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Biomedical subjects

F S Apple

Publications and source records attributed to F S Apple.

At least 73 records · Page 4Linked to original sources
PubMed1996

Cardiac troponin I and T concentrations in patients with cocaine-associated chest pain.

Patients with cocaine-related chest pain with electrocardiographic (ECG) abnormalities are often admitted to rule out acute myocardial infarction (AMI). Cardiac troponin I and T should be superior to measurement of creatine kinase (CK)-MB for detecting cardiac injury in patients with coexisting skeletal muscle injury. We prospectively evaluated 19 consecutive patients with acute chest pain related to cocaine use who were hospitalized to rule out AMI. The admission ECG was abnormal in 16 of 19 patients. Total CK and CK-MB were elevated during the hospital course in 14 and 3 patients, respectively. Cardiac troponin I and cardiac troponin T levels were within normal limits in all patients demonstrating that recent myocardial injury did not occur. Clinically, no patient had an AMI. Cocaine-induced thoracic skeletal muscle injury or transient cocaine-induced coronary vasospasm should be considered as alternative sources of chest pain in these patients.

Adult↗
PubMed1996

Serum cardiac troponin T concentrations in hospitalized patients without acute myocardial infarction.

The present study was designed to determine whether the measurement of serum levels of cardiac troponin T (cTnT) would establish the presence of myocardial injury in 79 patients, within 12 h of hospitalization, whose admission and final discharge diagnosis were not related to myocardial infarction. Independent classification by clinicians resulted in 35 (44%) patients characterized as having unsuspected myocardial injury and 44 (56%) without myocardial injury. Increased serum cTnT identified 94% of myocardial injury patients, compared to increased serum creatine kinase MB (CK-MB) mass which identified 69%. Negative serum cTnT and CK-MB concentrations respectively excluded 73 and 50% of patients evidently without myocardial injury, respectively. A total of 12 patients, 9 with and 3 without elevated CK-MB concentration, had unexplained cTnT elevations. While our findings show cardiac troponin T to be more efficient than CK-MB in determining and excluding myocardial injury, even in a randomly selected population with a very high probability, unexplained elevations of cardiac troponin T question its role as an absolute cardiospecific marker.

Biomarkers↗
PubMed1995

Cardiac troponin, CK-MB and myoglobin for the early detection of acute myocardial infarction and monitoring of reperfusion following thrombolytic therapy.

It is important to establish as soon as possible whether patients who present with chest pain are having an acute myocardial infarction (AMI). Ideally, sensitive and specific serum myocardial markers could provide the basis for early detection as well as determine the status of reperfusion following thrombolytic therapy. The present study examined the utility of cardiac troponin I (cTnI), CK-MB, and myoglobin for the sensitive and specific detection of AMI in 98 consecutive patients presenting to the emergency department (ED) with chest pain. In addition, cardiac troponin T (cTnT), CK-MB, and myoglobin samples were measured over a 90 min time period following thrombolytic therapy in nine separate AMI patients to assess reperfusion. In the ED study, CK-MB, myoglobin, and cTnI were equally sensitive (100%) for the detection of AMI in patients who presented 7.4-14 h after onset of chest pain. However, cTnI was the most specific serum marker (specificity 91.9% compared to CK-MB 85.6%, myoglobin 61.4%). Five of the six non-related AMI patients who had an elevated cTnI had clinically documented myocardial involvement. In the reperfusion study, cTnT, CK-MB and myoglobin, relative increases were greater in reperfused compared to non-reperfused patients. Within the reperfused group, the relative increase of cTnT was greater than CK-MB and myoglobin at 90 min following thrombolytic therapy. These findings show the clinical utility of cardiac-specific troponins as markers for the early detection of AMI and monitoring of reperfusion following thrombolytic therapy.

Creatine Kinase↗
PubMed1995

Cardiac troponin-I is not expressed in fetal and healthy or diseased adult human skeletal muscle tissue.

