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Biomedical subjects

J A Herd

Publications and source records attributed to J A Herd.

At least 19 recordsLinked to original sources
PubMed1999

A new pharmacological treatment for intermittent claudication: results of a randomized, multicenter trial.

BACKGROUND: Effective medication is limited for the relief of intermittent claudication, a common manifestation of arterial occlusive disease. Cilostazol is a potent inhibitor of platelet aggregation with vasodilation effects. OBJECTIVE: To evaluate the safety and efficacy of cilostazol for the treatment of intermittent claudication. METHODS: Thirty-seven outpatient vascular medicine clinics at regional tertiary and university hospitals in the United States participated in this multicenter, randomized, double-blind, placebo-controlled, parallel trial. Of the 663 screened volunteer patients with leg discomfort, a total of 516 men and women 40 years or older with a diagnosis of moderately severe chronic, stable, symptomatic intermittent claudication were randomized to receive cilostazol, 100 mg, cilostazol, 50 mg, or placebo twice a day orally for 24 weeks. Outcome measures included pain-free and maximal walking distances via treadmill testing, patient-based quality-of-life measures, global assessments by patient and physician, and cardiovascular morbidity and all-cause mortality survival analysis. RESULTS: The clinical and statistical superiority of active treatment over placebo was evident as early as week 4, with continued improvement at all subsequent time points. After 24 weeks, patients who received cilostazol, 100 mg, twice a day had a 51% geometric mean improvement in maximal walking distance (P<.001 vs placebo); those who received cilostazol, 50 mg, twice a day had a 38% geometric mean improvement in maximal walking distance (P<.001 vs placebo). These percentages translate into an arithmetic mean increase in distance walked, from 129.7 m at baseline to 258.8 m at week 24 for the cilostazol, 100 mg, group, and from 131.5 to 198.8 m for the cilostazol, 50 mg, group. Geometric mean change for pain-free walking distance increased by 59% (P<.001) and 48% (P<.001), respectively, in the cilostazol, 100 mg, and cilostazol, 50 mg, groups. These results were corroborated by the results of subjective quality-of-life assessments, functional status, and global evaluations. Headache, abnormal stool samples or diarrhea, dizziness, and palpitations were the most commonly reported potentially drug-related adverse events and were self-limited. A total of 75 patients (14.5%) withdrew because of any adverse event, which was equally distributed between all 3 treatment groups. Similarly, there were no differences between groups in the incidence of combined cardiovascular morbidity or all-cause mortality. CONCLUSION: Compared with placebo, long-term use of cilostazol, 100 mg or 50 mg, twice a day significantly improves walking distances in patients with intermittent claudication.

Adult↗
PubMed1999

Aggressive cholesterol lowering delays saphenous vein graft atherosclerosis in women, the elderly, and patients with associated risk factors. NHLBI post coronary artery bypass graft clinical trial. Post CABG Trial Investigators.

BACKGROUND: The NHLBI Post Coronary Artery Bypass Graft trial (Post CABG) showed that aggressive compared with moderate lowering of low-density lipoprotein-cholesterol (LDL-C) decreased obstructive changes in saphenous vein grafts (SVGs) by 31%.1 Using lovastatin and cholestyramine when necessary, the annually determined mean LDL-C level ranged from 93 to 97 mg/dL in aggressively treated patients and from 132 to 136 mg/dL in the others (P<0.001). METHODS AND RESULTS: The present study evaluated the treatment effect in subgroups defined by age, gender, and selected coronary heart disease (CHD) risk factors, ie, smoking, hypertension, diabetes mellitus, high-density lipoprotein cholesterol (HDL-C) <35 mg/dL, and triglyceride serum levels >/=200 mg/dL at baseline. As evidenced by similar odds ratio estimates of progression (lumen diameter decrease >/=0.6 mm) and lack of interactions with treatment, a similar beneficial effect of aggressive lowering was observed in elderly and young patients, in women and men, in patients with and without smoking, hypertension, or diabetes mellitus, and those with and without borderline high-risk triglyceride serum levels. The change in minimum lumen diameter was in the same direction for all subgroup categories, without significant interactions with treatment. CONCLUSIONS: Aggressive LDL-C lowering delays progression of atherosclerosis in SVGs irrespective of gender, age, and certain risk factors for CHD.

