X-ray and magnetic resonance imaging fusion for cardiac resynchronization therapy

Cardiac Resynchronization Therapy (CRT) can effectively treat left ventricle (LV) driven Heart Failure (HF). However, 30% of the CRT recipients do not experience symptomatic benefit. Recent studies show that the CRT response rate can reach 95% when the LV pacing lead is placed at an optimal site at a region of maximal LV dyssynchrony and away from myocardial scars. Cardiac Magnetic Resonance (CMR) can identify the optimal site in three dimensions (3D). 3D CMR data can be registered to clinical standard x-ray fluoroscopy to achieve an optimal pacing of the LV. We have developed a 3D CMR to 2D x-ray image registration method for CRT procedures. We have employed the LV pacing lead on x-ray images and coronary sinus on MR data as landmarks. The registration method makes use of a guidewire simulation algorithm, edge based image registration technique and x-ray C-arm tracking to register the coronary sinus and pacing lead landmarks.     

Transvenous implantation of a coronary sinus lead for left ventricular pacing after cutting balloon angioplasty

We describe a patient in whom a localized proximal vein stenosis at the only possible target vein precluded placement of a coronary sinus lead for left ventricular (LV) pacing. After multiple attempts to perform venoplasty with both compliant and noncompliant balloons, a cutting balloon relieved the obstruction, and an LV pacing lead was successfully placed in the midportion of this lateral vein.     

Left ventricular lead performance in cardiac resynchronization therapy: impact of lead localization and complications

INTRODUCTION: Cardiac resynchronization therapy (CRT) using left ventricular (LV) pacing from the coronary sinus tributary is increasingly and frequently used in patients with severe congestive heart failure. The present study investigates LV lead performance in different anatomic locations. METHODS: The LV pacing site was defined by bi-plane fluoroscopy. In the left anterior oblique view, the coronary sinus is encircling the mitral ring with the tributaries radiating out like the hands of a watch. Using this clockwise method, Group A had an LV pacing site before 3 o'clock and Group B at or after 3 o'clock. In right anterior oblique view, the LV was divided into three segments: basal, mid-ventricular, and apical. RESULTS: LV lead implantation was successful in all of 120 consecutive patients. Mean follow-up was 16.7 months. Implantation time decreased from mean 190 to 80 minutes during the period (P = 0.01). The mean LV lead stimulation threshold increased initially and stabilized afterwards. The threshold measured at last follow-up was higher than at implantation (2.3 vs 2.7 microJ, P = 0.04). Useful venograms were obtained in 94 patients. No significant difference in thresholds was observed between Groups A and B. Phrenic nerve stimulation was most commonly seen in Group B (8/70 vs 1/24, P = 0.001). CONCLUSION: Implantation of an LV lead for CRT is possible in patients with congestive heart failure and associated with an acceptable low complication rate. LV lead implantation is associated with a learning curve. At mid-term follow-up, LV lead performance is stable and unrelated to the LV implantation site.     

Simple access to the coronary venous system for left ventricular pacing

Implantation of the LV lead for biventricular pacing can be challenging, time consuming, and often requires extensive fluoroscopy time. A conventional diagnostic 5 Fr left Amplatz catheter was used to cannulate the coronary sinus in 15 consecutive patients undergoing implantation of a biventricular pacemaker. When the coronary sinus was cannulated, the proximal end of the Amplatz catheter was cut and the coronary sinus sheath was passed over the Amplatz catheter that was then removed. Coronary sinus cannulation was achieved in all 15 patients with a mean fluoroscopy time of 3.34 +/- 1.9 minutes. Subsequent implantation of a biventricular pacemaker was successful and free of complications in all the 15 patients.     

QRS Duration Widening: Reduced Synchronization of Endocardial Activation or Transseptal Conduction Time?

