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Ann Pharmacother. 2005 Feb 22; [Epub ahead of print]
Anasarca Edema with Amlodipine Treatment (April).
Sener D, Halil M, Yavuz BB, Cankurtaran M, Ariogul S.
Medical Faculty, Department of Internal Medicine, Hacettepe University, Ankara, Turkey.
OBJECTIVE: To report a case of anasarca edema associated with amlodipine use. CASE SUMMARY: A 77-year-old woman with essential hypertension who had not been treated with any other drug was prescribed amlodipine 10 mg/day to control her blood pressure. She developed anasarca edema soon after amlodipine treatment was initiated. Laboratory test results for possible etiologies were negative. Discontinuation of amlodipine resulted in dramatic improvement. DISCUSSION: To our knowledge, as of February 3, 2005, there have been no other reports of amlodipine-related anasarca edema in the English literature, and only one case was described in the Japanese literature. Pretibial edema is the most common adverse effect of amlodipine. Periocular and perioral edema have occurred less frequently, but anasarca edema has not emerged as a problem. An objective causality assessment revealed amlodipine to be a probable cause of anasarca edema. CONCLUSIONS: In rare instances, amlodipine may cause generalized edema, which will resolve upon discontinuation of the drug.


Expert Opin Pharmacother. 2004 Feb;5(2):459-68.
Amlodipine and atorvastatin in atherosclerosis: a review of the potential of combination therapy.
Jukema JW, van der Hoorn JW.
Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
Hypertension and hyperlipidaemia are major risk factors for the development of atherosclerosis. Calcium channel blockers (CCBs) have been used for decades and have established antihypertensive effects. Statins have been extensively used because of their potent lipid lowering properties. Amongst other factors, inflammation and oxidation are involved in enhanced progression of atherosclerosis and new lesion development. Therefore, research has been initiated focusing on the antioxidant and anti-inflammatory properties of CCBs and statins, beyond their primary effect, in order to evaluate the possible additive effects of combined treatment of CCBs with statins as antiatherosclerotic therapy. Clinical studies (e.g., the International Nifedipine Trial on Antiatherosclerotic Therapy [INTACT]) have demonstrated that the antiatherosclerotic action of CCBs is limited to the attenuation of the first stage of atherosclerogenesis (fatty streak formation or new lesion growth). The lesions that pre-existed at the start of CCB therapy did not demonstrate progression or regression on angiography. However, because the mechanisms of action of lipid-lowering drugs and CCBs, and their role in preventing the progression of atherosclerosis differ, it is conceivable to conclude that these two classes may have an additive or synergic effect, not only on new lesion formation but also on inhibiting the progression of established coronary atherosclerosis. Indeed, this combined effect of lipid-lowering therapy and CCBs on human coronary atherosclerosis has been reported in the Regression Growth Evaluation Statin Study (REGRESS) trial. This beneficial effect of combining CCBs with statins has now been replicated in transgenic atherosclerotic mice, where the combination of amlodipine and atorvastatin produced an additional 60% reduction of atherosclerosis compared with that observed with the statin alone. Serum markers of atherosclerosis and vascular integrity also improved most in the combination group. Synergistic effects of the combination of atorvastatin and amlodipine on acute nitric oxide release/endothelial function, and additive effects of the combination of amlodipine and atorvastatin in the improvement of arterial compliance in hypertensive hyperlipidaemic patients has been demonstrated. Collectively, these studies support the clinical antiatherosclerotic advantages of combination of CCBs and statins and in particular, of atorvastatin with amlodipine beyond their established antihyperlipidaemic and antihypertensive modes of action.


