Archives of Gerontology and Geriatrics
27 (1998) 127 – 139

Pharmacological treatment of atrial fibrillation: a
review on prevention of recurrences and control of
ventricular response
Giuseppe Boriani *, Mauro Biffi, Angelo Branzi, Bruno Magnani
Institute of Cardiology, Uni6ersity of Bologna, Policlinico S. Orsola, Via Massarenti 9,
40138 Bologna, Italy
Received 29 December 1997; received in revised form 17 April 1998; accepted 20 April 1998

Abstract
Atrial fibrillation is the most common sustained arrhythmia, however its treatment remains
controversial and problematic. Electrical or pharmacological cardioversion are able to restore
sinus rhythm in many patients but maintenance of sinus rhythm requires long term treatment
with antiarrrhythmic agents. Today there is major concern regarding the ventricular
proarrhythmic effects of antiarrhythmic drugs because they may increase mortality. Even
non-cardiac toxicity of these agents must be considered. An alternative strategy based on
pharmacological control of ventricular response rate coupled with antithromboembolic
prophylaxis can be followed. For rate control digoxin alone has some specific limitations,
therefore, use of calcium antagonists (verapamil or diltiazem) or i-blockers must be considered.
At the present time, the relative efficacy and risks of these two alternative strategies in specific
patients subgroups remain to be established. Today, non-pharmacological treatments, as
atrio-ventricular node ablation are also available. In elderly patients, moreover, advanced age,
underlying heart disease, concomitant systemic illnesses and patient compliance to treatments
condition our decision making and treatment needs to be individualized. Appropriate
knowledge of the advantages, of the limitations and of the costs of every pharmacological or
non-pharmacological treatment option is required for deciding in every patient in view of the
best risk-benefit and cost-benefit ratio. © 1998 Elsevier Science Ireland Ltd. All rights reserved.
Keywords: Antiarrhythmic drugs; Atrial fibrillation; Cardioversion; Prophylaxis

* Corresponding author. Tel.: +39 51 349858; fax: + 39 51 344859.
0167-4943/98/$ - see front matter © 1998 Elsevier Science Ireland Ltd. All rights reserved.
PII S0167-4943(98)00106-X

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1. Introduction
Atrial fibrillation is the most common sustained arrhythmia seen by the clinician
and both its prevalence and its incidence increase with age (Kannel et al., 1982;
Wolf et al., 1991). Atrial fibrillation can be recognized in 0.2–0.3% of subjects aged
25– 35, in 3 – 4% of those aged 55–60 and in 5–9% of those above the age of 60.
Overall, 4% of a general population has paroxysmal or chronic atrial fibrillation
(Kannel and Wolf, 1992).
Atrial fibrillation is usually associated with some form of concurrent cardiovascular disease and systemic hypertension is quite common. Non-cardiac factors related
to an increased likelihood of developing atrial fibrillation include hyperthyroidism
and diabetes (Kannel et al., 1982). Infrequently, there is no identifiable cause for
atrial fibrillation and the term idiopathic or ‘lone’ atrial fibrillation is employed. In
the elderly, atrial fibrillation can be the manifestation of a sick sinus syndrome, in
its so-called brady-tachy variant.
Atrial fibrillation is a major cause of stroke, especially in the elderly (Wolf et al.,
1991) and the risk of stroke is increased 6-fold in non-rheumatic atrial fibrillation,
and 15- to 20-fold in rheumatic valvular disease (Wolf et al., 1991).
The hemodynamic consequences of atrial fibrillation are related to: (i) loss of
atrial contribution to cardiac output, which may result in a 20–40% reduction of
stroke volume; and (ii) excessively rapid ventricular rate with irregular rhythm and
with alteration of normal ability to regulate cardiac rhythm according to physiological activities.
Patients symptoms may vary markedly, some patients being asymptomatic.
However, palpitations, dizziness, dyspnea and chest discomfort are common in
subjects with atrial fibrillation and may be related to reduced working capacity,
aggravation or induction of heart failure or aggravation of ischemic heart disease.
The relevance of atrial fibrillation is confirmed by considering that patients with
atrial fibrillation and constant high ventricular rate (\ 120 bpm) may develop a
tachycardia-induced cardiomyopathy with a pattern of severe congestive heart
failure (Peters and Kienzle, 1988; Grogan et al., 1992; Crijns et al., 1997).
The treatment of atrial fibrillation has different objectives, as reported in Table
1. Non-pharmacological approaches to atrial fibrillation treatment have been
proposed (Harvey and Morady, 1995; Nattel, 1996; Jung and DiMarco, 1998),
Table 1
Importance of treating atrial fibrillation
To relieve symptoms of congestive heart failure, hypotension or angina that can be directly
attributed to atrial fibrillation
To improve overall cardiac function
To improve exercise tolerance
To prevent atrial fibrillation recurrences and related symptoms
To reduce the risk of stroke and of thromboembolic events
To prevent morbidity related to atrial fibrillation
To prevent mortality related to atrial fibrillation

