Usefulness of Home Blood Pressure Measurement in the Morning in Type 1 Diabetic Patients

Recently, we reported that home blood pressure (BP) measurement in the morning has a stronger predictive power for micro- and macrovascular complications in type 2 diabetic patients than casual/clinic BP measurement (1). Here we report the results examined in the study of type 1 diabetic patients.

We studied 53 type 1 diabetic patients who regularly visited our clinics. The number of female patients (36) was twice that of male patients (17). The subjects were aged 23–81 years (mean 54 ± 17) and had a diabetes duration of 2–47 years (mean 17 ± 10). Their mean BMI was 22 ± 3 kg/m², HbA_1c 7.0 ± 0.9%, triglycerides 94 ± 44 mg/dl, total cholesterol 201 ± 32 mg/dl, LDL 107 ± 25 mg/dl, and HDL 75 ± 18 mg/dl. Of 53 patients, 38 (72%) were treated by multiple daily insulin injections and the remaining (28%) received subcutaneous continuous insulin infusion for diabetes. Twenty-two patients (42%) were treated with antihypertensive drugs at the beginning of the study.

The study design and analysis are the same as previously reported (1). BP was measured at the clinic during the day and at home after waking. Clinic hypertension and morning hypertension were defined as systolic BP (SBP) 130 mmHg and/or diastolic BP (DBP) 85 mmHg, whereas clinic normotension and morning normotension were SBP 130 mmHg and/or DBP 85 mmHg. Microalbuminuria and clinical albuminuria were defined as urinary albumin excretion 30 μg/mg creatinine and 300 μg/mg creatinine, respectively.

There were no significant differences in the prevalence of nephropathy (n = 4 in clinic hypertension vs. n = 7 in clinic normotension; odds ratio [OR] 1.3 [95% CI 0.3–5.1]) and retinopathy (n = 5 in clinic hypertension vs. n = 8 in clinic normotension; OR 1.5 [0.5–5.4]) between the two groups with clinic hypertension (n = 17) (mean SBP/DBP 152 ± 9/91 ± 17 mmHg) and with clinic normotension (n = 36) (mean SBP/DBP 118 ± 11/73 ± 11 mmHg). In contrast, the prevalence of nephropathy with eight microalbuminuria and three clinical albuminuria (mean albumin excretion 231 ± 437 μg/mg creatinine, n = 11) in the patients with morning hypertension (mean SBP/DBP 148 ± 16/82 ± 11 mmHg, n = 14) was significantly higher (OR 260 [12–5,404], P < 0.001) than that (n = 0) (mean albumin excretion 7.0 ± 6.1 μg/mg creatinine) with morning normotension (mean SBP/DBP 115 ± 12/70 ± 8 mmHg, n = 39). The prevalence of proliferative retinopathy (n = 4) in the patients with morning hypertension was significantly higher (OR 15.2 [1.5–152], P < 0.001) than that (n = 1) in those with morning normotension, although there was no significant difference in all types of retinopathy between two groups (n = 5 in morning hypertension and n = 8 in morning normotension). There was no occurrence of coronary heart disease or cerebral vascular disease in the two groups. Specifically, systolic morning hypertension made a significant (r = 0.66, P = 0.001) contribution to the occurrence of nephropathy by multiple regression analysis, whereas the difference is not related to age, sex, duration of diabetes, BMI, HbA_1c, and serum lipid concentrations or use of different methods of insulin therapy and antihypertensive drugs. Meanwhile, the duration of diabetes had a significant (r = 0.4, P = 0.001) contribution to the occurrence of retinopathy.

No relationships between SBP and DBP in home BP and clinic BP measurements were observed (morning SBP = 0.28, clinic SBP + 88 r = 0.07, P = 0.06 and morning DBP = 0.25, clinic DBP + 54 r = 0.14, P = 0.005). The area under the receiver-operating characteristic (ROC) curve (AUC) of morning SBP (0.99 ± 0.01) was significantly higher (P < 0.001) than that of clinic SBP (0.49 ± 0.10) in nephropathy. There was no statistical difference in AUC between them in other events. In nephropathy, sensitivities of 130-mmHg threshold in morning and clinic SBP were 1.0 (95% CI 1.0–1.0) and 0.55 (0.23–0.83), respectively, whereas those of 85-mmHg threshold in morning and clinic DBP were 0.64 (0.310.89) and 0.55 (0.23–0.83), respectively. Specificities of 130-mmHg threshold in morning and clinic SBP were 0.95 (0.84–0.99) and 0.48 (0.32–0.64), respectively, whereas those of 85-mmHg threshold in morning and clinic DBP were 0.14 (0.05–0.29) and 0.29 (0.16–0.45), respectively.

In type 1 diabetic patients, the prevalence of nephropathy in the patients with morning hypertension was significantly higher than in those without morning hypertension, even though they had clinic normotension (mean SBP/DBP 120 ± 11/75 ± 15 mmHg, n = 8). In contrast, the occurrence was not observed in those without morning hypertension, even though they had clinic hypertension (mean SBP/DBP 160 ± 8/85 ± 8 mmHg, n = 11). Specifically, nephropathy, including clinical albuminuria, was observed in patients with systolic morning hypertension but not in patients without morning hypertension. Analysis by ROC curves also indicates that home BP in the morning has a stronger predictive power than clinic BP, especially in nephropathy. The cut point of 130-mmHg morning SBP has higher sensitivity and higher specificity than that of clinic SBP. This finding indicates that nephropathy in type 1 diabetic patients may be strongly related to morning home BP rather than clinic BP, as in type 2 diabetic patients (1).

The reason may be explained by several factors, such as white coat hypertension, nondipper hypertension, and morning surge, as postulated in the type 2 diabetic patients (1). Particularly, an increase in nocturnal BP, as detected by ambulatory BP monitoring, in type 1 diabetes is related to the development of microalbuminuria (2,3). These phenomena are thought to be caused by many neuroendocrine and hematological factors, especially autonomic neuropathy (4–6). Although we did not measure 24-h ambulatory BP, the greater range in the relation of morning home BP and clinic BP may be partially explained by true and white coat hypertension, reverse-dipping hypertension, and the effects of treatment with antihypertensive drugs (1).

In contrast, the prevalence of retinopathy in type 1 diabetic patients did not relate to BP, including morning home BP, although the degree of retinopathy was strengthened by morning hypertension. The duration of diabetes contributed to retinopathy significantly. They support the hypothesis that sustained long-term hyperglycemia is the strongest predictor for developing retinopathy and that high morning home BP accelerates retinopathy (7).

In conclusion, elevations of morning home BP in type 1 diabetic patients are also strongly related to microvascular complications, especially nephropathy, and the control of morning hypertension may prevent vascular complications, as in type 2 diabetic patients (1).