Adv Perit Dial. 2003;19:10-4.
Effects of antihypertensive drugs on peritoneal vessels in hypertensive dogs with mild renal insufficiency.
Ishida Y, Tomori K, Nakamoto H, Imai H, Suzuki H.
Department of Nephrology, Saitama Medical School, Saitama, Japan.
The transport capacity of any membrane depends on its surface area and permeability. In addition, peritoneal capillaries are probably barriers to solute transport. Although no decisive use of antihypertensive drugs has been reported in continuous ambulatory peritoneal dialysis (CAPD) patients with hypertension, those drugs are known to have various effects on vessels. In the present study, we used a charge-coupled-device (CCD) camera in renovascular hypertensive dogs with mild renal insufficiency to investigate the effects of various antihypertensive drugs on the peritoneal capillaries. Renovascular hypertension was induced in the dogs by placing silver clips on both renal arteries to create 90% occlusion. After confirmation of elevation of blood pressure (usually 20 days after the operation), each dog's abdomen was opened while the animal was under general anesthesia. Using a CCD camera, the diameters of the small arteries of the peritoneum were measured after 3 days' oral administration of a placebo (n = 5); or of 8 mg CS866, a selective angiotensin II type 1 receptor blocker (n = 5); or of 10 mg benazepril, an angiotensin-converting enzyme inhibitor (n = 5); or of 10 mg amlodipine, a calcium antagonist (n = 5). In dogs receiving CS866, blood pressure decreased to 128 +/- 6 mmHg from 160 +/- 6 mmHg (p < 0.01). A similar decrease in blood pressure was observed with the use of the other drugs. The diameter of the small vessels increased by 28% +/- 6% in dogs receiving CS866 and by 24% +/- 5% in dogs receiving benazepril, as compared with 3% +/- 3% in dogs receiving the calcium antagonist. These data clearly demonstrate that blockade of the renin-angiotensin system produces an increase in solute clearance in hypertensive dogs with mild renal insufficiency and that such blockade may be applicable as therapy for hypertensive patients on CAPD.


Clin Ther. 2003 May;25(5):1469-89.
Comparison of the blood pressure-lowering effects and tolerability of Losartan- and Amlodipine-based regimens in patients with isolated systolic hypertension.
Volpe M, Junren Z, Maxwell T, Rodriguez A, Gamboa R, Gomez-Fernandez P, Ortega-Gonzalez G, Matadamas N, Rodriguez F, Dass B, Kyle C, Clarysse L, Bryce A, Moreno-Heredia E, Germano G, Gilles L, Smith RD, Sanderson JE; CDSP-944 Study Group.
Universita degli Studi di Roma "La Sapienza", Rome, Italy.
BACKGROUND: Elevated systolic blood pressure is a more important risk factor for cardiovascular and renal disease than elevated diastolic blood pressure. Isolated systolic hypertension (ISH) is the predominant form of hypertension in the elderly. Effects of angiotensin II on the vascular wall and endothelium may contribute to development of ISH. OBJECTIVE: The primary objective of this study was to compare the effects on trough sitting systolic blood pressure (SiSBP) of a regimen of losartan, a selective angiotensin II-receptor antagonist, and an amlodipine-based regimen in patients with ISH. METHODS: This multicenter, prospective, randomized, double-blind, parallel-group study consisted of a 4-week placebo phase and an 18-week active-treatment phase. The losartan-based regimen consisted of losartan 50 mg, increased as needed to losartan 50 mg/hydrochlorothiazide (HCTZ) 12.5 mg at week 6 and to losartan 100 mg/HCTZ 25 mg at week 12 to achieve a target SiSBP <140 mm Hg. the amlodipine-based regimen consisted of amlodipine 5 mg, increased as needed to amlodipine 10 mg at week 6 and to amlodipine 10 mg/HCTZ 25 mg at week 12. The primary efficacy measure was change in trough SiSBP from baseline to week 18. Information on the tolerability of study treatments was collected at each visit, including the investigator's and patient's observations of clinical adverse experiences (CAEs), laboratory adverse experiences, and responses to a symptom questionnaire. RESULTS: Eight hundred fifty-seven patients (65.6% female) were randomized to treatment, 432 in the losartan group and 425 in the amlodipine group. Their mean age was 67.6 years, and they had a mean duration of hypertension of 6.7 years at baseline. The losartan and amlodipine groups (intent-to-treat population) had baseline mean SiSBP values of 171.2 and 171.9 mm Hg, respectively. At week 18 (the primary end point), the mean change from baseline in SiSBP was -27.4 mm Hg for 426 patients who received losartan and -28.1 mm Hg for 419 patients who received amlodipine (estimated least-square mean difference, 0.3 mm Hg; 95% CI, -1.4 to 2.0), indicating that losartan's effect on systolic blood pressure was noninferior to that of amlodipine. The proportion of patients who responded (SiSBP <140 mm Hg or a > or =20-mm Hg decrease in SiSBP from baseline) was comparable between groups (73.9% losartan, 75.4% amlodipine). The incidence of CAEs and drug-related CAEs was significantly greater in the amlodipine group (amlodipine, 79.8% and 43.8%, respectively; losartan, 67.8% and 25.5%; P < or = 0.001). In addition, more patients in the amlodipine group discontinued therapy due to a drug-related CAE compared with patients in the losartan group (12.9% vs 4.4%, respectively; P < or = 0.001). Lower-extremity edema was the most common drug-related CAE in the amlodipine group (24.0% amlodipine, 2.5% losartan; P < or = 0.001); dizziness was the most common drug-related CAE in the losartan group (6.0% losartan, 4.0% amlodipine). CONCLUSIONS: In these patients with ISH, losartan and amlodipine produced comparable clinically relevant reductions in SiSBP; however, losartan was better tolerated, as evidenced by fewer CAEs and discontinuations compared with amlodipine. Losartan may be considered for the initial treatment of ISH.


