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Biomedical subjects

R L Jesse

Publications and source records attributed to R L Jesse.

33 records · Page 2Linked to original sources
PubMed1997

Use of the combination of myoglobin and CK-MB mass for the rapid diagnosis of acute myocardial infarction.

Early identification of patients presenting with myocardial infarction (MI) is necessary for rapid initiation of treatment. Currently, MI has been diagnosed using the combination of the history, electrocardiogram (ECG), and biochemical markers of myocardial necrosis. Unfortunately, all lack sufficient sensitivity and specificity to confidently identify most patients with MI in a timely enough fashion to influence early intervention. Development of newer immunochemical assays for CK-MB mass and myoglobin have allowed for earlier, more rapid diagnosis; however, each has important limitations. The diagnostic sensitivity of CK-MB mass, myoglobin, and the combination of both were analyzed at the time of presentation (0 hours) and again 4 hours later in 101 patients admitted from the emergency department (ED) with possible MI. Twenty patients were subsequently diagnosed as having MI. The sensitivity of the initial ECG was 60%, compared with the sensitivities of the initial myoglobin and CK-MB mass of 70% and 30%, respectively. By 4 hours the sensitivity of myoglobin had increased to 85% and CK-MB mass to 90%. The combination of the initial myoglobin and CK-MB mass had a sensitivity of 85%. Combining these two markers, using both the initial and 4-hour samples, raised the sensitivity to 100%, with a specificity of 100% and negative predictive value of 100%. When patients with diagnostic ECGs were excluded, the sensitivity of the combination at 0 hours was 80% with a specificity of 84%, while the use of the 0- and 4-hour markers had a sensitivity and specificity of 100% and 100%, respectively. We conclude that the combination of CK-MB mass and myoglobin can rapidly diagnose or exclude MI in as short as 4 hours after ED presentation, and accuracy is not different in patients without diagnostic ECGs. Application of this strategy could potentially lead to more rapid intervention in patients with MI, while also allowing early identification of lower risk patients.

Biomarkers↗
PubMed1995

Dehydroepiandrosterone inhibits human platelet aggregation in vitro and in vivo.

The hypothesis has been advanced that the adrenal steroids dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS) exert antiatherogenic and cardioprotective actions. Platelet activation has also been implicated in atherogenesis. To determine if DHEA and DHEAS affect platelet activation, the effects of these steroids on platelet aggregation were assessed both in vitro and in vivo. When DHEAS was added to pooled platelet-rich plasma before the addition of the agonist arachidonate, either the rate of platelet aggregation was slowed or aggregation was completely inhibited. Inhibition of platelet aggregation by DHEA was both dose- and time-dependent. Inhibition of platelet aggregation by DHEA was accompanied by reduced platelet thromboxane B2 (TxB2) production. Inhibition of platelet aggregation by DHEA was also demonstrated in vivo. In a randomized, double-blind trial, 10 normal men received either DHEA 300 mg (n = 5) or placebo capsule (n = 5) orally three times daily for 14 days. In one man in the DHEA group arachidonate-stimulated platelet aggregation was inhibited completely during DHEA administration, whereas in three other men in the DHEA group the rate of platelet aggregation was prolonged, and the sensitivity and responsiveness to agonist were reduced. None of the men in the placebo group manifested any change in platelet activity. These findings suggest that DHEA retards platelet aggregation in humans. Inhibition of platelet activity by DHEA may contribute to the putative antiatherogenic and cardioprotective effects of DHEA.

Dehydroepiandrosterone↗
PubMed1995

Sustained inhibition of nitric oxide by NG-nitro-L-arginine improves myocardial function following ischemia/reperfusion in isolated perfused rat heart.

