ADHERNCE to ORAL ANTICOAGULANTS AMONG PATIENTS with CHRONIC Atrial Fibrillation in Al-NASSIRIYA

ADHERNCE TO ORAL ANTICOAGULANTS AMONG PATIENTS WITH CHRONIC Atrial fibrillation IN Al-NASSIRIYA 2016

This study was submitted in partial fulfillment of the requirement for the M.B.Ch.B.

Faculty: Thi-Qar College of medicine/University of Thi-Qar.

By:

• Ousama Mohamad Jasim
• Mustafa Qusay Sagban

Supervised by:

• Assistant prof. Dr. Adnan Al-Ta’aan

Abstract

Health care professionals must be alert to the high prevalence of low adherence to treatment, because Low adherence increases morbidity and medical complications, contributes to poorer quality of life and an overuse of the health care system. Many different factors have an impact on adherence. However, critical factors to consider in teens are their developmental stage and challenges, emotional issues and family dysfunction. Direct and indirect methods have been described to assess adherence. Eliciting an adherence history is the most useful way for clinicians to evaluate adherence, and could be the beginning of a constructive dialogue with the adolescent. Interventions to improve adherence are multiple – managing mental health issues appropriately, building a strong relationship, customizing the treatment regimen if possible, empowering the adolescent to deal with adherence issues, providing information, ensuring family and peer support, and motivational enhancement therapy. Evaluation of adherence at regular intervals should be an important aspect of health care for adolescents.

The term adherence has been used more in recent literature, and is defined as “the extent to which a person’s behaviour, in terms of taking medications, following diets, or executing lifestyle changes, coincides with medical or health advice”. Although compliance and adherence are often used interchangeably, in the present article, adherence is used because it focuses on whether a person adheres to the regimen rather than passively follows the doctor’s orders. Rates of adherence in the adolescent population vary widely, from 10% to 89%, for chronic illnesses.

In this paper, we did a cross-sectional study conducted on 60-patients whom are known cases of chronic AF, with specially-constructed questionnaire to obtain information. The retrospective design, small number of patients & the non-randomized nature of the study and the non-homogeneity of the population leave the possibility of selection bias.

The results showed that adherence can be influenced by a number of factors, including: the patient’s gender, education ,the SES, the patient’s psychology & the presence of more comorbid illnesses.The recommendations for future are each patient should be provided with card contain full informations about patient illness and treatment , more studies should be done to discuss the cause of non-adherence to anti coagulants treatment and Giving tutorial programs about Anticoagulants drugs and risk of non adherence to therapy

Objective: This study aims to determine the adherence to guidelines on anticoagulant management among patients with chronic AF attend nasiriyah heart center ,CCU in hussain teaching hospital and their affection by demographic characteristics.

Introduction and literature review

Atrial fibrillation (AF) is the commonest cardiac arrhythmia. The incidence increases with age and affects 5% of UK population above the age of 65 yr and 10% above 75 yr.In the United States, AF accounts for more than 35% of all admissions for cardiac arrhhmytias(1,2).Men are 1.5 times more likely to develop AF than women(3). AF is often associated with structural heart disease, but in many patients it can occur with no detectable disease (lone AF). Thromboembolic events and heart failure resulting from AF lead to significant morbidity, mortality and increased cost of management.

Table 1

Causes and risk factors for AF

Acute causes / AF associated with cardiovascular disease
Alcohol binge drinking / Following myocardial infarction
Cardiac and non-cardiac surgery / Hypertension, especially if leftventricular hypertrophy
Myocarditis/pericarditis
Pulmonary embolism / Valvular heart disease (often mitral)
Pulmonary hypertension / Congenital heart disease, mainly atrial septal defects (ASD)
Chest infections / Sick sinus syndrome
Hyperthyroidism / Diabetes mellitus
Neurogenic AF / Familial AF
High vagal tone (nocturnal episodes) / Identified in a small group of patients11
High sympathetic tone (daytime episodes; associated with ischaemic heart disease, stress, excessive caffeine, alcohol)

Definition and electrocardiographic patterns

AF is a supraventricular arrhythmia characterised by complete absence of coordinated atrial contractions. On the electrocardiogram there is consistent absence ofPwaves which are replaced by fibrillatory waves. AF is associated with an irregular and frequently rapid ventricular response if atrioventricular conduction is intact. Regular R-R intervals are possible in the presence of atrioventricular block or interference by ventricular or junctional tachycardia.A wide QRS complex tachycardia that is rapid, irregular or sustained strongly suggests underlying bundle branch block or conduction over an accessory pathway (e.g. Wolf–Parkinson–White syndrome) especially if the ventricular rate is extremely rapid (over 200 beats min−1).(3)

