Hyponatremia.
Explore the source record for details and available documents.
False Positive Reactions↗
Biomedical subjects
J H Ladenson
Publications and source records attributed to J H Ladenson.
Direct comparison of early elevations of cardiac troponin T and I in patients with clinical unstable angina.
BACKGROUND: The aim of this study was to compare the prognostic efficacy of cardiac troponin T (cTnT) and I (cTnI) in patients with clinical unstable angina. METHODS: We studied 74 patients with chest pain at rest, electrocardiographic evidence of myocardial ischemia, and normal (<6.7 ng/mL) values of creatine kinase-MB. cTnT was measured with a commercial assay (cutoff level 0.1 ng/mL) and cTnI with a preliminary research application (cutoff level 3.1 ng/mL). All patients had blood drawn at baseline and 8 hours thereafter. The prospectively defined end point was the proportion of patients identified by each assay as having myocardial damage. RESULTS: cTnT and cTnI were elevated in the same percentage of patients (18 of 74; 24%). Overall, 23 patients had elevations of 1 or both markers. In 13 there were elevations of both. Ten patients had elevations of only one (5 for each marker). In 51 patients, no elevations were present. Death or nonfatal myocardial infarction was more frequent in patients with elevated cTnI (27.7% vs 5.3%; P =.02) than those with normal values. The prognostic influence of cTnT was less (17% vs 8.5%; P =.2). However, the difference between the 2 markers when compared directly was not statistically significant (27.7% vs 17%; P = NS). CONCLUSIONS: These data indicate that both markers identify myocardial damage in equal numbers of patients with clinical unstable angina. Patients with elevations had a worse short-term outcome. The significance of the minor differences in prognostic value will require additional studies.
Aged↗
Development, characterization, and use of monoclonal antibodies made to antigens expressed on the surface of fetal nucleated red blood cells.
BACKGROUND: Current methods for obtaining fetal cells for prenatal diagnosis are invasive and carry a small (0.5-1.0%) but definite risk of miscarriage. An attractive alternative would be isolation of fetal cells from peripheral maternal blood using antibodies with high specificity and avidity. METHODS: To generate antibodies, we purified nucleated red blood cells (NRBCs) from fetal livers and used them as the immunogen to generate monoclonal antibodies (mAbs) directed against surface antigens. RESULTS: The four antibodies recognized at least two conformationally sensitive epitopes of the transferrin receptor. Isolation of NRBCs from 252 maternal blood samples using these antibodies in magnetic activated cell sorting after an initial density gradient centrifugation yielded 0-419 NRBCs per 25 mL of maternal blood. One antibody, 2B7.4, not only isolated the highest number of NRBCs (>10 in 90% of the samples) but also isolated these NRBCs in 78 consecutive maternal samples. CONCLUSION: Antibody 2B7.4 shows promise for the isolation of NRBCs from maternal blood and should allow studies concerning the source of these cells, fetal vs maternal, and the factors controlling their prevalence.
Animals↗
Thyroid function during pregnancy.
BACKGROUND: This Case Conference reviews the normal changes in thyroid activity that occur during pregnancy and the proper use of laboratory tests for the diagnosis of thyroid dysfunction in the pregnant patient. CASE: A woman in the 18th week of pregnancy presented with tachycardia, increased blood pressure, severe vomiting, increased total and free thyroid hormone concentrations, a thyroid-stimulating hormone (TSH) concentration within the reference interval, and an increased human chorionic gonadotropin (hCG) beta-subunit concentration. ISSUES: During pregnancy, normal thyroid activity undergoes significant changes, including a two- to threefold increase in thyroxine-binding globulin concentrations, a 30-100% increase in total triiodothyronine and thyroxine concentrations, increased serum thyroglobulin, and increased renal iodide clearance. Furthermore, hCG has mild thyroid stimulating activity. Pregnancy produces an overall increase in thyroid activity, which allows the healthy individual to remain in a net euthyroid state. However, both hyper- and hypothyroidism can occur in pregnant patients. In addition, two pregnancy-specific conditions, hyperemesis gravidarum and gestational trophoblastic disease, can lead to clinical hyperthyroidism. The normal changes in thyroid activity and the association of pregnancy with conditions that can cause hyperthyroidism necessitates careful interpretation of thyroid function tests during pregnancy. CONCLUSION: Assessment of thyroid function during pregnancy should be done with a careful clinical evaluation of the patient's symptoms as well as measurement of TSH and free, not total, thyroid hormones. Measurement of thyroid autoantibodies may also be useful in selected cases to detect maternal Graves disease or Hashimoto thyroiditis and to assess risk of fetal or neonatal consequences of maternal thyroid dysfunction.
