A transmural approach for endocardial ventricular pacing

A transmural approach for endocardial ventricular pacing

congestiveheart failure, evidencefor increasedpulmonary blood flow and large pulmonary arteries. In all 3 patients a staged surgical approach replaced...

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congestiveheart failure, evidencefor increasedpulmonary blood flow and large pulmonary arteries. In all 3 patients a staged surgical approach replaced systemic collateral arteries with grafts to supply adequate but controlled perfusion, promotegrowth of the pulmonary arteries and protect against pulmonary vascular disease. Unifocalization simplified establishing perfusion from the newly constructed right ventricular outflow

A Transmural Approach Ventricular Pacing

tract at repair. Angiography between procedureshelped refine the surgical approach.By utilizing the newly created aortopulmonary connections,it was possibleto define the sourcesof pulmonary perfusion better than at the initial study. Postoperativeevaluation showedperfusion of the majority of bronchopulmonary segments and acceptableright/left ventricular systolic pressureratios. The clinical results were good in all 3 patients.

for Endocardial

thoracotomy and endocardial leads placed transvenously. At times, the usual transvenousapproachesare not feasible, such as in superior vena cava obstruction or impaired access to the right ventricle becauseof tricuspid stenosisor a mechanical prosthetic valve. Usually, such situations necessitateepicardial pacing, which sometimesis unsatisfactory because of poor thresholds or inadequate sensing with epicardial leads. We present a casein which a new method for endocardial ventricular lead placement was usedwhen both standard endocardial pacing and epicardial pacing were unsatisfactory.

The patient was asymptomatic over the following 4 years.

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Thorar Cardiouasc Surg 1987,94:91 l-914.

3. Millikan JS, Puga FJ, DanielsonGK, Schaff HV, Julsrud PR, Mair DD. Stagedsurgical repair of pulmonary atresia, ventricular septal defect, and hypeplastic,confluent pulmonary arteries. J Thorac Cardiocasc Surg 1986:91:818-825.

In 1988, the patient presented with progressive dyspnea and fatigue. Electrocardiographic and pacemaker analysis revealed complete heart block with a ventricular rate of 30 beats/min and failure to capture despite maximal energy settings (8.1 Vat 0.92-mspulse width).

Benjamin D. McCallister, Jr., MD, Ronald E. Vlietstra, MB, chB, Benjamin M. Westbrook, MD, and David L. Hayes, MD he 2 standard approaches to T placementof cardiac pacemaker leads are epicardial leads applied at

1. Sullivan ID, Wren C, Stard J, de Leval MR, Macartney FJ, Deanfield JE. Surgical unifocalization in pulmonary atresia and ventricular septal defect. Circulation 1988:(suppl 11l)78:111-5-111-13. 2. Barber@Marcia1M, Rizzo A, Lopes AAB, Bittencourt D, Junior JOA, Jatene AD. Correction of pulmonary atresia with ventricular septal defect in the absenceof the pulmonary trunk and the central pulmonary arteries (so-called truncus type IV). J

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A 63-year-old woman had StarrEdwards prosthetic valves in aortic, mitral and tricuspid positions. At age 59 she had developed complete heart block with a ventricular escape rate of 30 beatslmin that required epicardial lead placement because of the prosthetic tricuspid valve. Positioning of the lead was difficult because of high thresholds. Duringfollow-up, thepatient developedfailure to capture, but her intrinsic heart rate had increased to 50 beats/min. From the Division of Cardiovascular Diseases and Internal Medicine and the Division of Thoracic and Cardiovascular Surgery, Mayo Clinic and Mayo Foundation, 200 First Street SW, Rochester, Minnesota 55905. Manuscript received April 24, 1989; revised manuscript received and accepted September 1, 1989.

flGURE 1. Transmwal ventrkular had phement. Ventricular emhwardial bad is passodthroughrigM-wauandactivolyfixatedtorightvOlUbCaNiiUIll.Aprre~Iubre sesames lead in lighl ventrkular free wall. (By porddon of Mayo Foundation.) THE AMERICAN JOURNAL OF CARDIOLOGY JANUARY 15, 1990

