Accurate detection of segmental (regional) LV abnormalities in MRI is accepted as a predictor of cardiac diseases, the leading cause of death worldwide . In clinical practice, segmen- tal cardiac function (Fig. 1.2) is considered an essential diagnosis and follow-up component . It is often assessed visually following the AHA standard , which prescribes selecting representative 2D cardiac slices used to generate 17 standardized LV segments. Currently radi- ologists visually assess the 17 segments together. These practices, along with being subject to high inter-observer variability [5, 53], and are subjective and non-reproducible. For instance, the clinical study in  showed that the mean kappa measure of detecting regionalwall mo- tion abnormalities by three different radiologists could be as low as 0.43, the difficulties coming from the subtle visual differences between normal- and abnormal-segment motions. Automatic diagnosis of LV regional dysfunction has attracted significant research [15, 11, 21, 4, 14, 10]. Regardless of promising performances of the applied techniques, the results can still be im- proved in terms of accuracy. For instance, the recent publication in  reports an accuracy of 63.70% (base), 67.41% (middle), and 66.67% (apex) when visual wallmotion scoring is used as reference.
Cardiac dysfunction is associated with a variety of cardio- vascular conditions that lead to heart failure. Significant cardiac events such as those in infarcted or diabetic hearts are associated with impaired relaxation and contraction of myocardium or abnormalities in leftventricular (LV) wallmotion [1-5]. Tagged magnetic resonance imaging (tMRI) is an established cardiac imaging modality used to visual- ize regional myocardial motion within the LV wall  and references therein. Application of tMRI combined with sensitive motion estimation techniques, such as harmonic phase analysis (HARP), has proven to be feasible and diagnostically valuable in evaluating the performance of normal or diseased hearts in live subjects using conven- tional global and regional measures [7-11]. In the pres- ence of large motions, however, the current analysis techniques including HARP fail to accurately describe the absolute displacement of the myocardial tissue. This paper addresses this issue and offers a solution – provid- ing motion estimates with improved performance even when the tissue is subject to large movements. The solu- tion requires characterizing the LV wallmotion using a simple time-dependent model and performing time- reversal of tMRI data prior to analysis using HARP or other motion tracking techniques. In the following, we describe the forward LV model and give details of its implementa- tion and algorithms involved during a priori data process- ing steps. Next, we explain the time-reversal operation. Using examples with real and simulated data, we demon- strate how the time-reversal approach improves the com- puter-aided regional myocardial motion measurements by minimizing the errors made during the digital estima- tion process.
Leftventricular volumetry was performed in all patients and CMR sequences by one reader (CMR experience > 6 years) using the Argus software (Siemens Healthcare, Erlangen, Germany; employed standard values based upon ). Because excellent inter-rater agreement for leftventricular volumes has been re- peatedly reported for segmented compressed sensing cine SSFP sequences in breath-hold technique and during free breathing, we waived this subanalysis   . The papillary muscles and trabecullae were attributed to the ven- tricular cavity, and the most basal short-axis slice to be included into volumetry was defined by having at least 270˚ of the chamber circumference surrounded by visible myocardium  .
patients exhibited > 70 % luminal narrowing in a single coronary artery (often termed “single vessel coronary ar- tery disease”), a condition that may be more difficult to identify than multi-vessel disease . Subsequently, Jekic, et al., successfully used CMR in 20 volunteers without CAD to measure cardiac function and myocar- dial perfusion at peak stress after maximal exercise on a non-ferromagnetic treadmill inside the MRI room lo- cated just beyond the 2 Gauss line . While 100 % of our participants completed diagnostic imaging within 60 s using a treadmill outside of the CMR room, an add- itional 10 s could be gained by placing the treadmill in the same room as the MRI scanner as in the study used by Jekic, et al. A study by Thavendiranathan, et al. com- pared exercise CMR to echocardiography in 28 healthy volunteers, examining leftventricular endocardial wall visualization. They found that a greater proportion of the segments were visualized by CMR ; in our study 99 % of our participants’ LV myocardial segments were visualized. Finally, a study by Raman, et al. explored real time cine and myocardial perfusion with treadmill exer- cise stress CMR in individuals referred for stress SPECT imaging (single photon emission computed tomog- raphy). A follow up exam at 6 months indicated freedom from cardiovascular events in 29/29 CMR negative indi- vidual, while participants in our study without inducible LVWMA had a 2 % chance in 3 years of experiencing an event .