Adult↗
Patterns and potential value of cardiac troponin I elevations after pediatric cardiac operations.
BACKGROUND: Perioperative myocardial injury is a major determinant of postoperative cardiac dysfunction for congenital heart disease, but its assessment during this period is difficult. The objective of this study was to determine the suitability of using postoperative serum concentrations of cardiac troponin I (cTnI) for this purpose. METHODS: Cardiac troponin I levels were measured serially in the serum of patients undergoing uncomplicated repairs of atrial septal defect (n = 23), ventricular septal defect (n = 16) or tetralogy of Fallot (n = 16). The concentrations were correlated with intraoperative parameters (cardiopulmonary bypass time, aortic cross-clamp time, and cardiac bypass temperature), and postoperative parameters (magnitude of inotropic support, duration of intubation, and postoperative intensive care and hospital stay). RESULTS: Postoperative absolute cTnI levels were lesion specific, with a pattern of increase and decrease similar for each lesion. For the total cohort, significant correlations between postoperative cTnI levels at all times (r = 0.43 to 0.83, p < 0.05) until 72 hours were noted for all parameters, except for cardiac bypass temperature. When evaluated as individual procedure groups, no significant relationships were noted in the atrial septal defect group, whereas postoperative cTnI levels were more strongly correlated with all intraoperative and postoperative parameters in the ventricular septal defect group than in the tetralogy of Fallot group. CONCLUSIONS: This study suggests that cTnI values immediately after operation reflect the extent of myocardial damage from both incisional injury and intraoperative factors. Cardiac tropinin I levels in the first hours after operation for congenital heart disease are a potentially useful prognostic indicator for difficulty of recovery.
Body Temperature↗
Troponin I phosphorylation in the normal and failing adult human heart.
BACKGROUND: In the failing human heart myofibrillar calcium sensitivity of tension development is greater and maximal myofibrillar ATPase activity is less than in the normal heart. Phosphorylation of the cardiac troponin I (cTnI)-specific NH2-terminus decreases myofilament sensitivity to calcium, while phosphorylation of other cTnI sites decreases maximal myofibrillar ATPase activity. METHODS AND RESULTS: We examined cTnI phosphorylation in left ventricular myocardium collected from failing hearts at the time of transplant (n=20) and normal hearts from trauma victims (n=24). The relative amounts of actin, tropomyosin, and TnI did not differ between failing and normal myocardium. Using Western blot analysis with a monoclonal antibody (MAb) that recognizes the striated muscle TnI isoforms, we confirmed that the adult human heart expresses only cTnI. A cTnI-specific MAb recognized two bands of cTnI, designated cTnI1 and cTnI2, while a MAb whose epitope is located in the cTnI-specific NH2-terminus recognized only cTnI1. Alkaline phosphatase decreased the relative amount of cTnl1, while protein kinase A and protein kinase C increased cTnI1. The percentage of cTnI made up of cTnI1, the phosphorylated form of TnI, is greater in the normal than the failing human heart (P<.00). CONCLUSIONS: This phosphorylation difference could underlie the reported greater myofibrillar calcium sensitivity of failing myocardium. The functional consequence of this difference may be an adaptive or maladaptive response to the lower and longer calcium concentration transient of the failing heart, eg, enhancing force development or producing ventricular diastolic dysfunction.
Actins↗
Prognostic influence of elevated values of cardiac troponin I in patients with unstable angina.
