Serum enzymes and isoenzymes after surgery

Serum creatine kinase, aspartate transaminase, and hydroxybutyrate dehydrogenase activities were abnormal in 76, 50, and 28% respectively of 50 patients studied within 26 hours of surgery. No patient showed clinical evidence of myocardial infarction. Creatine kinase MB isoenzyme elevation, and lactate dehydrogenase LD1 activity greater than LD2 (LD) greater than LD2) were infrequent (6 and 10% respectively). No patient showed the combination of transient MB isoenzyme elevation and LD1 greater than LD2, although their rare association without infarction after surgery is to be anticipated.     

Pulmonary contusion: review of the clinical entity

Pulmonary contusion is a common lesion occurring in patients sustaining severe blunt chest trauma. Alveolar hemorrhage and parenchymal destruction are maximal during the first 24 hours after injury and then usually resolve within 7 days. The diagnosis of traumatic lung injury is usually made clinically with confirmation by chest x-ray films. The chest computed tomography scan is highly sensitive in identifying pulmonary contusion and may help predict the need for mechanical ventilation. Respiratory distress is common after lung trauma, with hypoxemia and hypercarbia greatest at about 72 hours. Although management of patients with pulmonary contusion is supportive, pneumonia and adult respiratory distress syndrome with long-term disability occur frequently.     

Myocardial infarction related atrial fibrillation: role of endogenous adenosine

Hyperglycemia and hypokalemia caused by catecholamine discharge have been reported to occur in patients after severe head trauma. The aim of this prospective study was to evaluate whether a similar neuroendocrine and metabolic response is found in children after minor head trauma such as brain concussion (Glasgow Coma Scale (GCS) > or = 13). One hundred fifty patients aged 2 to 14 years (average, 6 years) were divided into three groups (n = 50 in each group). Group 1 included patients admitted to the emergency department for brain concussion (Glasgow Coma Scale (GCS) > or = 13); group 2 included patients admitted for fractures of long bones without head injury; and group 3 were control patients electively admitted for hernia repair. All patients had complete physical and neurological examinations. Complete blood count and blood chemistry were obtained on admission. All blood tests were repeated at 6, 12, and 24 hours in patients belonging to group 1. An electrocardiogram was obtained in selected patients and catecholamine levels were measured in some patients. Statistical analysis was performed using analysis of variance (ANOVA). Serum potassium and sodium levels in patients with brain concussion (group 1) were 3.6 +/- 0.6 and 136 +/- 3 mEq/L, respectively and were significantly lower (P < 0.01) than those in patients belonging to group 2, 4 +/- 0.4 and 138 +/- 3, respectively, and the controls (group 3), 4.2 +/- 0.5 and 140 +/- 2, respectively. Serum glucose level was 124 +/- 34 and 118 +/- 32 mg% in groups 1 and 2 and was significantly higher than that of the controls (group 3), 90 +/- 23 mg%. There was no correlation between serum electrolytes and GCS. No electrocardiogram changes or elevation of serum catecholamines were found. Hypokalemia resolved spontaneously within 24 hours. All patients recovered without neurological sequalae. Transient hypokalemia frequently occurs in children even with minor head trauma. This hypokalemia resolves spontaneously, without treatment and within 24 hours.     

Influence of chronic administration of L-DOPA on event-related desynchronization of mu rhythm preceding voluntary movement in Parkinson''s disease

Casein zymographic assays were performed to identify changes in mu-calpain and m-calpain activity in naive, sham-injured, and injured rat cortex at 15 minutes, 3 hours, 6 hours, and 24 hours after unilateral cortical impact brain injury. Cortical samples ipsilateral and contralateral to the site of injury were separated into cytosolic and total membrane fractions. Marked increases in mu-calpain activity in cytosolic fractions in the ipsilateral cortex occurred as early as 15 minutes, became maximal at 6 hours, and decreased at 24 hours to levels observed at 15 minutes after injury. A similar temporal profile of cytosolic mu-calpain activity in the contralateral cortex was observed, although the increases in the contralateral cortex were substantially lower than those in the ipsilateral cortex. Differences were also noted between cytosolic and total membrane fractions. The detection of a shift in mu-calpain activity to the total membrane fraction first occurred at 3 hours after traumatic brain injury and became maximal at 24 hours after traumatic brain injury. This shift in mu-calpain activity between the two fractions could be due to the redistribution of mu-calpain from the cytosol to the membrane. m-Calpain activity was detected only in cytosolic fractions. m-Calpain activity in cytosolic fractions did not differ significantly between ipsilateral and contralateral cortices, and increased in both cortices from 15 minutes to 6 hours after injury. Relative magnitudes of m-calpain versus mu-calpain activity in cytosolic fractions differed at different time points after injury. These studies suggest that traumatic brain injury can activate both calpain isoforms and that calpain activity is not restricted to sites of focal contusion and cell death at the site of impact injury but may represent a more global response to injury.     