It has been postulated that nitric oxide (NO) can react with superoxide anion (.O2-) to generate hydroxyl (.OH) radical. If this is correct, inhibition of NO synthesis could attenuate .OH radical mediated ischemia/reperfusion injury. Therefore we studied the effects of NG-nitro-L-arginine (L-NNA), a competitive inhibitor of the NO synthase enzyme on ischemia/reperfusion injury injury in isolated perfused rat hearts. Three groups of rats (n = 12-15) were studied. Group I: Untreated ischemia/reperfusion control (37.5 min of global ischemia followed by 20 min reperfusion); Group II: ischemia/reperfusion with 25 microM NG-nitro-L-arginine; and Group III: ischemia/reperfusion in the presence of L-NNA and 2 mM L-arginine, the substrate for NO synthase. Coronary flow (in ml/min) and ventricular developed pressure, +dP/dt and -dP/dt were measured 5 min prior to ischemia and at the end of reperfusion. Baseline preischemic developed pressure was significantly lower in L-NNA perfused hearts than controls (76.8 +/- 5.9 v 97.6 +/- 2.9 mmHg, P < 0.05). However, the developed pressure following reperfusion was significantly greater in L-NNA perfused hearts (57.4 +/- 7.4 v 20.8 +/- 6.4 mmHg in control). This protective effect was reversed by the addition of L-arginine. Preischemic coronary flow was decreased significantly in the L-NNA group (6.4 +/- 0.5 ml/min) compared to controls (11.6 +/- 0.7 ml/min). The duration of sinus rhythm was significantly improved from 3.8 +/- 1.2 min in controls to 15.1 +/- 0.8 min in L-NNA perfused hearts. A corresponding significantly lower incidence of arrhythmias was observed (10.2 +/- 1.5 in ischemia/reperfusion group v 1.7 +/- 0.8 min with L-NNA).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1995

Left atrial appendage contractile function in atrial fibrillation. Influence of heart rate and cardioversion to sinus rhythm.

BACKGROUND: A high incidence of embolic phenomena is associated with atrial fibrillation (AF) and the left atrial appendage (LAA) is frequently the source of the emboli. Thrombus formation may be due to stasis within the fibrillating and inadequately emptying LAA. Because LAA emptying in AF may be the result of mechanical compression by the adjacent left ventricle, it is possible that left ventricular diastolic filling duration will importantly influence passive emptying of the LAA. We hypothesized that the magnitude of emptying of the LAA in AF is related to the duration of left ventricular diastolic filling which is determined by the ventricular response rate in AF. OBJECTIVE: The objective of our study was to determine the relationship of ventricular response rate in AF to LAA emptying and to assess the influence of sinus rhythm and heart rate on LAA emptying immediately after direct current cardioversion to sinus rhythm. METHODS: To study this, we used transesophageal echocardiography to measure LAA ejection fraction ([LAAmax-LAAmin]/LAAmax x 100%) and evaluated its relationship to left ventricular response rate (VRR) in 26 patients with AF (mean age, 65 +/- 7 [1 SD] years). RESULTS: There was a strong inverse relationship between LAA ejection fraction and VRR in AF (r = -0.73; p < 0.001). LAA ejection fraction during AF was 26 +/- 10%, and immediately after successful cardioversion, it increased to 46 +/- 12% (p < 0.001). However, during sinus rhythm there was no relationship between LAA ejection fraction and VRR (r = 0.06; p = NS) in the subgroup of patients who were successfully converted to sinus rhythm. There were poor relationships between LAA ejection fraction and peak transmitral flow velocity (r = -0.41; p = NS) or pulmonary venous flow velocity (r = -0.03; p = NS) in AF. CONCLUSION: These results indicate that the magnitude of LAA emptying in AF is strongly and inversely influenced by ventricular rate. Direct current cardioversion to sinus rhythm is associated with an increase in the magnitude of LAA emptying that is not influenced by heart rate. The magnitude of LAA emptying may be an important factor in the formation of thromboemboli in AF. The extent to which controlling the VRR in chronic AF will prevent stasis and LAA thrombus formation remains to be determined.

Aged↗
PubMed1994

Oxidant stress increases heat shock protein 70 mRNA in isolated perfused rat heart.

Ischemia/reperfusion (I/R) and preconditioning of the heart by coronary artery occlusions increase expression of heat shock protein 70 (HSP 70). Because free radicals are generated during I/R, we hypothesized that the oxidant stress might contribute to an increased expression of HSP 70. Isolated rat hearts were perfused with free radical-generating systems such as xanthine/xanthine oxidase (X/XO), irradiated rose bengal (RB) generating singlet oxygen, and H2O2 for 15 min followed by 30 min of recovery period. Significant decrease in developed pressure and coronary flow occurred after perfusion with X/XO, H2O2, and RB. During I/R, the developed pressure and coronary flow were 60 +/- 8 and 80 +/- 5%, respectively, of control, which improved significantly with superoxide dismutase. The expression of HSP 70 mRNA increased over 13-fold in hearts perfused with X/XO, 6- to 7-fold with RB, and over 5-fold with H2O2. With I/R, an over 10-fold increase in HSP 70 mRNA was observed, which decreased significantly in the presence of superoxide dismutase. These results demonstrate that oxidant stress directly increases HSP 70 mRNA in the rat heart. It is concluded that one of the potential mechanisms of expression of HSP 70 by I/R may be oxygen radicals.

