Disorders of 24-h rhythm of blood pressure in patients with chronic glomerulonephritis

AIM: To characterize 24-h profile of blood pressure (BP) and to clarify prognostic significance of 24-h BP variability in patients with chronic glomerulonephritis (CGN) with intact renal function and hypofunction of the kidneys. MATERIAL AND METHODS: A total of 38 hypertensive CGN patients (29 males and 9 females, mean age 37.9 +/- 12.4 years) entered the trial. All the patients had systolic BP (SBP) > 140 mm Hg and/or diastolic BP (DBP > 90 mm Hg. RESULTS: Twenty patients with renal hypofunction (creatinine > 1.4 mg/dl) had significantly higher (p < 0.05) SBP, day and 24-h SBP duration, high variability of day-time and 24-h SBP. Significantly higher mean day-time, night-time and 24-h SBP, SBP day-time and 24-h duration SBP duration, variability of SBP and DBP for a day and 24-h, respectively, were observed in 15 patients with left ventricular hypertrophy. Of prognostic significance in relation to renal survival estimated by Cox in 21 patients in multifactorial analysis were blood creatinine level, glomerular filtration rate, the patient's age, SBP duration for day, night and 24 hours. In multifactorial analysis, the final model included only age of the patient and blood creatinine. CONCLUSION: CGN patients with renal hypofunction had higher SBP and its variability associated with left ventricular variability.     

Significance of pharmacological blockade of angiotensin II type I receptors for correction of abnormal 24-hour blood pressure profile depending on its variability in patients with arterial hypertension stage II

AIM: To specify variable 24-h arterial hypertension (AH) stage II profile and to assess significance of pharmacological block of the end of the renin-angiotensin-aldosteron system for correction of the determined disorders. MATERIAL AND METHODS: The study was made of 46 men (mean age 42.8 +/- 3.28 years) with stage II AH and 25 normotensive controls (mean age 39.2 +/- 3.10 years). Depending on the magnitude of mean 24-h AP variability (APV), hypertensive patients were divided into two groups. Variability of systolic and/or diastolic AP (SAPV and DAPV, respectively) was considered high in at least 15.2 and/or 12.3 mm Hg variability, respectively, and normal at less values. RESULTS: AP 24-h profile in men with AH stage II and high APV compared to patients with normal APV is characterized by higher frequency of AP rise and less frequency of its night fall. In patients with high APV the drug eprosartan (teveten) is more effective in correction of hypertension and night fall of AP. CONCLUSION: Eprosartan has an adequate corrective activity in relation to absolute values of SAP and DAP in different hours. The highest hypotensive activity of the drug was seen in persons with initially high circadian AP variability within 24 hours.     

24-Hour blood pressure profile in patients with mild and moderate arterial hypertension and sleep apnea/hypopnea

AIM: To evaluate 24-hour blood pressure (BP) profile in arterial hypertension (AH) patients (pts) with desaturation signs of sleep apnea/hypopnea syndrome (SAHS). MATERIAL AND METHODS: We investigated 61 pts (44 males and 17 females) aged between 23-70 (52 +/- 2) years with mild to moderate AH. BP monitoring was performed with multisensor system TM-2425 (A&D, Japan). We assessed the following parameters: mean 24-h, awake, sleep systolic (S), diastolic (D) and pulse (P) BPs, systolic and diastolic BP loads ("normalized area under the curve"--NAUC). A normal circadian rhythm of BP was defined when nocturnal fall of SBP was > 10% and < 20%. The morning rise of BP we assessed by speed of increase of mean BP from 4 a.m. to 12 a.m. The nocturnal monitoring of arterial oxygen saturation(SaO2) was performed with pulseoximeter "NONIN 8500M" (USA). The analysis of the results was performed with the original program ARM-SaO2". The presence of SAHS was confirmed when the number of 4% desaturations were greater than 15 per hour or in the presence of group episodes of 4% desaturation below 90%. In 19 pts we revealed desaturation signs of SAHS. The comparison group included pts without SAHS (n = 42). We compared the groups regarding 24-h BP profile parameters. RESULTS: SAHS group had the following parameters significantly higher: mean 24-h (151.7 +/- 4.5 vs 142.9 +/- 2.4 mm Hg, p < 0.07) and sleep SBPs (142.8 +/- 5.1 vs 132.7 +/- 2.6 mm Hg, p < 0.05); mean 24-h (65.2 +/- 2.6 vs 55.9 +/- 1.9 mm Hg, p < 0.008), daytime (65.6 +/- 2.7 vs 56.6 +/- 2.0 mm Hg, p < 0.01) and sleep PBPs (64.1 +/- 2.7 vs 53.1 +/- 1.9 mm Hg, p < 0.002); 24-h (20.1 +/- 3.8 vs 12.6 +/- 1.8 mm Hg, p < 0.05) and sleep NAUC of SBP (24.6 +/- 4.4 vs 15.3 +/- 2.2 mm Hg, p < 0.03). In the group with SAHS were significantly higher the frequency of abnormal circadian rhythm of SBP (84 vs 57%, p < 0.05) and the speed of morning rise of mean BP (23.3 +/- 5.9 vs 8.5 +/- 2.8 mm Hg/h, p < 0.01). CONCLUSION: Our results suggest that pts with desaturation signs of SAHS are characterized by unfavourable changes in 24-h BP profile parameters, first of all owning to sleep systolic and pulse blood pressures with alteration of circadian rhythm and high speed of morning rise of BP.     

