Taru Kantola

7B.08: HIGH BLOOD PRESSURE AND ITS VARIATION AND THE USE OF BETA BLOCKING AGENTS AND STATINS DECREASE QUALITY OF LIFE IN DRUG-TREATED HYPERTENSIVE PATIENTS.

Objective: To clarify explanatory factors to quality of life in Finnish drug-treated hypertensive patients. Design and method: SF-36 questionnaire was filled out by 174 hypertensive patients (66 females, 108 males, aged 64.5(8.5)years). All used at least one antihypertensive agent. 24 hour ambulatory blood pressure(ABPM) and pulse wave- velocity(PWV) were performed and laboratory tests taken. Results: 24-hour ambulatory SBP was 132.1(12.6)mmHg and DBP 76.6(7.2) mmHg and LDL-cholesterol 2.6(0.7) mmol/l. Carotid-femoral-PWV was 11.3(3.7)m/s. The mean(SD) of the eight SF-36 questionnaire scores was 74.1(18.4) (maximum 100). All scores correlated significantly(p < 0.001)to each other. The use of beta-blockers correlated negatively to most of the quality of life parameters and the use of statins negatively to role-physical, general health and vitality. According to the regression model physical functioning was explained by lower ABPM nighttime pulse pressure(PP), daytime DBP standard deviation(SD) and home measured evening PP(model explained 83.6 % of the variation). Role-physical by not using either acetosalicylic acid or clopidogrel (25.5%). Bodily pain rate by lower ABPM daytime mean arterial pressure SD and higher SBP SD and 24 hour heart rate SD, lower age and not using diuretics(64.2%). General health by lower GHbA1c, not using beta-blockers and lower ABPM nighttime PP SD(22.6%). High vitality by lower carotid radial PWV and ABPM daytime DBP SD(41.3%). Social functioning by lower carotid radial PWV and not using ASA or clopidogrel (65.2%). High role-emotional by not using beta blockers or ASA or clopidogrel (54.4%). Mental health by lower carotid radial PWV(56.4%), Reported health transition by higher ABPM nighttime PP SD and the use of ASA or clopidogrel (14.6%). The mean of all the eight SF-36 questionnaire scores by lower home measured evening SBP and not using ASA or clopidogrel (61.2%). Conclusions: The SF-36 scores of the Finnish drug-treated hypertensive patients did not differ markedly from the same age American healthy population and hypertensive patients used in validation of questionnaire. High BP and its variation seemed to decrease quality of life. Also control of other cardiovascular risk factors seemed to be important. The use of beta- blocking agents and statins seemed to decrease quality of life.

HIGH CAROTID RADIAL PULSE WAVE VELOCITY MAY BE CONNECTED TO LOWER QUALITY OF LIFE MEASURED BY SF-36 QUESTIONNAIRE

Objective: To clarify correlation of carotid-femoral (C-F) and carotid-radial (C-R) pulse wave velocity (PWV) to quality of life measured by SF-36 questionnaire and the explanatory factors of C-F and C-R PWV in Finnish drug-treated hypertensive patients. Design and method: A Doppler ultrasonography device (Micro Medical PulseTrace PWV, Micro Medical Ltd, Rochester, Kent, UK) was used to measure C-F and C-R PWV in 133 Finnish drug-treated hypertensive patients, The mean age was 65.0 (8.8) years (59 females and 74 males). 24 hour ambulatory blood pressure monitoring (ABPM) was performed with a portable device (90207 Ambulatory Blood Pressure Monitor, SpaceLabs Inc., Washington, U.S.). SF-36 questionnaire was used in calculating quality of life. Fasting plasma glucose, GHbA1c, lipids and urine albumin/creatinine ratio were measured. Results: C-F PWV did not correlate to any SF-36 parameter. C-R PWV correlated inversely to SF-36 vitality, social functioning and mental health. The mean 24 hour systolic blood pressure (SBP) was 132.5 (12.1) and diastolic blood pressure (DBP) 76.4 (6.9) mmHg. The mean C-F PWV was 11.4 (3.8) m/s and C-R PWV 11.5 (2.5) m/s. C-F PWV correlated positively to age, office systolic blood pressure and serum creatinine. C-R PWV correlated positively to height, weight, waist-hip ratio, male gender and glycosylated haemoglobin A1c (GHbA1c) and negatively to SF-36 questionnaire vitality, social functioning and mental health, female gender, plasma total and LDL-cholesterol. According to stepwise linear regression analysis C-F PWV was explained by SF-36 bodily pain (t = 2.141, p = 0.038), office SBP (t = 3.056, p = 0.04) and 24 hour heart rate standard deviation (t = −2.244, p = 0.030) and C-R PWV by weight (t = 2.898, p = 0.005), GHbA1c (t = 2.700, p = 0.009) and male gender (t = 2.077, p = 0.041). Conclusions: Among treated Finnish hypertensive patients C-R PWV was correlated to SF-36 questionnaire parameters vitality, social functioning and mental health which may suggest that high C-R PWV may decrease quality of life of these patients. Also C-F PWV was partly explained by SF-36 bodily pain which suggest that C-F PWV might be high in patients with less pain.

