scholarly journals Physiology and Practicality of Left Ventricular Septal Pacing

2021 ◽  
Vol 10 (3) ◽  
pp. 165-171
Author(s):  
Luuk Heckman ◽  
Justin Luermans ◽  
Floor Salden ◽  
Antonius Martinus Wilhelmus van Stipdonk ◽  
Masih Mafi-Rad ◽  
...  

Left ventricular septal pacing (LVSP) and left bundle branch pacing (LBBP) have been introduced to maintain or correct interventricular and intraventricular (dys)synchrony. LVSP is hypothesised to produce a fairly physiological sequence of activation, since in the left ventricle (LV) the working myocardium is activated first at the LV endocardium in the low septal and anterior free-wall regions. Animal studies as well as patient studies have demonstrated that LV function is maintained during LVSP at levels comparable to sinus rhythm with normal conduction. Left ventricular activation is more synchronous during LBBP than LVSP, but LBBP produces a higher level of intraventricular dyssynchrony compared to LVSP. While LVSP is fairly straightforward to perform, targeting the left bundle branch area may be more challenging. Long-term effects of LVSP and LBBP are yet to be determined. This review focuses on the physiology and practicality of LVSP and provides a guide for permanent LVSP implantation.

2008 ◽  
Vol 294 (4) ◽  
pp. H1888-H1895 ◽  
Author(s):  
Eric Plante ◽  
Dominic Lachance ◽  
Serge Champetier ◽  
Marie-Claude Drolet ◽  
Élise Roussel ◽  
...  

The objective of this study was to assess the long-term effects of β-blockade on survival and left ventricular (LV) remodeling in rats with aortic valve regurgitation (AR). The pharmacological management of chronic AR remains controversial. No drug has been definitively proven to delay the need for valve replacement or to affect morbidity and/or mortality. Our group has reported that the adrenergic system is activated in an animal model of AR and that adrenergic blockade may help maintain normal LV function. The effects of prolonged treatment with a β-blocker are unknown. Forty Wistar rats with severe AR were divided into 2 groups of 20 animals each and treated with metoprolol (Met, 25 mg·kg−1·day−1) or left untreated for 1 yr. LV remodeling was evaluated by echocardiography. Survival was assessed by Kaplan-Meir curves. Hearts were harvested for tissue analysis. All Met-treated animals were alive after 6 mo vs. 70% of untreated animals. After 1 yr, 60% of Met-treated animals were alive vs. 35% of untreated animals ( P = 0.028). All deaths, except one, were sudden. There were no differences in LV ejection fraction (all >50%) or LV dimensions. LV mass tended to be lower in the Met-treated group. There was less subendocardial fibrosis in this group, as well as lower LV filling pressures (LV end-diastolic pressure). β-Adrenergic receptor ratio (β1/β2) was improved. One year of treatment with Met was well tolerated. Met improved 1-yr survival, minimized LV hypertrophy, improved LV filling pressures, decreased LV subendocardial fibrosis, and helped restore the β-adrenergic receptor ratio.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Robert W Mills ◽  
Larry J Mulligan ◽  
Arne van Hunnik ◽  
Marion Kuiper ◽  
Anniek Lampert ◽  
...  

Objective: Conventional right ventricular (RV) apex pacing is associated with asynchronous activation and reduced left ventricular (LV) pump function. Previous studies have shown acute hemodynamic benefits over RV apex pacing by LV septal or LV apex pacing. We investigated whether this improvement translates into a long-term benefit and how acute LV function during single site LV pacing compares to biventricular pacing. Methods: After AV-nodal ablation, mongrel dogs were randomized to receive 16 weeks of VDD pacing at the RV apex (n = 7), LV apex (n = 7), or LV mid-septum (n = 8; trans-ventricular septal approach). LV contractility (dP/dt max /P instantaneous ) was measured during normal ventricular conduction from atrial pacing (AP) and during ventricular pacing 1–3 hours and 16 weeks after implant. At 16 weeks, contractility was also measured after an acute switch from the implant site (IS) to the non-implanted apex (both for LV septal group) and to RV apex + LV lateral (BiV) pacing. Results: While acute and chronic RV apex pacing significantly reduced contractility (Figure a ; mean ± SD, *p<0.05 contrasted to 1), LV pacing maintained contractility near AP levels. After 16 weeks of RV apex pacing, switching to LV apex pacing (but not BiV pacing) increased contractility (Figure b ). After 16 weeks of LV pacing, switching to RV apex pacing decreased contractility. Collectively, acute LV apex pacing enhanced contractility over acute BiV (p<.001). Conclusions: Chronic LV apex and LV mid-septal pacing maintain contractility near normal levels, and at a higher level than RV apex pacing. Acutely, LV apex pacing improves contractility compared to BiV pacing.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Arnold Ng ◽  
Christine Allman ◽  
Jane Vidaic ◽  
Hui Tei ◽  
Andrew P Hopkins ◽  
...  

