Severe tricuspid valve stenosis secondary to pacemaker leads presenting as ascites and liver dysfunction: a complex problem requiring a multidisciplinary therapeutic approach

Tricuspid stenosis secondary to ventricular pacemaker leads is uncommon. We present a unique case of iatrogenic tricuspid stenosis secondary to fusion of the valve leaflets to transvenous implanted pacing leads. This occurred in an adult with childhood repaired Tetralogy of Fallot and high grade surgical heart block following multiple pacemaker procedures. The case was complicated by superior vena cava (SVC) and innominate vein stenosis secondary to implanted pacing leads, severe tricuspid valve (TV) stenosis, perforation of the heart by one of the implanted transvenous ventricular pacing leads, prolapse of the transvenous atrial pacing lead into the right ventricle, and unusual coronary sinus anatomy. We describe a multidisciplinary approach to management.     

Permanent pacing using a coronary sinus lead in a patient with univentricular physiology: an extended application of biventricular pacing technology.

In the past, patients requiring permanent pacing with difficult right ventricular (RV) access were usually subjected to epicardial pacing by a surgical approach. This report describes a young patient with univentricular physiology following repeated palliative surgery for complex congenital heart disease. The patient had symptomatic complete heart block and a dual chamber pacemaker with transvenous atrial and ventricular leads was implanted successfully. The ventricle was paced through the posterolateral cardiac vein with a lead specially designed for cardiac resynchronization therapy. This case illustrates an extended application of the recently developed coronary sinus lead in selected patients, when conventional RV endocardial pacing is impossible.     

Severe tricuspid regurgitation secondary to dislodgement of the atrial loop into the right ventricle: an unusual complication of pacemaker implantation in a young adult

Transvenous pacemaker leads may impair tricuspid valve function. Severe tricuspid regurgitation due to leaflet adhesion to the pacemaker lead has not been reported in a young adult patient in the literature. Our patient underwent a transvenous pacemaker implantation for symptoms of bradycardia. An atrial loop was created in the right atrium for future growth. After 10 years of follow-up, the patient was seen with severe tricuspid regurgitation and enlarged right heart structures due to migration of the atrial loop of the pacemaker lead into the right ventricle and adhesion of the lead to the tricuspid valve. Cardiac surgery and epicardial pacing was the chosen procedure to solve this problem. The venous system and right heart valves should be carefully observed during the follow-up of children who underwent transvenous pacing.     

Long-term transvenous AV-sequential pacing in a failing atriopulmonary Fontan patient

We report on a 32-year-old man with tricuspid atresia, pulmonary stenosis and hypoplastic right ventricle. He had received a Fontan-Kreutzer procedure (anastomosis between the right atrial appendage and the pulmonary artery) at the age of 14 years. At the age of 2 years, an abdominal VVI-pacemaker with an epicardial ventricular lead had been implanted because of symptomatic third degree AV-block. The patient was now hospitalized with symptoms of severe congestive heart failure. A least invasive approach restoration of AV-synchrony by a dual chamber pacer was performed. Therefore a complete transvenous approach to avoid thoracotomy was attempted. A specially designed CS lead was advanced via the CS to a left lateral ventricular vein for ventricular stimulation. After institution of dual chamber pacing the patient recovered of his heart failure. During a follow-up time of 20 months the patient was clinically stable in the AV-sequential pacing. Conclusion: Dual chamber pacing using a transvenously placed coronary sinus lead for ventricular stimulation may improve congestive heart failure in patients after the classic Fontan operation. The minimally invasive transvenous approach might be the best solution for patients who need a pacemaker and are not candidates for surgery or heart transplantation.     

Pacemaker-induced cardiovascular failure. Hemodynamic and angiographic observations

A 71 year old woman underwent permanent transvenous right ventricular pacemaker implantation for prolonged syncope and atrioventricular conduction defects. Each time the patient's heart rate spontaneously decreased to less than 70 beats/min, cardiovascular collapse with hypotension and reduced cardiac output occurred. Left ventricular cineangiography performed during both sinus rhythm and right ventricular pacing demonstrated reduced left ventricular end-diastolic volume, secondary to a loss of atrial contribution to left ventricular filling, and severe, acute mitral regurgitation with significantly decreased effective stroke volume and cardiac output. Pacing from the left ventricular endocardium had the same effect. The detrimental effects of cardiac pacing necessitated removal of the right ventricular pacemaker.     

