke index, and systemic vascular resistance index, showed significant improvement at 12 and 24 weeks after starting canagliflozin. The index of contractility (ICON™) increased significantly, but the other parameters of contractility, including left ventricular ejection time, pre-ejection time, and systolic time ratio, did not change. Unexpectedly, thoracic fluid content (TFC), which reflects the extravascular and intravascular fluid, increased from 24.6 ± 5.3 to 32.7 ± 7.1 k/Ω  increased erythropoiesis and hematocrit and helped reduce the risk of heart failure and ischemic heart disease20. The reduction of afterload by lowering blood pressure and decreasing vascular resistance likely contributed to the observed overall increase in hemodynamic parameters of blood flow, as well as the improvements in subclinical systolic functions. Studies have demonstrated that SGLT2 inhibitors can directly improver vascular function by inducing vasorelaxation and reducing endothelial cell dysfunction associated with atherogenesis22. Moreover, the “fuel hypothesis” suggests that SLGT2 inhibitors increase ketone bodies, thereby optimizing cardiac energy metabolism and cardiac function may ameliorate the outcomes24.The mechanisms underpinning the overwhelming effect of cardiorenal protection by SGLT2 inhibitors are not yet fully understood. It is postulated that SGLT2 inhibitors may augment erythropoiesis and suppress sympathetic hyperactivity25. The decrease in E/e′, indicative of decreased LV filling pressure and diastolic function improvement, is a consistent finding observed in this and other SGLT2 inhibitors’ studies28. In the IDDIA trial, E/e′ only decreased significantly during exercise in T2DM patients with dapagliflozin29. The other echocardiographic parameters for diastolic function, including LV mass, LA volume, and E/A ratio, are less sensitive. MRI imaging also did not detect an apparent change in the LA or LV geometry31. Nevertheless, our data from speckle tracking provided additional evidence suggesting beneficial effects on cardiac remodeling and function. LV GLS increased significantly while LVEF did not change, suggesting early and subclinical LV systolic improvement, which was similarly found in other studies33. The administration of canagliflozin was also associated with significant improvement in LA strain indices and LA stiffness.Elevated E/e′ is a valuable marker for diagnosing heart failure with preserved ejection fraction and predicting prognosis35. However, our findings contradicted previous studies that found empagliflozin and dapagliflozin had no effect on any hemodynamic parameters evaluated by ICG in T2DM patients at 3 months and 12 weeks, respectively36. Although all studies enrolled T2DM patients without overt heart failure, there were differences in baseline characteristics. Patients in our study were predominately female, had smaller BMIs, better diabetic control, greater reductions of SBP, and received less diuretic therapy. Additionally, the number of patients enrolled in these studies was limited.To our knowledge, few prior studies reported a comprehensive analysis of LA deformation with the administration of SGLT2 inhibitors. Decreased LA strain and increased LA stiffness have been strongly correlated with atrial fibrillation and adverse clinical outcomes in patients with heart failure with reduced EF (HFrEF) or HFpEF38. A previous study has shown oxidative stress was strongly associated with impaired myocardial performance and decreased GLS39. Dual SGLT1/2 inhibitor, sotagliflozin, has also been shown to reduce the overall risk of cardiovascular death, hospitalization for HF and emergent HF visit41. Thus, the additional SGLT1 inhibition may potentiate the hemodynamic effect of canagliflozin.Another possible explanation is that canagliflozin is more selective towards SGLT1 receptors, which are expressed abundantly in the distal proximal tubules of kidneys, the small intestine, and the cardiomyocytes. Suppression of SGLT1 can facilitate glucose uptake, decrease oxidative stress, reduce myocardial fibrosis and ventricular hypertrophy, and improve cardiac function44. Our data suggest that positive cardiac remodeling, improved LV systolic and diastolic functions, and reduced systemic vascular resistance contribute to the broad therapeutic efficacy of SGLT2 inhibitors. Although it is postulated that SGLT2 inhibitors exert a diuretic effect that removes interstitial fluid to reduce the risk of HF, this effect is transient and modest and cannot account for the long-term outcome in clinical trials. In our study cohort, baseline measurements revealed normal level of Nt-proBNP and relatively low TFC. Interestingly, the level of Nt-proBNP did not decrease, and TFC even exhibited an elevation, despite positive hemodynamic changes observed after 6 months of canagliflozin treatment. These findings suggest that other mechanisms may be responsible for the therapeutic effect of SGLT2 inhibitors. The