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Biomedical subjects

E Chesler

Publications and source records attributed to E Chesler.

At least 19 recordsLinked to original sources

Methodological aspects of the genetic dissection of gene expression.

MOTIVATION: Dissection of the genetics underlying gene expression utilizes techniques from microarray analyses as well as quantitative trait loci (QTL) mapping. Available QLT mapping methods are not tailored for the highly automated analyses required to deal with the thousand of gene transcripts encountered in the mapping of QTL affecting gene expression (sometimes referred to as eQTL). This report focuses on the adaptation of QTL mapping methodology to perform automated mapping of QTL affecting gene expression. RESULTS: The analyses of expression data on > 12,000 gene transcripts in BXD recombinant inbred mice found, on average, 629 QTL exceeding the genome-wide 5% threshold. Using additional information on trait repeatabilities and QTL location, 168 of these were classified as 'high confidence' QTL. Current sample sizes of genetical genomics studies make it possible to detect a reasonable number of QTL using simple genetic models, but considerably larger studies are needed to evaluate more complex genetic models. After extensive analyses of real data and additional simulated data (altogether > 300,000 genome scans) we make the following recommendations for detection of QTL for gene expression: (1) For populations with an unbalanced number of replicates on each genotype, weighted least squares should be preferred above ordinary least squares. Weights can be based on repeatability of the trait and the number of replicates. (2) A genome scan based on multiple marker information but analysing only at marker locations is a good approximation to a full interval mapping procedure. (3) Significance testing should be based on empirical genome-wide significance thresholds that are derived for each trait separately. (4) The significant QTL can be separated into high and low confidence QTL using a false discovery rate that incorporates prior information such as transcript repeatabilities and co-localization of gene-transcripts and QTL. (5) Including observations on the founder lines in the QTL analysis should be avoided as it inflates the test statistic and increases the Type I error. (6) To increase the computational efficiency of the study, use of parallel computing is advised. These recommendations are summarized in a possible strategy for mapping of QTL in a least squares framework. AVAILABILITY: The software used for this study is available on request from the authors.

Algorithms↗

Utility of positron emission tomography in predicting improved left ventricular ejection fraction after coronary artery bypass grafting among patients with ischemic cardiomyopathy.

The objective of this study was to determine whether preoperative estimates of regional myocardial uptake of (18)-F-fluorodeoxyglucose (FDG) could predict postoperative improvement in ejection fraction in patients undergoing coronary artery bypass grafting (CABG) for ischemic cardiomyopathy. 20 consecutive patients [left ventricular ejection fraction (LVEF) </=27%] were referred for preoperative positron emission tomography (PET) to measure regional myocardial FDG uptake and were deemed candidates for CABG. All individuals had technically adequate vessels and significant viability. The left anterior descending (LAD) coronary artery was severely diseased in all patients. Because of the importance of the anterior wall to overall ventricular performance, FDG uptake was semiquantitated in those regions and related to postoperative LVEF. 17 patients underwent CABG with an uneventful recovery. LVEF increased from 22 +/- 4 to 26 +/- 7% 2 weeks postsurgery (p < 0.05), with >/=5% change noted in 7 patients (group 1) and <5% noted in 10 patients (group 2). No preoperative or perioperative clinical variable could predict those with improved ventricular function. The relative amount of FDG uptake in the anterior wall was higher in group 1 compared with group 2 (93 +/- 9 vs. 81 +/- 13%; p < 0.05) and correlated with the change in LVEF post-CABG (r = 0.50; p < 0.05). >88% of FDG uptake in the LAD region had a positive predictive accuracy of 67% and negative predictive accuracy of 88% for improved LVEF postbypass. Late follow-up estimates of LVEF (median of 10 months) showed that early changes in function were sustained. In summary, among patients with severe coronary artery disease and depressed LVEF, ventricular function may improve early postrevascularization. PET estimates of relative FDG uptake in the anterior wall help predict those individuals who are likely to have the greatest increment in LVEF.

