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Non-invasive assessment of cardiac hypertrophy and function was made in 15 male patients with previous malignant hypertension as well as in 15 matched patients with ‘benign’ hypertension and 15 matched normotensive control subjects. In the group with previous malignant hypertension, echocardiography revealed increased (>1.3 cm) thickness of the interventricular septum in all but one patient (93%) as compared to 67% in the group with ‘benign’ hypertension and 7% in the control subjects. Other indices of left ventricular hypertrophy, including left ventricular mass, were also more pronounced in the hypertensive groups and significantly higher than in the control subjects. Conventional ECG appeared to be much less sensitive in detecting left ventricular hypertrophy, in particular the traditional ‘combined LVH criteria’ (high voltage+ST-T changes) which were positive in only 27% of the patients with previous malignant hypertension as compared to 0% in the other two groups. With less stringent and less specific criteria the diagnostic yield could be increased to 60 and 40% in the two hypertensive groups. Regarding left ventricular performance, an increased a/H ratio (15.4, 13.4 and 8.5%, respectively) and a lower E-F slope (67, 94 and 114 mm/s, respectively) indicated abnormal diastolic function in the hypertensive groups. On the other hand, indices of systolic function (ejection fraction and mean velocity of circumferential fiber shortening) were found to be normal in the hypertensive groups. In the patients with previous malignant hypertension these indices appeared to be ‘supranormal’ [i.e. significantly higher values were found (77 v. 70%, <0.01 and 1.31 v. 1.08 circ/s, <0.01, respectively) than in the normotensive control subjects]. [ABSTRACT FROM PUBLISHER]

1 In a double-blind study, 36 patients with essential hypertension were randomly allocated to treatment with either metoprolol, 100-300 mg/day, or pindolol, 5-15 mg/day for 6 months. Haemodynamic investigations were made on three separate occasions. Blood flow in the calves and in the forearm was determined by venous occlusion plethysmography after 6 weeks of placebo, after 6 weeks and again after 6 months of active therapy. 2 Both drugs reduced blood pressure significantly, by 17.1/11.8 mm Hg with metoprolol and 21.9/10.9 mm Hg with pindolol after 6 weeks (P less than 0.005). No further changes were seen after 6 months. 3 Heart rate after 6 weeks was significantly reduced by metoprolol (10.7 +/- 2.4 beats/min, P less than 0.001) but not by pindolol (4.4 +/- 2.3 beats/min, NS). After 6 months a significant reduction was seen also in the pindolol group (5.2 +/- 2.1 beats/min, P less than 0.05). 4 The vascular resistance in the calves at rest was reduced by pindolol (P less than 0.05), whereas resistance tended to increase with metoprolol. 5 Resting vascular resistance in the forearm after 6 months was significantly reduced in the metoprolol group (P less than 0.001) as well as in the pindolol group (P less than 0.02). The increase in forearm vascular resistance seen during leg exercise was not influenced by either drug. 6 Vascular resistance at maximal vasodilatation was unchanged in the calves, but a significant reduction (-17.4 +/- 5.7%, P less than 0.01) in the forearm vascular bed was seen after 6 months of pindolol. No change was observed with metoprolol. 7 It is concluded that pindolol reduces elevated blood pressure partly through peripheral vascular mechanism. Metoprolol, on the other hand, probably acts mainly via central cardiac mechanisms. [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate the incidence, complications, survival time and causes of death of patients with severe hypertension (S.H.) (grade III and grade IV) who were admitted to Landspítalinn (The University Hospital in Reykjavík med. Depart.) during the years 1957-1971. During this period 117 patients were found to have S.H. according to the grading of Keith and Wagener (20 patients with grade IV end 97 with grade III). It was found that relatively fewer patients with S.H. were admitted during the last 5 year period (1967-1971) compared to the two previous 5 year-period (1957-1966). The cases were analysed according to sex and age distribution, blood urea, electrocardiographic changes, heart size (by x-ray) and blood pressure readings at the time of admission. In relation to the above mentioned factors the incidence and type of complications, survival time and causes of death were evaluated. The main causes of death were cerebrovascular accidents (26,6%), myocardial infarction (22,8%) and uremia (22,8%). The survival calculations were done by the decremental method aim taken from patient age less than 66 years. Approximately 50% of the men and 60% of the women had a 5 year survival. Elevated blood urea values and signs of left ventricular hypertrophy in the electrocardiogram at the time of diagnosis of S.H. had an unfavorable influence on length of survival.

