Coronary artery disease is a major complication of hypertension; one of its manifestations is silent ischemia. The aim of this study was to assess the prevalence and circadian distribution of ST-segment depression together with concomitant blood pressure (BP) and heart rate variations. One hundred patients (male:female ratio 1:1) with a mean age (±SD) of 51 ± 8 years underwent ambulatory monitoring using the combined AMP 5600 monitor which simultaneously records a continuous Holler electrocardiogram and intermittent noninvasive BP measurements at 15-minute intervals, with extra measurements triggered by detection of a horizontal or downsloping ST depression (>1 mm and >60 seconds). Cardiovascular risk factors were fully evaluated in all patients; accurate and reliable echocardiogram enabled left ventricular mass index to be calculated in 52 patients. Twenty-three patients (15 men and 8 women) experienced a total of 72 episodes of ST depression. Duration of such episodes (mean ± SD) was 132 ± 65 seconds and amplitude was 1.51 ± 0.55 mm. Circadian distribution showed 2 peaks: on awakening and in the late afternoon periods. The mean ambulatory BP load was greater in the patients with than without ST-segment depression for both systolic and diastolic BP (135 ± 14 vs 129 ± 15 and 84 ± 8 vs 79 ± 10 mm Hg, respectively; p < 0.01). Plasma glucose (5.83 ± 0.70 vs 5.46 ± 0.71 mmol/L; p = 0.04) and self-rated work-related stress levels (22% vs 13%; p = 0.03) were also higher in patients with ST-segment depression. There were no significant differences between groups for clinical parameters, left ventricular mass index, and other cardiovascular risk factors. During ST depression episodes, systolic BP increased by 9 ± 15 mm Hg, diastolic BP by 7 ± 11 mm Hg, and heart rate by 5 ± 17 beats/min. Thus, 24-hour Hoher electrocardiographic monitoring showed ST depression episodes in 23 of 100 hypertensive patients (23%); ambulatory BP load was greater in these patients. BP variations, and mainly its elevation, may trigger such episodes of ST-segment depression.
The Tertatolol International Multicenter Study (T.I.M.S.) was aimed at assessing the efficacy and tolerability of 5 mg tertatolol (T) once daily over a one year period and at finding, among the clinical variables before treatment, parameters predicting a successful single beta-blocking therapy. The study was carried out in 230 patients (96 men, 134 women, mean age +/- standard error of the mean: (51.5 +/- 0.7 years) suffering from uncomplicated mild to moderate hypertension. After a one-month placebo run-in period (M0-M1) and a one-month double-blind placebo-controlled period (M1-M2), 213 patients entered and 166 completed the one-year open period (M2-M14). A diuretic (D) was added if blood pressure (BP) was inadequately controlled with the single therapy. After one year, 88.5% of patients were controlled (sitting diastolic BP less than or equal to 90 mm Hg): 56.3% on single therapy (T) and 32.2% on dual therapy (T + D), respectively. Statistical analysis performed on the controlled subjects showed that patients who were controlled with T alone had an initially lower standing diastolic BP and a higher standing heart rate, were younger and had a lower sitting systolic BP than those controlled with T + D. Using such discriminant parameters which are predictors, 83.5% patients (single therapy group) and 49% patients (dual therapy group) were classified in the therapeutic group to which they really belonged. This study confirms the antihypertensive efficacy of tertatolol, and highlights relevant parameters for a successful single beta-blocker therapy in clinical practice.
TIMS study group *Institut de Recherche Servier, Neuilly sur Seine, France †James Connolly Hospital, Dublin, Ireland.
Plasma renin activity (PRA) and aldosterone concentrations were measured simultaneously with urinary excretion of kallikrein and of four prostaglandins (PGE2, PGF2 alpha, 6-keto-PGF1 alpha and TXB2) in 23 patients with pregnancy-induced hypertension (PIH; 17 with permanent PIH (PH) and six with labile PIH (LH), i.e. patients whose hypertension was controlled only by home bed-rest) and in 16 normotensive pregnant women. Plasma renin activity was lower in PH than in controls or in LH. No difference between the three groups was observed for plasma aldosterone and urinary excretion of kallikrein and prostaglandins except that TXB2 was higher in LH than in PH. Thus patients with LH have a different biological profile from that of PH, since they have higher PRA and higher TXB2 excretion, an association that suggests a more pronounced ureteral compression by the gravid uterus in this group. Although no decreased synthesis of vasodilating prostaglandins was found in PH, a dysregulation of the renin-angiotensin-prostacyclin loop is suggested by a negative correlation between PRA and 6-keto-PGF1 alpha. An independent vasopressive substance which would stimulate PGI2 and suppress renin secretion is therefore postulated.
The plasma renin activity (PRA), plasma volume (PV), urinary excretion of Kallikrein (UK) and PGE2, PGF2 alpha, 6-keto PGF1 alpha and TXB2 were measured in 24 ambulant patients without treatment on normal sodium diets with pregnancy-induced hypertension (HT) (diastolic BP greater than or equal to 90 mmHg, appearing after 20 weeks' pregnancy and absent 2 months after delivery). The UK was measured by an esterase technique, prostaglandins by radioimmunological assay and PV by dye dilution (Evans blue). Two subgroups of patients were identified according to the evolution of their blood pressure at rest at home; the first (7 patients) with labile HT, and the second (14 patients) with permanent HT. The PRA was significantly lower (p less than 0,001) in patients with permanent compared to labile hypertension (4,7 +/- 0,3 compared to 12,2 +/- 0,8 ng/ml/h) and compared to a control group of normotensive pregnant women (6,5 +/- 0,5). The PV, expressed as a percentage of the theoretical volume with respect to the stage of pregnancy and body surface area was low in both groups. In permanent HT: 1) there was no correlation between PV and PRA, 2) a positive correlation between UK and urinary 6-keto PGF1 alpha (r = 0,62; p less than 0,001) and PGE2 (r = -0,51, p less than 0,05). Discriminative linear analysis showed that urinary 6-keto PGF1 alpha was mainly related to PRA and to a lesser degree to UK.(ABSTRACT TRUNCATED AT 250 WORDS)