When Patent Foramen Ovale (PFO) Can Cause Trouble—A Misplacement of Pacemaker Lead Into the Left Ventricle

Received June 17, 2008; accepted September 4, 2008. Idiopathic ventricular arrhythmias (VAs) arising from the left ventricle (LV) are often accessible for catheter ablation from the aortic sinuses of Valsalva or adjacent to the mitral annulus (MA).1 The aortic and mitral valves are direct apposition and attach to an elliptical opening at the base of the LV known as the LV ostium.2 The VAs arising from this region are being increasingly recognized as targets for catheter ablation.3–7 This review describes the anatomic features of the LV ostium and the electrocardiographic, electrophysiological, and angiographic characteristics that are relevant to the mapping and ablation of these arrhythmias. The dominant central structure of the heart is the junction of the aorta with the LV. Fundamental for understanding idiopathic VAs arising near the aortic and mitral valves are 2 concepts: first, these arrhythmias arise from the LV ostium (Figure 1); and second, the LV ostium is covered by the aorto-ventricular membrane, a tough fibrous structure which is perforated by the aorta anteriorly and the mitral valve (MV) posteriorly (Figure 2). The anatomic concept of the LV ostium and its covering, the aorto-ventricular membrane, are based on the pioneering work of McAlpine.2 Figure 1. The left ventricular ostium (postero-cranial view). The left panel includes the aortic root with the right coronary sinus (R), left coronary sinus (L), and noncoronary sinus (N). In the right panel, the root of the aorta has been removed to demonstrate the elliptical ostium of the left ventricle (LV) with the junction of the right coronary cusp (RCC), left coronary cusp (LCC), and LV summit demonstrated. APM indicates anterior papillary muscle; LA, left atrium; LAFT, left anterior fibrous trigone; LFT, left fibrous trigone; L-RCC, the junction between the LCC and RCC; PPM, posterior papillary muscle; PSP, postero-superior …

ORAL PRESENTATION

Sustained ventricular tachycardia (VT) is an important cause of morbidity and sudden death in patients with heart disease.1 Implantable cardioverter-defibrillators (ICDs) terminate VT episodes, reducing the risk of sudden death. Recurrent VT develops in 40% to 60% of patients who receive an ICD after an episode of spontaneous sustained VT. A first episode of VT occurs in ≈20% of patients within 3 to 5 years after ICD implantation for primary prevention of sudden death in high-risk groups.2–4 ICD shocks reduce quality of life and are associated with an increased risk of death.2–4 Antiarrhythmic drug therapy with amiodarone or sotalol reduces VT episodes but with disappointing incidence of side effects and efficacy.2 Catheter ablation is useful for reducing VT episodes and can be life-saving when VT is incessant.1,5,6 Idiopathic VTs occur in patients without structural heart disease and rarely cause sudden death. Electrophysiological study with catheter ablation is often warranted to confirm the diagnosis, to provide further evidence for the absence of ventricular scar or other disease, and often to cure the arrhythmia. Ablation is also an option for symptomatic nonsustained VT and frequent ventricular ectopy in these patients.1 The appearance of the VT on ECG often suggests its likely cause and associated heart disease (Figure 1). Monomorphic VT has the same QRS complex from beat to beat, indicating repetitive ventricular activation from a structural substrate or focus that can be targeted for ablation. Most are due to reentry through regions of ventricular scar.7 Figure 1. ECG types of VT and most common causes are shown with characteristic ECG features of selected VTs. LBBB indicates left bundle-branch block; LVOT, LV outflow tract; RBBB, right bundle-branch block; L, left; and R, right. Polymorphic VTs have a changing ventricular activation sequence that can be due to …

Left bundle pacing in transposition of the great arteries with previous atrial redirection operation

Objective: To determine the effect of multisite pacing on left ventricular function. Design: Prospective observational study. Patients: 18 patients with heart failure with a dilated poorly functioning left ventricle (LV)...