Spirapril - a new long-acting ACE inhibitor: efficacy and safety in patients with arterial hypertension in combination with diabetes mellitus and impaired kidney function

AIM: To examine effectiveness and safety of quadropril. MATERIAL AND METHODS: Changes in blood pressure (BP), heart rate (HR), levels of glucose, potassium and creatinine, creatinine clearance were studied in 120 patients (48 males and 72 females, mean age 60.6 +/- 0.7 years) with mild to moderate arterial hypertension (AH) with average duration 13.8 +/- 0.7 years. The patients were divided into 3 groups: with AH (n = 40), AH + noninsulindependent diabetes mellitus (DM) (n = 43), AH and nephropathy (n = 37). 8-week treatment was performed with a standard dose of 6 mg/day (1 tablet of quadropril). Control examinations were made 2, 4 and 8 weeks after the treatment. RESULTS: After 8 weeks of treatment a decrease in systolic blood pressure in AH group was 24.0 +/- 3.0 mm Hg and in diastolic blood pressure 16.3 +/- 1.3 mm Hg (P < 0.001). In the group with DM this decrease was 22.4 +/- 2.8 mm Hg and 15.7 +/- 1.4 mm Hg (p < 0.001), respectively. In the group with nephropathy this decrease was 26.4 +/- 2.4 and 16.5 +/- 1.3 mm Hg (p < 0.001), respectively. Heart rate changed significantly only in diabetics: from 75.1 +/- 1.7 to 72.9 +/- 1.3 beats/min. Biochemical parameters in the hypertensive and diabetic patients did not change significantly. In the nephropathy group there was a significant decrease in creatinine and increase in creatinine clearance. Their level of glucose and potassium changed insignificantly. CONCLUSION: The treatment with quadropril results in a significant decrease in blood pressure, does not influence parameters of carbohydrate metabolism, improves nitrogen eliminating function of the kidneys.     

Comparative study of spirapril (quadropril) and amlodipine efficacy. Results of randomized trial in patients with mild to moderate arterial hypertension

