The diagnosis of structural heart disease in athletes with ventricular arrhythmias (VAs) and an apparently normal heart can be very challenging. Several pieces of evidence demonstrate the importance of an extensive diagnostic work-up in apparently healthy young patients for the characterization of concealed cardiomyopathies. This study shows the various diagnostic levels and tools to help identify which athletes need deeper investigation in order to unmask possible underlying heart disease. Sudden cardiac death (SCD) is an unexpected, devastating event, especially when occurring in young athletes, who are generally considered healthy individuals. Recent studies ,2 have rAccording to comparative data from Italian studies, the risk of SCD in athletes is higher  with respect to non-athletes . This risk is also strongly related to underlying cardiovascular diseases .Up to 42% of athletes who suffer from SCD have an apparently normal heart and a negative toxicology screening . ExercisAccording to recent European Scociety of Cardiology (ESC) guidelines, screening strategies must be tailored to the target population and the specific disorders with the highest risk . SpecialIn Italy, the pre-participation clinical screening for competitive professional and non-professional athletes is established by Italian law and regional regulations . The firAn algorithm for the clinical management of athletes with premature ventricular beats (PVBs)  is proviECG represents an essential tool in the evaluation of athletes with PVBs. The most relevant ECG findings include repolarization abnormalities, such as T-wave inversion and ST-segment depression, pathological Q-waves, intraventricular conduction delays, ventricular pre-excitation, and a long QT interval. These ECG findings are classified as abnormal by current recommendations. Training-unrelated ECG findings warrant additional investigations to exclude myocardial disease [The  disease . The ass disease . exercise stress test. This exam is useful for the assessment of PVBs associated with increasing workloads [Following ECG examination, physicians must carry out an orkloads  and otheExercise-induced PVBs raise clinical suspicion because of their association with cardiomyopathy, myocarditis, and ion channel diseases, all of which are normally worsened by adrenergic stimulation ,14,15,1624 h ambulatory ECG monitoring must be obtained in order to study the frequency and morphology of ectopic beats during the day. This exam is able to evaluate the so-called “arrhythmic burden”, namely the number of PVBs in 24 h and the presence of complex arrhythmias . It was demonstrated that athletes with frequent PVBs or non-sustained VT have an underlying cardiovascular disease more frequently than athletes with rare and isolated PVBs [A ted PVBs . Howeverted PVBs ,22.There is scientific evidence that athletes have ventricular arrhythmic burdens similar to those of the general population ,23 and tEchocardiography is fundamental for the investigation of structural heart disease. With this exam, we can evaluate the heart’s global and regional function, both in systole and diastole, as well as wall motion abnormalities suggesting ischemic heart disease. It is also used to assess chamber size, valvular defects, and the presence of structural abnormalities suggestive of cardiomyopathy.Echocardiography is the basal screening modality for the characterization of congenital coronary artery anomalies, which are one of the leading causes of ischemia-induced VA and SCD in the athlete. Zeppilli et al.  demonstrHowever, echocardiography shows significant limitations in the evaluation of athletes with PVBs. It is unable to detect some conditions potentially associated with SCD during sports, with an apparently normal heart as the first presentation. Consequently, second-level diagnostic tools are needed for further evaluation.Cardiovascular magnetic resonance imaging (MRI) can be of great value in the differential diagnosis between various cardiomyopathies, including hypertrophic cardiomyopathy (HCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), left ventricle noncompaction cardiomyopathy (LVNC), and athlete’s heart [’s heart . This im’s heart .Cardiac MRI provides three-dimensional tomographic scans with high spatial and temporal resolution, allowing a clear delineation of endocardial and epicardial borders. Cardiac MRI can inspect the entire LV for abnormalities, including global/focal hypertrophy and wall motion disturbances. Late gadolinium-enhanced images (LGE) identify replacement myocardial fibrosis. Finally, the evaluation of pre-contrast (native) T1, post-contrast T1 mapping, and extracellular volume images (ECV) can identify diffuse myocardial edema. In particular, cardiac MRI is not useful in the definite diagnosis of early-stage cardiomyopathies, and some cardiac diseases, such as hypertrophic cardiomyopathy (HCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), and initial forms of myocarditis with arrhythmic phenotype, can be misdiagnosed as athlete’s heart .In a recent paper, we found that cardiac non-invasive imaging showed late gadolinium enhancement in only 30% of patients, with no difference between athletes and non-athletes . FurtherElectroanatomic mapping of ventricular substrate may help to identify concealed myocardial diseases in competitive athletes presenting with recent-onset VA and an apparently normal heart [al heart ,29. It h3D-EAM-guided EMB allowed histopathological diagnosis in 50% of athletes showing abnormal low voltage areas . SpecifiIn recent years, the advent of the Next Generation Sequencing (NGS) has made genetic testing in cardiology a useful diagnostic tool for detecting patients at high risk of SCD. Different sequencing panels have been developed to screen the main genes responsible for inherited cardiac conditions (ICC). In particular, more than 60 genes, including sarcomere and sarcomere-related genes, have been associated with inherited cardiomyopathies, but only a few of them are considered clinically actionable ,33 and rIt is important to highlight that, due to the limit in determining the clinical relevance of a variant and the variable yield of screening depending on the phenotype, genetic testing is highly recommended only in patients with an established clinical diagnosis or a strong suspicion of familial cardiomyopathy.This issue becomes even more complicated in professional athletes, in whom cardiac remodeling can be a physiological consequence of sports activity. In these cases, it is crucial to carefully assess all the clinical steps, as previously stated, and to undertake a pre-test genetic counseling, in order to collect the family history of the proband and to explain the limitations of the test. The identification of a pathogenic (P) or likely pathogenic (LP) variant in “definitive” genes can provide several benefits to the patients’ management by (1) improving diagnostic accuracy, (2) identifying the molecular etiology of disease, (3) improving the prognosis, and (4) supporting therapeutic choices. Furthermore, cascade screening is always recommended, especially in asymptomatic young patients, to select family members at high risk .Extensive diagnostic work-up, including first-, second-, and third-level diagnostic tools, could be very helpful in the diagnosis of cardiomyopathies in apparently healthy young athletes with ventricular arrhythmic phenotype, no structural cardiac abnormalities, and normal resting ECG. We suggest this extensive diagnostic work-up including CMR, 3D-EAM mapping, 3D-EAM-guided EMB, and genetic testing in the characterization of the arrhythmogenic substrate in young athletes with complex VA.


To understand the advantages and disadvantages of imaging techniques in identifying aetiology and mechanisms of mitral and aortic regurgitation.To understand the key echocardiographic methods of quantifying severity of mitral regurgitation (MR) and aortic regurgitation (AR), and their advantages and limitations.To be aware of the relative advantages and disadvantages of cardiac magnetic resonance in quantifying severity of MR and AR.Valvular heart disease (VHD) affects 1 in 50 of the general population and 1 in 3 of the over 65s, and is associated with increased morbidity and premature mortality.The severity of regurgitation through the MV and AV is governed by the Gorlin formula, which states that flow through an orifice varies by the square root of the pressure gradient across the orifice, the duration of flow and a discharge coefficient.Access to echocardiography is critical for diagnosis of valve disease.Once regurgitation has been detected, the key step is to determine the cause. This is particularly the case in the patient with MR, as the natural history, classification of severity and treatment choices all depend on whether regurgitation is ‘primary’, due to a fault in the valve apparatus, or ‘secondary’, due to disease of the LV . Most caIdentifying structural abnormalities leading to MR requires imaging of the leaflets, chordae, papillary muscles and annulus at high temporal and spatial resolution. 2D TTE is the main method to define leaflet thickening , leaflet mobility  or restricted), degree of leaflet coaptation, as well as extent and location of calcification . 3D TTE is of incremental value in identifying the lesion, leaflet involved and the specific valve segments affected, with an accuracy similar to multiplane 2D TOE.Visualisation of primary and secondary chordae requires good quality 2D TTE imaging in a modified apical two-chamber view to define location, length and thickening, with the transgastric long-axis view on 2D TOE also useful to perform these measurements and define interpapillary muscle distance. 3D TOE can improve on these measures but is mainly used to measure annulus size and detect annular remodelling that can be specific to a disease process, for example, to myxomatous or ischaemic MR.In the anatomical assessment of AR, 2D (and to some extent 3D) TTE remain the first step in the assessment of leaflet mobility, thickening and calcification required to determine mechanism and aetiology. When TTE provides inadequate visualisation of structures, or when high spatial and temporal resolution imaging is required to assess suitability for intervention, for example, with highly eccentric jets and when repair is considered, 2D and 3D TOEs provide incremental accuracy.When quantifying severity of a regurgitant lesion, it is important to consider the appearance of (1) the valve morphology and (2) the size, shape and function of the ventricle. For example, if the mitral valve leaflets are flail, it is highly likely there is severe regurgitation but if you do not think it is severe, make sure you have done all you can to be certain. Likewise, if the LV is dilated with spherical remodelling, if you are going to call any AR moderate, make sure you have done all you can to be certain.Good quality TTE with Doppler can provide all the core information required for evaluation of regurgitation severity but requires an experienced, motivated echocardiographer able to perform the necessary integrated assessment of multiple qualitative and quantitative parameters, in the knowledge that single measures are subject to variabilityLVOT–SVol MV) is subject to large interobserver variability.The assessment of AR severity with echocardiography is more challenging than that of MR. On TTE, the AR jet is seen with the highest resolution in the parasternal long-axis view, which can be used to measure vena contracta and jet width relative to the left ventricular outflow tract. In this view however, the PISA in AR is perpendicular to the angle of insonation (and therefore unreliable), and in the apical window it is in the far field and is often too small to measure reliably. In addition, the pulse Doppler method used to calculate stroke volumes across the mitral valve and left ventricular outflow tract  and flow quantification (for CMR) to identify the cause and mechanism of regurgitation, severity, and haemodynamic impact on ventricular and atrial remodelling, as well as the effect on pulmonary pressure. Transthoracic echocardiography remains the workhorse but requires careful integration of multiple parameters that vary in sensitivity and specificity, particularly when the aetiology is ischaemic, and the skill to use 3D regularly. Where data are conflicting, imaging is suboptimal or when intervention is under consideration, either transoesophageal echocardiography or CMR can be used, with 3D an integral component for complete TOE assessment.All imaging assessments in mitral or aortic regurgitation should include a statement on the quality of the scan, the size of the patient  and haemodynamic status .Transthoracic echocardiography remains the first-line imaging modality to determine cause and mechanism of regurgitation, quantify severity using multiple parameters, and impact of regurgitation on atrial and ventricular size and function.In cases where the above information is incomplete or is contradictory, transoesophageal echocardiography using 2D and 3D is the usual next step for detailed assessment of valve anatomy and helps with quantification.In those cases where regurgitation severity and the effects of regurgitation on chamber size and function are the primary source of concern, cardiovascular magnetic resonance (CMR) may be a better, less invasive alternative.Grading of severity by echocardiography and CMR differ, with thresholds for intervention lower using CMR, although there is a lack of data using these to guide intervention.Multislice CT is currently used mainly to image specific subsets of patients before intervention, such as those for percutaneous valve intervention and those requiring concomitant aortic surgery.Education in Heart articles are accredited for CME by various providers. To answer the accompanying multiple choice questions (MCQs) and obtain your credits, click on the 'Take the Test' link on the online version of the article. The MCQs are hosted on BMJ Learning. All users must complete a one-time registration on BMJ Learning and subsequently log in on every visit using their username and password to access modules and their CME record. Accreditation is only valid for 2 years from the date of publication. Printable CME certificates are available to users that achieve the minimum pass mark.10.1136/heartjnl-2019-316216.supp1Supplementary data


