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Dive into the research topics where James L. Pool is active.

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Featured researches published by James L. Pool.


American Journal of Cardiology | 1994

Expanded Clinical Evaluation of Lovastatin (EXCEL) study results: two-year efficacy and safety follow-up.

Reagan H. Bradford; Charles L. Shear; Athanassios N. Chremos; Carlos A. Dujovne; Frank A. Franklin; Ruth B. Grillo; James E. Higgins; Alexandra Langendorfer; David T. Nash; James L. Pool; Harold W. Schnaper

The Expanded Clinical Evaluation of Lovastatin study, a randomized, double-blind, placebo- and diet-controlled multicenter trial, evaluated the efficacy and tolerability of lovastatin over 48 weeks in 8,245 patients with moderately severe hypercholesterolemia. During year 1 of follow-up of the full cohort, lovastatin at 20 or 40 mg/day, or 20 or 40 mg twice daily, produced dose-dependent decreases in low-density lipoprotein (LDL) cholesterol (24% to 40%) and triglyceride levels (10% to 19%), and increases in high-density lipoprotein (HDL) cholesterol (6.6% to 9.5%). In all, 977 patients continued their original blinded treatment for an additional year. In year 2, the LDL cholesterol response to lovastatin was maintained, the triglyceride reductions were somewhat less, and the increases in HDL cholesterol were moderately greater than in year 1. Successive transaminase elevations > 3 times the upper limit of normal were observed in only 1 patient in year 2, yielding a cumulative 2-year incidence of from 0.1% (placebo or lovastatin 20 mg/day) to 1.9% (lovastatin 80 mg/day). Myopathy occurred in only 1 patient during year 2, and over the 2-year study was observed rarely and only at lovastatin dosages of 40 and 80 mg/day. This study indicates that lovastatin maintains its efficacy over long-term follow-up, particularly in effectively lowering LDL cholesterol, is generally well tolerated, and has a favorable safety profile.


American Journal of Hypertension | 1998

Dose-Related Antihypertensive Effects of Irbesartan in Patients With Mild-to-Moderate Hypertension

James L. Pool; Robert Guthrie; Thomas Littlejohn; Philip Raskin; Alexander M.M. Shephard; Michael A. Weber; Matthew R. Weir; Thomas W. Wilson; James R. Wright; Kenneth Kassler-Taub; Richard A. Reeves

Two multicenter, double-blind, placebo-controlled, parallel group studies were conducted to evaluate the efficacy, safety, pharmacokinetics, and pharmacodynamics of the angiotensin II receptor (AT1 subtype) antagonist irbesartan. The effect of irbesartan withdrawal and the effect of adding hydrochlorothiazide (HCTZ) to irbesartan were also assessed. After a placebo lead-in phase, all patients were randomized to 8 weeks of double-blind therapy with either placebo (n = 158) or irbesartan at doses of 1, 5, 10, 25, 50, 100, 200, or 300 mg (n = 731 total) orally once daily. Irbesartan reduced blood pressure in a dose-related manner. Reductions from baseline in trough seated diastolic blood pressure ranged from 7.5 mm Hg for 50 mg irbesartan to 11.6 mm Hg for 300 mg irbesartan. At week 8, statistically significant reductions over placebo were observed in trough seated blood pressure with all irbesartan doses > or = 50 mg. These reductions reached statistical significance versus placebo within 2 weeks with 100, 200, and 300 mg irbesartan. Plasma irbesartan concentrations correlated with dose. Angiotensin II and aldosterone levels generally showed dose-related changes, consistent with AT1 receptor blockade. In patients not controlled at 8 weeks, the addition of 12.5 mg HCTZ resulted in further dose-related reductions in blood pressure. Irbesartan demonstrated a placebo-like safety profile and no dose-related toxicity. Irbesartan, administered alone or in combination with HCTZ, was well tolerated. Withdrawal of irbesartan did not result in rebound hypertension or adverse events. Thus, once-daily irbesartan is both an effective and safe antihypertensive agent for the treatment of mild-to-moderate hypertension.


