National “Slow Down Day” 7.00hrs Friday 27 March to

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Appendix I:
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I.1 Lifestyle
I.1.1
Omega-3 fatty acids
Figure 15: Omega-3 fatty acids vs. placebo (post MI 100%) - all-cause mortality (hazard ratio)
Heterogeneity was detected at I2=60%. To investigate this, the papers were separated according to
whether they used food or a capsule form of omega-3 fatty acids and the timing of the onset of
treatment less than 3months vs. greater than 3 months following an MI. Relative risk data for allcause mortality is also provided since only presenting HR meant excluding a key paper in the field
(GISSI-P) that has influenced current practice.228
Figure 16: Omega-3 fatty acids vs. placebo – all-cause mortality (subgroup analysis of people
provided with a food or capsule form of treatment(hazard ratio))
The subgroup analysis shows it is unclear whether capsule form of omega-3 fatty acids reduces the
risk of all-cause mortality, while the food source of omega-3 fatty acids does not.
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Figure 17: Omega-3 fatty acids vs. placebo – all cause mortality (hazard ratio) (less than3 months
after an MI vs. greater than 3 months after an MI)
The subgroup analysis showed that initiating treatment within 3 months of having an MI may reduce
the risk of all-cause mortality but after 3 months the benefit is lost.
Figure 18: Omega-3 fatty acids vs. placebo (100% post MI) – cardiac mortality (hazard ratio)
Heterogeneity was not present in cardiac mortality but subgroup analysis was performed on food vs.
capsule form of omega-3-acid ethyl esters since the GDG expressed an interesting in exploring these
groups.
Figure 19: Omega-3 fatty acids vs. placebo - cardiac mortality (subgroup analysis of people who
received food or capsule source of omega-3 fatty acids) (hazard ratio))
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Figure 20: Omega-3 fatty acids vs. placebo – cardiac mortality (hazard ratio) (less than three
months 3 after MI vs. greater than 3 months after MI) (100% post MI)
Figure 21: Omega-3 fatty acids vs. placebo (100% post MI) - cardiac mortality (relative risk)
Figure 22: Omega-3 fatty acids vs. placebo (100% post MI) - cardiac mortality (relative risk)
(subgroup analysis of food vs. capsule form of omega-3 fatty acids)
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Figure 23: Omega-3 fatty acids vs. placebo (mixed population) - sudden death (hazard ratio)
Figure 24: Omega-3 fatty acids vs. placebo (mixed population) - sudden death (relative risk)
Figure 25: Omega-3 fatty acids vs. placebo (mixed population) -myocardial infarction (hazard
ratio)
Figure 26: Omega-3 fatty acids vs. placebo (mixed population) - myocardial infarction (relative
risk)
Figure 27: Omega-3 fatty acids vs. placebo (100% post MI) - revascularisation (hazard ratio)
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Figure 28: Omega-3 fatty acids vs. placebo (100% post MI) - revascularisation (relative risk)
Figure 29: Omega-3 fatty acids vs. placebo (mixed population) -stroke (hazard ratio)
Figure 30: Omega-3 fatty acids vs. placebo (mixed population) -stroke (relative risk)
Figure 31: Omega-3 fatty acids vs. placebo (100% post MI) - adverse events
Heterogeneity in adverse events (I2=92%) was investigated by separating the results into: 1) timing of
initiating treatment less than 3 months vs. greater than 3 months post MI; and 2) food vs. capsule
form of omega 3-fatty acids. Onset of treatment less than 3 months after an MI appeared to
increase the risk of adverse events compared with no difference in starting treatment greater than 3
months post MI. Capsule form of omega-3 fatty acids also appeared to increase the risk of adverse
events, whilst the food source did not.
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Figure 32: Omega-3 fatty acids vs. placebo – adverse events (subgroup analysis of adverse events
in patients who initiated treatment less than 3 or greater than 3 months after an MI
MI)
Figure 33: Omega-3 fatty acids vs. placebo (subgroup analysis of adverse events in people who
were treated with either a food or capsule source of omega-3 fatty acids)
Figure 34: Omega-3 fatty acids vs. placebo -hospitalisation (hazard ratio)
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I.1.2
Oily fish consumption
Figure 35: Oily fish vs. control diet in patients post MI -all-cause mortality (hazard ratio)
Figure 36: Oily fish vs. control diet in patients post MI - cardiac mortality (hazard ratio)
Figure 37: Oily fish vs. control diet in patients post MI - sudden death(hazard ratio)
Figure 38: Oily fish vs. control diet in patients post MI - reinfarction(relative risk)
Figure 39: Oily fish vs. control diet in patients post MI - stroke(hazard ratio)
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I.2 Cardiac rehabilitation
I.2.1
Interventions to increase uptake of and adherence to a cardiac rehabilitation programme
Figure 40: Early vs. late onset of cardiac rehabilitation programme - uptake
Study or Subgroup
1.2.2 RCT
Pack 2012
Subtotal (95% CI)
Early onset
Control
Events Total Events Total Weight
57
74
74
Total events
57
Heterogeneity: Not applicable
Test for overall effect: Z = 2.25 (P = 0.02)
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74 100.0%
74 100.0%
Risk Ratio
M-H, Fixed, 95% CI
Risk Ratio
M-H, Fixed, 95% CI
1.30 [1.03, 1.62]
1.30 [1.03, 1.62]
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0.1 0.2
0.5
1
2
5 10
Favours late onset Favour early onset
Test for subgroup differences: Not applicable
Figure 41: Early vs. late onset of cardiac rehabilitation programme - adherence
Figure 42: Gender tailored vs. traditional cardiac rehabilitation programme - adherence
Figure 43: Goal setting vs. usual care – uptake
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Figure 44: Planning and goal setting vs. usual care - adherence
Figure 45: Planning, goal setting and diary vs. usual care - adherence
Figure 46: Planning, goal setting and signed diary - adherence
Figure 47: Liaison referral vs. usual referral to cardiac rehabilitation programme - uptake
Figure 48: Liaison vs. usual referral to cardiac rehabilitation programme - percentage of classes
attended
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Figure 49: Automatic referral vs. usual referral to cardiac rehabilitation programme - uptake
Figure 50: Automatic referral vs. usual referral to cardiac rehabilitation programme - adherence
Figure 51: Automatic referral vs. usual referral to cardiac rehabilitation programme - percentage
of classes attended
Figure 52: Automatic and liaison referral vs. usual referral to cardiac rehabilitation programme uptake
Figure 53: Automatic and liaison referral vs. usual referral to cardiac rehabilitation programme percentage of classes attended
Figure 54: Short vs. long sessions - adherence
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Figure 55: Home vs. centre based cardiac rehabilitation - adherence
Figure 56: Behavioural letters vs. usual communication - uptake
Figure 57: Letters and telephone calls vs. usual communication - adherence
Heterogeneity:
The results from this meta-analysis show heterogeneity is present, I2=86% p =0.008. The protocol
states that the following parameters should be investigated if heterogeneity is detected: type of MI
(STEMI, NSTEMI), country (UK vs. non-UK), treatment (PCI, CABG, medical treatment) and comorbidity. Of these factors, the only parameter the papers provided sufficient data was the country
in which they were conducted. Wyer was conducted in the UK and Pinto in the USA. Whether this
explains the variations in the results it is not clear.