It is thought that heart failure (HF) patients may benefit from the evaluation of mechanical (dys)synchrony, and an independent inverse relationship between myocardial perfusion and ventricular synchrony has been suggested. We explore the relationship between quantitative myocardial perfusion and synchrony parameters when accounting for the presence and extent of fixed perfusion defects in patients with chronic HF.We studied 98 patients with chronic HF who underwent rest and stress Nitrogen-13 ammonia PET. Multivariate analyses of covariance were performed to determine relevant predictors of synchrony .p < .01), among other considered predictors including: age, sex, body mass index, smoking, diabetes mellitus, dyslipidemia, hypertension, rest myocardial blood flow (MBF), and myocardial perfusion reserve (MPR). Results were similar when considering stress MBF instead of MPR.In our population, there were 43 (44%) women and 55 men with a mean age of 71 ± 9.6 years. The SRS was the strongest independent predictor of mechanical synchrony variables , constitute a significant independent predictor of ventricular mechanical synchrony in patients with chronic HF.The online version of this article (10.1007/s12350-018-01507-9) contains supplementary material, which is available to authorized users. Heart failure (HF) represents a major issue with an estimate of 26 million patients worldwide.3HF research may benefit from techniques that provide evaluation of ventricular mechanical synchrony as well as from the evaluation of its determinants. On the one hand, because dyssynchrony may represent an earlier marker of a deteriorating ventricular function that conveys prognostic value for risk stratification,Quantitative PET myocardial perfusion imaging has robustly demonstrated its value in the evaluation of suspected ischemia in patients with and without history of cardiovascular events,14Notably, the link between quantitative PET myocardial perfusion and ventricular mechanical synchrony when considering the potential confounding influence of fixed perfusion defects, indicators of previous myocardial infarction [MI] and scarring, has not been investigated in HF patients. Hence, the present study aimed to explore the relationship between quantitative PET myocardial perfusion and peak stress ventricular mechanical synchrony when accounting for the presence and extent of pre-existing fixed perfusion defects in patients with chronic HF.We retrospectively analyzed data from 98 patients with chronic HF referred for Nitrogen-13 ammonia PET/CT imaging for suspected myocardial ischemia and followed in the Northwest Clinics in Alkmaar, the Netherlands. Demographic and clinical characteristics including sex, age, body mass index (BMI), as well as cardiovascular risk factors including arterial hypertension (HTN), dyslipidemia, smoking status, type 2 diabetes mellitus (DM), history of previous myocardial infarction (MI), and baseline HF descriptors  were extracted from the electronic file system.All patients gave written informed consent for use of their anonymous data for scientific purposes. Besides the standard imaging protocol and clinical management, no additional measurements or actions affecting the patient were performed. The study was approved by the institutional research department and approval of the local ethical committee for the present study was not necessary since the study does not fall within the scope of the Dutch Medical Research Involving Human Subjects Act .Every patient underwent a two-phase (rest and adenosine stress) PET scan using Nitrogen-13 ammonia as the perfusion radiotracer. All image data were acquired in list mode on a Siemens Biograph-16 TruePoint PET/CT  with the TrueV option . This 3D system consists of a 16-slice CT and a PET scanner with four rings of lutetium oxyorthosilicate (LSO) detectors. Patients were instructed to fast overnight and to avoid the consumption of methylxanthine-, caffeine-containing beverages, or medications for 24 hours before the study. Image acquisition parameters and scanning protocol were previously described in detail.15Based on the dynamic subsets, left ventricular contours were assigned automatically using the SyngoMBF software  with minimal observer intervention when appropriate. With a previously described 2-compartment kinetic model for Nitrogen-13 ammonia, stress and rest flow values in mL/g/minute were computed for each sample on the polar map through the resulting time-activity curves for global quantification.Pre-existing fixed perfusion defects were evaluated through semi-quantitative image analysis using the standard American Heart Association 17-segment modelECG-gated hyperemic stress images were analyzed with the QGS software package .21Briefly, BW conveys the time range that includes 95% of elements in the phase distribution, while SD corresponds to the standard deviation of the phase distribution. Thereon, E reflects the uniformity of the onset and progression of wall motion, expressed as a percentage. These measurements are understood as inversely proportional to ventricular synchrony and uniformity of contraction.All continuous variables were described as means ± SD, while categorical variables were expressed as frequencies and percentages. Univariate analyses were conducted through independent ANOVAs in order to evaluate trend differences in ventricular mechanical synchrony variables  across binned tertiles of quantitative PET perfusion variables (MPR and sMBF). Follow-up pairwise comparisons were corrected using the Bonferroni post hoc test.in the first model, with the addition of SRS in the second model, as independent  variables, while BW, SD, and E were simultaneously input as the dependent  variables. Pearson’s correlation coefficient was used to examine for and discard collinearity of predictors. Independent significance of the evaluated predictors was assessed through Pillai’s trace criterion with an approximate F statistic.p values for which < .05 was considered statistically significant. Multivariate analyses were repeated utilizing sMBF (instead of MPR) as the quantitative perfusion variable. Complementarily, all analyses were repeated in a per-vessel territory analysis.Prior evaluation of the biserial correlations between BW, SD, and E (utilizing Pearson’s correlation coefficient), two sequential (stepwise) multivariate analyses of covariance (MANCOVA) were performed including sex, age, BMI, HTN, dyslipidemia, DM, smoking status, rMBF, and MPR All statistical analyses were performed in SPSS .Baseline characteristics of the study sample of patients with chronic HF are shown in Table Mean quantitative PET MPR was below the generally applied pathological threshold of 2.0.22η2 = 0.17 vs 0.08, SDη2 = 0.15 vs 0.07, and Eη2 = 0.10 vs 0.08). Significant pairwise differences are graphically depicted in Figure There were significant differences in peak stress ventricular mechanical synchrony parameters across myocardial perfusion variable tertiles documenting a significant inversely proportional perfusion-synchrony relationship. Notably, these differences were more pronounced across tertiles of sMBF than of MPR according to the calculated effect sizes  is an independent predictor of stress ventricular mechanical synchrony accounting for a medium effect size (η2= 0.229), while dyslipidemia only demonstrated a trend towards significance and a rather discrete effect  and rMBF did not document a significant effect (p = .17). Further, when SRS was included into Model 2, MPR was no longer a significant predictor of the outcome variables. Conversely, SRS was found to be the strongest independent predictor of mechanical synchrony variables demonstrating a considerably higher absolute effect size  than the other considered predictors.A comprehensive pictorial representation of the MANCOVA results for all models is shown in Figure Model 1, dyslipidemia only demonstrated a trend towards a significant effect (p = .06), while sMBF (p = .01) was a significant predictor of stress mechanical synchrony variables. Conversely, SRS overshadowed (once again) sMBF as the strongest independent predictor  in Model 2. Consistently, rMBF did not demonstrate a significant effect in the models . Figure When the analyses were repeated considering sMBF as the quantitative myocardial perfusion variable, results were similar. In p = .06 and p = .07, respectively), and (2) rest MBF demonstrated a significant effect in Model 1 that included MPR as the perfusion parameter.The complementary results considering the perfusion and synchrony estimates at the coronary vessel-territory level demonstrated a similar behavior with SRS accounting for the predominating effect in the models. Two particular differences found in the supplementary analysis were (1) once SRS was included in the model, stress MBF and MPR showed a marginal trend towards significance in contrast with the global analysis .Based on our results, it became clear that even though the exploratory unadjusted comparisons of synchrony parameters  across worsening MPR and sMBF tertiles showed significant differences, the adjusted (multivariate) analysis demonstrated that SRS conveys the strongest independent association with the outcome variables, overshadowing the effect of quantitative perfusion parameters. Although this analysis may raise the uncertainty of whether such effect originates from a tight relationship between SRS and quantitative perfusion variables , the exploration of the SRS-MPR and SRS-sMBF correlations informed that collinearity did not hinder our analysis (p = .06), contrary to the multivariate results considering MPR (p = .23). We believe that these effects become readily patent in the pictorial representation of the MACONVA models’ results. The comparative weight of the correlation lines underscores the relevance of perfusion parameters while also demonstrating the major role of fixed perfusion defects. Of note, even though rMBF was considered in the reported analyses, as it may be the case that this parameter is found affected in the particular set of patients with HF, the univariate and multivariate estimates of effect did not support a major influence of this perfusion parameter on mechanical synchrony.An interesting finding in the univariate analysis was that ventricular synchrony parameters were considerably more sensitive to worsening values of sMBF than those of MPR. This collateral finding partially supports the perception suggested in previous reports of the superiority of sMBF as an absolute PET myocardial perfusion parameter.Patients with HF show lower quantitative myocardial perfusion estimatesA particular feature of our report is the incorporation and characterization of effect sizes in our interpretation of results. In fact, both the pictorial and