observed increase in TFC may be attributed to the counteracting mechanism of fluid regulation following the inhibition of SGLT2, as evident by the trending elevation in plasma renin activity45.Large clinical trials have recognized the effect of SGLT2 inhibitors in reducing the risk of hospitalization for heart failure, regardless of the presence of diabetes or glycemic control. Furthermore, SGLT2 inhibitors have been found to be effective in non-diabetic patients with HFrEF or HFpEF, who previously had no effective therapy46. A recent meta-analysis has indicated limitations in the inability of electrical cardiometry to measure absolute cardiac output values, and it may be applicable as a trend monitor if performed precisely47. Factors affecting the tissue and device conductivity, time and postural variability, and different algorithms may influence the calculated values. Nevertheless, our clinical and echocardiographic changes in response to canagliflozin treatment demonstrated favorable trends in positive cardiac remodeling, aligning with most available data in the literature.This study has several limitations. Firstly, the non-randomized, uncontrolled design affects the validity of our findings. Secondly, the small sample size and short follow-up duration may limit the generalizability of our results. A large randomized controlled trial is needed to confirm the positive hemodynamic effects of canagliflozin. The small percentage of patients with heart failure also made it difficult to detect the subclinical difference in some endpoints by conventional echocardiography over the 6-month period. Lastly, ICG utilizes the changes in electrical conductivity of the aortic arch blood flow detected by the skin sensors to estimate stroke volume and cardiac outputThis study suggests that canagliflozin has a positive impact on hemodynamics and cardiac function. Specifically, it increases cardiac index, reduces systemic vascular resistance, improves diastolic function, and promotes favorable LA remodeling. These findings may help explain the beneficial effects of SGLT2 inhibitors on cardiovascular outcomes.


Cardiac involvement is common in end-stage renal disease patients. The presenting study aimed to evaluate the global and segmental longitudinal strain in patients with advanced uremic cardiomyopathy (AUCM) and compare it to dilated cardiomyopathy (DCM).P value = 0.045). Comparing segmental strain showed a lower strain in mid inferoseptal , base and mid anterolateral , base and mid anteroseptal , base and mid inferior  and mid anterior  in patients with AUCM compared with DCM. In both groups, the segmental strain increased from base to apex.The mean global longitudinal strain (GLS) was significantly lower in AUCM (Segmental and GLSs in advanced uremic cardiomyopathy were significantly lower than those of dilated cardiomyopathy. In both groups, the segmental strain increased from base to apex. Cardiovascular complications are the important causes of mortality and morbidity in patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD) . “UremicSpeckle-tracking echocardiography (STE) allows the evaluation of myocardial deformation and heart mechanics , 5. In pMost of the presenting studies with STE focused on ESRD patients with normal left ventricular function. In this study, we focused on the advanced stages of UCM. The results of the presenting study compared the global and segmental longitudinal strain in advanced uremic cardiomyopathy with dilated cardiomyopathy.This single-center comparative observational study was performed between March 2017 and March 2019. Written informed consent was obtained from study participants. The ethics committee approved the study protocol. Twenty-five patients aged 18 to 70 years suffering from ESRD and advanced uremic cardiomyopathy (AUCM) were included. All the ESRD patients were on routine hemodialysis via arteriovenous fistula (AVF) and were candidates for kidney transplantation. The result of the invasive coronary angiography in ESRD patients was normal; an AVF-associated high-output cardiac failure was ruled out with echocardiography and ultrasonographic flow assessment of the fistula. Advanced uremic cardiomyopathy was arbitrarily defined as a left ventricular ejection fraction (LVEF) of less than 40%. Twenty-five known patients with dilated cardiomyopathy (DCM) matched with the same left ventricular ejection fraction ranges were enrolled as the control group. All the DCM patients had normal invasive coronary angiography results in their records.In patients with AUCM, several exclusion criteria were defined, including a history of heart failure or documented LVEF less than 50% before initiating renal replacement therapy (RRT), uncontrolled hypertension, congenital heart disease, pericardial disease, and history of autoimmune disorders.In both AUCM and DCM groups, a history of diabetes mellitus, permanent pacemaker, left bundle branch block, atrial fibrillation