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Biomedical subjects

S W Sharkey

Publications and source records attributed to S W Sharkey.

At least 19 recordsLinked to original sources
PubMed1995

Impact of a thrombolysis research trial on time to treatment for acute myocardial infarction in the emergency department.

Because time to treatment in AMI is a critical factor in long-term outcome, it is important that complex trials designed to improve reperfusion therapy do not delay the time to treatment. Participation in the TIMI 5 trial did not significantly prolong our door-to-needle time. These results indicate that, if done carefully, complex, labor-intensive studies can be performed within a reasonable time limit. Care should be taken to design protocols incorporating easy drug preparation, informed consent by the ED, and efficiency of trial initiation.

Clinical Trials as Topic↗
PubMed1995

Painless ischemia provoked by mental stress in the coronary care unit.

A 30-year-old man suffered a cardiac arrest after setting fire to his home. Continuous ST segment electrocardiographic monitoring in the Coronary Care Unit detected painless ST segment depression during an interview with a police officer. At angiography, the patient proved to have severe three-vessel coronary artery disease. This case demonstrates the clinical value of continuous ST segment monitoring in the ICU. In addition, the case illustrates that mental stress is a potential trigger for acute myocardial ischemia in the ICU.

Adult↗
PubMed1995

Human and canine cardiac troponin T and creatine kinase-MB distribution in normal and diseased myocardium. Infarct sizing using serum profiles.

OBJECTIVE: Cardiac troponin T (cTnT) has been suggested as a new, more specific marker of myocardial cellular damage. The objectives of this study were to examine the distribution of cTnT and creatine kinase (CK)-MB in normal and diseased heart tissue of dogs and humans, and to assess the use of serum cTnT for the estimation of infarct size in dogs. DESIGN: Serial serum specimens over 7 days were obtained from normal dogs (controls, n = 3) and dogs that underwent surgical coronary artery occlusion (n = 6). Heart muscle samples were obtained from the controls and after 3 weeks of occlusion in experimental dogs. Diseased human heart muscle samples were obtained at autopsy from patients who had died of acute myocardial infarction (n = 3). Normal heart muscle samples (n = 3) were obtained at autopsy from patients who died of non-cardiac-related illnesses. Tissues were sectioned and homogenized to harvest both cytosolic and myofibril-bound proteins. Serum samples and tissue homogenates were assayed for cTnT, CK-MB, and myoglobin (humans only). Total protein was assayed on homogenate samples and results were reported as milligrams per gram of total protein. RESULTS: The distributions of cTnT, CK-MB, and myoglobin were equivalent across 14 sites within normal human heart. Creatine kinase-MB and myoglobin were more than 99% cytosolic. Cardiac troponin T was 92% myofibril bound and 8% cytosolic. In the control dog hearts, cTnT was higher and CK-MB was lower in the right ventricle than in the left ventricle. While CK-MB and myoglobin were more than 99% cytosolic, cTnT was 98% myofibril bound and 2% cytosolic. Infarct sizing in dog hearts initially did not correlate well with serum cTnT or CK-MB concentrations. However, when the data were separated by infarct location (right coronary artery; left circumflex coronary artery), the correlations improved dramatically. Differences in tissue concentrations of cTnT and CK-MB between the left and right ventricle might explain the change in correlations. Coronary artery occlusion in dogs and humans resulted in decreased cytosolic and myofibril cTnT and increased CK-MB and myoglobin in diseased myocardial tissue. CONCLUSIONS: Our observed biochemical alterations suggest that the energy-producing proteins CK-MB and myoglobin are upregulated following cellular damage, while the structural and regulatory protein cTnT does not have a mechanism for replacement of lost protein following cell injury and necrosis.

Animals↗
PubMed1992

Effect of impression tray design upon the accuracy of stone casts produced from a single-phase medium-bodied polyvinyl siloxane impression material.

