Electromechanical Abnormalities Research Articles

Brugada syndrome: current concepts and genetic background

Brugada syndrome (BrS) is a hereditary clinical-electrocardiographic arrhythmic entity with low worldwide prevalence. The syndrome is caused by changes in the structure and function of certain cardiac ion channels and reduced expression of Connexin 43 (Cx43) in the Right Ventricle (RV), predominantly in the Right Ventricular Outflow Tract (VSVD), causing electromechanical abnormalities. The diagnosis is based on the presence of spontaneous or medicated ST elevation, characterized by boost of the J point and the ST segment ≥2 mm, of superior convexity "hollow type" (subtype 1A) or descending rectilinear model (subtype 1B). BrS is associated with an increased risk of syncope, palpitations, chest pain, convulsions, difficulty in breathing (nocturnal agonal breathing) and/or Sudden Cardiac Death (SCD) secondary to PVT/VF, unexplained cardiac arrest or documented PVT/VF or Paroxysmal atrial fibrillation (AF) in the absence of apparent macroscopic or structural heart disease, electrolyte disturbance, use of certain medications or coronary heart disease and fever. In less than three decades since the discovery of Brugada syndrome, the concept of Mendelian heredity has come undone. The enormous variants and mutations found mean that we are still far from being able to concretely clarify a genotype-phenotype relationship. There is no doubt that the entity is oligogenetic, associated with environmental factors, and that there are variants of uncertain significance, especially the rare variants of the SCN5A mutation, with European or Japanese ancestors, as well as a spontaneous type 1 or induced pattern, thanks to gnomAD (coalition) researchers who seek to aggregate and harmonize exome and genome sequencing data from a variety of large scale sequencing projects and make summary data available to the scientific community at large). Thus, we believe that this in depth analytical study of the countless mutations attributed to BrS may constitute a real cornerstone that will help to better understand this intriguing syndrome.

Left Ventricular Contraction Duration Is the Most Powerful Predictor of Cardiac Events in LQTS: A Systematic Review and Meta-Analysis.

Background: Long-QT syndrome (LQTS) is primarily an electrical disorder characterized by a prolonged myocardial action potential. The delay in cardiac repolarization leads to electromechanical (EM) abnormalities, which adds a diagnostic value for LQTS. Prolonged left ventricular (LV) contraction was identified as a potential risk for arrhythmia. The aim of this meta-analysis was to assess the best predictor of all EM parameters for cardiac events (CEs) in LQTS patients. Methods: We systematically searched all electronic databases up to March 2020, to select studies that assessed the relationship between echocardiographic indices—contraction duration (CD), mechanical dispersion (MD), QRS onset to peak systolic strain (QAoC), and the EM window (EMW); and electrical indices— corrected QT interval (QTC), QTC dispersion, RR interval in relation to CEs in LQTS. This meta-analysis included a total of 1041 patients and 373 controls recruited from 12 studies. Results: The meta-analysis showed that LQTS patients had electrical and mechanical abnormalities as compared to controls—QTC, WMD 72.8; QTC dispersion, WMD 31.7; RR interval, WMD 91.5; CD, WMD 49.2; MD, WMD 15.9; QAoC, WMD 27.8; and EMW, WMD −62.4. These mechanical abnormalities were more profound in symptomatic compared to asymptomatic patients in whom disturbances were already manifest, compared to controls. A CD ≥430 ms had a summary sensitivity (SS) of 71%, specificity of 84%, and diagnostic odds ratio (DOR) >19.5 in predicting CEs. EMW and QTC had a lower accuracy. Conclusions: LQTS is associated with pronounced EM abnormalities, particularly prolonged LV myocardial CD, which is profound in symptomatic patients. These findings highlight the significant role of EM indices like CD in managing LQTS patients.

Right ventricular electromechanical abnormalities in Brugada syndrome: is this a cardiomyopathy?