Safe right bundle branch block pattern during permanent right ventricular pacing

It is known that an electrocardiogram (ECG) after transvenous right ventricular (RV) pacing should yield left bundle branch block (LBBB) QRS patterns. When right bundle branch block (RBBB) pacing morphology appears in a patient with a permanent or temporary transvenous RV pacemaker, myocardial perforation or malposition of the pacing lead must be ruled out, even though the patient may be asymptomatic. We report a case of a 77-year-old man who underwent permanent transvenous VDD pacemaker implantation for symptomatic heart block. The postoperative ECG revealed a RBBB pacing configuration, but his chest X-ray and echocardiographic studies confirmed uncomplicated RV pacing. We review and discuss the literature concerning the differential diagnosis of such a safe RBBB ECG pattern.     

Ventricular fibrillation complicating pacemaker insertion in acute myocardial infarction

Temporary transvenous pacing catheters were placed in 101 patients with acute myocardial infarction (Ml) for the management of bradyarrhythmias or conduction disturbances. Fourteen (14%) patients (group A) developed ventricular fibrillation (VF) at the time of pacing catheter manipulation in the right ventricle. Compared to the remaining 87 (86%) patients (group B), the patients in group A were younger (56.1 vs 65.8 yrs, P = 0.007). Thirteen (92.8%) of 14 patients in group A had inferior MI compared to 58 (66.6%) of 87 patients in group B (P = 0.04). All but one patient in group A had pacemaker insertion within 24 h of the onset of symptoms of Ml compared to 55 (63%) of 87 in group B (P = 0.02). In 12 of the 14 patients in group A, following defibrillation and intravenous bolus administration of lidocaine, the pacing catheter was positioned in the right ventricle without further episodes of VF. It is concluded that (1) in patients with acute MI temporary transvenous pacemaker insertion may be complicated by VF; (2) VF is most likely to occur in younger patients with inferior MI infarction when the pacing catheter is inserted within 24 h of the onset of symptoms of infarction; and (3) administration of an intravenous bolus of lidocaine may be effective in preventing the induction of VF by catheter manipulation.     

Temporary coronary guidewire pacing during percutaneous coronary intervention.

Temporary pacing is occasionally required during percutaneous coronary artery interventions. This can be accomplished by the insertion of a temporary transvenous pacemaker wire into the right ventricle, but there is some risk and inconvenience associated with this approach. Temporary pacing using the coronary artery guidewire was described in 1985 but is used infrequently. Using currently available equipment, we evaluated guidewire pacing in 26 patients. Guidewire pacing was successful in all patients, but not with all coronary guidewires at acceptable ventricular capture thresholds. No complications occurred from guidewire pacing. Bench testing of multiple different wires showed several with very high resistances likely unsuitable for clinical use. Temporary guidewire pacing is easily performed and should be considered as an alternative to the separate placement of a temporary transvenous pacemaker.     

Transvenous ventricular pacing options in Ebstein's anomaly

Transvenous pacing in patients with Ebstein's anomaly is challenging due to anatomical abnormalities of the tricuspid valve and right heart chambers. This paper describes the various transvenous ventricular lead placement options for permanent pacing in patients with Ebstein's anomaly. In Ebstein's anomaly, stable long-term ventricular pacing can be achieved by positioning the lead either in the atrialised right ventricle, true right ventricle or the cardiac venous system. The pitfalls and advantages of pacing from these sites with the electrocardiographic and chest X-ray appearances are described.     

Diagnosis of inferior wall myocardial infarction during right ventricular apical pacing.

The diagnosis of inferior wall myocardial infarction is often masked during ventricular pacing. We observed paced ventricular beats with a qR pattern in leads 2,3, and aVF in a patient with acute inferior wall myocardial infarction and a temporary pacemaker at the apex of the right ventricle. Such a pattern might be specific for the diagnosis of inferior wall myocardial infarction, because it is never seen during uncomplicated pacing from anywhere within the right ventricular cavity.     

