scholarly journals Changes in left ventricular electromechanical relations during targeted hypothermia

2020 ◽  
Author(s):  
Kristin Wisløff-Aase ◽  
Viesturs Kerans ◽  
Kristina Haugaa ◽  
Per Steinar Halvorsen ◽  
Helge Skulstad ◽  
...  

Abstract Background:Targeted hypothermia, as used after cardiac arrest, increases electrical and mechanical systolic duration. Differences in duration of electrical and mechanical systole are correlated to ventricular arrhythmias. The electromechanical window (EMW) becomes negative when the electrical systole outlasts the mechanical systole. Prolonged electrical systole corresponds to prolonged QT interval, and is associated with increased dispersion of repolarization and mechanical dispersion. These three factors predispose for arrhythmias. The electromechanical relations during targeted hypothermia are unknown.We wanted to explore the electromechanical relations during hypothermia at 33 °C. We hypothesized that targeted hypothermia would increase electrical and mechanical systolic duration without an increase in EMW negativity, nor an increase in dispersion of repolarization and mechanical dispersion.Methods: In a porcine model (n = 14) we registered electrocardiogram (ECG) and echocardiographic recordings during 38 °C and 33 °C, at spontaneous and atrial paced heart rate 100 beats/min. EMW was calculated by subtracting electrical systole; QT interval, from the corresponding mechanical systole; QRS onset to aortic valve closure. Dispersion of repolarization was measured as time from peak to end of the ECG T wave. Mechanical dispersion was calculated by strain echocardiography as standard deviation of time to peak strain. Results:Electrical systole increased during hypothermia at spontaneous heart rate (p < 0.001) and heart rate 100 beats/min (p = 0.005). Mechanical systolic duration was prolonged and outlasted electrical systole independently of heart rate (p < 0.001). EMW changed from negative to positive value (-20 ± 19 to 27 ± 34 ms, p = 0.001). The positivity was even more pronounced at heart rate 100 beats/min (-25 ± 26 to 41 ± 18 ms, p < 0.001). Dispersion of repolarization decreased (p = 0.027 and p = 0.003), while mechanical dispersion did not differ (p = 0.078 and p = 0.297).Conclusion:Targeted hypothermia increased electrical and mechanical systolic duration, the electromechanical window became positive, dispersion of repolarization was slightly reduced and mechanical dispersion was unchanged. These alterations may have clinical importance. Further clinical studies are required to clarify whether corresponding electromechanical alterations are accommodating in humans.

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Kristin Wisløff-Aase ◽  
Viesturs Kerans ◽  
Kristina Haugaa ◽  
Per Steinar Halvorsen ◽  
Helge Skulstad ◽  
...  

Abstract Background Targeted hypothermia, as used after cardiac arrest, increases electrical and mechanical systolic duration. Differences in duration of electrical and mechanical systole are correlated to ventricular arrhythmias. The electromechanical window (EMW) becomes negative when the electrical systole outlasts the mechanical systole. Prolonged electrical systole corresponds to prolonged QT interval, and is associated with increased dispersion of repolarization and mechanical dispersion. These three factors predispose for arrhythmias. The electromechanical relations during targeted hypothermia are unknown. We wanted to explore the electromechanical relations during hypothermia at 33 °C. We hypothesized that targeted hypothermia would increase electrical and mechanical systolic duration without more profound EMW negativity, nor an increase in dispersion of repolarization and mechanical dispersion. Methods In a porcine model (n = 14), we registered electrocardiogram (ECG) and echocardiographic recordings during 38 °C and 33 °C, at spontaneous and atrial paced heart rate 100 beats/min. EMW was calculated by subtracting electrical systole; QT interval, from the corresponding mechanical systole; QRS onset to aortic valve closure. Dispersion of repolarization was measured as time from peak to end of the ECG T wave. Mechanical dispersion was calculated by strain echocardiography as standard deviation of time to peak strain. Results Electrical systole increased during hypothermia at spontaneous heart rate (p < 0.001) and heart rate 100 beats/min (p = 0.005). Mechanical systolic duration was prolonged and outlasted electrical systole independently of heart rate (p < 0.001). EMW changed from negative to positive value (− 20 ± 19 to 27 ± 34 ms, p = 0.001). The positivity was even more pronounced at heart rate 100 beats/min (− 25 ± 26 to 41 ± 18 ms, p < 0.001). Dispersion of repolarization decreased (p = 0.027 and p = 0.003), while mechanical dispersion did not differ (p = 0.078 and p = 0.297). Conclusion Targeted hypothermia increased electrical and mechanical systolic duration, the electromechanical window became positive, dispersion of repolarization was slightly reduced and mechanical dispersion was unchanged. These alterations may have clinical importance. Further clinical studies are required to clarify whether corresponding electromechanical alterations are accommodating in humans.