The American Journal of Medicine | 1991

Expanded clinical evaluation of lovastatin (EXCEL) study results: IV. Additional perspectives on the tolerability of lovastatin

Carlos A. Dujovne; A.N. Chremos; James L. Pool; Harold W. Schnaper; Reagan H. Bradford; Charles L. Shear; James E. Higgins; Maria Downton; Frank A. Franklin; David T. Nash; A. Lawrence Gould; Alexandra Langendorfer

This randomized, double-blind, multicenter, diet-and-placebo-controlled study was designed to clarify the dose-response relationship of lovastatin therapy to lipid-modifying efficacy and drug-related adverse events. Exclusion criteria were minimized so that study patients were representative of the majority of patients with moderate hypercholesterolemia seen in medical practice. After 6 weeks on the American Heart Association Step 1 Diet, a total of 8,245 patients were randomly assigned to 48 weeks of treatment with diet and placebo or lovastatin at dosages of 20 or 40 mg once a day or 20 or 40 mg twice a day. All adverse events were monitored, with particular attention to evaluation of liver and muscle. Liver transaminase elevations suggestive of possible hepatotoxicity, defined as successive elevations in either aspartate transaminase or alanine aminotransferase greater than 3 times the upper limit of normal, occurred in equal numbers of placebo and lovastatin 20 mg/day treated patients (0.1%). The frequencies were higher in lovastatin 40 mg/day and 80 mg/day patient groups (0.9 and 1.5%, respectively). No patient was diagnosed as having clinically symptomatic hepatic dysfunction. Creatinine kinase (CK) elevations above the upper limit of normal occurred frequently in placebo- (29%), as well as lovastatin-treated patients (29-35%), and muscle symptoms were reported with similar frequency in all groups (7-9%). The combination of muscle symptoms with marked CK elevations (greater than 10 times the upper limit of normal) was seen in only five patients: one in a 40 mg/day dose group and four in the 80 mg/day dose group. No patient developed rhabdomyolysis. The incidence of clinical and laboratory adverse events requiring discontinuation was 6% for the placebo group and from 7% (20 mg/day) to 9% (80 mg/day) for lovastatin treatment groups. No new types of adverse experiences related to lovastatin treatment were reported. Lovastatin, as an adjunct to diet for the reduction of elevated LDL cholesterol, was generally very well tolerated.


Journal of Vascular Surgery | 1988

The impact of renal fusion and ectopia on aortic surgery

E. Stanley Crawford; Joseph S. Coselli; Hazim J. Safi; Tomas D. Martin; James L. Pool

This article is concerned with observations in 17 patients with renal fusion and ectopic abnormalities: horseshoe kidney in 13 patients, crossed ectopia with fusion in two, pancake kidney in one, and pelvic kidney in one. Three patients had occlusive disease, one may have had renal artery occlusion, and 13 had aneurysms--three thoracoabdominal and 10 infrarenal. Rupture of aneurysm had occurred in one patient at each level and six patients had had one or more previous attempts at aneurysmal removal. Diagnosis and evaluation were made with the aid of intravenous pyelography, retrograde pyelography, CT scanning, and at operation (three patients). Three patients had two normally located right and left renal arteries. Twelve patients had one to three additional aberrant arteries arising from the aorta and iliac arteries. One patients renal blood supply arose from multiple aberrant arteries. Ureters crossed the midline in two patients. Treatment of occlusive disease consisted of endarterectomy in one patient and percutaneous transluminal angioplasty in two. Aneurysms were treated by graft replacement with retroperitoneal exposure in seven patients and transabdominal exposure in six. One patient was treated medically. Renal isthmus division was employed in only two patients and involved accessory arteries were reattached to the grafts in all cases. Death from myocardial infarction occurred in two patients (12%). Eleven patients subjected to operation were alive 6 months to 14 years later.


