BMJ  2003;327:97-100 (12 July), doi:10.1136/bmj.327.7406.97

Clinical review

ABC of interventional cardiology

Non-coronary percutaneous intervention

the Health Sciences Centre and St Boniface Hospital, Winnipeg, Manitoba, Canada, the University of Manitoba, Winnipeg.

Introduction

Although most percutaneous interventional procedures involve the coronary arteries, major developments in non-coronary transcatheter cardiac procedures have occurred in the past 20 years. In adults the commonest procedures are balloon mitral valvuloplasty, ethanol septal ablation, and septal defect closure. These problems were once treatable only by surgery, but selected patients may now be offered less invasive alternatives. Carrying out such transcatheter procedures requires supplementary training to that for coronary intervention.

Balloon mitral valvuloplasty

Acquired mitral stenosis is a consequence of rheumatic fever and is commonest in developing countries. Commissural fusion, thickening, and calcification of the mitral valve leaflets typically occur, as well as thickening and shortening of the chordae tendinae. The mitral valve stenosis leads to left atrial enlargement, which predisposes patients to atrial fibrillation and the formation of left atrial thrombus.

View larger version (142K): [in this window] [in a new window]   Stenotic mitral valve showing distorted, fused, and calcified valve leaflets. (AMVL=anterior mitral valve leaflet, PMVL=posterior mitral valve leaflet, LC=lateral commissure, MC=medial commissure)

 

In the 1980s percutaneous balloon valvuloplasty techniques were developed that could open the fused mitral commissures in a similar fashion to surgical commissurotomy. The resulting fall in pressure gradient and increase in mitral valve area led to symptomatic improvement. Today, this procedure is most often performed with the hourglass shaped Inoue balloon. This is introduced into the right atrium from the femoral vein, passed across the atrial septum by way of a septal puncture, and then positioned across the stenosed mitral valve before inflation.

Patient selection
In general, patients with moderate or severe mitral stenosis (valve area < 1.5 cm²) with symptomatic disease despite optimal medical treatment can be considered for this procedure. Further patient selection relies heavily on transthoracic and transoesophageal echocardiographic findings, which provide structural information about the mitral valve and subvalvar apparatus.

View larger version (82K): [in this window] [in a new window]   Top: Diagram of the Inoue balloon catheter positioned across a stenosed mitral valve. Bottom: Fluoroscopic image of the inflated Inoue balloon across the valve

 

A scoring system for predicting outcomes is commonly used to screen potential candidates. Four characteristics (valve mobility, leaflet thickening, subvalvar thickening, and calcification) are each graded 1 to 4. Patients with a score of < 8 are more likely to have to have a good result than those with scores of > 8. Thus, patients with pliable, non-calcified valves and minimal fusion of the subvalvar apparatus achieve the best immediate and long term results.

Relative contraindications are the presence of pre-existing significant mitral regurgitation and left atrial thrombus. Successful balloon valvuloplasty increases valve area to > 1.5 cm² without a substantial increase in mitral regurgitation, resulting in significant symptomatic improvement.

Complications—The major procedural complications are death (1%), haemopericardium (usually during transseptal catheterisation) (1%), cerebrovascular embolisation (1%), severe mitral regurgitation (due to a torn valve cusp) (2%), and atrial septal defect (although this closes or decreases in size in most patients) (10%). Immediate and long term results are similar to those with surgical valvotomy, and balloon valvuloplasty can be repeated if commissural restenosis (a gradual process with an incidence of 30-40% at 6-8 years) occurs.

In patients with suitable valvar anatomy, balloon valvuloplasty has become the treatment of choice for mitral stenosis, delaying the need for surgical intervention. It may also be of particular use in those patients who are at high risk of surgical intervention (because of pregnancy, age, or coexisting pulmonary or renal disease).

View larger version (135K): [in this window] [in a new window]   Postmortem appearance of a heart with hypertrophic cardiomyopathy showing massive ventricular and septal hypertrophy causing obstruction of the left ventricular outflow tract (LVOT). This is compounded by the anterior mitral valve leaflet (AMVL), which presses against the ventricular septum (VS). Note the coincidental right atrial (RAE) and right ventricular (RVE) pacing electrodes

 

In contrast, balloon valvuloplasty for adult aortic stenosis is associated with high complication rates and poor outcomes and is only rarely performed.

Ethanol septal ablation

Hypertrophic cardiomyopathy
Hypertrophic cardiomyopathy is a disease of the myocytes caused by mutations in any one of 10 genes encoding various components of the sarcomeres. It is the commonest genetic cardiovascular disease, being inherited as an autosomal dominant trait and affecting about 1 in 500 of the population. It has highly variable clinical and pathological presentations.