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129

however their reliability and their risk-benefit and cost-benefit ratios are still under
evaluation. Therefore, especially in elderly patients, the first approach to atrial
fibrillation treatment is based on drug therapy. In this paper prevention of
recurrences and pharmacological control of ventricular rate will be reviewed, with
special attention to the requirements of elderly patients.

2. Classification and management of atrial fibrillation
The temporal pattern of atrial fibrillation is of great importance in conditioning
the appropriate management of a patient with this arrhythmia. Acute atrial
fibrillation (onset within 48 – 72 h) is characterized by a high rate of spontaneous or
drug-induced cardioversion and, usually, by lack of need for anticoagulation.
Chronic atrial fibrillation can be distinguished into a paroxysmal form (spontaneous termination on at least one occasion), a persistent form (intervention
required to restore sinus rhythm) and a permanent form (resistence to cardioversion
attempts and recurrences prophylaxis) (Sopher and Camm, 1996).
In clinical practice, the key problem is how long should attempts be made to
restore and to maintain sinus rhythm as opposed to another treatment strategy
based on simple control of ventricular rate coupled with antithromboembolic
prophylaxis (Waktare and Camm, 1998). This problem applies mainly to patients
with persistent atrial fibrillation and is particularly difficult in elderly patients in
whom the risk-benefit and cost-benefit ratio of some treatment options may be
more unpredictable and less favorable than in younger patients.

3. Maintenance of sinus rhythm versus control of ventricular response
In patients with atrial fibrillation, restoration of sinus rhythm by electrical or
pharmacological cardioversion may eliminate palpitations, fatigue and dyspnea,
prevent left ventricular dysfunction and significantly reduce thromboembolic complications. Unfortunately, because of the high recurrence rate, only 30% of the
patients without antiarrhythmic drug prophylaxis, maintain sinus rhythm for 6
months or more (Crijns et al., 1994). Therefore, attempts to maintain sinus rhythm
by pharmacological prophylaxis of arrhythmia recurrences is required. Antiarrhythmic drugs may cause proarrhythmic effects or other adverse effects and for this
reason this prophylactic strategy must be considered in opposition to another
therapeutic strategy which is based only on ventricular rate control by appropriate
drugs associated with antithromboembolic prophylaxis. Advantages and disadvantages of every therapeutic option are reported in Table 2.
The impact of these two different approaches to atrial fibrillation management is
currently under evaluation in a controlled trial, named AFFIRM (Atrial Fibrillation Follow-up Investigation of Rhythm Management) (AFFIRM Planning and
Steering Committee for the NHLBI AFFIRM Investigators, 1997).

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Table 2
Alternative therapeutic strategies for atrial fibrillation management
Maintenance of sinus rhythm by
antiarrhythmic drugs

Control of ventricular rate+antithromboembolic
prophylaxis

Advantages
Better hemodynamics
Reduction in thromboembolic risk

Advantages
‘Natural history’
Absence of significant proarrhythmic effects

Disadvantages
Risk of proarrhythmic effects
Risk of other drug-related adverse effects
Need for repeated cardioversions (if partial
efficacy)

Disadvantages
Worsening hemodynamics
Hemorragic risks due to anticoagulants
Residual embolic risk

4. Drug prophylaxis of atrial fibrillation recurrences

4.1. Indications to antiarrhythmic drug prophylaxis
Drug prophylaxis of atrial fibrillation recurrences can be used in patients with
paroxysmal atrial fibrillation or following electrical cardioversion in patients presenting with permanent atrial fibrillation.
Following electrical cardioversion the risk of atrial fibrillation recurrences is
generally high in the first days and then declines. However some clinical factors are
helpful in identifying patients at higher risk of arrhythmia recurrences (Table 3).
The most important factors seem to be a long previous arrhythmia duration or a
long total arrhythmia history, a low functional capacity, a large left atrial size,
advanced age and mitral valve disease (Crijns et al., 1994).
Table 3
Risk of atrial fibrillation recurrence after cardioversion
Estimated risk
Duration of atrial fibrillation
\2 years
\1 year
Number of atrial fibrillation episodes
\1
\3
Age
Gender (female)
Alcohol
Mitral stenosis
Dilated cardiomyopathy
Left atrial diameter at echocardiogram
\60 mm
\45 mm
Previous ineffective antiarrhythmic drugs trials