Brugada syndrome (BrS) has been often described as a purely electrical disease. However, current dogma surrounding this concept has shifted to accept that BrS is associated with structural abnormalities. Brugada syndrome is now associated with epicardial surface and interstitial fibrosis, reduced gap junction expression, increased collagen, and reduced contractility. The ventricular arrhythmias observed in BrS have been linked to an arrhythmogenic substrate (AS) located rather consistently in the right ventricular outflow tract, sparking much debate as to the significance of this anatomical position. The size of the AS is dynamic and can be altered due to a number of factors. A larger AS is associated with reduced contractility, and this impaired mechanical function may be responsible for syncopal episodes in BrS patients in the absence of arrhythmic events. While BrS is generally regarded as a channelopathy, recent studies have now identified also mutations in genes encoding for sarcomeric proteins to be associated with BrS. Future studies should evaluate electromechanical coupling in BrS, including calcium handling and sarcomeric alterations, and evaluate whether BrS should be classified as a cardiomyopathy.

Cardiac Imaging in Liver Transplantation Candidates: Current Knowledge and Future Perspectives.

Cardiovascular dysfunction in cirrhotic patients is a recognized clinical entity commonly referred to as cirrhotic cardiomyopathy. Systematic inflammation, autonomic dysfunction, and activation of vasodilatory factors lead to hyperdynamic circulation with high cardiac output and low peripheral vascular resistance. Counter acting mechanisms as well as direct effects on cardiac cells led to systolic or diastolic dysfunction and electromechanical abnormalities, which are usually masked at rest but exposed at stress situations. While cardiovascular complications and mortality are common in patients undergoing liver transplantation, they cannot be adequately predicted by conventional cardiac examination including transthoracic echocardiography. Newer echocardiography indices and other imaging modalities such as cardiac magnetic resonance have shown increased diagnostic accuracy with predictive implications in cardiovascular diseases. The scope of this review was to describe the role of cardiac imaging in the preoperative assessment of liver transplantation candidates with comprehensive analysis of the future perspectives anticipated by the use of newer echocardiography indices and cardiac magnetic resonance applications.

New electromechanical substrate abnormalities in high-risk patients with Brugada syndrome

The relationship between the typical electrocardiographic pattern and electromechanical abnormalities has never been systematically explored in Brugada syndrome (BrS). The aims of this study were to characterize the electromechanical substrate in patients with BrS and to evaluate the relationship between electrical and mechanical abnormalities. We enrolled 50 consecutive high-risk patients with BrS (mean age 42 ± 7.2 years), with implantable cardioverter-defibrillator implantation for primary or secondary prevention of ventricular tachyarrhythmias (ventricular tachycardia/ventricular fibrillation [VT/VF]), undergoing substrate mapping and ablation. Patients underwent 3-dimensional (3D) echocardiography with 3D wall motion/deformation quantification and electroanatomic mapping before and after ajmaline administration (1 mg/kg in 5 minutes); 3D mechanical changes were compared with 50 age- and sex-matched controls. The effect of substrate ablation on electromechanical abnormalities was also assessed. In all patients, ajmaline administration induced Brugada type 1 pattern, with a significant increase in the electrical substrate (P < .001), particularly in patients with previous spontaneous VT/VF (P = .007). Induction of Brugada pattern was associated with lowering of right ventricular (RV) ejection fraction (P < .001) and worsening of 3D RV mechanical function (P < .001), particularly in the anterior free wall of the RV outflow tract, without changes in controls. RV electrical and mechanical abnormalities were highly correlated (r = 0.728, P < .001). By multivariate analysis, only the area of RV dysfunction was an independent predictor of spontaneous VT/VF (odds ratio 1.480; 95% confidence interval 1.159-1.889; P = .002). Substrate ablation abolished both BrS-electrocardiographic pattern and mechanical abnormalities, despite ajmaline rechallenge. BrS is an electromechanical disease affecting the RV. The typical BrS pattern reflects an extensive RV arrhythmic substrate, driving consistent RV mechanical abnormalities. Substrate ablation abolished both Brugada pattern and mechanical abnormalities.

Colonic Electromechanical Abnormalities Underlying Post-operative Ileus: A Systematic and Critical Review.

