Kristopher S. Cunningham, MD, PhD, University Health Network, University of Toronto, Department of Pathology, Toronto, ON.
Sharmi Shafi, BSc, University of Toronto, Toronto, ON.
Mellitta Mezony, MD, FRCPC, Mount Sinai Hospital, Department of Cardiology, Toronto, ON.
Molly Thangaroopan, MD, FRCPC, University Health Network, University of Toronto, Department of Cardiology, Toronto, ON.
Jagdish Butany, MBBS, MS, FRCPC, University Health Network, University of Toronto, Department of Pathology, Toronto, ON.

Pericardial inflammation is a familiar but uncommon cause of chest pain. The classic triad of retrosternal chest pain, pericardial friction rub, and serial ECG changes facilitates diagnosis of pericarditis, the etiology most often being idiopathic in nature. Because older adults more frequently contend with multiple conditions that may require cardiovascular surgical intervention, receive numerous medications, or result in an immunocompromised state, other important causes of pericarditis need to b e considered. This article considers pericarditis in the older population and emphasizes diagnosis and management of this condition. Situations common to this age group that require special attention to the appropriate treatment are also discussed.

Key words: pericarditis, pericardium, heart, inflammation, tamponade.

Editors: Valentin Fuster MD, PhD, R.Wayne Alexander MD, PhD, Robert A. O'Rourke MD

Reviewed by: Madhuri Reddy, MD
Associate Editor, Geriatrics & Aging

Thirty-five years after Dr. J. Willis Hurst published the first edition of Hurst's The Heart, the 10th edition has been released. The new edition covers the entire spectrum of cardiovascular disease, from basic science and molecular development, to clinical applications and the latest genetic therapies.

From the perspective of a clinician caring for the elderly, there is one particularly useful chapter, entitled "Cardiovascular aging in health and therapeutic considerations in older patients with cardiovascular diseases." It provides detailed descriptions of the anatomic and physiological changes in the normal aging heart, and explores their possible relationships with pathological states. Therapeutic options and evidence-based rationale are given for the most common disease states such as systolic hypertension, valvular disease and coronary syndromes.

Another practical chapter describes practice guidelines in cardiovascular care. It reviews, in straightforward charts and diagrams, guidelines for risk stratification and treatment for everything from blood pressure to cholesterol (in mg/dL rather than SI). Algorithms are given for treatment of chest pain, heart failure, valvular disease and preoperative assessment of cardiac risk.

A particularly timely chapter describes "Cost-effective strategies in cardiology." Costs are initially described from a societal perspective, with background provided on the different types of economic analyses used to study costs, and on cost-effectiveness in prevention, diagnosis and therapy in common areas such as hyperlipidemia, smoking cessation, anti-hypertensive screening and atrial fibrillation. This is a wonderful chapter, supplying practical information to the clinician (and non-health economist) and insight into public policy as it relates to cardiovascular medicine.

There are also a couple of interesting chapters on insurance and legal issues in patients with heart disease. Other chapters explore the effects of mood and anxiety disorders in cardiovascular disease and describe behavioural therapies.

Overall, this substantial text acts as an excellent reference for the non-cardiologist. It reviews common cardiovascular conditions in a clear, well-presented manner and provides a multitude of charts and graphs to display information. Chapters on history and cardiac auscultation will appeal to those clinicians early in their training, whereas chapters on MRI and PET (with superb imaging) and techniques of electrophysiology make wonderful reference for even the experienced clinician.

For some reason, the paradigm for death in our society seems to be cancer, and it is this disease that many elderly fear the most. Yet statistics still show that cardiac disease is by far the most common cause of death in western societies, despite the recent (40 years) age-adjusted decline in mortality for cardiac disease. What this means is that even though a 75-year-old man is less likely to die in the next year of heart disease than a similarly aged man would have in 1960, it is still the most likely cause of death. The greatest misconception is probably among women, who often think that breast cancer is a more common cause of death than heart disease.

Why is this the case? Although it is true that breast cancer can affect very young women, advancing age is the biggest risk for the prevalence of both cancer and cardiac disease. I think the more likely reason for the societal fear of cancer is the belief that cancer is likely to cause a particularly difficult death. This popular conception is based on two factors: a lack of appreciation of the effectiveness (and often a lack of availability) of modern palliative care, and a mistaken belief that cardiac death results in sudden death, usually in the setting of an acute myocardial infarction (MI). However, in the elderly, this is not usually the case.

