Effect of stent implantation on blood pressure control in adults with coarctation of the aorta

BackgroundStenting of coarctation of the aorta (CoA) generally results in good angiographic results and a decrease in transcoarctation pressure gradient. However, effect on blood pressure control is less clear. The goal of the current retrospective analysis was to investigate the effects of CoA stenting on blood pressure control.MethodsA retrospective analysis was conducted in consecutive adult patients with a CoA who underwent a percutaneous intervention at one of the three participating hospitals. Measurements included office blood pressure, invasive peak-to-peak systolic pressure over the CoA, diameter of the intima lumen at the narrowest part of the CoA and use of medication. The follow-up data were obtained, based on the most recent examination date.ResultsThere were 26 native CoA and 17 recurrent CoAs (total n = 43). Seven of them underwent two procedures. Mean peak-to-peak gradient decreased from 27 mmHg to 3 mmHg (p < 0.001), and minimal diameter increased from a mean of 11 mm to 18 mm (p < 0.001). Mean systolic blood pressure decreased from 151 ± 18 mmHg to 135 ± 19 mmHg at first follow-up of 3.8 ± 1.9 months and 137 ± 22 mmHg at latest follow-up of 19.5 ± 10.9 months (p = 0.001 and p = 0.009, compared to baseline, respectively). The total number of hypertensive patients decreased from 74% to 27% at latest follow-up. No significant change in antihypertensive medication was observed.ConclusionA clinically significant decrease in systolic blood pressure of approximately 16 mmHg was shown after (re)intervention in CoA patients, which sustained at follow-up. This sustained decrease of blood pressure can be expected to lead to less future adverse cardiovascular events.     

BLOOD PRESSURE REDUCTION IN THE MORNING YIELDS BENEFICIAL EFFECTS ON PROGRESSION OF CHRONIC RENAL INSUFFICIENCY WITH REGRESSION OF LEFT VENTRICULAR HYPERTROPHY

Self-monitoring values of blood pressure may better reflect the average long-term blood pressure value than sporadic measurements in the physician's office and be more useful for blood pressure control. In the present study, we compared the results of self-monitoring of blood pressure values, especially in the morning, with office blood pressure, and related these to progression of chronic renal insufficiency and left ventricular hypertrophy (LVH). Thirty-four patients were selected from 316 subjects with chronic renal insufficiency (average serum creatinine 1.72 ± 0.15 mg/dl, mean age 52.6 ± 3.5 yrs) in accordance with the following criteria office blood pressure was less than 140/90 mmHg, blood pressure was controlled with amlodipine (5–20 mg/day) combined with benazepril (2.5 mg/day), morning blood pressure was greater than 150/90 mmHg at 6–9 AM and LVH had been determined by echocardiography (posterior wall thickness; PWT ≥ 12 mm). The patients were assigned to 2 groups at random and were given: guanabenz (GB; 2–8 mg at 11 PM, n = 17) or placebo (n = 17). Two years later, the average blood pressure of both groups as measured in the office was not significantly different: however, BP in the morning was significantly reduced from 158 ± 6 to 134 ± 4 mmHg in GB treated group (P < 0.001). In 14 of 17 patients in GB treated group, LVH resolved and there was only mild progression of nephropathy (serum creatinine: 1.69 ± 0.18 to 1.81 ± 0.19 mg/dl). In 12 of 14 patients in placebo group, whose morning blood pressure remained at greater than 150/90 mmHg, LVH was retained and there was moderate progression of nephropathy (serum creatinine: 1.73 ± 0.14 to 2.62 ± 0.50 mg/dl). From these results, it is suggested that antihypertensive treatment with combination therapy based on self-monitoring BP is cardio-renoprotective in patients with chronic renal insufficiency and LVH.     