Informed of the situation, pregnant women vol- untarily accept abortion, which is permitted by Chinese law.The fetus of the induced labor was a male, and the development of the external features was normal (height: 40 cm; weight: 1500 g). Anatomy showed that the heart was in the normal position in the chest, with the atri- um in the correct position; right ventricular loop and enlarged left ventricle were also observed. The origins of the aorta and pulmonary artery were normal with coarse aorta. However, the morphology of the outflow tracts of the ascend- ing aorta and left ventricle was abnormal. Scissoring along the ascending aorta was observed, and the aortic lumen was divided into two parts by the carination structure at the center. One side of the lumen near the interven- tricular septum was smooth, and no valve-like structure was detected. While several short valves were observed on the other side of the lumen, the valves were thickened and contract- ed (Figure 5). The left and right ventricles were cleaved with an intact ventricular septum. Enlargement of the left ventricle and thickening of the endocardium were observed. The valve cusp of the mitral valve showed a malforma- tion, and the number of tendons was reduced. The tendons were directly connected to the ventricularwall, and a normal papillary muscle structure was not observed (Figure 6). No sig- nificant abnormalities were found in the right ventricle. The pathological diagnosis included aortic valve dysplasia and stenosis, ALVT, sec- ondary endocardial fibroelastosis, and mitral valve dysplasia. Endocardial fibroelastosis in Figure 1. The leftventricular endocardium showed
Additional file 2: Movie 1 B Apical four chamber and parasternal short axis view of a 37 years old male presenting with severe heart failure en left bundle branch block. Familial screening revealed several affected first degree relatives. Echocardiographically, there are prominent trabeculations with noncomapcted/compacted ratio > 2 at the parasternal short axis view in end systole. There is not only visual LV dyssynchrony, but also diffuse wallmotionabnormalities which are not only confined to the noncompacted segments. The systolic wall velocity with tissue Doppler imaging of the mitral annulus was respectively 4.8 cm/s (age/gender matched healthy control: 9.13 cm/s) and 6.3 cm/s (control: 9.4 cm/s) in septal wall and lateral wall.
Patients with a positive treadmill exercise test, and normal coronary angiography have long been recognised as an important problem in clinical practice [8-10]. These early studies identified many of the characteristics of what was subsequently characterized as syndrome X . The same denomination was also applied to a syndrome, character- ized by insulin resistance, hyperinsulinemia, and diabe- tes, that is associated with dyslipidemia, hypertension, and abdominal obesity. Hence a more specific terminol- ogy comes in use: angina with normal coronary arteriog- raphy . Patients with this entity, predominantly women , complain of pain that is frequently atypical. It may be precipitated by exertion, although the threshold for precipitating pain is highly variable . Its duration may be uncharacteristically long, and it may be unusually severe and is rarely associated with symptoms such as dia- phoresis. Perfusion abnormalities have been observed commonly in patients with chest pain and normal coro- nary arteriograms, but no consistent correlation could be made among the extent of the defect, the positivity of the exercise test, and exercise tolerance . Thus in many of this patients there is evidence of perfusion abnormalities that are attributed to abnormalities in the microvascula- ture . However stress echocardiography allways failled to demonstrate segmental wallabnormalities even show- ing hyperdinamic ventricles.