Age Factors↗
PubMed1999

Influence of low HDL on progression of coronary artery disease and response to fluvastatin therapy.

BACKGROUND--Patients with coronary artery disease (CAD) commonly have low HDL cholesterol (HDL-C) and mildly elevated LDL cholesterol (LDL-C), leading to uncertainty as to whether the appropriate goal of therapy should be lowering LDL-C or raising HDL-C. METHODS AND RESULTS--Patients in the Lipoprotein and Coronary Atherosclerosis Study (LCAS) had mildly to moderately elevated LDL-C; many also had low HDL-C, providing an opportunity to compare angiographic progression and the benefits of the HMG-CoA reductase inhibitor fluvastatin in patients with low versus patients with higher HDL-C. Of the 339 patients with biochemical and angiographic data, 68 had baseline HDL-C <0.91 mmol/L (35 mg/dL), mean 0.82+/-0.06 mmol/L (31. 7+/-2.2 mg/dL), versus 1.23+/-0.29 mmol/L (47.4+/-11.2 mg/dL) in patients with baseline HDL-C >/=0.91 mmol/L. Among patients on placebo, those with low HDL-C had significantly more angiographic progression than those with higher HDL-C. Fluvastatin significantly reduced progression among low-HDL-C patients: 0.065+/-0.036 mm versus 0.274+/-0.045 mm in placebo patients (P=0.0004); respective minimum lumen diameter decreases among higher-HDL-C patients were 0. 036+/-0.021 mm and 0.083+/-0.019 mm (P=0.09). The treatment effect of fluvastatin on minimum lumen diameter change was significantly greater among low-HDL-C patients than among higher-HDL-C patients (P=0.01); among low-HDL-C patients, fluvastatin patients had improved event-free survival compared with placebo patients. CONCLUSIONS--Although the predominant lipid-modifying effect of fluvastatin is to decrease LDL-C, patients with low HDL-C received the greatest angiographic and clinical benefit.

Adult↗
PubMed1999

Rationale and design of the Arterial Disease Multiple Intervention Trial (ADMIT) pilot study.

The primary objectives of the pilot study were to: (1) evaluate the feasibility of recruiting patients with peripheral arterial disease (PAD); (2) measure the efficacy and safety of high-density lipoprotein (HDL)-raising treatment, low-density lipoprotein (LDL)-lowering therapy, antioxidant therapy, antithrombotic therapy, and their combinations; and (3) assess adherence to a complex multiple drug regimen. Secondary objectives included measurement of the effect of the interventions on prespecified biochemical markers, maintenance of therapy masking (in particular with niacin), and measurement of the intervention's impact on functional status and on quality of life. To date, no secondary prevention trial has been conducted specifically among patients with PAD. Intermittent claudication affects about 0.5% to 1.0% of persons aged >35 years. There is a striking increase in incidence of PAD with age, particularly among those aged >50 years in both sexes, although men are twice as likely as women to develop PAD. The Arterial Disease Multiple Intervention Trial was a double-blind randomized pilot trial of 468 participants with documented PAD. A 2 x 2 x 2 factorial design was used to evaluate the effect of 3 interventions. The pilot incorporated several major novel design features: first, the use of a simple noninvasive method (measurement of ankle brachial index) to identify a population with either symptomatic or asymptomatic PAD; and second, a lipid modifying strategy to increase HDL with nicotinic acid in the intervention group while lowering LDL levels equally with an hydroxymethylglutaryl-coenzyme A reductase inhibitor as needed in the intervention and control group. Two other arms, the antioxidant arm (consisting of beta-carotene and vitamins E and C) and the antithrombotic arm (using warfarin) were also added. Adherence to therapy was measured by pill count, and success in treatment was measured by the proportion of values in target range for HDL, LDL, and the international normalized ratio.