Am Heart J. 2003 Jun;145(6):1030-5.
Effects of amlodipine on ischemia after percutaneous transluminal coronary angioplasty: secondary results of the Coronary Angioplasty Amlodipine Restenosis (CAPARES) Study.
Jorgensen B, Thaulow E; Coronary Angioplasty Amlodipine Restenosis Study.
Department of Cardiology, Rikshospitalet, University of Oslo, Oslo, Norway.
BACKGROUND: Despite successful coronary angioplasty (PTCA), patients may have ischemia after the procedure because of the overall coronary disease and luminal renarrowing at the lesion sites. The aim of this study was to examine the effects of the calcium-channel blocker amlodipine on post-PTCA ischemia. METHODS: In a prospective, double-blind design, patients were randomized to receive 10 mg of amlodipine or placebo 2 weeks before angioplasty. Exercise tests and 48-hour ambulatory electrocardiography recordings were performed in 405 patients, 2 weeks before and 2 and 20 weeks (early and late) after PTCA. RESULTS: There were no differences in clinical and angiographic baseline characteristics between the treatment groups. Ischemia and angina were equally distributed before PTCA, and no difference in restenosis was found between the groups at follow-up. The incidence of angina was significantly lower in the amlodipine group compared with the placebo group both early and late after PTCA (P =.04 and.03). Exercise-induced ischemia was reduced by 40% (P =.009) early and 34% (P =.02) late after PTCA in the amlodipine group, and ischemia on ambulatory electrocardiography was reduced by 18% early and 28% late after PTCA compared with placebo (P =.06 and P =.009). CONCLUSION: Ischemia and angina occurred after successful PTCA and were significantly reduced by amlodipine.