2020 ◽  
Author(s):  
Kristin Wisløff-Aase ◽  
Viesturs Kerans ◽  
Kristina Haugaa ◽  
Per Steinar Halvorsen ◽  
Helge Skulstad ◽  
...  

Abstract Background: Targeted hypothermia, as used after cardiac arrest, increases electrical and mechanical systolic duration. Differences in duration of mechanical and electrical systole are correlated to ventricular arrhythmias. The electromechanical window (EMW) becomes negative when electrical systole outlasts the mechanical systole. Prolonged electrical systole is also associated with electrical and mechanical dispersion, both predisposing for arrhythmias. The electromechanical relations during targeted hypothermia are unknown, but treatment after cardiac arrest has not demonstrated increased incidence of ventricular arrhythmic events.We wanted to explore the electromechanical relations during hypothermia at 33 °C. We hypothesized that targeted hypothermia would increase electrical and mechanical systolic duration without an increase in electromechanical negativity, nor an increase in electrical and mechanical dispersion. Methods: In a porcine model (n = 14) we registered electrocardiogram (ECG) and echocardiographic recordings during 38 °C and 33 °C, at spontaneous and atrial paced heart rate 100 beats/min. EMW was calculated by subtracting electrical systole, QT interval, from the corresponding mechanical systole, recorded from onset QRS to aortic valve closure. Electrical dispersion was measured as time from peak to end of the ECG T wave. Mechanical dispersion was calculated by strain echocardiography as standard deviation of time to peak strain. Results:Electrical systole increased during hypothermia at spontaneous heart rate (p < 0.001) and heart rate 100 beats/min (p = 0.005). Mechanical systolic duration was prolonged and outlasted electrical systole independently of heart rate (p < 0.001). EMW changed from negative to positive value (-20 ± 19 to 27 ± 34 ms, p = 0.001). The positivity was even more pronounced at heart rate 100 beats/min (-25 ± 26 to 41 ± 18 ms, p < 0.001). Electrical dispersion decreased (p = 0.027 and p = 0.003), while mechanical dispersion did not differ (p = 0.078 and p = 0.297).Conclusion: Targeted hypothermia increased electrical and mechanical systolic duration, the electromechanical window became positive, electrical dispersion was reduced and mechanical dispersion was unchanged. These alterations may have clinical importance. Further clinical studies are required to clarify whether corresponding electromechanical alterations are accommodating in humans.


2021 ◽  
Author(s):  
Kristin Wisløff-Aase ◽  
Helge Skulstad ◽  
Kristina Haugaa ◽  
Per Snorre Lingaas ◽  
Jan Otto Beitnes ◽  
...  