Aged↗

The influence of perioperative myocardial infarction on long-term prognosis following elective vascular surgery.

STUDY OBJECTIVE: The present study was performed to determine the influence of a perioperative myocardial infarction on long-term mortality in patients who have undergone elective vascular surgery. STUDY DESIGN: This was a 4-year follow-up of patients who had undergone elective vascular procedures at a Veterans Affairs Medical Center. Between January 1989 and December 1990, 115 consecutive patients underwent surgery for either an expanding abdominal aortic aneurysm (AAA) (38%) or for pain in the lower extremities (62%). RESULTS: Vital status at 4 years postsurgery was determined for all patients. Thirty-day postoperative mortality was 3%, while estimates at 1, 2, 3, and 4 years were 19%, 26%, 35%, and 39%, respectively. Of the 45 patients who died within 4 years following surgery, the major causes of death were cardiac (40%), cancer (18%), cerebrovascular (13%), and peripheral vascular disease (11%). Univariate predictors of 1-year mortality on preoperative evaluation were an abnormal ECG, moderate or greater sized exercise thallium defect and left ventricular ejection fraction < or =40%, and a perioperative myocardial infarction. Univariate predictors of 4-year mortality were non-AAA surgery and diabetes mellitus. Perioperative myocardial infarction was a marginally significant independent predictor of 1-year mortality (p=0.06), while the need for non-AAA surgery was a strong independent predictor at 4 years. CONCLUSIONS: Cardiac mortality is the major cause of late death among patients undergoing elective vascular surgery. Although preoperative indicators of symptomatic coronary artery disease and nonfatal perioperative myocardial infarction identified those individuals at increased mortality in the first postoperative year, the extent of vascular disease at presentation may be a more important determinant of long-term survival. A randomized trial in such patients is needed to assess the best strategy for treating patients with coexistent coronary artery and vascular diseases.

Aged↗

Usefulness of mean aortic valve gradient and left ventricular diastolic filling pattern for distinguishing symptomatic from asymptomatic patients.

Consecutive, symptomatic (n = 15) and asymptomatic (n = 25) men with aortic stenosis (valve area < 1.2 cm2) and no clinical evidence of myocardial ischemia underwent radionuclide angiography at rest and during supine bicycle ergometry. Ejection fraction, diastolic filling pattern and aortic valve area/gradient were measured on enrollment and when patients became symptomatic (n = 10) or underwent valve replacement (n = 22) during a 2-year follow-up period. Both groups had similar heart rate, blood pressure and ejection fractions, but mean aortic gradients were higher in symptomatic (53 +/- 4 mm Hg) than asymptomatic (37 +/- 2 mm Hg) subjects p < 0.01. Functional limitation evoked by exercise was prevalent even in the asymptomatic group but symptomatic patients exercised to lower work levels than asymptomatic subjects (184 +/- 27 and 307 +/- 32 kg.m/min, respectively, p = 0.02). Ejection fraction failed to increase with exercise in either group. Symptomatic subjects had supranormalization of early diastolic filling with shorter time to the peak filling rate than asymptomatic subjects (137 +/- 16 and 172 +/- 9 ms, respectively, p < 0.05) and a greater first 1/3 filling fraction. The 10 patients who became symptomatic during follow-up had higher first 1/3 filling fractions (53 +/- 7 and 42 +/- 5%, respectively) and mean gradients (41 +/- 4 and 33 +/- 2 mm Hg, respectively) than subjects who remained asymptomatic, p < 0.05. High mean aortic gradients, impaired exercise tolerance and enhanced early diastolic filling distinguish symptomatic from asymptomatic patients.

Adult↗

Angina and persistent exercise thallium defects: independent risk factors in elective vascular surgery.