Introduction: It has become increasingly popular to offer blood pressure measurements under circumstances that differ from the usual setting, for example measurements in supermarkets, pharmacies, at exhibitions etc. It is well known that environmental factors as well as doctor and patient relationship can affect blood pressure measurement. This must be considered in the diagnosis and treatment of hypertension. The aim of this study was to evaluate some of these phenomena., Material and Methods: Subjects attending local supermarket in a rural community were offered blood pressure measurement two Friday afternoons. All measurements were done in a sitting position with a fully automatic blood pressure recorder, AND UA-767. Hypertension was diagnosed if blood pres notsure exceeded 140 mm Hg systolic and/or 90 mmHg diastolic (according to WHO standards). Those who had hypertension were followed by two office and six home measurements. For the statistical analysis, a t-test for paired data was used. RESULTS are reported as means., Results: Total of 125 subjects had their blood pressure measured. By the WHO criteria 64 (51.2%) of the subjects had hypertension. Mean blood pressure was significantly higher in the supermarket compared to office both for systolic, 17.1 (C.I:12.8-21.4)mmHg, and diastolic, 5.2 (0.1:2.7-7.7) mmHg, blood pressure. Eighty per cent of the subjects had normal blood pressure at home. Compared to supermarket the mean blood pressure reduction was 29.3 (0.1:24.7-33.9) mmHg for systolic and 10.1 (0.1:7.2-13.0) mmHg for diastolic. A "white coat effect" (office vs. home BP) was present. Mean blood pressure reduction 12.9 mmHg (0.1:10.1-15.7) mmHg for systolic and 5.0 mmHg (0.1:3.4-6.6) for diastolic., Conclusions: This unconventional approach to blood pressure screening seems to be both cheap and acceptable for the public. Blood pressure measurements under these circumstances on the other hand are not directly comparable to the standard values given by WHO and should be looked on as reflecting the blood pressure each given time. Environmental factors therefore influence the blood pressure measurement greatly. The interaction between the physician and the patient seems to be a major factor in the office vs. home blood pressure difference, the so called white coat effect. On the other hand there must be another explanation for the difference between blood pressure measurement in supermarket "and at home. Different circumstances and their effect on reference values when offering blood pressure measurements must be taken into consideration. This should be kept in mind when diagnosing hypertension.

Raised blood pressure in the elderly is a frequent finding and is not a benign occurence. It should not be viewed as a normal or inevitable consequence of aging. Recent major intervention trials against hypertension in the elderly have showed clear benefits from actively lowering elevated arterial pressure in this group of patients and also in those with isolated systolic hypertension. This review emphasises the importance of antihypertensive treatment in the elderley and underlines the strategies and problems in the care of elderly patients with hypertension.

Background: Because of population stability, Tecumseh, a rural community in Michigan, was the site of health surveys over a period of three decades., Methods: In the recent survey anthropometrics, blood pressure (BP), blood chemistry, echo/Doppler cardiac exam, personality and exercise questionnaires were collected on site., Results: In this rural community 70% of subjects (447 men, 410 women, average age 30 years) do not engage in recreational exercise. Sedentary subjects were heavier (4 kg), had higher BP (2.3/2 mm Hg), faster heart rate (4 beats/min), and lower stroke volume (2 ml/m2) than physically more active subjects (p = 0.02 to 0.00001). Measures of cardiac structure and function were more favorable in exercising subjects. Cholesterol (+8 mg/dl), triglycerides (+15 mg/dl) and insulin (+2.4 microU/ml) were higher and HDL cholesterol was lower (-2 mg/dl) in the sedentary group (p = 0.04 to 0.003). Being sedentary was associated with more anxiety, anger and feeling time pressure (p = 0.001 to 0.00001). Exercise demands at work had no effect while even once a week recreational exercise was associated with a more favorable cardiovascular risk status. A difference in cardiovascular status between the sedentary and exercising subjects was not apparent throughout childhood, adolescence or early adult life, suggesting that subjects who exercise presently were not a priori healthier than presently sedentary subjects., Conclusions: Seventy percent of the residents studied in Tecumseh are physically inactive and have a less favorable cardiac risk profile. Enhancement of exercise habits may beneficially affect cardiovascular status and, presumably, the prognosis.