View this table: [in this window] [in a new window]   Characteristics of hypertrophic cardiomyopathy

 

It is usually diagnosed by echocardiography and is characterised by the presence of unexplained hypertrophy in a non-dilated left ventricle. In a quarter of cases septal enlargement may result in substantial obstruction of the left ventricular outflow tract. This is compounded by Venturi suction movement of the anterior mitral valve leaflet during ventricular systole, bringing it into contact with the hypertrophied septum. The systolic anterior motion of the anterior mitral valve leaflet also causes mitral regurgitation.

View larger version (63K): [in this window] [in a new window]   Echocardiogram showing anterior mitral valve leaflet (AMVL) and septal contact (***) during ventricular systole. Note marked left ventricular (LV) free wall and ventricular septal (VS) hypertrophy. Injection of an echocontrast agent down the septal artery results in an area of septal echo-brightness (dotted line). (LA=left atrium, AoV=aortic valve)

 

Treatment
Although hypertrophic cardiomyopathy is often asymptomatic, common symptoms are dyspnoea, angina, and exertional syncope, which may be related to the gradient in the left ventricular outflow tract. The aim of treatment of symptomatic patients is to improve functional disability, reduce the extent of obstruction of the left ventricular outflow tract, and improve diastolic filling. Treatments include negatively inotropic drugs such as blockers, verapamil, and disopyramide. However, 10% of symptomatic patients fail to respond to drugs, and surgery—ventricular myectomy (which usually involves removal of a small amount of septal muscle) or ethanol septal ablation—can be considered.

View larger version (361K): [in this window] [in a new window]   Angiograms showing ethanol septal ablation. The first septal artery (S1, top left) is occluded with a balloon catheter (top right) before ethanol injection. This results in permanent septal artery occlusion (bottom) and a localised septal myocardial infarction. (LAD=left anterior descending artery, TPW=temporary pacemaker wire)

 

The objective of ethanol septal ablation is to induce a localised septal myocardial infarction at the site of obstruction of the left ventricular outflow tract. The procedure involves threading a small balloon catheter into the septal artery supplying the culprit area of septum. Echocardiography with injection of an echocontrast agent down the septal artery allows the appropriate septal artery to be identified and reduces the number of unnecessary ethanol injections.

Once the appropriate artery is identified, the catheter balloon is inflated to completely occlude the vessel, and a small amount of dehydrated ethanol is injected through the central lumen of the catheter into the distal septal artery. This causes immediate vessel occlusion and localised myocardial infarction. The infarct reduces septal motion and thickness, enlarges the left ventricular outflow tract, and may decrease mitral valve systolic anterior motion, with consequent reduction in the gradient of the left ventricular outflow tract. Over the next few months the infarcted septum undergoes fibrosis and shrinkage, which may result in further symptomatic improvement.

The procedure is performed under local anaesthesia with sedation as required. Patients inevitably experience chest discomfort during ethanol injection, and treatment with intravenous opiate analgesics is essential. Patients are usually discharged after four or five days.

Complications
Heart block is a frequent acute complication, so a temporary pacing electrode is inserted via the femoral vein beforehand and is usually left in situ for 24 hours after the procedure, during which time the patient is monitored.

View larger version (139K): [in this window] [in a new window]   Micrograph of hypertrophied myocytes in haphazard alignments characteristic of hypertrophic cardiomyopathy. Interstitial collagen is also increased

 

The main procedural complications are persistent heart block requiring a permanent pacemaker (10%), coronary artery dissection and infarction requiring immediate coronary artery bypass grafting (2%), and death (1-2%). The procedural mortality and morbidity is similar to that for surgical myectomy, as is the reduction in left ventricular outflow tract gradient. Surgery and ethanol septal ablation have not as yet been directly compared in randomised studies.

View larger version (108K): [in this window] [in a new window]   Simultaneous aortic and left ventricular pressure waves before (left) and after (right) successful ethanol septal ablation. Note the difference between left ventricular peak pressure and aortic peak pressure, which represents the left ventricular outflow tract gradient, has been reduced from 80 mm Hg to 9 mm Hg

 

Septal defect closure

Atrial septal defects
Atrial septal defects are congenital abnormalities characterised by a structural deficiency of the atrial septum and account for about 10% of all congenital cardiac disease. The commonest atrial septal defects affect the ostium secundum (in the fossa ovalis), and most are suitable for transcatheter closure. Although atrial septal defects may be closed in childhood, they are the commonest form of congenital heart disease to become apparent in adulthood.

View this table: [in this window] [in a new window]   Indications and contraindications for percutaneous closure of atrial septal defects

 

Diagnosis is usually confirmed by echocardiography, allowing visualisation of the anatomy of the defect and Doppler estimation of the shunt size. The physiological importance of the defect depends on the duration and size of the shunt, as well as the response of the pulmonary vascular bed. Patients with significant shunts (defined as a ratio of pulmonary blood flow to systemic blood flow > 1.5) should be considered for closure when the diagnosis is made in later life because the defect reduces survival in adults who develop progressive pulmonary hypertension. They may also develop atrial tachyarrhythmias, which commonly precipitate heart failure.

