Kumar 2013.

Methods	RCT, parallel, (n3 EPA + DHA vs nil), 12 months Summary risk of bias: moderate or high
Participants	Adults > 60 years with sinoatrial node disease and dual chamber pacemakers N: 39 intervention, 39 control (only 18 vs 39 for 12‐month analyses) Level of risk for CVD: moderate/high Male %: 46% intervention, 56% control Mean age (SD): 78 (7) intervention, 77 (8) control Age range: not reported Smokers: not reported Hypertension: 72% Medications taken by ≥ 50% of those in the control group: statins, renin‐angiotensin system inhibitors Medications taken by 20%‐49% of those in the control group: anti‐arrhythmic drugs Medications taken by some, but < 20% of the control group: not reported Location: Australia Ethnicity: not reported
Interventions	Type: omega‐3 capsule Comparison: EPA + DHA vs nil Intervention: a triglyceride preparation containing a total of 6 g/day of omega‐3 PUFAs of which 1.8 g/day were n‐3 (1.02 g EPA and 0.72 g DHA) Control: no supplements Dose aim: increase 1.74 g/d EPA + DHA, 0.8% E n‐3, 0.8% E PUFA Baseline PUFA: unclear Compliance by biomarkers: phospholipid fatty acid status measured at randomisation and at 1‐3 months, DHA and EPA increased in intervention, not in control. No other PUFAs, or TC, reported Compliance by dietary intake: measured via weekly diet history, but no results reported Energy intake, kcal/d: not reported Total fat intake, % E: not reported SFA intake, %E: not reported PUFA intake, % E: not reported PUFA n‐3 intake: not reported PUFA n‐6 intake: not reported Trans fat intake: not reported MUFA intake, % E: not reported CHO intake, % E: not reported Sugars intake: not reported Protein intake, % E: not reported Alcohol intake, % E: not reported Compliance, other measures: measured by weekly pill count, results not reported Inclusion basis: no intention to increase total PUFA. Intention was to increase 1.74 g/d EPA + DHA, 0.8% E PUFA >10% greater than assumed baseline of 6% E. No biomarker, TC or intake data to confirm PUFA dose: 0.8% E Duration of intervention: median 378 days
Outcomes	Main trial outcome: AF burden Dropouts: 1 intervention, 0 control Available outcomes: all‐cause mortality, CV mortality, AF (frequency and duration but not recurrence so not used), adverse events Response to contact: written, no reply to date
Notes	Trial funding: unclear
Risk of bias
Bias	Authors' judgement	Support for judgement
Random sequence generation (selection bias)	Low risk	Randomisation was performed using sequentially numbered, opaque, sealed envelopes.
Allocation concealment (selection bias)	Low risk	As above
Blinding of participants and personnel (performance bias) All outcomes	High risk	Open‐label design
Blinding of outcome assessment (detection bias) All outcomes	High risk	Quote: “At each visit, stored AT/AF diagnostic data were retrieved in an un‐blinded fashion”
Incomplete outcome data (attrition bias) All outcomes	High risk	Only 1 lost, and reason explained. But group baseline size to cross‐over is huge. Doesn’t report just the 17 or 18 metrics at baseline, no idea why the 21 were the ones switched and mixed with the control
Selective reporting (reporting bias)	Low risk	Trial prospectively registered and outcomes stated were reported
Attention bias	Unclear risk	Only difference would be handing out the capsules, rest seems the same. However, one group is getting supplements and the other nil
Compliance	Unclear risk	Phospholipid fatty acid status measured at randomisation and at 1‐3 months, DHA and EPA increased in intervention, not in control. No other PUFAs, or TC, reported
Other bias	High risk	21 of the 39 randomised to the intervention were crossed over to control at six months so 12‐month outcomes are reported for 17/18 intervention group while baseline characteristics are reported for all 39 participants.