Animals↗
PubMed1992

Singlet oxygen: a potential culprit in myocardial injury?

The purpose of this study was to explore the role of singlet oxygen in cardiovascular injury. To accomplish this objective, we investigated the effect of singlet oxygen [generated from photoactivation of rose-bengal] on the calcium transport and Ca(2+)-ATPase activity of cardiac sarcoplasmic reticulum and compared these results with those obtained by superoxide radical, hydrogen peroxide and hydroxyl radical. Isolated cardiac SR exposed to rose bengal (10 nM) irradiated at (560 nm) produced a significant inhibition of Ca2+ uptake; from 2.27 +/- 0.05 to 0.62 +/- 0.05 mumol Ca2+/mg.min (mean +/- SE) (P less than 0.01) and Ca(2+)-ATPase activity from 2.08 +/- 0.05 mumol Pi/min.mg to 0.28 +/- 0.04 mumol Pi/min.mg (mean +/- SE) (P less than 0.01). The inhibition of calcium uptake and Ca(2+)-ATPase activity by rose bengal derived activated oxygen (singlet oxygen) was dependent on the duration of exposure and intensity of light. The singlet oxygen scavengers ascorbic acid and histidine significantly protected SR Ca(2+)-ATPase against rose bengal derived activated oxygen species but superoxide dismutase and catalase did not attenuate the inhibition. SDS-polyacrylamide gel electrophoresis of SR exposed to photoactivated rose bengal up to 14 min, demonstrated complete loss of Ca(2+)-ATPase monomer band which was significantly protected by histidine. Irradiation of rose bengal also caused an 18% loss of total sulfhydryl groups of SR. On the other hand, superoxide (generated from xanthine oxidase action on xanthine) and hydroxyl radical (0.5 mM H2O2 + Fe(2+)-EDTA) as well as H2O2 (12 mM) were without any effect on the 97,000 dalton Ca(2+)-ATPase band of sarcoplasmic reticulum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Oxidative damage to the myocardium: a fundamental mechanism of myocardial injury.

Certain pathophysiologic conditions are able to shift normal oxygen metabolism towards univalent reduction, resulting in the production of reduced oxygen intermediates, including free radicals and their metabolites. Oxygen free radicals have been implicated in a number of pathologic conditions, including myocardial injury. The possible sources of oxygen free radicals, the detection of the radicals during ischemia/reperfusion and possible mechanisms of free radical damage are discussed. The clinical implications of free radical damage and the experimental drug therapies at present under investigation are also reviewed.

Animals↗
PubMed1979

Modulation of purified phospholipase A2 activity from human platelets by calcium and indomethacin.

A membrane bound phospholipase A2 (phosphatide 2-acylhydrolase, EC 3.1.1.4) from human platelets has been purified 3500-fold, and partially characterized. Phospholipase A2 activity was assayed using [1(-14)C] oleate-labeled Escherichia coli or sonicated dispersions of synthetic phospholipids. The 2-acyl specificity of the phospholipase activity was confirmed using phosphatidylethanolamine labeled in the C-1 position as substrate. The purified enzyme was maximally active between pH 8.0 and 10.5, and had an absolute requirement for low concentrations of Ca2+. Indomethacin, but not aspirin, inhibited phospholipase A2 activity.

Blood Platelets↗
PubMed1976

Trypsin-induced phospholipase activity in human platelets.

Trypsin mediates a release of arachidonic acid with resultant increase in O2 consumption (a reflection of cyclo-oxygenase activity) by whole human platelets that is similar to thrombin's effect on these cells. The trypsin and thrombin effects can be differentiated in two ways: (1) at saturating concentrations the measured effects of trypsin greatly exceed those of thrombin; (2) EGTA [ethanedioxybis(ethylamine)-NNN'N'-tera-acetate] augments the effect of thrombin but not of trypsin. Thus trypsin and thrombin probably act at different loci in the pathway that induces phospholipase activity in human platelets.

