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Biomedical subjects

W H Haught

Publications and source records attributed to W H Haught.

10 recordsLinked to original sources
PubMed1996

Evaluation of heart failure patients: objective parameters to assess functional capacity.

Measures of disease severity used in the evaluation of patients with heart failure include survival data, the New York Heart Association classification, ejection fraction, functional assessments, exercise protocols, rest and exercise hemodynamic data, and biochemical parameters including catecholamine levels and serum sodium. Clinicians must integrate these multiple variables into an overall assessment. An overview of the clinical application of these techniques in the evaluation and treatment of patients with heart failure is presented.

Cardiac Output↗
PubMed1996

Alterations in circulating intercellular adhesion molecule-1 and L-selectin: further evidence for chronic inflammation in ischemic heart disease.

Atherosclerosis is increasingly thought to be a chronic inflammatory disease. Inflammation requires transmigration of leukocytes from the circulation to the tissues. Adhesion of leukocytes to endothelial calls is the initial event in an inflammatory response and is mediated by expression of several adhesion molecules. In this study we characterize the contribution of intercellular adhesion molecules (ICAM-1) and L-selectin in patients with different coronary artery disease syndromes. Serum concentrations of cICAM-1 and sL-selectin were measured by enzyme-linked immunosorbent assay in 31 patients with stable angina, 30 patients with unstable angina, 18 patients with acute myocardial infarction and 20 healthy subjects in a control group. All patients underwent coronary angiography. Mean (+/-SE) cICAM-1 levels were higher (p < 0.05) in patients with stable angina (249 +/- 6 ng/ml), unstable angina (260 +/- 16 ng/ml), or acute myocardial infarction (261 +/- 24 ng/ml) compared with those in subjects in the control group (171 +/- 11 ng/ml). In contrast, levels of sL-selectin were lower (p < 0.01) in patients with stable angina (1.2 +/- 0.1 microg/ml), unstable angina (1.1 +/- 0.6 microg/ml), or acute myocardial infarction (1.1 +/- 0.1 microg/ml) compared with those in subjects in the control group (1.8 +/- 0.1 microg/ml). No difference was found in cICAM-1 or sL-selectin levels among patients with stable angina, unstable angina, or acute myocardial infarction. No correlation was seen between cICAM-1 or sL-selectin levels and extent (or severity) of coronary artery disease or leukocyte count. L-selectin expression was observed to be depressed in patients with severe angina compared with that in members of the control group. To examine the mechanism of reduction in sL-selectin levels and L-selectin expression on leukocytes, leukocytes from the control group were stimulated in vitro. Stimulation of leukocytes resulted in a rapid downregulation of surface L-selectin expression, measured by flowcytometry, similar to the suppressed expression of L-selectin found on leukocytes from patients with coronary artery disease. In conclusion, altered cICAM-1 and sL-selectin levels in patients with coronary artery disease reflect the presence of a chronic inflammatory process. This inflammatory process results in downregulation of leukocyte expression of L-selectin and thus lower circulating sL-selectin levels.

Angina Pectoris↗
PubMed1996

Studies of vascular tolerance to nitroglycerin: effects of N-acetylcysteine, NG-monomethyl L-arginine, and endothelin-1.