Adult↗
PubMed1999

Change in estimated cerebral perfusion pressure after treatment with nimodipine or magnesium sulfate in patients with preeclampsia.

OBJECTIVE: Data are accumulating to suggest that cerebral perfusion pressure may be either abnormally high or low in preeclampsia and eclampsia. Little is known of the cerebral perfusion pressure effects of magnesium sulfate or nimodipine. Our objective in this study was to compare the change in cerebral perfusion pressure in patients with severe preeclampsia randomly selected to receive nimodipine or magnesium sulfate. STUDY DESIGN: Patients with severe preeclampsia were randomly selected to receive magnesium sulfate (6 g bolus and 2 g/hr intravenous infusion) or nimodipine (60 mg taken orally every 4 hours). Transcranial Doppler ultrasonography was used to measure flow velocities in the right and left middle cerebral arteries, and the results were averaged. Measurements were obtained before treatment (baseline) and 30 minutes after the magnesium sulfate bolus was completely infused or 30 minutes after the nimodipine was ingested. Studies were performed before any other intervention. The person performing the ultrasonography was unaware of the patient's group assignment. Estimated cerebral perfusion pressure was calculated with the following formula: Estimated cerebral perfusion pressure = Velocity(mean) x [(Blood pressure(mean ) - Blood pressure(diastolic ))/(Velocity(mean) - Velocity(diastolic ))]. The difference between estimated cerebral perfusion pressure at baseline and after treatment was compared between the 2 groups by means of the Mann-Whitney rank sum test. RESULTS: Nine patients were randomly selected to receive nimodipine and 12 to receive magnesium sulfate. Patient demographics and severity of condition were not significantly different between the 2 groups. The change in estimated cerebral perfusion pressure was significantly different between the groups. Estimated cerebral perfusion pressure increased after nimodipine use and decreased after magnesium sulfate use. CONCLUSION: Shortly after administration to patients with severe preeclampsia, nimodipine resulted in increased cerebral perfusion pressure in comparison with magnesium sulfate.

Adult↗
PubMed1999

Lipoprotein lipase gene mutations, plasma lipid levels, progression/regression of coronary atherosclerosis, response to therapy, and future clinical events. Lipoproteins and Coronary Atherosclerosis Study.

Mutations in human lipoprotein lipase (LPL) gene are potential risk factors for susceptibility to coronary artery disease (CAD). The objectives of this study were to determine the influence LPL mutations Asn291Ser and Ser447Ter on plasma lipid levels, regression and progression of CAD, clinical events rate, and response to fluvastatin therapy in the Lipoprotein and Coronary Atherosclerosis Study (LCAS) population. LCAS is a double blind, randomized, placebo-controlled study designed to test the influence of fluvastatin on progression or regression of CAD. The Asn291Ser and Ser447Ter genotypes were determined by polymerase chain reaction (PCR) and restriction enzyme digestion. Fasting plasma lipid profiles were measured and quantitative coronary angiography was performed at baseline and 2.5 years following randomization. Fatal and non-fatal cardiovascular events during the follow-up period were recorded. A total of 4% (14/363) and 18% (62/352) of the subjects had the Asn291Ser and Ser447Ter mutations, respectively. Overall, there was no statistically association between the Asn291Ser and Ser447Ter mutations and the baseline or final mean plasma levels of lipids, number of coronary lesions, total occlusions, the mean minimal lumen diameter (MLD) stenoses and the clinical events rate. However, patients with the Ser447Ter variant had a slightly higher baseline high density lipoprotein-cholesterol (HDL-C) level (46.2 +/- 12 vs 43.2 +/- 11, P = 0.057), less increase in plasma HDL levels in response to fluvastatin therapy (3 vs 11%, P = 0.056) and a higher cardiovascular events rate (23 vs 13%, P = 0.056). Thus, the Ser447Ter variant had a modest influence on plasma HDL levels and the rate of cardiovascular events. These changes were of borderline statistical significance. Neither the Ser447Ter nor the Asn291Ser mutation had a major impact on susceptibility to CAD, progression or regression of CAD, clinical events rate or response to fluvastatin therapy in LCAS population.