An estimate of arterial compliance--the stroke volume/pulse pressure ratio (SV/PP)--was studied in 801 participants in the Tecumseh Blood Pressure Study, a population-based ongoing cardiovascular, epidemiological investigation. The subjects were normal young adults (mean age 30 +/- 5.6 years) and 373 were females. Cardiac anatomy and function were studied by echo-Doppler methods, blood pressure being measured at the same time by the indirect method. The distribution of the SV/PP ratio was skewed toward higher values in larger subjects. After statistical adjustments for body surface area, this estimate of arterial compliance was found to be higher in females (2.00 +/- 0.62) than in males (1.90 +/- 0.58) (p < 0.05). When subjects were divided into tertiles, the group with the lowest estimated arterial compliance was normotensive but had higher systolic pressure, lower diastolic pressure, a similar mean arterial pressure, higher heart rate and higher left ventricular wall thickness ratio compared to subjects with higher arterial compliance. Indices of systolic ejection decreased and diastolic function was altered in the low compliance subjects. In addition, low compliance subjects also had higher fasting insulin levels. These findings suggest that the low arterial compliance in an otherwise normal population has negative cardiovascular correlates. The early association of decreased arterial compliance with anatomic, functional and biochemical aberrations suggests that estimates of arterial compliance might prove useful for prediction of cardiovascular complications.

The pathophysiology of the frequent association of insulin resistance and hypertension has not been elucidated. The skeletal muscle is the major site of insulin resistance; when stimulated with insulin, the hypertensive skeletal muscles extract less glucose than the normotensive. We postulate that hypertension-related changes in the skeletal muscle microcirculation contribute to the impaired glucose uptake in hypertension. Vascular rarefaction in hypertension impairs the delivery of insulin and glucose to muscle cells. Insulin resistance has been described both in human and experimental hypertension and both conditions are associated with vascular rarefaction. Functional studies (response to whole body or forearm exercise) and anatomic investigations (conjunctival photography, mesenteric and muscle biopsies) show vascular rarefaction in human hypertension. In addition, patients with hypertension are known to have a larger proportion of insulin resistant, poorly vascularized fast twitch muscle fibers. A few interventions can increase or decrease insulin resistance and these effects can be explained on hemodynamic grounds. Beta adrenergic blocking agents aggravate insulin resistance, and their main hemodynamic effect is a decrease of cardiac output. Converting enzyme inhibitors, alpha adrenergic blocking agents and possibly calcium antagonists decrease the insulin resistance, and their major hemodynamic effect is vasodilation. Physical training decreases insulin resistance; a higher capillary density in skeletal muscles is the hallmark of physical training. A hypothesis ought to rest on sufficient supporting data and its validity ought to lend itself to experimental verification. We believe our hypothesis meets both criteria. After outlining the supporting evidence we propose a number of tests to prove or disprove the hypothesis. In addition to the testable hypothesis we also speculate on the possible cause of the frequent association between hypertension and insulin resistance. We propose that both insulin resistance and blood pressure elevation represent a facet of the "defense reaction" which might have offered an early survival advantage and may, over evolutionary times, have fostered natural selection of subjects with both conditions.