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Lead impedance measured >2,500 ohms. At operation to investigate the pacemaker system, the generator functioned normally. The electrodemyocardial interface sites were markedly fibrotic. The ventricle was covered with a thick layer of epicardial fat, and multiple attempts to find adequate thresholds with 3-turn screw-in epicardial leads failed. A platinized ‘pshhook” epicardial lead (Medtrom’c 4951 -P) was placed with a threshold of 2 V, but adequate thresholds for a second 4951 -P lead could not be achieved. An active-fixation endocardial lead (Medtronic 6957) was then placed through the anterior wall of the right ventricle with the Seldinger technique and a IOFr peel-away introducer sheath. The screw-in unipolar endocardial lead tip was directed toward the apex of the right ventricle andfixated (Figure 1). Good thresholds were obtained (0.8 V at 0.6~ms pulse width). The insertion site through the right ventricular wall was secured with a pledgeted purse string suture of 3-O Prolene. The threshold in a bipolar configuration (endocardial lead negative, epicardial lead positive) was 1.2 Vat 0.6-ms pulse width. The 2

clude: the infeasibility of removing the lead percutaneously (e.g., if the lead were infected or had perforated the ventricular wall); the possibility of mural scarring and increasedarrhythmias; lead dislodgment, lead fracture or lead perforation, which could result becausethe lead is tetheredin the right ventricular free wall; and the risk of transmural hemorEndocardial lead placement rhage, especially if the patient has tendsto offer easierplacement,lower received anticoagulants. In view of these possible disadmorbidity and more reliable thresholds than epicardial lead systems.*v2 vantages and the lack of long-term Yet, situations arise in which the usu- follow-up in our patient, the transal transvenousapproach is inconve- mural approach to endocardial pacnient or not possible and epicardial ing should be consideredonly after pacing is inadequate.In the casepre standard approachesfail. In the case sented, a prosthetic tricuspid valve presented, transmural endocardial was in place and attempts at epicar- pacing, at least in the short term, ofdial pacing failed becauseof a fibrot- fered good lead stability and excelic, fatty epicardium. A ventricular lent thresholds and sensing. endocardial lead was placed through the wall of the right ventricle without 1. Henglein D, Gillette PC, Shannon C, Burns G. complication and with good sensing Long-term follow-up of pulse width threshold of and pacing thresholds. This is the transvenousand mywpicardiil leads.PACE 1984; first documentedcaseof transmural 3.7:203-214. Hayes DL, Holmes DR Jr, Maloney JD, Neuventricular pacing. The precedent bauer SA, Ritter DG, Danielson GK. Permanent for transmural endocardial pacing endocardial pacing in pediatric patients. J Thoruc Cwdimmc Surg 1983;aMl a-624. comes from atria1 lead systems 3. Hayes DL, Vlietstra RE, Puga FJ, Shub C. A placed transmurally that demon- novel approach to atria1 endocardial pacing. PACE strated goodfunction and stability.3v4 1989;i2:125-i30. Gordon R, Bode11BP, Pearson WT, Sacks JH. The theoretical problemsof using 4. Permanentatria1 electrode placement.Ann Thomc the transmural approach might in- surg i982:33:86-87.

leads were brought out through the subcostal area and connected to an activity-sensing, rate-modulating pulse generator (Medtronics 8402). The postoperative course was uncomplicated. At follow-up 3 months later, she had a pulse-width threshold of 0.25 ms at a 5-V setting. One year after operation, she was active and asymptomatic.

Severe Stenosis Involving a Congenitally Bicuspid Aortic Valve in the Tenth Decade of Life Dean G. Karalis, MD, Jeffrey M. Wahl, MD, Gary S. Mintz, MD, and Krishnaswamy Chandrasekaran, MD congenitally bicuspid aortic A valve (BAV) is present in at least 1%of persons.’The most com-

TABLE

Pressures (mm Hg) Right atrium (mean) Right ventricle (ps/ed) Pulmonary artery (ps/ed) Pulmonary artery wedge (mean) Left ventricle (ps/ed) Aorta (ps/ed) Aorta to left ventricle systolic gradient Aortic regurgitation Aortic valve calcium Cardiac index (liters/min/m2) Aortic valve area (cm2)

From the Likoff Cardiovascular Institute, Department of Medicine, Hahnemann University Hospital, 230 North Broad Street, MS 313, Philadelphia, Pennsylvania 19102. Manuscript receivedAugust 21, 1989;revisedmanuscript received and accepted September 1, 1989. THE AMERICAN

JOURNAL

OF CARDIOLOGY

Data

Catheterization

mon complication of a BAV is stenosis,and this congenital malformation representsthe most commoncauseof isolated aortic stenosisin the patient group aged 16 to 6L2 In patients over the ageof 65, aortic stenosissuperimposedon a BAV occurs with a fre-

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I Hemodynamic

*Calculated usingthe Goblinformula. ps/ed = peak systole/enddiastole.

VOLUME

65

4

50/s 55/26 22 185/2il 105/55

80(peak) 1+/4+ 3+/4+ 2.0 0.4*