Correlation Between Left Ventricular Electromechanical Delay and Body Mass Index

Aim To evaluate effect of body mass index on left ventricle electromechanical delay among adults with no history of cardiac disease. Obesity is a complex disorder involving an excessive amount of body fat. Being extremely obese increases the risk of diseases and health problems, such as heart disease, type 2 diabetes mellitus, hypertension and premature death. The assessment of LV dyssynchrony has been gaining interest because it is increasingly considered to indicate the risk of progression to heart failure in various populations. Ventricular electromechanical delay can be measured from the onset of the QRS complex on electrocardiogram to the onset or peak of ventricular contraction determined by tissue Doppler imaging. Methods 66 subjects divided into three groups with 22 subjects for each group with age range (≥18 years and < 60 years old) of either sex with no history of cardiac disease were classified according to BMI into three group; Group A: subjects with normal BMI (18.5 – 24.9 kg/m2|), Group B: overweight subjects with BMI (25-29.9 kg/m2), Group C: obese subjects with BMI (≥ 30 kg/m2). The study groups were age, gender and risk factors matched. The time from the beginning of the QRS complex (on electrocardiogram) to the onset of systolic velocities in the septum and lateral wall were assessed and the time from the beginning of the QRS complex (on electrocardiogram) to the peak of systolic velocities in the septum and lateral wall were assessed using the pulsed wave Tissue Doppler Imaging (PW-TDI) by placing the sample volume in the middle of the basal portions of the LV septal and lateral walls in the apical four-chamber view at end-expiratory at a sweep speed of 100 mm/s, The difference between time recorded from septal and that recorded from lateral walls was referred as the lateral-to-septal delay. Results There was significant difference between the three groups regarding (lateral to septal delay) from onset of QRS to onset of S'(23.36±7.6 ms vs. 24.05±5.9ms vs. 35.18±9.3ms respectively, P < 0.0001), also there was a significant difference between study groups regarding (lateral to septal delay) from onset of QRS to peak of S'(39.41±9 ms vs. 48±10.4ms vs. 62.82±15.3ms respectively, P < 0.0001). There was a direct correlation between BMI and (lateral to septal delay) onset of QRS to peak of S' (r = 0.633, P < 0.0001) as well as (lateral to septal delay) onset of QRS to onset of S'(r = 0.64, P < 0.0001). Conclusion We present an interesting finding of left ventricular electromechanical delay in asymptomatic obese subjects with sinus rhythm and no history of cardiac disease. It would be speculative to say that the intraventricular dyssynchrony seen in asymptomatic obese individuals is related to cardiac electrical remodeling occurs with obesity and gives a proposal to understand pathophysiology of heart failure occurring in obese patients.

Effects of Plyometric Training on Electromechanical Delay of College Women

The article's abstract is not available.

Sensitivity Analysis of Ion Channel Conductance on Myocardial Electromechanical Delay: Computational Study

It is well known that cardiac electromechanical delay (EMD) can cause dyssynchronous heart failure (DHF), a prominent cardiovascular disease (CVD). This work computationally assesses the conductance variation of every ion channel on the cardiac cell to give rise to EMD prolongation. The electrical and mechanical models of human ventricular tissue were simulated, using a population approach with four conductance reductions for each ion channel. Then, EMD was calculated by determining the difference between the onset of action potential and the start of cell shortening. Finally, EMD data were put into the optimized conductance dimensional stacking to show which ion channel has the most influence in elongating the EMD. We found that major ion channels, such as L-type calcium (CaL), slow-delayed rectifier potassium (Ks), rapid-delayed rectifier potassium (Kr), and inward rectifier potassium (K1), can significantly extend the action potential duration (APD) up to 580 ms. Additionally, the maximum intracellular calcium (Cai) concentration is greatly affected by the reduction in channel CaL, Ks, background calcium, and Kr. However, among the aforementioned major ion channels, only the CaL channel can play a superior role in prolonging the EMD up to 83 ms. Furthermore, ventricular cells with long EMD have been shown to inherit insignificant mechanical response (in terms of how strong the tension can grow and how far length shortening can go) compared with that in normal cells. In conclusion, despite all variations in every ion channel conductance, only the CaL channel can play a significant role in extending EMD. In addition, cardiac cells with long EMD tend to have inferior mechanical responses due to a lack of Cai compared with normal conditions, which are highly likely to result in a compromised pump function of the heart.