Antegrade activation of the His-Purkinje system (HPS) results in synchronized activation of the right ventricular (RV) and left ventricular (LV) endocardia forming normal, narrow QRS duration (QRSD). An alteration in septal activation and transseptal conduction time have been reported to be the causes for QRSD widening seen with bundle branch block. However, reduced synchronization of activation ofRVand LV endocardia as another potential mechanism for QRSD widening has not been systematically studied. Fifteen consecutive patients underwent radiofrequency ablation (RFA) for treatment of supraventricular tachycardia. After RFA, mean QRSD in normal sinus rhythm was 86 ± 8 ms with mean HV interval of 40 ± 5 ms. Right atrial (RA), coronary sinus (CS), simultaneous (S) RA-CS, RVapex (RVA), LV apex (LVA), and SRVA-LVA pacing were performed. Mean QRSD with RA, CS, SRA-CS pacing was similar to normal sinus rhythm (87 ± 7, 87 ± 8 and 88 ± 8 ms respectively). Mean QRSD was significantly longer with SRVA-LVA and either RVA or LVA pacing alone compared to normal sinus rhythm (106 t 8, 146 ± 12 and 157 ± 13 ms, respectively). However, QRSD was significantly shorter with SRVA-LVA pacing compared to either RVA or LVA pacing alone (P < 0.0001). We conclude that shorter QRSD with SRVA-LVA pacing compared to either RVA or LVA pacing alone is due to elimination of transseptal conduction delay; longer QRSD with SRVA-LVA pacing compared to sinus or atrial paced rhythm is due to reduced synchronization of endocardial activation secondary to ectopic entry of impulses into the HPS network and inability to take advantage of the branching structure of the HPS. Therefore, in addition to transseptal conduction delay, reduced synchronization of endocardial activation is another potential mechanism for QRSD widening.     

Quad‐Site Pacing Using a Quadripolar Left Ventricular Pacing Lead

Pacing the left ventricle (LV) from multiple sites simultaneously may result in a better response to cardiac resynchronization therapy (CRT). We sought to assess whether multisite pacing using a quadripolar LV lead improves acute hemodynamic response (AHR) to CRT. We paced four ventricular sites simultaneously using two vectors of a Quartet lead, a right ventricular apical lead, and an additional LV lead temporarily placed in an anterior branch of the coronary sinus. Multisite pacing using the Quartet lead alone did not improve the AHR but “quad‐site” pacing using an additional temporary LV lead did increase dP/dt_max. (PACE 2013; 36:e48–e50)     

Permanent nonselective His bundle pacing in an adult with L‐transposition of the great arteries and complete AV block

We report the placement of a permanent transvenous nonselective His bundle pacing lead in conjunction with a transvenous pacemaker/implantable cardioverter‐defibrillator in an adult with Levo‐Transposition of the Great Arteries (L‐TGA) and a stenotic coronary sinus (CS) ostium, which would not accommodate a transvenous left ventricular (LV) pacing lead. Nonselective His bundle pacing provided a nearly identical ventricular activation pattern in this previously unpaced patient. Many L‐TGA patients will have an eventual need for permanent pacing and, given the challenges of CS cannulation, His bundle pacing may represent a preferred modality rather than pure morphologic LV pacing or surgical systemic ventricular lead placement to achieve optimal electrical synchrony.     

A Method for Permanent Transvenous Left Ventricular Pacing

LV-based pacing has recently been reported to be of benefit in patients with severe cardiac failure and left bundle branch block. LV permanent pacing has been reported using epicardial leads but the surgical mortality is excessive. A transvenous approach is now favored. In this regard, cannulation of the coronary sinus and of one of its tributaries using only the permanent electrode is feasible but technically challenging. We describe a "long guiding sheath" method using catheterization, and a long radiopaque and peelable sheath. Once the coronaiy sinus is cannulated with the electrophysiological catheter, the long sheath is advanced to the mid-part of the coronary sinus. The permanent pacing electrode is then placed through the sheath and into a tributary of the coronary sinus. This method has been attempted in 10 patients and was successful in 8, with an average lead insertion time of 21 ± 5.5 minutes and an average fluoroscopic time of 11 ± 5.5 minutes. In conclusion, although transvenous left ventricular pacing remains a challenge, the "long guiding sheath" approach appears to facilitate this procedure with both a high success rate and an acceptable procedure time.     