++++
+++
++
+++
++
+
++
+++
+
++++
+++
+++

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131

Table 4
Guidelines to drug prophylaxis of atrial fibrillation recurrences
Indications
Recurrent atrial fibrillation (at least two episodes) requiring hospitalisation
Symptomatic recurrent atrial fibrillation
Atrial fibrillation with arrhythmia-related hemodynamic impairment
Recurrent atrial fibrillation with thromboembolic episodes
Atrial fibrillation successfully treated by electrical cardioversion
Atrial fibrillation in Wolff–Parkinson–White (even only one episode) (indeed transcatheter ablation
can be the most appropriate choice)
Contraindications
Severe left ventricular dysfunction
Congestive heart failure
Sick sinus syndrome
Non indications
Asymptomatic recurrent self-terminating atrial fibrillation

Infrequent recurrences of atrial fibrillation (less or equal to 2–3 episodes per
year) can be managed by episodic drug treatment (Margolis et al., 1980; Capucci et
al., 1994; Boriani et al., 1995, 1997) and do not require, in our view, continuous
drug prophylaxis.
Indeed, proper indications to pharmacological prophylaxis are required in order
to minimize the risks of adverse effects and particular attention is mandatory in
elderly patients due to concomitant heart diseases, decreased compliance to treatments and greater sensitivity to drug-related adverse effects. General indications
and contraindications to drug prophylaxis are reported in Table 4.

4.2. Efficacy of antiarrhythmic drugs
The prophylactic efficacy of antiarrhythmic drugs can be asssessed by evaluating
the capacity to prevent atrial fibrillation recurrences after effective cardioversion. In
Table 5, a summary of data from literature is reported. As shown, the percentage
of patients who maintain sinus rhythm, without arrhythmia recurrence, under
placebo treatment is around 30% after 3 months and around 20–25% after 12
months. Antiarrhythmic agents may increase the percentage of patients who
maintain sinus rhythm, however, the overall efficacy is limited and, except for
amiodarone, no more than 50% of the treated patients are free from arrhythmia
recurrences after 6 – 12 months. For amiodarone efficacy rates of 75–78.5% at 6
months and of 50 – 73% at 12 months have been reported (Middlekauff et al., 1992),
however, prospective large sale trials on the risk-benefit ratio of low dose amiodarone in atrial fibrillation are still lacking. Although amiodarone may be effective
where other agents have failed, there is major concern about its use because it
carries the risk of severe and sometimes irreversible adverse effects.
Data from the literature indicate how a serial approach to drug therapy may be
the most successful strategy: for example, 40% of patients with recurrences on a

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132

class 1A agent remained in sinus rhythm after 1 year with sotalol or propafenone
(Reimold et al., 1993), whereas in another experience, the sequential use of
flecainide, sotalol or quinidine and amiodarone allowed 63% of the treated patients
to maintain sinus rhythm at 2 years, although with a mean of 1.8 cardioversions per
patient (Crijns et al., 1991).

4.3. Proarrhythmic effects
Today there is major concern over the risk of potentially lethal ventricular
proarrhythmic effects caused by antiarrhythmic agents employed for a relatively
benign arrhythmia, as atrial fibrillation (Falk, 1992; Waldo and Prystowsky, 1998).
Indeed, one of the most important advances in this field has been the awareness of
the risks related to drugs used for maintaining sinus rhythm.
The proarrhythmic risks of quinidine were assessed by a meta-analysis of six
randomized trials on quinidine after atrial fibrillation cardioversion (Coplen et al.,
1990). Although more effective in preventing recurrences than placebo, quinidine
was associated with a 3-fold increase in mortality risk (2.9% versus 0.8%). Caution
has been suggested in interpreting these data in view of the limitations of metaanalysis, the possibility that concomitant treatment with digoxin or diuretics may
have conditioned quinidine-related risks, the finding that the precise mode of death
was not available in a significant proportion of deaths, and that sudden death
occurred only in three out of 12 patients who died on quinidine.
The most typical quinidine-related proarrhythmic effect is torsade de pointe,
whose occurrence is associated with marked QT interval prolongation and is
favored by hypokalemia, but is not related to quinidine dose (Falk, 1992). Torsade
de pointe occurrence is favored by bradycardia or by a relatively slow heart rate
and for this reason during treatment with class 1A agents (quinidine, dysopiramide,
procainamide) it occurs more often after termination of AF, when sinus rhythm is
restored.
Table 5
Efficacy of antiarrhythmic drugs in preventing atrial fibrillation recurrences after electrical cardioversion (summary from literature)
Drug