Patients within certain parameters can be selected for transcatheter closure with a septal occluder. In those who are unsuitable for the procedure, surgical closure may be considered.

View larger version (77K): [in this window] [in a new window]   Deployment sequence of the Amplatzer septal occluder for closing an atrial septal defect

 

Patent foramen ovale
A patent foramen ovale is a persistent flap-like opening between the atrial septum primum and secundum which occurs in roughly 25% of adults. With microbubbles injected into a peripheral vein during echocardiography, a patent foramen ovale can be demonstrated by the patient performing and releasing a prolonged Valsalva manoeuvre. Visualisation of microbubbles crossing into the left atrium reveals a right-to-left shunt mediated by transient reversal of the interatrial pressure gradient.

Although a patent foramen ovale (or an atrial septal aneurysm) has no clinical importance in otherwise healthy adults, it may cause paradoxical embolism in patients with cryptogenic transient ischaemic attack or stroke (up to half of whom have a patent foramen ovale), decompression illness in divers, and right-to-left shunting in patients with right ventricular infarction or severe pulmonary hypertension. Patients with patent foramen ovale and paradoxical embolism have an approximate 3.5% yearly risk of recurrent cerebrovascular events.

View larger version (296K): [in this window] [in a new window]   Amplatzer occluder devices for patent foramen ovale (left) and muscular ventricular septal defects (right)

 

Secondary preventive strategies are drug treatment (aspirin, clopidogrel, or warfarin), surgery, or percutaneous closure using a dedicated occluding device. A lack of randomised clinical trials directly comparing these options means optimal treatment remains uncertain. However, percutaneous closure offers a less invasive alternative to traditional surgery and allows patients to avoid potential side effects associated with anticoagulants and interactions with other drugs. In addition, divers taking anticoagulants may experience haemorrhage in the ear, sinus, or lung from barotrauma.

Congenital ventricular septal defects
Untreated congenital ventricular septal defects that require intervention are rare in adults. Recently, there has been interest in percutaneous device closure of ventricular septal defects acquired as a complication of acute myocardial infarction. However, more experience is necessary to assess the role of this procedure as a primary closure technique or as a bridge to subsequent surgery.

Further reading • Inoue K, Lau K-W, Hung J-S. Percutaneous transvenous mitral commissurotomy. In: Grech ED, Ramsdale DR, eds. Practical interventional cardiology. 2nd ed. London: Martin Dunitz, 2002: 373-87 • Bonow RO, Carabello B, de Leon AC, Edmunds LH Jr, Fedderly BJ, Freed MD, et al. ACC/AHA guidelines for the management of patients with valvular heart disease: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients with Valvular Heart Disease). J Am Coll Cardiol 1998;32: 1486-582[Free Full Text] • Wilkins GT, Weyman AE, Abascal VM, Bloch PC, Palacios IF. Percutaneous balloon dilatation of the mitral valve: an analysis of echocardiographic variables related to outcome and the mechanism of dilatation. Br Heart J 1998;60: 299-308[CrossRef] • Wigle ED, Rakowski H, Kimball BP, Williams WG. Hypertrophic cardiomyopathy: clinical spectrum and treatment. Circulation 1995;92: 1680-92[Free Full Text] • Nagueh SF, Ommen SR, Lakkis NM, Killip D, Zoghbi WA, Schaff HV, et al. Comparison of ethanol septal reduction therapy with surgical myectomy for the treatment of hypertrophic obstructive cardiomyopathy. J Am Coll Cardiol 2001;38: 1701-6[Abstract/Free Full Text] • Braun MU, Fassbender D, Schoen SP, Haass M, Schraeder R, Scholtz W, et al. Transcatheter closure of patent foramen ovale in patients with cerebral ischaemia. J Am Coll Cardiol 2002;39: 2019-25[Abstract/Free Full Text] • Waight DJ, Cao Q-L, Hijazi ZM. Interventional cardiac catheterisation in adults with congenital heart disease. In: Grech ED, Ramsdale DR, eds. Practical interventional cardiology. 2nd ed. London: Martin Dunitz, 2002: 390-406

 

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The ABC of interventional cardiology is edited by Ever D Grech and will be published as a book in summer 2003.

The picture of a stenotic mitral valve and micrograph of myocytes showing hypertrophic cardiomyopathy were provided by C Littman, consultant histopathologist at the Health Sciences Centre, Winnipeg, Manitoba, Canada. The postmortem picture of a heart with hypertrophic cardiomyopathy was provided by T Balachandra, chief medical examiner for the Province of Manitoba, Winnipeg. The pictures of Amplatzer occluder devices were provided by AGA Medical Corporation, Minnesota, USA.

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