Radionuclide angiography (RNA) permits analysis of contractility and conduction abnormalities. We determined the parameters of normal ventricular synchronization, assessed the reproducibility of the technique, and compared first harmonic (1H) and third harmonic (3H) analysis. Forty-four normal subjects (28 men and 16 women) were studied. RNA was performed in left anterior oblique (LAO) and left lateral (LL) projections. The onset (To), mean time (Tm), total contraction time (Tt) for right ventricle (RV) and left ventricle (LV), interventricular time (T(RV-LV) = Tm(LV - Tm(RV)) in LAO, and the apex-to-base time (T(a-b)) in LL were measured on the histograms of the time-activity curve. Reproducibility (R) was tested by studying 26 consecutive patients with two successive RNAs. RV starts contracting 25 ms before LV (To(RV) = 29 +/- 37 ms; To(LV) = 54 +/- 39 ms; mean +/- SD) with a 37 ms longer total contraction time. T(RV-LV) is 3 +/- 16 ms. In LL projection, apex and base contract synchronously: T(a-b) = 2 +/- 16 ms. 3H analysis enlarges all duration parameters (To, Tm and Tt), but does not alter synchronization (deltaT(a-b) and deltaT(RV-LV) between 1H and 3H <1%, p = NS). Reproducibility of the duration (T(tLV) and T(tRv)) and synchronization parameters (T(a-b) and T(RV-LV)) is high (R < or = 2.2%). In conclusion, the simultaneous contraction of right and left ventricles and of apex and base can be quantified by RNA phase analysis with high reproducibility. These results, consistent with published electrophysiological data, provide the basis for further non-invasive investigations of ventricular resynchronization in patients with basal electrical or mechanical asynchrony.

Supravalvar ablation has now been well documented to be the ideal mode for ablating specific forms of ventricular tachycardia, atrial tachycardia, and accessory pathways. A studied appreciation of the anatomy of the supravalvar region is a prerequisite for electrophysiologists to safely and effectively approach these arrhythmias. In addition, the consistent ability to correlate the recorded electrograms with fluoroscopic anatomy and intracardiac ultrasound images enhances the chance of successful elimination of supravalvar arrhythmias.

Laser Extraction of Pacemaker Lead Traversing a Patent Foramen Ovale and the Mitral Valve

Prolonged right ventricular (RV) apical pacing produces dysynchronous ventricular contraction, which may result in left ventricular (LV) dysfunction, whereas septal pacing sites might reflect a more synchronous LV activation. This study examined a method of evaluating alternate RV pacing sites using a template scoring system based on measuring the angle of lead attachment in the 40° left anterior oblique (LAO) fluoroscopic view and its effect on altering the loop of lead in the RV. Twenty-three consecutive patients for RV pacing were enrolled. Conventional active fixation leads were positioned in either the RV outflow tract (RVOT) or mid RV using a stylet designed for septal placement (Model 4140, St. Jude Medical, St. Paul, MN, USA). Using LAO cine fluoroscopy, a generous loop of lead was inserted into the RV chamber and the change in angle of attachment determined. Successful positioning of pacing leads at the RVOT septum (18 patients) and mid-RV septum (five patients) was achieved. With introduction of more lead into the RV chamber, the angle of attachment in the LAO projection altered over a range of 6°-32° for all patients with a mean of 14.6 ± 6.6°. In 87% of patients, the range was predominantly within the same template score with only minor overlap into another zone. This study shows that the angle of lead attachment in the RV is altered by introducing more lead, but in most cases, the template score remains the same. Further studies are required to determine the accuracy and efficacy of the templates.