AF can be commonly associated with other arrhythmias such as atrial flutter or atrial tachycardia. Atrial flutter is a more organised and regular form of atrial activation resulting in a saw-tooth pattern or flutter waves (f) on the electrocardiogram. Atrial flutter can arise during treatment of AF with antiarrhythmic drugs. Atrial flutter itself can degenerate into AF, can be triggered by AF or the pattern can alternate between AF and flutter. Other atrial arrhythmias can also trigger AF and are identified by the presence ofPwaves which are separated by an isoelectric baseline.

Classification

Classification of AF has always been controversial.The current classification is based on two important elements: patterns of evolution of arrhythmia and the response to treatment (3,4,5) .

First onsetAF is the first clinical presentation where the patient is still in AF and the episode has been present for less than 48 h.

ParoxysmalAF is the occurrence of recurrent episodes that typically last minutes to hours, occasionally days, but eventually self-terminate.

PersistentAF is present when arrhythmia is not self-terminating, but pharmacological or electrical cardioversion is required to restore sinus rhythm.

AF ispermanentwhen all attempts to restore sinus rhythm have been abandoned because of physician or patient decision, frequent recurrence, or inability to cardiovert the patient.

Pathophysiology and mechanisms

The mechanisms of AF are not fully clear, but at least three aspects seem to be important in its genesis and maintenance:

• There may be enhanced automaticity within ‘sleeves’ of atrial tissue that extend into the pulmonary veins or vena caval junctions.These foci can act as trigger points to generate multiple atrial ectopics leading to AF and their elimination by means of ablation may possibly provide a permanent cure, particularly in those with structurally normal hearts.(6)
• In chronic AF, maintenance of arrhythmia is sustained by multiple re-entering and randomly circulating wavelets that collide and divide into ‘daughter-wavelets’ thus maintaining the chaotic electrical state.(8,9)
• The longer the duration of AF, the more difficult it is to restore sinus rhythm and prevent recurrences. This is due to electrical and structural remodelling of atrial tissue resulting in shortening of effective refractory periods, thereby maintaining and increasing the duration of AF.(8,9)

Causes and risk factors

As described above, the risk of developing AF increases with age. Whilst rheumatic valvular disease remains the most common cause for AF in developing countries, most patients develop AF on the basis of coronary artery disease and systemic hypertension. Clinically important causes and risk factors for AF are summarised inTable 1. Echocardiographic predictors include large atria, diminished ventricular function and increased left ventricular wall thickness. When AF occurs in normal hearts without signs of any demonstrable cardiovascular disease, it is termed ‘lone atrial fibrillation’

Principles of management

The management of AF still represents one of the major therapeutic challenges in medicine. Based on current evidence and guidelines, there are four main principles (3) :

1. Restoration of sinus rhythm by pharmacological or electrical means.
2. Control of ventricular rate during paroxysmal or persistent AF, and chronically in those with permanent AF.
3. Prevention of recurrence of paroxysmal or persistent AF following successful restoration of sinus rhythm.
4. Prevention of thromboembolic phenomena.

When a patient is seen in the emergency setting, the main priority is to control the fast ventricular response and, depending on the haemodynamic status of patient, this can be achieved either by urgently restoring sinus rhythm or by controlling the ventricular rate. Immediate electrical cardioversion is indicated in patients with a rapid ventricular rate who are either haemodynamically unstable or have evidence of acute myocardial ischaemia or heart failure that do not respond promptly to pharmacological measures. In less acute situations, pharmacological cardioversion can be attempted, thereby avoiding the requirement for general anaesthesia.

Cardioversion by either means carries a risk of thromboembolism, particularly when the arrhythmia has been present for longer than 48 h; anticoagulation prophylaxis must be initiated before the procedure. In the long-run, it may become appropriate to accept the arrhythmia as permanent.