Abstract BackgroundTargeted temperature management is recommended after cardiac arrest, but the beneficial effects are controversial. The recently published TTM2 study reports that arrhythmias causing hemodynamic compromise are more common during moderate hypothermia. The causation is not explored. Experimentally, moderate hypothermia attenuates electromechanical relations with pro-arrhythmic impact. Mechanical systole outlasts the electrical systole to a greater extent giving increased electromechanical window positivity, and dispersion of electrical and mechanical activity are unaltered. In this prospective clinical study, we explored the effect of moderate hypothermia on electromechanical relations in un-insulted left ventricles. We hypothesized that during moderate hypothermia, prolongation of systolic duration would exceed electrical duration without dispersed electrical- or mechanical activity. Methods20 patients with normal left ventricular function, undergoing surgery on the ascending aorta and connected to cardiopulmonary bypass, were included. Measurements were obtained at 36 °C and 32 °C prior to aortic-repair, and at 36 °C after repair at spontaneous and paced heart rate 90 bpm. Comparable loading conditions were ensured and cardiopulmonary bypass was reduced to 20% of estimated maximum during the measurements. Global cardiac function was measured invasively and with echocardiography. Electromechanical window, dispersion of repolarization by ECG and mechanical dispersion by echocardiography, were calculated. ResultsAt moderate hypothermia (32°C), mechanical systolic prolongation exceeded electrical prolongation so that electromechanical window increased (29 ± 30 to 86 ± 50 ms, p <0.001). Dispersion of repolarization and mechanical dispersion remained unchanged. Myocardial function was preserved with maintained strain, fractional shortening and stroke volume. Similar electromechanical relations were present also at comparable increased heart rate during moderate hypothermia. After rewarming to 36°C, electromechanical alterations were reversed. ConclusionModerate hypothermia increased electromechanical window positivity. Dispersion of repolarisation, mechanical dispersion, and myocardial function were unchanged. Moderate hypothermia did not induce adverse electromechanical changes in the left ventricle during standardized conditions, but rather an attenuation of pro-arrhythmic electromechanical relations.


2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
V Marinho ◽  
P Alves ◽  
C Domingues ◽  
J Ferreira ◽  
J Milner ◽  
...  

Abstract Introduction Hypertrophic cardiomyopathy (HCM) is characterized by a heterogeneous clinical expression with increased risk of sudden cardiac death (SCD) from ventricular arrhythmias (VAs).Several studies have shown that patients with malignant arrhythmias have increased electrical dispersion and in homogeneity of intraventricular conduction. Strain by echocardiography is an excellent tool for assessing regional and global left ventricular (LV) function and mechanical dispersion reflects heterogeneous myocardial contraction. We aimed to explore the value of strain parameters in prediction of VAs in HCM with LV preserved systolic function. Methods Retrospective observational study including all patients with HCM and ICD implanted in setting of primary prevention in our centre. Patients with LVEF &lt; 40% or coronary artery disease were excluded. LV GLS was defined as the average of peak longitudinal strains from a 16 LV segments model, obtained from three apical views. Time to peak strain was defined as the time from onset Q/R wave on ECG to peak negative longitudinal strain during the entire cardiac cycle. Mechanical dispersion was defined as the standard deviation of time to peak negative strain in 16 LV segments. Patients with VA (group1) and patients without VA (group2) were compared. Results The study population included 48 patients, 63.3% of male gender. A family history of HCM was present in 64 pts (43%). All patients were under anti arrhythmic therapy (BB in 95.6%, other anti-arrhythmic in 28.2%). VAs (sustained and non sustained) were documented in 27 (55%) patients. The study groups did not differ regarding to mean age (54 ± 12 vs 56 ± 12 years, p = 0.67), male gender (54% vs 56%, p = 0.87) and BB therapy (91% vs 96%,p = 0.07). Mean LVEF was 58% in group 1 and 61% in group 1, p = 0.56; a LVOT gradient &gt;30mmHg was present in 52% of group 1 pts and 45% of group 2 pts, p = 0.06. Mean wall thickness was 22mm vs 18 mm, p = 0.03, respectively. GLS was significantly lower in group 1 (- 13.9 ±3.4 vs -16.1 ±3.5, p = 0.02), mechanic dispersion was significantly higher in group 1(81 ± 14 vs 60 ± 12ms, respectively, p = 0.01. Using a multivariate logistic regression model including variables included in SCD HCM risk score proposed by ESC mechanical dispersion (OR: 1.54 (1.03–8.7), p = 0,03) was a strong and independent risk predictor of VA. Using optimal cut-off values from ROC analyses, patients with mechanical dispersion &gt;67 ms (AUC = 0.82, p= 0.02) had more VAs. Conclusions Mechanical dispersion and GLS may help to identify HCM patients with high risk of VAs and SCD. Abstract P1541 Figure 1


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T F Cianciulli ◽  
M C Saccheri ◽  
A M Risolo ◽  
J A Lax ◽  
R J Mendez ◽  
...  