Poorer Exercise Accommodation of Regional Systolic Myocardial Motion after Spironolactone Treatment in Heart Failure Patients with Preserved Ejection Fraction and Ventricular Dyssynchrony

Patients with heart failure and preserved ejection fraction (HFpEF) are known to have reduced systolic myocardial velocity (Sm) with impaired accommodation to exercise. We tested the impact of an aldosterone antagonist on Sm at rest and post-exercise. Forty-nine HFpEF patients (65 ± 11 years, 24 male) with HF signs/symptoms, mitral E/Ea (annular early diastolic velocity) > 8, and left ventricular (LV) EF > 50% were randomized to spironolactone (25 mg/day, 25 patients) or the Control. At baseline and 6 months, we analyzed Sm of basal LV segments at rest and after a 6 min treadmill exercise. At 6 months, post-exercise mean Sm in the spironolactone group became greater than that in the Control (9.2 ± 1.6 vs. 8.3 ± 1.0 cm/s, p = 0.021), mainly due to the increment of post-exercise % increase of lateral Sm (44 ± 30 vs. 30 ± 19% at baseline, p = 0.045). Further analyses showed the presence of systolic dyssynchrony (standard deviation of electromechanical delay of 6-basal LV segments > 35 ms) was independently associated with a poorer response to spironolactone, defined as a post-exercise % increase of lateral Sm < 50% (OR = 2.7, 95% CI = 1.8–4.2) and the increment of Ea < 1.5 cm/s (OR = 1.5, 95% CI = 1.1–2.3). Spironolactone could improve exercise accommodation of regional systolic myocardial velocity for HFpEF patients. However, its benefits could be decreased in those with ventricular dyssynchrony. This suggested possible therapeutic impacts from underlying heterogeneity within HFpEF patients.

Excitation and Contraction of the Failing Human Heart In Situ and Effects of Cardiac Resynchronization Therapy: Application of Electrocardiographic Imaging and Speckle Tracking Echo-Cardiography

Despite the success of cardiac resynchronization therapy (CRT) for treating heart failure (HF), the rate of nonresponders remains 30%. Improvements to CRT require understanding of reverse remodeling and the relationship between electrical and mechanical measures of synchrony. The objective was to utilize electrocardiographic imaging (ECGI, a method for noninvasive cardiac electrophysiology mapping) and speckle tracking echocardiography (STE) to study the physiology of HF and reverse remodeling induced by CRT. We imaged 30 patients (63% male, mean age 63.7 years) longitudinally using ECGI and STE. We quantified CRT-induced remodeling of electromechanical parameters and evaluated a novel index, the electromechanical delay (EMD, the delay from activation to peak contraction). We also measured dyssynchrony using ECGI and STE and compared their effectiveness for predicting response to CRT. EMD values were elevated in HF patients compared to controls. However, the EMD values were dependent on the activation sequence (CRT-paced vs. un-paced), indicating that the EMD is not intrinsic to the local tissue, but is influenced by factors such as opposing wall contractions. After 6 months of CRT, patients had increased contraction in native rhythm compared to baseline pre-CRT (baseline: −8.55%, 6 months: −10.14%, p = 0.008). They also had prolonged repolarization at the location of the LV pacing lead. The pre-CRT delay between mean lateral LV and RV electrical activation time was the best predictor of beneficial reduction in LV end systolic volume by CRT (Spearman’s Rho: −0.722, p < 0.001); it outperformed mechanical indices and 12-lead ECG criteria. HF patients have abnormal EMD. The EMD depends upon the activation sequence and is not predictive of response to CRT. ECGI-measured LV activation delay is an effective index for CRT patient selection. CRT causes persistent improvements in contractile function.