OBJECTIVES: In this study, we assessed the utility of exercise thallium-201 scintigraphy and other clinical factors in predicting perioperative cardiac complications in patients undergoing elective vascular surgery. BACKGROUND: The risk of cardiac complications among such patients is very high. METHODS: The study group comprised 116 men (mean age 67 years). Fifty patients (43%) had a history of coronary artery disease, including angina pectoris in 26 (22%), myocardial infarction in 32 (28%) and coronary artery bypass surgery in 19 (16%). RESULTS: There were a total of 22 perioperative myocardial infarctions (18.9%), including 2 cardiac deaths (1.7%). A significantly greater proportion (p < 0.05) of patients with than without perioperative complications had a history of coronary artery disease (77% vs. 35%), angina (59% vs. 14%), prior myocardial infarction (50% vs. 22%), abnormal electrocardiogram (68% vs. 40%) and abnormal exercise thallium test (75% vs. 47%). The patient group with complications also had a significantly lower mean rest ejection fraction (45 +/- 3% vs. 55 +/- 2%, p < 0.005). Independent predictors of complication, as determined by straight logistic regression, were angina and fixed thallium defects after exercise. CONCLUSIONS: Our data indicate that angina and the presence of fixed thallium defects after exercise are independent predictors of cardiac risk in patients undergoing elective vascular surgery. These findings are compatible with other studies showing that nonredistribution on standard 3- to 4-h delayed studies cannot exclude viable myocardium at risk.

Adult↗

Saphenous vein graft patency 1 year after coronary artery bypass surgery and effects of antiplatelet therapy. Results of a Veterans Administration Cooperative Study.

To determine whether antiplatelet therapies improve saphenous vein graft patency after coronary artery bypass grafting, we compared 1) aspirin (325 mg once daily), 2) aspirin (325 mg three times daily), 3) aspirin and dipyridamole (325 mg and 75 mg, respectively, three times daily), 4) sulfinpyrazone (267 mg three times daily), and 5) placebo (three times daily). Therapy with dipyridamole and sulfinpyrazone was started 48 hours before bypass graft surgery, and aspirin treatment was begun 12 hours before surgery as a single 325-mg dose. Postoperative treatment was started 6 hours after surgery and continued for 1 year. Graft patency data were obtained early (median, 9 days) and late (median, 367 days) after surgery. The early graft occlusion rate was decreased with all aspirin treatment regimens compared with that of the placebo regimen. At 1 year, in 406 patients with 1,315 grafts, the graft occlusion rate in all of the aspirin groups combined was 15.8% compared with 22.6% for the placebo group (p = 0.029). The patients taking aspirin once daily had a lower occlusion rate (13.2%) compared with the patients receiving placebo (p = 0.050). At 1 year, in the vein grafts placed to vessels less than or equal to 2.0 mm in diameter (804 distal sites), the graft occlusion rate in all of the aspirin groups was 20.1% compared with 32.3% for the placebo group (p = 0.008). In the vein grafts placed to vessels greater than 2.0 mm in diameter (511 distal sites), there was no difference in the occlusion rates between aspirin and the placebo group at 1 year (8.7% vs. 9.0%, p = 0.918).(ABSTRACT TRUNCATED AT 250 WORDS)

Aspirin↗

The statistical analysis of graft patency data in a clinical trial of antiplatelet agents following coronary artery bypass grafting.

Because most coronary artery bypass patients receive more than one graft at surgery, it is most important to determine whether statistical analysis of graft patency should be performed on the premise that the multiple grafts within patients are dependent or independent experimental units. Veterans Administration Cooperative Study No. 207 was a multicenter clinical trial comparing four different antiplatelet regimens to placebo in the prevention of graft occlusion following coronary artery bypass grafting. Using the results from the 1-week postoperative angiograms from the Veterans Administration Cooperative Study No. 207, in which there were 3.2 distal anastomoses per patient, we have tested the hypothesis that grafts within patients tend to act dependently with respect to patency or occlusion by comparing the graft patency data to a binomial distribution (i.e., that distribution that would have been manifest if grafts were independent). Because the graft patency results in Study No. 207 significantly deviated from the binomial distribution (p = 0.0003), a more appropriate analysis for graft patency data was applied using a ratio estimate as applied to cluster sampling. The statistical methods used in 11 previous clinical trials of antithrombotic therapy after coronary artery bypass grafting were examined. Only one of the previous studies used such an analysis, and three additional reports attempted to correct for dependency of grafts within patients in their analyses using other statistical methods. In seven of the studies the investigators did not address the potential problem of a dependent relationship between multiple grafts within patients. We conclude that grafts within patients act as dependent experimental units and that the ratio estimate as applied to cluster sampling may be appropriately applied to these data.