Methods Find Exp Clin Pharmacol. 2003 Apr;25(3):209-13.
Effect of amlodipine and hormone replacement therapy on blood pressure and bone markers in menopause.
Zacharieva S, Shigarminova R, Nachev E, Kamenov Z, Atanassova I, Orbetzova M, Stoynev A, Doncheva N, Borissova AM.
Clinical Centre of Endocrinology and Gerontology, Medical University, Sofia, Bulgaria.
The aim of this study was to observe the effect of an 8-week treatment with amlodipine, alone or in combination with hormone replacement therapy (HRT), on blood pressure (BP), serum osteocalcin, bone-specific alkaline phosphatase (B-ALP) and urine deoxypiridinoline in postmenopausal osteoporotic women with mild-to-moderate arterial hypertension. Both conventional clinical BP measurements and ambulatory blood pressure monitoring (ABPM) were used. Twenty hypertensive menopausal women with osteoporosis were randomly divided in two groups according to the treatment regimens: amlodipine and amlodipine + HRT. Neither treatment regimen significantly changed bone formation or bone resorption markers. There were no significant differences in levels of serum and urinary calcium and phosphorous or serum cholesterol and low-density lipoprotein (LDL)-cholesterol after treatment with amlodipine alone or in combination with HRT. Triglycerides were significantly decreased and high-density lipoprotein (HDL)-cholesterol was significantly increased after amlodipine treatment. Both treatment regimens significantly decreased conventionally measured BP to a similar extent. Amlodipine given alone lowered the midline estimating statistic of rhythm (MESOR; mean 24-level) of systolic BP and induced phase advances of the circadian rhythms of systolic, diastolic and mean BP. When combined with HRT, amlodipine lowered the MESOR and reduced the amplitude of systolic BP without any phase change. In conclusion, amlodipine is effective in reducing BP in postmenopausal women. The maintenance of a normal circadian BP pattern is also influenced by supplementation with 17beta-estradiol. The 8-week treatment with amlodipine alone and in combination with HRT is not associated with a marked influence on bone metabolism.


Clin Ther. 2003 Jan;25(1):35-57.
Effect of amlodipine on systolic blood pressure.
Levine CB, Fahrbach KR, Frame D, Connelly JE, Estok RP, Stone LR, Ludensky V.
MetaWorks Inc., Medford, Massachusetts 02155, USA.
BACKGROUND: Systolic hypertension is the most common form of hypertension, particularly in people aged >60 years. Caused by decreased compliance of large arteries, systolic hypertension is an independent risk factor for cardiovascular disease. Recent studies have demonstrated that it is more important to control systolic blood pressure (SBP) than diastolic blood pressure (DBP). OBJECTIVE: The objective of this study was to perform a systematic literature review to examine the effectiveness of amlodipine in lowering SBP in a variety of patient subgroups and clinical settings. METHODS: The literature review methodology included identifying, selecting, appraising, extracting, and synthesizing primary research studies. Following an a priori protocol, published literature was searched from 1980 to 2001 using 3 electronic databases. A manual review of the reference lists of recent review articles and all accepted studies was performed. Parallel-group, randomized, controlled trials that included at least 10 adults with baseline hypertension (SBP>or=140 mm Hg, DBP>or=90 mm Hg, or both), included at least 1 arm randomized to initial treatment with amlodipine monotherapy, had a minimum treatment duration of 8 weeks, and reported baseline and end-point blood pressure were included. RESULTS: Of 696 citations identified, 85 primary studies met all inclusion criteria. Comparable treatment arms were pooled, and weightd mean SBP was calculated. In the amlodipine monotherapy arms, which included >5000 patients, SBP decreased by a mean of 17.5 mm Hg from baseline. The effect of amlodipine in reducing SBP was greater in elderly patients (age>or=60 years) and patients with author-defined isolated systolic hypertension. The dose was titrated to achieve the target blood pressure in 73 of 89 amlodipine treatment arms, whereas 16 treatment arms reported fixed doses. The median daily dose was 5 mg (range, 1.25-15 mg) in both the fixed-dose and dose-titration groups. CONCLUSIONS: In this review of the published literature, amlodipine monotherapy was effective in reducing SBP. Antihypertensive agents such as amlodipine warrant consideration for the management of patients with inadequately controlled SBP.