Home blood pressure readings by self-monitoring (14 readings in 7 days) have been compared to readings taken in the clinic in 937 participants of the Tecumseh Blood Pressure Study. In the absence of firm criteria "hypertension at home" was defined as having home readings in the upper decile of the whole population. If a clinic reading exceeded 140 and/or 90 mmHg a subject was categorized as having clinic "hypertension". Two hypertensive groups emerged; one with both clinic and home hypertension ("sustained" N = 47) and one with high clinic but normal home blood pressure ("white coat" N = 50). Groups with "white coat" and "sustained" hypertension were very similar. Both groups were overweight, had faster heart rates, elevated cholesterol, insulin, triglyceride and decreased HDL levels. Blood pressure readings at previous exams (age 5, 8, 21 and 22) were elevated in both the "sustained" and white coat hypertension group compared to the normotensive controls. Subjects with white coat hypertension were not hyperresponders to the stress of mental arrythmetrics or to isometric exercise. The white coat hypertensives did not show abnormal anger, excessive submissiveness, or anxiety. The pathophysiology of the reproducible elevation of the clinic blood pressure in the white coat hypertensives remains unclear. Because of a higher risk of coronary heart disease and a risk for late development of sustained hypertension, subjects with white coat hypertension should be counselled on nonpharmacologic methods to control the blood pressure elevation and to ameliorate coronary risk factors.

Whereas this review is based on the available evidence, interpretation of the data is entirely hypothetical and subjective. To a large degree the review reflects our long-standing fascination with the role of the sympathetic overactivity in hypertension. The basic tenet is that sympathetic overactivity in hypertension may lead to a number of secondary changes, all of which are conductive to coronary heart disease. We also propose that insulin resistance and hypertension are associated through an underlying hemodynamic abnormality and again find good evidence for a possible role of sympathetics in the genesis of such hemodynamic changes. Future research in our laboratory will be oriented toward experimental testing of various aspects of the proposed sympathetic overactivity/hypertension/insulin resistance hypothesis.

Patients with stable, effort-induced angina pectoris and a typical combination of anginal pain and ischemic ST depression in exercise tolerance tests were randomized to treatment for 8 weeks with nicorandil (a newly developed antianginal and anti-ischemic drug) or nifedipine. After 4 weeks, the dosage of nicorandil was increased from 10 mg b.i.d. to 20 mg b.i.d., but the recommended dosage of nifedipine, 20 mg b.i.d., was kept constant during the study period. Double-blind treatment was preceded by a 2-week prephase during which patients were treated with isosorbide dinitrate. During the study period, patients were asked to report the rate of anginal attacks and consumption of sublingual nitroglycerin. Measurements of blood pressure and heart rate at rest and during exercise always were performed 2 h after drug intake. Fifty-eight patients were randomized--29 to nicorandil and 29 to nifedipine. There were large individual variations in anginal attack rates, which makes group comparisons difficult, but in the nicorandil group, the anginal attack rate decreased significantly compared with baseline frequency. Systolic blood pressure at rest was reduced significantly only with the highest dose of nicorandil, but nifedipine had a significant effect on both systolic and diastolic blood pressures as well as on the heart rate. Both treatments significantly increased exercise duration, time to onset of angina pectoris, and time to 1-mm ST depression. In the nicorandil group, an improvement was noted with the 20-mg dose compared with the 10-mg dose, but no significant differences were noted between the nicorandil and nifedipine groups after either 4 or 8 weeks of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

It has been suggested that the failure of thiazide therapy, administered to treat high blood pressure, to prevent coronary heart disease is related to the metabolic adverse effects of these drugs. The almost consistent observation of reduced serum potassium and total body potassium associated with diuretics appears to be of clinical importance. It may cause not only an increased risk of cardiac arrhythmias but also impaired glucose tolerance and abnormal lipid metabolism, while replacement of potassium has been shown to eliminate the risk of arrhythmias as well as thiazide-induced hyperglycaemia. The effect of the thiazide-induced short-term changes in serum lipids is unclear. Present experience suggests that thiazide-induced impairment of glucose tolerance is due to both reduced glucose-stimulated insulin release and increased peripheral resistance to the action of insulin. The blunted initial response of the pancreatic beta-cells to glucose is clearly dependent on serum potassium, and may cause postprandial hyperglycaemia during most of the day and night. This hypothesis is supported by the observation of enhanced glucose and insulin levels after an overnight fast, as well as 60-120 min after glucose challenges. Increased average levels of insulin may eventually cause down-regulation of cellular insulin receptors, i.e. insulin resistance. It is also conceivable that elevated insulin levels may cause hypertriglyceridaemia and possibly other abnormalities of lipid metabolism. Some recent observations indicate that the prognosis in treated hypertensive patients improves if both blood pressure and cholesterol levels are successfully controlled. We therefore emphasize the importance of normalizing serum potassium when using diuretic-based therapies in the treatment of hypertension.