Post-operative ileus (POI) is an inevitable consequence of major abdominal surgery, and may be prolonged in up to 30% of patients. Ileus is commonly presumed to result from paralysis of the GI tract, though there is little direct evidence to support this view. The aim of this review is to systematically search and critically review the literature investigating post-operative colonic electrical and mechanical activity. MEDLINE and Embase databases were systematically searched for articles investigating post-operative colonic motor or electrical activity in human patients. Nineteen original articles investigating post-operative colonic motor or electrical activity were identified. Most studies have used low-resolution techniques, with intermittent recordings of colonic motility. Numerous studies have shown that colonic electrical and motor activity does not cease routinely following surgery, but is of abnormal character for 3–6 days following laparotomy. One recent high-resolution manometry study identified hyperactive cyclic motor patterns occurring in the distal colon on the first post-operative day. Low-resolution studies have shown colonic slow waves are not inhibited by surgery, and are present even in the immediate post-operative period. Recovery of normal motility appears to occur in a proximal to distal direction and is temporally correlated with the clinical return of bowel function. No studies have investigated motility specifically in prolonged POI. Future studies should use high-resolution techniques to accurately characterise abnormalities in electrical and mechanical function underlying POI, and correlate these changes with clinical recovery of bowel function.

Increased oxidative stress and CaMKII activity contribute to electro-mechanical defects in cardiomyocytes from a murine model of Huntington's disease.

Huntington's disease (HD) is a neurodegenerative genetic disorder. Although described as a brain pathology, there is evidence suggesting that defects in other systems can contribute to disease progression. In line with this, cardiovascular defects are a major cause of death in HD. To date, relatively little is known about the peripheral abnormalities associated with the disease. Here, we applied a range of assays to evaluate cardiac electro-mechanical properties invivo, using a previously characterized mouse model of HD (BACHD), and invitro, using cardiomyocytes isolated from the same mice. We observed conduction disturbances including QT interval prolongation in BACHD mice, indicative of cardiac dysfunction. Cardiomyocytes from these mice demonstrated cellular electro-mechanical abnormalities, including a prolonged action potential, arrhythmic contractions, and relaxation disturbances. Cellular arrhythmia was accompanied by an increase in calcium waves and increased Ca2+ /calmodulin-dependent protein kinase II activity, suggesting that disruption of calcium homeostasis plays a key part. We also described structural abnormalities in the mitochondria of BACHD-derived cardiomyocytes, indicative of oxidative stress. Consistent with this, imbalances in superoxide dismutase and glutathione peroxidase activities were detected. Our data provide an invivo demonstration of cardiac abnormalities in HD together with new insights into the cellular mechanistic basis, providing a possible explanation for the higher cardiovascular risk in HD.

Uniqueness of local myocardial strain patterns with respect to activation time and contractility of the failing heart: a computational study

BackgroundMyocardial deformation measured by strain is used to detect electro-mechanical abnormalities in cardiac tissue. Estimation of myocardial properties from regional strain patterns when multiple pathologies are present is therefore a promising application of computer modelling. However, if different tissue properties lead to indistinguishable strain patterns (‘degeneracy’), the applicability of any such method will be limited. We investigated whether estimation of local activation time (AT) and contractility from myocardial strain patterns is theoretically possible.MethodsFor four different global cardiac pathologies local myocardial strain patterns for 1025 combinations of AT and contractility were simulated with a computational model (CircAdapt). For each strain pattern, a cohort of similar patterns was found within estimated measurement error using the sum of least-squared differences. Cohort members came from (1) the same pathology only, and (2) all four pathologies. Uncertainty was calculated as accuracy and precision of cohort members in parameter space. Connectedness within the cohorts was also studied.ResultsWe found that cohorts drawn from one pathology had parameters with adjacent values although their distribution was neither constant nor symmetrical. In comparison cohorts drawn from four pathologies had disconnected components with drastically different parameter values and accuracy and precision values up to three times higher.ConclusionsGlobal pathology must be known when extracting AT and contractility from strain patterns, otherwise degeneracy occurs causing unacceptable uncertainty in derived parameters.

In silico electro-mechanical window shortening and repolarisation abnormalities predict clinical risk of torsade de pointes for 40 reference compounds

In silico electro-mechanical window shortening and repolarisation abnormalities predict clinical risk of torsade de pointes for 40 reference compounds

Pretransplant increases in left ventricular volume and mass are associated with QT prolongation during pediatric liver transplantation.