Recent studies have pointed out that rate controlling the AF could be at least as effective as restoration of sinus rhythm in terms of symptom control and survival, particularly in stable patients aged approximately 60 years old

Restoration of sinus rhythm

Direct current cardioversion

Direct current cardioversion (DCC) involves a synchronised direct current electrical shock delivered across the chest wall. Sinus rhythm can be restored in a significant proportion of patients with success rates varying between 65% and 90%. The success of DCC appears to be greater with anterior-posterior positioning of paddles (sternum and left scapular) than with anterior-lateral (ventricular apex and right infraclavicular). Other factors include nature of heart disease, transthoracic resistance and output waveform (monophasic or biphasic).(1,2,3)

Elective DCC is performed under adequate short-acting anaesthesia. In an emergency situation, the need for anaesthesia depends on the nature of the emergency and conscious level of the patient; it is reasonable to perform DCC under conscious sedation if the urgency of the situation is such that there can be no delay. In a recent report, elective DCC performed under conscious sedation was also shown to be safe and not associated with any intolerable discomfort to the patient.(12)

Devices that deliver a monophasic waveform of current have been conventionally used for cardioversion. Initial shock energy of 200 J is recommended for cardioversion of AF using a monophasic device. The sequence of energy commonly used is: 200 J; 200 J; 300 J; and 360 J.3Biphasic machines achieve cardioversion at much lower energy levels and are increasingly replacing monophasic devices.

It is safe to cardiovert patients with implanted devices such as permanent pacemaker or internal defibrillator provided the implanted device is interrogated immediately before and after cardioversion to assess any malfunction. The paddles used for cardioversion should be placed as far as possible from the implanted device, preferably in the anterior-posterior position.

Brief arrhythmias can arise immediately following DCC. These are mainly ventricular and supraventricular premature beats, bradycardia and short periods of sinus arrest.

Ventricular tachycardia or fibrillation can be precipitated in patients with hypokalaemia and digitalis intoxication. Patients with underlying conduction defects are at risk of developing profound bradycardia, complete heart block or asystolic periods following cardioversion. These patients are identified by having a slow ventricular response to AF in the absence of rate-reducing medications and facilities for temporary external or endocardial pacing must be made available prior to attempting cardioversion.

Electrical cardioversion can also lead to transient ST segment elevation with a rise in blood concentrations of cardiac troponins and CK-MB, even without cardiac damage. The rate of relapse after DCC is high unless anti-arrhythmic drug therapy to maintain sinus rhythm is given concomitantly. However, prophylactic therapy to prevent recurrences following DCC should be considered individually for each patient.

Pharmacological restoration of sinus rhythm

Prior to considering any anti-arrhythmic therapy, it is important to realise that up to 60% of patients with recent onset AF spontaneously revert to sinus rhythm within 24 h to a few days.Pharmacological cardioversion is considered in patients who are haemodynamically stable; it is often successful in AF of <48 h.(13)

Anti-arrhythmic drugs are classified according to the Vaughan Williams classification (Table 2). Current guidelines on the management of AF3recommend use of propafenone, flecainide, ibutilide or dofetilide as first choice for pharmacological cardioversion of AF of <7 days duration (conversion rates of up to 90%).Flecainide and propafenone are safe in patients who do not have evidence of ischaemic heart disease or myocardial dysfunction. Dofetilide and ibutilide are relatively new class III agents and are most useful for cardioverting atrial flutter. However, there is an increased incidence of torsade de points or polymorphic ventricular tachycardia with use of these drugs.(13)

Table 2

Vaughan Williams Classification of Antiarrhythmic Drugs

Class / Action / Drugs
I / Sodium channel blockade
IA / Prolong repolarisation / Quinidine, procainamide, disopyramide
IB / Shorten repolarisation / Lidocaine, mexiletine, tocainide, phenytoin
IC / Little effect on repolarisation / Encainide, flecainide, propafenone
II / Beta-adrenergic blockade / Propanolol, esmolol, acebutolol,l-sotalol
III / Prolong repolarisation (potassium channel blockade; other) / Amiodarone, bretylium,d,l-sotalol, ibutilide
IV / Calcium channel blockade / Verapamil, diltiazem, bepridil
Miscellaneous / Miscellaneous Actions / Adenosine, digitalis,