Atrial pacing lead location alters the effects of atrioventricular delay on atrial and ventricular hemodynamics

The combined role of atrial pacing lead location and AV timing on cardiovascular performance has not been defined. This study tested the hypothesis that atrial pacing lead location can change the dependence of LA and LV hemodynamics on AV timing in vivo. Dogs anesthetized with isoflurane (n = 8) were instrumented for measurement of hemodynamics including LA pressure, LA volume, and pulmonary venous bloodflow. Data were recorded during normal sinus rhythm, and atrial overdrive pacing from the right atrial appendage (RAA), proximal coronary sinus (CS), and LA lateral wall (LAW). The AV node was then ablated and measurements repeated during synchronous ventricular pacing and during dual chamber pacing from each atrial lead location at various AV delays (20, 60, 120, 180, 240, and 350 ms). Hemodynamics during intrinsic sinus rhythm and overdrive atrial pacing from different sites were similar. In contrast, ventricular or dual chamber pacing caused significant (P < 0.05) changes in cardiac output with different AV timing during RAA (3.5 +/- 0.2 vs 2.9 +/- 0.2 L/min at 120 and 350 ms, respectively) and LAW pacing but not CS pacing. A significant interaction between atrial lead location and AV delay was observed for changes in stroke volume, pulmonary venous blood transport, LA volume, and LV preload. The results indicate that the atrial contribution to cardiac output depends on AV timing and atrial lead location in isoflurane-anesthetized dogs with AV nodal conduction block.     

Coronary Sinus Aneurysm and Left Ventricular‐Coronary Sinus Fistula. Implantation of CRT Device

We describe a 72‐year‐old man referred for implantation of a cardiac resynchronization therapy device who had previously undergone repeated operations to replace the mitral valve. Retrograde venography of the coronary sinus (CS) to implant the left ventricular (LV) pacing lead revealed aneurysmal dilatation of the CS with LV‐CS fistula that hindered—but did not prevent—complete implantation of the system. (PACE 2013; 36:e38–e40)     

The Left Ventricular Apex is the Optimal Site for Pediatric Pacing:

Pacing at the commonly used right ventricular (RV) apex results in impaired ventricular performance. Previous animal studies indicated that the left ventricular (LV) apex is a superior pacing site. The purpose of this study was to investigate in dogs whether this good performance is associated with a more synchronous electrical activation pattern of the LV and whether the LV apex is also a good pacing site in children. In 11 healthy dogs and 8 children undergoing cardiac surgery, dual chamber pacing was performed at the RV apex, LV apex and LV lateral free wall (LVFW). In dogs, a basket electrode was inserted into the LV to assess pattern and timing of LV endocardial activation. In the children, hemodynamic measurements were performed immediately after recovery from cardiopulmonary bypass. In dogs, LV apex pacing resulted in synchronous activation around the LV circumference whereas RV apex and LVFW pacing resulted in asynchrony of activation between the septum and LVFW. In both canine and children's hearts most hemodynamic variables remained at sinus rhythm level during LV apex pacing, but LVdPdtmax, stroke work (dogs), and pulse pressure (children) were reduced as compared with sinus rhythm during RV apex and LVFW pacing. LV apex pacing results in synchronous activation of the LV and is, in adult dogs and in children, associated with superior hemodynamic performance. (PACE 2004; 27 [Pt. II]:837–843)     

The ECG Lead I Paradox in Cardiac Resynchronization Therapy

Background: In cardiac resynchronization therapy (CRT), the morphology of the QRS complex plays an important role in the determination of the pacing site and effectiveness of stimulation. Patients and Methods: Review of the electrocardiograms (ECGs) of 737 patients with a CRT device showed a negative QRS complex in lead I during right ventricular (RV) pacing and a positive QRS complex during left ventricular (LV) pacing in four patients. The RV lead was positioned in the high RV septum and the coronary sinus leads in a posterior or postero‐lateral basal level. Reversed ECG lead or pacemaker lead connection, anodal RV stimulation, and scar tissue‐related depolarization abnormalities were excluded as possible causes. Conclusion: Pacing from the high RV septum may rarely lead to a negative QRS complex and basal positions of the LV lead to a positive QRS complex in lead I during LV pacing. The lead I paradox becomes obvious when both phenomena, that are not interrelated, are present in the same patient.     