There has been a recent dramatic increase in the prevalence of congestive heart failure in the elderly, partially at least as a result of modern advances in treatment of acute MI that allows more patients to survive the acute incident. Patients with Grade IV ventricular function have a 50% annual mortality rate, worse than many cancers. Patients can be severely symptomatic and have very poor quality of life. Frequently in these patients, palliative care would seem to be appropriate, and yet it is not often 'prescribed.' Part of the reasoning is that for many of us the word 'palliative' is only associated with cancer. As well, our ability to predict survival in specific individuals with congestive heart failure is poor, thus making them inappropriate for some palliative care services that expect a very limited time frame per patient.

This topic was recently discussed in the British Medical Journal in an article entitled 'Cancer isn't the only malignant disease.1 The case described a man with incurable and severe peripheral vascular disease, and the reasons for lack of a palliative focus in his management. Fortunately, in this case the physicians eventually recognized the need for palliation, and the patient was able to die at home. The article is definitely worth reading and the BMJ (like Geriatrics & Aging!) is one of the few journals available on line (at bmj.com) in its entirety at no cost to the user.

This month's journal focuses on some of the key issues primary care doctors face in managing the cardiovascular problems of their patients. Current issues in heart failure management are discussed and there are articles on the management of multi-vessel coronary artery disease (stenting vs. bypass). The internationally renowned expert in geriatric cardiology, Dr. W.S. Aronow, has contributed an article on the controversies in treatment of low HDL cholesterol levels and elevated triglycerides.

The issue also contains articles on frontotemporal dementias, treatment of depression in the elderly, acute urinary retention and screening for urogenital cancers in elderly women. Dr. Madhuri Reddy has contributed an article on the difficulties inherent in making long term predictions of patients' needs, and Dr. Mark Clarfield has provided an entertaining article on the history of geriatrics. Enjoy this issue.

Reference

1. Moulder E. Cancer isn't the only malignant disease. BMJ 2002;324:07.

New evidence from Germany suggests that infections may contribute to the pathogenesis of atherosclerosis. Researchers studied a group of 572 patients and measured their IgG or IgA antibodies to eight different pathogens, including herpes simplex virus 1 and 2, cytomegalovirus, Epstein-Barr virus, Hemophilus influenzae, Chlamydia pneumoniae, Mycoplasma pneumoniae and Helicobacter pylori. Patients underwent coronary angiography, carotid duplex sonography and evaluation of the ankle-arm index, to determine the extent of atherosclerosis. What the researchers found was a correlation between infectious burden and the presence of advanced atherosclerosis. After a follow-up of three years, the mortality rate in patients with advanced atherosclerosis who were seropositive for up to three pathogens was only 7%, compared to a rate of 20% in those patients with between six and eight pathogens.

Further study will be required to determine whether the infections are actually causal for atherosclerosis, or whether they merely serve as a marker for poor health.

Source

1. Espinola-Klein C, Rupprecht HJ, Blankenberg S, et al. Impact of infectious burden on extent and long-term prognosis of atherosclerosis. Circulation. 2002;105:15-21.

D'Arcy Little, MD, CCFP
Director of Medical Education,
York Community Services, Toronto, ON. 

Introduction
Atrial fibrillation (AF) is the most common, chronic arrhythmia seen in clinical practice,^1,2 and is a common cause of morbidity, mortality and health care expenditure. The prevalence of the arrhythmia increases dramatically with age; it is estimated to have a prevalence of 5% in individuals aged 60 to 70 and of 22% in persons aged 91 to 103 years.^2,3 AF commonly causes symptoms in elderly patients, including palpitations, shortness of breath, fatigue and exercise intolerance.⁴ In addition, the presence of AF is an independent risk factor for stroke, especially in older persons.⁴ The risk of stroke is increased six-fold in patients with AF, even those without coexistent rheumatic heart disease. Further, it is estimated that over one-third of all strokes in the elderly are a consequence of AF.^2,4,5,6

Approach to Treatment with Electrical Cardioversion
The goals of therapy in patients with AF are to control the patient's symptoms and to reduce the risk of complications from thrombo-embolism.¹ Conversion of AF back to normal sinus rhythm will accomplish the first goal immediately and the second goal, theoretically, over the long term if sinus rhythm can be maintained post conversion. These results are thought to be due to the return and maintenance of atrial mechanical function.¹

Atrial fibrillation (AF) is characterized by the irregular and very rapid beating of the heart's atrial chambers. It results from a malfunction of the electrical conduction system of the atria, leading to chaotic electrical signals. The regular pumping action of the atria is replaced by irregular and disorganized spasms of atrial tissue, leading to reduced blood flow, blood clots (thrombi), stroke and even death.