BACKGROUND: Elevations of the MB isoform of creatine kinase (CK) and cardiac troponin T seem to confer an adverse prognosis in unstable angina. We examined whether this prognostic influence is also present for cardiac troponin I (cTnI), a new and even more specific marker of myocardial injury. METHODS AND RESULTS: We studied 106 patients with the clinical diagnosis of unstable angina showing chest discomfort at rest within 48 hours of admission, ECG evidence of myocardial ischemia, and normal values of total CK over the initial 16 hours of observation. The primary end point was death or nonfatal myocardial infarction (MI) at 30 days; the secondary end point was the incidence of cardiac events at 1 year. Blood was drawn every 8 hours for 3 days. Thirteen patients were excluded because of increased CK-MB mass concentrations within 16 hours of admission (non-Q-wave MI) and 2 because of inadequate blood sampling. Of the remaining 91 patients, 22 had cTnI elevations on admission (n=7) or after 8 hours (n=15). At 30 days, no deaths (0%) and 4 MIs (5.8%) occurred in the 69 patients with normal cTnI compared with 2 deaths (9.1%) and 4 MIs (18.2%) in the 22 patients with elevated cTnI. The combined incidence of death and nonfatal MI was 5.8% and 27.3%, respectively (P=.02). At 1 year, only 68% of patients with elevated cTnI were free of cardiac events, compared with 90% of those without elevations (P=.01). CONCLUSIONS: These data indicate that cTnI is an important prognostic variable in patients with unstable angina. Elevations of cTnI predict an adverse short- and long-term prognosis.
Aged↗
Elevations of cardiac troponin I associated with myocarditis. Experimental and clinical correlates.
BACKGROUND: Endomyocardial biopsy is currently the standard method used to diagnose myocarditis. However, it is invasive and has a low diagnostic yield. Because the histological diagnosis of myocarditis requires the presence of myocyte injury, we sought to determine whether measurement of cardiac troponin I (cTnI), which is a serum marker with high sensitivity and specificity for cardiac myocyte injury, could aid in the diagnosis of myocarditis. METHODS AND RESULTS: To validate this approach, cTnI values were first measured in mice with autoimmune myocarditis. cTnI values were elevated in 24 of 26 mice with myocarditis but were not elevated in any of the control animals (P < .001). Next, cTnI values were measured in the sera from 88 patients referred to the Myocarditis Treatment Trial and were compared with creatine kinase-MB (CK-MB) values measured in the same patients. cTnI values were elevated in 18 (34%) of 53 patients with myocarditis and in only 4 (11%) of 35 patients without myocarditis (P = .01). In contrast, CK-MB values were elevated in only 3 (5.7%) of 53 patients with myocarditis and 0 of 35 patients without myocarditis (P = .27). Thus, elevations of cTnI occurred more frequently than did elevations of CK-MB in patients with biopsy-proven myocarditis (P = .001). Importantly, elevations of cTnI in patients with myocarditis were significantly correlated with < or = 1 month duration of heart failure symptoms (P = .02), suggesting that the majority of myocyte necrosis occurs early, and thus the window for diagnosis and treatment may be relatively brief. CONCLUSIONS: cTnI was superior to CK-MB for detection of myocyte injury in myocarditis, and cTnI elevations were substantially more common in the first month after the onset of heart failure symptoms.
Animals↗
Cardiac troponin I in pediatrics: normal values and potential use in the assessment of cardiac injury.
OBJECTIVE: To establish normal values and determine the impact of congenital or acquired heart disease on serum cardiac troponin I (cTnI). METHODS: Concentrations of cTnI were measured in two groups of children. Group A represented ambulatory pediatric patients with no apparent cardiac disease (n = 120) and patients in stable condition with known congenital or acquired cardiac abnormalities (n = 96); group B was composed of patients admitted to intensive care units with normal echocardiograms (n = 16), with abnormal echocardiograms (n = 36), and those with blunt chest trauma who were thought to have cardiac contusions (n = 7). RESULTS: The cTnI concentrations were generally less than 2.0 ng/ml in group A and frequently below the level of detection for the assay (1.5 ng/ml). There was no statistical difference between the two outpatient subgroups (p = 0.66). Nine intensive care patients had cTnI values greater than 2.0 ng/ml. Six of these patients, all with abnormal echocardiograms, had values less than 7.7 ng/ml. All improved and had subsequent normal cTnI concentrations. None of the three remaining patients (two with systemic illness (trauma and sepsis) and one with severe pulmonary hypertension), all with values greater than 8.0 ng/ml, survived. Three of the four patients with high likelihood of cardiac contusion had cTnI concentrations greater than 2.0 ng/ml (including one patient who died). CONCLUSIONS: Cardiac troponin-I values are generally not elevated in children with stable cardiac disease or general pediatric conditions. In the context of severe acute illness, significant elevation of cTnI may be an indicator of poor outcome. Elevation of cTnI may also have diagnostic value in cases when cardiac contusion is suspected.
Adolescent↗
Prolonged exercise decreases serum leptin concentrations.