numerical effect sizes provided by the multivariate analyses attest the comparative relevance of quantitative perfusion and of the presence/extent of fixed defects by demonstrating that although SRS was clearly the strongest independent predictor of synchrony (with a large effect), the magnitude of the effect sizes of MPR and sMBF were the second largest overall and mostly fall in the category of medium effects.Fixed perfusion defects can be caused by a previous MI, but in our sample only 40% of patients had a medical history of MI. Still, all patients had the associated diagnosis of chronic HF and were referred to PET due to suspected (chronic) ischemia. Although myocardial scarring after major events such as MI is generally considered in the horizon of HF of suspected ischemic origin, it is also considered that physiopathological levels of chronic ischemia (probably at the microvascular level) can negatively influence myocardial architecture and ultimately its function. Moreover, it is also understood that a discrete proportion of MI events can be overlooked due to atypical symptomatology such as in diabetic patients and expectedly, the prevalence of DM in our sample was substantial. Consequently, we aimed to account for existing fixed perfusion defects rather than only on the history of previous MI. This means that, while we do not account for the particular origin or composition of the documented fixed perfusion defects, one can still argue that such non-reversible defects seem to be by far more influential on the integral axis of mechanical synchrony than the quantitative myocardial perfusion status obtained in absolute terms with PET. In fact, this notion was sustained when the analysis was repeated at a per-vessel territory  level. Of course, we still believe that a regional analysis is relevant for the particular exploration of suspected localized ischemia and in the characterization of potentially viable residual tissue.Nitrogen-13 ammonia PET allows for the evaluation of absolute myocardial perfusion and mechanical synchrony at real time-peak hyperemic stress, which confers an advantage over traditional post-stress SPECT acquisitions. Nevertheless, as non-invasive imaging advances the refinement of its implementations, we believe that multimodality imaging (considering other powerful techniques such as CMR) will benefit patient classification optimization by providing complementary information that, in the case of HF and its management, is currently incomplete.Finally, it is worth considering that either if mechanical synchrony is viewed as a marker of disease,The present study carries all the limitations of a retrospective analysis. Furthermore, we have mentioned that the mechanistic nature of the fixed perfusion defects was not accounted for in every case and it is possible that a small proportion of artifacts may have factored into the SRS estimates. However, this may represent a minor issue given the superior quality of PET imaging when compared with traditional SPECT. Another limitation may be found in the sample size and constitution, it could be possible that the significance of perfusion estimates as determinants of ventricular synchrony was attenuated by the number of subjects included and by a mixture of possible etiologies. Yet, this report studied patients with the commonality of clinically-classified chronic HF evaluated in our institution by a dedicated clinic. Moreover, in the case of this sample, patients were referred for PET imaging when there was doubt of whether an ischemic component was present beyond the assumed etiology. Finally, our results have included effect sizes for the studied relations and we exhort the reader to bear such estimates in mind given their stability against sample size differences.The existence and extent of fixed perfusion defects, but not the quantitative PET myocardial perfusion parameters (sMBF and MPR), constitute a significant independent predictor of resulting peak-stress ventricular mechanical synchrony in patients with chronic HF.Among patients with chronic HF referred to Nitrogen-13 ammonia PET/CT imaging, the presence and extent of pre-existing fixed perfusion defects, but not quantitative myocardial perfusion parameters, constitute a significant independent determinant of resulting peak-stress ventricular mechanical synchrony.Supplementary material 1 (DOCX 24 kb)Supplementary material 2 (PPTX 320 kb)Below is the link to the electronic supplementary material.


The aim is to measure and analyze the wave amplitudes and time intervals of differential graphs of reconstructed impedance cardiography (RICG).180 adults with normal cardiac function between the ages of 18–78 were included in the study. Six mingled impedance changes on chest surface were simultaneously detected for each subject. The differential graphs of five impedance change components of RICG were obtained through waveform separation and software differentiation. The amplitudes of C, X, O, b waves and time intervals of Q‐b and Q‐C were measured and statistically analyzed.p < .01), while the Q‐C intervals of the female group were shorter than that of the male group (p < .01). Among five impedance change components, the wave amplitude of AO was larger than those of PL and PR (p < .01), and wave amplitudes of PL and PR were bigger than those of LV and RV (p < .01). Q‐C intervals of LV and RV were longer than those of AO, PL and PR (p < .01), while the Q‐b intervals of LV and RV were shorter than the Q‐C intervals of AO, PL, and PR.The amplitudes of C and X waves in PL, PR, AO, and that of C, O, b waves in LV and RV, all decrease as age increases. Wave amplitudes of the female group were bigger than those of the male group (The differential graphs of RICG could reflect indirectly the physiological activities and pathological changes of the heart and of the large blood vessels in thorax. It includes the affluent information concerning the physiological activity and pathological changes in the heart and of the large blood vessels in thorax. Now, the ICG is generally measured by means of Kubicek's method , left lung vasculature (PL), right lung vasculature (PR), left ventricle (LV), and right ventricle (RV) from six mingled impedance changes measured on the chest surface through waveform separation  for four consecutive cardiac cycles by artificial operation, correct the basic lines of thoracic mixed impedance changes, separate five impedance change components of AO, PL, PR, LV, and RV of RICG from six mingled impedance changes measured on chest surface through establishing and solving the thoracic impedance equations, make the differential treatment for each component, measure the waveform parameters of each differential graph, display, and print the waveform graphs and parameters.Our research group developed the measurement instrument used in the present study. As shown in Figure 2.1.3Zs1, ΔZs2, ΔZs3, ΔZs4, ΔZs5, and ΔZs6) and basal impedances  of all six leads, as well as the ECG and PCG, were detected and displayed simultaneously.Height, weight, chest circumference, blood pressure, as well as name, sex, age, and other relevant information were entered into the instrument prior to the measurement. The chest circumference was measured on the chest surface at the xiphoid level. A supine position was adopted for the measurement. The electrodes for sensing the ECG were attached to the right upper arm and left and right lower legs . The transducer for sensing the PCG was placed at the cardiac apex on chest surface. The subject was asked to hold his/her breath for the duration of recording the waveform graphs. Thoracic mixed impedance changes , middle (45–59 year), and elder (60–78 year). 30 males and 30 females were included in each age group.2.3t test. If p‐value < .05, there was a significant difference between two averages.Statistical analysis was performed by means of SPSS12.0 software. The measurement results of C, X, O, b wave amplitudes, as well as the Q‐b and Q‐C time intervals, were all expressed with the average value and standard deviation. The difference level between two averages was judged by 3The waveform of PL, PR, and AO was upward in systolic phase, but that of LV and RV was downward. This shows that the waveforms of both were in opposite phases.p < .05), except for X wave of PR (p > .40). The waveform amplitudes of the female group were larger than those of the male group, p < .05.The waveform amplitudes of C and X waves of various components, as well as that of b and O waves of LV and RV, all decreased as age increased Tables , and 3, p < .01 .C wave amplitude of AO is related to the contractile force and stroke volume of the left ventricle. If C wave amplitude is larger, it suggests that the myocardial contractility of the subject is stronger and that stroke volume is larger. Thus, C wave amplitude of AO is an important parameter reflecting the contractile function of the left ventricle. The contractile function of left ventricle generally decreases as age increases. The C wave amplitude of AO also decreases as age increases see Table, and theIn addition, the C wave amplitudes of 196 patients were also measured. The C wave amplitude of 36 patients with coronary heart disease (first group) was 1.145 ± 0.360 Ω/s, that of 35 patients with hypertension (second group) is 1.216 ± 0.441 Ω/s, that of 72 patients with cardiac insufficiency (third group) is 0.760 ± 0.300 Ω/s, and that of 53 patients with hyperthyroidism (fourth group) is 3.029 ± 1.139 Ω/s. These data show that the contractile function of patients in the first, second, and third groups is remarkably decreased, while that of the fourth group is abnormally strengthened. Thus, C wave amplitude of AO can reflect the pathological changes of patients.2. The X wave is caused by the recovery of aortal volume, and it reflects indirectly the speed change of aortal recovery. The mean of X wave amplitude in 180 normal adults was −0.882 ± 0.294 Ω/s (see Table The X wave of AO is a negative wave after the C wave and is in the later stage of left ventricle contraction. Its negative peak point X is in the vicinity of S4.2p < .001).Figure p < .001).There is also a negative X wave in PL and PR, and it is approximately in time phase of the X wave of AO. The X waves of PL and PR are a result of volume recovery of the pulmonary arteries and reflect indirectly the speed change of volume recovery of pulmonary arteries. The average X wave amplitudes of PL and PR are 0.413 ± 0.138 Ω/s and 0.299 ± 0.111 Ω/s, respectively , because b wave peak point of LV and RV is in front of C wave peak point of AO, PL, and PR in time phase. On the basis of physiological principles and resistance law, if the ventricle volume diminishes, its impedance should increase as the ventricle ejects the blood. However, the positive b wave in Figure As shown in Figure p < .001. C wave amplitudes of LV and RV are −0.545 ± 0.194 Ω/s and −0.455 ± 0.168 Ω/s in 180 normal adults, respectively . The O wave amplitudes in RV and LV decrease as the age increases, and there is a significant difference between the measured data of the younger and elder groups (p < .01). O wave amplitudes of RV and LV for patients with cardiac insufficiency are remarkably decreased. For instance, the O wave amplitudes of RV and LV for 72 patients with cardiac insufficiency are −0.130 ± 0.090 Ω/s and −0.109 ± 0.105 Ω/s, respectively, and they are smaller than that of the adults with normal function (see Table. p < .001).The O wave of RV and LV appears after S4.42 occurs and the ventricular volume is minimal. In Figure 2. This means that the time phase of the negative peak point of the impedance change components of LV and RV corresponds with that of minimal ventricular volume  is smaller , in which, the square root formula for measuring the cardiac output had been published in Med. Phys (Kuang et al., 5The differential graphs of each impedance change component of RICG for 180 normal adults were measured in this paper, and statistical analysis was performed according to the different age and sex groups. C and X wave amplitudes of various components all decrease as age increases. The wave amplitudes of the male group were smaller than those of the female group, while the Q‐C interval of the male group was longer than that of the female group. C wave amplitude of AO was largest, that of PL and PR was next, and that of LV and RV was smallest. The differential waveform graphs of various impedance change components of RICG may reflect indirectly the physiological activity and pathological changes of the heart and of the large blood vessels in thorax.