AIM: To compare in the non-blind randomised parallel study the efficiency of quadropril and amlodipine in the treatment of mild to moderate arterial hypertension. MATERIAL AND METHODS: A total of 80 patients (57.6 +/- 1.0 years) were included in this study. The patients were randomised in two groups, 40 patients each. Patients of group 1 received monotherapy with quadropril, while those of group 2 were treated with amlodipine. The treatment duration was 8 weeks in both groups. Quadropril was given in a fixed dose of 6 mg once daily. The initial dose of amlodipine was 5 mg/day. In case of insufficient effect the dose was elevated to 10 mg/day. The efficacy was evaluated by changes in blood pressure (BP) measured at rest. Moreover, in 50 randomly chosen patients 24-h monitoring of BP was performed at the start and end of the treatment. RESULTS: In the quadropril group baseline systolic BP reached 158.6 +/- 2.1 mm Hg, diastolic BP--101.8 +/- 0.8 mm Hg, heart rate was 74.3 +/- 1.6 beats/min. In the amlodipine group baseline systolic BP was 159.9 +/- 2.4 mm Hg, diastolic BP--101.8 +/- 1.0 mm Hg, heart rate was 71.3 +/- 1.0 beats/min. Systolic BP decreased at the end of quadropril therapy to 138.5 +/- 2.2 mm Hg, diastolic BP to 88.1 +/- 1.4 mm Hg. No significant change of the heart rate was observed. Under 5 mg of amlodipine systolic BP decreased to 137.9 +/- 2.5 mm Hg and diastolic BP to 87.1 +/- 1.6 mm Hg. Heart rate increased to 73.3 +/- 2.2 beats/min. Under therapy with 10 mg amlodipine systolic BP decreased to 145.9 +/- 3.8 mm Hg, diastolic BP to 89.7 +/- 3.4 mm Hg. Heart rate increased to 77.3 +/- 4.0 beats/min (p < 0.01). The hypotensive effect of quadropril remained stable while the effect of amlodipine decreased by the 8th week of therapy (p < 0.01). Side effects were observed significantly more often in the amlodipine group, then in the quadropril group. The main quadropril side effect was cough. Side effects observed in the amlodipine group were edemas, tachycardia, weakness. CONCLUSION: Both quadropril and amlodipine demonstrated a comparable antihypertensive effect although in 11 of 40 patients in the amlodipine group a dose increase was necessary and tolerability of quadropril was better.     

24-hour arterial hypertension profile and heart rhythm variability in patients with arterial hypertension and NIDDM

The study covered 72 patients with non-insulin-dependent diabetes mellitus (NIDDM) whose mean age was 54.2 +/- 0.8 years, duration of the disease 8.6 +/- 3.6 years. They had also mild or moderate arterial hypertension mean duration of which was 12.4 +/- 4.3 years. The examination of the patients consisted of 24-h arterial pressure (AP) monitoring, Holter ECG monitoring, cardiointervalography. For eight weeks 19 patients received enalapril (5-20 mg/day), 14 patients were given felodipin (5-10 mg/day) and 15 patients were treated with valsartan (80-160 mg/day). Enhanced activity of the sympathetic nervous system in hypertensive subjects with NIDDM raises daily average values of systolic and diastolic AP, variability and speed of AP morning rise. In NIDDM patients with moderate arterial hypertension vegetative regulation of AP was more stressed than in mild hypertension. Optimal medication of NIDDM patients' arterial hypertension may consist of ACE inhibitors and antagonists of angiotensin II receptors. These drug lower stress of the sympathetic nervous system and thus promote normalization of daily profile of AP.     

Daily profile of arterial pressure in patients with arterial hypertension,continuously living in Tyumen polar region

AIM: To study a 24-h profile of arterial hypertension and affection of target organs in hypertensive population of the Tyumen North. MATERIAL AND METHODS: 62 patients (43 men and 19 women, age 18-50 years) with arterial hypertension (AH) living in the North of the Tyumen region entered the test group. The control group consisted of 56 AH patients (36 men and 20 women) matched by age. They lived in the zone of moderate climate (in Tyumen). 24-h arterial pressure (AP) monitoring was made starting on day 2 of the patients' arrival in Tyumen. Echocardiography was made on the arrival day. The examination of the groups was conducted against "clean" background. RESULTS: The groups did not differ significantly by age, sex, AH duration, office systolic and diastolic pressure (SP, DP). However, 37 patients from the test group on arrival in Tyumen showed normalization of both office AP and mean 24-h AP. 25 patients from this group sustained high office and mean 24-h AP. An abnormal 24-h AP profile with nocturnal hypertension was recorded in 76.6% of the test group and 28.31% patients of the control group. Left ventricular hypertrophy was significantly more pronounced in the test group than in the control one. CONCLUSION: In 2/3 patients from the North with AH stage 1 and 2 office AP and mean 24-h AP normalized upon their arrival to the zone of moderate climate but their left ventricular hypertrophy was more severe and changes in a 24-h AP profile with nocturnal hypertension persisted.     