Antiproteinuric Effect of an N-Type Calcium Channel Blocker,Cilnidipine

The objective of the present study was to determine antiproteinuric effect of an N-type calcium channel blocker—cilnidipine. Subjects were 43 essential or renal hypertensive subjects who had been taking calcium channel blockers other than cilnidipine for at least 6 months. All patients had proteinuria greater than 0.2 g/day in spite of fair blood pressure control (< 150/90 mmHg). Calcium channel blockers in 25 patients (62 ± 3 years) were switched to cilnidipine (cilnidipine group), whereas other 18 patients (58 ± 3 years) continued to take originally prescribed calcium channel blockers (control group). The 24-hr urine collections were done at baseline and after 6 months of the follow-up period. Baseline characteristics including age, blood pressure levels, body mass index and creatinine clearance were similar between cilnidipine and control groups. Urinary protein excretion also was comparable between cilnidipine (0.61 ± 0.10 g/day) and control (0.86 ± 0.17 g/day) groups. Urinary protein significantly decreased after 6 months in cilnidipine group (? 0.21 ± 0.11 g/day, ? 36%, p < 0.01), whereas it did not change in control group (+ 0.01 ± 0.15 g/day, 0.4%, ns). There were no significant changes in blood pressure, serum creatinine, creatinine clearance, estimated protein intake, and urinary salt excretion during the follow-up period in either group. The reduction of urinary protein by cilnidipine was evident in essential hypertensives (? 54 ± 9%, n = 18, p < 0.01) but not in renal hypertensives (+ 10 ± 35%, n = 7, ns). Results suggest that cilnidipine has an antiproteinuric effect especially in patients with essential hypertension.     

Efficacy of once-daily lisinopril monotherapy in systemic hypertension

Lisinopril is a new, long-acting angiotensin-converting enzyme inhibitor formulated for once-daily treatment of hypertension. This study assessed the 24-h efficacy and tolerability of lisinopril in Chinese patients with mild to moderate hypertension of World Health Organization Stages I to II. A total of 30 patients aged 30 to 60 years (mean 47 ± 9) entered a 2-week washout period. All patients had ambulatory diastolic blood pressure (BP) > 90 mmHg and were given active treatment with lisinopril for 4 to 7 weeks. The dose of lisinopril was titrated from 10 to 40 mg daily (at 8-9 A. M.). In each patient, 24-h ambulatory blood pressure (BP) monitoring (SpaceLabs 90202) was performed twice, once before and once following treatment. Mean 24-hour systolic/diastolic BPs after lisinopril were significantly decreased compared with baseline values (132 ± 12/86 ± 7 vs. 150 ± 11/98 ± 7 mmHg; p < 0.0005/ 0.0005). The average dose of lisinopril was 14.5 ± 5 mg daily after a titration period of 5 weeks of treatment. Mean daytime (6 A. M. to 6 P. M.) BP decreased from 152 ± 11/100 ± 8 to 134 ± 12/87 ± 8 mmHg (p < 0.0005/0.0005) and nighttime (6 P.M. to 6 A. M.) BP from 147 ± 14/95 ± 9 to 128 ± 14/83 ± 8 mmHg ( p < 0.0005/0.0005). BP reduction was more pronounced during the night. Before treatment, the circadian variation showed a peak BP at 11 A. M. and nadir at 3 P. M. After treatment, significant BP reduction (p < 0.0005/0.0005) was seen throughout the 24-h period. The circadian rhythm of BP was preserved as indicated by similar BP standard deviations (14 ± 3/11 ± 2 vs. 13 ± 3/10 ± 2 mmHg). Mean heart rate increased from 76 to 80 beats/min (p < 0.05). Four patients reported having a nonproductive cough. Thus, lisinopril administered as once-daily monotherapy provided effective BP control over a 24-h period with preserved circadian rhythm.     

Anti-Albuminuric Effects of the Angiotensin AT1 Receptor Blocker Telmisartan in Hypertensive Patients

We evaluated the anti-hypertensive and anti-albuminuric effect of the angiotensin receptor blocker telmisartan alone and in combination with torasemide and amlodipine. Patients were hypertensive, both diabetics and non-diabetics with persistent microalbuminuria. Our primary endpoint was a change in microalbuminuria levels, while the secondary endpoints were changes in systolic blood pressure (SBP), diastolic blood pressure (DBP), serum creatinine levels, and glomerular filtration rate.After the 16-week treatment period, the patients significantly reduced microalbuminuria levels (76.4 ± 52.4 μg/min; p < 0.001), SBP (16.4 ± 8.7 mmHg; p < 0.001) and DBP (17.7 ± 5.9 mmHg; p < 0.001). Both diabetics and non-diabetics showed an identical pattern of significance with respect to the whole population. Systolic blood pressure, DBP, and microalbuminuria were significantly reduced as a consequence of therapy, both in diabetics and non-diabetics.     

