scholarly journals Comparison of Electromechanical Delay during Ventricular Tachycardia and Fibrillation under Different Conductivity Conditions Using Computational Modeling

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Aulia K. Heikhmakhtiar ◽  
Ki M. Lim
Keyword(s):  
Heart Failure ◽  
Ventricular Fibrillation ◽  
Sinus Rhythm ◽  
Realistic Model ◽  
Time Interval ◽  
Electromechanical Delay ◽  
Conduction Velocities ◽  
Ventricular Tachycardia And Fibrillation ◽  
Failure Conditions ◽  
Action Potential Duration Restitution

Electromechanical delay (EMD) is the time interval between local myocyte depolarization and the onset of myofiber shortening. Previously, researchers measured EMD during sinus rhythm and ectopic pacing in normal and heart failure conditions. However, to our knowledge, there are no reports regarding EMD during another type of rhythms or arrhythmia. The goal of this study was to quantify EMD during sinus rhythm, tachycardia, and ventricular fibrillation conditions. We hypothesized that EMD under sinus rhythm is longer due to isovolumetric contraction which is imprecise during arrhythmia. We used a realistic model of 3D electromechanical ventricles. During sinus rhythm, EMD was measured in the last cycle of cardiac systole under steady conditions. EMD under tachycardia and fibrillation conditions was measured during the entire simulation, resulting in multiple EMD values. We assessed EMD for the following 3 conduction velocities (CVs): 31 cm/s, 51 cm/s, and 69 cm/s. The average EMD during fibrillation condition was the shortest corresponding to 53.45 ms, 55.07 ms, and 50.77 ms, for the CVs of 31 cm/s, 51 cm/s, and 69 cm/s, respectively. The average EMD during tachycardia was 58.61 ms, 58.33 ms, and 52.50 ms for the three CVs. Under sinus rhythm with action potential duration restitution (APDR) slope 0.7, the average EMD was 66.35 ms, 66.41 ms, and 66.60 ms in line with the three CVs. This result supports our hypothesis that EMD under sinus rhythm is longer than that under tachyarrhythmia conditions. In conclusion, this study observed and quantified EMD under tachycardia and ventricular fibrillation conditions. This simulation study has widened our understanding of EMD in 3D ventricles under chaotic conditions.

scholarly journals Mechanistic insight into prolonged electromechanical delay in dyssynchronous heart failure: a computational study

2013 ◽  
Vol 305 (8) ◽  
pp. H1265-H1273 ◽  
Author(s):  
Jason Constantino ◽  
Yuxuan Hu ◽  
Albert C. Lardo ◽  
Natalia A. Trayanova
Keyword(s):  
Heart Failure ◽  
Left Bundle Branch Block ◽  
Computational Study ◽  
Electrical Activation ◽  
Block Type ◽  
Time Interval ◽  
Electromechanical Delay ◽  
Bundle Branch Block ◽  
Wall Stiffness ◽  
Dyssynchronous Heart Failure

In addition to the left bundle branch block type of electrical activation, there are further remodeling aspects associated with dyssynchronous heart failure (HF) that affect the electromechanical behavior of the heart. Among the most important are altered ventricular structure (both geometry and fiber/sheet orientation), abnormal Ca2+ handling, slowed conduction, and reduced wall stiffness. In dyssynchronous HF, the electromechanical delay (EMD), the time interval between local myocyte depolarization and myofiber shortening onset, is prolonged. However, the contributions of the four major HF remodeling aspects in extending EMD in the dyssynchronous failing heart remain unknown. The goal of this study was to determine the individual and combined contributions of HF-induced remodeling aspects to EMD prolongation. We used MRI-based models of dyssynchronous nonfailing and HF canine electromechanics and constructed additional models in which varying combinations of the four remodeling aspects were represented. A left bundle branch block electrical activation sequence was simulated in all models. The simulation results revealed that deranged Ca2+ handling is the primary culprit in extending EMD in dyssynchronous HF, with the other aspects of remodeling contributing insignificantly. Mechanistically, we found that abnormal Ca2+ handling in dyssynchronous HF slows myofiber shortening velocity at the early-activated septum and depresses both myofiber shortening and stretch rate at the late-activated lateral wall. These changes in myofiber dynamics delay the onset of myofiber shortening, thus giving rise to prolonged EMD in dyssynchronous HF.