Since the arterial d P /d t reflects the force of LV ejection and it is the major stress acting on the aortic wall that contributes to both genesis and subsequent propa- gation of dissection, its diminution and reduction of systolic blood pressure are the two primary goals of pharmacological therapy. Acute dissection generally pre- sents as a hypertensive emergency and the prime consideration of medical man- agement is to maintain the mean arterial pressure around 60 to 75 mmHg and the systolic blood pressure to be reduced to values between 100 and 120 mmHg with an initial decrease should be at 20% . Historically, Wheat et al.  first introduced the aggressive drug therapy for aortic dissection by originally using reserpine and guanethidine. A combination of beta blocker and a vasodilator (so- dium nitroprusside) remains as a standard medical therapy recently. To reduce the d P /d t , an intravenous beta blocker, preferably propranolol 1 mg every 3 to 5 minutes (0.15 mg/kg) until a satisfactory beta blockade (heart rate 60 to 80 beats/minute) up to a total dose of 2 to 6 mg and then at 4 to 6 hours interval to maintain the adequate heat rate. In patients with labile arterial pressure or ob- structive pulmonary disease, an ultra-short-acting beta blocker esmolol 500 mcg/kg IV bolus, followed by continuous infusion at a rate of 50 mcg/kg/minute and titrated up to 200 mcg/kg/minute is useful especially if surgery is to be planned. Labetalol, an alpha and beta adrenergic receptor antagonist is an alter- native drug to lower both d P /d t and arterial pressure. It is given in an initial dose 20 mg IV over 2 minutes period, followed by 40 to 80 mg every 10 to 15 minutes until the heart rate and blood pressure have been controlled and then a main- tenance dose of 2 mg/minute.
microvascular dysfunction is a primary or secondary phenomenon. Coronary epicardial spasm has been docu- mented in a significant proportion of Japanese patients [1,2], but is rare in Caucasian patients [3-6,19]. During the acute phase a transient dynamic intraventricular gra- dient was documented in 18% of patients in the largest population of LVBS so far reported ; in other smaller studies the prevalence of dynamic obstruction in the acute phase ranged from 12.5%  to 23% . These findings and the association of dobutamine-induced dynamic intraventricular gradient with worsening of api- cal wallmotion recently reported in 2 patients with LVBS and septal hypertrophy  suggested a possible pathoge- netic role for dynamic intraventricular obstruction in LVBS. The prevalence of dobutamine-induced dynamic obstruction in our patients with LVBS is similar to that reported by previous studies in patients undergoing dob- utamine stress echocardiography for evaluation of coro- nary artery disease [8-11,20-22], that showed a prevalence ranging from 13% in the study by Heinle et al  to 53% by Wagner et al . Therefore, the develop- ment of a mild to moderate intraventricular gradient dur- ing dobutamine stress is frequent and may have no major clinical significance in the majority of patients with LVBS as in the general population. The significant association found in our patients between dynamic intraventricular gradient and septal hypertrophy is in keeping with the studies by Khanal et al  and Wagner et al , who showed that dobutamine-induced LV cavity obliteration was associated with female sex and LV hypertrophy. Thus, the dynamic intraventricular obstruction docu- mented in our patients does not seem to be a specific fea- ture of LVBS, but rather depends upon the presence of a localized septal hypertrophy that is frequently found in
volume, and end-diastolic volume and pressure did not change significantly after surgery in the presence of patent or occluded grafts (P greater than 0.05). Statistically significant increases occurred in the peak rate of systolic wall thickening regions supplied by patent bypass grafts, and significant decreases occurred in regions with occluded grafts (P less than 0.01). Of 42 preoperatively hypokinetic regions (pdTw/dt greater than 0 less than 5.0 cm/s) supplied by a patent graft, 30 improved by an average of 2.6 cm/s after operation; 18 returned to normal. Failure of 24 hypokinetic regions to improve to normal was associated with myocardial infarction in 11 or with late postoperative graft blood flows of less than 60 ml/min measured by videodensitometry, in 10. All seven preoperatively akinetic (pdTw/dt=0) or dyskinetic (pdTw/dt less than 0) regions did not improve after the operation despite the fact that, in five of the seven, coronary bypass flows were over 60 ml/min. All eight
8. Brown L, Cragoe EJ Jr, Abel KC, Manley SW, and Bourke JR. Amiloride analogues induce responses in isolated rat cardiovascular tissues by inhibition of Na + /Ca 2+ exchange. Naunyn Schmiedebergs Arch Pharmacol 344: 220–224, 1991. 9. Brown L, Duce B, Miric G, and Sernia C. Reversal of cardiac fibrosis in
transmural pressure-volume relation that assesses the amount of ventricular chamber distension under pressure, the stress-strain relation represents the resistance of the myocardium influenced by the configuration of the left ventricle. However, calculation of stress requires the use of a geometrical model of the left ventricle, and calculation of strain requires assumption of the unstressed leftventricular volume. In addition to these potential theoretical limitations, these calculations require accurate measurements over a wide range of leftventricular pressures and volumes. Measurements made during rapid filling may be inappropriately influenced by active myocardial relaxation and viscoelastic effects. Observations during diastasis and atrial systole do not have this problem, but they may not supply a wide enough range of data points. The theoretical problems and the technical difficulties in determining myocardial stress-strain relations have limited their clinical applications.