Blood Pressure Response to Sodium Restriction and Potassium Supplementation in Healthy Normotensive Children

To examine the effects of dietary sodium on blood pressure 149 healthy, normotensive children (64 males, 85 females) participated in a study to restrict sodium intake to 60 mEq/day or half of the usual intake for 3 months. Sodium excretion was significantly decreased during the study period (100.6 ± 3.4 mEq vs 46.5 ± 2.0 mEq, P<.001). As a group there was no significant change in systolic and a small decrease in diastolic blood pressure (54.2 ± 0.8 mmHg vs 53.0 ± 0.7 mmHg, p<.03, one tailed). Adjustment of blood pressure for weight and age and analysis of residuals yielded significant decreases in both mean arterial (p <.05) and diastolic blood pressure (p<.05). In the potassium supplement study, comparison of supplementation to post-supplement periods in 31 children (13 male, 18 female) showed a significantly lower (p <.05) systolic blood pressure during supplementation (101.3 ± 2.1 mmHg vs 103.3 ± 20 mmHg). Analyses of diastolic pressures, sodium excretion and weight were not significant. These studies show heterogeneity in the blood pressure response to sodium restriction and suggest that sodium restriction and potassium supplementation have different effects on blood pressure in children.     

Blood Pressure and Metabolic Effects of Cortisol and Deoxycorticosterone in Man

We have previously shown that ACTH administration (1 mg/day) for 5 days raises systolic blood pressure (BP) by some 20 mmHg in both normotensive and hypertensive subjects, accompanied by hypokalaemia, urinary Na retention, a rise in fasting blood glucose and a fall in plasma renin concentration (PRC). In the present study cortisol and deoxycorticosterone (DOC) were infused for 5 days in 7 and 6 subjects respectively at rates appropriate for conditions of ACTH stimulation to determine whether the effects of ACTH could be reproduced by either steroid. Cortisol infusion increased systolic BP from a control of 108 ± 7 mmHg to 129 ± 7 mmHg on day 5, p < 0.001. Plasma [Na] increased from 137 ± 1 to 139 ± 1 mmol/1 (p < 0.01), plasma [K] fell from 3.8 ± 0.1 to 3.6 ± 0.1 mmol/1 (p < 0.05); blood glucose rose from 3.9 ± 0.2 to 4.7 ± 0.2 mmol/1 (p < 0.001); PRC fell from 26 ± 7 to 12 ± 3 μiu/ml (p < 0.05); renin substrate rose from 1629 ± 140 to 2206 ± 453 pmol AI/ml, (p < 0.05); urine Na excretion fell from 93 ± 19 to 41 ± 10 mmol on day 2 (p < 0.05) and rose to 209 ± 31 mmol 48 hrs after infusion (p < 0.001); urine output rose from 2.0 ± 0.35 to 2.89 ± 0.46 L on day 5, (p < 0.01). Plasma cortisol levels were similar to those seen with ACTH treatment. DOC infusion was associated with a fall in diastolic BP (control 64.2 ± 4.0 mmHg, day 5 57.0 ± 4.2 mmHg, p < 0.01). Urine Na excretion fell from 77 ± 1 2 mmol/day to 49 ± 8 mmol/day on day 1, (p=0.06) and body weight rose from 76.0 ± 5.8 kg to 76.8 ± 5.9 kg day 5 (p < 0.001). Thus in man, cortisol infusion (in contrast to DOC) at rates appropriate for conditions of ACTH stimulation reproduces both the BP and metabolic effects of ACTH. Whether cortisol acts to raise blood pressure by a classical glucocorticoid mechanism or by a hypertensinogenic mechanism is not known.     

Plasma and Blood Vessel Endothelin-1 Concentrations in Hypertensive Uremic Rats Treated with Erythropoietin