Journal of Human Hypertension | 1999

Dose-response efficacy of valsartan, a new angiotensin II receptor blocker

James L. Pool; Glazer R; Chiang Yt; Gatlin M

Objective: To study the efficacy and tolerability of a range of valsartan doses in patients with mild-to-moderate hypertension. Design: 122 adult out-patients were randomised in equal numbers to receive valsartan 10 mg, 40 mg, 80 mg, 160 mg or placebo once daily (OD) for 4 weeks in this multicentre, double-blind, fixed-dose, parallel trial. Patients were assessed at 0, 2 and 4 weeks. Main outcome measures: The primary efficacy variable was change from baseline in trough mean supine diastolic blood pressure (MSuDBP). Other variables included change from baseline in trough mean supine systolic blood pressure (MSuSBP), responder rates and trough/peak ratio. Results: All treatments significantly reduced MSuDBP and MSuSBP at 4-week end-point compared to baseline (P < 0.001). the magnitude of blood pressure lowering was greater with increasing doses of valsartan (least square mean change from baseline for placebo, valsartan 10 mg, 40 mg, 80 mg, 160 mg respectively: msudbp −4.4 mm hg, −4.9 mm hg, −6.5 mm hg, −8.2 mm hg, −9.1 mm hg; msusbp −1.3 mm hg, −3.6 mm hg, −7.0 mm hg, −11.1 mm hg, −11.9 mm hg). a fitted quadratic curve, to predict relationship between dose and change from baseline in trough msudbp, indicated a positive dose response. responder rates were 16%, 24%, 33%, 46%, 54% for placebo, valsartan 10 mg, 40 mg, 80 mg, 160 mg respectively, which also indicated a positive dose response in the dose range of 10 mg to 160 mg. greater than 50% of the antihypertensive effect measured at peak persisted at trough for each of the four active treatment groups, confirming efficacy over a 24-h period. no dose-related adverse experiences were observed, with overall incidence (regardless of relationship to trial medication) of 44% with placebo and 44%, 36%, 22%, 21% for valsartan 10 mg, 40 mg, 80 mg, 160 mg respectively. the most common adverse experience reported was headache which occurred most frequently with placebo (12%). no trial drug-related cough was observed. treatment with valsartan did not produce clinically significant orthostatic changes in diastolic or systolic blood pressure. one case of symptomatic orthostatic hypotension was observed on placebo. Conclusions: The results of this trial show valsartan to effectively lower blood pressure in patients with mild-to-moderate hypertension, and demonstrate that the reduction in blood pressure increases with increasing dose levels.


The American Journal of Medicine | 1987

Mitral valve prolapse with symptoms of beta-adrenergic hypersensitivity: Beta2-adrenergic receptor supercoupling with desensitization on isoproterenol exposure☆

Albert O. Davies; Adolph Mares; James L. Pool; Addison A. Taylor

Autonomic nervous system dysfunction has recently been identified in a subset of patients with mitral valve prolapse. These autonomic nervous system abnormalities may correspond, in part, to biochemical alterations in beta-adrenergic receptors. Nine women with mitral valve prolapse and symptoms and signs of beta-adrenergic hypersensitivity and seven normal volunteer women were studied. Quiet standing (five minutes) increased both heart rate and plasma norepinephrine (p less than 0.05) in symptomatic patients with mitral valve prolapse compared with normal subjects. The dose of isoproterenol required either to increase heart rate 25 beats/minute (0.5 +/- 0.3 microgram versus 1.0 +/- 0.3 microgram) or to decrease mean arterial pressure 20 mm Hg (11.1 +/- 4.8 versus 78.2 +/- 25.2 micrograms) was significantly less in the patients with mitral valve prolapse than in the volunteers. Symptomatic patients with mitral valve prolapse were desensitized by a four-hour isoproterenol infusion, whereas sensitivity in normal control subjects did not change. In the patients with mitral valve prolapse, baseline beta-adrenergic receptor coupling was elevated compared with that in control subjects (220 +/- 7 versus 81 +/- 2; p less than 0.001). Isoproterenol infusion induced uncoupling in these patients (KL/KH = 35 +/- 3, p less than 0.05) but did not alter coupling in normal volunteers. This study demonstrates physiologic and pharmacologic beta-adrenergic hypersensitivity in vivo directly corresponding to biochemical supercoupling in a subset of patients with mitral valve prolapse.