Takotsubo syndrome (TTS) is a complex and still poorly recognized heart disease with a wide spectrum of possible clinical presentations. Despite its reversibility, it is associated with serious adverse in-hospital events and high complication rates during follow-up. Multimodality imaging is helpful for establishing the diagnosis, guiding therapy, and stratifying prognosis of TTS patients in both the acute and post-acute phase. Echocardiography plays a key role, particularly in the acute care setting, allowing for the assessment of left ventricular (LV) systolic and diastolic function and the identification of the typical apical-midventricular ballooning pattern, as well as the circumferential pattern of wall motion abnormalities. It is also useful in the early detection of complications  and monitoring of systolic function recovery. Left ventriculography allows the evaluation of LV function and morphology, identifying the typical TTS patterns when echocardiography is not available or wall motion abnormalities cannot be properly assessed with ultrasound. Cardiac magnetic resonance provides a more comprehensive depiction of cardiac morphology and function and tissue characterization and offers additional value to other imaging modalities for differential diagnosis . Coronary computed tomography angiography has a substantial role in the diagnostic workup of patients with acute chest pain and a doubtful TTS diagnosis to rule out other medical conditions. It can be considered as a non-invasive appropriate alternative to coronary angiography in several clinical scenarios. Although the role of nuclear imaging in TTS has not yet been well established, the combination of perfusion and metabolic imaging may provide useful information on myocardial function in both the acute and post-acutephase.The online version of this article (10.1007/s12574-020-00480-y) contains supplementary material, which is available to authorized users. Takotsubo syndrome (TTS), also known as takotsubo cardiomyopathy, stress-induced cardiomyopathy, or apical ballooning syndrome, is an acute and transient heart failure syndrome originally reported by Dr Sato in 1991 in a Japanese textbook and by Pavin et al. in Europe in 1997 . Chest pRecently, a classification of TTS according to the type of triggering event has been proposed Table  4].Tab.Tab4].Electrocardiographic abnormalities (ST-T elevation in the majority of cases) resembling those detectable in acute coronary syndromes are common, as well as increased biomarkers reflecting myocyte damage despite unobstructed coronary arteries. For this reason, TTS has been classified as ‘myocardial injury’ in the last universal definition of myocardial infarction and categorized as myocardial infarction with non-obstructive coronary arteries (MINOCA) . The patOwing to the wide spectrum of clinical presentations, diagnosis of TTS is often challenging. However, early recognition of this syndrome is key to adopting an appropriate therapy. Multimodality imaging is helpful in reinforcing the clinical suspicion of TTS in the early phase, allowing confirmation of the diagnosis, even retrospectively, after ruling out other clinical entities that should be considered in the differential diagnosis. The aim of this consensus document is to discuss and review the utility of multimodality imaging, including left ventriculography, echocardiography, computed tomography (CT), magnetic resonance imaging, and nuclear imaging, in the diagnostic workup of TTS.Several diagnostic criteria for TTS have been proposed, including those issued by the Mayo Clinic, the Japanese guidelines , the TakAlthough initial studies suggested that prognosis of TTS is benign  , 14, recCoronary arteries are generally normal or near-normal in TTS. Although echocardiography is the first-line imaging modality in patients with suspicion of TTS, assessment of coronary anatomy is crucial in TTS diagnostic workup to rule out alternative diagnoses. As recommended by current guidelines on acute coronary syndromes (ACS), cardiac catheterization should be performed in all patients with acute cardiac ischaemia and ST-segment elevation or in patients without ST-segment elevation according to the individual risk profile, especially for patients with a low-intermediate probability of TTS , 17–21.Coronary anatomy should be carefully evaluated using multiple angiographic views, ensuring that all lesions have been assessed in at least two orthogonal projections. Obstructive atherosclerotic plaques can be observed in about 1 in 10 of TTS patients , 18. It The diagnosis of TTS can also be established during cardiac catheterization through LV opacification. Biplane left ventriculography in the right and left anterior oblique projections allows for the assessment of nine LV segments and differentiation of TTS from anterior ST-elevation myocardial infarction (STEMI) in the majority of cases , 22. TheAlthough not specific for TTS, coronary anatomical variants, including myocardial bridging or long and tortuous arteries, are common findings on CA . LikewisKey pointsCA should be performed in ACS according to guidelines in all STEMI and intermediate to very high-risk non-STEMI presentations.Obstructive coronary stenosis does not represent an absolute exclusion criteria for TTS, but if coronary artery disease is present, it should not be sufficient to explain the observed regional WMAs.Biplane left ventriculography allows assessment of LV function and morphology in TTS.In selected cases, intravascular imaging and functional testing to rule out vasospasm may be helpful for the differential diagnosis.Transthoracic echocardiography (TTE) is the first-line imaging modality for the evaluation of patients with TTS . If suspFirstly, TTE may help to detect the distribution of WMAs and determine the morphologic anatomical variant , 34.Videos S1 and S2) .In clinical practice, the most important application of contrast echocardiography is LV cavity opacification for the detection of WMAs  Fig. 1010 and thOf note, myocardial contrast echocardiography performed within 24 h after TTS onset revealed reversible perfusion defects in involved segments, which improved faster than WMAs .3D echocardiography is a useful method to quantify chamber measurements with higher accuracy and reproducibility than 2D echocardiography  Figs. 11 and 12.These ‘advanced’ echocardiography techniques, including strain imaging, coronary flow assessment, contrast echocardiography, and 3D echocardiography, are emerging and hold promise in improving our understanding of the pathophysiology underlying TTS. However, it should be acknowledged that the clinical utility of these techniques has not been fully established and physicians should not make clinical decisions solely on this basis.Key pointsLV mechanics are profoundly and transiently impaired in TTS, in a pattern that differs from AMI.Whilst EF and WMAs resolve in TTS, some subtle wall strain abnormalities can persist.The coronary microcirculation is transiently compromised in TTS, but its physiological role is still unclear.Contrast echocardiography should be used in patients with poor acoustic window to better define WMAs and the presence of intraventricular thrombus.Compared to 2D echocardiography, 3D echocardiography enables more accurate assessment of regional WMAs and may be a useful tool to better detect and assess RV involvement, even in the acute care setting.As an additional prognostic tool, RV strain could be useful in assessing the extent of RV involvement.Although echocardiography and left ventriculography have mainly been used to diagnose LV WMAs in patients with TTS, CMR plays an important role in the comprehensive assessment of the functional and structural changes that occur in patients with clinical suspicion of TTS . CMR repVideos S7–S10). These planes enable precise visualization of the contractile dysfunction pattern  including short-axis plane covering the entire left ventricle and three long-axis planes , should be systematically performed during CMR  , 97.Recently, CMR-feature tracking (FT) has been introduced as a new method to quantify regional LV deformation similarly to speckle tracking echocardiography, providing a more reliable and accurate assessment of (dys-)synchrony as well as rotational parameters . In TTS CMR has the advantage of enabling multiparametric myocardial tissue characterization. Specifically, CMR can rule out ischaemic myocardial injury or myocarditis using late gadolinium-enhancement (LGE) imaging Fig.  96]. Wh. Wh96]. Although patchy areas of LGE can be detected in TTS patients using low SI thresholds, the transient nature of this myocardial injury, which generally disappears within few days or weeks, as well as the absence of LGE at high SI thresholds are distinctive patterns that differentiate TTS from AMI and myocarditis. It has been suggested that an increase of extracellular matrix rich in collagen-1, as a finding of transient fibrosis, might be accountable for the LGE observed in TTS .In conclusion, these evidences suggest that the absence of LGE at high SI thresholds is still a diagnostic criterion for TTS, keeping in mind that small amounts of reversible patchy areas of LGE can be transiently detected using low SI thresholds and do not represent an absolute exclusion criterion during diagnostic work-up.The impact of LGE on clinical outcomes in TTS remains controversial. Although some authors have reported worse clinical prognosis in patients with LGE, no differences in clinical outcomes between patients with and without LGE have been found in a multicentre prospective registry , 103.T1 mapping techniques, where T1 time of injured myocardium is quantitatively and