Clinical Trials as Topic↗

Improvement in early saphenous vein graft patency after coronary artery bypass surgery with antiplatelet therapy: results of a Veterans Administration Cooperative Study.

To determine whether specific antiplatelet therapies improved vein graft patency after coronary artery bypass grafting (CABG) we compared (1) aspirin, 325 mg daily, (2) aspirin, 325 mg three times daily, (3) aspirin plus dipyridamole (325 mg and 75 mg, respectively, three times daily), (4) sulfinpyrazone (267 mg three times daily), and (5) placebo (three times daily). Therapy, except aspirin, was started 48 hr before CABG. When aspirin was a treatment, one 325 mg dose was given 12 hr before surgery and therapy was maintained thereafter according to the assigned regimen. Angiographic graft patency data were obtained within 60 days of surgery. Analysis of early graft patency in 555 patients (1781 grafts), revealed the following graft patency rates: aspirin daily, 93.5%; aspirin three times daily, 92.3%; aspirin and dipyridamole, 91.9%; and sulfinpyrazone, 90.2%. All aspirin-containing therapeutic regimens improved (p less than .05) graft patency compared with placebo (85.2%). Chest tube drainage measured within the first 35 hr after CABG revealed that the median loss with aspirin daily (965 ml), aspirin three times daily (1175 ml), and aspirin plus dipyridamole (1000 ml) exceeded (p less than .02) that with placebo (805 ml), while median loss with sulfinpyrazone (775 ml) did not. The reoperation rate was greater (p less than .01) in all the treatment groups that received aspirin (6.5%) compared with the two nonaspirin groups (1.7%). Overall operative mortality was 2.3%, without significant differences among treatment groups. Transient renal insufficiency occurred in 5.3% of patients taking sulfinpyrazone. Thus, early vein graft patency was improved after CABG with all aspirin-containing drug regimens.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Trials as Topic↗

ZK 36-374, a stable analog of prostacyclin, prevents acute hypoxic pulmonary hypertension in the dog.

Vasodilator therapy in pulmonary hypertension is limited by the lack of an agent selective for the pulmonary circulation. The effects of intravenous prostacyclin and two stable prostaglandin analogs, ZK 36-374 and CL 115,347, were assessed on the preconstricted pulmonary vasculature of the anesthetized dog. During hypoxic vasoconstriction ZK 36-374 (0.4 micrograms/kg per min) markedly reduced pulmonary artery pressure (26 +/- 3 to 13 +/- 1 mm Hg) (p less than 0.05) and pulmonary vascular resistance (6.2 +/- 1.1 to 2.8 +/- 0.2 mm Hg/liter per min) (p less than 0.01). There was no significant effect on cardiac output, aortic pressure or arterial blood gases. Pulmonary vasoconstriction induced by prostaglandin F2 alpha was similarly affected by ZK 36-374, and in this instance the aortic pressure was also reduced (158 +/- 11 to 129 +/- 11 mm Hg) (p less than 0.01). ZK 36-374 (0.2 micrograms/kg per min) was more effective in lowering hypoxic pulmonary vascular resistance (from 6.5 +/- 0.6 to 3.0 +/- 0.3 mm Hg/liter per min) than was prostacyclin (0.75 micrograms/kg per min) (from 6.3 +/- 0.6 to 4.2 +/- 0.4 mm Hg/liter per min) (p less than 0.05) and resulted in a smaller fall in aortic pressure (p less than 0.05). CL 115,347 (1.0 micrograms/kg per min) had no effect on the pulmonary vasculature during normoxia or when preconstricted by prostaglandin F2 alpha or hypoxia, but reduced aortic pressure and total systemic resistance (p less than 0.05). It appears to be a selective systemic vasodilator with no pulmonary vascular activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Pulmonary vascular tone is increased by a voltage-dependent calcium channel potentiator.