Am J Hypertens. 2002 Dec;15(12):1042-9.
Effects of amlodipine fosinopril combination on microalbuminuria in hypertensive type 2 diabetic patients.
Fogari R, Preti P, Zoppi A, Rinaldi A, Corradi L, Pasotti C, Poletti L, Marasi G, Derosa G, Mugellini A, Voglini C, Lazzari P.
Department of Internal Medicine and Therapeutics, Clinica Medica IRCCS Policlinico S. Matteo, University of Pavia, Pavia, Italy.
BACKGROUND: The aim of this study is to compare the long-term effect of amlodipine and fosinopril in monotherapy or in combination on urinary albumin excretion (UAE) in hypertensive diabetic patients. METHODS: We selected 453 hypertensive patients with type 2 diabetes and microalbuminuria and randomized them to amlodipine (5 to 15 mg/day), fosinopril (10 to 30 mg/day), or amlodipine plus fosinopril (5/10 to 15/30 mg/day) for a 3-month titration period. The nonresponder patients or those complaining of side effects during the titration period were discontinued (n = 144); the remaining 309 patients were enrolled in the trial and treated with the same therapy for 4 years. Every 6 months, blood pressure (BP), heart rate (HR), UAE, creatinine clearance, and glycosylated hemoglobin (HbA1c) were evaluated. RESULTS: The combination therapy was more effective in reducing BP than either drug alone at any time of the study without affecting glucose homeostasis. All three treatments provided a significant decrease in UAE during the 48-month study period. However, this effect was more pronounced and became evident earlier with fosinopril than with amlodipine monotherapy (after 3 v 18 months of therapy). In addition, the combination therapy provided a greater antialbuminuric effect than the single drugs. This could be due to the greater antihypertensive effects, although other drug-specific effects cannot be excluded. The cardiovascular outcomes were similar in the amlodipine and in the fosinopril group, but they were lower in the combination group. CONCLUSIONS: These results strengthen the rationale to use a calcium-antagonist/angiotensin converting enzyme inhibitor combination in the treatment of hypertensive patients with type 2 diabetes.


Z Kardiol. 2002 Oct;91(10):833-9.
The effect of amlodipine on exercise-induced pulmonary hypertension and right heart function in patients with chronic obstructive pulmonary disease.
Franz IW, Van Der Meyden J, Schaupp S, Tonnesmann U.
Klinik Wehrawald, BfA Schwarzenbacher Strasse 3 79682 Todtmoos, Germany.
The aim of the study was to investigate the pulmonary vasodilator effect of the dihydropyridine calcium channel blocker amlodipine in patients with clinically stable chronic obstructive pulmonary disease (COPD) and pulmonary hypertension (PH). Many patients with COPD develop chronic PH and this may predict mortality in this disorder. The treatment with calcium channel blockers is accepted as a therapeutic strategy for primary pulmonary hypertension. In twenty male patients (mean age 57+/-7 years) with clinically stable COPD and PH, we investigated whether amlodipine could effectively decrease pulmonary vascular resistance (PVR) and pulmonary arterial pressure (PAP) and improve right heart function. PAP was recorded by a balloon-tipped thermodilution catheter and cardiac output was determined in triplicate by thermodilution at rest and during exercise. In addition, blood gas values were determined from the capillary blood of the earlobe. All measurements were done under identical conditions before and after 18 days of chronic treatment: with 10 mg amlodipine once daily starting with 5mg in the first week. At a mean maximal achieved workload of 71.3+/-20 Watts, amlodipine achieved a significant reduction in PVR (-13.4%; p<0.01) and PAP (-12.1%; p<0.001) implying an improved right heart function assessed by a significant reduction in mean right atrial pressure (-20.6%; p<0.05). During the action of amlodipine there were no significant changes in pulmonary gas exchange and pulmonary capillary wedge pressure. Amlodipine given as a single daily oral dose of 10mg is a safe and effective pulmonary vasodilator in COPD patients with PH and leads to an improvement in right heart function.