more objectively assessed, can be useful to detect very subtle areas of damage in patients with TTS Fig. . AssessmUp to date, cut-off values of native T1 mapping have not been established in this setting. This technique is still considered a research tool and its impact on clinical practice and outcome needs to be further investigated.in vivo the acuity, extent, and severity of myocardial stunning in TTS [Myocardial oedema is another distinctive feature of TTS. The exact pathophysiological mechanisms underlying the development of myocardial oedema in TTS is still unclear. Increased LV wall stress and/or transient ischaemia seem to be responsible for inflammatory injury of cell membrane, with subsequent transmembranous leakage of water and large molecules leading to extracellular oedema. It can be detected by T2 weighted black blood imaging (T2BB) or newer mapping techniques (i.e. native T1 mapping and T2 mapping). T2BB allows to recognize oedema due to the suppression of both fat and flowing blood signal. In T2BB imaging, a triple inversion recovery fast-spin echo sequence is used in contiguous short-axis views of the left ventricle. A ratio of mean SI of the myocardium compared with that of the skeletal muscle (T2 SI ratio) ≥1.9 is generally accepted to define oedema. Myocardial oedema is generally localized in segments with abnormal contraction (a-hypokinesis) showing a diffuse or transmural distribution. Its acute extent also correlates with acute release of both catecholamines and N-terminal pro-B-type natriuretic peptide . It is ag in TTS  . Additionally, CMR is recommended in case of incomplete recovery (persisting ECG changes and/or WMAs at echocardiography) and atypical presentation  to assess tissue characterization and definitively corroborate TTS diagnosis.Key pointsCMR can visualize the entire spectrum of functional and structural changes that occur in patients with TTS.typical regional WMAs ;presence of reversible tissue injury (oedema);CMR provides additional value to other imaging modalities for differential diagnosis , pathophysiological insights, and detection of complications (e.g. LV thrombi) in TTS.In the acute phase, CMR is recommended in doubtful TTS cases, especially if diagnosis of another type of MINOCA (e.g. myocarditis) requires a different therapeutic approach.In the post-acute phase, CMR is mandatory in all patients within 2 months, especially in case of persisting ECG abnormalities and/or regional WMAs at echocardiography, in order to definitively confirm the diagnosis of TTS.absence of irreversible tissue injury (LGE) when SI thresholds of 5 standard deviations are used.CMR diagnostic criteria for TTS include the combination of:Technological developments over recent years have emphasized the role of coronary computed tomography angiography (CCTA) in the evaluation of patients with suspected TTS .An advantage of both CCTA and CMR is the ability to evaluate the heart in any potential plane, overcoming the limitations imposed by suboptimal acoustic windows on echocardiography . MoreoveCCTA has been proposed as a non-invasive alternative to CA in stable and pain-free patients with no ST-segment elevation at onset and convincing clinical  and echocardiographic  findings consistent with TTS. This approach could be advantageous, particularly in patients with delayed presentation (>48 h after chest pain onset) or when CA is not available on site .Cardiac CT, beyond coronary artery disease, allows assessment of LV function and WMAs. Nowadays, cardiac CT also provides myocardial characterization with late iodine enhancement imaging comparable with that obtained from CMR .Owing to multiplanar imaging , 116 thaUp to date there is no evidence for delaying invasive CA in patients with ongoing acute chest pain and acute ECG changes. In such a clinical scenario, patients should be managed according to current guidelines for STEMI or ACS until culprit coronary artery disease has been ruled out , 21.in stable patients with low suspicion of ACS;in patients with suspected TTS recurrence;in other conditions generally associated with TTS such as critical illnesses .CCTA may be chosen instead of CA:Moreover, CCTA can be considered as a non-invasive valuable alternative in life-threatening conditions where CA is highly likely to cause complications .Key pointsThe main indication for CCTA in TTS patients relates to the assessment of the epicardial coronary arteries and the ruling out of coronary artery disease.Cardiac CT also plays an important role in the diagnostic workup of patients with acute chest pain and doubtful TTS diagnosis to exclude other conditions such as pulmonary embolism and aortic dissection.Stable patients with low suspicion of ACS;Patients with a history of TTS and suspected recurrence;Critical clinical conditions usually associated with TTS  or where CA is highly likely to cause complications .CCTA may be chosen instead of CA in some peculiar situations:Although the role of nuclear imaging in TTS has not yet been well established in clinical practice, nuclear imaging can provide assessments of myocardial perfusion and metabolic activity, improving our understanding of the pathophysiology of TTS and potentially aiding diagnosis.123I-beta-methy-iodophenyl pentadecanoic acid (123I-BMIPP) single-photon emission computed tomography (SPECT) was more severely impaired than myocardial perfusion depicted by 201thallium scintigraphy in acute TTS patients [Some studies have reported that fatty acid metabolism depicted by patients , 120. Re123I metaiodobenzyl guanidine (MIBG) scintigraphy can assess myocardial sympathetic nerve terminal activity and detect adrenal and ectopic pheochromocytoma. Even in the subacute phase, the adrenergic hyperactivity observed in TTS results in decreased uptake and increased washout of 123I-MIBG from the heart  shows abnormal glucose metabolism alongside normal myocardial perfusion in TTS. Recently, some studies have been conducted at different phases during the TTS time course [Cardiac positron emission tomography (PET) using [e course , 124. InThe pathophysiology of TTS remains challenging and controversial. Several hypotheses have been proposed to explain this unique cardiac disorder , 125–128Key pointsAlthough the role of nuclear imaging in TTS has not yet been well established in clinical practice, myocardial perfusion and sympathetic nerve innervation can be assessed by SPECT and MIBG.123I-MIBG scintigraphy) may allow diagnosis of TTS in patients with delayed presentation, even within a few months of the suspected triggering episode.In the context of normalized LV wall motion, the delayed recovery of glucose metabolism (by FDG-PET) and sympathetic innervation (by Coronavirus disease 2019 (COVID-19) is a tremendous infectious disease firstly recognized in Wuhan, Hubei, China, that has spread throughout to other provinces in China and impetuously involved worldwide many countries causing a pandemic and a public health crisis of global proportions in 2020. Cardiovascular involvement, including acute coronary syndromes, myopericarditis, and pulmonary embolism, has been associated to the clinical course of a substantial proportion of patients affected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Myocardial injury emerged as an important predictor of worst outcome. Shi et al. report a prevalence of 19.7% of cardiac injury, defined by high blood levels of high-sensitivity troponin I, among 416 patients with confirmed diagnosis of SARS-CoV-2 . In thisAs with other coronaviruses, an intense systemic inflammatory response secondary to SARS-CoV-2 may produce demand ischaemia and/or possible coronary plaque disruption. Moreover, the detection of increased levels of multiple cytokines and chemokines in patients hospitalized in intensive care unit, suggests a direct myocardial damage as an alternative potential mechanism .Noteworthy septic status, hypoxaemia, and metabolic acidosis; complications often detected in SARS-CoV-2 patients, are established triggers for secondary TTS.Owing to the detection of myocardial inflammatory infiltrates documented in TTS patients, possible shared pathophysiological pathways in occurrence of myocardial dysfunction might be hypothesized in patients with SARS-CoV2 experiencing myocardial injury . TTS andImaging diagnostic tests are not routinely used in the emergency context of pandemic disease, the European Association of Cardiovascular Imaging recommend performing echocardiography at least in patients with laboratory or electrocardiographic signs of cardiac injury . The susAlthough the current challenging clinical scenario makes serial invasive and not invasive diagnostic testing difficult, whenever possible multimodality imaging should be performed in patients with SARS-CoV-2 and cardiac injury to distinguish type II myocardial infarction, myocarditis, and TTS, and to adopt the most appropriate therapeutic strategy.TTS is a complex clinical entity, with a wide spectrum of clinical presentations and varying levels of risk and haemodynamic stability, which requires tailored management strategies depending on the different scenarios. Multimodality imaging plays a key role in establishing the diagnosis, guiding therapy and stratifying prognosis in both the acute and post-acute phases of TTS Figs. ; Table 5Supplementary file1 (AVI 2875 kb)Supplementary file2 (AVI 2992 kb)Supplementary file3 (AVI 11181 kb)Supplementary file4 (MP4 1033 kb)Supplementary file5 (MP4 1028 kb)Supplementary file6 (MP4 1231 kb)Supplementary file7 (AVI 2389 kb)Supplementary file8 (AVI 18591 kb)Supplementary file9 (AVI 2065 kb)Supplementary file10 (AVI 2053 kb)Below is the link to the electronic supplementary material.