Structural alterations in the cirrhotic heart may contribute to electromechanical abnormalities, represented by QT prolongation. The aim of this study was to investigate the changes in QTc according to the operative stage during pediatric LT and to identify which baseline echocardiographic parameters were associated with intraoperative QTc prolongation. Data were evaluated from 39 children undergoing LT for chronic liver disease (median age 9months). In 19 patients (48.7%), baseline QTc was prolonged ≥440ms (462±19ms). Through the period of post-reperfusion, QTI, QTc, and JTI progressively increased, although values partially recovered toward the end of surgery. High LVMI (≥82.51g/m2 ) was associated with baseline QTc≥440ms (OR=1.034, P=.032). In the 5minutes post-reperfusion stage, marked QTc prolongation (defined as QTc≥500ms; n=24, 61.5%) was significantly associated with high EDVI (OR=1.060, P=.027) and SVI (OR=1.075, P=.026). In children with chronic liver disease, increased ventricular volumes and mass may increase the risk of QTc prolongation during LT, suggesting that repolarization abnormalities might be contributed by structural changes characteristic of cirrhotic cardiomyopathy.

AN UNUSUAL CAUSE OF DYSPNEA: CIRRHOTIC CARDIOMYOPATHY WITH CONCOMITANT HEPATOPULMONARY SYNDROME AND PORTOPULMONARY HYPERTENSION

Cirrhotic Cardiomyopathy (CCM) is a new clinical phenotype, characterized by suboptimal ventricular response to stress, systolic and/or diastolic dysfunction and electromechanical abnormalities. Relative hypovolemia from pooling of blood in splanchnic circulation in cirrhosis leads to CCM. We

Clinical Utility of Atrial Electromechanical Conduction Time Measured with Speckle Tracking Echocardiography after Catheter Ablation in Patients with Atrial Fibrillation: A Validation Study with Electroanatomical Mapping.

Our recent report demonstrated that atrial electromechanical conduction time (EMT-ε) measured with speckle tracking echocardiography could predict cardiac events in patients with pathological left ventricular hypertrophy. This study aimed to validate EMT-ε by comparison with electroanatomical mapping and to investigate the clinical utility of EMT-ε in patients with atrial fibrillation (AF) undergoing catheter ablation. Forty-six patients with preserved LV ejection fraction (LVEF ≥ 50%) undergoing pulmonary vein isolation (PVI) for AF were studied. Atrial electrical conduction delay was determined by measuring atrial electrical activation time (EAT) using three-dimensional electroanatomical mapping just after PVI. Echocardiographic parameters were acquired within 24 hours and at 6 months after PVI. The study also included 10 control subjects. AF patients had a larger left atrial (LA) volume index (LAVI) and more prolonged EMT-ε compared with control subjects. According to the validation study, EAT was closely related to EMT-ε and a', and this association was independent of LAVI and the presence of persistent AF (EMT-ε: R(2) = 0.342, P < 0.0001, a': R(2) = 0.337, P < 0.0001). At 6 months after PVI, LAVI and EMT-ε were significantly improved. During continued follow-up beyond 6 months (total follow-up, 26 ± 12 months), the EMT-ε shortening at 6 months after PVI was significantly greater in AF-free patients than patients with AF recurrence. This study suggested that the EMT-ε could be a useful echocardiographic marker of LA electromechanical abnormalities in patients with AF.

Assessment of atrial electromechanical delay and P-wave dispersion in patients with type 2 diabetes mellitus

ObjectivesDiabetes mellitus is an independent and strong risk factor for development of atrial fibrillation (AF). Electrophysiologic and electromechanical abnormalities are associated with a higher risk of AF. In this study we aimed to determine the correlation of atrial conduction abnormalities between the surface electrocardiographic and tissue Doppler echocardiographic measurements in type 2 diabetes mellitus (T2DM) patients. MethodsA total of 88 consecutive T2DM patients and 49 age-, gender-, and body mass index-matched healthy volunteers were included in the present study. Baseline characteristics were recorded and 24-hour ambulatory blood pressure monitoring, transthoracic echocardiography, and 12-lead surface electrocardiography were performed for all study participants. Atrial electromechanical delay (EMD) intervals were measured. ResultsMaximum P-wave duration and P-wave dispersion (Pd) were significantly higher in patients with T2DM (105.7±10.2ms vs. 102.2±7.5ms, p=0.02; 40.6±7.6ms vs. 33.6±5.9ms, p<0.001, respectively). Interatrial, intraatrial, and intraleft atrial EMD were significantly higher in the T2DM patients when compared with the controls (16.5±7.8ms vs.11.2±4.4ms, p<0.001; 9.0±7.3ms vs. 6.0±3.8ms, p=0.002, and 7.4±5.2ms vs. 5.1±3.2ms, p=0.002 respectively). Correlation analysis showed a positive correlation between interatrial EMD and Pd (r=0.429, p<0.001) and left atrial volume (r=0.428, p<0.001). ConclusionsIn this study, there was significant EMD and Pd in patients with T2DM as compared with healthy volunteers. Additionally, interatrial EMD was correlated with Pd and left atrial volume index.

