Table 2: Prospective Studies Comparing HBPM and Office BPM in Terms of Stroke and Cardiovascular Risk.
| Study Type | Study Population | Findings | Reference |
|---|---|---|---|
| Prospective cohort study, n=1,769, mean 6.6 years | Age ≥40 years | Average of multiple (taken more than three times) home SBP but not screening values was significantly and strongly related to the CV mortality risk according to Cox model | Ohkubo et al., 1998[38] |
| Longitudinal study, n=209 | Age 31–86 | Correlation between LVMI, HBP and OBP was closer for HPB | Tsuonda, 2002[26] |
| Prospective cohort study, n=4,939, mean 3.2 years | Age 70 ± 6.5 years | For BP self-measurement at home, each 10 mmHg increase in SBP increased the risk of a cardiovascular event by 17.2 % (95 % CI 11.0 %–23.8 %); each 5 mmHg increase in diastolic BP increased that risk by 11.7 % (95 % CI 5.7 %-18.1 %). The same increase in BP observed using office measurement was not associated with a significant increase in the risk of a cardiovascular event | Bobrie et al., 2004[36] |
| Prospective cohort study, n=1,702, mean 11 years | Age ≥40 years | The JNC-7 classification had a stronger predictive power of stroke using HBP-based classification compared with CBP-based classification | Asayama et al., 2004[42] |
| Prospective cohort study, n=2,051, mean 131 months | Age 25–74 years | Office, home and ambulatory BP values showed a significant exponential direct relationship with risk of CV or all-cause death, greater for systolic than for diastolic BP and for night than for day BP, but not better for home or ambulatory than for office BP. The slope of the relationship, however, was progressively greater from office to home and ambulatory BP | Sega, 2005[40] |
| Prospective cohort study, n=391, median 10.9 years | Age 71 ± 9 years; | Incidence of major CV events (cardiovascular death, MI and stroke) was related to the BPs by use of multivariate Cox regression analysis. Prognostic value of home BP was better than that of office BP | Fagard et al., 2005[37] |
| Prospective cohort study, n=163, compared OBPM, ABPM and HPBM | Age 53.9 ± 14.5 years | In a multivariate regression analysis in which age, sex, body mass index, OBP, awake ABP and HBPM were included, only age, sex and HBP were significant predictors of LVMI | Shimbo et al., 2007[24] |
| Cross-sectional study, n=662, compared OBPM and HPBM | Mean age 54.1 ± 17.6 years | HBPM and office BPM were both significant predictors of cardiovascular risk but there was no significant prognostic superiority of HBPM over office BPM | Stergiou et al., 2007[41] |
| Prospective cohort study, n=2,081, median 6.8 years | Age 45–74 years | HBPM (HR 1.22/1.15, 95 % CI 1.09 to 1.37/1.05 to 1.26), but not office BP (HR 1.01/1.06, 95 % CI 0.92 to 1.12/0.97 to 1.16), was predictive of cardiovascular events. Systolic home BP was the sole predictor of total mortality (HR 1.11; 95 % CI 1.01/1.23) | Niiranen et al., 2010[39] |
| Meta-analysis, n=5,008, median 8.3 years | Mean age 57.1 years | HBPM substantially refines risk stratification at office BPM levels assumed to carry no or only mildly increased risk, in particular in the presence of masked hypertension | Asayama et al., 2014[31] |
| RCT, n=778 Intervention = usual care (control), HBPM monitoring + website training (group 1), or HBPM + website training plus pharmacist care management delivered through website (group 2). | Aged 25–75 years with uncontrolled hypertension | Group 1: non-significant increase in controlled BP 36 % [95 % CI 58, 30 %–42 %] versus 31 % (95 % CI 25 %–37 %); 0 = 0.21). Group 2: controlled BP in 56 %; 95 % CI 49 %–62% (p0<0.001) SBP decreased stepwise from control to group 1 to group 2. DBP decreased only group 2 |
Green et al., 2008[57] |
| 2 × 2 RCT, n=636 intervention = usual care, behavioural intervention (group 1), HBPM (group 2) or HPPM + behavioural intervention (group 3), 24 months | Mean age was 61 years, 49 % were African American, and 19 % reported having inadequate incomes | Improvements in BP control in 4.3 % (95 % CI -4.5 % to 12.9 %) of group 1, 7.6 % (CI -1.9 % to 17.0 %) of group 2, and 11.0 % (CI 1.9 %, 19.8 %) in group 3. Change in SBP was -0.6 mmHg (CI -2.2 to 3.4 mmHg) in group 1, -0.6 mmHg (CI -3.6 to 2.3 mmHg) in group 2, and -3.9 mmHg (CI -6.9 to -0.9 mmHg) in group 3; patterns were similar for DBP | Bosworth et al., 2009[58] |
