Pathology of Cardiac Devices and Interventions



Pathology of Cardiac Devices and Interventions


Joseph J. Maleszewski, M.D.

Allen P. Burke, M.D.



Introduction

Open and percutaneous interventions performed on the heart and thoracic aorta are relatively commonplace. They are typically done in order to restore normal blood flow. Procedures can involve the valves (Chapter 41), coronary arteries (Chapters 16 and 17), thoracic aorta and branches (Chapter 53), as well as the myocardium itself (such as in congenital heart disease or cardiomyopathies) (Chapters 3, 19, 20, and 25).

This chapter addresses (1) interventions used in the treatment of arrhythmias, including placement of indwelling leads for pacing or defibrillation, and direct ablation of arrhythmogenic foci within the myocardium; (2) common interventions used in the treatment of heart failure; and (3) unexpected thoracic complications of percutaneous interventions.

At autopsy, the pathologist should describe the intervention, pathology in and around the intervened site, and any sequelae. Some interventions result in unexpected consequences that may be incidentally noted, for example, embolization of catheter-based hydrophilic polymers.

Pathologic reactions to treatments and devices have a common pathway of wound healing, which progresses through phases of acute and chronic inflammation, granulation tissue, and fibrosis, often with a tissue reaction to foreign material. In the case of intravascular interventions, there is a progression of acute thrombosis (composed of fibrin and platelets) to early organization with endothelialization and persistent fibrin and to mature organization often with recanalization. There may or may not be foreign body/inflammatory reactions complicating the healing process.


Pacemakers and AICDs

There are myriad devices implanted in the heart for treatment of arrhythmias, including pacemakers and automatic implantable cardiac defibrillators. Indications for cardiac pacing include acquired atrioventricular block such as seen after atrioventricular nodal ablation, myocardial infarction, or a number of syndromic states.

Pacemakers are generally either single chamber (lead in either right atrium or right ventricle) or dual chamber (leads in both right atrium and right ventricle). Each lead communicates with the pacemaker and provides pacing and/or monitoring capabilities. Pacemakers may be used in conjunction with defibrillators, which are similar in appearance. In patients with heart failure, a third pacing wire in the left ventricle, inserted through the coronary sinus and anterior cardiac vein, results in better contractility via synchronous biventricular contraction (cardiac resynchronization therapy).1

At autopsy, leads are identified in the heart, entering through the superior vena cava (Fig. 142.1). They can be separated from the device itself by cutting the wires within the superior vena cava. The device is usually positioned subcutaneously in the upper chest. The lead may be adherent to the tricuspid valve, which in some instances may tether the valve and cause significant hemodynamic regurgitation. Occasionally, tricuspid valve replacement is necessary in order to surgically extract an indwelling right ventricular lead or if the lead becomes infected.2,3 A hollow, cylindrical, lead tract may be present extending from the tricuspid valve to the insertion in the ventricular wall (Fig. 142.2). This tract consists of endocardium that has grown around the foreign object.2,3

Care should be taken to avoid electric shocks to the prosecting pathologist or assistant. The status of the leads and their tips should be
ascertained, including their position and associated pathology (if any). Interrogation of the device can provide important clues as to the functioning of the device at the time of death and/or the terminal rhythm. Such interrogation can usually be performed by electrophysiology personnel or the device manufacturer and can be done without the leads being attached.4






FIGURE 142.1 ▲ Pacemaker device seen at autopsy, postmortem radiography. The pacer is dual chamber, with one lead in the right atrium and the other in the right ventricle. The indication in this patient was acquired third-degree heart block.


Cardiac Ablations


General

Endocardial cardiac ablations are performed for a variety of indications. These include ablation of bypass tracts, re-entrant pathways, and arrhythmogenic foci determined by electrophysiologic mapping (Table 142.1). Arrhythmias that are treated include atrial and ventricular tachycardias and atrial fibrillation.






FIGURE 142.2 ▲ Right ventricular scar at site of indwelling lead. Right ventricular catheter site, manifest as hole from catheter, incidental finding. The arrow indicates the site where the catheter tip was pulled at explant. There is a fibrous capsule around the catheter lead, which had been removed from its entanglement in the tricuspid valve.