Non-cardiac surgery in a high-risk patient with severe mitral stenosis (MS) and severe pulmonary hypertension (PH) presents a significant anesthetic challenge. Guidelines recommend using advanced hemodynamic monitors for specific cardiovascular goals. The gold standard for intraoperative monitoring in these cases is the pulmonary artery catheter (PAC) and transesophageal echocardiography (TEE). This case discusses the successful management of a severe MS patient undergoing cystoprostatectomy using a minimally invasive cardiovascular monitor (MICM) incorporating several hemodynamic parameters.  The etiology of mitral stenosis (MS) includes rheumatic fever and degenerative mitral valve (MV) disease . Per AmeA 78-year-old man with squamous cell bladder carcinoma and high-grade prostate cancer presented for radical cystoprostatectomy, lymph node dissection, and ileal conduit. His medical history included hypertension (HTN), transient ischemic attack (TIA) x 1, and gastroesophageal reflux disease (GERD). In the preanesthesia testing clinic, a 2/6 diastolic murmur was auscultated. An externally performed transthoracic echocardiogram (TTE) showed an ejection fraction (EF) of 65%-70%, dilated right ventricle (RV) with normal systolic function, severely dilated left atrium, heavily calcified mitral annulus and valve leaflets, and severe MS . There was concurrent mild aortic stenosis , mild mitral regurgitation (MR), moderate tricuspid regurgitation (TR), and a right ventricular systolic pressure of 67 mmHg. Given his aggressive cancers and lack of symptoms, a decision was made to proceed to the operating room (OR) without further testing or intervention. Initial preoperative vitals were blood pressure (BP) 134/77 mmHg, heart rate (HR) 85 beats per minutes (bpm), and oxygen saturation (SpO2) 94% on room air. His electrocardiogram (EKG) showed sinus rhythm (SR) with first-degree atrioventricular (AV) block and right bundle branch block (RBBB).In the OR, standard American Society of Anesthesiologists (ASA) monitors were applied. Defibrillator pads were placed, and amiodarone was available. A pre-induction arterial line was placed with 1% subcutaneous lidocaine. After preoxygenation, the patient was induced and intubated with intravenous (IV) lidocaine 60 mg, etomidate 20 mg, succinylcholine 100 mg, and fentanyl 250 mcg in rapid succession. Esmolol was given for a total of 40 mg IV to maintain a heart rate less than 70 bpm during laryngoscopy. The patient was placed on a low tidal volume strategy 6 mL/kg, relatively high respiratory rate, an inspiratory to expiratory (I:E) ratio of 1:2, and a positive end-expiratory pressure (PEEP) of 4. The goal was to keep intrathoracic pressures low to avoid increasing RV afterload and pulmonary vascular resistance (PVR) and decreasing RV preload. An arterial blood gas was obtained 30 minutes after intubation to calibrate the end tidal CO2 to the pCO2 and check the pH. Norepinephrine and epinephrine bolus syringes and infusions were prepared. An eight-French (FR), 16-cm double lumen central venous line was inserted into the right internal jugular vein using ultrasound. The arterial and central lines were connected to an MICM device.Initial readings showed central venous pressure (CVP) of 21 mmHg, cardiac index (CI) of 2.5 L/min/m2, stroke volume variation (SVV) of 3, systemic vascular resistance (SVR) of 1296 dynes-s/cm5, and mean arterial pressure (MAP) of 94 mmHg  depending on surgical blood loss. CVP and SVR parameters were further used to guide fluid and pressor use as follows: If SVV was > 13% but SVR was < 20% of baseline or if SVV was < 13% but CVP dropped > 20% baseline, a combination of albumin and phenylephrine was given  filling to maintain cardiac output. This was accomplished by avoiding tachycardia and hypovolemia as well as maintaining SR and the atrial kick. These patients are predisposed to atrial fibrillation due to left atrial enlargement. Afterload was maintained for coronary perfusion and preventing ischemia. An epidural, while not absolutely contraindicated, was not placed to avoid precipitous drops in preload and afterload. The concurrent severe PH from increased left atrial pressures could precipitate right heart failure. Hence, to avoid increasing pulmonary artery (PA) and RV pressures, care was taken to avoid hypercarbia, hypoxia, acidosis, and excessive preload. Increased intrathoracic pressure from positive pressure ventilation and PEEP can be deleterious to RV function, thus necessitating low PEEP and tidal volumes with higher respiratory rates. Inotropic agents were available in case of suspected RV failure . For intraoperative monitoring in MS patients with severe PH, guidelines recommend TEE or a PAC to assess volume, biventricular function, and cardiac output . HoweverIn this case, a MICM device was used to monitor preload, CO, and afterload by trending SVV, CI, SV, and SVR using an arterial line and central line. The reliability of non-invasive monitoring has been explored in recent literature. One study comparing MICM to a PAC found that SVV correlated better with right ventricular end diastolic volume index than PA diastolic pressure, suggesting it was an accurate preload monitor . Other sHowever, few studies address the efficacy of non-invasive hemodynamic monitors in patients with significant valvulopathies. Case reports describe using the MICM for management of severe aortic stenosis during hip surgery and severe MR during cerebral aneurysm surgery ,12. HoweThis case report describes a unique MICM algorithm incorporating MAP, SVV, SVR, and CVP for intraoperative management of severe MS with severe PH. Of note, CVP has been shown to poorly predict responsiveness to a fluid challenge and should not be used alone to guide therapy . HoweverMinimally invasive cardiac monitoring devices have the potential to lower complications and may serve as a less invasive alternative for intraoperative hemodynamic monitoring. The high-risk patient population may especially benefit from such an approach to non-cardiac surgeries. Further clinical studies are needed to elucidate the utility of MICM in comparison to the PA catheter in similar high-risk patients.


Left bundle branch block (LBBB) and left ventricular (LV) dyssynchrony likely contribute to progressive systolic dysfunction. The evaluation of newly recognized LBBB includes screening for structural heart abnormalities and coronary artery disease (CAD). In patients whose LV ejection fraction (EF) is preserved during initial testing, the incidence of subsequent cardiomyopathy is not firmly established.The risk of developing LV systolic dysfunction among LBBB patients with preserved LVEF is high enough to warrant serial imaging.We screened records of 1000 consecutive patients with LBBB from our ECG database and identified subjects with an initially preserved LVEF (≥45%) without clinically relevant CAD or other cause for cardiomyopathy. Baseline imaging, clinical data, and follow‐up imaging were recorded to determine the risk of subsequent LV systolic dysfunction (LVEF ≤40%).(Data are mean + SD) 784 subjects were excluded, the majority for CAD or depressed LVEF upon initial imaging. Of the remaining 216, 37 (17%) developed a decline in LVEF(≤40%) over a mean follow‐up of 55 ± 31 months; 94% of these patients had a baseline LVEF≤60% and LV end systolic diameter (ESD) ≥ 2.9 cm indicating that these measures may be useful to define which patients warrant longitudinal follow‐up. The negative predictive value of a LVEF>60% and LVESD <2.9 cm was 98%.Seventeen percent of patients with LBBB and initial preserved LVEF develop dyssynchrony cardiomyopathy. We believe the risk of developing dyssynchrony cardiomyopathy is high enough to warrant serial assessment of LV systolic function in this high‐risk population. BNPbrain natriuretic peptideCADcoronary artery diseaseCRTcardiac resynchronization therapyEDDend diastolic dimensionEFejection fractionESDend systolic dimensionLBBBleft bundle branch blockLVleft ventricular1The prevalence of left bundle branch block (LBBB) in the general population ranges from approximately 0.1% to 1.0%, the incidence increasing with age.22.1This study was approved by the Institutional investigational review board. We obtained subjects by screening our ECG database from September 2011 to September 2012 for all studies in which LBBB was included in the official interpretation. This time period represents the earliest computerized tracings for review in our database to assure as long a follow‐up period as possible. The ECG was analyzed for evidence of a left bundle branch block using conventional criteria that included native QRS duration ≥120 ms, broad R waves in leads I, aVL, V5, or V6, and absent q waves in leads I, V5, and V6.Patients were included if they demonstrated an initially preserved LVEF prospectively defined as ≥45% by any imaging modality obtained after the earliest identified LBBB tracing with at least one follow‐up assessment of LV function. Transthoracic echocardiography was the imaging method used for 205 out of 216 subjects (95%). A LVEF of 45% was chosen as the lower limit because dyssynchrony alone acutely lowers the EF in patients with rate‐related LBBB and no other structural heart abnormalities.2.2Medical records were reviewed whereby clinical data were recorded at the time of initial diagnosis including age, gender, comorbid conditions , and laboratory data . The initial and follow‐up EKGs were reviewed for underlying rhythm, QRS axis, and duration. We obtained echocardiographic measurements  from echocardiographic reports. Chamber dimensions were only available for those patients whose initial LVEFs were assessed by echocardiography and whose reports were available for review . Our institution follows the chamber quantification guidelines for these measures.2.3t test. Chi square analysis was used to compare differences in the frequencies of categorical variables between the two groups. Differences were considered statistically significant if the P‐value was less than .05. Odds ratio, sensitivity, specificity, and negative predictive values were calculated using standard formulas. We utilized Kaplan‐Meyer analysis to chart the time course of the development of LV systolic dysfunction among those patients who developed a cardiomyopathy during the follow‐up period. The Symstat software (version 13.2) was used for these analyses.Two groups were compared: patients whose LVEF remained preserved (≥45) upon subsequent imaging—Group 1; and those who exhibited a decline in LVEF (≤40%) on subsequent imaging—Group 2. Continuous variables were expressed as mean ± SD. Comparisons were made with the student 3We reviewed a total of 1000 consecutive subjects within our ECG database, between September 2011 and September 2012 with a LBBB. Of these, 786 were excluded for reasons shown in Figure P < .01). The baseline mean QRS durations and QRS axes were similar. The follow‐up QRS durations in the decline in EF group, Group 2, were slightly and significantly higher than those in the preserved LVEF group, Group 1. The initial assessments of LVEF differed significantly with a statistically lower mean LVEF in those with subsequent deterioration of LV systolic function vs those who maintained a preserved LVEF. Coinciding with the LVEF measures, the initial LVEDD and LVESD measurements were higher in the group whose LVEF declined. Data pertaining to baseline LVEFs and LVESDs are shown graphically as scatter plots in Figure Table Figure 4Significant interest has been placed on dyssynchrony cardiomyopathyBecause of the need for sequential imaging to document an initially preserved LVEF with subsequent deterioration, retrospective analyses are wrought with selection bias. To reduce this bias, we included patients with a single assessment of LV systolic function if that subject's LVEF was preserved and the assessment occurred more than 1 year following the earliest LBBB ECG. By identifying the earliest time at which the LBBB was identified we were able to achieve a relatively long follow‐up duration that extended to more than 10 years with a mean of more than 5 years. Henceforth, we report here that 17% of patients with LBBB and an initial preserved LVEF develop subsequent LV systolic dysfunction (LVEF≤40%) indicative of dyssynchrony cardiomyopathy.Other groups have tried to answer this question using varied approaches. In a landmark study, Vaillant et al.An important strength of our study lies in the identification of the earliest LBBB‐ECG in each subject, labeling this as time zero. The time for the development of dyssynchrony cardiomyopathy among subjects in our population would therefore be applicable to how such patients are identified and followed in clinical practice. All 37 patients within this cohort developed LV systolic dysfunction within 10.5 years. Importantly, 117 patients from our original 1000 subject database had a reduced LVEF on their earliest imaging assessment with no other identifiable cause for their cardiomyopathy. It is possible, therefore, that many if not the majority of these patients had LV systolic dysfunction driven by dyssynchrony.A correlate of dyssynchrony cardiomyopathy is the decline in LVEF observed with chronic right ventricular (RV) pacing. RV pacing was recognized as a potential causative factor in heart failure progression in the DAVID trialWithin the present study, there were no specific clinical or ECG variables that predicted which patients would subsequently develop a reduction in LVEF. However, some potentially important findings were noted within the echocardiographic data. For instance, none of the patients who developed a cardiomyopathy had a LVEF greater than 60% at their initial imaging evaluation. Moreover, within the cardiomyopathy cohort, all of the patients had an LVESD ≥2.5 cm and the majority of patients (94%) had an LVESD ≥2.9 cm on their initial echocardiogram. These data support those subjects with LBBB, who develop a decline in LV systolic function display features of early adverse LV remodeling as indicated by greater chamber size and slightly lower initial LVEF. To our knowledge, this is the first such report whereby these readily available echocardiographic measures aid in identifying those with LBBB at greatest risk for developing dyssynchrony cardiomyopathy.It is well established that a depressed LVEF is an independent risk factor for cardiovascular morbidity and mortality.To date, there are no guideline statements to address how patients with LBBB are managed longitudinally. Based on our data and that from others,5Since inclusion within our database required serial assessments of LVEF after the diagnosis of LBBB, the possibility of selection bias remains. Moreover, despite screening 1000 subjects with LBBB, over 75% were excluded from the data reducing our sample size. We were also unable to include morbidity or mortality assessments within our population as these data could not be obtained reliably. Moreover, medication data were only inconsistently available; it is possible; therefore, that differences in background medical therapy  may have influenced our findings. Finally, echocardiographic data were extracted from written reports and were not subjected to core‐lab verification.6Dyssynchrony cardiomyopathy occurs in 17% of patients with LBBB and preserved LVEF on initial assessment over a mean follow‐up period of 55 months. An initial LVEF between 45% and 60% and an LVESD ≥2.9 cm are associated with much greater risk of developing LV systolic dysfunction among patients with LBBB. Our findings support that patients with LBBB and a preserved LVEF undergo serial imaging and clinical assessments.The authors declare no potential conflict of interests.