External transcutaneous pacemakers in interhospital transport of cardiac patients

From October 1985 to April 1988, 297 patients with presumed unstable angina, acute myocardial infarction, or permanent pacemaker failure were transferred by helicopter from community hospitals to our medical center for tertiary care. Fifty-six patients (19%) experienced treatable bradycardia (heart rate of less than 50) and hypotension (systolic pressure of less than 80 mm Hg); nine patients (16%) improved without treatment, 24 (43%) responded to atropine, and 23 (41%) were unresponsive to atropine. An external transcutaneous pacemaker (EXTP) was applied to patients unresponsive to atropine if a transvenous pacemaker could not be placed. In the atropine-unresponsive group, 11 (48%) had a transvenous pacemaker placed successfully, two (9%) had poor transvenous pacemaker capture (followed by EXTP capture), and ten (43%) were treated with EXTP alone. Eleven patients experienced EXTP capture and improved. Six had profound bradycardia and apnea before EXTP application. Of the 297 patients, 23 (8%) required transvenous or external pacing, and 12 of these patients (52%) survived. The availability of external pacing during interhospital transport of high-risk cardiac patients seems necessary for the management of symptomatic bradycardia and hypotension.     

Two- and three-dimensional echocardiographic imaging of massive left intraventricular thrombosis complicating fatal heart failure

Management of severe autonomic dysfunction in patients with Guillain-Barre syndrome (GBS) or its variant Miller-Fisher syndrome (MFS) include placement of permanent pacemaker. We report a case of MFS with severe bradycardia and asystole treated initially with an external permanent (temporary-permanent) pacemaker with a transvenous, active fixation right ventricular lead placement as a "bridge" to permanent pacing.     

Chronic bundle branch block and use of temporary transvenous pacemakers during coronary arteriography

A retrospective analysis of 217 consecutive patients with chronic bundle branch blocks undergoing cardiac catheterization was done to evaluate the need for temporary transvenous pacing during coronary arteriography. In patients without temporary right ventricular pacemakers (n = 185), only one episode of high-grade atrioventricular block occurred during coronary arteriography which required the urgent use of temporary pacing. All other bradyarrhythmias, including five episodes of transient asystole (greater than 3-sec pause) and four episodes of atrioventricular block (second degree or higher) were successfully managed without pacemaker utilization. Patients with prophylactic right ventricular pacemakers (n = 32) had a greater prevalence of ventricular fibrillation than those without pacing electrodes located in the right ventricle (2% vs. 9% respectively; P less than 0.05). These findings suggest that routing prophylactic pacemaker insertion during coronary arteriography in patients with chronic bundle branch block is not warranted and may place the patient at risk for developing iatrogenic ventricular arrhythmias.     

Pacemaker catheter induced systolic murmurs in two patients

Although extracardiac sounds secondary to cardiac pacing have been well known, the murmurs originating in the heart after permanent pacemaker implantation and then disappearance after exchanging a temporary to permanent lead have rarely been reported. In this paper, two patients revealing a musical systolic murmur after placement of a transvenous endocardial pacemaker in the absence of any complications were documented. Case 1: A 43-year-old man with episodes of dizziness and brady-tachycardiac atrial fibrillation. Immediately after the implantation of a temporary transvenous right ventricular pacemaker, a high-pitched systolic musical murmur was heard at the lower left sternal border. No murmur was however gullible after a permanent pacemaker implantation in this case. Case 2 was a 83-year-old female with coronary heart disease associated with sick sinus syndrome to whom a permanent transvenous right ventricular pacemaker was inserted. A musical systolic murmur occurring immediately after the procedure was best audible at the apex. Although numerous papers concerning the mechanisms of these cardiac murmurs have been reported without reaching conclusive explanations, our data based on two cases examined with Doppler echocardiography did not support the idea of tricuspid regurgitation as one of causative factors. In the first case, this murmur appeared only a temporary pacing was performed and disappeared after implantation of a permanent pacemaker lead. On the contrary, however, the 2nd case revealed after the implantation of the permanent pacemaker with a relatively rigid bipolar lead. It is concluded that these murmurs might be produced by vibrations caused by the pacing catheters and physical properties could be related the mechanism of this phenomenon.     