Cardiac contusion in a 2 1/2-year-old child

This case was unique in that we were seeing signs and symptoms of a cardiac contusion 11 hours after injury, when cellular edema was causing lethal bradyarrhythmias and hypotension. Keeping the possibility of a cardiac contusion in mind when caring for pediatric patients with trauma and including a 12-lead EKG more routinely for pediatric patients with chest trauma would increase identification of potential problems as early as possible. Although cardiac contusion is not common in children, it must not be overlooked.     

The role of xanthine dehydrogenase (xanthine oxidase) in ischemia-reperfusion injury in rat kidney

Xanthine dehydrogenase (XDH) and xanthine oxidase (XO) are enzymes involved in the metabolism of purines in various organisms. XO produces superoxide radicals, suggesting that is responsible for tissue ischemia-reperfusion injury. To test this notion further studies were performed on rat kidneys and the time course of changes in purine nucleotides, oxypurines and XDH and XO activity was determined. At 24 hours after reperfusion subsequent to 30-minute ischemia, serum creatinine increased to 0.83 +/- 0.74 mg/dl from 0.28 +/- 0.06 mg/dl (the level prior to ischemia, the control). Renal ATP and ADP contents were reduced after ischemia lasting for 30 minutes and restored 10 minutes after reperfusion following 30 minutes of ischemia. The renal AMP content increased after 30 minutes of ischemia and recovered within 10 minutes after reperfusion. The total adenine nucleotide (TAN) content was reduced gradually during ischemia-reperfusion in the rat kidney. Although the energy charge was reduced following 30 minutes of ischemia, it was restored to the control level 10 minutes following reperfusion. Hypoxanthine (HX) and xanthine (X), which had accumulated at 30 minutes after ischemia, were reduced to the control levels 10 minutes after reperfusion. There were no significant changes in the pre-ischemia values of total XDH and XO activities or XDH/XO ratio during the period nor at various time intervals (up to 24 hours) during reperfusion. It was shown that HX and X accumulate without significant conversion of XDH to XO during ischemia. Therefore the putative role of XO in ischemia-reperfusion injury seems to more complex than initially predicted.     

Delayed cytokine expression in rat brain following experimental contusion

Proinflammatory cytokines mediate brain injury in experimental studies. This study was undertaken to analyze the production of proinflammatory cytokines in experimental contusion. A brain contusion causing delayed edema was mimicked experimentally in rats using a weight-drop model. Intracerebral expression of the cytokines interleukin (IL)-1 beta, tumor necrosis factor-alpha (TNF alpha), IL-6, and interferon-gamma (IFN gamma) was studied by in situ hybridization and immunohistochemistry. The animals were killed at 6 hours or 1, 2, 4, 6, 8, or 16 days postinjury. In the injured area, no messenger (m)RNA expression was seen during the first 2 days after the trauma. On Days 4 to 6 posttrauma, however, strong IL-1 beta, TNF alpha, and IL-6 mRNA expression was detected in mononuclear cells surrounding the contusion. Expression of IFN gamma was not detected. Immunohistochemical double labeling confirmed the in situ hybridization results and demonstrated that mononuclear phagocytes and astrocytes produced IL-1 beta and that mainly astrocytes produced TNF alpha. The findings showed, somewhat unexpectedly, a late peak of intracerebral cytokine production in the injured area and in the contralateral corpus callosum, allowing for both local and global effects on the brain. An unexpected difference in the cellular sources of TNF alpha and IL-1 beta was detected. The cytokine pattern differs from that seen in other central nervous system inflammatory diseases and trauma models, suggesting that the intracerebral immune response is not a uniform event. The dominance of late cytokine production indicates that many cytokine effects are late events in an experimental contusion: Different pathogenic mechanisms may thus be operative at different times after brain injury.     