Objective To assess the effect of ultrasound contrast agent SonoVue on the dimensions and systolic function of left and right ventricle in pigs. Methods Sixteen pigs were randomly assigned to two groups. Intravenous injection of 1 ml of SonoVue were given in study group, and repeated 20 min later. The control group was given the same doses of saline. Before and after the administration of contrast agent, the end-diastolic dimension (LVEDD, RVEDD). end-systolic dimension ( LVESD, RVESD) and fractional shortening(LVFS,RVFS) of left and right ventricle were measured. The time to reach the extreme value of these parameters and the time to return to the baseline were recorded. Results There was no significant difference regarding the parameters at baseline between the two groups. After injection of SonoVue,RVEDD significantly increased from (25. 88 ± 1. 38) mm at baseline to its maximum of (33. 26 ± 0. 99)mm( P < 0. 05). Accordingly,RVFS significantly increased from (26. 90 ± 1. 92) % to (33. 92 ± 2. 53) % ( P <0. 05). Meanwhile,LVEDD remarkably decreased from (38.10 ± 1. 39)mm at baseline to its minimum of (26.25 ± 0. 65)mm( P <0. 05) and LVFS remarkably decreased from (36. 24 ± 1. 93) % to (29.13 ± 3.00) % ( P < 0. 05). There was no change in the control group after administration of the saline. When SonoVue was given repeatedly, the maximum RVEDD and RVFS was (29. 98 ± 1. 23) mm and (31. 09 + 1.90) % , respectively, which had less increase compared to the first time. Minimum LVEDD and LVFS was (31. 91 ± 1, 64)mm and (32. 17 ± 2. 31)%,respectively,with less decrease compared with which at first injection. It took (10. 15±0. 59) min for the right and left ventricle to reach the extreme value and (9.00± 0. 56) min to return to the baseline at the first injection. The time used for the right and left ventricle to reach its peak change and back to baseline after second injection of SonoVue were shorter [(8.73± 0.55) min and (6.89± 0.43) min, respectively,both P <0.05]. Conclusions Administration of SonoVue was associated with acute, transient dilation of right ventricle and compression of left ventricle. The influence of SonoVue on the right and left ventricle became less at it second injection. Key words: Echocardiography; Microbubbles/adverse effects; Ventricular function

Cardiac resynchronization therapy (CRT) aims to correct delayed left ventricle (LV) activation resulting from left bundle branch block (LBBB). The source of LV activation delay resides in the septum and/or anterior LV. LV pacing, timed with intrinsic right bundle branch (RBB) conduction, may restore "physiological" biventricular activation. This is not assured because LV paced wavefronts themselves propagate unpredictably. Less studied are effects of right ventricle (RV) pacing on LV activation in heart failure (HF) patients with LBBB. In this case RV pacing pre-excited precisely the region left behind during LV pacing. Consequently, biventricular pacing produced confluent LV depolarization (the patient "responded" to this with reverse remodeling). Successful electrical resynchronization requires best combination and timing of paced/intrinsic wavefront(s). This demands individualization. Sometimes, an RV paced wavefront may be valuable to resynchronization.

Background pacemaker induced cardiomyopathy or transient impairment of the left ventricle (LV) function could be common collateral effects of the prolonged right ventricle (RV) pacing in patients with a pacemaker (PM) and pre-existing intra-ventricular conduction disturbances. However, the impact of RV pacing-site on RV performance of patients with right bundle branch block(RBBB) is still under-investigated. Purpose to study the effects of RV pacing in the mid-septal versus apical site on the morpho-functional performance of RV in patients undergoing permanent PM implantation. Methods We prospectively enrolled consecutive patients with a pre-existent complete RBBB and undergoing dual-chamber PM implantation in our institution. We randomized the patients 1:1 to receive the RV catheter fixed either in the apex or in the mid-septal position. Patients with LV systolic dysfunction (LVEF &amp;lt;50%), severe valvulopathies, left bundle branch block (LBBB), or preserved intraventricular conduction were excluded. Patients who received PM implantation were evaluated both at baseline and after two months with a 12-lead ECG, 2D, and 3D echocardiogram with analysis focused on RV performance according to the guidelines of the European Association of Cardiovascular Imaging. Results a total of 22 patients were randomized in the study, 11 (50%) received RV catheter positioned in the apex and 11 (50%) in the mid-septum, respectively. No baseline differences were recorded between the two groups in clinical characteristics, ECG and echocardiographic parameters. At 2 months follow up, there were no statistically significant difference in the % of RV pacing between the two groups. Nonetheless, RV mid-septal group showed significantly shorter duration of the stimulated QRS (146 ± 12 msec vs. 161 ± 20 msec, p = 0.05), significantly reductions in the RV dimensions (pre: 42 ± 8 mm vs. post: 37 ± 7 mm, p = 0.05) telediastolic area (pre: 12 ± 3 cm2/m2 vs post: 9 ± 4 cm2/ m2, p = 0.02) telediastolic volume (pre: 55 ± 16 ml/m2 vs post: 50 ± 17 ml/m2, p = 0.02) and a significant improvement of RV ejection fraction (pre: 54 ± 9% vs post: 57 ± 11%, p = 0.02) than patients in the RV-apical group. Moreover, patients in the RV-apical group showed significant lowering in the GLS of the LV (pre: -16 ± 3% vs post: -11.7 ± 3%, p &amp;lt;0.001) and in the TAPSE (pre: 23 ± 5 mm vs post: 21 ± 2, p = 0.07) at follow up. Conclusions In this study, mid-septal pacing seems associated with a better morpho-functional RV performance than apical pacing in patients with pre-existent RBBB undergoing permanent PM implantation.