Arachidonic Acids↗
PubMed1976

Arachidonic acid release from diacyl phosphatidylethanolamine by human platelet membranes.

At pH9.5 in the presence of 10 mM-Ca2+, human platelet membranes released 22% (167 of 785 nmol) of arachidonic acid that was esterified to phospholipids. With the use of synthetic choline (dinonadecanoyl) and ethanolamine (diheptadecanoyl) phosphoglycerides as internal reference compounds, 115 nmol of the released arachidonic acid was shown to be derived from endogenous breakdown of the phosphatidylethanolamine fraction. Further, the lysophosphatidylethanolamine that was released along with the arachidonic acid was shown virtually to lack fatty aldehydes and to contain a preponderance of fatty acids that have a preference for esterification at the 1-position of naturally occurring phosphatidylethanolamine of human platelets. These findings ruled out plasmalogen phosphatidylethanolamine as the source of the released arachidonic acid. We conclude that diacyl phosphatidylethanolamine was the principal source of arachidonic acid released by human platelet membranes under the conditions described.

Aldehydes↗
PubMed1976

Initiation of phospholipase A2 activity in human platelets by the calcium ion ionophore A23187.

Phospholipase A2 activity in a suspension of intact platelets was induced by addition of a Ca2+-ionophore, A23187. This action of ionophore A23187 was enhanced by EGTA and inhibited by an excess of Ca2+ in the medium, findings which suggest that A23187 is able to mobilize intracellular Ca2+ for the latter's role as an essential cofactor for phospholipase A2 activity.

Anti-Bacterial Agents↗
PubMedDate not supplied

Cost-effectiveness of cardiac troponin I in a systematic chest pain evaluation protocol: use of cardiac troponin I lowers length of stay for low-risk cardiac patients.

We evaluated several measures of clinical and fiscal interest to assess the effect of adding an automated cardiac troponin I (c-TnI) assay to our current cardiac panel, which consists of creatine kinase MB (CK-MB), myoglobin, total CK activity, and a calculated CK-MB relative index. Samples were collected on admission and at 3, 6, and 8 hours after admission as part of our diagnostic protocol. Our study was designed to collect data on a control group of patients, implement a change (i.e., c-TnI testing), and then measure the effect of the change on a test population having otherwise equivalent diagnostic and therapeutic pathways. We assessed differences in patient hospital and cardiac care unit length of stay (LOS), time to cardiac catheterization, and hospital and laboratory charges and costs. We found that adding c-TnI to our testing regimen decreased LOS for the large test population. Within this large test population, patients classified as low risk for acute myocardial infarction experienced statistically and clinically significant shorter LOS and lower total and variable hospital costs; for patients with unstable angina, there was an increase (though not statistically significant) in laboratory costs.

Adult↗
PubMedDate not supplied

Noninvasive detection of transplant coronary artery disease by dobutamine stress echocardiography.

Coronary artery disease has emerged as the leading cause of late morbidity and mortality in heart transplant recipients. The incidence of allograft coronary artery disease has been reported to be as high as 40% to 50% by 5 years. Coronary angiography remains the standard approach for surveillance of coronary artery disease in this patient population. However, the detection and surveillance of allograft coronary disease by noninvasive methods remains a challenge. The purpose of this study was to determine the value of dobutamine stress echocardiography as a noninvasive screening test to rule out the presence of anatomically significant allograft coronary artery disease and to assess its prognostic power. Dobutamine stress echocardiography was carried out according to a standard protocol in which dobutamine was infused at 5, 10, 20, 30, and 40 micrograms/kg/min intravenously at 5-minute stages with 12-lead electrocardiogram and blood pressure monitoring. Left ventricular wall motion was analyzed at baseline and at peak dobutamine dose. Mean age (+/- standard error of the mean) of the study population was 50.5 +/- 1.5 years, and mean duration (+/- standard error of the mean) since transplantation was 57 +/- 5 months. The sensitivity, specificity, and positive and negative predictive accuracy of dobutamine stress echocardiography were 95%, 55%, 69%, and 92%, respectively. In the 12-month follow-up study 12 patients with abnormal dobutamine stress echocardiographic findings had 15 major cardiac events whereas no event occurred in patients with normal dobutamine stress echocardiograms.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