Adult↗
PubMed1999

The effect of aggressive and moderate lowering of LDL-cholesterol and low dose anticoagulation on plasma lipids, apolipoproteins and lipoprotein families in post coronary artery bypass graft trial.

The reported results (The Post Coronary Artery Bypass Graft Trial Investigators. The effect of aggressive lowering of low-density lipoprotein cholesterol levels and low-dose anticoagulation on obstructive changes in saphenous-vein coronary-artery bypass grafts. New Engl J Med 1997;336:153-162) of the Post Coronary Artery Bypass Graft (Post CABG) trial have shown that aggressive lowering was more effective than moderate lowering of low density lipoprotein (LDL) cholesterol in reducing the progression of atherosclerosis in saphenous-vein grafts (27 vs. 39%; P < 0.001); low dose warfarin had no effect on the progression of atherosclerosis. The present report describes the effect of long-term (an average of 4.3 years) aggressive treatment with high (40-80 mg/day) and moderate treatment with low (2.5-5 mg/day) doses of lovastatin on lipids, apolipoproteins (apo) and apoA- and apoB-containing lipoprotein families. To achieve the target LDL-cholesterol levels (60-85 mg/dl for aggressive group and 134-140 mg/dl for moderate group), cholestyramine (8 g/day) was given to 25% of subjects on aggressive and 5% of subjects on moderate treatment. Although with both treatment strategies there were significant decreases (P<0.001) in the levels of total cholesterol, LDL-cholesterol, apoB, LDL-apoB and cholesterol-rich Lp-B family, percent changes in the levels of these variables were greater in the aggressive- than in the moderate-treatment groups. These treatments had only marginal effects in increasing the levels of high density lipoprotein cholesterol, apoA-I and Lp-A-I and Lp-A-I:A-II families. The long-term aggressive treatment exerted no effect on the concentrations of triglycerides, apoC-IlI, apoC-III in VLDL + LDL and triglyceride-rich Lp-Bc families. Neither treatment affected the levels of Lp(a). The potentially modifying influence of warfarin and apoE phenotypes on lovastatin-induced changes in lipoprotein variables was found to be of little significance. It is likely that the beneficial effect of lovastatin in reducing the progression of atherosclerosis in grafts is mediated through its specific lowering effect on cholesterol-rich Lp-B particles.

Anticholesteremic Agents↗
PubMed1999

Association of cerebral perfusion pressure with headache in women with pre-eclampsia.

OBJECTIVE: To study estimated cerebral perfusion pressure and its relation to headache and scotomata in women with pre-eclampsia. DESIGN: Prospective, observational study. SETTING: University teaching hospitals. POPULATION: Seventy-nine pre-eclamptic women with (n = 42) and without (n = 37) headache. Patients with scotomata were also studied separately. METHODS: Transcranial Doppler ultrasound was used to estimate the resistance index, pulsatility index, and estimated cerebral perfusion pressure in the middle cerebral artery. eCPP data were plotted on the same axes as the mean (and 5th and 95th% prediction limits) eCPP data from 63 normal pregnant women followed longitudinally through pregnancy. Data outside of the 95% prediction limits were regarded as abnormal. Data from the pre-eclamptic women were also expressed in terms of the number of standard deviations from the mean value established for normal pregnancy (multiples of the standard deviation: MOS). All studies were prior to labour, under similar conditions, and before volume expansion or treatment. Analysis of data was performed using Student's t test, Mann-Whitney U test, ANOVA, and Fisher's exact test with two-tailed P < 0.05, and receiver operating characteristic curve analysis with a one-tailed P < 0.05. MAIN OUTCOME MEASURES: Resistance index, pulsatility index, and eCPP. RESULTS: Pre-eclamptic women with headache were much more likely to have abnormal eCPP (34/42; 88%) than those without headache (18/37; 49%), P = 0.004, OR 4.5 (95% CI 1.5 to 13.9). There were no differences in terms of MOS in the resistance index or pulsatility index between the two groups, but estimated perfusion pressure, expressed as multiples of the standard deviation in the group with headache, was significantly higher than in the women without. Headache was noted in both over-perfusion and under-perfusion states. Only women with headache had scotomata, and their presence was not related to the severity of the headache or any difference in resistance indices or eCPP. CONCLUSIONS: Headache in women with pre-eclampsia is strongly associated with the presence of abnormal cerebral perfusion pressure. This information may be of use in clinical management.