Figure 58: Home visit vs. telephone calls – uptake
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Figure 59: Education of staff vs. usual care - uptake
Figure 60: Telephone calls vs. usual care - uptake
Figure 61: Letters and telephone calls vs. letters – mean attendance
Figure 62: Pre-approved referral strategy vs. usual referral to cardiac rehabilitation programmeuptake
Figure 63: Pre-approved referral strategy vs. usual referral to cardiac rehabilitation programme –
mean attendance
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Figure 64: Pre-booked referral strategy vs. usual referral to cardiac rehabilitation programme uptake
Figure 65: Pre-booked referral strategy vs. usual referral to cardiac rehabilitation programme –
mean attendance
Figure 66: Early education vs. usual referral to cardiac rehabilitation programme - uptake
Figure 67: Early education vs. usual referral to cardiac rehabilitation programme – mean
attendance
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I.3 Drug therapy
I.3.1
I.3.1.1
ACE inhibitor vs. placebo and optimal duration of ACE inhibitor therapy
People who have had an MI with LVSD
Figure 68: ACE inhibitor vs. placebo in people who have had an MI with LVSD – all-cause mortality
Figure 69: ACE inhibitor vs. placebo in people who have had an MI with LVSD – cardiac mortality
Heterogeneity
Heterogeneity was detected (I2=90%, p<0.0001) for the effects of ACE inhibitors on the risk of cardiac
mortality in post MI patients for the first 12 months of treatment. The results show the same trend
for all three papers, but one paper shows a much larger effect than the other two paper and if this is
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removed heterogeneity is also removed. However, there is no justification to remove this paper nor
do any of the subgroups explain any differences. For this reason the results are presented as random
effects rather than fixed effects.
Figure 70: ACE inhibitor vs. placebo in people who have had an MI with LVSD – sudden death
Figure 71: ACE inhibitor vs. placebo in people who have had an MI with LVSD - revascularisation
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Figure 72: ACE inhibitor vs. placebo in people who have had an MI patients with LVSD reinfarction
Figure 73: ACE inhibitor vs. placebo in people who have had an MI patients with LVSD hospitalisation
Heterogeneity
Heterogeneity was detected (I2=66%, p<0.09) for the effects of ACE inhibitors on the risk of
rehospitalisation in post MI patients for the first 12 months of treatment. The results show the same
trend for the two papers, but one paper shows a much larger effect than the other and if this is
removed heterogeneity is also removed. However, there is no justification to remove this paper nor
do any of the subgroups explain any differences. For this reason the results are presented as random
effects rather than fixed effects.
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Figure 74: ACE inhibitor vs. placebo in people who have had an MI patients with LVSD - stroke
Figure 75: ACE inhibitor vs. placebo in people who have had an MI patients with LVSD – adverse
events
Figure 76: ACE inhibitor vs. placebo in people who have had an MI patients with LVSD – renal
dysfunction
Figure 77: ACE inhibitor vs. placebo in people who have had an MI patients with LVSD –
hypotension
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Figure 78: ACE inhibitor vs. placebo in people who have had an MI patients with LVSD –
dizziness/fainting
I.3.1.2
People who have had an MI without heart failure
Figure 79: ACE inhibitor vs. placebo in people who have had an MI patients without heart failure–
all-cause mortality
Figure 80: ACE inhibitor vs. placebo in people who have had an MI without heart failure reinfarction
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Figure 81: ACE inhibitor vs. placebo in people who have had an MI without heart failure hospitalisation
Figure 82: ACE inhibitor vs. placebo in people who have had an MI without heart failure – adverse
events
Figure 83: ACE inhibitor vs. placebo in people who have had an MI without heart failure – CV
death, non-fatal MI, cardiac arrest
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Figure 84: ACE inhibitor vs. placebo in people who have had an MI without heart failure - CV
death, MI, stroke
Figure 85: ACE inhibitor vs. placebo in people who have had an MI without heart failure (indirect
population) – cardiac mortality
Figure 86: ACE inhibitor vs. placebo in people who have had an MI without heart failure (indirect
population) - stroke
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