Clinical Therapeutics | 1997

Valsartan, a new angiotensin II antagonist: antihypertensive effects over 24 hours

Joel M. Neutel; Michael A. Weber; James L. Pool; David Woodruff Smith; Sheila Fitzsimmons; Yanntong Chiang; Majorie Gatlin

This study was done to assess the antihypertensive efficacy of once-daily valsartan 20 mg, 80 mg, 160 mg, and 320 mg over 24 hours using ambulatory blood pressure monitoring (ABPM). A total of 217 adult outpatients with uncomplicated essential hypertension (office mean sitting diastolic blood pressure [DBP] of > or = 95 to < or = 115 mm Hg) participated in this multicenter, double-masked, placebo-controlled study. Patients were randomized to receive valsartan 20 mg, 80 mg, 160 mg, 320 mg, or placebo for 8 weeks. Twenty-four-hour ABPM was done at baseline and after 8 weeks of treatment. All valsartan doses produced significant decreases in average ambulatory systolic blood pressure (SBP) and DBP over 24 hours compared with placebo. A trend to greater reductions compared with placebo was observed for doses of valsartan 80 mg and greater (80 mg, -6.61 mm Hg DBP, -11.04 mm Hg SBP; 160 mg, -5.51 mm Hg DBP, -10.61 mm Hg SBP; 320 mg, -8.44 mm Hg DBP, -14.34 mm Hg SBP) compared with valsartan 20 mg (-3.52 mm Hg DBP, -5.92 mm Hg SBP). Valsartan produced consistent reductions compared with placebo during both day (> 6 AM to < or = 10 PM) and night (> 10 PM to < or = 6 AM). However, in all groups, the circadian pattern of blood pressure over 24 hours was preserved and was similar to that observed at baseline (but shifted into the normotensive range in a parallel fashion). The data show that single daily doses of valsartan 80 mg and greater provide effective control of both DBP and SBP over a 24-hour period without loss of diurnal variation.


The American Journal of Medicine | 1991

Expanded clinical evaluation of lovastatin (EXCEL) study results: III. Efficacy in modifying lipoproteins and implications for managing patients with moderate hypercholesterolemia

Reagan H. Bradford; Charles L. Shear; A.N. Chremos; Frank A. Franklin; David T. Nash; Dennis P. Hurley; Carlos A. Dujovne; James L. Pool; Harold W. Schnaper; Michael Hesney; Alexandra Langendorfer

In the multicenter, double-blind EXCEL (Expanded Clinical Evaluation of Lovastatin) study the efficacy of lovastatin in modifying plasma lipids and lipoproteins in 8,245 participants with moderate primary hypercholesterolemia was evaluated. Patients were randomly assigned to 48 weeks of treatment with diet and placebo or diet and lovastatin 20 or 40 mg once a day, or 20 or 40 mg twice a day. At all of these dosages, lovastatin produced substantial dose-dependent reductions in low-density-lipoprotein (LDL)-cholesterol levels, averaging 24% (20 mg/day) to 40% (80 mg/day). The magnitude of the effect of this lipoprotein was further reflected by the percentage of patients who achieved National Cholesterol Education Program (NCEP) goals. In the absence of coronary artery disease (CAD) or two other CAD risk factors, the LDL-cholesterol goal of 4.14 mmol/L (160 mg/dL) was attained by 22% of patients in the placebo group and between 81% (20 mg/day) and 96% (80 mg/day) of those treated with lovastatin. For those with CAD or at least two other CAD risk factors, the LDL-cholesterol goal of 3.36 mmol/L (130 mg/dL) was attained by 4% of placebo patients and between 38% (20 mg/day) and 83% (80 mg/day) of those treated with lovastatin. Lovastatin also increased high-density-lipoprotein cholesterol (7-10%) and decreased triglycerides (10-19%) in a dose-dependent manner. Thus, when used as an adjunct to a prudent diet, lovastatin produces favorable changes in the entire lipoprotein profile and is a highly effective agent for managing patients with primary hypercholesterolemia.


