FIT Heart 2008.

Methods	Design: RCT Setting: secondary care, New York, USA Dates: recruitment January 2005 ‐ June 2007 Follow‐up: 1 year
Participants	3649 screened N randomised: 501 Intervention n = 250 Control n = 251 Healthy. Family members of cardiac patients admitted to a secondary care centre with acute atherosclerotic CVD (including catheter procedures and CABG) English/Spanish speaking adults aged 20 ‐ 79 who lived within 3 hours of medical centre. Had to be family member (= blood relative, spouse or other cohabitant for ≥ 1 year in last 5 years, or for 10 years in the past) – only 1 family member per index case was randomised into study. Exclusions: current/planned pregnancy, known CVD/ diabetes, active liver disease, chronic kidney disease, life expectancy < 5 years, on specialised diet not compatible with the programme intervention, or part of a drug trial in last 3 months. Framingham absolute risk ≥ 10% ‐ 21/250 (8.5%) intervention, 23/251 (9.2%) control Mean age: intervention 30, control 30 % men: intervention 34, control 33 Ethnicity: intervention 64% white, control 64% white. Total cholesterol, mmol/l, mean (SD): intervention 5.24 (0.95), control 5.32 (1.0) HDL cholesterol, mmol/l, mean (SD): intervention 1.51 (0.45), control 1.55 (0.48) LDL cholesterol, mmol/l, mean (SD): intervention 3.32 (0.88), control 3.38 (0.95) Triglycerides, mmol/l, mean (SD): intervention 1.30 (0.72), control 1.33 (0.95) SBP, mm Hg, mean (SD): intervention 126.7 (14.69), control 126.4 (15.46) DBP, mm Hg, mean (SD): intervention 77.9 (10.82), control 77.0 (11.98) Statin therapy: 31/250 (13%) intervention, 40 (16%) control Antihypertensive therapy: 52/250 (21%) intervention, 53/251 (21%) control
Interventions	Setting: not clear All participants received baseline and 1‐year assessments of diet, lifestyle, and risk factors: demographics, medical Hx, family Hx, drug Hx, lifestyle habits, SBP, DBP, height, weight, waist circumference, BMI, physical activity level, smoking status (with carbon monoxide monitoring). Fasting blood samples collected for total cholesterol, HDL‐C, triglyceride, glucose, LDL‐C, CRP. Intervention: Personalised CVD risk factor screening with immediate feedback by health educator, behavioural counselling, taught lifestyle approaches to risk reduction including way to improve total blood cholesterol. Diet counselling focused on foods rather than nutrient intake. Encouraged to do physical activity, stop smoking (and referred to cessation programme). Had regular contact with educator (by person/phone) at 2 weeks, 6 weeks, 3 months, 6 months and 9 months. All visits 30 ‐ 60 minutes long. Risk factor results given to primary care providers as written report. In addition, those with abnormal lipids were offered fingerprick lipid testing and 3‐, 6‐, 9‐month testing with immediate feedback. Control: Received a 1‐page handout to 1) avoid tobacco, 2) choose good nutrition, 3) be more active. Brief prevention message and a letter sent to their healthcare provider only if they had a critical risk factor level. i.e. BP ≥ 140/90, LDL‐C ≥ 190 mg/dL, HDL‐C < 25 mg/dl, triglycerides ≥ 500 mg/dl, total cholesterol > 300 mg/dl
Outcomes	SBP, DBP, lipid levels, attendance rates, case‐finding rates
Notes	Number (%) lost to follow‐up: intervention: 18 (7.2%); control 19 (7.6%)
Risk of bias
Bias	Authors' judgement	Support for judgement
Random sequence generation (selection bias)	Low risk	Web‐based programme, blocks based on sex and race
Allocation concealment (selection bias)	Low risk	Web‐based programme
Blinding of participants and personnel (performance bias) All outcomes	Unclear risk	Not reported
Blinding of outcome assessment (detection bias) All outcomes	Low risk	States research assistants blind to group assignments collected the 1‐year outcome data
Incomplete outcome data (attrition bias) All outcomes	Low risk	Reported and similar between groups
Selective reporting (reporting bias)	Unclear risk	Unclear
Other bias	Unclear risk	Unclear