Muscle Contractile Characteristics During Exhaustive Dynamic Exercise and Recovery

Our aim was to provide an in vivo assessment of human muscle twitch characteristics during and following an exhaustive dynamic exercise to explore temporal alterations of the rate of force development (RFD) and relaxation (RFR). Eleven healthy participants (mean age ± SD: 24 ± 3 years) completed a dynamic knee-extensor exercise in randomized order at three different intensities, eliciting exhaustion after ∼9 min (56 ± 10 W), ∼6 min (60 ± 10 W), and ∼4 min (63 ± 10 W), in addition to a low-intensity (28 ± 5 W) bout. In a novel setup, an electrical doublet stimulation of m. vastus lateralis was applied during exercise (every 30 s) and recovery for frequent evaluation of key contractile properties (maximal force, RFD, RFR, and electromechanical delay) in addition to M-wave characteristics. RFD and RFR remained stable throughout the low-intensity trial but declined in all exhaustive trials to reach a similar level of ∼40% of pre-exercise values at task failure but with the exponential decay augmented by intensity. Following exhaustion, there was a fast initial recovery of RFD and RFR to ∼80% of pre-exercise values within 1 min, followed by a longer suppression at this level. The M-wave characteristics remained unchanged during all trials. In conclusion, this is the first study to quantify the intensity-dependent alterations of RFD and RFR during and after exhaustive dynamic exercise in humans. A hypothesized reduction and fast reversion of RFD was confirmed, and a surprising compromised RFR is reported. The present unique experimental approach allows for novel insight to exercise-induced alterations in human muscle contractile properties which is relevant in health and disease.

THE VALUE OF ATRIAL ELECTROMECHANICAL DELAY IN PREDICTING ATRIAL FIBRILLATION DEVELOPMENT AFTER CORONARY ARTERY BYPASS SURGERY

Objective: Predicting postoperative atrial fibrillation (PoAF) in the preoperative period will provide a serious advantage in preventing the morbidity and mortality associated with this arrhythmia and in planning the treatment. In this study, we investigated the value of atrial electromechanical delay (AEMD) in predicting the development of PoAF. Methods: A total of 93 patients who underwent isolated coronary artery bypass grafting (CABG) operation were included in this prospective study. Patients’ demographic characteristics, laboratory parameters, echocardiographic data, and AEMD durations that could be measured by the co-use of electrocardiography and echocardiography were recorded. The patients at sinus rhythm during the postoperative period were identified as “Group 1”, and those who developed PoAF were identified as “Group 2”. Results: PoAF incidence was 26.88% (n=25). Left ventricle (LV) lateral AEMD, LV medial AEMD, right ventricle lateral AEMD, and left atrium (LA) lateral AEMD durations of Group 2 were significantly higher than Group 1 (p<0.001, p=0.004, p=0.004, p<0.001; respectively). In Univariate Logistic Regression Analysis, the age, hypertension, LA maximum volume, LA lateral AEMD and pulmonary artery pressure were significantly associated with PoAF development (p=0.01, p=0.004, p=0.004, p=0.001, p=0.01; respectively). However, only LA lateral AEMD was found as an independent predictive factor for the development of PoAF in the Multivariate Logistic Regression Analysis (OR:1.03, 95% CI:1,001-1.06, p=0.04). AUC was 0.741 for LA lateral AEMD in ROC Curve Analysis (95% CI:0.633-0.849, p<0.001). Conclusions: The development of PoAF can be predicted by AEMD durations measured in the preoperative period in patients undergoing isolated CABG.

The Influence of Growth, Maturation and Resistance Training on Muscle-Tendon and Neuromuscular Adaptations: A Narrative Review

The purpose of this article is to provide an overview of the growth, maturation and resistance training-related changes in muscle-tendon and neuromuscular mechanisms in youth, and the subsequent effect on performance. Sprinting, jumping, kicking, and throwing are common movements in sport that have been shown to develop naturally with age, with improvements in performance being attributed to growth and maturity-related changes in neuromuscular mechanisms. These changes include moderate to very large increases in muscle physiological cross-sectional area (CSA), muscle volume and thickness, tendon CSA and stiffness, fascicle length, muscle activation, pre-activation, stretch reflex control accompanied by large reductions in electro-mechanical delay and co-contraction. Furthermore, a limited number of training studies examining neuromuscular changes following four to 20 weeks of resistance training have reported trivial to moderate differences in tendon stiffness, muscle CSA, muscle thickness, and motor unit activation accompanied by reductions in electromechanical delay (EMD) in pre-pubertal children. However, the interaction of maturity- and training-related neuromuscular adaptions remains unclear. An understanding of how different neuromuscular mechanisms adapt in response to growth, maturation and training is important in order to optimise training responsiveness in youth populations. Additionally, the impact that these muscle-tendon and neuromuscular changes have on force producing capabilities underpinning performance is unclear.