TABLE 142.1 Sites of Ablation, by Common Types of Arrhythmia




























Common Sites of Ablation


Atrial fibrillation Paroxysmal Chronic


Pulmonary vein sleeve


Linear posterior left atrial ablations (maze)


Atrial fibrillation, control of ventricular response


Atrioventricular junction ablation (insertion of pacemaker)


Atrial flutter


Isthmus between coronary sinus and inferior vena cava


Supraventricular atrial re-entrant tachycardia


Coronary sinus


WPW preexcitation syndrome


Atrioventricular groove, especially left atrial free wall > right atrial free wall


Supraventricular nodal re-entrant tachycardia


Atrioventricular node


Monomorphic ventricular tachycardia, monomorphic premature ventricular contractions


Left ventricular outflow near aortic valve and near any of the 4 valves (especially dilated cardiomyopathy) including outflow tracts


Epicardial sites


Areas of scar (ischemic cardiomyopathy)


Ablation is most frequently accomplished by radiofrequency waves, but lasers, microwaves, and cryoablation have also been used. Radiofrequency causes thermal injury using alternating current and is usually delivered percutaneously via catheter. Cryoablation produces myocardial injury with tissue freezing and thawing. Cryoablation, which is more frequently done by open procedure, produces less endothelial or endocardial injury possibly with less endocardial thrombus.

An electrophysiologic study records electrical activity and determines where catheter ablation may eliminate cardiac arrhythmias. The success of catheter ablation is high for atrioventricular nodal reentry, accessory pathways, atrial flutter, and idiopathic ventricular tachycardia. The success rate is lower in patients with atrial fibrillation or structural heart disease.5


Atrioventricular Nodal Ablation

Atrioventricular nodal ablation is performed in patients who have atrial fibrillation with a rapid ventricular response who do not respond to medical treatment. Complete atrioventricular node ablation requires implantation of a permanent pacemaker. At autopsy, there will be scarring in the region of the membranous septum (Fig. 142.3).


Wolff-Parkinson-White Syndrome

Wolff-Parkinson-White (WPW) syndrome is a preexcitation syndrome caused by atrioventricular bypass tracts that are most common in the left free wall, followed by the right free wall and the posteroseptal region (see Chapter 4). Most patients are asymptomatic and do not require treatment. Catheter ablation is performed in patients who are refractory to drugs and are symptomatic with atrioventricular reentrant tachycardia or paroxysmal atrial fibrillation. In the past, open surgical procedures were performed to interrupt the pathway, and currently, catheter-based radiofrequency ablation is used, with a success rate of near 100%.6

Of note, patients with certain types of congenital heart disease (e.g., Ebstein anomaly) (Chapter 34) have a high incidence of WPW and may have ablations in addition to their underlying structural heart disease.


Atrial Arrhythmias

Supraventricular arrhythmias are frequently treated with ablation and are often caused by reentry, especially near the coronary sinus. Of atrial arrhythmias in children, supraventricular re-entrant tachycardia
accounts for over 60%, the remainder including atrioventricular nodal re-entrant tachycardia, atrial tachycardia, and atrial flutter.7,8,9 Supraventricular tachycardias also occur in adults, and ablation sites can be anywhere in the atria but most frequently in the area of the atrioventricular node and posteriorly at the coronary sinus. In junctional reciprocating tachycardia, the accessory pathway is often the posteroseptal area.10 Occasionally, they may be associated with coronary sinus aneurysms (Fig. 142.4).






FIGURE 142.3 ▲ Ablation scarring, atrioventricular nodal area. Scarring under tricuspid valve after remote atrioventricular nodal ablation. This section is more anterior or distal, in the area of right bundle branch, which is completely scarred.

Atrial flutter is classified as counterclockwise or clockwise and is a re-entrant arrhythmia, which often involves the isthmus between the tricuspid valve and the inferior vena cava; this area is used for treatment of atrial flutter, and ablation sites may be present in this area at autopsy from patients with prior treatment.






FIGURE 142.4 ▲ Coronary sinus seen from right atrium. There is marked endocardial fibrosis from remote endocardial ablation, performed in the coronary sinus area. This region is a common site of ablations for atrial tachycardias and atrial flutter (the latter typically at the isthmus between the coronary sinus and inferior vena cava).