Abstract Background Fabry disease is a rare X-linked storage disorder caused by a deficiency of the lysosomal enzyme α-galactosidase A and generally causes multi-organ dysfunction. Heart disease is the main cause of death, due to severe left ventricular (LV) systolic dysfunction and sudden death. In several heart diseases, the LV systolic dysfunction and ventricular arrhythmias are associated with mechanical dispersion (MD). The presence of MD in patients with FD has not been studied yet. In this cross-sectional study, we investigated the prevalence of MD in patients with FD. Methods Complete echocardiographic and speckle tracking echocardiographic (STE) data were collected. MD is an index of inter-segmental discoordination of contraction which has been used to quantify LV dyssynchrony and was defined as the standard deviation (SD) of time to peak negative strain in 17 left ventricular segments. Patients were divided into two groups according to whether or not they had left ventricular hypertrophy (LVH). MD was defined as an SD >49 msec. Results We studied 108 patients with FD, 24 patients (22%) were excluded due to inadequate imaging quality or presence of comorbidities, so the final study population consisted of 84 patients (mean age 33.3±14.6 years, 60.7% women). LVH in FD appears at older ages than in patients without LVH (48±12.5 y/o vs 27.8±11.1 y/o, p<0.0001). Patients with FD without LVH (Group I) showed normal global longitudinal peak strain (GLPS) (21.2±2.5%) and no MD (32.7±8.8 msec). In Group II (n=23) patients with FD with LVH, 17 (73.9%) had MD >49 msec prolonged mechanical dispersion (73.3±20.7 msec) and reduced GLPS (13.6±4.0%). MD was more pronounced in Fabry patients with LVH than in patients without LVH (63.4±24.7 msec vs. 32.7±8.8 msec, p<0.0001). GLPS was lower in Fabry patients with LVH than in patients without LVH (15.3±4.7% vs 21.2±2.5%, p<0.0001). Figure 1 Conclusions To our knowledge, this is the first study to demonstrate the prevalence of mechanical dispersion in patients with FD. Mechanical dispersion was seen in 73.9% of patients with FD with LVH. This dyssynchrony should be taken into account in patients who develop heart failure or life-threatening ventricular tachyarrhythmias.


Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Elsayed Z Soliman ◽  
George Howard ◽  
George Howard ◽  
Mary Cushman ◽  
Brett Kissela ◽  
...  

Background: Prolongation of heart rate-corrected QT interval (QTc) is a well established predictor of cardiovascular morbidity and mortality. Little is known, however, about the relationship between this simple electrocardiographic (ECG) marker and risk of stroke. Methods: A total of 27,411 participants aged > 45 years without prior stroke from the REasons for Geographic and Racial Differences in Stroke (REGARDS) study were included in this analysis. QTc was calculated using Framingham formula (QTcFram). Stroke cases were identified and adjudicated during an up to 7 years of follow-up (median 2.7 years). Cox proportional hazards analysis was used to estimate the hazard ratios for incident stroke associated with prolonged QTcFram interval (vs. normal) and per 1 standard deviation (SD) increase, separately, in a series of incremental models. Results: The risk of incident stroke in the study participants with baseline prolonged QTcFram was almost 3 times the risk in those with normal QTcFram [HR (95% CI): 2.88 (2.12, 3.92), p<0.0001]. After adjustment for age, race, sex, antihypertensive medication use, systolic blood pressure, current smoking, diabetes, left ventricular hypertrophy, atrial fibrillation, prior cardiovascular disease, QRS duration, warfarin use, and QT-prolonging drugs (full model), the risk of stroke remained significantly high [HR (95% CI): 1.67 (1.16, 2.41), p=0.0060)], and was consistent across several subgroups of REGARDS participants. When the risk of stroke was estimated per 1 SD increase in QTcFram, a 24% increased risk was observed [HR (95% CI): 1.24 (1.16, 1.33), p<0.0001)]. This risk remained significant in the fully adjusted model [HR (95% CI): 1.12 (1.03, 1.21), p=0.0055]. Similar results were obtained when other QTc correction formulas including Hodge’s, Bazett’s and Fridericia’s were used. Conclusions: QTc prolongation is associated with a significantly increased risk of incident stroke independently from known stroke risk factors. In light of our results, examining the risk of stroke associated with QT-prolonging drugs may be warranted.