The change in quality of life in drug-treated hypertensive patients after 10 years of antihypertensive treatment

Background: Non-specific ST-T change in electrocardiogram, a marker of impaired repolarization in the myocardium, can be observed among hypertensive patients; however, relationship between non-specific ST-T change and myocardial regional wall motion at inner and outer layers remains was unclear. Methods: In 288 hypertensive patients undergoing echocardiography for the screening of hypertensive heart disease, we evaluated 2D speckletracking stain. In electrocardiogram, major ST-T change was defined as ST depression >1⁄4 0.1mV, and non-specific ST-T change was defined as minor ST-T depression (<0.1mV) or flat T wave in any leads. Results:Mean age was 63.4 13.2 years (male 47.9%). There were 29.6 % of patients with non-specific ST-T change and 5.6 % of those with major ST-T change. Patients with non-specific ST-T change had greater Cornell product (P1⁄40.018), Sokolow-Lyon voltage (P<0.001), left ventricular mass index (LVMI) (P1⁄40.014), septal E/e’ (P1⁄40.019). The patient with non-specific ST-T change had greater global longitudinal strain (GLS) (-12.8 3.0 vs. -14.0 2.6, P1⁄40.010) and the relationship was similar in both inner and outer layer. Patients with non-specific ST-T change had greater GLS than those without even after adjustment for conventional risk factors and LVMI (P1⁄40.042). There were no significant differences in radial or circumferential strain between patients with and without non-specific ST-T change. Results: Non-specific ST-T change in electrocardiogram was associated with global longitudinal strain in both inner and outer myocardial layer.

[PP.13.14] QUALITY OF LIFE MEASURED BY SF-36 DID NOT CHANGE DURING SIX MONTHS AFTER STARTING ANTIHYPERTENSIVE MEDICATION

Objective: To clarify the change in quality of life during six months after starting the antihypertensive treatment in hypertensive patients. Design and method: The patients were non-treated and participated during the years 1999–2002 in a six-month study where their antihypertensive treatment was titrated during six months according to a predetermined schedule to reach the target pressure. SF-36 questionnaire was filled out every six weeks by 88 patients (49 females and 39 males, aged 55.4 (7.8), 36–71 years). After six months they used at least one antihypertensive agent. Blood pressure was measured every six weeks by using 24 hour ambulatory measurement. Results: Daytime systolic blood pressure (SBP) decreased from 144.8 (11.6) to 129.8 (10.1) mmHg (p = 0.001) and diastolic blood pressure (DBP) from 94.1 (7.0) to 82.2 (6.4) mmHg (p = 0.001). Nocturnal SBP decreased from 128.5 (12.8) to 113.2 (10.3) mmHg (p = 0.001) and DBP from 77.9 (7.8) to 67.4 (6.9) mmHg (p = 0.001). Daytime heart rate (HR) changed from 72.7 (9.5) to 72.0 (8.3) beats/min (p = 0.09) and nocturnal HR decreased from 62.0 (7.8) to 60.5 (6.7) beats /min (p = 0.001). None of the eight SF-36 parameters nor their mean value changed significantly during the six months of the study. The change in physical functioning and role physical were negatively explained by daytime SBP in the beginning, in bodily pain negatively by daytime SBP and nocturnal HR at the end, in general health negatively by 24 hour SBP in the beginning, in role emotional negatively by daytime SBP at the end. Vitality, social functioning and mental health were explained by none of the parameters. The mean of the parameters of SF-36 questionnaire was explained negatively by daytime SBP in the beginning. Conclusions: According to our results quality of life did not change significantly during the six months after starting antihypertensive medication although blood pressure decreased significantly. Low change in the SF-36 physical parameters was mostly explained by high systolic blood pressure in the beginning of the study. Mental SF-36 parameters were not explained by any of the measured parameters.

825 CAROTID-FEMORAL PULSE WAVE VELOCITY IN FINNISH HYPERTENSIVE PATIENTS WAS EXPLAINED BY AGE AND CARDIOVASCULAR RISK FACTORS

Objective: To clarify the explanatory factors of carotid-femoral (C-F) and carotid-radial (C-R) pulse wave velocity (PWV) in Finnish drug-treated hypertensive patients. Design and methods: A Doppler ultrasonography device (Micro Medical PulseTrace PWV, Micro Medical Ltd; Rochester, Kent, UK) was used to measure both C-F and C-R PWV in 119 Finnish drug-treated hypertensive patients (mean age 65.2 (7.4) years, 45 females and 74 males). C-F and C-R distances were measured manually according to guidelines. The 24 h ambulatory blood pressure monitoring (ABPM) was performed with a portable device (90207 Ambulatory Blood Pressure Monitor, SpaceLabs Inc.; Washington, U.S.A.). Fasting plasma creatinine, glucose, GHbA1c and lipids were measured. Results: The mean 24 hour systolic blood pressure was 130.8 (13.5) and diastolic blood pressure 76.7 (7.1) mmHg. The mean C-F PWV was 11.0 (3.0) m/s and mean C-R PWV 11.4 (3.0) m/s (r = 0.458, p = 0.0001). According to logistic stepwise regression analysis C-F PWV was explained by waist circumference, office systolic blood pressure and heart rate, and age. C-R PWV was explained by weight and office diastolic blood pressure. Conclusions: According to our results C-F PWV was explained by waist circumference, systolic blood pressure and age as also seen in previous studies. Instead C-R PWV was explained by diastolic blood pressure and weight. The correlations of C-R PWV have not been studied largely. Plasma lipids or glucose and the use of statins or antiplatelet medication did not correlate to either PWV.