| Cochrane review of interventions to control BP in hypertension, 72 RCT | Mixed | HBPM was associated with reduction in SBP (-2.5 mmHg, 95 % CI -3.7 to -1.3 mmHg) and DBP (-1.8 mmHg, 95 % CI: -2.4 to -1.2 mmHg) | Glynn et al., 2010[51] |
| RCT, n=527, 12 month Intervention = HBPM + telemonitoring | Aged 35–85 years, BP >140/90 mmHg despite antihypertensive treatment | Mean SBP decreased by 12.9 mmHg (95 % CI 10.4–15.5) at 6 month in self-management group and by 9.2 mmHg (6.7–11.8) in control group (p=0.013). At 12 months, SBP decreased by 17.6 mmHg (14.9-20.3) in self-management group and by 12.2 mmHg (9.5-14.9) in control group (p=0.0004) | McManus et al., 2010[61] |
| Meta analysis, 25 RCTs, | Mixed | HBPM was associated with reduction of SBP of -3.82 mmHg (95% confidence interval -5.61 to -2.03), and DBP -1.45 mmHg (-1.95 to -0.94). Self-monitoring increased the chance of meeting office BP targets RR = 1.09 (1.02 to 1.16)). Significant heterogeneity was observed between studies | Bray et al., 2010[49] |
| Meta analysis, 37 RCTs, n=9449 | Mixed | HPBM was associated with reductions in SBP (-2.63 mmHg; 95% CI -4.24, -1.02), DBP (-1.68 mmHg; 95% CI -2.58, -0.79 reductions in antihypertensive medication (RR 2.02 [95% CI 1.32 to 3.11]) and less therapeutic inertia defined as unchanged medication despite elevated BP (RR for unchanged medication, 0.82 [95% CI 0.68 to 0.99]) | Agarwal et al., 2011[50] |
| Cluster randomised trial, n=450, 12 month intervention and 6-month post-intervention follow up. Intervention = HBPM + telemonitoring | Uncontrolled BP, mean age 61.1±14 years | BP was controlled at 6 and 12 month in 57.2 % (95 % CI 44.8 % to 68.7 %) of intervention group versus 30.0 % (95 % CI 23.2 % to 37.8 %) of usual care (p = 0.001). At 18 mo, BP was controlled in 71.8 % (95 % CI 65.0 % to 77.8 %) of intervention group versus 57.1 % (95 % CI 51.5% to 62.6%) of usual care group (p = 0.003). SBP decreased more in intervention group at 6 months (-10.7 mmHg [95 % CI -14.3 to -7.3 mmHg]; p<.001), at 12 months (-9.7 mmHg [95 % CI -13.4 to -6.0 mmHg]; p<0.001), and at 18 months (-6.6 mmHg [95% CI -10.7 to -2.5 mmHg]; p=0.004). DBP decreased at 6 months (-6.0 mmHg [95 % CI -8.6 to -3.4 mmHg]; p<0.001), at 12 months (-5.1 mmHg [95 % CI -7.4 to -2.8 mmHg]; p<0.001), and at 18 months (-3.0 mmHg [95 % CI -6.3 to 0.3 mmHg]; p =0 .07) | Margolis et al., 2013[62] |
| Prospective cohort study. 9 months | Predominantly black and Hispanic adults with uncontrolled hypertentsion from clinics in low-income, medically underserved communities | 53 % of the patients had controlled hypertension at follow-up. Systolic and DBP decreased by 18.7 mmHg and 8.5 mmHg, respectively, at follow-up | Angell et al., 2013[52] |
| Randomised controlled trial, n=552, 12 months | History of stroke, coronary heart disease, diabetes, or CKD and with baseline blood pressure of at least 130/80 mmHg | Mean SBP decreased by 9.2 mmHg (95 % CI 5.7-12.7) in systolic and diastolic by 3.4 mmHg (95 % CI 1.8-5.0) | McManus et al., 2014[54] |
| Randomised controlled trial, n=900, 9 months | Predominantly black and Hispanic adults with uncontrolled hypertension from clinics in low-income, medically underserved communities | SBP decreased (intervention, 14.7 mmHg; control, 14.1 mmHg; p=0.70). Control was achieved in 38.9 % of intervention and 39.1% of control participants at the end of follow-up. No significant difference between groups | Yi et al., 2015[53] |
CI = confidence interval; CKD = chronic kidney disease; DBP = diastolic blood pressure; HBPM = home blood pressure monitoring; HR = hazard ratio; JNC-7 = Joint National Committee 7; LVMI = left ventricular mass index; RCT = randomised controlled trial; RR = relative risk; SBP = systolic blood pressure.