Cardiac troponin-I (cTnI) is not found in sera of patients with skeletal muscle disease in the absence of myocardial injury. It is not known, however, whether trace amounts of cTnI are expressed in regenerating human skeletal muscle, as has been observed with creatine kinase MB. Using immunohistochemical and biochemical techniques, we investigated cTnI expression in various human muscle tissues: human heart tissue (n = 5), normal adult skeletal muscle (n = 3), and fetal heart (n = 3) and skeletal muscle (n = 3) obtained, respectively, during heart transplant, from autopsy, or from a tissue bank. Specimens from diagnostic tissue biopsies were used as diseased skeletal muscle: polymyositis (PM), n = 13; Duchenne muscular dystrophy (DMD), n = 6. Frozen sections 8 microns thick were stained immunohistochemically for either cTnI or TnI (cardiac or skeletal) by using monoclonal antibodies (MAb) 2B1.9 (cTnI specific) or 3C5.10 (reactive with all TnI isoforms), respectively. cTnI was measured in tissue homogenates by an immunofluorometric assay. Cardiac muscle was stained by both MAbs. Normal fetal and adult skeletal muscle, and samples from all of the PM and DMD patients, stained only with the nonspecific MAb (3C5.10), confirming the sole presence of skeletal TnI. No cTnI was detectable by immunoassay in any skeletal muscle sample. We conclude that cTnI is not expressed in human skeletal muscle during development or during regenerative muscle disease processes such as PM or DMD.

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↗
PubMed1994

Expression of creatine kinase M and B mRNAs in treadmill trained rat skeletal muscle.

Gastrocnemius muscle from treadmill trained rats was analyzed for creatine kinase (CK) isoenzyme activities by agarose electrophoresis and M and B CK mRNA levels by Northern blot analysis. Total CK activity in exercise-trained (143 (SD 15) U/g) and control (154 (SD 16) U/g) muscles did not differ. CK-MB increased 220% in exercised-trained muscle compared to controls. CK-B subunit mRNA increased 40%, while CK-M subunit mRNA decreased 42% in exercised-trained muscle compared to control. Thus, gene expression of CK isoenzymes appears to be partially controlled at the level of transcription following exercise training.

Animals↗
PubMed1994

Clinical implementation of a rapid, automated assay for assessing fetal lung maturity.

We retrospectively determined cutoff levels and implemented the use of the TDxFLx assay in assessing the likelihood or absence of respiratory distress syndrome or fetal lung maturity (FLM) in a high-risk obstetric setting when compared to the lecithin/sphingomyelin (L/S) ratio and disaturated lecithin (DSL) measurements. Using a mature TDxFLx cutoff value of > or = 50 mg/g and an immature cutoff value of < 20 mg/g, 88% of L/S ratio and DSL measurements could be eliminated without compromise to the patient. The > or = 50 mg/g TDxFLx cutoff value resulted in a sensitivity of 100% and specificity of 88%. We also recommend the use of the TDxFLx assay as a screening test in diabetic pregnancies. More timely patient care occurred when the rapid TDxFLx assay was implemented by the laboratory and used by clinicians.

Albumins↗
PubMed1994

TNF-alpha effect on oxygen free radical scavenging and generating enzymes in rat liver.

The presence of cancer induces metabolic alterations in distant, tumor-free tissues and organs of the host. A remote humoral effect of cancer growing extrahepatically is an increase in the activity of oxidant and a decrease of antioxidant enzymes in the liver of the tumor-bearing animal. We speculated that TNF-alpha, produced by host cells, the cancer, or both, is responsible for these changes. When human recombinant TNF-alpha, 100 micrograms/kg/d i.p. for 5 days, was injected in groups of rats fed ad libitum, starved, or pair-fed, a decrease in the activity of superoxide dismutase and glutathione peroxidase and an increase in xanthine oxidase was observed, particularly with pair-fed controls. It is concluded that TNF-alpha, directly or indirectly, causes these enzyme alterations in the tumor-free liver of a tumor-bearing host.

Analysis of Variance↗
PubMed1994

Cardiac troponin-T immunoassay for diagnosis of acute myocardial infarction.

We evaluated the analytical and clinical performance of an immunoassay for cardiac troponin T (cTnT). Within-run and total imprecision ranged from 1.6 to 11.3%. The sensitivity and linear range was 0.015 and 13 micrograms/L, respectively. Frozen samples were stable for at least 8 weeks. No interferences were seen with lipids or bilirubin (total and conjugated). Hemoglobin caused a negative bias at concentrations > 4 g/L. Heparinized plasma showed a 6% negative bias compared with serum. The clinical utility of cTnT was compared with that of creatine kinase (CK)-MB (mass assay). The sensitivity of cTnT measurements from 63 patients with acute myocardial infarction (AMI) (cTnT cutoff 0.1 microgram/L) was 60% at 0-3 h, 59% at 3-6 h, 94% at 6-9 h, 90% at 9-12 h, 99% at 12-24 h, 92% at 24-48 h, 83% at 48-72 h, and 100% at 72-96 h. Corresponding results for CK-MB (cutoff 5.0 micrograms/L and 2.5% relative index) were 45%, 64%, 82%, 97%, 87%, 81%, 54%, and 59%. The specificity of the markers from 49 non-AMI patients was 46% and 79% for cTnT and CK-MB, respectively. We show that CK-MB is more specific for diagnosis of AMI, and propose that cTnT is more sensitive to myocardial injury.