Efficacy of valsartan in patients aged > or =65 years with systolic hypertension

OBJECTIVE: This randomized, double-blind, placebo-controlled, parallel-group, multicenter trial investigated the effects of valsartan, an angiotensin II receptor blocker, on systolic blood pressure (SBP) in patients aged > or =65 years with systolic hypertension, with or without diastolic hypertension. BACKGROUND: Hypertension in older persons is a public health problem of epidemic proportions. SBP, which increases with age, is a better predictor of cardiovascular morbidity and all-cause mortality than is diastolic blood pressure (DBP). SBP is now thought to be a major modifiable risk factor for cardiovascular disease. METHODS: The study population consisted of 146 outpatients (74 female and 72 male) with a mean (+/- SD) age of 73.0+/-6.7 years and a trough mean sitting SBP > or =160 mm Hg; 88.4% were white. Patients with clinically relevant cardiac valvular disease, documented or suspected renal artery stenosis, and a serum creatinine level >2.5 mg/dL were excluded from the study. After a 2- to 4-week, single-blind, placebo run-in period, patients were randomly assigned to receive valsartan 80 mg or placebo once daily for 4 weeks and were then force-titrated to valsartan 160 mg or matching placebo once daily for an additional 4 weeks. Median DBP was 90 mm Hg, and >50% of the patients had isolated systolic hypertension. RESULTS: For the primary efficacy variable, the change from baseline to end point in trough mean sitting SBP, treatment with valsartan was superior to placebo, with reductions of 19.2 mm Hg compared with 8.8 mm Hg, respectively (P < 0.001, 95% CI -15.7, -5.5). Valsartan also produced superior reductions in trough mean sitting DBP (5.2 mm Hg and 1.2 mm Hg for valsartan and placebo, respectively; P < 0.001, 95% CI -6.4, -2.3). The tolerability of valsartan was comparable to that of placebo, with adverse events occurring in 31 (42.5%) valsartan-treated patients compared with 28 (38.4%) patients who received placebo. CONCLUSIONS: In this patient population of hypertensive patients aged > or =65 years, valsartan was effective and well tolerated and offers a promising new approach to the treatment of systolic hypertension.     

Assessment of the efficacy and tolerance of delayed-action nifedipine as the monotherapy or in combination with metoprolol in patients with arterial hypertension

AIM: To compare efficacy and safety of nifedipin-retard (cordaflex-retard, Egis, Hungary) used in monotherapy and in combination with metoprolol (egilok, Egis, Hungary) in patients with arterial hypertension (AH). MATERIAL AND METHODS: The study included 20 patients with AH stage I-II (12 males, 8 females, mean age 57.3 years, mean duration of the disease 8.6 years). Nifedipin-retard was given in a daily dose 40 mg/day (20 mg twice a day) in monotherapy and 20 mg/day in combination with metoprolol which was administered 50 mg twice a day (a daily dose 100 mg/day). The control examination consisted of a physical examination, measurement of arterial pressure (AP) by Korotkov, registration of heart rate, ECG, 24-h AP monitoring, echocardiography. RESULTS: By 24-h AP monitoring, a 4-week treatment with nifedipin-retard alone resulted in lowering of systolic arterial pressure. The combined treatment produced a more pronounced fall both in systolic and diastolic pressure. Diastolic left-ventricular function improved in combined therapy. Side effects observed in nifedipin-retard monotherapy got much more weaker when this drug combined with metoprolol. CONCLUSION: Combination of nifedipin-retard with metoprolol provides better clinical response and tolerance than monotherapy with nifedipin-retard.     

Evaluation of the evenness of the antihypertensive effect of losartan and captopril by using a 24-hour monitoring of arterial pressure

AIM: To investigate 24-h evenness of an antihypertensive effect of angiotensin II receptor blocker losartan vs captopril by four parameters of arterial pressure (AP) monitoring. MATERIAL AND METHODS: An open, cross-over, placebo-controlled trial was made in 22 patients with mild/moderate arterial hypertension (AH). Four parameters of AP monitoring were assessed: TPR, SI, rate of AP morning rise, index of AP morning rise. RESULTS: In losartan treatment TPR for systolic and diastolic AP were 61.5 and 61.3%, respectively, IS made up 0.74 +/- 0.13 and 0.64 +/- 0.09, respectively. For captopril these values reached 21.2 and 26.9%, 0.51 +/- 0.14 and 0.47 +/- 0.10, respectively. Differences by SI between the two drugs were statistically insignificant. Both drugs did not raise the rate and index of AP morning rise significantly. CONCLUSION: When administered in a single daily dose 100 mg, losartan produced a regular antihypertensive effect throughout 24 hours. Captopril (twice a day in a dose 50 mg) effect was not regular enough. This means that some patients need a three-times-a day regimen of captopril. Of the four parameters, SI is most informative for evaluation of antihypertensive effect evenness.     