Excitation of the intrinsic conduction system through his and interventricular septal pacing

BACKGROUND: Direct His bundle pacing results in rapid synchronous ventricular activation. However, clinical experiences with such pacing have been associated with long procedure times and compromised pacing and sensing performance. METHODS: We evaluated myocardial activation sequences (AS) for pacing of the His bundle and peri-His region and assessed acute pacing performance using custom-designed plunge electrodes. Unipolar pacing was performed in isolated swine hearts (n = 10) using four quadripolar stimulation/sensing electrodes implanted into the interventricular septum and equally spaced between the membranous septum and the coronary sinus ostium (zones 1-4, respectively; electrode depth (ED) 1 = most distal, ED 4 = most proximal). Optimal pacing sites were defined as: pacing thresholds < or = 1.5 V, a P-R ratio of < or = 0.5, and > or = 50% occurrence of an intrinsic midseptal left ventricular (LV) endocardial electrical breakout (BO) and activation pattern. RESULTS: Pacing thresholds improved with greater depth of electrode location within the septum (ED 1: 1.51 +/- 0.8 V vs ED 4: 5.2 +/- 3.8 V, P < 0.001), as did the P-R ratio (0.34 +/- 0.6 vs 0.78 +/- 1.0, P < 0.05). His potentials were only observed in zone 1 and 2 electrodes (0.12 and 0.02 mV, respectively). Only electrodes in zones 1 and 2 produced LV endocardial electrical BOs in the midseptal region that demonstrated an intrinsic-like endocardial AS. Depth 1 and 2 electrodes (11.75 and 8.75 mm, respectively) in zone 1 satisfied all three optimal pacing site requirements. CONCLUSIONS: This study has shown that LV activation patterns similar to sinus rhythm may be achieved without direct activation of the His bundle, while maintaining acceptable pacing and sensing performance. These data indicate that pacing systems designed to stimulate the tissues below the point at which the His bundle penetrates the central fibrous body may provide improved system efficiency and LV performance in comparison to both direct His bundle pacing and traditional pacing sites.     

Effect of Ventricular Pacing on Coronary Blood Flow in Patients with Normal Coronary Arteries

Although ventricular pacing is thought to produce impairment of left ventricular function by altering the sequence of ventricular activation and AV dyssynchrony, little is known about the effect of ventricular pacing on coronary blood flow. We measured coronary blood flow and coronary flow reserve in the left anterior descending coronary artery during sinus rhythm, and during both atrial and ventricular pacing at a rate of 100 ppm in 14 patients with normal coronary arteries. The double product increased significantly during both types of pacing. Coronary arterial diameter during ventricular pacing significantly increased compared to that during both sinus rhythm and atrial pacing. Coronary flow velocity during ventricular pacing was significantly lower compared to that during both sinus rhythm and atrial pacing. Coronary blood flow increased significantly during atriai pacing (30.7%± 12.1%; P < 0.001), but not significantly during ventricular pacing (23.6%± 47.0%; P = ns). While coronary flow re-serve during both atrial (3.9 ± 1.3) and ventricular pacing (3.8 ± 0.9) was lower compared to its value during sinus rhythm (4,5 ± 1.5), the difference was not significant. There was a significant positive correlation between the coronary flow reserve during sinus rhythm and the increase of coronary blood flow during ventricular pacing (R²= 0.78; P < 0.001). We concluded that an increase in coronary blood flow during ventricular pacing is not a common finding regardless of the increase in metabolic demand. The increase of coronary blood flow during ventricular pacing was less in patients with a reduced coronary flow reserve. These findings suggest that preservation of AV synchrony and the presence of a normal sequence of ventricular activation may play an important role in preserving coranary blaod flow in this subset of patients.     

Abolition of Diaphragmatic Pacing by Nonsurgical Retraction of a Left Ventricular Lead

This report describes the nonsurgical elimination of intractable diaphragmatic stimulation by partial withdrawal of a left ventricular (LV) pacing lead (in the coronary venous system) with resultant preservation of LV pacing. The procedure entailed the use of a deflectable catheter in the right atrium for ensnaring the LV lead. At the 3-month follow-up, the absence of diaphragmatic stimulation was associated with a satisfactory LV pacing threshold and dramatic clinical improvement from effectual biventricular pacing.     