Background: Right ventricular (RV) septal pacing has been advocated as an alternative to RV apical pacing to avoid long term detrimental effects. There is conflicting evidence on the benefits of RV septal pacing. No studies have previously compared left ventricular (LV) strain and dyssynchrony between different pacing sites and utilized echocardiography to determine pacing sites. Methods: 55 patients (22 normal controls, 17 RV septal and 17 RV apical pacing) were recruited. LV circumferential and radial strain were determined in the midventricular short axis views. Circumferential and radial strain synchrony, and longitudinal systolic (SDTs) and diastolic (SDTe) dyssynchrony indices were determined. Echocardiographic determination of pacing sites were compared with ECG and chest x-ray (CXR). Results: The median pacing durations were 436 days for RV septal and 2398 days for RV apical pacing. Mean QRS duration were significantly shorter for septal than apical pacing and normal controls (139.8 ± 22.6 vs. 162.4 ± 22.9 vs. 85.9 ± 15.2 msec respectively, p < 0.001). LV mass index, end-systolic volume index and ejection fraction were more impaired in RV septal than apical pacing (108.2 ± 27.2 vs. 91.5 ± 15.4 g/m 2 , 21.3 ± 3.7 vs. 19.4 ± 9.3mL/m 2 , 47.6 ± 8.5 vs. 54.2 ± 7.8% respectively, all p < 0.05). RV septal pacing was associated with more impaired circumferential strain (p < 0.001) and worse circumferential strain dyssynchrony (p = 0.02) than apical pacing and normal controls. There were no significant differences in radial strain, radial strain dyssynchrony or SDTs. RV septal pacing consisted of a heterogeneous group of different pacing sites on echocardiography, and there was only modest agreement between echocardiographic, ECG and CXR determinations of pacing sites. Conclusions: RV septal pacing was associated with poorer long term LV function and greater dyssynchrony than RV apical pacing and normal controls.


Circulation ◽  
2001 ◽  
Vol 104 (suppl_1) ◽  
Author(s):  
Takeshi Nishina ◽  
Kazunobu Nishimura ◽  
Sadatoshi Yuasa ◽  
Senri Miwa ◽  
Takuya Nomoto ◽  
...  

Background Long term effects of left ventricle (LV) repair surgery (LVR) for ischemic cardiomyopathy are not well understood. Methods and Results Sixty-nine rats developed ischemic cardiomyopathy with large akinetic LV area 4 weeks after the left anterior descending artery was ligated. In a second surgery 4 weeks later, 33 rats underwent LVR by plication of the akinetic LV area (LVR group), and 36 underwent rethoracotomy alone (sham group). No medication was used in either group. All rats survived the second surgery. LV end-diastolic dimension as measured by echocardiography, LV fractional shortening, and the maximal end-systolic pressure-volume relationship (E max ) as calculated from the data by catheter-tipped manometer and echocardiography improved in the LVR group after the second surgery, but LV end-diastolic dimension and E max gradually deteriorated as time passed. LV end-diastolic pressure improved 1 week after LVR but rose significantly 4 weeks after LVR. Brain natriuretic peptide mRNA was lower in the LVR group than in the sham group 1 week after LVR but not 4 weeks postoperatively. Conclusions Initial improvement in LV function and neurohormonal status after LVR did not last for 4 weeks in this rat model when untreated medically. The mechanism of deterioration should be elucidated to improve long-term results of LVR.