Prolonged right ventricular ejection delay identifies high risk patients and gender differences in Brugada syndrome

Background and objectivesRight ventricular (RV) conduction delay has been suggested as an underlying pathophysiological mechanism in Brugada syndrome (BS). In this cross-sectional study we non-invasively assessed the value of echocardiographic markers reflecting ventricular ejection delay to further assess electromechanical abnormalities in BS and to identify patients at risk for life-threatening arrhythmic events. Furthermore, we sought to assess differences in ejection delays between genders because male BS patients demonstrate a more malignant clinical phenotype. Methods124 BS patients (57.3% males) and 62 controls (CTR) (48.4% males) were included. Using Tissue Velocity Imaging, the ejection delay, determined as the time from QRS onset to the onset of the sustained systolic contraction, was measured for both RV free wall (RVED) and lateral LV wall (LVED). From these parameters, the interventricular ejection delay between both walls (IVED) was calculated. ResultsBS patients had longer RVEDs and IVEDs compared to the CTR. BS patients with a previous history of syncope or spontaneous ventricular arrhythmia showed the longest RVEDs and IVEDs. Male BS patients demonstrated longer RVEDs and IVEDs than females. Male BS patients with malignant events had the longest delays. No significant differences regarding LVED were observed between BS patients and CTR. ConclusionsWe demonstrated that a previous history of malignant events was associated with longer RVEDs. Our findings supported the RV conduction delay mechanism behind BS and demonstrated for the first time that the predominant malignant male Brugada phenotype might also be the result of a more delayed RV conduction in males.

Assessment of diastolic function in the management of patients with cirrhosis.

For many years, it has been known that impaired liver function and portal hypertension are associated with a pronounced splanchnic vasodilatation. This leads to important circulatory changes with displacement of the circulating blood volume resulting in central hypovolemia [1]. The combination of effective hypovolemia, arterial hypotension, and baroreceptor-activation of potent vasoconstricting systems such as the sympathetic nervous system leads to a hyperdynamic circulation and a multi-organ failure including impaired function of the heart [2]. In a patient with a full-blown decompensated state of cirrhosis, the heart rate and cardiac output are typically increased [1]. Both experimental and clinical studies have shown that the dimensions of the cirrhotic heart are augmented and the contractility and electromechanical function are impaired [3, 4]. This condition has been termed cirrhotic cardiomyopathy, which designates a cardiac dysfunction that includes impaired cardiac contractility with systolic and diastolic dysfunction and electromechanical abnormalities in the absence of other known causes of cardiac disease [4]. Cirrhotic cardiomyopathy can be demasked by physical or pharmacological stress, which may reveal in particular a systolic dysfunction, which seems to contribute to several cirrhotic complications such as the formation of ascites [5, 6] and the development of hepatic nephropathy [7, 8]. Additionally, cirrhotic cardiomyopathy seems associated with the development of heart failure in relation to invasive procedures such as shunt insertion and liver transplantation [9, 10]. Abnormal left ventricular diastolic function, caused by decreased left ventricular compliance and relaxation, implies an abnormal filling pattern of the ventricles. The transmitral blood flow is changed, with an increased atrial contribution to the late ventricular filling [4]. The pathophysiological background of the diastolic dysfunction in cirrhosis is an increased stiffness of the myocardial wall, most likely because of a combination of mild myocardial hypertrophy, fibrosis, and subendothelial edema [2, 3]. The increase in myocardial stiffness is also reflected by other parameters of diastolic dysfunction, such as a prolonged time for the ventricles to relax after diastolic filling at a specific end-diastolic volume, which reflects an increased resistance to the ventricular inflow [4]. Natriuretic peptides are regarded as markers of volume overload and impaired contractility, and are released by stretch of the atrial fibers such as in patients with ascites where the right atrium has been reported increased partly because of volume overload with expanded blood volume [1, 4]. However, the interpretation of increased natriuretic peptides in patients who from a functional point of view suffer from effective hypovolemia is complex. Activation of the renin–angiotensin–aldosterone system (RAAS) is associated with cardiac disease such as hypertrophy and heart failure, and seems to be related to diastolic dysfunction in both cirrhotic and non-cirrhotic patients with portal hypertension [11]. Furthermore, RAAS may induce fibrosis, and there is evidence of relationships between plasma aldosterone and E/A ratio; thus, RAAS may be both directly and indirectly involved in diastolic dysfunction [4]. Echocardiography is the method more frequently utilised for the detection of left ventricular diastolic dysfunction. Diastolic dysfunction is expressed as a decreased S. Moller (&) Department of Clinical Physiology and Nuclear Medicine 239, Faculty of Health Sciences, Hvidovre Hospital, Centre of Functional Imaging and Research, University of Copenhagen, 2650 Hvidovre, Denmark e-mail: soeren.moeller@regionh.dk