The study examined the accuracy of stone casts produced from impressions taken in stock polycarbonate trays, some of which had been strengthened with autopolymerizing polymethyl methacrylate resin and four designs of custom-made trays. Impressions of an acrylic master model of the mandibular arch on which two extracoronal crown preparations and one intracoronal inlay preparation had been carried out were taken using a medium-bodied polyvinyl siloxane material. Each preparation had been intended with a reference point for later measurement. Five impressions were taken for each type of tray and these were cast in die-stone after 24 h. The distances between the points were measured with a reflex microscope and the means determined for each design of tray. The mean difference between casts produced from the various tray designs and the acrylic master model were determined for each of the distances between the three measuring points. Statistical analysis showed that, with the stock trays, there were no significant differences between any of the modifications, or between them and the acrylic model, for any of the three distances (P greater than 0.1). When the results from the custom-made trays were analysed there were statistical differences between the acrylic model and the casts from the unperforated tray with no stops (P = 0.02), and between the unperforated tray with no stops and the perforated with stops for the distance A-B (P less than 0.01). There were no other significant differences.(ABSTRACT TRUNCATED AT 250 WORDS)

Dental Impression Materials↗
PubMed1991

Cocaine and chest pain: clinical features and outcome of patients hospitalized to rule out myocardial infarction.

OBJECTIVE: To investigate the clinical features, electrocardiographic findings, and hospital course in patients admitted with acute chest pain temporally related to cocaine use. DESIGN: Retrospective data analysis. SETTING: A 485-bed county hospital. PATIENTS: One hundred and one consecutive patients with cocaine-related chest pain admitted to the hospital to rule out myocardial infarction. MEASUREMENTS AND MAIN RESULTS: The quality of the chest pain frequently suggested myocardial ischemia. Dyspnea was common (56%). The onset of chest pain occurred during cocaine use in 21% of patients, within 1 hour of use in 37%, and after 1 hour of use in 42%. Admission electrocardiographic findings were interpreted as normal in 32% of patients; as acute myocardial injury in 8%; as early repolarization variant in 32%; as left ventricular hypertrophy in 16%; and as "other" in 12%. Forty-three percent of patients had ST-segment elevation meeting the electrocardiographic criteria for use of thrombolytic therapy, but such elevation was usually due to the early repolarization variant. The initial total creatine kinase was elevated more than 3.3 mu kat/L (200 U/L) in 43% of patients, and an elevated total creatine kinase was recorded at some time during the hospital course in 47% of patients. The creatine kinase MB fraction was less than 0.02 in all patients. Myocardial infarction was ruled out in all patients. No patient experienced in-hospital cardiovascular complications. CONCLUSION: The quality of acute chest pain related to cocaine use is indistinguishable from that experienced in acute myocardial ischemia. Abnormal or normal variant electrocardiographic findings are common in patients with chest pain related to cocaine use, but nevertheless the incidence of acute myocardial infarction is low. The ST-segment and T-wave changes can mimic acute myocardial injury and are most likely normal findings in young black men that can be readily recognized in the emergency department. Most of these patients do not require admission to an intensive care unit.

Adolescent↗
PubMed1991

Effect of impression tray design and impression technique upon the accuracy of stone casts produced from a putty-wash polyvinyl siloxane impression material.

This study examined the accuracy of stone casts produced from impressions taken in stock polycarbonate trays, some of which had been strengthened with autopolymerizing polymethyl methacrylate resin. Three techniques were used to make the impression of an acrylic master model of the mandibular arch on which two extracoronal preparations for bridgework and one intracoronal inlay preparation had been carried out. Each preparation had been indented with a reference point for later measurement. The impression material was a putty-wash polyvinyl siloxane material. Five impressions were taken for each type of tray for each impression technique and these were cast in die-stone after 24 h. The distances between the points were measured with a reflex microscope and the means determined for each design of tray. The mean difference between casts produced from the various tray designs and the acrylic master model were determined for each of the distances between the three measuring points for the various impression techniques. Statistical analysis showed that, with the polycarbonate stock trays, there were significant differences between some of the modifications and between them and the acrylic model, for the three distances (P less than 0.05). These differences were limited to one measurement for one design of tray for each of the two-stage impression methods. With the one-stage technique the unreinforced tray and those reinforced with acrylic, over the heels and anteriorly, and the barred design were statistically significantly different from the acrylic model for measurement A-B.(ABSTRACT TRUNCATED AT 250 WORDS)

Adhesives↗
PubMed1991

Occlusal abnormalities, pericranial muscle and joint tenderness and tooth wear in a group of migraine patients.

Seventy-two migraine sufferers, whose attacks normally begin during or soon after waking from sleep, were compared with 37 age- and sex-matched controls to establish whether signs of mandibular dysfunction, occlusal discrepancies and known clenching or grinding habits were any more frequent among the former group. Temporomandibular joint tenderness or pain history, masticatory muscle tenderness and known clenching or grinding habits were found to occur at significantly increased levels in the migraine sufferers, with two-thirds of these patients reporting a parafunctional habit. Occlusal abnormalities, including non-working side or protrusive interferences and slides of greater than 1 mm to the intercuspal position, were found to occur at similar frequencies in the two groups. Assessment of wear of the occlusal surfaces also showed no difference, suggesting that any nocturnal habit with a role in migraine is more likely to be clenching in nature. In conclusion, evidence was found to support an aetiological role for nocturnal tooth clenching or grinding in migraine characterized by attacks that start predominantly during sleep or soon after waking, but no evidence of a link with occlusal factors was found in these patients.