Anadolu Kardiyol Derg. 2001 Mar;1(1):14-6.
The effects of amlodipine on cerebral circulatory values in patients with essential hypertension.
Alizade IG, Karayeva NT.
Department of Cardiology, Hospital of Ministry of Internal Affairs, Baku, Azerbaijan.
OBJECTIVE: This study assessed the effects of calcium channel blocker Amlodipine on the cerebral circulation in patients with essential hypertension. METHODS: Cerebral circulation in 37 patients with essential hypertension and 10 healthy subjects was assessed using rheoplethysmography. In patients with essential hypertension cerebral circulation values were also re-estimated after treatment with Amlodipine (5-10 mg daily). RESULTS: The cerebral circulatory parameters in hypertensive patients before treatment with Amlodipine were different from those in healthy persons. Amlodipine along with the reduction in systemic blood pressure caused attenuation of cerebrovascular abnormalities: decrease in spastic signs and increase in cerebral blood supply in patients with essential hypertension. CONCLUSION: Amlodipine causes reduction of cerebral vascular resistance and promotes improvement in arterial blood filling in patients with essential hypertension. These changes in cerebral circulation may be secondary to the increase of cardiac output--known effect of Amlodipine.


Ann Cardiol Angeiol (Paris). 2000 Oct;49(7):423-30.
Validation of the therapeutic role of amlodipine in 31,946 French hypertensive patients.
Dievart F, Pasquie JL, Bernaud C, Grolleau-Raoux R.
Clinique Villette, 18, rue Parmentier, 59240 Dunkerque, France.
Amlodipine, a dihydropyridine calcium channel blocker (CCB), with a long duration of action, has been the subject of numerous controlled studies which showed its effectiveness and good tolerance in arterial hypertension in once-daily doses. We report the results of a large, multicentric, French, prospective phase IV study which evaluated the effectiveness and tolerance of amlodipine administered at a rate of 5 to 10 mg in only one daily dose. We also assess the evolution of the quality of life after 12 weeks of treatment among 31,946 hypertensive patients followed up to the ambulatory stage by general practitioners. The response rate--defined as the patients having had a reduction of 10 mmHg or more diastolic blood pressure--was 88%. The blood pressure standardization--defined by a diastolic blood pressure lower than 90 mmHg--was achieved for 70% of the patients. Amlodipine was administered in stand-alone therapy in 78% of the cases. The occurrence of an undesirable event was noted in the course of treatment in 12% of the patients and justified interruption of the treatment for 3.7% of the total population. The index average of quality of life was improved by the end of the 12-week treatment. This study carried out on a significant number of hypertensive patients (n = 31,946) under real prescription conditions confirms the efficacy and good tolerance of amlodipine, as has already been demonstrated in the preliminary developmental studies.


Can J Cardiol. 2000 Jul;16 Suppl D:5D-7D.
Overview of the prospective randomized evaluation of the vascular effects of Norvasc (amlodipine) trial: PREVENT.
Mancini GB.
Vancouver Hospital and Health Sciences Centre, Vancouver, Canada.
The Prospective Randomized Evaluation of the Vascular Effects of Norvase (amlodipine) Trial (PREVENT) was designed specifically to assess if amlodipine can be shown to inhibit angiographic progression of lesions 30% or less diameter stenosis. A carotid ultrasound substudy was also undertaken. The antiatherosclerotic effects were discordant in that minor coronary lesions were not affected, whereas carotid intima-media thickness showed significantly less progression in the amlodipine-treated patients. Moreover, significant cardiac events, particularly admissions to hospital for unstable angina and intervention, were significantly reduced in the amlodipine-treated patients. This brief report provides an overview and assessment of the implications of these findings.