Development of vascular tolerance to nitroglycerin (NTG) has been attributed to sulfhydryl (SH) depletion, guanylate cyclase desensitization, or both. Controversy regarding the precise contribution of these mechanisms may be due to variations in experimental design. To examine further the biochemical basis of NTG tolerance, norepinephrine (NE)-precontracted rat aortic rings were exposed to NTG (10(-5)M), which resulted in 84 +/- 6% relaxation. Other rings were first superfused with NTG (10(-6)M) and then contracted with NE. These rings showed a marked tolerance to the vasorelaxant effects of NTG (maximal relaxation 20 +/- 5%, n = 15, p < 0.001 vs. control rings). Similar tolerance to NTG was observed when the vascular rings were first superfused with acetylcholine (ACh 10(-6)M), indicating cross-tolerance between ACh and NTG. Treatment of NTG-tolerant rings with N-acetylcysteine (NAC) (10(-5)M) did not restore vascular smooth muscle (VSM) relaxation in response to NTG (maximal relaxation 23 +/- 5%, n = 8), suggesting that SH depletion may not be the basis of NTG tolerance in these experiments. Parallel sets of NTG-tolerant aortic rings were contracted with endothelin-1 (ET-1, n = 5) or the endothelium-derived relaxing factor (EDRF) synthase inhibitor NG-monomethyl L-arginine (L-NMMA, 10(-4)M, n = 8). In both ET-1- and L-NMMA-contracted rings, vascular relaxation in response to NTG was preserved (80 +/- 6 and 88 +/- 8% relaxation, respectively). Measurement of cyclic GMP in aortic rings showed marked accumulation on initial exposure of tissues to NTG (310 +/- 10 fmol/mg), whereas the NTG-tolerant rings showed much less cyclic GMP accumulation (48 +/- 29 fmol/mg). Rings contracted with L-NMMA or ET-1, but not NE, accumulated cyclic GMP when exposed to NTG (280 +/- 20 fmol/mg). These data indicate that NTG tolerance develops on exposure of vascular rings superfused with NTG or ACh and is probably not related to tissue SH depletion. Contraction of NTG-tolerant rings with ET-1 or L-NMMA restores NTG-mediated relaxation.

Acetylcysteine↗
PubMed1995

Decrease in hematocrit after coronary stent placement and dextran therapy.

In summary, dextran 40, when given after coronary stent placement, results in a marked decrease in hematocrit within 24 hours. Hematocrit often returns to near baseline levels within 48 hours of stopping dextran. This phenomenon most likely reflects dextran-related hemodilution. This hemodilutional decrease in hematocrit is often misinterpreted as acute blood loss and may result in blood transfusion in patients with low baseline hematocrit. However, far less aggressive anticoagulation regimens, which do not include dextran, are under investigation in patients undergoing coronary stent placement.

Angioplasty, Balloon, Coronary↗
PubMed1995

Emergency intracardiac defibrillation for refractory ventricular fibrillation.

Hemodynamically unstable ventricular arrhythmias induced during electrophysiologic testing almost always respond to prompt application of direct current transthoracic shocks. In rare cases, however, ventricular fibrillation may be refractory to conventional treatment. Recently, a technique of intracardiac defibrillation has been successfully used to resuscitate patients with ventricular fibrillation refractory to transthoracic defibrillation. We describe two patients with a history of myocardial infarction and left ventricular dysfunction who were admitted with symptomatic episodes of ventricular tachycardia. Both had inducible sustained monomorphic ventricular tachycardia. During a repeat electrophysiologic study in Patient No. 1 on procainamide and at the initial study in Patient No. 2, right ventricular burst pacing to terminate ventricular tachycardia resulted in ventricular fibrillation refractory to resuscitation efforts, including transthoracic defibrillation with 360 J. Emergency intracardiac defibrillation with 200 and 360 J, respectively, successfully converted both patients to sinus rhythm. Both patients were subsequently discharged from the hospital on amiodarone. These cases illustrate the life-saving capabilities of intracardiac defibrillation.

Aged↗
PubMed1993

Case report: bacillary angiomatosis with massive visceral lymphadenopathy.

Bacillary angiomatosis is a newly characterized infectious disease occurring mainly in patients with AIDS. Most patients have cutaneous angiomatosis lesions resembling Kaposi's sarcoma or pyogenic granuloma. Although the disease may be life-threatening if not treated, it is curable with appropriate antibiotic therapy. A patient had a fever, nightsweats, abdominal pain, pleural effusions, and asymmetric peripheral lymphadenopathy. Computed tomography of the chest and abdomen revealed a unique pattern of enhancement of lymph nodes that, to this research team's knowledge, has not been reported previously with this condition. Appropriate antibiotic therapy resulted in a complete resolution of the disease. Included is a discussion of the clinical presentation, etiology, histology, and treatment of bacillary angiomatosis.