2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Takaaki Furihata ◽  
Satoshi Maekawa ◽  
Shingo Takada ◽  
Naoya Kakutani ◽  
Hideo Nambu ◽  
...  

Abstract Background Doxorubicin (DOX) is widely used as an effective chemotherapeutic agent for cancers; however, DOX induces cardiac toxicity, called DOX-induced cardiomyopathy. Although DOX-induced cardiomyopathy is known to be associated with a high cumulative dose of DOX, the mechanisms of its long-term effects have not been completely elucidated. Pioglitazone (Pio) is presently contraindicated in patients with symptomatic heart failure owing to the side effects. The concept of drug repositioning led us to hypothesize the potential effects of Pio as a premedication before DOX treatment, and to analyze this hypothesis in mice. Methods First, for the hyperacute (day 1) and acute (day 7) DOX-induced dysfunction models, mice were fed a standard diet with or without 0.02% (wt/wt) Pio for 5 days before DOX treatment (15 mg/kg body weight [BW] via intraperitoneal [i.p.] administration). The following 3 treatment groups were analyzed: standard diet + vehicle (Vehicle), standard diet + DOX (DOX), and Pio + DOX. Next, for the chronic model (day 35), the mice were administrated DOX once a week for 5 weeks (5 mg/kg BW/week, i.p.). Results In the acute phase after DOX treatment, the percent fractional shortening of the left ventricle (LV) was significantly decreased in DOX mice. This cardiac malfunction was improved in Pio + DOX mice. In the chronic phase, we observed that LV function was preserved in Pio + DOX mice. Conclusions Our findings may provide a new pathophysiological explanation by which Pio plays a role in the treatment of DOX-induced cardiomyopathy, but the molecular links between Pio and DOX-induced LV dysfunction remain largely elusive.


2021 ◽  
Vol 10 (6) ◽  
pp. 1273
Author(s):  
Georgios Chatzis ◽  
Styliani Syntila ◽  
Harald Schuett ◽  
Christian Waechter ◽  
Holger Ahrens ◽  
...  

Although the use of microaxilar mechanical circulatory support systems may improve the outcome of patients with cardiogenic shock (CS), little is known about its effect on the long-term structural integrity of left ventricular (LV) valves as well as on the development of LV-architecture. Therefore, we aimed to study the integrity of the LV valves and architecture and function after Impella support. Thus, 84 consecutive patients were monitored over two years having received ImpellaTM CP (n = 24) or 2.5 (n = 60) for refractory CS (n = 62) or for high-risk percutaneous coronary interventions (n = 22) followed by optimal medical treatment. Beside a significant increase in LV ejection fraction after two years (p ≤ 0.03 vs. pre-implantation), we observed a statistically significant decrease in LV dilation (p < 0.001) and severity of mitral valve regurgitation (p = 0.007) in the two-year follow-up period, suggesting an improved LV architecture. Neither the duration of support, nor the size of the Impella device or the indication for its use revealed any devastating impact on aortic or mitral valve integrity. These findings indicate that Impella device is a safe means of support of LV-function without detrimental long-term effects on the structural integrity of LV valves regardless of the size of the device or the indication of support.


Author(s):  
Philippe C. Wouters ◽  
Geert E. Leenders ◽  
Maarten J. Cramer ◽  
Mathias Meine ◽  
Frits W. Prinzen ◽  
...  