Considerations Prior to Electrical Cardioversion

Spontaneous Cardioversion
In up to 48% of cases of recent-onset AF, spontaneous reversion to sinus rhythm occurs. The most important factor in determining whether spontaneous reversion can occur is the duration of the AF. AF of less than 72 hours duration has a spontaneous conversion rate of approximately 40%.¹

Emergent Cardioversion
Immediate, direct current (DC) cardioversion should be performed in patients who are unstable with serious signs or symptoms. This can be the case in atrial fibrillation with a very rapid ventricular rate (greater than 150 bpm) contributing to acute myocardial infarction, angina, congestive heart failure, hypotension or syncope.²

Elective Cardioversion:

Contraindications
The treatment or elimination of any reversible, predisposing conditions should be undertaken prior to elective cardioversion. Such precipitating causes include hyperthyroidism, pneumonia, acute myocardial infarction, pulmonary embolism and pericarditis. Conditions that are relatively unfavourable for elective DC cardioversion, or where elective DC cardioversion is contraindicated, should also be investigated. These conditions are listed in Table 1. However, a recent study suggested that the duration of AF may have less of an influence on the ability of AF to be cardioverted to, and maintained in normal sinus rhythm in the absence of coexisting significant heart disease.⁷ Appropriate initial blood work includes complete blood count, creatinine, electrolytes and thyroid function (sTSH).¹ Age does not influence the success of cardioversion. Congestive heart failure, poor LV function and increased left atrial size have been found by some but not all investigators to decrease success.⁸

TABLE 1 Unfavourable Conditions for Elective Cardioversion of Chronic Atrial Fibrillation

Duration of atrial fibrillation of more than 1 year (see text) Moderate to severe cardiomegaly Echocardiographic left atrial dimension >45 mm Digitalis toxicity (contraindication) Slow ventricular rate (contraindication) Sick sinus syndrome (contraindication) Mitral valve disease Congestive heart failure COPD Recurrent atrial fibrillation despite anti-arrhythmic drugs Inability to tolerate anti-arrhythmic drugs

Modified from: Aronow WS. Management of atrial fibrillation, ventricular arrhythmias and pacemakers in older persons: Management of the older person with atrial fibrillation. JAGS 1999;47(6):740-8.

Anticoagulation
Patients with AF have an increased risk of thrombo-embolism. Cardioversion from AF to sinus rhythm in a patient with prolonged AF who is not anticoagulated is associated with a 5-7% risk of stroke.⁸ While there are no randomized trials evaluating the efficacy of anticoagulation with warfarin, several large studies suggest that, with prior anticoagulation, systemic embolism associated with cardioversion is reduced to 0-1.1%.^1,8 As a result, it is recommended that in patients with AF of longer than 48 hours, oral anticoagulant therapy with warfarin should be administered (goal for INR of 2.0 to 3.0) for a minimum of three weeks before cardioversion. In addition, because the return of atrial mechanical activity may be delayed for several weeks after the restoration of sinus rhythm, it is recommended that anticoagulation be continued for a minimum of four weeks after cardioversion. This will also decrease the chances of embolism if AF recurs.¹

Transesophageal echocardiography (TEE) has been advocated by some as a screening tool to identify patients with AF of greater than 48 hours duration where there is no evidence of left atrial clot, allowing these patients to be cardioverted without prophylactic anticoagulation. However, studies have revealed that this technique is associated with a significant incidence of thromboembolic complications, resulting in current recommendations for anticoagulation in these patients.^1,9,10 In addition, prior to cardioversion, even patients whose AF has lasted less than 48 hours should be anticoagulated with intravenous heparin, in order to cover the delays that may be encountered during medical treatment.¹