Adult↗
PubMed1992

Slow channel calcium blockers attenuate reoxygenation-mediated vascular contraction, but augment anoxia-mediated vascular contraction.

Anoxia and reoxygenation modulate vasomotor tone. To determine the effect of the slow channel calcium blockers verapamil and diltiazem in vascular smooth muscle contraction during states of altered oxygenation, rat aortic rings with intact endothelium were contracted with norepinephrine (NE) or the thromboxane A2 mimic U46,619 and then exposed abruptly to anoxia (switch from 95% O2 to 95% N2) for 30 min and then reoxygenated (switch from 95% N2 to 95% O2). Anoxia caused a transient 40 +/- 9% (mean +/- SE, n = 15) increase in contraction, whereas reoxygenation resulted in an initial decrease followed by a large (83 +/- 21%) increase in contraction. Treatment of vascular rings with verapamil or diltiazem (1 microgram/ml or 2 microM) decreased contractile response to the agonists (p less than 0.01). Both these agents consistently augmented the magnitude and duration of anoxia-induced contraction (p less than 0.01). In other experiments, pretreatment of vascular rings with NG-monomethyl-L-arginine (L-NMMA), an inhibitor of endothelium-derived relaxing factor (EDRF) synthesis, or with oxyhemoglobin, an inhibitor of EDRF activity, or de-endothelialization resulted in marked (p less than 0.01) decrease in anoxic contraction, indicating that anoxia-induced contraction is caused by modulation of EDRF. Treatment of aortic rings with verapamil also reduced acetylcholine-mediated relaxation (from 86 +/- 6% to 45 +/- 5%, p less than 0.02) and cyclic GMP accumulation (from 192 +/- 53 to 111 +/- 35 fmol/mg, p less than 0.02), indicating reduction in EDRF synthesis or activity by verapamil.(ABSTRACT TRUNCATED AT 250 WORDS)

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1991

Familial recurring cardiac myxoma.

A 34-year-old woman presented with her fourth occurrence of an atrial myxoma and a right lower lung field mass. Her surgical history was extensive. In addition to resection of three previous atrial myxomas, she had undergone resection of her adrenal glands as a teenager because of Cushing's syndrome, and a hysterectomy at age 26 revealed a myxoid leiomyoma. Family history was remarkable as a maternal uncle and daughter died from embolic complications of left atrial myxomas and her sister previously had a left atrial myxoma resected. The patient underwent uncomplicated removal of the myxoma, and resection of the lung mass revealed a granuloma. A review of typical and atypical aspects of cardiac myxomas is provided including a rare and recently described syndrome of familial cardiac myxoma associated with Cushing's syndrome, spotty skin pigmentation and other myxoid tumors.

Adult↗
PubMed1991

Role of superoxide radicals in anoxia reoxygenation-mediated vascular contraction.

To determine the mechanism of anoxic vasoconstriction, precontracted rat aortic rings were exposed to 95% N2, which caused additional contraction. Reoxygenation (95% O2) resulted in initial relaxation followed by contraction. Indomethacin did not affect anoxic contraction or reoxygenation-mediated events, but NG-monomethyl-1-arginine, which inhibits EDRF synthesis, and oxyhemoglobin, which reduces EDRF activity, markedly decreased anoxic contraction and reoxygenation relaxation, and potentiated subsequent contraction. Superoxide dismutase did not affect anoxic contraction, but potentiated reoxygenation relaxation and attenuated subsequent contraction. Endothelin concentrations remained unchanged throughout anoxia and reoxygenation. Thus, anoxic contraction and reoxygenation-mediated early relaxation appear to be due to changes in EDRF. On the other hand, reoxygenation-induced contraction appears related to release of superoxide radicals.

Animals↗