Malignant hypertension: new aspects of an old clinical entity.

Malignant hypertension (MHT), also known as accelerated-malignant hypertension or malignant-phase hypertension, is the most severe form of arterial hypertension. It is defined clinically as high blood pressure (BP) levels associated with lesions of the retinal fundus (flame-shaped hemorrhages, exudates, or cotton wool spots, with or without papilledema). Despite the availability of a vast range of antihypertensive agents, MHT continues to be a significant clinical challenge. Although its prevalence is very low, the absolute number of new cases has not changed over the past decades. While the role of the activation of the renin-angiotensin-aldosterone system and endothelial dysfunction in the pathogenesis of MHT has been well described, recent studies have indicated that the immune system may also play an important role in the development of this condition. Patients with MHT are characterized by pronounced target organ damage, including structural and functional cardiac abnormalities. MHT is frequently complicated by renal insufficiency and end-stage renal disease. The survival rates for patients with MHT have improved considerably with increased availability of antihypertensive treatment. However, renal insufficiency and end-stage renal disease still remain a significant cause of morbidity and mortality in this patient group. In conclusion, MHT is not a "vanishing disease" because there is a relatively stable number of new cases per year. Nonetheless, prognosis and survival rates in these patients have improved significantly owing to earlier detection, stricter BP control, lower BP targets, better choice of antihypertensive drugs, and availability of hemodialysis and renal transplantation.

[Pathogenesis of essential hypertension--a half of the century perspective]. / Patogeneza nadcisnienia pierwotnego z perspektywy ponad pólwiecza.

Over the past 60 years a great progress has been made in our understanding of the pathogenesis of essential hypertension. The contribution of excessive sympathetic nerves activity in the development of hypertension and target organ damage has been demonstrated in experimental and clinical studies. Also the important role of the renin-angiotensin-aldosteron in the pathophysiology of arterial hypertension has been confirmed in many studies. During the last three decades many studies revealed the relationship between low birth weight and arterial hypertension. Sleep disturbances--short sleep duration, insomnia are proposed as a possible pathophysiological factor of hypertension. The novel concept that immune system may play an important role in the pathogenesis of essential hypertension has gained support in recent years. The multifactorial nature of essential hypertension is now widely accepted.

Primary aldosteronism - recent progress and current concepts.

Primary aldosteronism is the commonest form of hormone-related hypertension, with an estimated prevalence of 6-13% in the generalpopulation of hypertensive patients. Among patients with resistant hypertension, the proportion of PA is even higher. Through intensiveresearch in the field of basic science and the creation of large registries of patients with PA, it is possible to understand the effect ofexcess aldosterone not only on the cardiovascular system but also on the morphology and function of the other organs. Recent researchhas highlighted the differences in the regulation of calcium metabolism in patients with adrenal adenomas and PA. A lot of attention hasbeen paid to the improvement of diagnostic methods, with particular emphasis on adrenal vein sampling, which is becoming increasinglyimportant. In recent years there have been many publications on the prevalence of mutations in the potassium channel in patients withadrenal tumours and PA. A new form of familial hyperaldosteronism - FIII, has also been distinguished. Treatment of patients with PAstill relies on the use of mineralocorticoid receptor antagonists or adrenalectomy, preferably preceded by a confirmation of aldosteronesecretion lateralisation by adrenal vein sampling.

Felodipine-metoprolol combination tablet: maintained health-related quality of life in the presence of substantial blood pressure reduction.

BACKGROUND: Most treated hypertensive patients do not achieve adequate blood pressure (BP) control. Initiating therapy with two drugs has been suggested when BP is >20/10 mm Hg above goal. To ensure patients' compliance, such treatment needs to be well tolerated and must not compromise health-related quality of life (HRQL). The primary objective of this study was to compare the effects on HRQL of initiating treatment with felodipine + metoprolol (F+M) fixed combination tablets, or enalapril (E), or placebo (P). METHODS: A total of 947 patients of both sexes with primary hypertension (diastolic BP 95 to 110 mm Hg), aged 20 to 70 years, participated in this randomized, double-blind, parallel group, 12-week, multicenter trial. Treatment was initiated with F+M 5 + 50 mg, or E 10 mg, or P. Doses were doubled after 4 or 8 weeks if diastolic BP was >90 mm Hg. The HRQL was measured at baseline and at the last visit using two validated questionnaires: the Psychological General Well-being Index (PGWB) and the Subjective Symptom Assessment Profile (SSA-P). Office BP was measured at trough, that is, 24 h after the previous dose. RESULTS: The HRQL was high at baseline and generally well maintained during the study. For example, the mean (SD) PGWB total score was 104 (16) at baseline and 105 (16) at 12 weeks in all three treatment groups. The BP reductions after F+M (18/14 mm Hg) and E (12/9 mm Hg) were significantly greater than after P (7/7 mm Hg), and the reduction after F+M was significantly greater than after E. CONCLUSIONS: The HRQL is maintained in the presence of substantial BP reduction during antihypertensive treatment with F+M fixed combination tablets.