The present study was designed to evaluate whether changes in plasma and blood vessel endothelin-1 (ET-1) concentrations may play a role in the enhanced blood pressure response to recombinant human erythropoietin (r-HuEPO) replacement therapy in uremia. Renal failure was induced by 5/6 nephrectomy (Nx). Uremic rats received either r-HuEPO (100 u s.c. three times a week) or the vehicle for 5 weeks. They were compared to control rats receiving the vehicle. Systolic blood pressure (tail cuff method), hematocrit, serum creatinine, plasma and tissue ET-1 were measured at the end of the protocol. Immunoreactive ET-1 (ir-ET-1) was determined by radioimmunoassay of acid-extracts from the plasma, thoracic aorta and mesenteric arterial bed. Creatinine increased about three fold in Nx animals. Blood pressure in control rats was 120 ± 3 mmHg compared to 161 ± 6 mmHg in the Nx + vehicle group (p<0.01) and 199 ± 9 mmHg in the Nx + r-HuEPO group (p±0.01). Plasma ir-ET-1 levals were similar in the Nx + vehicle and Nx + r-HuEPO Groups (7.9 ± 1.0 and 7.8 ± 0.8 pg/ml). In contrast, thoracic aorta ir-Et-1 content was significantly higher in the Nx + r-HuEPO group than in the Nx + vehicle group (20.3 ± 2.9 vs 13.4 ± 1.9 pg, p<0.05). Simlar results were obtained in the mesenteric arterial bed. There were significant ocrrelations between blood pressure and ir-ET-1 content in the thoracic aorta (r=0.045, p<0.05) and in the mesenteric arterial bed (r=0.41, p<0.05). Vascular ET-1 content but not plasma levels are increased in uremic rats treated with r-HuEPO suggesting an increase in blood vessel ET-1 production which may play a role in the pathogenesis of r-HuEPO-induced hypertension     

Uremia Enhances the Blood Pressure Response to Erythropoietin

To investigate the role of uremia in the development of human recombinant erythropoietin (r-HuEPO)-induced hypertension, Wistar rats were divided into a uremic (subtotal nephrectomy) and a control group. After three weeks, both groups were again divided and each subgroup received either r-HuEPO (100 u/kg s.c., 3 times weekly) or the vehicle for a further 3 weeks. Hematocrit, blood pressure and blood chemistry were measured prior to surgery, before either vehicle or r-HuEPO treatment and before euthanasia. The uremic group developed anemia, hypertension and all the biochemical features observed in humans with end-stage renal disease. r-HuEPO therapy increased hematocrit from 29 ± 2.5% to 46 ± 2% (p < 0.01) in the uremic rats. The mean baseline blood pressure was 119 ± 10 mmHg. At week 3, mean blood pressure was unchanged in control rats, but it was increased to 151 & 5 mmHg (p CO.01) in the nephrectomized group. At week 6, mean blood pressure in the untreated uremic rats remained unchanged from week 3, but blood pressure in the uremic animals treated with r-HuEPO increased significantly to 187 & 8 mmHg (p CO.01). There was no significant correlation between hematocrit and blood pressure in the r-HuEPO treated uremic group (r=0.01, NS). r-HuEPO had no effect on blood pressure in control rats despite a significant increase in hematocrit. These results indicate that the blood pressure response to r-HuEPO is enhanced in rats with chronic renal failure.     

Living donor nephrectomy: follow-up renal function, blood pressure, and urine protein excretion

PURPOSE: To assess the effect of donor nephrectomy on blood pressure, 24-hour urine protein excretion, and renal function. MATERIALS AND METHODS: Of the 198 individuals who donated a kidney between 1991-1996, 101 had their blood pressure, 24-hour urine protein excretion, and serum creatinine concentration levels measured. The mean duration of follow-up was 3.2 +/- 1.6 years (range: 8.5 months to 6.5 years). RESULTS: Serum creatinine concentration was significantly higher (p<.001) at follow-up (107 +/- 20 umol/L) compared to before donation (86 +/- 18 umol/L). When follow-up serum creatinine concentrations were expressed as percentages of their pre-operative values, a gradual decline was observed with time (R= -.380). Diastolic blood pressures (p<.05) and 24-hour urine protein levels (p<.001) were significantly higher at follow-up, however, neither increased with time. The prevalence of hypertension and proteinuria in our donors was no different from that of the general population. CONCLUSIONS: Donor nephrectomy does not impair renal function or result in a progressive rise in blood pressure or urine protein excretion up to 6.5 years after nephrectomy.     