The effect of the atrial pacing site on the total atrial activation time

The effect of dual site pacing for prevention of atrial fibrillation may be due to synchronization of right and left atrial activation. Little is known, however, about the effect of pacing from single right atrial sites on differences in interatrial conduction. Twenty-eight patients without structural heart disease were studied following radiofrequency catheter ablation of supraventricular arrhythmias. Pacing was performed using standard multipolar catheters from the presumed insertion site of Bachmann's bundle, the coronary sinus ostium, the high lateral right atrium, and the right atrial appendage (n = 8 patients). Bipolar recording was performed from the distal coronary sinus, the high and low lateral right atrium, and the posterolateral left atrium (n = 13 patients). The longest conduction time from each pacing to each recording site was considered the total atrial activation time for the respective pacing site. During high right atrial pacing, the total atrial activation time was determined by the conduction to the distal coronary sinus (118 +/- 18 ms), during coronary sinus ostium pacing by the conduction to the high right atrium (94 +/- 18 ms), and during Bachmann's bundle pacing by the conduction to the distal coronary sinus (74 +/- 18 ms). The total atrial activation time was significantly shorter during pacing from Bachmann's bundle, as compared to pacing from other right atrial sites. Thus, in normal atria, pacing from the insertion of Bachmann's bundle causes a shorter total atrial activation time and less interatrial conduction delay, as compared to pacing from other right atrial sites. These findings may have implications for alternative pacing sites for prevention of atrial fibrillation.     

Long-Term Follow-Up of Biventricular Pacing Using a Totally Endocardial Approach in Patients with End-Stage Cardiac Failure

Background: Besides standard left ventricular (LV) stimulation via the coronary sinus, a transseptal approach allows left ventricular endocardial stimulation. We report our long-term observations with biventricular stimulation, using a strictly endocardial system for patients presenting with severe congestive heart failure .
Methods: Six patients with nonischemic cardiomyopathy (mean age = 60 ± 9.6 years, women) in New York Heart Association (NYHA) functional class III (n = 5) or IV, despite optimal drug therapy, and a mean LV ejection fraction of 24 ± 3%, underwent implantation of biventricular stimulation systems between April 1998 and March 1999. All presented with left bundle branch block and an increased LV end-diastolic diameter (mean = 66 ± 5 mm). In all patients, a bipolar pacing lead was implanted in the lateral LV wall using a direct transseptal approach. After implantation, all patients received oral anticoagulation.
Results: QRS duration decreased from 184 ± 22 ms to 108 ± 11 ms. NYHA functional class decreased to II in all patients within 1 month. Over a 85 ± 5 month follow-up, two patients underwent cardiac transplantation, 2 and 4 years after device implantation, respectively; two patients died of end-stage heart failure 4 years after system implantation; and two patients were alive in functional class II. One patient, who experienced syncope due to fast ventricular, underwent implantation of an ICD. One transient ischemic attack occurred in a patient whose anticoagulation was temporarily interrupted .
Conclusions: Long-term endocardial biventricular stimulation via a transseptal approach was safe and effective in this small population. This approach needs to be further compared with conventional epicardial pacing via the coronary sinus     

Biventricular Pacing via a Persistent Left Superior Vena Cava: Report of Four Cases