Serum leptin and free fatty acid concentrations were determined in two groups of subjects undergoing strenuous exercise: 12 men who fasted overnight and then pedaled a stationary ergometer for 2 hours, and 14 nonfasting ultramarathon runners. Blood samples were collected before exercise, immediately after cessation of exercise, and 6 to 24 hours after the end of the exercise period. Two hours of strenuous pedaling following an overnight fast significantly reduced mean leptin levels by 8.3%; free fatty acids were highly increased and correlated well with the decrease in serum leptin (r = .737, P = .01). After 6 hours of rest and refeeding, leptin concentrations recovered to preexercise levels and free fatty acid concentrations were decreased to less than preexercise levels. A similar decrease in serum leptin levels (12.3%) occurred in subjects who fasted overnight and then for a period corresponding to the cycle exercise period. The prolonged exercise of an ultramarathon significantly reduced leptin concentrations by 32% in comparison to prerace levels; free fatty acid concentrations were highly increased, but did not correlate with the change in serum leptin concentrations (r = .366, P = .20). Leptin and free fatty acid concentrations all trended toward prerace levels in blood samples collected 18 to 24 hours after cessation of racing. The results suggest that the negative energy balance of exercise can reduce serum leptin concentrations, but that the significant decrease occurs only at extremes of severity/duration of the exercise-induced negative balance. The possible physiological role of reduced leptin concentrations in response to energy balance and the role of free fatty acids in mediating the response are discussed.
Adult↗
Transient right but not left ventricular dysfunction after strenuous exercise at high altitude.
OBJECTIVES: We sought to evaluate whether prolonged exercise in ultramarathon runners results in left ventricular (LV) damage. BACKGROUND: Strenuous exercise has been reported to cause LV damage. METHODS: Fourteen runners who completed an ultramarathon at high altitude underwent echocardiography, finger-tip oximetry and blood measurements of cardiac troponin I (cTnI) and creatine kinase, MB fraction (CK-MB) levels before, immediately after and 1 day after the race. RESULTS: At baseline, the echocardiograms showed normal LV and right ventricular (RV) size and function in all subjects, as well as mild tricuspid regurgitation in nine subjects, with normal estimated pulmonary artery systolic pressure (mean 28 mm Hg). At baseline, all oxymetric readings and CK-MB measurements were normal, and cTnI was undetectable. Immediately after the race, the echocardiograms showed the expected augmentation of global and segmental LV function in all subjects. Although the RV was normal in nine subjects, five developed marked RV dilation and hypokinesia, paradoxic septal motion, pulmonary hypertension and wheezing. CK-MB values were elevated in all subjects. In all but one subject cTnI was undetectable. In that subject there was a small elevation in cTnI accompanied by severe RV dysfunction and pulmonary hypertension. At the 1-day follow-up study, the echocardiographic measurements had normalized in all subjects. CONCLUSIONS: In trained athletes, strenuous exercise at high altitude did not result in LV damage. However, wheezing, reversible pulmonary hypertension and RV dysfunction occurred in a third of those completing the race. The incidence and pathogenesis of these findings remain to be determined.
Adult↗
Cardiac troponin I levels are normal or minimally elevated after transthoracic cardioversion.
OBJECTIVES: The present study was designed to assess the impact of direct current shocks on cardiac troponin I (cTnI), which has greater sensitivity and specificity than creatine kinase (CK) for the diagnosis of myocardial injury. BACKGROUND: Transthoracic direct current shocks can cause myocardial injury. They also cause elevations of total CK and CK-MB fraction (CK-MB). METHODS: We obtained measurements of cTnI total CK and CK-MB before and after elective cardioversions in 38 patients. Blood samples were drawn before and 8, 16, 24 and 48 h after cardioversion. Shock energy, current, impedance and number of shocks delivered were tabulated. RESULTS: Patients received a mean (+/-SD) of 2.1 +/- 1.2 shocks with a median cumulative energy of 300 J (range 50 to 1,580). Three patients had minimal elevations (1.5, 1.2 and 0.8 ng/ml, normal < or = 0.6 ng/ml) of cTnI. Two of these patients had impaired left ventricular contractility by echocardiography. Thirty-five of the 38 patients had no elevations of cTnI. Sixty-two percent of patients had an increase in CK after cardioversion, but CK-MB was elevated to an abnormal level of 12.7 ng/ml (normal < 6.7) in only one patient after cardioversion. CONCLUSIONS: Cardiac troponin I levels are either normal or minimally elevated after elective direct current cardioversion, suggesting that subtle myocardial injury can be caused by direct current transthoracic shocks. However, substantial elevations of cTnI after cardioversion suggest the presence of myocardial injury from causes unrelated to the direct current shocks administered for cardioversion.