The Development of the Transvenous Automatic Defibrillator

The transvenous automatic defibrillator is a device which automatically recognizes and treats ventricular fibrillation. The initial clinical prototype resembles an external pacemaker: the electronic components and power supply are external to the body, the sensing and defibrillating elements being contained in a transvenous catheter. The sensors monitor intracardiac R waves and cardiac contraction. Absence of both signals identifies the arrhythmia and triggers the defibrillatory shock, delivered through the right ventricular electrode and another more proximal on the catheter. If needed, the device recycles automatically. It is also adaptable for pacing and for elective intraatrial cardioversion. Results of animal experiments were successful, and tests are currently being done on patients requiring defl‐brillation during open heart surgery. The clinical indications for the device are numerous and it is hoped that this approach will decrease the present prohibitive mortality from coronary heart disease.     

Ventricular pacing from the coronary sinus of a patient with a Fontan circulation.

Permanent pacing of the left ventricle was achieved by transvenous implantation of a steroid-eluting electrode into the coronary sinus in a patient who had undergone a Fontan operation. This approach to endocardial pacemaker implantation is potentially of considerable value in patients who do not have transvenous access to the right ventricle.     

Sudden death of a patient with a pacemaker caused by heart rupture in a "cloisonné" pericardium

Myocardial infarction is sometimes accompanied by bradycardia requiring either temporary or permanent cardiac pacing. In addition an MI reduces the amplitude of endocardial action potentials which produces the conditions for defective detection of spontaneous ventricular complexes by the pacemaker. In this particular condition, the competing cardiac rhythm which arises frequently causes malignant arrhythmias which are potentially fatal. This danger is increased even further by endocardial stimulation of the right ventricle with myocardial infarction of the right ventricle. We have reported in this paper the instructive case of a patient with coronary heart disease, hospitalized for third degree AV block with syncope which developed following a massive postero-diaphragmatic MI, but with few symptoms. After secondary extension of the necrotic area, the artificial pacemaker implanted manifested defective firing which resulted in development of ventricular fibrillation. The latter was controlled by cardioversion, but the patient died from disordered conduction after 30 seconds of complete asystole. For one minute, the pacemaker did not stimulate the ventricle because of "electrical stunt to the myocardium", caused by the shock from the defibrillator. Anatomical examination (at autopsy) confirmed the cardiac rupture.     

Right ventricular enlargement mimicking electrocardiographic left ventricular pacing

Electrocardiographic right bundle branch block morphology during cardiac pacing is occasionally the result of accidental placement of pacemaker or defibrillator leads into the left ventricle. Inadvertent lead placement in the left heart is associated with a risk of systemic embolism. Previous authors have attempted to define safe (right ventricular origin) and unsafe (left ventricular origin) patterns of right bundle branch block during pacing. We report a case of a patient with severe dilated cardiomyopathy and a correctly positioned pacemaker-defibrillator lead in the right ventricular apex, who meets electrocardiographic criteria for lead implantation into the left ventricle.     

Entanglement of embolised thrombus with an endocardial lead causing pacemaker malfunction and subsequent pulmonary embolism.

A 67 year old woman with a permanent pacemaker was admitted with pulmonary oedema and mitral valve incompetence two months after a myocardial infarction. Echocardiograms showed good left ventricular function and a large coil of apparent thrombus in the right atrium prolapsing into the right ventricle. Intermittent loss of pacemaker sensing and capture was noticed on admission and probably caused the supraventricular tachycardia and ventricular fibrillation that occurred before an exploratory bypass operation. At operation rupture of the papillary muscle was found and the mitral valve was replaced. A large piece of thrombus was retrieved from the right pulmonary artery. The right heart contained no clot and the pacemaker wire was not displaced. It is envisaged that the strand of venous thrombus was caught in the permanent pacing wire at the tricuspid valve level resulting in an unusual case of pacemaker malfunction. The eventual poor outcome was almost certainly influenced by the arrhythmias and pulmonary embolism caused by the clot and might have been avoided by early operation.