Adult↗
PubMed1999

Ethnicity affects the postprandial regulation of glycogenolysis.

We investigated the effect of nutrient intake on glucose metabolism in normal Mexican-Americans (n = 6) and European-Americans (n = 6). Subjects were studied after an 18-h fast and after 5-6 h of ingestion of hourly meals that supplied 6.35 or 12.75 micromol glucose. kg(-1). min(-1). Endogenous glucose production (EGP), gluconeogenesis (GNG), and glycogenolysis (GLY) were estimated by mass isotopomer analysis with [U-(13)C]glucose infusions. Fasting EGP, GNG, and GLY did not differ between the groups. Food ingestion lowered the molar rate of GNG by only 31%. However, while consuming the lower quantity of nutrients, Mexican-Americans had higher plasma glucose (P < 0.05), a 39% higher rate of EGP (P < 0.05), and a 68% (P < 0.025) higher rate of GLY than the European-Americans. At the higher intake, EGP and GLY were suppressed completely in both groups. There was a linear relationship between insulin concentrations, EGP, and GLY in both groups, but the slope of the line was significantly (P < 0.05) greater in the European-Americans. We conclude that the sensitivity of GLY to nutrient intake differs between ethnic groups and that this may play a role in the increased predisposition of Mexican-Americans to type II diabetes.

Adult↗
PubMed1998

Relation of clinical benefit to metabolic effects in lipid-lowering therapy.

Studies of lipid-modifying therapy show that inhibition of cholesterol synthesis is required in at least 2 sites-in hepatic cells and in cells located in the walls of coronary arteries-if the progression of coronary atherosclerosis is to be decreased in patients with relatively normal levels of low-density lipoprotein (LDL) cholesterol. This is clinically important, because the majority of patients with coronary artery disease do not have severely elevated LDL cholesterol levels. Of the 2 angiographic trials of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors ("statins") in patients with coronary artery disease and average cholesterol levels, only the Lipoprotein and Atherosclerosis Study (LCAS) of fluvastatin reported slowed angiographic progression of coronary artery disease in these patients. The change in LDL cholesterol levels during treatment with fluvastatin did not predict the extent of change in coronary atherosclerosis or incidence of clinical cardiac events. Apparently, the metabolic effects of treatment with fluvastatin were more important than the extent to which blood cholesterol levels were lowered. The clinical benefits of treatment with statins should be directly compared in randomized controlled clinical trials among patients with average cholesterol levels.

Animals↗
PubMed1998

The lipoprotein and coronary atherosclerosis study (LCAS): lipid and metabolic factors related to atheroma and clinical events.

Studies of lipid-lowering therapy are usually conducted in patients with severely elevated cholesterol levels. However, most individuals who develop clinically significant coronary artery disease (CAD) have total cholesterol levels <240 mg/dL and low-density lipoprotein (LDL) cholesterol levels similar to individuals who do not develop significant CAD. The Lipoprotein and Coronary Atherosclerosis Study (LCAS) was conducted to determine whether lipid-lowering therapy with fluvastatin would reduce the progression or induce the regression of coronary atherosclerotic lesions and/or reduce new lesion formation in patients with CAD and mildly to moderately elevated LDL cholesterol. The LCAS was the first angiographically monitored trial of this 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor. All 429 men and women (mean age, 58.8 years) had angiographic evidence of CAD and LDL cholesterol levels of 115-190 mg/dL (mean 145.6 mg/dL). Patients were randomized to fluvastatin 20 mg twice daily or placebo. Patients whose prerandomization LDL cholesterol was > or = 160 mg/dL also received open-label cholestyramine. Lipid-lowering therapy with fluvastatin significantly slowed CAD progression. After 2.5 years, the mean LDL cholesterol decreased by 23.9% in all fluvastatin-treated patients (+/-cholestyramine) and by 22.5% in patients treated with fluvastatin monotherapy. There was significantly less lesion progression in fluvastatin versus placebo-treated patients (p <0.01). There also were fewer clinical events in fluvastatin-treated patients. Findings suggest that fluvastatin may improve arterial and arteriolar function within a few weeks of beginning therapy.

