The normal diurnal BP pattern in primary aldosteronism was detected despite the highest casual and 24 h BP levels. It is therefore unlikely that the differences in the severity of hypertension contribute to the observed circadian BP differences.
The severity of hypertension in PA patients corresponds to earlier findings . Surprisingly, slightly lower BP values were observed in SH patients. The reason for this is not clear and may involve a higher incidence of the paroxysmal mode of catecholamine release in our pacients or milder forms of the disease in some patients.
The alteration of circadian BP rhythm in CS patients is in accordance with a study by Imai et al . This phenomenon may be the consequence of high glucocorticoid levels rather than ACTH overproduction because a similar reduction of circadian BP rhythm was observed in central, peripheral and ectopic forms. In addition, exogenous glucocorticoid administration abolished the circadian BP rhythm in patients with chronic glomerulonephritis or systemic lupus erythematosus. On the other hand, the altered circadian BP pattern in Cushmg’s syndrome may be caused by an interaction bet tween glucocorticoids and the sympathetic nervous system.
This study revealed a significantly lower night-time BP fall in SH and CS patients. It therefore seems that the cirt cadian BP rhythm is suppressed in these diseases. PA and A patients showed, in contrast, a normal pattern of circadian BP rhythm, similar to that in PH patients and controls. These results, in agreement with those of previous studies , indicate that the circadian BP rhythm may be influenced mainly by the tone of the sympathetic nervous system and the system involving adrenocorticotropic hormone (ACTH) and cortisol. The renin-angiotensin-aldosterone system and growth hormone, in contrast, may not contribute to the variations in circadian BP levels.
No statistically significant differences were detected in heart rate, which was 81±3 beats/min in the PA group; 84±3 in SH; 81±3 in CS; 79±4 in A; 84±4 in PH; and 79±4 in controls.
Figure 2 shows circadian BP rhythm in all groups expressed as the potential nocturnal BP fall. This parameter was calculated as the ratio of mean night:mean day BP and expressed as a percentage. Significantly higher values were found in SH and CS than in all other groups. No differences were, however, noted among PA, A, PH and controls.
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Table 2 shows the calcutated patameters from 24 h BP monitoring. The highest BP and BP load were recorded in PA.
Figure 1 shows mean 24 h systolic and diastolic BP in the studied groups. As with casual BP, these values were significantly higher in PA and PH. As expected, all studied groups revealed higher BP levels than controls.
The following parameters were determined: mean 24 h systolic and diastolic BP, mean daytime (06:00 to 22:00) and night-time (22:00 to 06:00) systolic and diastolic BP, and 24 h BP load (percentage of BP values exceeding 140/90 mmHg). Circadian BP rhythm was characterized by the potential differences of the mean BP during the day (06:00 to 22:00) and during the night (22:00 to 06:00). This difference was determined as the ratio of mean night-time:daytime BP (as a percentage). Finally, 24 h variability of BP was assessed by calculation of the SD of mean 24 h systolic and diastolic BP.
All results are reported as mean values + SEM. For statistical purposes, analysis of variance was used. Continue reading
All investitated subj ects were found to be otherwise healthy on routine examination.
Patients with idiopathic aldosteronism presented with bilateral adrenal hyperplasia on computed tomography together with a laboratory picture typical of primary aldosteronism (suppressed plasma renin activity and higher plasma aldosterone values, higher aldosterone:renin ratio, responsiveness to postural stimulation). The possibility of dexamethasone-suppressible hyperaldosteronism was excluded by dexamethasone suppression test (ie, demonstration of a marked suppression of BP and plasma aldosterone after four days’ dexamethasone [0.5 mg four times a day]).
Patients were divided into the following groups: primary aldosteronism (PA, n=25, mean age 47±2 years, comprising 12 patients with aldosterone-producing adenoma, 12 with idiopathic aldosteronism and one with aldosterone-producing carcinoma); sympathoadrenal hypertension (SH, n=14, mean age 46+4 years, comprising 13 patients with pheochromocytoma and one with neuroblastoma; seven had noradrenaline, three had adrenaline, and four had noradrenaline and adrenaline overproduction); Cushing’s syndrome (CS, n=11, mean age 44+5 years, comprising seven patients with central subtype, three with peripheral subtype and one with ectopic form); actomegaly (A, n=10, mean age 44+5 years; all had hypophyseal adenoma); essential hypertension of second- to third-degree World Health Organization criteria (PH, n=11, mean age 42+5 years); and a control group composed of healthy subjects (n=10, mean age 43+7 years).
PATIENTS AND METHODS
Noninvasive blood pressure (BP) monitoring has become a valuable method for evaluation of hypertensive patients and for diagnosis, assessment and treatmentof essential hypertension. Only few and conflicting data are, however, available regarding the use of BP monitoring in the evaluation and diagnosis of various types of endocrine hypertension . Because potential alterations in 24 h BP profile may be expected in endocrine hypertension (mainly changes in circadian BP rhythm and in BP variability), the purpose of this study was to investigate patients with primary hypertension as well as different types of endocrine diseases with frequent occurrence of secondary hypertension (primary aldosteronism, sympathoadrenal hypertension, Cushing’s syndrome, acromegaly). Two points were addressed: possible differences in 24 h BP profiles in different types of endocrine diseases; and the potential contribution of 24 h BP monitoring to the diagnosis of endocrine diseases. Continue reading