Cardioversion Technique
Elective DC cardioversion has a higher rate of success in converting AF to sinus rhythm than does medical cardioversion,^2,6 making it the most reliable means to restore sinus rhythm.¹ The technique works by delivering an R-wave synchronized shock between two thoracic electrode paddles in an anesthetized patient. The paddles can be oriented anterolaterally or anteroposteriorly. A success rate of over 90% is achieved with either configuration.¹ However, some data suggest that with regards to technical success, an anteroposterior defibrillator paddle position is superior to an anterolateral position and permits lower energy usage.¹¹ Digoxin is usually stopped 24h before cardioversion, or at least a level is checked prior to cardioversion, since digitalis toxicity increases the risk of malignant ventricular arrhythmias.¹ Generally, energy requirements depend on the duration of the AF (for instance, recent AF has coarser fibrillatory waves and requires lower energy). The first attempt at cardioversion is made with 200J. Increments of 100J are used if preceding shocks are not successful.¹ Some studies have suggested that phamacologic agents, such as ibutilide, facilitate successful cardioversion of AF in patients who failed conventional external cardioversion. The medication is administered and cardioversion is attempted again.¹² Internal cardioversion (beyond the scope of this article) is an option if external cardioversion has not been successful, and some studies indicate that this technique may work for AF of duration greater than one year but less than three years.¹³

Complications
A variety of short-lived arrhythmias can follow cardioversion, including premature atrial and ventricular beats, sinus pauses and junctional escape rhythms. These usually do not require treatment. There is a small risk of ventricular fibrillation, especially if there is poor synchronization of the DC shock and the native QRS complex. Pulmonary edema can also be a rare complication in the context of severely depressed left ventricular function.¹⁴ Thrombo-embolic complications are discussed above.¹

Clinical Decisions
The decision to cardiovert a patient from atrial fibrillation to sinus rhythm is a clinical one. The most symptomatic patients will gain the most relief.1 Patients who have had atrial fibrillation for a shorter period will likely have less left atrial dilatation; therefore they have a greater probability of being maintained in sinus rhythm.

A reasonable approach is to attempt to cardiovert patients with AF of recent onset. Patients with chronic AF have two broad therapeutic options: 1) rate control and anticoagulation; and 2) cardioversion and maintenance of sinus rhythm. The comparative value of these approaches is still under investigation,⁸ although it might be reasonable to attempt to convert symptomatic patients to sinus rhythm. Conversion to sinus rhythm improves a patient's hemodynamic status and, as a result, his or her exercise tolerance. The left ventricular stroke volume and ejection fraction increase immediately after cardioversion, while the cardiac contractility remains unchanged. This implies that the improvement in hemodynamics is secondary to enhanced left ventricular diastolic filling, due to an increased cycle length and to the return of left atrial mechanical function (atrial "kick").¹⁵ This could be very important for patients with reduced left ventricular function.⁷ Other studies have demonstrated that changes in atrial electrophysiology and the atrial dilatation associated with chronic AF are reversible after cardioversion.^16,17

Maintenance of Sinus Rhythm
While electrical cardioversion of AF to normal sinus rhythm is successful in more than 80% of cases, without antiarrythmic therapy, only 25% of patients will remain in sinus rhythm after one year.18 A cost-benefit analysis in the Annals of Internal Medicine suggests that cardioversion alone should be the initial management strategy for persistent, non-valvular atrial fibrillation. For a relapse of the arrhythmia, repeated cardioversion plus low-dose amiodarone was found to be cost-effective for patients at moderate to high risk for ischemic stroke.¹⁹ Another study has demonstrated that amiodarone is more effective than sotalol and propafenone for the prevention of recurrences of atrial fibrillation²⁰ (see article).

Conclusions
Atrial fibrillation is a common, significant arrhythmia in the elderly. DC cardioversion is used in unstable cases, and as an elective procedure in cases of recent onset, to convert the patient to normal sinus rhythm. To avoid thromboembolic complications, patients with AF of greater than 48 hours duration should be anticoagulated with warfarin for three weeks prior to, and four weeks after cardioversion. Repeat cardioversion can be used for recurrent atrial fibrillation, and antiarrhythmic therapy, such as amiodarone, can be initiated to help maintain sinus rhythm. Cardioversion can also be used in symptomatic cases of AF of long duration, as duration has been shown to be less important than underlying heart disease in the success of conversion and maintenance of sinus rhythm.