Sinus rhythm maintenance
At 1 month (%)

Quinidine
Disopyramide
Procainamide
Propafenone
Flecainide
Amiodarone
Sotalol
Placebo

At 3 months (%)

At 6 months (%)

At 12 months (%)

65

44– 75
72
39
44
44

27 – 58
44 – 50

23 – 51
54
25

54

58

49– 50
15– 56

40
75 – 78.5
46 – 50
19 – 35

34 – 42
50 – 73
37 – 46
0 – 45

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133

The role of underlying heart disease and functional status in worsening the
proarrhythmic risk of antiarrhythmic agents, mainly class 1A drugs, has been
stressed by a post hoc analysis of the Stroke Prevention in Atrial Fibrillation
(SPAF) trial (Stroke Prevention in Atrial Fibrillation Investigators, 1991) on
warfarin and aspirin in non valvular atrial fibrillation (Flaker et al., 1992). In this
paper use of antiarrhythmic agents was associated with a 2.5-fold increase in the
risk of arrhythmic death and this increased to 5.8-fold in patients with congestive
heart failure.
In view of these findings, the use of quinidine has been restricted in recent years,
and in patients who need to be treated with this drug, careful monitoring of QT
interval changes in the first days of treatment is required. Initiation of treatment
during in-hospital stay is recommended in patients at higher risk (Prystovsky, 1994;
Waldo and Prystowsky, 1998).
Sotalol, a i-blocker with class 3 antiarrhythmic activity, also may cause torsade
de pointes, but the risk is dose-dependent, being around 1% for dosages between
160 and 240 mg daily and 4 – 5% for dosages higher than 480 mg daily (Falk, 1992).
Class 1C antiarrhythmic drugs (flecainide, propafenone and encainide) have a
marked effect on conduction velocity, and like class 1A agents, may organize and
slow the rate of atrial fibrillation, converting it into atrial flutter. In some cases, the
atrial rate is slow enough to allow 1:1 atrio-ventricular conduction, thus with rapid
ventricular response, wide QRS complexes simulating ventricular tachycardia and
risk of hemodynamic impairment (Falk, 1992). This proarrhythmic effect is favoured by adrenergic stimulation and has been reported in 3–5% of patients treated
with flecainide or propafenone (Falk, 1992).
The risk of ventricular proarrhythmia, like sustained ventricular tachycardia or
ventricular fibrillation, during treatment with antiarrhythmics for supraventricular
arrhythmias seems to be generally low, however patients with significant left
ventricular dysfunction are at potentially higher risk.
For amiodarone, a low risk of ventricular proarrhythmic effects has been
reported, even in patients with structural heart disease (Middlekauff et al., 1992).
Amiodarone has little or no negative inotropic effect and is usually tolerated in
patients with congestive heart failure. The mortality rate associated with amiodarone treatment is around 0.4%, comparable to that of control patients. However,
controlled trials are required to evaluate the effective risks related to non-cardiac
adverse effects (Middlekauff et al., 1992).
Other proarrhythmic effects, as aggravation of sinus node disease in the bradytachy syndrome or occurrence of high degree atrio-ventricular block in patients
with previous conduction disease, may occur virtually with any antiarrhythmic drug
and are of great importance in elderly subjects.
In clinical practice, awareness of the problem of proarrhythmic effects is essential
in order to prevent them, to identify them promptly and to solve them. Some
categories of patients who are at higher risk of proarrhythmia and can be identified
are: (i) patients with previous myocardial infarction; (ii) patients with overt or
previous congestive heart failure; (iii) patients with significant left ventricular
dysfunction; (iv) patients with previous conduction disease or sinus node dysfunc-

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tion; (v) patients with electrolytes impairment; (vi) patients with concomitant renal
or hepatic insufficiency; and (vii) patients with advanced age. For these patients
effective need for antiarrhythmic treatment must be evaluated, and selection of
most appropriate drug is required (Cobbe, 1997; Waldo and Prystowsky, 1998)
together with close monitoring of the patient in the first 2–3 days of treatment. For
some patients initiation of treatment during hospitalization has been recommended
(Prystovsky, 1994; Waldo and Prystowsky, 1998).