In this cross-sectional study, we enrolled 54 patients with Chagas’ heart disease to undergo CMR. Patients with serologic confirmed Chagas’ disease diagnosis were referred to the study from our cardiomyopathy out- patient clinic. Exclusion criteria were history of myocar- dial infarction or coronary artery disease, more than two risk factors for CAD or diabetes mellitus (for those patients without anatomical confirmation of coronary ar- teries free of significant stenosis, by invasive coronary angiography or by coronary computed tomography angi- ography), valvular heart disease, previous viral myocardi- tis, other phases of cardiomyopathy, creatinine clearance below 30 ml/min/1.72 m 2 and a contraindication to per- form CMR. All patients underwent a brief interview prior to the MRI exam, which included information on height, weight, medical history and previous exams. We enrolled three subgroups at different stages of disease progression based on a classification of Chagas’ disease and grouped by the outpatient clinic: 1) a group of 16 patients without evidence of cardiac involvement by ECG, chest radiography and echocardiography called in- determinate phase of Chagas’ disease (IND), 2) a group of 17 patients who had cardiac phase without left ven- tricular systolic dysfunction (CPND), determined by ejection fraction equal or superior to 55 % by a routine clinical echocardiography analysis and electrocardio- graphic abnormalities (right bundle branch block with left anterior hemiblock) or 3) a group of 21 patients with the cardiac phase with leftventricular systolic dysfunc- tion determined by ejection fraction inferior to 55 % by echocardiography analysis (CPD). The use of echocardi- ography for the definition of the leftventricular dysfunc- tion and for the classification of chagasic cardiopathy phase followed the recommendation of the current guidelines for Chagas heart disease . All CMR scans and image acquisitions were uneventful. All patients signed written informed consent approved by our local ethic committee (Comissão de Ética para Análise de Pro- jetos de Pesquisa (CAPPesq) do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo) under number 0054/11.
An iE33 ultrasound system equipped with an S3 transducer (Philips Medical Systems, Andover, MA) was used. Mea- surements were performed with an experienced sonogra- pher blinded to patients’ clinical data. Peak transaortic velocity and mean transaortic pressure gradient were mea- sured using continuous-wave Doppler echocardiography. Standard LV volume and mass and left atrial volume were measured according to current recommendations . LV end-diastolic volume and end-systolic volume were measured using Simpson’s biplane method to calculate LV ejection fraction. LV sphericity index was calculated as the ratio of short to long axis on end-systolic apical four-chamber view. LV hypertrophy was determined using LV mass/height 2.7 (cutoffs: 47 g/m 2.7 in women, 49 g/m 2.7 in men) . Mitral inflow and pulmonary ven- ous velocities were recorded using pulsed-wave Doppler echocardiography in the apical four-chamber view. Trans- mitral early (E) and late (A) diastolic velocities and decel- eration time were measured at the leaflet tips. Pulmonary venous systolic (S) and diastolic (D) velocities were re- corded with the sample volume placed at the orifice of the right superior pulmonary vein in the left atrium. The ratio of E wave to early diastolic mitral annular velocity (E/e’) was determined using color-coded tissue Doppler imaging with the sample volume positioned in the septal mitral annulus.
Materials and Methods: It was a prospective study done in PSG Institute of Medical Sciences and Research, Coimbatore, Tamil Nadu, India, from January 2014 to September 2014. Patients aged above 18 years admitted with first episode of ST EMI as per the inclusion and exclusion criteria were recruited for the study. Presence of reciprocal changes and QRS amplitude was measured from ECG. Presence of LeftVentricular Dysfunction (LVD) and wallmotion score were calculated from ECG along with clinical outcome during first follow up visit. Statistical analysis was done using SPSS software. Probability was calculated using chi-square test, independent t-test and ANOVA analysis. Results: A total of 120 patients were recruited for the study of which six were excluded based on the exclusion criteria. Among 114 patients analysed, 55 had reciprocal changes; 38 of them developed LVD which was statistically significant (p=0.002). Of
that this was not controlled. The change in left ven- tricular wall stress seen after food intake are about the same magnitude as the differences seen between differ- ent populations (for example, athletes or hypertensive subjects versus controls) in some investigations [3,24]. While it is difficult to control patients’ food intake in clinical echocardiography, one should be aware of the effect that food intake has on these echocardiographic parameters, affecting in this case both ESS and cESS. The influence of food consumption should be consid- ered in studies, especially when a small sample size is involved.