Adolescent↗
PubMed1991

Canine myocardial creatine kinase isoenzymes after chronic coronary artery occlusion.

BACKGROUND: Creatine kinase (CK) exists as three cytosolic isoenzymes, CK-MM, CK-MB, and CK-BB, and one mitochondrial isoenzyme. Animal and human observations suggest that the CK-MB content of myocardium is dynamic and may increase in response to ischemia, but the response of the myocardial CK system to chronic coronary artery occlusion is not well-defined. METHODS AND RESULTS: We measured serial changes in myocardial total CK, percent CK-MB, and percent CK-BB before and 3 weeks after coronary artery occlusion in 17 pentobarbital-anesthetized dogs. Tissue biopsies were obtained from the left anterior descending (LAD) coronary artery myocardium, the right coronary artery (RCA) myocardium, and the circumflex coronary artery myocardium at baseline and 3 weeks after LAD occlusion (n = 6), RCA occlusion (n = 5), and no coronary artery occlusion (n = 6). Tissue samples were assayed for total CK, percent CK-MB, and percent CK-BB. Samples were also examined by electron microscopy for evidence of ischemic myopathy. Total myocardial CK activity did not change over 3 weeks. Percent CK-MB increased significantly in the tissue supplied by the occluded artery (4.1-fold in dogs with LAD occlusion and 6.7-fold in dogs with RCA occlusion). Percent CK-BB did not change. Dogs with LAD occlusion had ultrastructural evidence of myopathic fibers interspersed with normal fibers in the LAD myocardium. Dogs with RCA occlusion had no ultrastructural evidence of myopathic fibers in the RCA myocardium. CONCLUSIONS: Chronic coronary artery occlusion causes a pronounced change in the canine myocardial CK system that is limited to the tissue supplied by the occluded coronary artery. These biochemical alterations do not correlate with any cellular ultrastructural changes. Myocardial CK-MB content is dynamic, varies geographically within the heart, and increases rapidly after coronary artery occlusion.

Animals↗
PubMed1989

An analysis of time delays preceding thrombolysis for acute myocardial infarction.

For a patient to derive maximal benefit from intravenous thrombolytic therapy for acute myocardial infarction, early treatment is essential. As part of the Thrombolysis in Myocardial Infarction II trial, this study investigated the time delays that preceded treatment of 236 consecutive patients with intravenous tissue-plasminogen activator (TPA) during acute myocardial infarction. The average (+/- SD) time from the onset of symptoms to treatment with TPA was 153 +/- 54 minutes. After arrival in the emergency department, patients waited an average of 19.9 +/- 17.8 minutes for the initial electrocardiogram. Following the diagnosis of acute myocardial infarction by electrocardiogram, an additional 70 +/- 40 minutes elapsed before thrombolytic therapy began. The interval between the initial electrocardiogram and initiation of treatment with TPA was less when the drug was first administered in the emergency department (46.8 +/- 23.4 minutes) rather than after transfer to the coronary care unit (82.1 +/- 34.7 minutes). In-hospital delays at the two academic and two private hospitals accounted for more than half of the total time from the onset of symptoms to initiation of thrombolytic therapy. We conclude that significant in-hospital delays are likely to occur before a patient receives thrombolytic therapy for acute myocardial infarction. Various factors conspire to create these delays, but a well-organized team approach to treatment will help to minimize delays in the implementation of this new form of therapy.

Adult↗
PubMed1989

Canine myocardial creatine kinase isoenzyme response to coronary artery occlusion.