AbstractPurpose: Cardiac resynchronisation therapy (CRT) improves left ventricular (LV) function acutely, with further improvements and reverse remodelling during chronic CRT. The current study investigated the relation between acute improvement of LV systolic function, acute mechanical recoordination, and long-term reverse remodelling after CRT. Methods: In 35 patients, LV speckle tracking longitudinal strain, LV volumes & ejection fraction (LVEF) were assessed by echocardiography before, acutely within three days, and 6 months after CRT. A subgroup of 25 patients underwent invasive assessment of the maximal rate of LV pressure rise (dP/dtmax,) during CRT-implantation. The acute change in dP/dtmax, LVEF, systolic discoordination (internal stretch fraction [ISF] and LV systolic rebound stretch [SRSlv]) and systolic dyssynchrony (standard deviation of peak strain times [2DS-SD18]) was studied, and their association with long-term reverse remodelling were determined. Results: CRT induced acute and ongoing recoordination (ISF from 45 ± 18 to 27 ± 11 and 23 ± 12%, p < 0.001; SRS from 2.27 ± 1.33 to 0.74 ± 0.50 and 0.71 ± 0.43%, p < 0.001) and improved LV function (dP/dtmax 668 ± 185 vs. 817 ± 198 mmHg/s, p < 0.001; stroke volume 46 ± 15 vs. 54 ± 20 and 52 ± 16 ml; LVEF 19 ± 7 vs. 23 ± 8 and 27 ± 10%, p < 0.001). Acute recoordination related to reverse remodelling (r = 0.601 and r = 0.765 for ISF & SRSlv, respectively, p < 0.001). Acute functional improvements of LV systolic function however, neither related to reverse remodelling nor to the extent of acute recoordination. Conclusion: Long-term reverse remodelling after CRT is likely determined by (acute) recoordination rather than by acute hemodynamic improvements. Discoordination may therefore be a more important CRT-substrate that can be assessed and, acutely restored.


2021 ◽  
Vol 10 (4) ◽  
pp. 822
Author(s):  
Luuk I.B. Heckman ◽  
Justin G.L.M. Luermans ◽  
Karol Curila ◽  
Antonius M.W. Van Stipdonk ◽  
Sjoerd Westra ◽  
...  

Background: Left bundle branch area pacing (LBBAP) has recently been introduced as a novel physiological pacing strategy. Within LBBAP, distinction is made between left bundle branch pacing (LBBP) and left ventricular septal pacing (LVSP, no left bundle capture). Objective: To investigate acute electrophysiological effects of LBBP and LVSP as compared to intrinsic ventricular conduction. Methods: Fifty patients with normal cardiac function and pacemaker indication for bradycardia underwent LBBAP. Electrocardiography (ECG) characteristics were evaluated during pacing at various depths within the septum: starting at the right ventricular (RV) side of the septum: the last position with QS morphology, the first position with r’ morphology, LVSP and—in patients where left bundle branch (LBB) capture was achieved—LBBP. From the ECG’s QRS duration and QRS morphology in lead V1, the stimulus- left ventricular activation time left ventricular activation time (LVAT) interval were measured. After conversion of the ECG into vectorcardiogram (VCG) (Kors conversion matrix), QRS area and QRS vector in transverse plane (Azimuth) were determined. Results: QRS area significantly decreased from 82 ± 29 µVs during RV septal pacing (RVSP) to 46 ± 12 µVs during LVSP. In the subgroup where LBB capture was achieved (n = 31), QRS area significantly decreased from 46 ± 17 µVs during LVSP to 38 ± 15 µVs during LBBP, while LVAT was not significantly different between LVSP and LBBP. In patients with normal ventricular activation and narrow QRS, QRS area during LBBP was not significantly different from that during intrinsic activation (37 ± 16 vs. 35 ± 19 µVs, respectively). The Azimuth significantly changed from RVSP (−46 ± 33°) to LVSP (19 ± 16°) and LBBP (−22 ± 14°). The Azimuth during both LVSP and LBBP were not significantly different from normal ventricular activation. QRS area and LVAT correlated moderately (Spearman’s R = 0.58). Conclusions: ECG and VCG indices demonstrate that both LVSP and LBBP improve ventricular dyssynchrony considerably as compared to RVSP, to values close to normal ventricular activation. LBBP seems to result in a small, but significant, improvement in ventricular synchrony as compared to LVSP.


Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Aline M De Souza ◽  
Jonathas Almeida ◽  
Nataliia Shults ◽  
Hong Ji ◽  
Kathryn Sandberg

Severe caloric restriction (sCR) increases the risk for acute cardiovascular disease. Less understood are the long-term effects on cardiovascular disease risk after the sCR period has ended. We investigated the effects of sCR on heart structure and function months after refeeding (sCR-Refed). Female Fischer rats (3-months-old) were maintained on (CT) ad libitum or a 60% caloric restricted diet for 2 weeks. Thereafter, all rats received ad libitum chow for 3 months and they were analyzed by precision ultrasound to assess their heart function. After imaging, the animals were sacrificed and the hearts were subjected to ischemia-reperfusion (I/R) using a Langendorff preparation. After 2 weeks of sCR, rats lost 15% of their initial body weight (BW) [% (100*(Final-Initial/Initial)): CT, 1.5±0.8 vs sCR, -15.4±1.1; p<0.001;n=8]. After 3 months of refeeding, there was no detectable difference in BW between CT and sFR-Refed groups. Isolated hearts from the sCR-Refed rats exhibited worse myocardial pathology after I/R compared to CT rats. The parallel orientation of myofibers and striations normally present in cardiomyocytes was lost in sCR-Refed rats. Further analysis revealed uneven blood-filling of the microcirculatory vessels and prominent interstitial edema of the myocardium. Hearts from sCR-Refed rats had more atrophied cardiomyocytes than CT [Atrophied/Total (%): CT, 0.2±0.1 vs sCR-Refed, 50.6±1.1; p<0.001; n=5]. The number of arrhythmic events during a 30 min ischemic interval in isolated hearts doubled after 2 weeks on the sCR diet ( data not shown ) and remained doubled 3 months later [Arrhythmias (% of time): CT, 34±8 vs sCR-Refed, 68±9; p=0.02; n=8]. Ultrasound imaging showed no difference in stroke volume, coronary perfusion pressure and left ventricular mass. However, the thickness of the left ventricular posterior wall was significantly reduced in sCR-Refed rats [(mm): CT, 2.55 ±0.03 vs sCR-Refed, 2.10±0.04; p=0.002; n=4]. These findings indicate heart structure and function remained damaged months after the sCR period ended and BW was restored. These studies have adverse cardiovascular risk implications for who are subjected either voluntarily (crash diets) or involuntarily (very low food security) to periods of inadequate caloric intake.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Daniela Ravizzoni Dartora ◽  
Adrien Flahualt ◽  
Carolina Nobre Pontes ◽  
Gabriel Altit ◽  
Alyson Deprez ◽  
...  

Introduction: Preterm (PT) birth is associated with increased risk of cardiovascular diseases (CVD) and heart failure. We previously reported left ventricular (LV) mitochondrial dysfunction in a rat model mimicking the deleterious conditions associated with PT birth. Whether mitochondrial function is altered in humans born PT and associated with LV function changes is unknown. We aimed to determine if serum humanin levels, a mitochondrial-derived peptide with cytoprotective effects, are altered in humans born PT and are associated with impaired myocardial function. Methods: Data were obtained from 55 young adults born PT (<30 weeks of gestational age, GA) compared to 54 full-term (T) controls of the same age. Serum humanin levels were determined by ELISA and LV ejection fraction (LVEF) by echocardiography. Results are shown as median (interquartile range) and comparisons between groups were performed using non-parametric tests. Results: Individuals were evaluated at 23.3 (21.4, 25.3) years, and age and sex distribution were similar between groups. Median GA was 27.5 (26.2, 28.4) weeks in the PT group. Humanin levels (pg/ml) were 132.9 (105.1, 189.3) and 161.1 (123.6, 252) in the PT and the T groups, respectively (p=0.0414). LVEF was within the normal range and similar between groups. Lower LVEF was associated with lower humanin levels (p<0.001), and this association was observed both in the term (p=0.002) and the preterm (p=0.047) groups. Conclusions: Serum humanin levels are lower in adult born PT. Since lower humanin levels are also associated with lower LVEF, our results suggest that mitochondrial alterations could play a role in the long-term adverse cardiovascular consequences of PT birth. Humanin analogs improve LV function in experimental models. Our results pave the way for future studies exploring humanin as a therapeutic avenue for the prevention and treatment of CVD in individuals born PT.


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