Time interval from left ventricular stimulation to QRS onset is a predictor of mortality in patients with cardiac resynchronization therapy

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
D Yagishita ◽  
Y Yagishita ◽  
S Kataoka ◽  
K Yazaki ◽  
M Kanai ◽  
...  
Keyword(s):  
Heart Failure ◽  
Independent Predictor ◽  
Total Mortality ◽  
Left Ventricular ◽  
Cardiac Resynchronization ◽  
Time Interval ◽  
Heart Failure Hospitalization ◽  
Conduction Disturbance ◽  
Secondary Endpoints ◽  
Fibrotic Lesion

Abstract Introduction In our previous report, the time interval from left ventricular (LV) pacing to the earliest onset of QRS (S-QRS interval) has been found to be an independent predictor of mechanical response to cardiac resynchronization therapy (CRT). The S-QRS interval may indicate the conduction disturbance relevant to the localized tissue property such as scar or fibrotic lesion. Therefore, S-QRS interval longer than 37ms was associated with poor response to CRT, and proposed as suboptimal LV lead position. Then, we hypothesized that the longer S-QRS interval at the LV pacing site could be related to long term mortality and heart failure events in patients with CRT. Methods This retrospective study included 82 consecutive heart failure patients with sinus rhythm, reduced LV ejection fraction (≤35%), and a wide QRS complex (≥120ms), who undergone CRT implantation between 2012 January and 2017 December. Patients were divided into Short S-QRS group (<37ms, SS-QRS) and Long S-QRS group (≥37ms, LS-QRS) according to the previously reported optimal cut off value. A responder was defined as one with ≥15% reduction in LV end-systolic volume assessed by echocardiography at 6 months after CRT. The primary endpoint was total mortality, which included LV assist device implantation or heart transplantation. The secondary endpoints included the composite endpoint of total mortality or heart failure hospitalization. Results The study patients were divided into SS-QRS (N=43, age 65.9±13.2 years, 77% male) and LS-QRS (N=39, age 63.0±13.4, 85% male). In the electrocardiographic measurements, there were no significant differences in baseline QRS duration (162.4±30.3ms in SS-QRS vs. 154.5±31.6ms in LS-QRS, P=0.19) and LV local activation time assessed as Q-LV interval (118.3±34.3ms in SS-QRS vs. 115.3±32.0ms in LS-QRS, P=0.71). S-QRS interval was 25.9±5.3ms in SS-QRS and 51.5±13.7ms in LS-QRS (P<0.01), and the responder rate was significantly higher in SS-QRS compared with LS-QRS (79% vs. 29%, P<0.01). During mean follow up of 47.7±22.4 months, 24 patients (29%) reached to the primary endpoint, while the secondary endpoints were observed in 47 patients (57%). LS-QRS patients had significantly worse event-free survival for both primary and secondary endpoints (Figure). After the multivariate Cox regression analysis, LS-QRS (≥37ms) was an independent predictor of total mortality (HR=2.6, 95% CI: 1.11 to 6.12, P=0.03) and the secondary composite events (HR=2.4, 95% CI: 1.31 to 4.33, P<0.01). Conclusion The S-QRS interval longer than 37ms, which may reflect the conduction disturbance relevant to the scar or fibrotic lesion at the LV pacing site, was a significant predictor of the total mortality and heart failure hospitalization. These findings have implications for the optimal LV lead placement in patients with CRT device. Clinical outcomes according to S-QRS Funding Acknowledgement Type of funding source: None

scholarly journals Heart Rate–Induced Myocardial Ca 2+ Retention and Left Ventricular Volume Loss in Patients With Heart Failure With Preserved Ejection Fraction

2020 ◽  
Vol 9 (17) ◽  
Author(s):  
Daniel N. Silverman ◽  
Mehdi Rambod ◽  
Daniel L. Lustgarten ◽  
Robert Lobel ◽  
Martin M. LeWinter ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Ejection Fraction ◽  
Sinus Rhythm ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Preserved Ejection Fraction ◽  
Volume Loss ◽  
Heart Rates ◽  
Patients With Heart Failure

Background Increases in heart rate are thought to result in incomplete left ventricular (LV) relaxation and elevated filling pressures in patients with heart failure with preserved ejection fraction (HFpEF). Experimental studies in isolated human myocardium have suggested that incomplete relaxation is a result of cellular Ca 2+ overload caused by increased myocardial Na + levels. We tested these heart rate paradigms in patients with HFpEF and referent controls without hypertension. Methods and Results In 22 fully sedated and instrumented patients (12 controls and 10 patients with HFpEF) in sinus rhythm with a preserved ejection fraction (≥50%) we assessed left‐sided filling pressures and volumes in sinus rhythm and with atrial pacing (95 beats per minute and 125 beats per minute) before atrial fibrillation ablation. Coronary sinus blood samples and flow measurements were also obtained. Seven women and 15 men were studied (aged 59±10 years, ejection fraction 61%±4%). Patients with HFpEF had a history of hypertension, dyspnea on exertion, concentric LV remodeling and a dilated left atrium, whereas controls did not. Pacing at 125 beats per minute lowered the mean LV end‐diastolic pressure in both groups (controls −4.3±4.1 mm Hg versus patients with HFpEF −8.5±6.0 mm Hg, P =0.08). Pacing also reduced LV end‐diastolic volumes. The volume loss was about twice as much in the HFpEF group (controls −15%±14% versus patients with HFpEF −32%±11%, P =0.009). Coronary venous [Ca 2+ ] increased after pacing at 125 beats per minute in patients with HFpEF but not in controls. [Na + ] did not change. Conclusions Higher resting heart rates are associated with lower filling pressures in patients with and without HFpEF. Incomplete relaxation and LV filling at high heart rates lead to a reduction in LV volumes that is more pronounced in patients with HFpEF and may be associated with myocardial Ca 2+ retention.