Borderline hypertension was the topic of one of the "Hypertension seminars" arranged by the Hypertension Section at the Ostra Hospital, Göteborg, Sweden. On that occasion Professor Stevo Julius, Ann Arbor, Michigan USA, was an invited guest. During the seminar, various aspects of borderline hypertension were discussed, e.g. the natural history, hemodynamics and management of this condition. The present review is based on these discussions.

beta-Adrenoceptor blocking drugs are generally recognized as being effective in the treatment of hypertension. The mechanisms whereby these drugs reduce blood pressure are, however, not fully understood. In a double-blind, randomized study either metoprolol, 100--300 mg/day, or pindolol, 5--15 mg/day, was given for 6 months and the effects on blood pressure, heart rate and vascular resistance in the calf and forearm were investigated. Measurements were made at rest, during and after physical exercise, and during postischaemic hyperaemia. Both drugs reduced blood pressure to the same extent both at rest and during and after exercise. Metoprolol reduced heart rate to a greater extent than pindolol at rest and after exercise, whereas no difference was seen during physical exercise. Pindolol reduced the vascular resistance in the calf at rest by 14% (p less than 0.05), whereas metoprolol tended to increase vascular resistance, the difference in effect being highly significant (p less than 0.005). During and after leg exercise, there was no difference in forearm vascular resistance between the two drugs. It may be concluded that pindolol reduced resting blood pressure partly through peripheral vasodilatation. This was probably an effect of beta 2-adrenoceptor stimulation linked to the pronounced intrinsic sympathomimetic activity (ISA) of pindolol. Metoprolol on the other hand, acted mainly through cardiac mechanisms, as suggested by its pronounced reduction of heart rate.

The aim of this study was to evaluate the number, outcome, survival time, and causes of death of patients with severe arterial hypertension who were admitted to the Department of Medicine at Landspitalinn (National Hospital) in Reykjavik during the years 1957 to 1971. During this period 117 patients were found to have severe arterial hypertension (12.6% of all cases of hypertension diagnosed) according to the grading of Keith and Wagener, 20 patients with grade IV retinopathy and 97 patients with grade III. The case histories were analysed according to age and sex distribution, blood urea, electrocardiographic changes, heart size by X-ray at the time of diagnosis and final outcome. The survival calculations were done by the decrement method (life tables) and aim taken from patient age 65 years and less. Relatively fewer patients with severe arterial hypertension were admitted during the last five year period (1967-1971) than during the two previous five year periods. The main causes of death were cerebrovascular accidents (26.6%), myocardial infarctions (22.8%), and renal failure (22.8%). Approximately 50% of the men and 60% of the women survived five years. Elevated blood urea values and signs of left ventricular hypertrophy on ECG at the time of diagnosis carried a more sinister prognosis.

Renal function was evaluated in a group of 24 patients (21 men and 3 women, mean age 47 years) who had survived the malignant phase of hypertension during the period of 1969-1979. Five had grade III retinopathy (haemorrhages and exudates) and 19 had grade IV changes (papilloedema, FH IV) at diagnosis. Highest recorded blood pressure was 248 +/- 4/152 +/- 3 mmHg (mean +/- S.E.M.). Renal function rapidly deteriorated in 7 cases with progression to terminal uraemia. All patients in this group had a marked elevation in serum creatinine at diagnosis (448 +/- 105 mumol/l) and inadequate blood pressure control. Two of these 7 patients died and 5 underwent renal transplantation. The other 17 patients initially had serum creatinine less than or equal to 250 mumol/l (169 +/- 19 mumol/l-glomerular filtration rate (GFR) 51 +/- 7 ml/min). All except one were reinvestigated after a mean time of 6 years (range 6 months-11 years) with evaluation of blood pressure and determination of GFR by 51Cr-EDTA clearance. At follow-up their blood pressure was fairly well controlled (153 +/- 3/99 +/- 2 mmHg). Their GFR was 62 +/- 6 ml/min. Of the 11 patients in whom two GFR determinations were available (one initially and one at follow-up), six patients showed a marked increase in GFR while 5 patients showed only slight or no improvement in spite of fairly good blood pressure control. In malignant hypertension adequate antihypertensive treatment can lead to a pronounced improvement in GFR unless renal function has deteriorated gravely.