Aged↗
Time course of lysophosphatidylcholine release from ischemic human myocardium parallels the time course of early ischemic ventricular arrhythmia.
BACKGROUND: We determined the kinetics of the release of lysophosphatidylcholine (LPC) into the coronary sinus of patients undergoing stress tests after coronary artery bypass grafting. The kinetics were consistent with a role for this amphiphile in the pathogenesis of ischemic ventricular arrhythmia, a major cause of sudden death. METHODS: Stress testing was initiated in the operating suite by pacing at a rate of 160 beats/min for 2 min. Ischemia was then induced by clamping the bypass grafts to the anterior wall for a maximal time of 4 min. RESULTS: The pacing procedure induced a prompt but reversible increase in coronary sinus LPC concentration from a baseline of 60.9 +/- 2.5 to 83.8 +/- 5.0 mumol/l via pacing alone, and a further increase to 101.8 +/- 6.7 mumol/l when the grafts were clamped for 2 min (P < 0.01). Six minutes after the cessation of pacing, LPC concentration returned to 67.5 +/- 4.4 mumol/l. CONCLUSIONS: These results demonstrate that severe myocardial ischemia is an agonist for rapid release of LPC from the myocardium. Kinetics of this release paralleled the time-course of early onset of electrophysiologic changes in isolated myocytes and perfused heart preparations in vitro. These results indicate that LPC may have an important role in the pathogenesis of ischemic ventricular arrhythmia in patients.
Aged↗
Clinically recognized cardiac dysfunction: an independent determinant of mortality among critically ill patients. Is there a role for serial measurement of cardiac troponin I?
OBJECTIVE: To determine the relative importance of clinically recognized cardiac dysfunction and unrecognized cardiac injury to hospital mortality. DESIGN: Prospective, blinded, single-center study. SETTING: Medical ICU of Barnes-Jewish Hospital, St. Louis, a university-affiliated teaching hospital. PATIENTS: Two hundred sixty adult patients requiring admission to the medical ICU. INTERVENTIONS: Daily blood collection. MAIN OUTCOME MEASURES: The presence of cardiac dysfunction (myocardial infarction, unstable angina, cardiac arrest, or congestive heart failure) as determined by the physicians responsible for the care of the patient. Daily measurement of levels of cardiac troponin I, a sensitive, highly specific, and long-lived marker of myocardial injury. RESULTS: Fifty-five (21.2%) patients had clinical evidence of cardiac dysfunction, among whom 22 (40%) had an elevated level of cardiac troponin I. A total of 41 (15.8%) patients had evidence of acute myocardial injury based on elevated levels of cardiac troponin I. Patients with clinically recognized cardiac dysfunction had a significantly greater hospital mortality rate compared to patients without clinically recognized cardiac dysfunction (45.5% vs 10.2%; p < 0.001). Similarly, patients with elevated blood levels of cardiac troponin I had a greater hospital mortality rate compared to patients without elevated blood levels of cardiac troponin I (26.8% vs 16.0%; p = 0.095). Multiple logistic-regression analysis controlling for potential confounding variables demonstrated that the presence of clinically recognized cardiac dysfunction was independently associated with hospital mortality (adjusted odds ratio = 3.0; 95% confidence interval = 1.9 to 4.8; p = 0.016). However, having an elevated blood level of cardiac troponin I was not found to be an independent determinant of hospital mortality. CONCLUSION: Among critically ill medical patients, clinically recognized cardiac dysfunction is an independent determinant of hospital mortality. The identification of unrecognized cardiac injury, using serial measurements of cardiac troponin I, did not independently contribute to the prediction of hospital mortality.
Adult↗
Differential reactivity of cardiac and skeletal muscle from various species in a cardiac troponin I immunoassay.
