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.

Morris Sherman, MB BCh, PhD, FRCP(C)
University of Toronto and,
University Health Network,
Toronto, ON.

Introduction
Although hepatocellular carcinoma (HCC) is not a common cancer in North America, it is the fifth most common cancer in the world.¹ Age standardized incidence rates vary from three per 100,000 in North American men to 80 per 100,000 in China.^1,2 HCC affects people of all ages. However, as with many cancers, the incidence of this disease increases with age, so that the peak incidence is at about age 67-70, (M Sherman, submitted) regardless of the underlying etiology. In Canada, the incidence of HCC is largely driven by three chronic liver diseases: chronic hepatitis B, chronic hepatitis C and alcoholic cirrhosis. In Toronto, hepatitis B is the single most common cause of HCC, accounting for nearly half of all cases, while elsewhere in Ontario hepatitis C and alcohol are the major causes. (M Sherman, submitted)

Prognosis
HCC causes substantial morbidity and mortality. In the absence of early detection programs, most HCC present late, with advanced incurable disease. The reported survival rates for untreated symptomatic HCC varies from 0% at four months to 1% at two years.^3-5 The prognosis for small, untreated HCC--lesions that are the target of surveillance--is not well described. However, two-year survival in excess of 50% is not unusual.

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.

Bob Chaudhuri, MD
Resident in Psychiatry,
Department of Psychiatry,
University of Toronto.

In 1990, three million members of the US population were 85 years of age or older. By the year 2050, it is expected that the numbers of these very elderly people will reach 20 million. However, the percentage of older people in the US is less than that in most European nations. If one considers developing nations, 250 million Chinese will be over the age of 60 by the year 2020, and the number of people in developing nations over the age of 60 will be greater than that number in all the countries in Europe. Importantly, the number of people over the age of 80 continues to grow in proportion to the nation's population.¹ Given these demographic numbers,² the sequella of aging is relevant to psychiatry in general and geriatric psychiatry specifically. There is no specific Canadian data on this subpopulation.

Dementia is primarily a disease of later life, affecting approximately 5% of people over the age of 65, and in some populations studied, almost 50% of those over the age of 85. The essential features of dementia include the development of multiple cognitive deficits including, memory impairment, disturbance in executive functioning, and at least one of aphasia, apraxia or agnosia.

Eileen P. Sloan, PhD, MD
Resident in Psychiatry,
Department of Psychiatry,
University of Toronto.

Introduction
Agitation is an aspect of dementia that can have serious emotional, medical and health-care system consequences. It results in decreased quality of life for both patient and caregiver and is often cited as the reason for the patient being admitted to a long-term care facility. Within the nursing home setting, agitation may often result in increased use of physical and/or chemical restraints, with concomitant problems such as physical injury and falls. Medical care of the agitated patient can be compromised and nursing staff is required to spend greater amounts of time caring for the agitated patient.

Definition and Prevalence
Allen (1999) points out that "agitation" is not a diagnosis but refers to a constellation of symptoms.¹ Cohen-Mansfield and Billing (1986)² define agitation as "inappropriate verbal, vocal or motor activity unexplained by apparent needs or confusion." These authors divide the symptoms of agitation into three: aggressive behaviours (hitting, kicking, verbal aggression, spitting); inappropriate physically non-aggressive behaviours (pacing, repetitious mannerisms, robing and disrobing); and inappropriate verbal agitated behaviours (screaming, complaining, constant demands for attention).

A. Mark Clarfield

The fact that dementia is finally beginning to receive the attention that it deserves is evidenced by the editors of Geriatrics & Aging wisely deciding to devote most of this issue to the subject. Dementia is primarily associated with memory loss; this means, unfortunately, that professionals often pay far less attention to the other symptoms that can accompany the syndrome. In fact, caregivers tell us that their loved one's problem with memory is usually far less burdensome than are the behavioural symptoms. Two of these symptoms are featured in this issue: agitation, by Dr. Elizabeth Sloan (a resident in Psychiatry at the U of T); and wandering, written by Dr. Bob Chaudhari, of the same department.

Dr. Sloan reminds us that agitation--sometimes accompanied by other symptoms such as screaming and aggression--is not a diagnosis per se but rather consists of a "constellation of symptoms." In geriatric care we are not afraid of such terminology, even if the terms are not always easily found in the index of Harrison's Textbook of Medicine. The same, of course, would hold for falls or incontinence.

As is the case with many of the non-specific ("atypical") presentations of disease in the elderly, Sloan points out, an underlying medical illness must never be overlooked as a possible causal factor. As I like to teach my medical students, "Take a history before prescribing haldol." (Unfortunately, now that the older anti-psychotic medications are increasingly being replaced by less toxic molecules, I'll have to figure out a new alliteration to go with, for example, risperidone--now what starts with an "r"? "rectum", no; "respiratory system"--doesn't ring true.) But I digress.

Dr. Sloan goes on to offer a great deal of good advice and the interested reader is advised to consult the references in her comprehensive bibliography.

Dr. Chaudhuri tackles the related problem of wandering, where he offers an interesting tri-partite classification which I admit that I have not seen before: volitional (depressive), motivational (anxious) and repetitive behavioural (irritable) wandering. Perhaps as a geriatrician, I am used to a more "medical" classification; but the author, not surprisingly as he is a psychiatrist, offers a more psychodynamic approach.

Like Sloan, Dr. Chaudhuri points out that management must take into account the patient's environment. Appropriately, he does not spend much time on a pharmacological approach, which is not usually an effective method unless, of course, your aim is to drug the patient into a stupor.