Plasma Endothelin Levels and Blood Pressure in Hemodialysis and in Capd Patients. Effect of Subcutaneous Erythropoietin Replacement Therapy

We investigated plasma endothelin (ET) concentration and blood pressure in 44 patients with end stage renal failure chronically treated with either hemodialysis (n = 24) or continuous ambulatory peritoneal dialysis (CAPD) (n = 20). Half of the subjects were on chronic erythropoietin (r-HuEPO) replacement therapy (30-60 U/kg) subcutaneously, 3 times weekly. The mean plasma ET level of the whole group was about five fold higher than the normal range. Plasma ET concentration and mean blood pressure were higher in hemodialysis than in CAPD patients (33.3 ± 2.1 vs 24.8 ± 1.2 pg/ml, p < 0.01, and 101 ± 2.4 vs 91 ± 3 mmHg, p < 0.025). There was a significant correlation between plasma ET levels and systolic blood pressures in both groups (r = 0.45, p < 0.05). Patients (hemodialysis and CAPD) receiving subcutaneous r-HuEPO had higher mean blood pressure (99 f 3 vs 85 Ifi 4 mmHg, p < 0.01), while their plasma ET levels were similar to untreated patients independent of the dialysis mode. However, a statistically significant correlation between plasma ET and systolic blood pressure was present only in the r-HuEPO treated group (r = 0.46, p < 0.05 vs r = 0.29, N.S., for the untreated group). These results show that plasma ET levels are markedly increased on both dialysis mode, but the values are lower in CAPD patients. Plasma ET concentrations significantly correlated with systolic blood pressures in the whole group of patients, and also in those receiving r-HuEPO replacement therapy.     

Urinary kallikrein excretion after renal transplantation: Relationship to hypertension,graft source,and renal function

The role of the renal kallikrein-kinin system in the pathogenesis of hypertension and various forms of renal dysfunction after human renal transplantation has been assessed by measurement of urinary kallikrein activity in 41 renal transplant recipients. The urinary tosyl arginine methyl esterase assay was used. The urinary kallikrein in these patients appeared to originate from the transplanted kidney and not their own diseased kidneys. Twenty-three recipients had hypertension (mean blood pressure 156 ± 3/98 ± 2 mm Hg) and excreted less kallikrein (4.0 ± 1.2 versus 12.5 ± 4.0 esterase units [EU] per 24 hours, p < 0.05) than their 18 normotensive counterparts (mean blood pressure 132 ± 2/77 ± 1 mm Hg, both p < 0.01). Subjects with renal complications of transplantation (acute tubular necrosis [ATN], nine patients, or acute rejection [AR], eight patients) also excreted less kallikrein than the 28 subjects without such complications (3.4 ± 0.9 versus 10.3 ± 2.7 EU/24 hours, p < 0.02). Among those with acute renal complications, subjects with ATN excreted less kallikrein than those with AR (1.3 ± 0.3 versus 5.7 ± 1.7 EU/24 hours, p < 0.02). Cadaver graft recipients excreted less kallikrein than living related donor graft recipients (2.1 ± 0.4 versus 13.0 ± 3.5 EU/24 hours, p < 0.01), perhaps reflecting their higher blood pressures (mean systolic pressure 151 ± 3 versus 140 ± 3 mm Hg, p < 0.04), relatively impaired renal function (creatinine clearance values 42 ± 8 versus 62 ± 5 ml/min, p < 0.04), and higher incidence of ATN (nine cases versus none). The kallikrein-kinin system may be involved in the pathogenesis of hypertension and some forms of renal dysfunction after renal transplantation.     

Hypertension in cyclosporin A-treated patients is independent of circulating endothelin levels

Abstract. Objectives. To measure blood pressure (BP), plasma endothelin-1 (ET-1), atrial natriuretic peptide (ANP), antidiuretic hormone (ADH) and aldosterone (ALDO) concentration, and plasma renin activity (PRA) in patients treated with a low-dose cyclosporin A (CyA). Design. An open study of patients with rheumatoid arthritis (RA) or palmoplantar pustulosis (PPP). Setting. Out-patient clinics at the Central Hospital of Jyväskylä and Helsinki University Central Hospital. Subjects. CyA was given to 25 patients with RA and to 10 patients with PPP. Intervention. RA patients were given CyA at a dose of 2.5±0.13 mg kg^?1 body weight (BW) to 3.47±0.79 mg kg^?1 BW (mean values±SD) at the start of the study and after 6 months, respectively, and the CyA dose was 2.67±0.13 mg kg^?1 BW decreasing to 2.07±0.96 mg kg^?1 (P < 0.001) after 4 months in PPP subjects. Results. Systolic (sBP) and diastolic blood pressure (dBP) increased from 127.8±13.6/79.7±8.4 mmHg to 140.0±19.8/83.8±9.7 mmHg during the study (P < 0.03). Plasma ET-1, ANP, ALDO and ADH concentration and PRA did not change during 4 to 6 months of CyA treatment. The plasma ANP concentration was constantly higher in CyA-treated RA patients (112±87 ng l^?1) to 118±78 ng l^?1) than in PPP patients (37.3±26 ng l^?1 to 47.7±39.9 ng l^?1; P < 0.02). The serum creatinine concentration remained within the normal range, but increased from baseline (76.7±11.9 μmol l^?1), to 90±15.4 μmol l^?1 (P < 0.001). The serum magnesium concentration decreased significantly (P < 0.005) after 6 months of CyA treatment in RA patients. No correlation was found between serum creatinine and plasma ET-1 concentration. Conclusions. Increased blood pressure during CyA treatment was independent of circulating ET-1 levels. A low dose of CyA did not induce increased ET-1 synthesis as judged from plasma samples. The high plasma ANP level observed in RA patients could be due to fluid retention caused by concomitant treatment with non-steroid anti-inflammatory drugs. Fluid retention and decreased magnesium levels could also be involved in the development of hypertension in CyA-treated subjects.     