Heart ◽  
2019 ◽  
Vol 105 (14) ◽  
pp. 1063-1069 ◽  
Author(s):  
Simon Ermakov ◽  
Radhika Gulhar ◽  
Lisa Lim ◽  
Dwight Bibby ◽  
Qizhi Fang ◽  
...  

ObjectiveBileaflet mitral valve prolapse (MVP) with either focal or diffuse myocardial fibrosis has been linked to ventricular arrhythmia and/or sudden cardiac arrest. Left ventricular (LV) mechanical dispersion by speckle-tracking echocardiography (STE) is a measure of heterogeneity of ventricular contraction previously associated with myocardial fibrosis. The aim of this study is to determine whether mechanical dispersion can identify MVP at higher arrhythmic risk.MethodsWe identified 32 consecutive arrhythmic MVPs (A-MVP) with a history of complex ventricular ectopy on Holter/event monitor (n=23) or defibrillator placement (n=9) along with 27 MVPs without arrhythmic complications (NA-MVP) and 39 controls. STE was performed to calculate global longitudinal strain (GLS) as the average peak longitudinal strain from an 18-segment LV model and mechanical dispersion as the SD of the time to peak strain of each segment.ResultsMVPs had significantly higher mechanical dispersion compared with controls (52 vs 42 ms, p=0.005) despite similar LV ejection fraction (62% vs 63%, p=0.42) and GLS (−19.7 vs −21, p=0.045). A-MVP and NA-MVP had similar demographics, LV ejection fraction and GLS (all p>0.05). A-MVP had more bileaflet prolapse (69% vs 44%, p=0.031) with a similar degree of mitral regurgitation (mostly trace or mild in both groups) (p>0.05). A-MVP exhibited greater mechanical dispersion when compared with NA-MVP (59 vs 43 ms, p=0.0002). Mechanical dispersion was the only significant predictor of arrhythmic risk on multivariate analysis (OR 1.1, 95% CI 1.02 to 1.11, p=0.006).ConclusionsSTE-derived mechanical dispersion may help identify MVP patients at higher arrhythmic risk.


2013 ◽  
Vol 60 (2) ◽  
pp. 15-21
Author(s):  
Kráľová E. ◽  
Jankyová S. ◽  
Pekárik A. ◽  
Čuboň J. ◽  
Stankovičová T.

Abstract We observed the changes in electrical activity, biometric and haemodynamic parameters of hearts in animals with experimental diabetes mellitus (DM). As well the effect of carvedilol, PycnogenolR and its combination with carvedilol on DM heart function was tested. DM was induced by streptozotocin over three sequential days at a dose of 25 mg/kg body weight i.p. We started therapy by suspension of carvedilol, PycnogenolR and their combination for six weeks. Blood pressure was measured using tail cuff plethysmography. ECG, haemodynamic and biometric parameters were measured in isolated hearts perfused according to the Langendorff. DM rats had increased systolic arterial blood pressure, thicker free wall of left ventricle but weakened myocardial contractility compared with controls. In contrast to controls, electrophysiological parameters showed prolonged QT interval and increased incidence of dysrhythmias in DM rats. The PycnogenolR administration induced regression of left ventricular hypertrophy, improved left ventriculi contraction and increased coronary flow; however, it did not improve the electrical activity of the myocardium compared with DM ones. Carvedilol also reversed the myocardial remodelling, shortened the duration of QT interval and suppressed the incidence of dysrhythmias. The common combination of drugs improved biometric and haemodynamic parameters compared with DM animals, however, not so significantly as monotherapy. On the other hand, the combination of carvedilol and PycnogenolR significantly reduced the duration of the QT interval and shortened the incidence of dysrhythmias. We can conclude that the administration of PycnogenolR effectively improved haemodynamic parameters, and carvedilol affected biometric parameters and also electrical parameters in DM animals. We observed the marked synergic effect of the combination of both drugs on the electrical activity of myocardium. This combination shortened the most pathologically prolonged QT interval and reduced the number of dysrhythmias.


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