The leftventricular (LV) hypertrophy (LVH) is a well-known clinical and morphological parameter that is considered to be the important risk factor for heart failure [5, 8]. It occurs typically in response to the haemodynamic overload in some physiological and pathological conditions, and hypertension is the most important reason for LVH development . The infiltrative cardiomyopathies are the next well-known reason of LVH. This is a diverse group of cardiac dis- eases characterised by the deposition of abnormal substances within the heart tissue that causes the ventricular walls to develop either diastolic or, less common, systolic dysfunction. Recently the growing interest of scientists in this issue affects hereditary haemochromatosis (HH), which is characterised by the excess deposition of iron mostly due to HFE gene mutation [1, 12, 14]. Dysfunction of molecules that control iron homeostasis leads to excessive iron ab- sorption in the duodenum and upper section of the small intestine, as well as its maldistribution. As there is no regulatory mechanism for iron excretion from the human body, iron is deposited in a variety of tissues and organs (liver, pancreas, skin, joints, heart) over the course of the disease [1, 11, 16]. Bioactive iron ions produce oxidative stress that destroys involved tissues [6, 13, 15]. Cardiomyocytes, due to intense iron intake, are very susceptible to this type of damage . Symptoms of HH are nonspecific and typically absent in the early stages, therefore a high degree of clinical suspicion is key to making the diagnosis.
So far, the role of EAT and its contribution to the devel- opment of cardiac pathology is quite ambiguous. There is growing evidence of a close functional and anatomical relationship between the adipose tissue and muscular components of the heart. Its close proximity to the myo- cardium suggests that EAT as a metabolically active organ and a source of several bioactive molecules may influence cardiac morphology and function [1,11,12]. Under physio- logical conditions EAT is supposed to act as a buffering system between the myocardium and the local vascular bed [13,14]. Increased EAT could serve as a scavenger of excess fatty free acids which interfere with the generation and propagation of the contractile circle of the heart, may cause ventricular arrhythmias and are supposed to alter cardiac repolarization [15,16]. On the other hand, EAT possesses a high lipolytic activity so that it is able to serve as a ready source of free fatty acids under conditions of an increased myocardial energy demand .
This pilot study showed that very few echocardiography parameters correlated with BNP or NT-proBNP levels in a population of patients with poorly regulated T2D. The exception was LAVI, which showed a moderate correlation with BNP or NT-proBNP levels. Moreover, significant differences in BNP and NT-proBNP levels were found between those with normal and those with abnormal leftventricular diastolic function according to current classifications. Larger studies are warranted to confirm these findings. There is a need for tools to help clinicians to risk stratify subsets of patients who are likely to have particularly unfavorable prognoses, using readily identifiable clinical and laboratory factors. Knowledge is increasing in this field and, hopefully, the results will enable clinicians to identify patients with increased risk of developing adverse events, thereby choosing an individualized treatment and monitoring scheme for each patient. Data on patients with poorly regulated T2D are scarce and the findings in the present investigation points out a direction for further larger studies.
Introduction: Septic shock is the most severe manifestation of sepsis. It is characterized as a hypotensive cardiovascular state associated with multiorgan dysfunction and metabolic disturbances. Management of septic shock is targeted at preserving adequate organ perfusion pressure without precipitating pulmonary edema or massive volume overload. Cardiac dysfunction often occurs in septic shock patients and can significantly affect outcomes. One physiologic approach to detect the interaction between the heart and the circulation when both are affected is to examine ventriculoarterial coupling, which is defined by the ratio of arterial elastance (Ea) to leftventricular end-systolic elastance (Ees). In this study, we analyzed ventriculoarterial coupling in a cohort of patients admitted to ICUs who presented with vs without septic shock.