Antihypertensive Therapy in Elderly Patients with Isolated Systolic Hypertension: Third Progress Report of the Syst-Eur Trial

The Syst-Eur trial is a randomised, double-blind, placebo-controlled trial that examines the hypothesis that antihyper-tensive treatment can prevent or delay cardiovascular complications in elderly patients (> 60 years) with isolated systolic hypertension. On March, 1st 1993 a total of 1395 patients with a sitting systolic blood pressure on placebo averaging 160–219 mmHg and a diastolic blood pressure < 95 mmHg were randomised into this trial. The placebo and active treatment groups were similar at randomisation with respect to age (7 2 ±7 years, mean ± SD), percentage of women (68%), percentage of patients with cardiovascular complications (30%) and sitting blood pressures (175±12/85±6 mmHg). The fall in sitting systolic and diastolic blood pressures from baseline to 2 years was significantly more pronounced (p<0.001) in the actively treated (-22±18/-6±9 mmHg) as compared with the placebo treated Syst-Eur patients (-10±20/- 1±9 mmHg). Active treatment consists of nitrendipine if necessary associated with a converting-enzyme inhibitor and a thiazide. Whether treatment with these antihypertensive agents results in a clinically meaningful reduction of cardiovascular morbidity and mortality is the subject of investigation in this trial.     

Predictive factors of resistance to antihypertensive treatment

Results of antihypertensive treatment were analyzed in a group of 5,209 hypertensive patients referred in two hypertension Clinics in Paris from 1976 to 1985. Patients were included in the study if they fulfilled the following criteria: 1) at least four visits in the clinic, 2) follow-up period greater than 6 months, 3) initial diastolic blood pressure greater than or equal to 90 mmHg and/or presence of an antihypertensive treatment. After a mean follow-up period of 43 months, blood pressure was reduced from 177/105 mmHg to 148/89 mmHg. However, in spite of at least two antihypertensive drugs, 16.7 p. 100 of these patients had a diastolic blood pressure above 95 mmHg at the end of the follow-up period and were defined as uncontrolled hypertensives (UH). By comparison with controlled hypertensives (CH), UH patients were more frequently males (67.9 vs 56.6 p. 100, p less than 0.001), had a greater known duration of hypertension (11.6 vs 8.7 years, p less than 0.001), and presented at the first visit with higher blood pressures (188/113 vs 174/103 mmHg, p less than 0.001/p less than 0.001), despite a higher rate of antihypertensive treatment (66.6 vs 53.8 p. cent, p less than 0.001), a higher ponderal index (26.3 vs 25.3/kg/m2, p less than 0.01) and a higher prevalence of end-organ damage (23.2 vs 16.3 p. 100, p less than 0.001). Sokolov index, serum creatinine and uric acid levels were higher among UH than among CH patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute effects of ethanol on myocardial blood flow in the nonischemic and ischemic heart