Bilirubin↗
PubMed1993

Cardiac troponin I. A marker with high specificity for cardiac injury.

BACKGROUND: Levels of MBCK can be increased in patients with skeletal muscle injury or renal failure in the absence of myocardial injury, causing diagnostic confusion. This study was designed to determine whether measurement of cardiac troponin I (cTnI), a myocardial regulatory protein with comparable sensitivity to MBCK, has sufficient specificity to clarify the etiology of MBCK elevations in patients with acute or chronic skeletal muscle disease or renal failure. METHODS AND RESULTS: Of the patients (n = 215) studied, 37 had acute skeletal muscle injury, 10 had chronic muscle disease, nine were marathon runners, and 159 were chronic dialysis patients. Patients were evaluated clinically, by ECG, and by two-dimensional echocardiography. Total creatine kinase (normal, < 170 IU/L) was determined spectrophotometrically, and cTnI (normal, < 3.1 ng/mL) and MBCK (normal, < 6.7 ng/mL) were determined with specific monoclonal antibodies. Values above the upper reference limit were considered "elevated." Elevations of total creatine kinase were common, and elevations of MBCK occurred in 59% of patients with acute muscle injury, 78% of patients with chronic muscle disease and marathon runners, and 3.8% of patients with chronic renal failure. Some of the patients were critically ill; five patients were found to have had myocardial infarctions and one had a myocardial contusion. cTnI was elevated only in these patients. CONCLUSIONS: Elevations of cTnI are highly specific for myocardial injury. Use of cTnI should facilitate distinguishing whether elevations of MBCK are due to myocardial or skeletal muscle injury.

Adult↗
PubMed1992

Glycerol interference in serum lipase assay falsely indicates pancreas injury.

The measurement of serum lipase activity has been shown to be a very sensitive and specific marker for the diagnosis of pancreatic injury. Two case reports are presented showing that glycerol ingested coincidentally in the formulation of several medications taken therapeutically and given in the emergency room causes a falsely elevated serum lipase activity when measured on the Kodak Ektachem 700 clinical analyzer (Eastman Kodak Co., Rochester, NY). The transient but falsely elevated serum lipase activity could potentially affect the differential diagnosis of patients by the admitting physician.

Acute Disease↗
PubMed1992

Acute myocardial infarction and coronary reperfusion. Serum cardiac markers for the 1990s.

Early detection of AMI and reperfusion offers advantages to emergency department physicians when making diagnostic, therapeutic, and triage decisions. The measurement of serial CK-MB in serum remains the gold standard clinical laboratory test. A recommended enzyme ordering pattern scheme is described in Table 5. Rapidly available CK-MB results (two values separated by 30 to 180 minutes) may (1) prevent emergency department discharge of patients with AMI having nondiagnostic electrocardiographs and (2) allow more rapid use and assessment of thrombolytic therapy with AMI in patients not having diagnostic electrocardiographs. Technology no longer limits the availability of a stat CK-MB from the laboratory. However, each institution will have to assess the real value of a stat CK-MB. The future potential and clinical utility of troponin isoenzymes, CK isoforms, and myoglobin for diagnostic and therapeutic purposes still remain to be shown in real time settings.

Animals↗
PubMed1992

The creatine kinase system in the serum of runners following a doubling of training mileage.

This study examined the response of the serum creatine kinase (CK) isoenzyme/isoform system following the stress of successive weeks of increased training. Four highly-trained male long-distance runners doubled their training mileage [45.0 (SD 3.5) to 81.2 (4.7) miles] for 3 weeks. Venous blood samples were obtained prior to the start of the increased training period and at the end of each week, days 7, 14, and 21, 12 h after a training run. All runners experienced a significant increase in training perception difficulty, which correlated with the significant increase in training mileage. While total CK activities did not become significantly elevated until day 14, the tissue isoform CK-MM3, as well as the ratio of CK-MM3 to MM1 (final CK-MM degradation isoform) became significantly elevated at day 7 and remained elevated throughout day 21. These findings demonstrate that an increase in training mileage caused a significant and continuous release of tissue CK activity from skeletal muscle into the circulation.

Adult↗