Arch Intern Med. 2000 Feb 14;160(3):343-7.
Sex bias and underutilization of lipid-lowering therapy in patients with coronary artery disease at academic medical centers in the United States and Canada. Prospective Randomized Evaluation of the Vascular Effects of Norvasc Trial (PREVENT) Investigators.
Miller M, Byington R, Hunninghake D, Pitt B, Furberg CD.
Department of Medicine, University of Maryland Medical Center, Baltimore, USA.
BACKGROUND: The efficacy of lipid-lowering therapy (LLT) has been well established for patients with preexisting coronary artery disease (CAD). However, limited information is available assessing the extent to which these medications are prescribed in academic medical centers. METHODS: The use of LLT for patients with CAD was prospectively evaluated in 825 men and women who were recruited from 16 academic medical centers in the United States and Canada to participate in the Prospective Evaluation of the Vascular Events of Norvasc Trial (PREVENT). The assessment of LLT use during the 3-year trial was evaluated in patients receiving amlodipine therapy and placebo; levels of low-density lipoprotein cholesterol (LDL-C) were used to assess the impact of LLT. RESULTS: Despite a baseline prevalence of LLT in 42% of men (38% in 1994), half of the patients had high levels of LDL-C (>3.36 mmol [>130 mg/dL]). During the subsequent 3 years, the prevalence of elevated LDL-C levels dropped in men (29%) but remained stagnant in women (48%). These changes were associated with increased LLT in men (55%) but not in women (35%) (P = .04). In 1994, the LDL-C target goal (<2.59 mmol/L [<100 mg/dL]) was attained in 17% of men and 6% of women (P = .006). At study completion in 1997, the LDL-C target goal was achieved in 31% of men and only 12% of women (P = .001). CONCLUSIONS: This study highlights the relatively low treatment rates of hyperlipidemia among patients with CAD overall and women in particular who were participating in a clinical trial at academic medical centers in the United States and Canada. Because LLT has been proven to reduce future cardiovascular events, these results suggest that more intensive efforts should be promoted in order to maximize CAD reduction.


J Cardiovasc Pharmacol. 1999;33 Suppl 2:S17-22.
Atheroprotection with amlodipine: cells to lesions and the PREVENT trial. Prospective Randomized Evaluation of the Vascular Effects of Norvasc Trial.
Tulenko TN, Brown J, Laury-Kleintop L, Khan M, Walter MF, Mason RP.
Department of Physiology, Biochemistry and Surgery, Allegheny University of the Health Sciences, Philadelphia, Pennsylvania 19129, USA.
Oxidized lipid and calcium regulatory abnormalities appear to play important roles in early atherogenesis secondary to cholesterol enrichment of the cell membrane in endothelial and arterial smooth muscle cells (SMCs). However, the link between the two is poorly understood. The findings reviewed here demonstrate that amlodipine has membrane-modifying and antioxidant actions at the cell membrane level in addition to its classical calcium channel blocking properties. These multiple pharmacologic actions may explain the cellular mechanisms of the atheroprotective effects of amlodipine in spontaneous atherogenesis and in accelerated atherosclerotic syndromes. Recent animal model studies have demonstrated that amlodipine inhibits the progression of atherosclerotic lesions and protects against restenosis after angioplasty. Amlodipine inhibits the cholesterol-induced increase in calcium permeability in SMCs, and has been shown to repair abnormalities in SMC membrane structure. Recent data have also demonstrated that amlodipine has a marked antioxidant action in membrane bilayers enriched with polyunsaturated fatty acids. However, these findings have been in animal models only; the efficacy of amlodipine in atheroprotection in humans cannot be predicted. The PREVENT trial has therefore been launched to examine the atheroprotective potential of amlodipine in spontaneous lesion development in humans with ischemic heart disease and in the prevention of restenosis after angioplasty.


Rev Med Panama. 1993 Sep;18(3):233-7.
Experience with amlodipine (Norvasc) in the management of arterial hypertension.
Rodriguez N, Dominguez B.
Servicio de Medicina Interna y Cardiologia, Complejo Hospitalario Dr. Arnulfo Arias M., Caja de Seguro Social.
The authors report the results of therapy with amlodipine in 20 patients with mild or moderate hypertension (diastolic pressure between 95 and 115 mmHg). Amlodopine was administered in a dose of either 5 or 10 mg once a day for 12 weeks. None of the patients had a history of congestive heart failure. Eleven patients were men between 27 and 89 years of age (average age was 52.6 years). There was a significant decrease in systolic blood pressure (from 161 to 141 mm Hg or -12.4%) and in diastolic blood pressure (from 103 to 86 mm Hg or -16.5%). Heart rate remained between 78 and 77 beats per minute. Only one patient experienced palpitations and two complained of mild, transient giddiness while on this therapy.