GASPARINI, M., et al .: Biventricular Pacing via a Persistent Left Superior Vena Cava: Report of Four Cases. Persistence of left superior vena cava (LSVC) is an uncommon finding during pacemaker implantation, which may be particularly relevant in performing LV transvenous pacing. Rarely, it is further complicated by the presence of atresia of the coronary sinus ostium (CSO). This article reports the authors experience with biventricular pacing (Biv-P) in this unusual clinical setting. From October 1999 to April 2002, 158 patients underwent biventricular pacing. In four of them (mean age 62.2 years), the presence of a persistent LSVC draining into the coronary sinus (CS) was detected at implantation, associated with atresia of the CSO in two patients. A common characteristic was the angiographic finding of a large CS with few tributaries. The LV leads were successfully positioned in the middle cardiac vein in three patients and in a posterolateral vein in one patient. All vessels were large and their cannulation via downstream CS catheterization required the lead to be manipulated through sharp angles. Mean fluoroscopic exposure and procedural times were not significantly different from the overall Biv-P population. In all patients, at a mean follow-up of 11 months, sensing and capture threshold remained stable and a significant decrease in NYHA functional class and increase in LVEF were noted. The direct lead placement in large CS tributaries in the presence of persistent LSVC was feasible and safe. The leads remained stable up to a mean follow-up of nearly 1 year. (PACE 2003; 26[Pt. II]:192–196)     

Permanent Left Ventricular Pacing With Transvenous Leads Inserted Into The Coronary Veins

This paper describes a preliminary experiment - conducted jointly by 2 centers - of permanent left ventricular pacing using leads inserted by the transvenous route and through the coronary sinus into the cardiac veins of the left ventricle free wall. The aim was to obtain permanent biventricular pacing in a totally endocavitary configuration in pattents with severe LV dysfunction and drug-refractory heart failure. Two types of leads were used: nonspecific unipolar leads at the beginning of the experiment, followed by leads specifically designed to be used in the coronary sinus in a second step. The electrode could be fitted in an adequate location in 35 of the 47 patients (75.4%), with a 1.15±0.7 V acute pactng threshold and 11.8±5.7 mV R wave amplitude. The success rate was significantly higher with the specific electrodes (81.8% vs 53,3%, p < 0.001). The pacing and sensing thresholds upon implantation were not influenced by the type of lead or by the localization of the cardiac vein that was catheterized (great cardiac vein, lateral vein, postero-lateral or posterior vein, mid cardiac vein). In contrast, the pacing threshold was significantly lower (0.8 ± 0.2 vs L8 ± 0.8 V; p = 0.002) and the R wave amplitude tended to be greater (13.1 ± 4.5 mV vs 9.3 ± 6.5 mV; p = 0.07) when the tip electrode could be inserted distally into the vein, by comparison with a proximal site near the ostium. At the end of follow-up (10.2 ± 8.7 months), 34 out of the 35 leads were still fully functional, with a chronic pacing threshold of 1.8 ± 0.7 V and a R wave amplitude of 10.7 ± 6 mV. To conclude, permanent LV pacing via the transvenous route is possible in most patients, with excellent safety and long-term results.     

Morphology of the RV electrogram during LV pacing is related to the hemodynamic effect in cardiac resynchronization therapy

Background: Biventricular (BiV) pacing and left ventricular (LV) pacing both improve LV function in patients with heart failure and LV dyssynchrony. We studied the hemodynamic effect of the atrioventricular (AV) interval and the associated changes in the right ventricular (RV) electrogram (EGM) during LV pacing and compared this with the hemodynamic effect of optimized sequential BiV pacing.
Methods: In 16 patients with New York Heart Association (NYHA) class II to IV, sinus rhythm with normal AV conduction, left bundle branch block (LBBB), QRS > 130 ms, and optimal medical therapy, the changes in RV EGM during LV pacing with varying AV intervals were studied. The hemodynamic effect associated with these changes was evaluated by invasive measurement of LVdP/dt_max and compared with the result of optimized sequential BiV pacing in the same patient.
Results: All patients showed electrocardiographic fusion during LV pacing. The morphology of the RV EGM showed changes in the RV activation that indicated a shift in the extent of fusion from LV pacing. These changes were associated with significant changes in LVdP/dt_max. Baseline LV dP/dt_max was 734 ± 177 mmHg/s, which increased to 927 ± 202 mmHg/s (P<0.0001) with optimized LV pacing and to 920 ± 209 mmHg/s (P<0.0001) with optimized sequential BiV pacing.
Conclusion: The RV EGM is a proper indicator for intrinsic activation over the right bundle during LV pacing and reveals the transition to fusion in the RV EGM that is associated with a decrease in LVdP/dt_max. The hemodynamic effect of optimized LV pacing is equal to optimized sequential BiV pacing.