4.4. Non-cardiac ad6erse effects
Non-cardiac adverse effects cause intolerance, thus limiting patient’s compliance.
However, these effects are usually reversible after drug withdrawal. For amiodarone
non-cardiac toxicity has limited the widespread use of this drug. Some side effects
of amiodarone, including hypo or hyperthyroidism, are not dose-related. The most
serious adverse effect of amiodarone is pulmonary toxicity, which occurs more
frequently in older patients and when daily dose is higher than 300 mg daily
(Antman, 1996). Unfortunately, for amiodarone the lowest effective dose which ca
be considered at very low risk of toxicity remains to be defined.

4.5. Choice of antiarrhythmic drugs
At the present time, selection of an antiarrhythmic drug for atrial fibrillation
prophylaxis is largely an empiric process and different agents are used sequentially
with a trial and error approach. Knowledge of pharmacokinetics and pharmacodynamics of every agent is required for choosing the most appropriate drug in a
specific patient. An approach based on the characteristics of atrial fibrillation in
terms of autonomic influences (vagal or adrenergic atrial fibrillation) is difficult to
translate in clinical practice and has never be validated by a controlled trial.

5. Control of ventricular response

5.1. Importance of rate control
Control of ventricular rate is very important for reducing symptoms related to
atrial fibrillation and for preventing left ventricular dysfunction secondary to
constantly high ventricular rates (Grogan et al., 1992; Crijns et al., 1997; Waktare
and Camm, 1998). Avoidance of antiarrhythmic agents for prophylaxis of recurrences, limiting drug treatment to agents for rate control, coupled with antithromboembolic prophylaxis, seems to be a reasonable choice, at least in some patients
(Table 6). In these patients permanent atrial fibrillation can be the best option,
provided that appropriate ventricular rate control is achieved.
Three categories of drugs are used to block the atrio-ventricular node in order to
slow ventricular response in atrial fibrillation: (i) digoxin; (ii) calcium antagonists
(verapamil and diltiazem); and (iii) i-blockers.

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135

Table 6
Indications to ventricular rate control plus antithromboembolic prophylaxis instead of attempts to
prevent atrial fibrillation recurrences with antiarrhythmic drugs (‘permanent atrial fibrillation as a
choice’)
Atrial fibrillation lasting more than 2 years
Marked left atrial enlargement
Contraindications to antiarrhythmic drugs
Frequent recurrences of atrial fibrillation despite prophylaxis with antiarrhythmic drugs

5.2. Limitations of digoxin for rate control
Digoxin has a traditional role for controlling the ventricular rate and is widely
used because this effect is coupled with a positive inotropic effect. Digoxin slows
the ventricular response by enhancing vagal effects on the atrio-ventricular node
and thereby prolonging nodal refractoriness (Sarter and Marchlinski, 1992). In
conditions characterised by low vagal tone, as exercise, thyrotoxicosis or hyperadrenergic states, digoxin efficacy in controlling ventricular rate is limited (Nattel,
1996). Indeed, in the past few controlled studies were available and in clinical
practice digoxin dosages and serum levels are often below required therapeutic
levels. Digoxin may effectively slow ventricular rate at rest but there is no
relationship between this effect and the ability to control ventricular rates during
exercise (Cobbe, 1997). Overall, the slowing effect on ventricular rates during peak
exercise is very weak and a reduction in heart rate of 3–8% compared to controls
has been demonstrated (Sarter and Marchlinski, 1992).
Control of ventricular rate at rest can be achieved with intravenous digoxin in a
relatively long time and this is another limitation in comparison to calcium-antagonists and i-blockers which are effective within a few minutes. In a study evaluating
effectiveness and costs of digoxin treatment for controlling heart rate in atrial
fibrillation and flutter, long hospital stay and consequently high costs were demonstrated when digoxin alone was used and this finding stresses the need for a more
aggressive approach to this problem (Roberts et al., 1993).
In view of these limitations, the role of digoxin for rate control in atrial
fibrillation has been redefined. Because of positive inotropic effects, it remains the
agent of choice in patients with atrial fibrillation in the setting of significant left
ventricular dysfunction. However, in the absence of left ventricular dysfunction
digoxin should be considered as a second-line therapy and eventually can be used
in association with calcium antagonists or i-blockers.