Effect of losartan plus hydrochlorothiazide on nitric oxide status in 'nondipper' hypertensive patients

The objective of this study was to investigate the effects of losartan (100 mg) plus hydrochlorothiazide (HCTZ; 25 mg) on nitric oxide (NO) production and blood pressure (BP) in "nondipper" severe hypertensive patients. Twelve hypertensive "nondipper patients" (6 of each gender) with sitting systolic/diastolic BP of 188.0 +/- 5.2/116.2 +/- 1.2 mm Hg were studied by 24-hour ambulatory blood pressure monitoring (ABPM) after daily administration of 100 mg losartan plus 25 mg HCTZ for a period of 12 weeks. Office and mean 24-hour, as well as mean awake- and sleep-time systolic/diastolic BP, serum NO levels, and urinary excretion of NO were measured after the placebo period (3 weeks) and after 12 weeks of therapy. At the end of the 12-week treatment period, the mean 24-hour systolic/diastolic BP decreased significantly from 158.6 +/- 4.7/102.2 +/- 2.6 mm Hg (placebo period) to 140.3 +/- 4.8/90.9 +/- 3.3 mm Hg (P = 0.001/< or = 0.002). The mean BP (systolic/diastolic) during the waking period was reduced from 159.3 +/- 4.4/103.0 +/- 2.5 mm Hg to 135.0 +/- 4.4/88.2 +/- 3.1 (P < or = 0.007/P < or = 0.002), whereas the mean BP (systolic/diastolic) during the sleeping hours changed from 154.9 +/- 5.3/98.9 +/- 3.1 to 140.9 +/- 4.6 (P = 0.035)/91.7 +/- 3.2 mm Hg (P = 0.035/P = 0.051). Serum NO levels increased from 40.89 +/- 5.69 microM/L (placebo period) to 67.35 +/- 6.96 microM/L (posttreatment; P < or = 0.007), whereas the 24-hour urinary NO excretion did not change significantly (69.71 +/- 3.68 microM/L [placebo period] vs 79.64 +/- 4.25 microM/L [posttreatment]; P < or = 0.16). Urinary clearance of NO also did not change. Serum NO levels increased significantly without a significant change in urinary NO excretion. BP was significantly reduced but without modifying the nondipper pattern in these patients.     

The role of hypersympathycotony in development of arterial hypertension in patients with metabolic syndrome: potential of pathogenetically sound therapy

AIM: To assess hypotensive efficacy and metabolic neutrality of moxonidine (physiotenz)--a selective agonist of imidasoline receptors--in patients with mild and moderate arterial hypertension (AH) associated with diabetes mellitus (DM) type 2. MATERIAL AND METHODS: Follow-up and treatment were conducted in 30 hypertensive diabetics (mean age 52.43 +/- 4.65 years). Mean duration of DM and AH was 4.77 +/- 2.69 and 6.93 +/- 2.98 years, respectively. The study was made of lipid exchange, glycemia, levels of glycosylated hemoglobin (GH), fasting and postprandial immunoreactive insulin. Hypotensive efficacy was examined by 24-h monitoring of arterial pressure after 16 weeks of therapy. RESULTS: Mean 24-h systolic arterial pressure fell by 8.02%, diastolic arterial pressure--by 6.47%. The drug had a good effect on a 24-h profile of arterial pressure: a significant decrease of day and night pressure load index, lowering of initially high 24-h variability of systolic and diastolic arterial pressure, normalization of two-phase profile of arterial pressure. Carbohydrate metabolism improved also: GH, glycemia, immunoreactive insulin decreased. There was a significant trend to a change in qualitative composition of blood lipid--a decrease in lipoproteins atherogenic fractions and a rise in HDLP. CONCLUSION: Physiotens is a highly effective hypotensive drug for use in mild and moderate AH in DM of type 2.     