Prevalence and outcome of diastolic dysfunction in liver transplantation recipients

Objective Cirrhotic cardiomyopathy (CCMP) denotes a chronic cardiac dysfunction in cirrhotic patients. It is characterized by systolic (SD) and diastolic dysfunction (DD), and electromechanical abnormalities, in the absence of other cardiac diseases. Liver transplantation (LTx) has a favourable effect on CCMP, but CCMP is in itself a risk factor. Aims of the study were (1) to estimate the prevalence of DD among LTx candidates, (2) to compare outcome between patients with and without DD, and (3) to determine if tricuspid regurgitation (TR) is a predictor of post-transplantation outcome.Methods 173 LTx recipients were retrospectively evaluated. Diagnostic criteria for SD and DD were a resting ejection fraction < 55% and an E/A ratio < 1 or a deceleration time > 200 msec on echocardiography, respectively, according to the criteria proposed during the World Congress of Gastroenterology in Montreal, 2005. The difference in outcome between patients with and without DD was evaluated in terms of mortality and cardiovascular complications post-transplantation.Results SD and DD were diagnosed in 3 (2%) and 74 (43%) patients, respectively. Patients with DD had significantly older age (P < 0.0001). Regarding outcome, no statistically significant difference could be documented. Moderate/severe TR is, in contrast to no or mild TR, associated with worse posttransplantation outcome (P = 0.01 short-term, P= 0.02 long-term).Conclusion In this study population, a prevalence of SD and DD of 2% and 43%, respectively, was registered. Outcome does not seem to be strongly affected by the presence of DD. Tricuspid regurgitation severity on echocardiography is predictive of survival.

Atrial electromechanical abnormalities in hypertensive patients with diastolic dysfunction

It was to compare atrial electromechanical delays (AEMDs) by pulsed tissue Doppler echocardiography between hypertensive patients and healthy controls. It was used as a predictor for development of atrial arrhythmias as proved by other studies. We examined 60 subjects; 20 normotensive (Controls), 20 hypertensive with LV diastolic dysfunction (Group I) and 20 hypertensive without LV diastolic dysfunction (Group II). Exclusion criteria were: receiving B-blockers or non-dihydropyridine calcium channel blockers, Diabetes mellitus, Coronary heart disease and Systolic heart failure. All were examined to assess BP, left atrium and ventricle, and mitral valve flow. The Pulsed wave tissue Doppler imaging is used to assess diastolic function and AEMDs. In apical 4-chamber view, using the pulse wave Doppler, Time intervals from the onset of P wave on surface electrocardiography to the beginning of A wave (PA) were obtained from lateral mitral annulus, septal mitral annulus, and lateral tricuspid annulus and named as lateral PA, septal PA, and RV PA, respectively. The difference between septal PA and RV PA was defined as Intra-right AEMD. The difference between lateral PA and septal PA was defined as Intra-left AEMD .The difference between lateral PA and RV PA was defined as Inter-AEMD. The Inter-AEMD was significantly higher in Group I compared with Group II and Controls. The Intra-Left AEMD was significantly higher in Group I and Group II compared with Controls. There was no significant difference between Controls and Groups as regard to Intra-Right AEMD. There was a positive correlation between systolic blood pressure, LA diameter and volume, LV mass, E/E′ from one side and Inter-AEMD and Intra-Left AEMD from the other side. There was a negative correlation between E wave, E/A ratio and E′ wave from one side and Inter-AEMD and Intra-LeftAEMD from the other side. The Inter-AEMD and the Intra-Left AEMD were significantly higher in subjects with LV hypertrophy than those without. There was no significant correlation between the Intra-Right AEMD and left ventricular hypertrophy. The Inter-AEMD was significantly higher in hypertensive patients with diastolic dysfunction compared with those without diastolic dysfunction and controls. Intra-left AEMD was significantly higher in hypertensive patients with diastolic dysfunction and without diastolic dysfunction compared with normotensives, suggesting that diastolic dysfunction is associated with atrial electromechanical abnormalities.