The response of the myocardial creatine kinase system to acute coronary artery occlusion is not well defined. In the present study, we measured serial changes in myocardial creatine kinase and creatine kinase-MB activities after acute occlusion of the left anterior descending (LAD) coronary artery in 20 open-chest pentobarbital-anesthetized dogs. Tissue samples were obtained from both ischemic and nonischemic left ventricular myocardium at base line and 1-, 3-, and 5-h intervals after LAD occlusion and assayed for total creatine kinase and the isoenzymes creatine kinase-MM, and creatine kinase-MB. Total creatine kinase activity declined significantly in both the ischemic and the nonischemic tissue because of a decline in creatine kinase-MM activity. Concomitantly, creatine kinase-MB activity increased significantly in both the ischemic and the nonischemic tissue. These changes were observed when the duration of the LAD occlusion was 3 h or longer, but not when the duration of the occlusion was 1 h. Thus acute myocardial ischemia causes pronounced changes in the canine myocardial creatine kinase system. These rapid biochemical alterations occur both locally in ischemic tissue and remotely in nonischemic tissue.

Animals↗
PubMed1988

Serial changes in left ventricular wall motion by two-dimensional echocardiography following anterior myocardial infarction.

To evaluate the time course of spontaneous changes in wall motion following anterior infarction, we prospectively performed serial apical four-chamber two-dimensional echocardiography on 45 consecutive long-term survivors of initial transmural anterior infarction. Studies were performed on admission (1 +/- 1 days), 1 week after admission (6 +/- 2 days), at discharge (15 +/- 8 days), and at long-term follow-up (235 +/- 186 days). Ventricular size was expressed as end-diastolic area in square centimeters. Wall motion for this tomographic section was evaluated as the percent change in left ventricular area from end diastole to end systole (% LVA). Patients were grouped on the basis of significant differences for %LVA between the first and fourth studies. Group I (n = 14) had improved wall motion (23 +/- 5% to 38 +/- 9%); group II (n = 23) did not change (22 +/- 9% to 23 +/- 11%); and group III (n = 8) had worsened wall motion (28 +/- 6% to 18 +/- 7%). End-diastolic area did not change over the study period for groups I and II but increased significantly for group III (30 +/- 6 to 35 +/- 4 cm2, p less than 0.05). Most of the increase in end-diastolic area for group III was between the third and fourth study. The percent improvement (%IMP) in wall motion for patients in group I who did not have ventricular fibrillation outside the hospital expressed in days (t) following infarction fit an exponential curve (%IMP = 100-100e-(.108t) that predicts that 70% of eventual recovery will occur in the first 15 days post-infarction. We conclude that changes in left ventricular size and wall motion occur following anterior infarction with improvement or worsening occurring spontaneously in some patients. If improvement occurs, it should be evident within 2 weeks of infarction; infarct expansion in this select group of long-term survivors occurred primarily after discharge.

Clinical Enzyme Tests↗
PubMed1988

Early peak of creatine kinase-MB in acute myocardial infarction with a nondiagnostic electrocardiogram.

This study compared the time from the onset of symptoms to the peak of the creatine kinase-myocardial band (CK-MB) in 34 consecutive patients with acute myocardial infarction. Patients were separated into two groups: group 1 (n = 21) had diagnostic (greater than or equal to 0.1 mV) ST segment elevation on the initial ECG, and group 2 (n = 13) did not have diagnostic ST segment elevation on the initial ECG. In group 1 the time to the peak CK-MB was 16.2 +/- 50 hours vs 10.0 +/- 2.0 hours for group 2 (p = 0.0001). Peak CK-MB was 331 +/- 276 IU/L in group 1 vs 81 +/- 54 IU/L in group 2 (p less than 0.005). In group 1 there were 16 patients who subsequently had a Q wave myocardial infarction as opposed to one patient in group 2 (p = 0.0001). Patients who do not have diagnostic ST segment elevation on the initial ECG have an early but low peak of CK-MB and typically have a non-Q wave infarction. These findings are consistent with early spontaneous restoration of blood flow during the infarction process in these patients. This early restoration of blood flow may provide the substrate for the high incidence of recurrent ischemic events noted in patients with non-Q wave myocardial infarction.

Aged↗
PubMed1987

Beyond the wedge: clinical physiology and the Swan-Ganz catheter.

The Swan-Ganz catheter was introduced into general clinical medicine in 1970 and quickly gained widespread use in the management of critically ill patients. The device offers highly sophisticated physiologic information; however, in many instances, only the wedge pressure and the cardiac output are utilized when managing acutely ill patients. The purpose of this review is to illustrate and explain the array of physiologic data available from the Swan-Ganz catheter in most circumstances. A basic understanding of the information that can be obtained with the Swan-Ganz catheter is quite useful in the diagnosis and management of a variety of cardiovascular disorders. In addition, the Swan-Ganz catheter can be a helpful tool for teaching cardiovascular pathophysiology.

Acute Disease↗