References

1. Beamish RE. (Ed.) Canadian Cardiovascular Society Consensus Conference on Atrial Fibrillation. Can J Cardiol 1996;12A:1A-61A.
2. Aronow WS. Management of atrial fibrillation, ventricular arrhythmias and pacemakers in older persons: Management of the older person with atrial fibrillation. JAGS 1999;47(6): 740-8.
3. Aronow WS, Ahn C, Gutstein H. Prevalence of atrial fibrillation and association of atrial fibrillation with prior and new thromboembolic stroke in older patients. J Am Geriatr Soc 1996;44:521-3.
4. English KM, Channer KS. Managing atrial fibrillation in elderly people: Active management of atrial fibrillation should include elderly people. BMJ 1999;318:1088-9.
5. Hampton JR. The management of atrial fibrillation in elderly patients. Age and Ageing 1999;28:249-50.
6. Morris JJ Jr, Peter RH, McIntosh HD. Electrical conversion of atrial fibrillation: Immediate and long-term results and selection of patients. Ann Intern Med 1966;65:216-31.
7. Nakazawa H, et al. Is there a place for late cardioversion of atrial fibrillation? Eur Heart J 2000;21:327-33.
8. Lampert R, Ezekowitz MD. Management of arrhythmias. Clin in Ger Med 2000;16(3):593-618.
9. Warren J, et al. Cardioversion from atrial fibrillation without prolonged anticoagulation with use of transesophageal echocardiography to exclude the presence of atrial thrombi NEJM 1993;328(11):750-5.
10. Black IW, et al. Exclusion of atrial thrombus by transesophageal echocardiography does not preclude embolism after cardioversion of atrial fibrillation. A multicentre study. Circ 1994;89:2509-13.
11. Botto GL, Politi A, Bonini W, Broffoni, T, Bonatti R. External cardioversion of atrial fibrillation: role of paddle position on technical efficacy and energy requirements. Heart 1999;82:726-30.
12. Li H, et al. Usefulness of ibutilide in facilitating successful external cardioversion of refractory atrial fibrillation. Am J Cardiol. 1999;84:1096-8.
13. Tse HF, et al. Long-term outcome in patients with chronic atrial fibrillation after successful internal cardioversion. Am J Cardiol. 1999;83:607-9.
14. Levy S, et al. Atrial fibrillation: current knowledge and recommendations for management. Eur Heart J. 1998;19:1294-1320.
15. Raymond RJ, et al. Cardiac performance early after cardioversion from atrial fibrillation. Am Heart J 1998;136(3):435-42.
16. Hobbs WJC, et al. Reversal of atrial electrical remodeling after cardioversion of persistent atrial fibrillation in humans. Circ 2000:101;1145-51.
17. Mattioli AV, et al. Serial evaluation of left atrial dimension after cardioversion for atrial fibrillation and relation to atrial function. Am J Cardiol. 2000;85:832-36.
18. Coumel P, Thomas O, Leenhardt A. Drug therapy for prevention of atrial fibrillation. Am J Cardiol 1996;77(3):3A-9A.
19. Catherwood E, et al. Cost-effectiveness of cardioversion and antiarrhythmic therapy in non-valvular atrial fibrillation. 1999;130(8):625-36.
20. Roy D, et al. Amiodarone to prevent recurrence of atrial fibrillation. N Engl J Med 2000;342:913-20.

Kimby N. Barton, MSc
Associate Editor,
Geriatrics & Aging.

If you have ever known anyone with any degree of heart trouble you may be aware of the options available for the treatment of heart disease. We have medications that treat hypertension, medications that lower lipids and medications to prevent clotting. We can use diet and exercise to keep our arteries clear and our heart muscle healthy. But can we repair a heart once cells have been lost? Coronary heart disease accounts for 50% of all cardiovascular deaths and nearly 40% of the incidence of heart failure. Heart attacks lead to the death of vital cardiac myocytes and impair cardiac performance. The cells that survive an MI are unable to reconstitute the tissue that is lost, and eventually the heart begins to deteriorate. The victims of heart attack and their caregivers are well aware of the slow progression from heart attack to heart failure, and the lack of available therapies to stop this progression.

What if there was a way to re-vitalize the damaged cell population or to replace the cells that are lost? Unfortunately, in order to form a functional cardiac unit, the replacement cells must be able to survive, mature, electromechanically couple with pre-existing heart cells and have a beneficial effect on the function of the damaged heart.