Introduction Cardiac perforation with leadless pacemakers (LPM) remains a concern. Non-septal placement seems to be the main cause, with frequent delivery in the right ventricular (RV) free wall when using standard 30-40º left anterior oblique (LAO) projections. Thus, individualized angulations might be considered, because distinguishing septal from free-wall location with standard projections has been proved to be unreliable: previous studies have shown frequent RV free wall position misclassified as septal when using 30-40º LAO. Methods This is a single-center, observational pilot study, comparing a 60º LAO approach LPM (VR or VDD) implant technique with the standard one. All consecutive patients who received LPM using non-standard LAO projections (study cohort) were compared with an immediately retrospective cohort of consecutive patients who received LPM using only standard projections in the same institution (control cohort). In the study group, sequential 30-40º and 60º LAO projections were performed, and a RV transvenous reference was also considered in cases with preexisting pacing leads or by placing an electrophysiological catheter into an apical-septum position upon implanter´s criterion. The primary endpoint was the need of repositioning the delivery catheter in the study cohort, due to unproper position in the 30-40º LAO angulation. The secondary endpoints were: 1) procedural characteristics (procedure and fluoroscopy times, final fluoroscopic device position and number of deployments); 2) procedure related complications (the composite of vascular complications, implant failure, cardiac perforation, and device dislodgement); 3) acute pacing parameters. Results Twenty-one patients who received LPM using both 30-40º and 60º LAO (study cohort) were compared with 84 patients who received LPM using only 30-40º LAO. Delivery catheter repositioning was needed in 73,7% of patients (n=16/21) in the study cohort, most of them (n=14/16, 77,5%) due to catheter towards RV free wall, distinguished with 60º LAO from 30-40º LAO. Placement in non-midseptal locations was more common in the control group compared to the study group (74.7% vs. 42.8%, p=0.006). The median number of delivery attempts was higher in the study group (1.8±1.3 vs. 1.3±0.9, p=0.010), with longer procedural times. Threshold tended to be higher in the study group (0.8±0.7Vx0.4ms vs. 0.5±0.3Vx0.4ms, p=0.063), with smaller R-wave sensing (9.2±3.7mV vs. 11.4±4.4mV, p=0.038) and impedance (757±207ohms vs. 1026±314ohms, p&amp;lt;0.001). Conclusion 60º LAO frequently identified catheter mislocations using 30-40º LAO, helping to avoid RV free wall LPM deployment. This intervention resulted in longer procedures, possibly due to a higher number of repositions and delivery attempts. Pacing parameters remained adequate, although there was a trend for higher threshold, meanwhile sensing and impedance were lower, maybe related to worse myocardial contact when true septal placement is achieved.Study group implant sequenceBaseline and procedural characteristics

