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To evaluate the effect on decrease in blood pressure of modifying risk factors for stroke, such as blood lipid profiles, diet habits and indices of body weight, through a family-based nutrition health education programme among hypertensive patients and pre-hypertensive subjects without taking any antihypertensive drugs.
Design and setting
This was a community-based prospective study. The study population was randomly selected from communities in Taipei; potential subjects were invited by telephone to participate.
After excluding subjects whose blood pressure was normal and those using antihypertensive drugs, there were 390 participants included in the study. Subjects in the intervention group (n 293) received nutrition health education on blood pressure control and stroke-related risk factor modification at each visit. Non-intervention subjects (n 97) only acquired a general education sheet available in clinics. The blood pressure of study subjects was measured at baseline and 6-month follow-up to evaluate the intervention’s effect on decrease in blood pressure.
Significant decreases of 2·0 mmHg and 5·9 mmHg in systolic blood pressure were observed both in pre-hypertensive and hypertensive subjects in the intervention group. Additionally, intervention subjects with improvement of total cholesterol and LDL cholesterol, decrease in indices of body weight and increase in consumption of fruit and vegetables also had significant lowering of blood pressure.
The present study provided evidence that the blood pressure of pre-hypertensive and hypertensive subjects could decrease significantly, without taking antihypertensive drugs, after modifying blood lipid profiles and waist by dietary habits changed through a family-based nutrition heath education programme, resulting in a significant effect on stroke risk reduction.
A total of 80 patients, diagnosed by echocardiography as having ventricular septal defect with aortic valvar prolapse, underwent cardiac catheterization and surgery. Echocardiographic and angiographic results were compared with surgical findings. The ventricular septal defects as observed during surgery were found to be doubly committed and subarterial in 49 (61%), muscular outlet in 10 (13%), and perimembranous in 21(26%). The location had been erroneously categorized by echocardiography and angiography in 12 (15%) and in 15 (19%) patients, respectively. Prolapse of the right coronary leaflet of the aortic valve, as documented by echocardiography, was confirmed by angiography in all but two cases. Prolapse of the noncoronary leaflet was detected by both imaging modalities in three patients. Prolapse of the right coronary and noncoronary leaflets was observed at surgery in 49 and three patients, respectively. The mean size of the ventricular septal defect, when measured by echocardiography, was significantly smaller than that found following surgical measurements (3.3±1.3 vs 8.4±3.8 mm, p<0.001). Our study showed that the ventricular septal defect was erroneously classified in the presence of prolapse of the aortic valve in 15% and 19% of our cases by echocardiography and angiography, respectively. The herniated sinus of Valsalva forming the “roof” of the ventricular septal defect probably redirected the jet across the defect to cause the errors in interpretation. Echocardiography, nevertheless, is as reliable as angiography in our hands in the follow-up of patients with ventricular septal defect opening to the outlet of the right ventricle.
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