Injury to a target organ is sensed by distant stem cells; these cells migrate to the site of damage and then differentiate, promoting structural and functional repair.

Sheldon Singh, BSc

Valvular heart disease is an increasingly common cause of congestive heart failure in the elderly population. Stenosis of the aortic valve is one type of valvular heart disease that can lead to congestive heart failure. Approximately 28,000 aortic valve replacements were performed in the United States in 1994. Sixty-one per cent of these were performed in individuals over age 65. This procedure is the second most common open-heart procedure performed in the elderly after coronary bypass grafting.

In adults, aortic stenosis may be due to previous rheumatic disease or calcification of a congenital bicuspid valve or normal tricuspid aortic valve. Although common worldwide, rheumatic disease is uncommon in North America and Europe. However, because of the increasing aging population, degenerative aortic valve calcification constitutes a substantial health problem.¹

Anatomy
A normal aortic valve is tricuspid. Each leaflet is flexible and composed of three layers covered with endothelium on each side. Degenerative calcific disease is characterized by discrete focal lesions on the aortic side of the leaflet. It is typically an active inflammatory process that bears some resemblance to atherosclerosis; there are protein and lipid infiltration as well as macrophages, foam cells, and the occasional T cell.² The risk factors for aortic valve disease include age, male gender, lipoprotein a, hypertension, smoking, cholesterol and diabetes.

SMH Alibhai, MD, FRCPC

As any physician knows, stroke is a common cause of morbidity and mortality in older patients. Strokes can be divided into three major aetiological groups--haemorrhagic, thromboembolic, and lacunar. Practically speaking, if neuroimaging does not show evidence of haemorrhage, physicians will generally treat patients who present with an acute stroke (or a transient ischaemic attack (TIA), for that matter) with either antiplatelet or anticoagulant therapy. For patients with a well-documented embolic source (e.g. atrial fibrillation), warfarin is the treatment of choice. For all other patients with non-haemorrhagic stroke, the treatment is traditionally antiplatelet therapy.

However, there are several options within antiplatelet therapy. The standard drug has been acetylsalicylic acid (ASA), or aspirin. At least four large randomized controlled trials revealed Ticlopidine to be slightly more effective in reducing the incidence of strokes and TIAs than aspirin, although it was more costly and more toxic.¹ However, a later meta-analysis of 145 studies suggested ticlopidine was probably as equally effective as aspirin.² Although newer antiplatelet agents are on the horizon (e.g.

D'Arcy L. Little, MD
Chief Resident, Family Medicine, Sunnybrook Health Science Centre, North York, Ontario

Background

Angiotensin Converting Enzyme inhibitors (ACE inhibitors) interact with the body's renin-angiotensin-aldosterone axis. Angiotensinogen (alpha-2 globulin) is converted to angiotensin I or AG-I (inactive) by renin released by the kidney in response to renal ischemia, hypotension, hypovolemia or depletion of sodium ions. ACE inhibitors block the conversion of AG-I to AG-II. AG-II is a powerful vasoconstrictor, as well as a releaser of aldosterone (an adrenal cortical hormone that leads to sodium retention in the kidney), see Figure 1.

 

FIGURE 1

Despite the fact that elderly patients have lower levels of plasma renin than their younger counterparts, ACE inhibitors have been evolving as important agents in the treatment of several cardiovascular diseases in both younger and older patients.

Jaye Waggoner, BAA

Heart disease and stroke are the top killers of Canadians. There are currently more than 500 cardiovascular disease-related research studies underway in Canada, in an effort to reduce the numbers who succumb to these conditions.

Despite the statistics, not all are doomed to a date with a heart attack. Even those who have already fallen victim to some aspect of heart disease can turn their health around with the right professional help. This help can be found at Cardiac Rehabilitation Centres, through the varied rehabilitation programs that they and other organizations offer.

Although the focus has changed since its doors opened in 1922, when its main function was meeting the rehabilitation needs of Canadians wounded in the First World War, The Toronto Rehabilitation Centre is still striving to help patients. The Centre has since split in half, with the Toronto Cardiac Rehabilitation Centre now specializing in recovery for heart patients. It was the first of its kind and is today the largest centre of its kind in North America.

Accepting referrals, the Centre's mandate is to assist cardiac patients to reach their "optimal physical, cognitive, functional and social potential and in doing so to improve their quality of life.