The mechanism of hypoxia-induced pulmonary vasoconstriction remains unknown. To explore the possible dependence of the hypoxic response on voltage-activated calcium (Ca2+) channels, the effects of BAY K 8644 (BAY), a voltage-dependent Ca2+ channel potentiator, were observed on the pulmonary vascular response to hypoxia of both the intact anesthetized dog and the perfused isolated rat lung. In six rat lungs given BAY (1 X 10(-6)M), hypoxia increased mean pulmonary arterial pressure (Ppa) to 30.5 +/- 1.7 (SEM) Torr compared with 14.8 +/- 1.2 Torr for six untreated rat lungs (P less than 0.01). After nifedipine, the maximum Ppa during hypoxia fell 14.1 +/- 2.4 Torr from the previous hypoxic challenge in the BAY-stimulated rats (P less than 0.01). BAY (1.2 X 10(-7) mol/kg) given during normoxia in seven dogs increased pulmonary vascular resistance 2.5 +/- 0.3 to 5.0 +/- 1.2 Torr X 1(-1) X min (P less than 0.05), and systemic vascular resistance 55 +/- 4.9 to 126 +/- 20.7 Torr X 1(-1) X min (P less than 0.05). Systemic mean arterial pressure rose 68 Torr, whereas Ppa remained unchanged. Administration of BAY during hypoxia produced an increase in Ppa: 28 +/- 1.5 to 33 +/- 1.9 Torr (P less than 0.05). Thus BAY, a Ca2+ channel potentiator, enhances the hypoxic pulmonary response in vitro and in vivo. This, together with the effect of nifedipine on BAY potentiation, suggests that increased Ca2+ channel activity may be important in the mechanism of hypoxic pulmonary vasoconstriction.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

The effects of substance P on the preconstricted pulmonary vasculature of the anesthetized dog.

Substance P is a vasoactive peptide. Nerve fibers containing substance P are present in the media of pulmonary arteries but the physiologic function of substance P in the pulmonary vasculature is unknown. Several doses of substance P were infused intravenously in the anesthetized dog to ascertain its effects on the pulmonary vasculature, both during normoxia and following preconstriction with hypoxia (F1O2 0.1) or prostaglandin F2 alpha (PGF2 alpha 5 mug/kg/min). Substance P resulted in systemic vasodilation during normoxia but had minimal effect on the pulmonary vasculature. During hypoxia and PGF2 alpha-induced pulmonary vasoconstriction, substance P significantly lowered pulmonary artery pressure, pulmonary vascular resistance, mean aortic pressure, and total systemic resistance. It had no effect on cardiac output, wedge pressure, and arterial blood gases. To investigate possible mechanisms for substance P-induced vasodilation, substance P was studied following pretreatment with N-acetylcysteine (a radical scavenging agent), methylene blue (an inhibitor of guanylate cyclase), meclofenamate (a cyclooxygenase inhibitor), and atropine (a muscarinic receptor antagonist). None of these agents impaired substance P-induced vasodilation. Substance P given intravenously is a nonselective vasodilator in the dog but the mechanism of its action remains uncertain.

Acetylcysteine↗

Long-term efficacy of bepridil in patients with chronic stable angina pectoris: results of a multicenter, placebo-controlled study of extended bepridil use.