In clinical practice, amiodarone is a reasonable alternative to class Ic agents and is the drug of choice in patients with ventricular dysfunction and ischaemic heart disease. Amiodarone also has an added advantage of providing prompt rate control in addition to its anti-arrhythmic effect. This rate controlling effect (beta blockade and calcium channel blockade properties) is observed early following i.v. loading; the class III anti-arrhythmic properties take effect at 8–24 h. Most of the toxicity of amiodarone is dose-dependent and related to chronic treatment; however, it should be used with caution in patients with acute ischaemia or myocardial dysfunction, as profound hypotension may be induced by i.v. or high-dose oral loading. There is emerging evidence that i.v. and oral amiodarone have different electrophysiological properties and it may be possible to administer i.v. amiodarone to cardiovert AF in patients who are already on chronic oral treatment.(14)

Maintenance of sinus rhythm

The relapse rate of AF following initial cardioversion is high (25–50% at 1 month). Maintenance of sinus rhythm after successful cardioversion is achieved by continuation of oral therapy with class I or III anti-arrhythmic drugs. Pre-treatment with these drugs also improves success rates of repeated DCC. Sotalol is useful for preventing recurrences of paroxysmal AF. However, it is vital to be aware of the pro-arrhythmic effects of these agents; they can prolong the QT interval and lead to dangerous ventricular arrhythmias. Thus, regular monitoring of corrected QT interval (QTc) and QRS duration is important during outpatient reviews. Renal insufficiency and electrolyte imbalance also predispose to polymorphic ventricular tachycardia.

Rate control of atrial fibrillation

It is necessary to control the ventricular rate in persistent AF. Also, rate control may be a preferred strategy in patients with paroxysmal AF who are stable at presentation, as 60% of these patients can spontaneously revert to sinus rhythm within 24 h.

The aim of rate control in AF is to improve symptoms and prevent worsening of ventricular dysfunction. Recent evidence from randomised trials (AFFIRM,(15)PIAF,(16)RACE,(17)STAF (18) ) has shown that rate control is at least as effective as rhythm control in improving symptoms and functional capacity, particularly in those over 65 yr of age. What is considered adequate rate control remains controversial. Heart rate should neither be too high (leads to tachycardia induced cardiomyopathy) or too low (facilitates heart failure); it is considered to be controlled when the ventricular rate is 60–80 bpm at rest and 90–115 bpm during exercise.

Rate control is achieved by drugs which predominantly affect conduction through the AV node. Commonly used agents are digoxin, beta-blockers (atenolol, propranolol, metoprolol, esmolol) and non-dihydropyridine calcium channel blockers (verapamil and diltiazem). In permanent AF, digoxin can usually provide adequate rate control. However, digoxin does not prevent excessive heart rates during exercise and combination therapy with beta-blockers or calcium antagonists may be necessary, especially in younger active individuals. In stable patients with acute AF, calcium antagonists or beta-blockers (oral or i.v.) are preferred to digoxin due to their rapid onset of action (3–7 min). Digoxin is the drug of choice for rate control in patients with heart failure, though there is emerging evidence in support of beta-blockers.

Patients with sick sinus syndrome with AF and present with episodes of bradycardia, usually require the support of a permanent pacemaker to allow the use of rate controlling medications. Drugs acting on the AV node are contraindicated in patients with accessory conduction pathways (e.g. Wolf–Parkinson–White syndrome) as they can result in dangerously fast ventricular rates by increasing the conduction via the accessory pathway. In these situations amiodarone, flecainide or procainamide are drugs of choice.

Prevention of thromboembolism

Chronic AF is associated with a 3–7% annual risk of ischaemic stroke from thromboembolism. Guidelines(3) recommend administration of heparin prior to, or concurrently during, immediate electrical or pharmacological cardioversion. If AF has been present for longer than 48 h or the duration is unknown, warfarin should be given for 3–4 weeks following successful cardioversion. Patients admitted for elective cardioversion require adequate anticoagulation with warfarin 3–4 weeks before and after the procedure (INR 2–3). Those patients who cannot be anticoagulated due to contraindications prior to cardioversion should undergo transoesophageal echocardiographic examination to exclude the presence of thrombus.

In chronic AF, the risks and benefits of antithrombotic therapy (aspirin, warfarin) must be considered in each individual patient. Chronic hypertension, age >65 yr, diabetes mellitus, previous ischaemic stroke, ventricular dysfunction and co-existent ischaemic or valvular heart disease are considered as high risk factors for thromboembolism in AF. All such high risk patients must receive warfarin unless contraindicated. In the absence of these factors (low risk patients) or when warfarin cannot be given, aspirin 300 mg daily is an alternative. Young patients with AF who do not have any clinical or echocardiographic evidence of heart disease (‘lone AF’) are also at low risk of thromboembolism.