Background Left ventricle (LV) dysfunction after chronic right ventricle (RV) pacing, also known as pacemaker induced cardiomyopathy (PICM) is a relatively common finding, ranging from 15–20% of patients. It has been associated to a high burden RV pacing, age, male gender and intrinsic and paced QRS duration. However, clinical relevance of LV dysfunction in this population has not been studied. Purpose The aim of the study was to identify predictors of heart failure (HF) hospitalization and cardiovascular (CV) mortality in patients with RV pacing. Methods Retrospective and unicentric study. We studied 2418 patients undergoing single or dual-chamber pacemaker implantation between 2012–2018. Patients were included if they had an echocardiogram prior to implantation and a repeated echocardiogram &amp;gt;3 months after implantation. Baseline LV ejection fraction (LVEF) had to be &amp;gt;50%. PICM was defined as ≥10% decrease in LVEF, resulting in LVEF &amp;lt;50%. Alternative causes of LV dysfunction were excluded. Primary endpoint was heart failure hospitalization. Secondary endpoint was cardiovascular mortality. Competing-risk regression analysis was performed to identify predictors of HFH and CV mortality. Results Of 2418 patients, 495 meeting study criteria and 105 (21.2%) met PICM criteria. Follow-up period was 56.1±28.5months. There were no differences in basal LVEF (60.1±0.5% in non-PICM patients vs 59.5±0.5 in PICM patients, p=0.51). Mean LVEF at follow-up was 37.7±0.9 vs 56.7±0.3, p&amp;lt;0.001. After logistic multivariable analysis, factors associated with PICM were alcohol consumption (OR 3.0, 95% CI 1.1–8.0,p=0.032), right bundle branch block (RBBB) (OR 1.9, 95% CI 1.06–3.51,p=0.031), higher RV pacing burden (OR 1.0, 95% CI 1.0–1.1,p=0.008) and higher basal LV end-diastolic diameter (OR 1.1, 95% CI 1.0–1.1,p=0.016). HFH occurred in 144 patients (29.1%). Factors associated with HFH after multivariable analysis were any decrease in LVEF (LVEF&amp;gt;55% as reference: LVEF 46–55% (HR 2.1, 95% CI 1.3–3.3,p=0.002); LVEF 36–45% (HR=1.5, 95% CI 0.7–3.0; p=0.306), LVEF≤35% (HR 2.44, 95% CI 1.11–5.37,p=0.027), age (HR 1.0, 95% CI 1.0–1.1,p=0.037), alcohol consumption (HR 3.4, 95% CI 1.9–6.1,p&amp;lt;0.001), presence of atrial fibrillation (HR 1.7, 95% CI 1.06–2.70,p=0.027) and paced QRS duration (HR 1.0, 95% CI 1.0–1.02,p=0.031). CV mortality occurred in 54 patients (10.9%). Factors associated with CV mortality after multivariable analysis were a decrease in LVEF (LVEF 46–55% (HR 1.6, 95% CI 0.8–3.2,p=0.217); LVEF 36–45% (HR=1.6, 95% CI 0.6–4.2,p=0.33); LVEF≤35% (HR 4.6, 95% CI 2.0–10.7,p&amp;lt;0.001), RBBB (HR 2.1, 95% CI 1.1–3.9,p=0.026) and lower haemoglobin (HR 0.8, 95% CI 0.7–0.99,p=0.033). Conclusion In patients with RV pacing, factors associated with PICM were alcohol consumption, RBBB, RV pacing burden and basal LV end-diastolic diameter. HF hospitalization and CV mortality are common (29.1% and 10.9%). Any decrease in LVEF is associated with an increase in CV events. Funding Acknowledgement Type of funding sources: None.

The implantable cardioverter-defibrillator (ICD) was devised to satisfy the unmet need for an effective, instantaneous therapy to prevent sudden cardiac death (SCD) due to ventricular fibrillation (VF) in at-risk, ambulatory patients. That therapy was a high-voltage electric shock delivered directly into the heart muscle. More than 3 decades later, shocks are still the defining operating characteristic of ICDs, and no other instantaneously effective therapy for VF exists. This elite status was clinched by large randomized clinical trials1,2 which demonstrated that ICDs improved mortality in patients with reduced left ventricular ejection fraction, regardless of pathogenesis or accompanying symptoms of heart failure (HF), by primary prevention of SCD due to ventricular tachyarrhythmia (VTA). Like bradycardia pacemakers for asystole, the ICD resides as a therapy genre of one, with no peer, and no competitor on the horizon. These sibling therapies for lethal heart rhythm disturbances will stand prominently among the greatest medical achievements of the 20th century. The ICD is a mature technology, and neither the technique nor the tools have changed much for several decades. Despite a certain evolutionary elegance of the operating system, the ICD is still a blunt instrument. Although it is true that some innovation has occurred, it is still a matter of a shock delivered by insulated metal conductors residing somewhere in direct proximity to the heart. No innovation beyond the fundamental of a timed shock for VF has proven to enhance mortality benefit. The basic design persists simply because no one can think of a suitable alternative and the self-satisfying aphorism that “shocks save lives.” Yet there is a growing intellectual dissatisfaction with the unintended consequences of this powerful, irreplaceable therapy. The stimulus for this self-inspection is an awareness of the very high morbidity risk overhead borne by the primary prevention patient, in particular, …