Mitral valve prolapse is a common cardiac condition, with an estimated prevalence between 1% and 3%. Most patients have a benign course, but ever since its initial description mitral valve prolapse has been associated to sudden cardiac death. Although the causal relationship between mitral valve prolapse and sudden cardiac death has never been clearly demonstrated, different factors have been implicated in arrhythmogenesis in patients with mitral valve prolapse. In this work, we offer a comprehensive overview of the etiology and the genetic background, epidemiology, pathophysiology, and we focus on the state-of-the-art imaging-based diagnosis of mitral valve prolapse. Going beyond the classical, well-described clinical factors, such as young age, female gender and auscultatory findings, we investigate multimodality imaging features, such as alterations of anatomy and function of the mitral valve and its leaflets, the structural and contractile anomalies of the myocardium, all of which have been associated to sudden cardiac death. Mitral valve (MV) is a complex three-dimensional (3D) structure composed of valvular  and sub-valvular  components .The pivotal study by Levine and colleagues demonstrated that the mitral annulus (MA) is a saddle-shaped structure with its most apical points being located medially and laterally, while its most basal points are located anteriorly and posteriorly  Figure . Later sThe motion of the MA is passive and is functionally related to the contraction-relaxation cycle of adjacent atrial and ventricular musculature, as well as the motion of the aortic root . During The leaflets of the MV differ: The mural (posterior) leaflet is narrower and presents indentations forming three segments; while the aortic (anterior) leaflet is broader, semi-circular, and presents two distinct zones (a rough and a clear one) . The broThe classical work of Lam and colleagues defined the anatomy of the sub-valvular apparatus. They found that chordae tendineae arise from the tips of the papillary muscles  and depending on the site of insertion can be classified as primary , secondary (those that ventricular surface of the body of the leaflet) and tertiary  . The posMitral valve prolapse (MVP) is a spectrum of clinical entities characterized by superior displacement of one or both leaflets into the left atrium (LA)  Figure .At the present time, MVP is commonly classified as primary  or secondary . Familial studies have suggested that heritability is common , and thuFLNC) mutation (p. Pro637Gln) as the first MVP gene in a large French Caucasian family [FLNC mutations (two missense and one large deletion) in three unrelated families  [The initial hypothesis of X-linked inheritance had been put forth in the late 1960s , but almn family . These iChinese) .MMVP1 [MMVP2 [MMVP3 [DCHS1 gene [MMVP2 locus, have been described in two non-related families with a strong family history of MVP.Additionally, linkage studies identified three loci with an autosomal dominant inheritance: MMVP1 , MMVP2 [1 [MMVP2  and MMVP2 [MMVP3  mapping HS1 gene  coding fSecondary MVP is typically associated to a range of connective tissue disorders such as Marfan syndrome , Loeys-DInitial description of MVP had been provided by Barlow and Bosman in 1966 as an “auscultatory-electrocardiographic syndrome” : Apical In the early days of echocardiography, extremely high prevalence rates have been identified, with up to a third of healthy children being affected . One of MVP is a considered a common condition, with an estimated community-based prevalence between 1%  and 2.4%Since the first description, MVP had been associated to ventricular arrhythmias (VA)  and suddCardiac imaging represents the gold standard for the diagnosis of MVP, and has largely supplanted the auscultatory signs, with most diagnoses being made using echocardiography.The 2013 European Society of Cardiology recommendations define the MVP as an abnormal systolic displacement of one or both mitral leaflets more than 2 mm below the annular plane, superiorly into the left atrium, as seen in the parasternal or eventually the apical long-axis view  on two-dIn 2006, the data from this laboratory, in a cohort of 112 patients with an established diagnosis of severe MR due to degenerative MVP, demonstrated that trans-esophageal echocardiography (TEE) provides the most accurate localization of pathology, assuming surgical findings as reference , and should be considered the gold standard for surgical planning  Figure . Indepen2 and regurgitant volume greater or equal to 60 mL/beat are consistent for severe MR. Lastly, a novel and complementary method for the identification of severe MR that has been suggested recently is the average pixel intensity method, with a cut-off greater than 125 au proposed for the identification of severe MR [The diagnosis of MVP must always be accompanied with an extensive research for the potential presence of MR, and ultimately, a robust quantification of its severity . Echocarevere MR .Importantly, both regional and global LV systolic function should always be evaluated using echocardiography, according to the 2017 ESC Guidelines .Cardiovascular magnetic resonance (CMR) is considered a robust noninvasive technique that can provide comprehensive assessment of the MV . The addThe pioneering work of Han and colleagues established that a 2 mm threshold for leaflet excursion into the LA, identical to echocardiography criteria, in the LV outflow tract long-axis view yielded 100% sensitivity and 100% specificity  Figure .Later on, the work by Delling and colleagues identified anterior leaflet length, posterior leaflet displacement, posterior leaflet thickness, and the presence of flail leaflet as the best CMR valvular determinants of MVP-related MR .The 2020 AHA/ACC Guidelines suggest that the use of CMR is appropriate for the assessment of LV volumes, function and MR severity, especially when TTE does not address these issues satisfactorily .r = 0.84, p < 0.0001) and non-invasive echocardiographic assessment  [2, CMR detected MR with sensitivity and specificity of 94% and 94%, respectively [In terms of quantitative assessment, CMR planimetry of the EROA has been shown to be feasible and in good agreement with invasive angiographic grading ( 0.0001) . Importaectively . CMR alsectively .Novel techniques such as 4D-flow CMR offer great promise for an accurate qualitative assessment of MR, especially for eccentric jets .The evidence of CMR capability to detect tissue changes in MVP patients was published in recent studies which demonstrated that only patients with MVP had a significant reduction of papillary muscle signal compared to LV parietal myocardium . InteresLast, cardiac computed tomography (cCT) is another feasible, but under-investigated method for the diagnosis of MVP. It boasts excellent specificity (95%), but as compared to echocardiography, cCT has a significantly lower sensitivity (80% versus 87%), which is particularly marked in bileaflet MVP  Figure .In different series, MVP is found in approximately 2–4% of all causes of SCD in the young, both in the general population and in competitive athletes. Albeit SCD has been associated with MVP since the earliest descriptions of the condition ,33, the Demographic parameters, such as young age and female gender , as wellIn this section, we will offer a deep-dive into four broad, overlapping and non-exclusive groups of imaging-based risk factors: mitral valve leaflet alterations, mitral valve annulus alterations, myocardial structural abnormalities, myocardial contraction alterations; and their interactions with the electrophysiologic risk factors .One of the first series, compiled by Dr. Jeresaty in 1976, described a number of MV characteristics that would later be confirmed as risk factors for SCD in patients with MVP. Namely, in the series of 12 patients ) from a larger cohort of 240 patients who had died suddenly, redundant myxomatous mitral leaflets, mitral regurgitation (86%) and bilateral prolapse (70%) were significantly overrepresented .The first prognostic factor investigated for risk stratification was leaflet redundancy  , it is eAlthough sporadic reports of bileaflet MVP  associatThe work by the Padua group supports the high prevalence of bileaflet MVP in patients with SCD. In their cohort 43/650 (7%) patients died suddenly at an age <40 years of age: In 70% of them, bileaflet involvement was identified .In select cohorts (5 patients), preliminary data seem to hint at the reduction, but not complete abolishment, of the burden of malignant arrhythmias and the rate of appropriate shocks following the surgical correction of bileaflet MVP , suggestDifferent alterations involving the MA itself have been extensively studied, but have been only indirectly implicated as risk factors for SCD: As precursors  for the Perhaps the most important aspect of mitral annular dysfunction in MVP is mitral annular disjunction MAD; . MAD is MAD has profound implications on the dynamic behavior of the MV shape and recent works have suggest that it may be both an anatomic feature of the MA itself  and an iA correlation between the severity of MAD and the occurrence of VA has been demonstrated: MAD > 8.5 mm was a strong predictor for non-sustained ventricular tachycardia (NSVT) . ConsideInitial observations linking intramyocardial fibrosis to MVP and SCD were made in the histological studies and have been subsequently confirmed by robust CMR studies. Namely, in the work by the Padua group, histological evidence of LV fibrosis had been found in papillary muscles (43/43 SCD victims) and the infero-basal wall  . These fA mechanicistic insight into the molecular pathophysiology of mechanical stress-induced fibrosis has been offered by Blomme and colleagues in 2019 who showed a transient upregulation of transforming growth factor β2 (TGF-β2) and a longer lasting connective tissue growth factor (CTGF) expression, a known downstream effector of TGF-β . These f1 times (pT1) when compared with controls (334 ± 52 vs. 363 ± 58 ms). Additionally, the same group identified that patients with MVP and VA had longer pT1 compared to the patients with MVP and without VA (324 (IQR: 296 to 348 ms) vs. 354 (IQR: 327 to 376 ms)). Our group provided evidence for the prolongation of global native T1 times (nT1) in patients with MVP compared to healthy controls (1124.9 ± 97.5 ms vs. 1007.4 ± 26.1 ms) [1 prolongation reflected the “typical” sites: nT1 times were significantly higher in the basal and mid-LV inferolateral walls [1 times, signifying that diffuse fibrosis in patients with MVP  . We founal walls . Importawith MVP  is likelThese observations suggest that even though macroscopic, focal fibrosis clearly serves as electrophysiological substrate for malignant VA, as evidenced with the highest arrhythmic burden in patients with LGE , it is pIn addition to the aforementioned morphological myocardial anomalies, a range of myocardial contraction abnormalities have also been implicated as potential risk factors for SCD in patients with MVP, but no data corroborating these hypotheses exist at the present