Quality control in ultrasound studies on atherosclerosis.

This review discusses the quality control of equipment and technician performance in long term, multicentre trials using ultrasound detection and quantification of atherosclerosis. Examples on how such quality control measures could be implemented are given. Based on our own experience and that of other groups we suggest the following items as being important when planning for quality control in this type of study. 1. Write down the specifications demanded with regard to the ultrasound equipment and reading stations. 2. Compare the commercially available equipment on those characteristics by means of in-vitro and/or in-vivo testing. 3. Select the most suitable equipment for all centres and check it before shipping. 4. Sign a full maintenance agreement for all centres. 5. Evaluate the ultrasound devices and reading stations regularly during the study using phantoms. 6. Train sonographer and readers thoroughly before the start of the study. Certify those who successfully complete the training programme and demonstrate proficiency in scanning or reading. 7. Determine each sonographer's/reader's variability before and repeatedly during the study. Give feedback on performance to the sonographer/reader. 8. Create a regular retraining programme for all sonographers/readers and extend for those with poor performance. 9. Feed all the above information to a Data Quality Control Committee, having the ultimate responsibility for the quality control in the study.

The J-shaped relationship between coronary heart disease and achieved blood pressure level in treated hypertension: further analyses of 12 years of follow-up of treated hypertensives in the Primary Prevention Trial in Gothenburg, Sweden.

The relationship between the blood pressure level achieved through antihypertensive treatment and the incidence of coronary heart disease (CHD) was studied in 686 middle-aged hypertensive men. The patients studied came from a random population sample and were followed-up for 12 years, yielding a total of 6563 patient-years for the study. Eighty-seven patients suffered a non-fatal myocardial infarction or died from CHD. The incidence of CHD showed a J-shaped distribution in relation to achieved treated systolic and diastolic blood pressure levels. The incidence of CHD, adjusted for entry characteristics, age, serum cholesterol, blood pressure and smoking habits, decreased with reductions in blood pressure achieved through treatment, to a level of about 150/85 mmHg, below which the incidence rate again increased. This J-shaped pattern was also observed when data from patients with pre-existing signs or symptoms of ischemic heart disease at entry were excluded. Using a quadratic term as the best fit to the observed relationship between achieved treated diastolic blood pressure level and the incidence of CHD, a Cox regression analysis showed that the nadir of the J-shaped incidence curve was at a diastolic blood pressure value of 81 mmHg. There did not seem to be any association between the absolute size of the blood pressure reduction during treatment and the incidence of CHD. Although we cannot exclude the possibility that the increased incidence of CHD in patients with a low treated blood pressure is due primarily to pre-existing but subclinical ischemic heart disease, our findings indicate that an excessive lowering of blood pressure in hypertensive patients may be harmful.(ABSTRACT TRUNCATED AT 250 WORDS)

Mortality and morbidity in relation to systolic blood pressure in two populations with different management of hypertension: The Study of Men Born in 1913 and the Multifactorial Primary Prevention Trial.

Total mortality and cardiovascular disease (CVD) mortality and morbidity during 10 years of follow-up in relation to systolic blood pressure (SBP) at entry were compared between a random sample of 7455 men, aged 47-54 years at entry, in whom multifactorial risk-factor intervention including intense efforts to detect and treat hypertension had been performed [the Primary Prevention Trial (PPT)], and a similar population (from an observational study) in which intervention, on CVD risk factors was kept to a minimum (the Study of Men Born in 1913). Total mortality, CVD mortality, coronary heart disease (CHD) and stroke incidence increased with SBP in both populations, but levelled off above the cut-off point for antihypertensive treatment in the population subjected to multifactorial CVD risk factor intervention. In this population total mortality was reduced by 30%, CVD mortality by 37%, CHD morbidity by 13% and stroke morbidity by 30% above the cut-off point for blood pressure intervention compared with the incidence predicted from the observational study. These findings indicate that multifactorial intervention, and especially antihypertensive treatment, have preventive effects in the hypertensive part of the middle-aged male population.

Left ventricular wall stress and systolic function in untreated primary hypertension.

A noninvasive investigation was undertaken in four blood pressure (BP) groups of untreated 49-year-old men derived by screening a random population sample: normotensive men (n = 20) and subjects with borderline (n = 30), mild (n = 45), or moderate BP elevation (n = 24). We here report the findings regarding left ventricular (LV) wall stress, LV wall thickness, and LV systolic function. Although there was an increase in LV wall thickness with hypertension, the raised BP was not compensated for by a sufficient degree of LV wall thickening to keep wall stress within normal limits in the hypertensive groups. Among a subset of individuals with pronounced increase in wall thickness peak systolic wall stress approached the normal range, but end-systolic wall stress was still high. In spite of high wall stress LV systolic function was normal or supranormal in the hypertensive men. The LV ejection phase indices showed a close inverse correlation with end-systolic wall stress (r = -0.67 to -0.84) in all four BP groups, but no correlation or only a weak correlation with peak systolic wall stress (r = 0.18 to -0.40). As judged from the relationship between end-systolic wall stress and ejection phase indices of LV function in the normotensive controls, all hypertensive groups had higher than expected values for LV ejection phase indices, which indicates an increased myocardial contractility secondary to adrenergic stimulation or to a more efficient contractile machinery in the myocardial cells.

Calf muscle haemodynamics and the renin-angiotensin-aldosterone system in normotensive subjects with a familial predisposition to hypertension: changes during increased salt intake.

Blood pressure, plethysmographically determined muscle blood flow in the calf at rest and during maximal dilatation, plasma renin activity, angiotensin II and plasma and urinary aldosterone were determined in normotensive men with a positive family history of hypertension (n = 17) and in an age- and weight-matched control group (n = 15) during usual sodium intake and after four weeks of increased salt intake. On normal salt intake resting muscle blood flow was significantly lower and resting resistance and resting vascular tone significantly higher in those with a positive family history, reflecting a stronger smooth muscle contraction of the resistance vessels in the calf at rest. Flow and resistance at maximal dilatation did not differ between the groups, indicating no difference in the structural design of the resistance vessels in the calf. Plasma angiotensin II and urinary aldosterone were not significantly different between the two groups. Plasma renin activity was, however, significantly higher in those with a positive family history which might be interpreted as increased renal sympathetic activity in the genetically predisposed subjects. After four weeks of increased salt intake no significant changes were noted in blood pressure, muscle blood flow and resistance at rest or at maximal dilatation in either of the two groups. Plasma renin activity and angiotensin II decreased significantly in both groups after 10 days of increased salt but tended to return to normal values at the end of the fourth week. Plasma aldosterone and urinary aldosterone excretion were equally and significantly decreased in both groups giving no evidence for an inadequate suppression of aldosterone in subjects genetically predisposed to hypertension.