Atrial fibrillation is the most common arrhythmia treated by intervention. It may be chronic or paroxysmal and is frequently associated with organic heart disease, such as cardiomyopathy or ischemia. Chronic atrial fibrillation has been classified as persistent (>7 days) or permanent. Occasionally, there are no predisposing diseases (lone atrial fibrillation). Noncardiac conditions that increase the risk of atrial fibrillation include hypertension, lung disease, and hyperthyroidism. The most common cardiac conditions are mitral valve disease, especially stenosis, ischemic heart disease, and cardiomyopathy.

Patients with atrial fibrillation are treated with anticoagulation, because there is a sevenfold increase in the risk of stroke from embolized mural thrombosis. Other complications include heart failure and palpitations; the ventricular response is treated with beta-blockers and calcium channel blockers. Occasionally, ablation of the atrioventricular node is necessary, with dual-chamber pacing.

There are no specific pathologic findings in atrial fibrillation, but nonspecific features are commonly encountered such as gross atrial dilatation (which may be primary or secondary to the arrhythmic state) and histologic hypertrophy and fibrosis. These latter findings have been shown to have some correlation with recurrence of atrial fibrillation following the Cox maze procedure.11 Mural thrombi are common findings in markedly dilated atria.

The arrhythmia is believed to propagate in the area of the pulmonary valve sleeves, or regions of smooth muscle that extend from the pulmonary vein media into the left atrial body. The sleeve length ranges from 2 to 25 mm and is longest in the upper veins. The concept of interruption of left atrial tracts has led to a variety of surgical approaches, which are generally termed “maze” procedure, after the irregular incisions made above the posterior leaflet of the mitral valve. Patients with atrial fibrillation due to mitral valve disease often undergo mitral valve replacement or repair. Approximately 40% of these patients have surgical ablation either by incisions or by other methods of ablation, typically cryotherapy (cryomaze). The latter procedure has been associated with over 75% freedom from recurrent atrial fibrillation at 1 year.12 In general, the success of the maze procedure is correlated to the degree of atrial dilatation and is most successful if the atrium is <50 mm in diameter.


Ventricular Tachycardia in the Absence of Structural Heart Disease

Monomorphic ventricular tachycardias and premature ventricular impulses occur anywhere in the ventricles but most frequently in the left ventricular outflow tract beneath the aortic valve cusps,13 right ventricular outflow tract,14 and tricuspid annulus.15 Ablation has a good success rate of ameliorating symptoms with prevention of recurrent arrhythmias. In patients with a history of ventricular ablation, these are sites that are likely to have been treated with prior ablations, which appear as white endocardial scars.


Ventricular Tachycardia in Structural and Ischemic Heart Disease

Cardiomyopathies, including hypertrophic and dilated cardiomyopathy, are prone to the development of monomorphic ventricular tachycardias that are amenable to ablation.16 In dilated cardiomyopathy, they may be endocardial based, especially near a valve annulus, or deep and subepicardial.17 The latter may be approached percutaneously by introducing the catheter to the epicardium through the pericardium. Ventricular tachycardia associated with healed myocardial infarction is also associated with areas of low-voltage scar. Histologic sections of these areas at autopsy show transmural scars in most cases.18 Common ablation sites for monomorphic ventricular tachycardias in ischemic cardiomyopathy are the posterior papillary muscle and ventricular septum.19







FIGURE 142.5 ▲ Complication of right ventricular outflow ablation. Months after a right ventricular outflow ablation for ventricular tachycardia, there was rupture of a pseudoaneurysm resulting in hemopericardium and sudden death. Perforation and sudden death rarely occurs and may happen years after procedure (from a published case report).20


Pathologic Findings

Radiofrequency ablation results in endocardial injury generally 5 to 6 mm diameter and up to 3 mm deep, sometimes associated with mural thrombus. Grossly, lesions are acutely pale and progress to fibrosis, which may disappear on gross inspection. Acutely, there is coagulative necrosis surrounded by neutrophils and then macrophages and granulation tissue, as in any wound healing response. In areas of healed injury, there may be transmural coagulation necrosis of meshlike fibrotic tissue, with interspersed islands of myocardial cells, up to a maximum depth of 7 mm.18 Chronically, there is fibrosis, which is nonspecific as to etiology.



Aug 19, 2016 | Posted by in CARDIOLOGY | Comments Off on Pathology of Cardiac Devices and Interventions

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