Adult↗
PubMed1998

Safety of coronary arteriography in clinically stable patients following coronary bypass surgery. Post CABG Clinical Trial Investigators.

The frequent use of diagnostic coronary arteriography and its importance in evaluating results of intervention in clinical trials emphasize the necessity of continued assessment of procedural risk. Several studies have described such risks, but they have often included a diverse group of patients with varying levels of clinical stability. Furthermore, this risk has not been well established in a population of patients with saphenous vein bypass grafts. There is need to define the risk of coronary arteriography in a group of patients who are both clinically similar and stable, and to evaluate the influence of improved technology and increased operator experience on the risk of the procedure. The National Heart, Lung, and Blood Institute-funded Post Coronary Artery Bypass Graft Trial offered the opportunity to evaluate the risk of elective diagnostic coronary arteriography in clinically stable patients studied at two points in time: pre-enrollment and 4-5 years after study entry. In this group of 2,635 angiograms from clinically stable patients over 5 years there were no deaths and the risk of myocardial infarction was 0.08%, while 0.7% had clinically important complications. Non-elective, urgent studies (311 angiograms) on unstable patients were more likely to include angioplasty and were associated with a risk of death of 0.6% and myocardial infarction of 1.3%. Complications did not vary with age or gender. Vascular trauma was more likely to occur using the brachial than the femoral artery entry sites. These results indicate that elective angiography on stable patients can be accomplished with a very low risk of mortality (0% in this study) or serious cardiovascular complication. This supports the safety and usefulness of angiography for clinical intervention trials.

Aged↗
PubMed1998

Effect of cilostazol on walking distances in patients with intermittent claudication caused by peripheral vascular disease.

PURPOSE: This study evaluated the effects of cilostazol on walking distances in patients with intermittent claudication (IC) caused by peripheral arterial occlusive disease. METHODS: The study was a multicenter, randomized, double-blind, placebo-controlled trial. Two hundred thirty-nine patients with IC were randomly assigned to receive cilostazol (100 mg b.i.d.) or a placebo for 16 weeks. All patients underwent serial, variable-grade, constant-speed treadmill testing. Absolute claudication distance (ACD), assessed at the end of the 12-hour dosing interval (trough), was the primary end point. Secondary end points included ACD assessed 3 to 4 hours after dosing (peak) and initial claudication distances (trough and peak). Functional status measures, including the Medical Outcomes Scale (SF-36) and Walking Impairment Questionnaire, were used to assess subjective changes over the 16-week treatment period. Ankle-brachial indexes were calculated from Doppler-measured systolic pressures at every visit with treadmill testing. RESULTS: Patients treated with cilostazol demonstrated significant improvements over the placebo patients in ACD at all three time points tested after baseline (weeks 8, 12, and 16). Peak treadmill testing at weeks 8 and 12 also showed significant improvement in walking distances for cilostazol-treated patients over placebo-treated patients. At week 16, patients in the cilostazol group had a 96.4-meter (47%) increase in ACD compared with 31.4 meters (12.9%) for the placebo group (p < 0.001). In the SF-36, significant improvement was observed in the physical component subscale and the composite physical component score. In the Walking Impairment Questionnaire, improvements were significant in patient reports of walking speed and specific measures of walking difficulty. Ankle-brachial indexes improved in the cilostazol group (0.64 +/- 0.02 to 0.70 +/- 0.02) compared with the placebo group (0.68 +/- 0.02 to 0.69 +/- 0.02) (p < 0.0125). The most frequent adverse events were headache, abnormal stools (e.g. loose stools), diarrhea, and dizziness. CONCLUSIONS: Cilostazol significantly increased ACD at all measured time points and initial claudication distances at most time points. This agent may represent a new treatment option for patients with intermittent claudication.