The antihypertensive efficacy of hydrochlorothiazide is not prostacyclin dependent

We tested the hypothesis that vascular prostacyclin synthesis is stimulated by hydrochlorothiazide and could account for some of the drug's antihypertensive effect. We studied 13 patients with mild essential hypertension in a randomized, double-blind design to assess the effects of indomethacin on hydrochlorothiazide's ability to lower blood pressure, alter body weight, stimulate plasma renin activity, and modulate vascular prostacyclin biosynthesis as assessed by the urinary excretion of the major enzymatically produced metabolite of prostacyclin, 2,3-dinor-6-keto-prostaglandin F1 alpha (PGF1 alpha), measured by GC/MS. Administration of hydrochlorothiazide, 50 mg daily for 2 weeks, was associated with a significant decrease in both systolic and diastolic blood pressure in both supine (systolic, 148 +/- 3 to 136 +/- 3 mm Hg; diastolic, 97 +/- 2 to 94 +/- 3 mm Hg) and upright (systolic, 151 +/- 4 to 131 +/- 2 mm Hg; diastolic, 103 +/- 2 to 97 +/- 3 mm Hg) positions. Hydrochlorothiazide administration resulted in a 1 kg weight loss and stimulation of plasma renin activity from 1.7 +/- 0.4 to 5.3 +/- 1.1 ng angiotensin I/ml/hr. However, the urinary excretion of 2,3-dinor-6-keto-PGF1 alpha was unchanged after administration of hydrochlorothiazide (86 +/- 13/ng/gm creatinine during placebo, 74 +/- 13 ng/gm during week 1 of hydrochlorothiazide, and 70 +/- 9 ng/gm during week 2 of the drug). Administration of indomethacin, 50 mg twice a day, resulted in greater than 60% inhibition of 2,3-dinor-6-keto-PGF1 alpha excretion but did not affect the antihypertensive response to hydrochlorothiazide. Indomethacin did not oppose the diuretic effect of hydrochlorothiazide as assessed by weight loss but did attenuate the rise in plasma renin activity. Our data demonstrate that the blood pressure-lowering effect of a thiazide diuretic does not require enhanced prostacyclin synthesis and the cyclooxygenase inhibitor indomethacin does not antagonize the antihypertensive efficacy of hydrochlorothiazide.     

Thiaside diuretics in combination with inhibitors of angiotensin-converting enzyme in patients with diabetes mellitus type 2 comorbid with arterial hypertension

AIM: To study the effect of co-renitek monotherapy for 16 weeks on parameters of 24-h monitoring of arterial pressure, carbohydrate, lipid, purin metabolism in patients with mild and moderate arterial hypertension (AH) and diabetes mellitus (DM) type 2. MATERIAL AND METHODS: 20 patients with DM type 2, mild or moderate AH received co-renitek (1-2 tablets a day) for 16 weeks. Before the treatment and 16 weeks later the patients were examined (24-h AH monitoring, carbohydrate, lipid, purin, electrolyte metabolism). RESULTS: Co-renitek treatment of DM type 2 patients with hypertension led to a significant lowering of mean systolic and diastolic pressure, improvement of 24-h AP profile and reduction of fasting glucose level. Co-renitek proved to be metabolically neutral in relation to lipid, purin and electrolyte metabolism. CONCLUSION: Co-renitek is effective and safe antihypertensive drug for treatment of arterial hypertension in patients with diabetes mellitus type 2.     

Diastolic dysfunction--predictor of cardiac remodeling in arterial hypertension in young males

For the study of the state of central hemodynamics and diastolic function of the left and right ventricle in formation of arterial hypertension (AH) with method of computer polyrheocardiography 76 males of mean age of 35.1 +/- 3.2 years were examined. The first group included 26 cases with high normal BP (systolic BP (SBP) 130-139 mm Hg, diastolic (DBP) 85-89 mm Hg--prehypertension, the second group was consisted of 30 cases with essential AH 1 stage (SBP 140-159 mm Hg, DBP 90-99 mm Hg), who did not receive antihypertensive therapy. The control group was consisted of 20 practically health young males. As a result of performed study at early stages of AH there were revealed lop-sided changes both of central hemodynamics and a diastolic function of both ventricles, which progressively increase along with elevation of AH stage. Diastolic dysfunction of left and right ventricle appears at the prehypertension stage and stage 1 arterial hypertension and precedes heart remodeling.     