To determine the effects of ethanol on myocardial blood flow in the non-ischemic and ischemic heart, coronary blood flow was measured with radionuclide-tagged microspheres in the anesthetized dog before and after intravenous administration of 1.7 g/kg body weight of ethanol. In non-ischemic dogs, at an average peak blood ethanol level of 225 ± 8 mg/dl (mean ± standard error of the mean), left atrial pressure increased from 5.7 ± 0.6 to 7.7 ± 0.8 mm Hg (p <0.01) and heart rate slowed from 179 ± 8 to 171 ± 8 min^?1 (p <0.001) but mean aortic pressure and cardiac output were unchanged. Average myocardial blood flow increased from 122 ± 5 to 143 ± 8 ml/min per 100 g (p <0.001). In dogs given ethanol after coronary occlusion, at an average peak blood ethanol level of 201 ± 13 mg/dl, left atrlal pressure increased from 6.3 ± 0.6 to 7.4 ± 1.4 mm Hg (p <0.05) but there was no significant change in heart rate, mean aortic pressure or peak positive first derivative of left ventricular pressure ($\text{dP}\text{dt}$). In these dogs, there was a significant change (F = 6.47, p <0.001) in the distribution of myocardial blood flow. In the nonischemic zone, blood flow increased from 118 ± 7 to 148 ± 14 ml/min per 100 g (p <0.005), whereas in the ischemie zone it declined from 30 ± 6 to 20 ± 5 ml/min per 100 g (p <0.02). Myocardial tissue demonstrating myocardial perfusion equal to or greater than 80 percent of preligation levels showed a significant increment of blood flow after ethanol; by contrast, myocardial tissue having blood flow levels equal to or less than 60 percent of preligation levels showed a significant decline in blood flow.Thus, ethanol increases coronary blood flow in the nonischemic myocardium. However, in the acutely ischemic heart, ethanol produces an unfavorable redistribution of myocardial blood flow with flow in the non-ischemic myocardium increasing, at least in part, at the expense of blood flow to ischemic myocardium, producing in effect a “coronary steal.”     

COMPARISON OF THE EFFECTS OF AMLODIPINE AND LOSARTAN ON 24-HOUR AMBULATORY BLOOD PRESSURE IN HYPERTENSIVE PATIENTS

Effects of amlodipine (AML), a long-acting calcium antagonist, and losartan (LOS), an angiotensin II receptor antagonist, on 24-hr blood pressure profile were compared in 15 patients with essential hypertension. After 4 weeks of placebo period, the patients were treated with AML or LOS in a random cross-over design for 12–16 weeks each. Either drug was given once daily at 0800 and the doses were titrated so that the office blood pressure was reduced lower than 140/90 mmHg. At the end of each period, 24-hr blood pressure was monitored. Average office blood pressure was lowered from 158 ± 2/ 98 ± 2 mmHg to 134 ± 1/87 ± 1 mmHg by AML and 134 ± 2/88 ± 1 mmHg by LOS. Average 24-hr blood pressure was also reduced from 144 ± 3/ 92 ± 2 mmHg to 131 ± 2/84 ± 2 mmHg by AML and 135 ± 3/85 ± 2 mmHg by LOS. The averaged 24-hr systolic blood pressure was significantly lower in AML than in LOS (p < 0.05). Then, the 24-hr blood pressure was analyzed for four segments; morning (0530–0900 h), daytime (0930–1800 h), evening (1830–2300 h) and night (2330–0500 h). Although the daytime blood pressure was comparable between AML and LOS, systolic blood pressure in the evening and morning hours were lower in AML than in LOS (133 ± 2 vs. 138 ± 3 mmHg, p < 0.01; 129 ± 3 vs. 134 ± 4, p < 0.05). Trough to peak ratio of antihypertensive effect on systolic blood pressure was significantly greater in AML than in LOS (62 ± 5% vs. 55 ± 4%, p < 0.05). Either drug did not cause reflective increase in pulse rate over 24 hours. These results suggest that both AML and LOS are equally effective in lowering daytime blood pressure without eliciting reflex tachycardia, however, the antihypertensive effect of AML lasts longer than that of LOS. Such information seems important to achieve 24-hr blood pressure control using these drugs.     

