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C20 Cardiology and Cardiac Surgery
Lenient versus Strict Rate Control in Patients with Atrial Fibrillation
NEJM 362:1363-1373
Study: Randomized, multi-centre Netherlands prospective study, follow-up for at least 2 yr Population: 614 patients with permanent atrial fibrillation.
Intervention: Lenient control (resting HR <110 bpm) or strict control (resting HR <80 bpm) Primary Outcomes: Death from cardiovascular causes, hospitalization for heart failure, and stroke, systemic embolism, bleeding, and life-threatening arrhythmic events.
Results: Goal of the study was to establish whether lenient control was equivalent to strict control for prevention of primary outcomes. Resulting hazard ratios were not significantly different between
the treatment groups (P = 0.001). Frequencies
of hospitalization and adverse effects were also similar. More patients were able to maintain lenient targets (97.7%) compared to strict targets (67%). Conclusion: Lenient control was equivalent to strict control for prevention of primary outcomes in patients with atrial fibrillation. Furthermore, lenient control was more easily achieved.
Rivaroxaban for Stroke Prevention in AFib – ROCKET-AF Trial
NEJM 2011;365:883-891
Study: Prospective, non-inferiority, double blind, RCT, median follow-up of 1.9 yr.
Population: 14,264 patients with AFib (mean CHADS2=3.5). Patients either had previous thromboembolism or ≥3 risk factors.
Intervention: Patients were randomized to receiving rivaroxaban or warfarin.
Outcome: Composite of strokes and systemic thromboembolic event (STE).
Results: The hazard ratio of the primary outcome for rivaroxaban compared to warfarin was 0.88; 95% CI 0.74-1.03; p<0.001 for noninferiority; p=0.12 for superiority. Furthermore, the hazard ratio for major and non-major, but clinically relevant, bleeding was 1.03; 95% CI 0.96-1.11; p=0.44). There were also significant reductions in intracranial hemorrhage (0.5% vs. 0.7%, p=0.02) and fatal bleeding (0.2% vs. 0.5%, p=0.003) for rivaroxaban.
Conclusions: In patients with AFib, rivaroxaban is non-inferior to warfarin for stroke prevention and major and non-major bleeding.
Arrhythmias Toronto Notes 2019 Table 5. CHADS2 Risk Prediction for Non-Valvular AFib and Refer to AHA/ACC/HRS AFib Guidelines 2014 for
more details
Risk Factor
Congestive Heart Failure Hypertension
Age >75
Diabetes
Points CHADS2 Score
1 0 1 1 1 2-3 1 4-6
Stroke Risk (%/Yr)
1.9 (low)
2.8 (low-mod) 4.0-5.9 (mod) 8.5-18.2 (high)
Stroke/TIA (prior) 2
JAMA 2001;285:2864-70 and Can J Cardiol 2014 Oct;30(10):1114-30.
• ECG findings
■ noorganizedPwavesduetorapidatrialactivity(350-600bpm)causingachaoticfibrillatorybaseline
■ irregularly irregular ventricular response (typically 100-180 bpm), narrow QRS (unless aberrancy or
previous BBB)
■ wide QRS complexes due to aberrancy may occur following a long-short cycle sequence (“Ashman
phenomenon”)
■ loss of atrial contraction, thus no “a” wave seen in JVP, no S4 on auscultation
Figure 26. Atrial fibrillation (lead II)
• management(adaptedfromCCSAtrialFibrillationGuidelines2016) ■ the primary goal is symptom control
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major objectives (RACE): all patients with AFib (paroxysmal, persistent, or permanent), should be stratified using a predictive index for stroke risk and for the risk of bleeding, and most patients should receive either an oral anticoagulant or ASA (see below)
1. Rate control: β-blockers, diltiazem, verapamil (in patients with heart failure: digoxin, amiodarone) – digoxin can be considered as a therapeutic option to achieve rate control in patients whose
response to β-blockers and/or calcium channel blockers is inadequate, contraindicated or
not tolerated
2. Anticoagulation: use either warfarin or novel oral anticoagulant (NOACs) e.g. apixaban,
dabigatran, rivaroxaban, edoxaban to prevent thromboembolism
– for patients with non-valvular AF (NVAF): oral anticoagulant (OAC) is recommended for
most patients aged >65 yr or CHADS2 >= 1. ASA 81 mg is recommended only for patients with none of the risk outlined in the CCS algorithm (age <65 and no CHADS2 risk factors) who have arterial disease (coronary, aortic, or peripheral). Novel oral anticoagulant (NOAC) is to be used in preference to warfarin
3. Cardioversion (electrical)
– if AFib <24-48 h, can usually cardiovert without anticoagulation
– if AFib >24-48 h, anticoagulate for 3 wk prior and 4 wk after cardioversion due to risk of
unstable intra-atrial thrombus
– if patient unstable (hypotensive, active angina due to tachycardia, uncontrolled heart failure)
should cardiovert immediately 4. Etiology
– HTN, CAD, valvular disease, pericarditis, cardiomyopathy, myocarditis, ASD, post- operative, PE, COPD, thyrotoxicosis, sick sinus syndrome, alcohol (“holiday heart”)
– may present in young patients without demonstrable disease (“lone AFib”) and in the elderly without underlying heart disease
studies of patients with AFib suggest that there is no difference in long-term survival when treating patients with a rhythm-control versus rate-control strategy
however, many patients with a significant underlying structural heart lesion (e.g. valve disease, cardiomyopathy) will not tolerate AFib well (since may be dependent on atrial kick) and these patients should be cardioverted (chemical or electrical) as soon as possible
newlydiscoveredAFib
◆ anticoagulants may be beneficial if high risk for stroke
◆ if the episode is self-limited and not associated with severe symptoms, no need for
antiarrhythmic drugs
◆ if AFib persists, 2 options:
1. rate control and anticoagulation (as indicated above)
2. cardioversion (as above)
◆ recurrent or permanent AFib
◆ if episodes are brief or minimally symptomatic, antiarrhythmic drugs may be avoided; rate
control and anticoagulation are appropriate
◆ patients who have undergone at least one attempt to restore sinus rhythm may remain in AFib
after recurrence; permanent AFib may be accepted (with rate control and antithrombotics as
indicated by CHADS2 score) in certain clinical situations
◆ if symptoms are bothersome or episodes are prolonged, antiarrhythmic drugs should be used
– no or minimal heart disease: flecainide, propafenone once proven to have no underlying CAD (usually by exercise stress testing)
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