Cilostazol↗
PubMed1998

Effect of the novel antiplatelet agent cilostazol on plasma lipoproteins in patients with intermittent claudication.

Cilostazol is an antiplatelet agent and vasodilator marketed in Japan for treatment of ischemic symptoms of peripheral vascular disease. It is currently being evaluated in the United States for treatment of symptomatic intermittent claudication (IC). Cilostazol has been shown to improve walking distance in patients with IC. In addition to its reported vasodilator and antiplatelet effects, cilostazol has been proposed to have beneficial effects on plasma lipoproteins. We examined the effect of cilostazol versus placebo on plasma lipoproteins in 189 patients with IC. After 12 weeks of therapy with 100 mg cilostazol BID, plasma triglycerides decreased 15% (P<0.001). Cilostazol also increased plasma high density lipoprotein cholesterol (HDL-C) (10%) and apolipoprotein (apo) A1 (5.7%) significantly (P<0.001 and P<0.01, respectively). Both HDL3 and HDL2 subfractions were increased by cilostazol; however, the greatest percentage increase was observed in HDL2. Individuals with baseline hypertriglyceridemia (>140 mg/dL) experienced the greatest changes in both HDL-C and triglycerides with cilostazol treatment. In that subset of patients, HDL-C was increased 12.2% and triglycerides were decreased 23%. With cilostazol, there was a trend (3%) toward decreased apoB as well as increased apoA1, resulting in a significant (9.8%, P<0.002) increase in the apoA1 to apoB ratio. Low density lipoprotein cholesterol and lipoprotein(a) concentrations were unaffected. Cilostazol treatment resulted in a 35% increase in treadmill walking time (P=0.0015) and a 9.03% increase in ankle-brachial index (P<0.001). These results indicate that in addition to improving the symptoms of IC, cilostazol also favorably modifies plasma lipoproteins in patients with peripheral arterial disease. The mechanism of this effect is currently unknown.

Adrenergic beta-Antagonists↗
PubMed1997

Effects of fluvastatin on coronary atherosclerosis in patients with mild to moderate cholesterol elevations (Lipoprotein and Coronary Atherosclerosis Study [LCAS]).

Despite the potential for reduced morbidity and mortality, aggressive intervention against mild to moderate hypercholesterolemia in patients with coronary heart disease (CHD) remains controversial and infrequently practiced. Eligible patients in the 2.5-year Lipoprotein and Coronary Atherosclerosis Study were men and women aged 35 to 75 years with angiographic CHD and mean low-density lipoprotein (LDL) cholesterol of 115 to 190 mg/dl despite diet. Patients (n = 429; 19% women) were randomized to fluvastatin 20 mg twice daily or placebo. One fourth of patients were also assigned open-label adjunctive cholestyramine up to 12 g/day because prerandomization LDL cholesterol remained > or = 160 mg/dl. The primary end point, assessed by quantitative coronary angiography, was within-patient per-lesion change in minimum lumen diameter (MLD) of qualifying lesions. Across 2.5 years, mean LDL cholesterol was reduced by 23.9% in all fluvastatin patients (+/- cholestyramine) (146 to 111 mg/dl) and by 22.5% in the fluvastatin only subgroup (137 to 106 mg/dl). Primary end point analysis (340 patients) showed significantly less lesion progression in all fluvastatin versus all placebo patients, deltaMLD -0.028 versus -0.100 mm (p <0.01), and for fluvastatin alone versus placebo alone, deltaMLD -0.024 versus -0.094 mm (p <0.02). A consistent angiographic benefit with treatment was seen whether baseline LDL cholesterol was above or below 160 or 130 mg/dl. Beneficial trends with treatment were also consistently seen in clinical event rates but were not statistically significant. Thus, lipid lowering by fluvastatin in patients with mildly to moderately elevated LDL cholesterol significantly slowed CHD progression.