Cirrhotic cardiomyopathy: pathogenesis and clinical relevance

Cirrhosis is known to cause alterations in the systemic haemodynamic system. Cirrhotic cardiomyopathy designates a cardiac dysfunction that includes impaired cardiac contractility with systolic and diastolic dysfunction, as well as electromechanical abnormalities in the absence of other known causes of cardiac disease. This condition is primarily revealed by inducing physical or pharmacological stress, but echocardiography is excellent at revealing diastolic dysfunction and might also be used to detect systolic dysfunction at rest. Furthermore, measurement of circulating levels of cardiac biomarkers could improve the diagnostic assessm+ent. Cirrhotic cardiomyopathy contributes to various complications in cirrhosis, especially as an important factor in the development of hepatic nephropathy. Additionally, cirrhotic cardiomyopathy seems to be associated with the development of heart failure in relation to invasive procedures such as shunt insertion and liver transplantation. Current pharmacological treatment is nonspecific and directed towards left ventricular failure, and liver transplantation is currently the only proven treatment with specific effect on cirrhotic cardiomyopathy.

Evaluation of Correlation between Aortic Elastic Parameters and Atrial Electromechanical Abnormalities in Hypertensive Patients

Arterial hypertension leads to instability and heterogeneity in atrial conduction by these hemodynamic and morphological changes in heart and aorta. These changes can be evaluated by transthoracic echocardiography. The aim of this study was to evaluate the correlation of aortic elastic parameters and atrial electromechanical delay (AEMD) parameters in patients with hypertension. Eighty-one hypertensive patients and 55 control subjects were included in the study. All subjects underwent transthoracic echocardiography for detecting aortic elastic parameters and AEMD parameters. There was no difference between HT and control groups regarding age and gender. Aortic strain (8.1±4.3% vs. 10.3±5.1%, P=0.008) and aortic distensibility (0.35±0.18cm(2) /dyn vs. 0.45±0.23cm(2) /dyn, P=0.003) were decreased in hypertensive patients than in controls. Intra-left AEMD (25.5±7.3 vs. 21.8±9.2 P<0.009) was significantly higher in hypertensive patients compared to control subjects. No statistically significant difference was found in intra-right AEMD and inter-AEMD between the groups. There was a positive significant moderate correlation between aortic strain and intra-left AEMD (r=0.501, P<0.001). This study demonstrated that intra-left AEMD was increased in hypertensive patients and aortic elastic parameters was correlated with intra-left AEMD. These findings may be related to similar structural and functional changes in heart and aorta in hypertension.

Atrial Electromechanical Coupling Interval and P-Wave Dispersion in Patients With White Coat Hypertension

Background. The aim of our study was to investigate the effect of white coat hypertension (WCH) to atrial conduction abnormalities by electrocardiographic P-wave analysis and echocardiographic electromechanical coupling (EMC) interval measurement. Methods. The study consisted of sex-, age-, and body mass index-matched 24 patients with WCH, 24 patients with sustained hypertension (SH), and 24 subjects with normotension (NT). The difference between the maximum (Pmax) and minimum P-wave durations on 12-lead electrocardiography was defined as P-wave dispersion (PD). Intra- and inter-atrial EMC were measured by tissue Doppler imaging. Results. Pmax and PD of subjects with WCH were significantly higher than those of normotensives and lower than those of patients with SH. Inter-atrial EMC and left atrial EMC values of WCH group were intermediate between NT and SH groups. There was a significant correlation between left atrial diameter, PD, Pmax, left ventricle mass index, left atrial EMC, and inter-atrial EMC. Conclusion. White coat hypertension is an intermediate group between SH and NT in terms of atrial electromechanical abnormalities which may be associated with the risk of atrial fibrillation.