To evaluate whether bepridil once a day provides effective antianginal therapy during extended use, a placebo-controlled withdrawal study was conducted in 33 patients with chronic stable angina. Each patient studied had previously had a favorable response to short-term administration of bepridil and had been taking the drug once daily for greater than or equal to 9 months of continuous use. Patients were then randomly assigned to receive either continued bepridil or a placebo substitution once daily during a 4-week, double-blind, parallel-group comparison. Dosage for the bepridil group was constantly maintained for each patient at a level observed to be clinically effective. The study consisted of a comparison of angina frequency and nitroglycerin tablet consumption obtained from patient diaries and results from maximal-graded multistage treadmill tests. Patients randomized to continue receiving bepridil remained stable in terms of angina frequency and exercise performance. Discontinuation of long-term bepridil significantly increased angina frequency and nitroglycerin tablet consumption and reduced exercise capacity. Four patients (24%), all receiving placebo treatment, had increases in angina frequency and had the study terminated. Bepridil was reinstituted in these patients with resolution of symptoms and no untoward effects. The results of this placebo-controlled, double-blind, randomized study confirm that bepridil continues to provide antianginal benefit during long-term administration.

Adult↗

Normal catecholamine and hemodynamic responses to orthostatic tilt in subjects with mitral valve prolapse. Correlation with psychologic testing.

Various functional abnormalities of the autonomic nervous system have been reported in symptomatic patients with mitral valve prolapse. It has also been suggested that mitral valve prolapse may be a component of a neurovascular endocrine abnormality and a marker for anxiety. Eleven consecutive patients with mitral valve prolapse (six men and five women), five of whom were asymptomatic, were studied. In comparison with 11 control subjects matched for age and sex who underwent 60-degree upright tilt, there was no significant difference between plasma norepinephrine levels, heart rate, and blood pressure, before, during, and after tilting. Psychologic testing for anxiety neurosis in both groups showed no significant difference on any of these measurements. There was therefore no evidence of autonomic dysfunction or neurosis in the patients with mitral valve prolapse. This variance with the findings of other investigators is probably related to their study of patient groups skewed by a disproportionate number of symptomatic females; the patients in the study reported herein are more representative of mitral valve prolapse in the general population. The symptoms attributed to mitral valve prolapse are quite likely adrenergically mediated and precipitated by anxiety, but this probably represents a coincidence of two common conditions encountered in medical practice.

Adult↗

Redox status and pulmonary vascular reactivity.

Oxygen radicals are produced during oxidative metabolism in proportion to the tissue oxygen tension. The studies reported here have shown that oxygen radicals or the sulfhydryl oxidant, diamide, caused pulmonary vasodilatation in the isolated perfused rat lung. Could oxygen radicals play a role in the physiologic control of pulmonary vascular smooth muscle tone?

Allopurinol↗

Comparative effects of nisoldipine, nifedipine and bepridil on experimental pulmonary hypertension.

Calcium channel blockers sometimes reduce pulmonary vascular resistance (PVR) in patients with pulmonary hypertension. This study compares the pulmonary vasodilator effect of two new calcium channel blockers, nisoldipine and bepridil, to that of nifedipine in three groups of anesthetized dogs (n = 8 for each group). In each group the normoxic hemodynamics were recorded before and after low, medium and high doses of the respective agents given i.v. In addition, the effect of these doses on the pulmonary pressor responses to hypoxia and prostaglandin F2 alpha (PGF 2 alpha) was measured. During normoxia all doses of bepridil caused brief increases in cardiac output. However, during the hypoxic and PGF 2 alpha challenges cardiac output fell and PVR rose above predrug responses, rather than being reduced. Nisoldipine produced a sustained increase in cardiac output throughout the experiment. During hypoxia, at high dose, it decreased pulmonary arterial pressure, unlike the two other agents. However, in common with them, nisoldipine also caused systemic hypotension. After medium and high dose nisoldipine and after high dose nifedipine, PVR remained close to normoxic control levels during both hypoxic and PGF 2 alpha challenges. Both medium dose nisoldipine (5 X 10(-8) M/kg) and high dose nifedipine (5 X 10(-7) M/kg) reduced hypoxic PVR by 39% of the untreated hypoxic value. Although nisoldipine is more effective in reducing pulmonary hypertension than nifedipine or bepridil, it also causes marked systemic hypotension. This lack of specificity may limit the therapeutic potential of this agent when given i.v.

Animals↗