5.3. Calcium antagonists
Diltiazem and verapamil significantly slow atrio-ventricular nodal conduction
and prolong atrio-ventricular node refractoriness. Their effects on ventricular rate
during atrial fibrillation may be potentiated by the association with digoxin and
ventricular rate at rest and during submaximal exercise can be reduced by 17–28%

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in comparison with controls, whereas during maximal exercise the reduction is
around 12 – 20% (Sarter and Marchlinski, 1992).
Diltiazem and verapamil can be administered intravenously and a more rapid
effect can be achieved in comparison with digoxin. Both these agents have potentially negative inotropic effects but these effects are counterbalanced by the
beneficial effects related to mean ventricular rate slowing and left ventricular
afterload reduction. Diltiazem has been employed safely even in patients with left
ventricular dysfunction and congestive heart failure (Heywood et al., 1991), however, caution is required in these cases.
During long term oral administration of diltiazem or verapamil an improvement
in exercise tolerance has been demonstrated in comparison with digoxin (Sarter and
Marchlinski, 1992).

5.4. i-blockers
i-Blockers counteract the facilitating effects of catecholamines on atrio-ventricular node transmission of atrial imputs, thus they may be of limited efficacy when
i-adrenergic tone is low, and of greatest efficacy in situations of enhanced
sympathetic tone. The slowing of the ventricular rate is around 15–30% at rest or
during submaximal exercise and around 27–31% during maximal exercise (Sarter
and Marchlinski, 1992). i-Blockers have negative inotropic properties and a
reduction in exercise capacity has been demonstrated (Sarter and Marchlinski,
1992; Sopher and Camm, 1996). i-Blockers can be used acutely or for long term
treatment. For acute treatment esmolol, a short-acting agent, seems to have a better
safety profile than long-acting agents as propranolol or metoprolol (Platia et al.,
1989).

5.5. Combination therapy
The addition of a calcium antagonist or a i-blocker to digoxin resulted in a
significant reduction in resting heart rate and heart rate during exercise in several
studies (Sarter and Marchlinski, 1992).

5.6. Rate control in elderly patients
Calcium channel antagonists and i-blockers alone or in combination with
digoxin may obtain a more appropriate control of ventricular rate during exercise
than digoxin alone; however, their use in elderly patients implies more risks than in
younger subjects. These risks are related to the possibility of inducing excessive
sinus bradycardia or unmasking a sick sinus syndrome, to the possibility of
inducing atrio-ventricular blocks or to potential negative inotropic effects. Moreover, the use of i-blockers in the elderly may have some limitations because they
are contraindicated in patients with severe bronchospasm and may worsen symptoms of peripheral vascular insufficiency, two common conditions in advanced age.

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137

A satisfactory rate control is particularly difficult to achieve in patients with
chronic obstructive pulmonary disease, in brady-tachy syndromes and in
thyrotoxicosis.
In some selected patients, in whom drugs are ineffective or contraindicated,
non-pharmacologic treatments as atrio-ventricular node ablation followed by implantation of a ventricular pacemaker with rate-responsiveness (so-called VVIR
pacemakers) or atrio-ventricular node modulation can be appropriate even in
elderly subjects (Harvey and Morady, 1995; Crijns et al., 1997; Jung and DiMarco,
1998).

6. Conclusions
Atrial fibrillation is the most common sustained arrhythmia, however, its treatment remains controversial and problematic. Electrical or pharmacological cardioversion are able to restore sinus rhythm in many patients with atrial fibrillation
but maintenance of sinus rhythm requires long term treatment with antiarrrhythmic
agents. Today there is major concern regarding the ventricular proarrhythmic
effects of antiarrhythmic drugs because they may increase mortality. An alternative
strategy based on pharmacological control of ventricular response rate coupled with
antithromboembolic prophylaxis can be followed. At the present time, the relative
efficacy and risks of these strategies in specific patient subgroups remain to be
established and also non-pharmacological options as atrio-ventricular node ablation are currently available. In elderly patients, advanced age, underlying heart
disease, concomitant systemic illnesses and patient compliance to treatments condition our decision making and treatment need to be individualized. Appropriate
knowledge of the advantages, limitations and costs of every pharmacological or
non-pharmacological treatment option is required for assessing in every patient the
best risk-benefit and cost-benefit ratio.

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