MMW Fortschr Med. 2004 Dec 9;146:115-21.
[Safety and antihypertensive efficacy of the dihydropyridine calcium antagonist Amlodipine besylate--results from an observational study in 9,672 patients] [Article in German]
Keck M, Sauerbrey-Wullkopf N, Regourd E, Clemens A.
Fachklinik fur Herz- und Kreislaufkrankheiten, Drei-Burgen-Klinik, Bad Munster am Stein.
OBJECTIVES: This observational study investigated prescription behavior and the efficacy and safety of Amlodipine besylate in hypertensive patients. METHODS: 9,672 hypertensive patients were treated with Amlodipine besylate 5-10 mg/day for 12 weeks. At the end of the observation period, the participating physicians were asked to give their subjective evaluation of the efficacy and safety of treatment with Amlodipine besylate as well as their therapeutic considerations regarding the use of Amlodipine besylate. RESULTS: 55.2% of the patients received Amlodipine besylate in combination with other antihypertensive agents. The mean baseline blood pressure was 168.0/96.7 mmHg and the mean blood pressure reduction achieved at the end of the observation period was -28.5/-14.5 mmHg. In 80.3% of the total population, a reduction to diastolic blood pressure values of < 90 mmHg was achieved. A reduction to systolic blood pressure values of < 140 mmHg was obtained in 41.6% of the patients. Adverse events were reported by only 1.2% of the patients. For the vast majority of the patients, efficacy (96.6%) and safety (98.9%) were rated "very good" or "good" by their physicians. 24-hour efficacy with once daily dosing was given as the most important argument for using Amlodipine besylate. CONCLUSION: The observation study confirmsthat Amlodipine besylate is an effective and safe antihypertensive drug both in mono and combination therapy.



 
 
- ACARBOSE
- ACCUPRIL-ACCUPRO
- ADALAT
- ADAMANTAN
- ALENDRONATE
- MANTADINE
- AMARYL
- AMLODIPINE
- ARAVA
- ARICEPT
- ATAMET
- ATORVASTATIN
- AVANDIA
- AZITHROMYCIN
- BENAZEPRIL
- BEXTRA
- CARBIDOPA
- CIPRO
- CIPROBAY
- CIPROFLOXACIN
- CLOPIDOGREL
- DEPRENYL
- DONEPEZIL
- DOXYCYCLINE
- ECDYSTEN
- ECDYSTERONE
- ELDEPRYL
- EVISTA
- FARESTON
- FAT BURNER
- FINASTERIDE
- FLOMAX
- FLUVASTATIN
- FOLIC ACID
- FOSAMAX
- GEROVITAL
- GLIMEPERIDE
- GLUCOBAY
- GLUCOPHAGE
- HUMALOG
- OMNIC
- IODIDE
- ISOPRINOSINE
- LAMISIL
- LARODOPA
- LESCOL
- LEUZEA
- LEVODOPA
- LIPITOR
- LIPOIC ACID
- LOTENSIN
- LOVASTATIN
- MADOPAR
- MELOXICAM
- METFORMIN
- MEVACOR
- MILGAMMA
- MIRAPEX
- MOBIC-MOVALIS
- NOLVADEX
- NOOTROPYL
- NORVASC
- ORLISTAT
- PIRACETAM
- PLAVIX
- PRAMIPEXOLE
- PRECOSE
- PROSCAR
- QUINAPRIL
- RALOXIFENE
- RHAPONTICUM
- RHODIOLA
- ROSIGLITAZONE
- SELEGILINE
- SELENIUM
- SIMVASTATIN
- SINEMET
- SUMAMED
- TAMOXIFEN
- TAMSULOSIN
- TERBINAFINE
- TOREMIFENE
- VALDECOXIB
- VINPOCETINE
- VIREGYT
- XENICAL
- ZITHROMAX
- ZOCOR



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