American Heart Journal | 1991

Effects of doxazosin on serum lipids: A review of the clinical data and molecular basis for altered lipid metabolism

James L. Pool

The goal of antihypertensive treatment must be not only the reduction of high blood pressure, but also the effective management of elevated cholesterol levels and other risk factors of coronary heart disease (CHD). In controlled clinical trials, doxazosin has been shown to have antihypertensive efficacy comparable with other classes of antihypertensive agents and to lower the levels of total cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides while increasing the levels of high-density lipoprotein cholesterol. Doxazosin appears to inhibit the development of CHD on two fronts. First, doxazosin binds to the alpha 1-adrenoreceptor and inhibits the receptor-mediated responses to epinephrine and norepinephrine. Second, doxazosin has direct and indirect effects on lipid metabolism by increasing LDL receptor activity, decreasing intracellular LDL synthesis, reducing the synthesis and secretion of very low-density lipoprotein cholesterol, and stimulating lipoprotein lipase activity. Doxazosin may also inhibit platelet aggregation. Long-term studies will determine how these actions translate into reductions in the morbidity and mortality rates of CHD. First-year results from the Treatment of Mild Hypertension Study (TOMHS) have demonstrated expected reductions in blood pressure for all antihypertensive agents studied. The lipid changes have varied with the type of antihypertensive treatment and have been favorable for doxazosin.


American Journal of Cardiology | 1987

Plasma lipid lowering effects of doxazosin, a new selective alpha1 adrenergic inhibitor for systemic hypertension

James L. Pool

Hypertension and hypercholesterolemia are 2 major risk factors for atherosclerotic coronary artery disease (CAD). Elevations of both blood pressure and serum cholesterol levels should be reduced to control CAD risk. Doxazosin is a once-daily, long-acting, selective alpha 1-adrenergic inhibitor that is effective for the treatment of essential hypertension. During controlled studies of doxazosins antihypertensive efficacy, 3 serum lipid parameters were measured; total cholesterol, total triglyceride and high density lipoprotein (HDL) cholesterol. In 10- to 12-week placebo-controlled studies, 142 doxazosin-treated patients were compared with 155 placebo-controlled subjects. Doxazosin patients had an increase of 8.9% in the HDL/total cholesterol ratio (p less than 0.05), whereas total cholesterol, HDL cholesterol and triglyceride levels were not significantly different between the 2 study groups. During a 52-week comparison of doxazosin versus atenolol, doxazosin treatment was associated with a significant decrease in total triglyceride levels (5%; p less than 0.001) and increases in HDL cholesterol levels (3.9%; p less than 0.01) and HDL/total cholesterol ratio (5.4%; p less than 0.0001). Doxazosin is an effective antihypertensive agent that has a favorable impact on serum lipid levels, thereby promoting a beneficial effect on 2 major CAD risk factors.

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Addison A. Taylor

Baylor College of Medicine

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Edward B. Nelson

Baylor College of Medicine

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Frank A. Franklin

University of Alabama at Birmingham

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Harold W. Schnaper

University of Alabama at Birmingham

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Jerry R. Mitchell

Baylor College of Medicine

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Reagan H. Bradford

Oklahoma Medical Research Foundation

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David T. Nash

State University of New York System

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