Atrial fibrillation followed by torsade de pointes degenerated into ventricular fibrillation spontaneously terminated and restored sinus rhythm

2013 ◽  
Vol 166 (3) ◽  
pp. e39-e40 ◽  
Author(s):  
Francesco Santoro ◽  
Riccardo Ieva ◽  
Armando Ferraretti ◽  
Luisa De Gennaro ◽  
Matteo Di Biase ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Ventricular Fibrillation ◽  
Sinus Rhythm ◽  
Torsade De Pointes

scholarly journals Stroke in Heart Failure in Sinus Rhythm: The Warfarin versus Aspirin in Reduced Cardiac Ejection Fraction Trial

2013 ◽  
Vol 36 (1) ◽  
pp. 74-78 ◽  
Author(s):  
Patrick M. Pullicino ◽  
John L.P. Thompson ◽  
Ralph L. Sacco ◽  
Alexandra R. Sanford ◽  
Min Qian ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Sinus Rhythm ◽  
Cardiac Ejection Fraction

scholarly journals Age independently predicts hemodynamic, but not arrhythmic STEMI-related complications. Data from a cohort study on 848 STEMI patients

2021 ◽  
Vol 10 (Supplement_1) ◽  
Author(s):  
RC Serban ◽  
L Hadadi ◽  
I Sus ◽  
EK Lakatos ◽  
Z Demjen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Coronary Intervention ◽  
Hospital Death ◽  
High Risk Population ◽  
Time Interval ◽  
Killip Class ◽  
St Segment Elevation ◽  
Catheterization Laboratory ◽  
Cardiac Stimulation ◽  
Cardiac Catheterization Laboratory

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Romanian Ministry of Education and Research, CNCS-UEFISCDI BACKGROUND Age is one of the most relevant prognostic factors in patients presenting with ST-segment elevation myocardial infarction (STEMI). However, it remains unknown whether this impaired prognosis is due to the occurrence of hemodynamic and/or arrhythmic STEMI-related complications. Understanding the mechanisms involved in STEMI-related complications with advancing age could significantly improve outcomes in this high-risk population. PURPOSE We aimed to investigate the contribution of advanced age to the occurrence of hemodynamic and arrhythmic complications in STEMI patients. METHODS A total of 848 consecutive patients treated by primary percutaneous coronary intervention for STEMI were evaluated. Heart failure, cardiogenic shock, asystole, inotropic and diuretic use, and kidney dysfunction were used as in-hospital markers of hemodynamic complications. Ventricular fibrillation, conduction disorders, cardiac stimulation, and antiarrhythmic drugs use were used as markers of arrhythmic complications. The relationship between age and the occurrence of hemodynamic and arrhythmic complications was evaluated. The contribution of age to in-hospital death was also assessed. RESULTS In-hospital death occurred in 50 (5.8%) patients; patients who deceased were significantly older than their non-deceased counterparts (70.9 ± 10.9 vs. 61.2 ± 11.8 years; p< 0.0001). There was no association between age and the occurrence of any of the evaluated arrhythmic complications (all p >0.05). However, patients who presented hemodynamic complications were significantly older than those who did not (all p< 0.05). Age >60 years was a significant predictor of hemodynamic complications (p< 0.0001) with 61.7% sensitivity and 60.4% specificity. The association between age and hemodynamic complications remained significant after correction for additional risk factors (i.e., hypertension, diabetes mellitus, pre-existing heart failure, Killip class on admission, symptom onset-to-cardiac catheterization laboratory time interval). CONCLUSIONS In the present study, age was identified as an independent predictor of STEMI-related hemodynamic, but not arrhythmic complications. These data indicate that whereas age does not seem to affect the occurrence of STEMI-related rhythm disorders, patients above the age of 60 should particularly benefit from closer follow-up and more intensive strategies to prevent life-threating hemodynamic complications.

Sign in / Sign up

Export Citation Format

Share Document