To identify a blood test that can differentiate cardiac from skeletal muscle injury in animals, we compared tissue reactivities for various species with the use of an immunoassay for human cardiac troponin I (cTnI). Tissue reactivity varied as a function of the homology of tissue troponin with human cTnI. Cardiac reactivity in large mammals was equivalent to cTnI, 9.8 +/- 0.6 mg/g, and was 2-fold, 10-fold, and 100-fold greater than in small mammals, birds, and fish, respectively. Skeletal muscle reactivity was equivalent to cTnI, 5.1 +/- 0.6 micrograms/g, in all species except fish, in which it was 50% lower. The ratio of reactivities of cardiac and skeletal muscle was: 1800 in large mammals, 1100 in small mammals, 230 in birds, and 43 in fish. We conclude that cTnI is a powerful candidate in mammals, a possible candidate in birds, but unlikely to be of use in fish as a sensitive and tissue-selective diagnostic test for cardiac injury.
Animals↗
Creatine kinase brain isoenzyme (BB-CK) presence in serum distinguishes osteopetroses among the sclerosing bone disorders.
Creatine kinase (CK) isoenzyme BB-CK is predominantly found in brain and is not normally detected in the blood. A few recent reports, however, have described BB-CK in serum from several patients with osteopetrosis (OP). To evaluate the presence and specificity of BB-CK in serum in the osteopetroses among disorders that increase skeletal mass, we quantitated total CK activity and CK isoenzymes in 15 patients representing the five major clinical forms of OP (2 infantile, 3 intermediate, 7 adult [2 type I, 5 type II], and 3 carbonic anhydrase II [CA II] deficiency cases) and in 22 patients representing 14 other types of sclerosing bone disease. All OP patients (except the two adult type I subjects) had BB-CK readily detected in their serum. Conversely, only 1 of the 22 patients with other sclerosing bone disorders had detectable BB-CK in serum (1 of 3 patients with fibrodysplasia [myositis] ossificans progressiva who had barely measurable activity). In three OP patients (one of two with the infantile form and two of five with adult, type II disease), BB-CK values were sufficiently high that serum total CK activity was elevated. In a newborn with malignant OP, both cord blood plasma and peripheral blood serum had substantial amounts of BB-CK. In three subjects (with adult type II OP), who were restudied 2-6 years later, BB-CK was still elevated in their blood. BB-CK in serum appears to distinguish the osteopetroses among the sclerosing bone disorders. Absence of serum BB-CK in adult type I disease suggests that this condition may not be a genuine form of OP. Assay of BB-CK in fetal blood could be studied as a means for prenatal diagnosis of malignant OP. Why the osteoclast failure that characterizes all true forms of OP is associated with BB-CK in the circulation is a new question for skeletal biologists.
Adolescent↗
Improved detection of cardiac contusion with cardiac troponin I.
Detecting cardiac injury in patients with chest trauma is difficult because the level of the MB isoenzyme of creatine kinase (MBCK) can be elevated from skeletal muscle injury alone. However, the level of cardiac troponin I (cTnl) is not elevated by skeletal muscle injury. To determine whether its measurement would improve the ability to detect cardiac injury in patients with blunt chest trauma, 44 patients were studied. Serial echocardiograms and serial blood samples were obtained. Six patients had evidence of cardiac injury by echocardiography; all had elevations of MBCK and cTnl. One patient had elevations of both MBCK and cTnl with only a pericardial effusion. Twenty-six of the 37 patients without contusion had elevations of MBCK; none had elevations of cTnl. The ratio of MBCK to total creatine kinase improved specificity at the expense of sensitivity. Measurement of cTnl accurately detects cardiac injury in patients with blunt chest trauma and should facilitate the diagnosis and management of such patients.
Case-Control Studies↗
Comparative sensitivity of cardiac troponin I and lactate dehydrogenase isoenzymes for diagnosing acute myocardial infarction.
Criteria for the retrospective diagnosis of acute myocardial infarction rely heavily on increases in lactate dehydrogenase (LD) isoenzymes. However, increases of LD isoenzyme activities are not specific for myocardial injury. Recently, increased concentrations of cardiac troponin I (cTnI) have been shown to be highly specific for myocardial damage and to have sensitivity comparable with that of creatine kinase MB isoenzyme for detecting cardiac injury. Furthermore, increases of cTnI persist in plasma for at least several days. The present study was designed to determine the relative sensitivities of cTnI and LD isoenzymes over time for the diagnosis of infarction. The results indicate that cTnI values are at least as sensitive as LD isoenzymes: 90% of patients with myocardial infarction had above-normal concentrations of cTnI on the 4th day after admission to the coronary care unit. Criteria based on cTnI should improve the accuracy of retrospective diagnoses of acute myocardial infarction.
Animals↗