Plasma neuropeptide Y immunoreactivity influences left ventricular mass in pheochromocytoma.

UNLABELLED: Left ventricular hypertrophy (LVH) in patients with arterial hypertension is closely related to the levels of blood pressure (BP), catecholamines, angiotensin II and other mitogenic peptides. Pheochromocytoma (pheo) is a type of hypertension caused by excessive production of catecholamines. The aim of this study was to determinate if left ventricular hypertrophy in patients with pheochromocytoma is related to catecholamines and neuropeptide Y (NPY). METHODS: 29 patients with pheochromocytoma (22 F, age 40 +/- 13 years), plasma concentration of neuropeptide Y immunoreactivity, noradrenaline (NA), and adrenaline (A) were determined. Twenty-four hour urine collection for determination of noradrenaline and adrenaline were performed. Every patient had echocardiographic examination and 24 h ambulatory blood pressure monitoring. RESULTS: Left ventricular hypertrophy was diagnosed in 14 patients. No differences in systolic and diastolic blood pressure in patients with and without left ventricular hypertrophy were found. Plasma noradrenaline and adrenaline levels did not differ between both groups, while plasma neuropeptide Y immunoreactivity was higher in patients with left ventricular hypertrophy than in patients without left ventricular hypertrophy (18.46 +/- 13.26 vs. 9.3 +/- 5.9 fmol/ml (p = 0.02)). Left ventricular mass index (LVMI) correlated with plasma neuropeptide Y-immunoreactivity (r = 0.42 p = 0.023), however, no relationship between left ventricular mass index and plasma or urine noradrenaline and adrenaline levels were found. CONCLUSION: Our results indicate that mitogenic effect of neuropeptide Y may play a role in pathogenesis of left ventricular hypertrophy in patients with pheochromocytoma.

The effects of genetic factors on selected indicators of the activity of the sympathoadrenal system and the renin-angiotensin-aldosterone system in twins.

BACKGROUND: There are numerous data indicating a significant role of the sympathoadrenal system and the reninangiotensin- aldosterone system in the regulation of blood pressure and the pathogenesis of essential hypertension. However, the genetic background of essential hypertension remains unclear. AIM: To determine the effects of genetic factors on selected indicators of the activity of the sympathoadrenal system and the renin-angiotensin-aldosterone system in twins. METHODS: We studied 39 monozygotic twin pairs (age 33+/-7 years) and 37 same-gender dizygotic twin pairs (age 36+/-7 years). We measured blood and urine adrenaline (A), noradrenaline (NA), dopamine (DA) and aldosterone (ALD) levels, as well as plasma renin activity (PRA) and serum angiotensin-converting enzyme (ACE) activity. Parameters of the genetic models for age- and gender-adjusted data were estimated by model fitting and path analysis technique using LISREL 8. RESULTS: The effects of genetic factors on the variability of blood and urine catecholamine levels were 69% and 65% for A, 42% and 76% for NA, and 58% and 40% for DA, respectively. We also found shared environmental components for blood NA (28%) and urine DA (17%). Genetic factors accounted for 36% of the variability of PRA and 80% of the variability of ACE. ALD levels were related only to environmental factors (including a shared environmental component, estimated at 25%, for urine ALD). CONCLUSIONS: We found significant effects of genetic factors on the activity of the sympathoadrenal system, as indicated by blood and urine catecholamine levels. We also found the effect of genetic factors on PRA and ACE, but not on aldosterone levels.

[Rare forms of hypertension]. / Rzadkie postacie nadcisnienia tetniczego.

In recent years there has been a growing interest in rare forms of secondary hypertension. Data from these studies enlarge our knowledge of hypertension pathophysiology and make possible establishing new possibilities of hypertension treatment. Primary reninism, Liddle's syndrome and neurovascular contact has been presented in the article. The pathogenesis, clinical symptoms and treatment of these rare forms of hypertension is discussed in this article.

Do catecholamines influence the level of plasma leptin in patients with phaeochromocytoma?

The relationship between plasma leptin and catecholamine concentrations during chronic and acute catecholamine excess is studied. Patients with phaeochromocytoma, divided according to gender, were examined under basal conditions (n = 18) and at selected time-points during surgical removal of the tumour (n = 12). Appropriate controls were used (n = 23) for the basal study. Plasma leptin was determined by radioimmunoassay (RIA) and plasma noradrenaline (NA) and adrenaline (A) by high-performance liquid chromatography (HPLC). Statistical evaluation employed Student's t-test, Wicoxon test and Spearman's correlation coefficient. Gender-related differences in plasma leptin in normal subjects was confirmed, and these were maintained in the patients. Phaeochromocytoma patients had normal plasma leptin levels in the basal state and decreased levels following the massive catecholamine surge provoked by surgery. Plasma leptin concentration did not correlate with plasma NA or A in either group studied. In the patients with phaeochromocytoma, acute but not chronic catecholamine excess affected plasma leptin, suggesting a role for sympathetic activity in modulating leptin release.