Co-renitek treatment of patients with moderate and severe forms of hypertensive disease

AIM: To evaluate efficacy and tolerance of a compound drug co-renitec combining an ACE inhibitor enalapril maleate and diuretic hydrochlorothiazide co-renitec taken for 16 weeks in essential hypertension (EH). MATERIAL AND METHODS: 28 patients with EH (16 males and 12 females aged 47-74 years) of mean duration 13.1 +/- 1.6 years. Blood pressure (BP) was monitored for 24 hours with the device SL 90207 (SpaceLabs Medical, USA). Microalbuminuria (MAU) was estimated with the use of immunoturbodimetric test. RESULTS: By 24-hour monitoring, co-renitec reduced day BP by 14.9/8.9 +/- 3/2 mm Hg, nocturnal BP lowered by 18.6/11.4 +/- 3/2 mmHg, pulse pressure also fell. Coefficient T/P was 53.5% for systolic BP (SBP) and 59.6% for diastolic BP (DBP). The target SBP was reached in 77% patients, target DBP--in 69%. Co-renitec significantly decreased MAU, albumines excretion normalized in 46% patients. CONCLUSION: Co-renitec lowers both day and nocturnal blood pressure, improves 24-h rhythm of BP, has a positive effect on the kidneys. This allows its recommendation as a first-line drug in patients with moderate and severe EH.     

Clinico-genetic aspects of the hypotensive response and regression of left ventricular hypertrophy in arterial hypertension patients

AIM: To study clinicogenetic determinants of left ventricular hypertrophy (LVH) regress in 52-week antihypertensive therapy to achieve the target arterial pressure (AP) < 140/90 mm Hg. MATERIAL AND METHODS: I/D-polymorphism of angiotensin converting enzyme gene, T174M-polymorphism of angiotensinogen gene, A1166C-polymorphism of angiotensin II ATI-receptor gene (ATII), 4a/b-polymorphism of endothelial NO-synthetase gene (eNOS) were determined in 64 patients (24 males, 40 females, mean age 54 +/- 1.1 years) with arterial hypertension (AH) and LVH. Echocardiography, laboratory tests, clinical measurements of blood pressure (BP) and 24-h AP monitoring were made after 4 weeks of placebo and 52 weeks of treatment. RESULTS: Baseline values of LV myocardium mass index (LVMMI) correlated significantly with mean 24 hour and night systolic arterial pressure; 24-h, day and night pulse pressure (PP). In patients with regress of LVH the degree of LVMMI reduction significantly correlated with lowering of day and night PP, baseline level of neutrophils, uric acid and creatinine 52 weeks after treatment. Groups made by polymorphism, did not significantly differ by initial LVMMI, frequency of achievement of target AP. In patients with genotypes ID/II and aa, the level of achieved diastolic arterial pressure was significantly lower than in other groups. Resistant LVH was seen in 42.2% patients. Frequency of AP normalization was higher in the group of patients with LVH regress (48.6% vs 25.9%; p < 0.05). Resistant LVH occurred more frequently in patients with genotype DD (64.0 vs 28.2% in patients with II/ID, p < 0.05) and in patients with genotype 4ab (62.9 vs 30.4% in patients with genotype aa and 21.4%--with genotype bb; p < 0.05 in both cases). In patients with resistant LVH frequency of DD genotype increased (59.3 vs 24.3% in patients with regress of LVH; p < 0.01), genotype AA (74.5 vs 48.6%; p < 0.01) and genotype ab (63.0 vs 27.0%, p < 0.01). CONCLUSION: Regress of LVH in AH patients depends on dynamics and complex interactions of some hemodynamic, laboratory and genetic parameters.     