My own experience is that the wandering (pacing) patient with dementia must be allowed his/her own space. Obviously, as is also the case at the other end of the age spectrum with the toddler, wanderers must be protected against the obvious dangers involved. However, when all is said and done, the milieu extérieur seems to me to be of more importance than the milieu intérieur.

Dr. Clarfield is the Chief of Academic Affairs at the Herzog Hospital in Jerusalem, Director of Geriatrics in the Ministry of Health, and on staff in the Division of Geriatric Medicine, Sir Mortimer B. Davis-Jewish General Hospital, McGill University, Montreal.

Clinical and Ethical Perspectives

Michael Gordon, MD, MSc, FRCPC
Vice President of Medical Services,
Baycrest Centre for Geriatric Care,
Professor of Medicine,
University of Toronto,
Toronto, ON.

David Goldstein, PhD
Director, Centre for Knowledge Transfer,
Baycrest Centre for Geriatric Care,
Professor of Psychology,
University of Toronto,
Toronto, ON.

The daughter told me (MG) that Dr. L. was prescribing Donepezil to her 87-year-old mother. "Do you agree with her decision?" she queried, then added, "We won't use the "A" word will we?" This recent exchange reflects the anxiety and fear that accompanies the communication of a diagnosis of Alzheimer's disease. It presents many complex clinical, legal and ethical problems, which may be challenging to many physicians.

Physicians are generally expected to communicate honestly and directly with their patients on matters of clinical significance. For patients suffering from Alzheimer's and other dementias, such straightforward communication may not always be appropriate. The patient may not be aware of his or her own cognitive changes and family members may balk at the idea of communicating such a devastating diagnosis. The physician may be left with a clinical and ethical conundrum: the desire to communicate honestly with the patient may conflict with the compelling desire to concur with the wishes of the patient's family.

Since I have my pen in hand, I hope that you will indulge me if I make a couple of personal remarks in response to our Editor-in-Chief's kind words about me.

It is true that Barry and I trained together but he is senior to me by a year or two. And, as those of us who have worked with and were trained by him can attest, he is no slouch himself! Physician, teacher, administrator and editor--each role acted out with his usual calm and panache. But perhaps the highest compliment that I can pay the good doctor is to recount a short anecdote. When I was an intern, and Barry a medical resident, I brought my father--who was suffering from chest pain--into the ER of Toronto's Mt. Sinai Hospital, where Barry and I were both in training. As my mother and I waited anxiously in the anteroom for word of his fate, I was scared to death that my dad would die.

To my great relief and good fortune, who should rush past but Dr. Goldlist, who had been called in by the ER staff to have a look at my father. As Dr. Goldlist walked through the ER doors on his way to examine my father, I turned to my mother and said, "Don't worry, Mom, one of the hospital's best doctors is going to be taking care of Dad. We've got nothing to worry about."

And so it was. Almost 30 years later--there Barry, it's out--my father is still hale and hearty.

By coincidence, another important influence on my professional life and career choice is also well represented in this issue. The prolific and dynamic Dr. Michael Gordon, Medical Director of the world-renowned Baycrest Hospital, was a couple of years senior to both Barry and me and, as Barry points out, in his role as chief medical resident at Mt. Sinai, he had a powerful effect on all of us. It would be safe to say that no one had more influence on my decision to enter the field than did Michael, and all of us continue to enjoy his special blend of qualities.

I encourage the readers to read Dr. Gordon's articles and the rest of the informative articles in this special issue of Geriatrics & Aging. Thanks again to the editors for allowing me to blather on and, above all, for the opportunity to contribute to this important issue.

A. Mark Clarfield

Margaret MacAdam, PhD
Senior Vice President and Vice President,
Community Services,
Baycrest Centre for Geriatric Care,
Toronto, ON.

Two of the biggest problems facing patients with cognitive impairment and their families are access to a safe and appropriate physical environment, and access to supportive services throughout the course of the patient's disease. These problems arise because it may become increasingly difficult for the patient to obtain an appropriate level of care in his or her original residence. The options that are currently available to these patients vary widely from province to province but include staying at home, moving to one of the supportive housing projects that are becoming available in many communities, or moving to a long-term care facility. To determine which of these options is most appropriate, one must take into account the needs of the individual patient, his or her prognosis and the resources that are available to the family for maintaining their relative in the community. Because of the progressive nature of many forms of cognitive impairment, housing and care decisions are subject to change during the patient's life span.

The first step in deciding what type of housing is most appropriate is to make an assessment of the individual's needs.

Michael Gordon, MD, MSc, FRCPC
Vice President of Medical Services,
Baycrest Centre for Geriatric Care,
Professor of Medicine,
University of Toronto,
Toronto, ON.

The husband looked to his wife when he was asked if he would allow me to refer him to participate in a research trial. He admitted that he had some "memory" problems but was not really aware of the degree of his cognitive decline. His wife said she would consider it and discuss it with her husband and their children. She was distraught about the diagnosis of Alzheimer's disease and the future implications for his function and the requirements for his care. She wanted to know if the trial might help him. I explained the principles of a double-blind randomized drug trial and suggested that she discuss her concerns with the researcher conducting it.

Without research there is no progress in Medicine. Most people support the concepts of, and need for, medical research. Throughout history, some form of medical research has occurred. As an outcome of the horrific experiments done on involuntary subjects during the Nazi regime, and the more contemporary American studies on poor black syphilis victims in the Tuskegee experiment and the Willowbrook hepatitis study, a more rigorous and protective approach to human research has been developed.

Contemporary medical researchers are expected to understand the basic ethical principles that govern clinical research.