Does Short Sleep Duration in Daily Life Affect Morning Home Blood Pressure? Evaluation in Japanese People

A short sleep duration is expected to elevate blood pressure the next morning, but no report has evaluated this in detail using home blood pressure measurement. In this study, the relation between sleep duration and morning and evening home blood pressure and heart rate during seven consecutive days was evaluated. From 630 volunteers not receiving antihypertensive agents, we selected 478 subjects (318 male, 160 female; mean age: 39.0 years) whose 2–7 days of data consisted of 7–8 hours sleep duration (proper sleep period phase; mean sleep duration: 7.3 ± 0.3 hours) and less than 7 hours (short sleep period phase; 5.7 ± 4.9 hours). In the morning, systolic blood pressure and heart rate in the short sleep period phase (117.7 ± 14.9 mmHg, 67.3 ± 9.6/min) were significantly (p < 0.01) higher than those in the proper sleep period phase (116.9 ± 14.9 mmHg, 66.5 ± 9.1/min). However, there was no difference in morning diastolic blood pressure. Although the difference in morning systolic blood pressure had disappeared by the time of measurement before going to bed, the difference in heart rate was maintained (proper sleep period phase: 70.4 ± 10.2/min, short sleep period phase: 71.7 ± 10.7/min, p < 0.01). In conclusion, days with sleep duration of less than 7 hours showed higher morning systolic blood pressure and heart rate compared with days with sleep duration between 7 and 8 hours, but no difference was found in diastolic blood pressure. Moreover, although the difference in morning systolic blood pressure had disappeared at night, the difference in heart rate was still maintained.     

Role of Renin-Angiotensin and Sympathetic Nervous Systems in the Chronic Phase of Two-kidney,One-Clip Hypertension in Rats

The purpose of the present study was to examine the role of the renin-angiotensin and the sympathetic nervous systems during the chronic phase (>16 weeks) of two-kidney, one-clip hypertension in conscious unrestrained rats. During this phase, the mean arterial pressure (MAP) (p < 0.001) and plasma angiotensin II (31.9 ± 1.5 to 125.8 ± 19.9 pg/m1, p < 0.005) were significantly increased as compared to normotensive group. Converting enzyme inhibition by captopril produced a significant decrease of MAP (181.2 ± 8.2 to 140.0 ± 5.5 mmHg, p < 0.001). This hypotensive response was similar when aprotinin (a Kallikrein inhibitor) and captopril were infused simultaneously. Alpha1-adrenergic receptor blockade by phenoxybenzamine (POB) significantly decreased but did not normalize MAP (179.8 ± 12.4 to 135.8 ± 10.4 mmHg, p < 0.001). However, when infused after POB, captopril induced a further decrease of MAP to 86.7 ± 9.4 mmHg (p < 0.001). This MAP level was not different from that found in normotensive rats after infusion of the two drugs (83.2 ± 5.3 mmHg).

These results suggest that both the renin-angiotensin system and the sympathetic nervous system, by activating peripheral α1-adrenergic receptors, maintain the high blood pressure during the chronic phase (>16 weeks) of two-kidney, one-clip hypertension in conscious rats.     

Improvement of Multiple Organ Functions in Hepatorenal Syndrome During Albumin Dialysis with the Molecular Adsorbent Recirculating System

Abstract: Recently, significant improvement of renal function and prolongation of survival were reported in hepatorenal syndrome (HRS) patients treated with the Molecular Adsorbent Recirculating System (MARS). As no impact on extrarenal organ function was documented, this trial looked into multiple organ function changes during MARS in HRS patients. Eight HRS patients (4 male, mean age 42. 1 years, range 30–58, all United Network for Organ Sharing [UNOS] status 2A) were treated intermittendly 4–14 times (total 47, mean 5.9 ± 3.4) between 4 and 8 h/single treatment. The following changes were observed pre‐ and posttreatment: bilirubin 466 ± 146 to 284 ± 134 γmol/L, creatinine 380 ± 182 to 163 ± 119 μmol/L, urea 26.4 ± 10.3 to 12.9 ± 4.9 mmol/L, plasma sodium 127.5 ± 7.7 to 137.5 ± 4.8 mmol/L (all p < 0.01). Mean arterial pressure (MAP) increased from 71.9 ± 12.8 to 95.6 ± 7.8 Torr (p < 0.001). Oliguria or anuria, present in all patients, was successfully reverted. Ascites, present in all patients, was not detectable after the treatment period. The hepatic encephalopathy grade decreased from 2.8 ± 0.8 to 0.8 ± 0.7 (p < 0.0001). Child‐Index decreased from 13.25 ± 1.3 to 9.4 ± 1.8 (p < 0.001). The hospital survival rate was 62%. One man underwent successful liver transplantation 18 months after the treatment. We conclude that MARS can improve multiple organ functions in patients with HRS.