time.In an echocardiography study, Muthukumar and colleagues described a high-velocity systolic signal using tissue Doppler imaging (TDI) and coined the term “Pickelhaube sign” , for the1 times, suggesting a nexus between the two [Recently published data from this laboratory demonstrated strain alterations using CMR feature tracking (CMR-FT). Patients with MVP showed reduced radial and circumferential strain values in basal and mid-ventricular inferolateral segments, as compared to other segments  Figure . Additio the two .Additional strain-derived indices have been assessed as risk factors, such as mechanical dispersion. Interestingly, mechanical dispersion, was not merely significantly higher in patients with arrhythmic MVP, but also an independent predictor of arrhythmic risk .The baseline electrocardiogram is often characterized by the presence of repolarization abnormalities in the infero-lateral leads (T wave inversion) ,85 and mThe stretch-induced afterdepolarizations may occur due to the contact of the prolapsing leaflets with the ventricular myocardium during diastole, due to the stretch of the leaflet itself or at the site of the insertion of papillary muscle . RegardlIn fact, a recent meta-analysis demonstrated that PVC-triggered ventricular fibrillation (VF)  seems toThe European Society of Cardiology guidelines for the management of ventricular arrhythmias and the prevention of sudden cardiac death do not pose specific indications for the risk stratification in patients with MVP. In fact, a granular risk stratification is still not possible, in the absence of large prospective studies on well-characterized cohorts of patients in primary prevention of sudden cardiac death.Some experts have suggested that patients with MVP should undergo a focused work-up with 12-lead ECG, exercise stress test, 24-hour ambulatory ECG Holter and an echocardiogram . In the MVP represents a common cardiac condition, with an estimated prevalence between 1% to 3%. Most patients with MVP have a benign course, but MVP has often been associated to SCD. Notwithstanding the fact that the causal relationship between MVP and SCD has never been clearly documented, the data we have presented suggest that there are different factors which may contribute to arrhythmogenesis in patients with MVP.primum movens for the occurrence of arrhythmias in patients with MVP. The results of the mechanical dysfunction are multifaceted and are likely to represent a pathophysiological spectrum. Mechanical dysfunction, resulting in sharp tugging of the papillary muscle and the LV wall, can represent an arrhythmogenic trigger, with the electrical mechanism implicated seems to be mediated by stretch-induced afterdepolarizations. The resultant triggered activity may induce PVCs, typically located in the proximity of the papillary muscles and can be the trigger for VF. On the other hand, the aforementioned mechanical dysfunction may arise in mechanical stress-induced fibrosis via a TGF-β-mediated pathway in the long run, which can manifest as either focal or diffuse fibrosis, which in turn act as a pathological substrate. Lastly, an important consequence of MVP is the development of MR, a strong risk factor for SCD.Current literature suggests that the alterations of the MV leaflets (leaflet redundancy and bileaflet prolapse) and the MA , may be interdependent and might represent the real It is clear how accurate multimodality imaging plays a central role in MVP. Using the variety of techniques at our disposal, we can study the complex valvular anatomy, detecting and quantifying the degree of MVP; assess the presence and severity of MR; identify the myocardial contraction abnormalities; and characterize the myocardial structural abnormalities, such as focal and/or diffuse fibrosis. Given the link between mechanical dysfunction and electrophysiology, imaging represents the most powerful tool at our disposal for the identification of risk factors that have been suggested to predispose patients with MVP to SCD.


Intramyocardial dissecting hematoma (IMDH) is an uncommon fatal complication after acute myocardial infarction. It is usually under identified. Transthoracic echocardiography is the first-line modality that can detect IMDH. Cardiac magnetic resonance could confirm the diagnosis. In this paper, we reported a unique partially thrombosed large left ventricle IMDH that mimics thrombosed true aneurysm aiming to highlight the supporting diagnostic transthoracic echocardiography and cardiac magnetic resonance criteria of IMDH. However, cardiovascular magnetic resonance (CMR) imaging is very beneficial to confirm the diagnosis. We will present transthoracic echocardiography (TTE) and CMR findings of an LV anterior wall and apex IMDH of our patient, who was treated conservatively.Intramyocardial dissecting hematoma (IMDH) is a rare prognostically poor form of cardiac rupture with a haemorrhagic dissection through the myocardium.A 60-years-old male patient admitted to our centre as a case of anterior wall myocardial infarction with pulmonary oedema. He had a history of ischaemic heart disease, no history of hypertension, and he is not diabetic.Bedside TTE was performed on the same day of admission and showed  & Suppl–3 LV api–Supplementary Video 1.Click here for additional data file.Supplementary Video 2.Click here for additional data file.Supplementary Video 3.Click here for additional data file.1 weighted double inversion recovery and T2 weighted double inversion recovery with fat suppression were applied in the axial chest plane. Contrast MRA (magnetic resonance angiography) was performed with hree-dimensional reformates then late gadolinium enhancement (LGE) images were acquired in the short axis, four-chamber, and two-chamber planes.CMR was performed on the next day of admission on a 1.5 T system . Retrospectively gated breath-hold steady-state free precession sequences (SSFP-FIESTA) were obtained in the four-chamber and two-chamber long axes, then in the short axis slabs from the LV base to the apex and axial chest slabs covering the heart. T1 weighted and T2 weighted images. On the LGE sequence, the cystic lesion displayed homogenous signal void signal intensity outlined by the enhanced myocardium toward the pericardium. There was no detectable endomyocardial tear. Contrast-enhanced MRA showed no contrast leakage from the LV cavity into the hematoma. A rim of pericardial effusion was noted. The patient was treated conservatively according to the consensus of the heart team, including cardiologists, cardiovascular surgeons, interventional cardiologists, and anaesthesiologist. They went with the conservative approach due to the high risk of surgery, the large size and wide extension of the IMDH, and the poor LV function.CMR images are presented in  & Suppl and 5. CSupplementary Video 4.Click here for additional data file.Supplementary Video 5.Click here for additional data file.The patient was treated medically with anti-failure medications. Anticoagulants were not used for fear of increasing the size of the hematoma. Follow-up TTE after 4 months showed no significant change as regards the size and the echo pattern of the hematoma in the last TTE before discharge. The patient was haemodynamically stable.5 LV free wall rupture is the third most common cause of death after acute myocardial infarction, and immediate surgical repair is the treatment of choice. In such cases, a tear from the endocardium through the myocardium and epicardium leads to cardiac tamponade, imminent left ventricle failure, and death.6 If the tear is confined to the myocardium, an intramyocardial hematoma (IMH) can be formed as a neocavitation enclosed by the myocardium. The hematoma was thought to be due to the rupture of the intramyocardial vessels, diminished tensile strength of the infarcted myocardium, or due to sudden increased perfusion pressure.7The worldwide incidence of IMDH has not been adequately reported. It is an uncommon but under recognised complication of myocardial infarction.8 Some previous variable publications suggested the establishment of IMDH diagnosis echocardiographically if the patient had at least three of the following supporting findings:(1) formation of a neocavitation with central echolucency (2) mobile contracting endomyocardial border (3) the neocavity is outlined by the myocardium from outside (4) continuity between the ventricular cavity and the dissecting hematoma (5) detection of Doppler coloured flow within the cavity (6) changing of the echo pattern of the neocavity on follow-up (7) partial or complete absorption of the cystic cavity.1,8TTE is the most commonly used first-time imaging modality, but CT or CMR is advised if the patient is clinically stable.9 Kali et al reported that T2* is more suitable than T2 weighted CMR in the detection of the acute IMH.10 While Pedersen et al study concluded that T1 weighted inversion recovery sequences (T1WIR) have high sensitivity and specificity in the detection of experimental IMH in porcine myocardium as compared to T2 short tau inversion recovery and T2*-weighted sequences.11 In our case, the IMDH was well-depicted in the cine FIESTA, and in the DIR (both T1- and T2 weighted). In the conventional LGE, the enhanced infarcted inner endomyocardial layer could not be differentiated from the adjacent bright LV blood. So, we recommend using the novel dark-blood LGE method to nullify the LV blood magnetisation for better detection of the ischaemic myocardial scar in such similar cases. It had been published that dark blood LGE imaging improved the depiction of myocardial fibrosis in the cases with low contrast with the contiguous blood pool.12,13CMR is the only imaging modality that can detect precisely IMH owing to the characteristic signal intensity of the blood products. However, the optimal CMR sequences to identify IMDH are still a matter of debate. Kumar et al, in his paper, concluded that T2*-CMR could adequately quantify the myocardium reperfusion haemorrhage.5,10 Conservative management is a suitable viable approach for patients with haemodynamic stability, large-sized dissecting area, or those with reduced LV function and dilated cardiomyopathy.14 Till now, the short-to-midterm prognosis of IMDH in patients who were not treated surgically is poor. However, many IMDH cases treated conservatively were published showed a fair mid-to-long-term survival.14,15The management of patients with IMDH, either via surgical or conservative approach, depends on various factors: the haemodynamic stability status of the patient, the size of the dissecting hematoma, LV function, and the experience of each surgical centre.Herein, we represent a rare case of a large LV partially thrombosed IMDH. The lesion is suspected by TTE and very well characterised in CMR.Intramyocardial dissecting hematoma is an uncommon and under recognised complication of myocardial infarction.Echocardiography and CMR deliver an accurate diagnosis of IMDH.Conservative management is a viable approach for IMDH patients who are haemodynamically stable, with a large-sized IMDH, or those with impaired LV function.