In a double-blind randomized study, hydralazine (n = 59) or the new dihydropyridine calcium antagonist felodipine (n = 61) was added to previous treatment with beta-adrenoceptor blocking agents in a group of 120 patients with essential hypertension. Active treatment with either hydralazine or felodipine was given for 8 weeks after a 4-week placebo run-in period, at the end of which all patients had supine diastolic blood pressures greater than 95 mm Hg. Assessment of the results according to the intention to treat principle showed that felodipine was significantly more effective than hydralazine at the doses employed, reducing systolic blood pressure 10-19 mm Hg more than hydralazine and reducing diastolic blood pressure 5-11 mm Hg more than hydralazine (95% confidence intervals). The number of patients complaining of side effects, the number of complaints, and the number of patients that had to be withdrawn from treatment were numerically higher during treatment with hydralazine than with felodipine, but these differences were not statistically significant. Against this background it is concluded that felodipine is superior to hydralazine when added to an antihypertensive regimen consisting of beta-adrenoceptor blocking agents.

In a randomized double-blind trial 36 patients with essential hypertension were treated with either metoprolol or pindolol for 6 months following a 6-week placebo period. At the end of the placebo period and after 6 weeks and 6 months of active therapy peripheral hemodynamics at rest and during maximal vasodilatation were studied. Exercise heart rate was reduced to the same extent with both metoprolol and pindolol, indicating that the doses used (metoprolol average 179 mg/day; pindolol average 12 mg/day) were equipotent as regards beta-adrenoceptor blocking effect. The antihypertensive effect was identical with both compounds. However, metoprolol caused a significant reduction of heart rate at rest both at 6 weeks and 6 months. With pindolol the reduction in heart rate was not significant at 6 weeks, and it was clearly much less than with metoprolol. On the other hand, no change in calf vascular resistance was seen during metoprolol therapy, whereas a marked and statistically significant reduction was caused by pindolol. Resistance at maximal dilatation in the forearm did not change with metoprolol, but tended to fall with pindolol after 6 weeks and was significantly reduced after 6 months. This indicates that although metoprolol and pindolol have the same antihypertensive potency, the two agents appear to reduce blood pressure through different mechanisms. Thus, cardiac mechanisms seem to play the most important role with metoprolol, whereas pindolol mainly acts by a reduction in vascular resistance. It also seems that treatment with pindolol normalizes the structural arteriolar abnormality present in hypertension as indicated by the reduction in resistance at maximal vasodilation.

Increased T-lymphocyte reactivity against human arterial antigen was significantly more common in a group of 20 patients with previously malignant essential hypertension than in matched control subjects. Serum-levels of IgG and IgM and the prevalence of autoantibodies were also significantly higher in the patients. It is suggested that these changes, whether primary or secondary, may contribute to or aggravate the vascular damage in this condition and are therefore of pathogenetic importance.

A review on the effects of ageing on cardiovascular function, with special reference to high blood pressure (BP), is given in this seminar. In most western populations the diastolic and especially the systolic BP increases with age in both sexes and this has been observed both in cross-sectional and longitudinal studies. Over the age of 60 the diastolic BP decreases. Of the different risk factors for cardiovascular diseases, only BP has been shown consistently to be an independent risk indicator in subjects 70 years or older. Hypotensive drugs used in the treatment of middle-aged hypertensive patients can also reduce the BP in elderly hypertensive patients can also reduce the BP in elderly hypertensive patients but are likely to produce more adverse reactions such as electrolyte disturbances and glucose intolerance by thiazides, depression by reserpine, orthostatic hypotension by methyldopa and excessive bradycardia by beta-blockers. A prolongation of life expectancy in hypertensive patients 60 years or older by hypotensive drug therapy has not been shown conclusively in controlled trials.