Adult↗
PubMed1997

Comparison of preoperative characteristics of men and women undergoing coronary artery bypass grafting (the Post Coronary Artery Bypass Graft [CABG] Biobehavioral Study).

A cohort of 759 coronary artery bypass grafting (CABG) patients (269 women and 490 men) was enrolled in the prospective POST CABG Biobehavioral Study at 5 clinical centers in the United States and Canada. Sociodemographic and medical data were obtained by interview and from medical charts. Health-related quality of life and psychosocial data were ascertained preoperatively by interview and questionnaire for those patients whose condition allowed preoperative assessment and was compared among patients from hospitals enrolling both male and female patients (143 women and 267 men). Women enrolled in the Biobehavioral Study were older than men (65.4 +/- 9.0 vs 61.8 +/- 9.7 years, p < 0.001) and more likely to have a preoperative medical condition which precluded biobehavioral evaluation (47% vs 34%, p < 0.001). Women were less likely to be high school graduates (59% vs 74%, p < 0.001), were less likely to be earning > or = $25,000 per year (39% vs 69%, p < 0.001), and were married less often at the time of surgery (59% vs 85%, p < 0.001). Fewer women than men were able to perform basic self-care activities (p < 0.001) and social activities (p < 0.001). Women were also less able to perform the more demanding activities required for independent living, recreation, and maintaining a household (p < 0.001). Women were also more anxious (p = 0.01) and reported more depressive symptoms (p < 0.001) than men. These data suggest that plans for perioperative and convalescent care for women undergoing CABG should take into account their less favorable medical and psychosocial status relative to men.

Activities of Daily Living↗
PubMed1997

Persistent cerebrovascular changes in postpartum preeclamptic women: a Doppler evaluation.

OBJECTIVE: Our goal was to evaluate the cerebral vasculature in postpartum normotensive and preeclamptic women. STUDY DESIGN: Nineteen previously preeclamptic women and 19 matched normotensive controls were studied at 6 weeks, and 8 preeclamptic women and 28 normotensive controls were studied at 12 weeks post partum. Systolic, diastolic, and mean velocities, as well as resistance and pulsatility indexes, of the middle cerebral, ophthalmic, and central retinal arteries were recorded. Data are presented as median and range. Statistical significance was set at p < 0.05. RESULTS: There were no differences in maternal age, parity, heart rate, mean arterial pressure, and proteinuria between the two groups at 6 and 12 weeks post partum. At 6 weeks post partum the preeclamptic group had higher ophthalmic artery diastolic velocity (9.0 cm/sec, 3.1 to 22.3, vs 5.4 cm/sec, 3.0 to 20.1; p = 0.008), ophthalmic artery mean velocity (6.0 cm/sec, 8.8 to 34.8, vs 12.5 cm/sec, 6.8 to 35.4; p = 0.03), and central retinal artery systolic velocity (10.0 cm/sec, 7.6 to 28.0, vs 8.4 cm/sec, 5.2 to 18.3; p = 0.02). The ophthalmic artery resistance index (0.72, 0.43 to 0.88, vs 0.79, 0.66 to 0.90; p = 0.03) and ophthalmic artery pulsatility index (1.56, 0.94 to 2.82, vs 2.03, vs 1.13 to 3.10; p = 0.04) were lower in the preeclamptic group. At 12 weeks post partum the preeclamptic group had elevated ophthalmic artery mean velocity (14.5 cm/sec, 7.9 to 20.2, vs 10.9 cm/sec, 5.5 to 15.4 p = 0.01), central retinal artery systolic velocity (11.1 cm/sec, 6.8 to 15.9, vs 8.5, 5.1 to 15.3; p = 0.02), and central retinal artery diastolic velocity (3.9 cm/sec, 1.2 to 5.2, vs 3.0, 1.4 to 5.8; p < 0.05). CONCLUSION: In the postpartum period preeclamptic women show persistently elevated central retinal artery systolic velocity, which suggests distal vasoconstriction.

Adolescent↗