rhythm, and inadequate acoustic window was considered exclusion criteria.Transthoracic echocardiography was performed by Vivid E9 echo vendor (GE company). In ESRD patients, echocardiographic interrogation was done 6–24 h after the last hemodialysis session. All the ESRD patients had controlled blood pressure(systolic blood pressure less than 140 mmHg) at the time of echocardiography. A Cardiologist with a fellowship in echocardiography performed two-dimensional, color Doppler echocardiography, tissue Doppler imaging (TDI), and 2D STE. The left ventricular dimensions were measured by 2D echocardiography. The modified Simpson's method assessed left ventricular volumes and systolic function. Right ventricular systolic function was evaluated by tricuspid annular plane systolic excursion (TAPSE), right ventricular fractional area change (RVFAC), and right ventricular peak systolic myocardial velocity (RVSm). Valvular heart disease severity was assessed based on the latest ASE guidelines . Global Global longitudinal strain, segmental longitudinal strain, and all echocardiographic measurements were compared between the two groups as the study endpoints.Descriptive analysis was used to describe the data, including mean ± standard deviation (SD) for quantitative variables and frequency (percentage) for categorical variables. The Chi-square, t-test, or Mann–Whitney U tests were used to compare variables. The statistical software IBM SPSS Statistics for Windows version 22.0  was used for the statistical analysis. P values < 0.05 were considered statistically significant.P = 0.877). The mean age of the AUCM group was lower than DCM . Compelling cardiovascular risk profile, 23 patients in advanced uremic cardiomyopathy had a history of hypertension versus one in the DCM group . No difference was found between the two groups in the history of smoking and hyperlipidemia (Table This study enrolled 25 patients with ESRD and advanced uremic cardiomyopathy (AUCM as the case group) and 25 DCM patients (as the control group). Regarding demographic characteristics, the male gender was 76.0% in AUCM and 72.0% in the DCM group (P = 0.045). A comparison of segmental longitudinal strain in 17 segments was provided (Table P = 0.048), base anterolateral (P = 0.026), mid anterolateral (P = 0.001), base inferior (P = 0.015), mid inferior (P = 0.034), mid anterior (P = 0.015), base anteroseptal (P = 0.005), and mid anteroseptal (P = 0.009) in AUCM and DCM. The segmental strain increased in both groups from the basal to the apex.Echocardiographic data were compared in Table ed Table , Fig. 2.P = 0.011). Systolic PAP in AUCM was 43.00 ± 11.99 mmHg versus 34.52 ± 11.13 mmHg in the DCM group (P = 0.015).Also, those suffering from AUCM had significantly lower mitral E wave deceleration time  and between RRT duration and GLS .No correlation was found between age and GLS  and compared this group of patients with DCM. The results showed that the global longitudinal strain was lower in AUCM versus DCM. Despite a lower strain in some myocardial segments in AUCM, both groups showed increased segmental longitudinal strain from base to apex. There was no specific segmental left ventricular strain pattern using speckle tracking to differentiate advanced uremic cardiomyopathy from DCM. GLS was reduced in advanced uremic cardiomyopathy and may indicate a more severe myocardial injury. The major limitation of this conclusion is the significant difference between the age of study participants in AUCM and DCM in our study; AUCM patients were one decade younger than DCM. The important question is the effect of aging on GLS values. In one meta-analysis, the effect of aging on GLS was assessed. The decrease in GLS was most pronounced after sixty in the normal population . The lowVarious studies have evaluated and compared echocardiographic parameters between patients with uremic cardiomyopathy and healthy individuals. In the study by Tamulnait et al., diastolic dysfunction was reported in 81.6% of patients with ERSD. Also, the ESRD group's mean GLS and global circumferential strain (GCS) were significantly lower than healthy controls. RV GLS was significantly lower in ESRD patients than in healthy controls . In a stThe study's main limitations were the small number of patients and the absence of long-term follow-up for comparing cardiovascular events and mortality. The advanced uremic and dilated cardiomyopathy were not matched properly regarding the age of the study population. The study did not include the duration of the severe decline of the eGFR to the initiation of the first hemodialysis session. Meanwhile, data on mean arterial noninvasive blood pressure measurement, renal function tests, mean eGFR, and hemoglobin levels in both groups needed to be documented.Myocardial injury in patients with advanced uremic cardiomyopathy is more severe than DCM. There is no specific pattern of segmental strain to differentiate uremic cardiomyopathy and DCM.