Tests for cell membrane destabilization in assessing activity-progression of chronic glomerulonephritis

AIM: To study the role of cell membrane destabilization (MD) in the serum and urine in assessing activity/progression of primary chronic glomerulonephritis (CGN). MATERIAL AND METHODS: The trial entered 163 patients (mean age 38 +/- 7.3 years) with primary CGN in active phase, 64 patients with CGN in remission and 24 controls. The groups were compared by MD (urine phospholipids--PL, blood and urine ethanolamine--EA), indexes of activity and sclerosis (AI and SI), lipid peroxidation (LPO), etc. RESULTS: In active glomerulonephritis (GN) vs inactive one there were high levels of 24-h proteinuria, AI, PL and EA in the urine, malonic dialdehyde (MDA) and hydroperoxides (HP) in the blood. SI was similar in both groups. In active GN significant correlations were found between urinary SI, systolic and diastolic pressure, elevated levels of beta-lipoproteins and triglycerides; between blood EA and 24-h proteinuria, blood platelets, beta-lipoproteins, triglycerides, MDA, urine EA. CONCLUSION: LPO and MD play an essential role in GN pathogenesis. They reflect activity of inflammation in GN irrespective of the activity type and clinicomorphological form of GN, absence or presence of CRF.     

The effect of sodium on hemodynamic changes during coronary angiography with nonionic contrast media

To investigate the effect of sodium on cardiac hemodynamics, sodium chloride was added to nonionic contrast media to a 0.9% concentration and was compared with the standard media iohexol, iopamidol, and ioversol. Left coronary angiography was performed in 10 closed-chest, atrial-paced dogs with 10 ml injections of each preparation in a randomized and blinded fashion. The maximum changes in left ventricular systolic pressure, mean aortic pressure, left ventricular and diastolic pressure, and maximal rise of left ventricular pressure were measured. The left ventricular systolic pressure and mean aortic pressure decreased by 17 +/- 7 mm Hg and by 12 +/- 5 mm Hg with iohexol plus 0.9% NaCl, but only by 5 +/- 4 mm Hg and by 4 +/- 3 mm Hg with iohexol alone (p less than 0.001). The left ventricular and end diastolic pressure increased by 2.2 +/- 0.6 mm Hg with iohexol plus 0.9% NaCl, but did not change with iohexol alone (p less than 0.001). Left ventricular dp/dt decreased by 204 +/- 161 mm Hg/sec with iohexol plus 0.9% NaCl but increased by 392 +/- 122 mm Hg/sec with iohexol alone (p less than 0.001). Similar results were obtained from experiments with iopamidol versus iopamidol plus 0.9% NaCl and ioversol versus ioversol plus 0.9% NaCl. Ioversol plus 5% dextrose or ioversol plus 2.1% choline chloride (isomolar to ioversol plus 0.9% NaCl) produced a significant increase in left ventricular systolic pressure and left ventricular dp/dt (versus ioversol plus 0.9% NaCl, p less than 0.001). Thus, sodium, but not the osmolality or chloride, contributed to the negative inotropic effect of the contrast media.(ABSTRACT TRUNCATED AT 250 WORDS)     

Blood pressure elevation in a patient treated with salsalate

OBJECTIVE: To report a case of increased blood pressure associated with the use of salsalate in an elderly patient with no prior history of hypertension. CASE SUMMARY: A 78-year-old white man with no prior history of hypertension initiated salsalate therapy for low-back pain. Over the 15 months prior to the initiation of salsalate, his blood pressure averaged 127 +/- 7 mm Hg systolic and 84 +/- 6 mm Hg diastolic (mean +/- SD). After initiation of salsalate, he experienced significant elevations in blood pressure, which led to a preliminary diagnosis of hypertension. Blood pressure after initiation of salsalate averaged 150 +/- 13 mm Hg systolic and 95 +/- 5 mm Hg diastolic. No changes in medications or medication doses (with the exception of warfarin) occurred in the 18 months prior to or during salsalate therapy. His weight remained stable. A detailed review of his medical records and history revealed no other causes for these elevations in blood pressure. Salsalate therapy was discontinued and his blood pressure returned to normotensive levels (119 +/- 2 mm Hg systolic and 81 +/- 2 mm Hg diastolic). DISCUSSION: Nonsteroidal antiinflammatory drug (NSAID)-induced elevations in blood pressure have been well documented in patients receiving antihypertensive medications. Due to its relative weak inhibition of cyclooxygenase and lack of published literature in hypertensive patients, salsalate is considered to have little or no effect on blood pressure. Our report documents a possible case of salsalate-induced hypertension in a previously normotensive elderly man. Observational studies suggest that NSAID use may increase the risk of developing hypertension in older patients. CONCLUSIONS: Clinicians should be aware of the possible effects of NSAIDs on blood pressure. Blood pressure monitoring following the initiation of salsalate may be warranted, particularly in older patients.