Evaluation of the effects of various factors on the serum alpha hydroxybutyrate dehydrogenase activity in young females

In this study, for determining the influence of different life style on the serum alpha hydroxybutyrate dehydrogenase activity (alpha HBD), we carried out surveys and laboratory studies on the relationships of the nutritional intake, physical activity, cigarette smoking and alcohol consumption of young females with their serum alpha HBD activity. There are significant positive correlation between alpha HBD and GOT, GPT, LDH, CPK, phospholipids, total cholesterol, and HDL-cholesterol, and significant negative correlation between alpha HBD/LDH and GOT, GPT, and gamma GTP. There are significant positive or negative correlation between alpha HBD and systolic pressure, diastolic pressure, cardiac index, stoke volume and total periperal resistance, and significant negative correlation between alpha HBD/LDH and vital capacity in young females. The serum alpha HBD activity levels of nonsmokers was significant higher than those of smokers (p < 0.05). There are significant positive correlations between serum alpha HBD activity and beverage consumption, and between alpha HBD/LDH and protein, calcium, vitamin A, B1, B2, C, pulses, vegetables and milk in young females. The finding shows that the group of serum alpha HBD activity level of 240 or more units exhibited higher level of rate of those who exercised sometimes+usually than the other group in young females. However, the serum alpha HBD activity level did not show significant correlation with energy expenditures per day. Exercise at 50 and 70% VO2 max may produce a significant increase in their serum alpha HBD activity. There is a possibility that serum alpha HBD activity may serve as an indicator for ones health condition. It is undeniable that observation of variation of serum alpha HBD activity is highly significant in health maintenance.     

Open capsulorrhaphy with suture anchors for recurrent anterior dislocation of the shoulder

OBJECTIVE: The aim of this study was to index the frequency of occurrence of acute stress disorder following mild traumatic brain injury and to determine its utility in predicting posttraumatic stress disorder (PTSD). METHOD: Consecutive adult patients who sustained a mild traumatic brain injury following a motor vehicle accident (N = 79) were assessed for acute stress disorder within 1 month of their trauma with the Acute Stress Disorder Inventory, a structured clinical interview based on DSM-IV criteria. Patients were followed up 6 months after the trauma (N = 63) and were administered the PTSD module of the Composite International Diagnostic Interview. RESULTS: Acute stress disorder was diagnosed in 14% of patients, and at follow-up 24% satisfied criteria for PTSD. Six months after the trauma PTSD was diagnosed in 82% of patients who had been diagnosed with acute stress disorder and in 11% of those who had not been diagnosed with acute stress disorder. CONCLUSIONS: These findings point to the frequency of PTSD following mild traumatic brain injury. While the criteria for acute stress disorder are useful in identifying those individuals who are at risk of developing chronic PTSD, the findings suggest that current criteria require modification in order to optimally predict PTSD following mild traumatic brain injury.     

Early neutrophil sequestration after injury: a pathogenic mechanism for multiple organ failure

Polymorphonuclear neutrophils (PMNs) play a pivotal role in the inflammation that precedes multiple organ failure (MOF). In a rat model of MOF, PMNs become primed for enhanced superoxide anion (O2-) release and CD11b expression, sequester in end organs, and produce organ failure. Therefore, we hypothesized that circulating PMNs harvested in the first 24 hours after injury from trauma patients at risk for MOF would (1) exhibit a primed O2- release, (2) upregulate CD11b expression, and (3) show evidence of sequestration in tissues. Extracellular PMN O2- release and CD11b receptor expression were measured at 3, 6, 12, and 24 hours after injury in 33 torso trauma patients with Injury Severity Scores > 15; eight patients (24%) developed MOF. Healthy adults served as controls. PMNs after injury were primed for enhanced in vitro O2- release at 3, 6, 12, and 24 hours after injury, indicating prior in vivo priming. CD11b expression was also increased at 6, 12, and 24 hours after injury. Circulating PMN numbers increased sharply at 3 hours after injury, before decreasing dramatically at 6 and 12 hours, suggesting end organ sequestration. At 12 hours after injury, declines in circulating PMNs were significantly greater in MOF than in non-MOF patients (p < 0.05). These data indicate that PMNs are quickly mobilized into the circulation after injury and then primed for enhanced O2- release and CD11b expression. PMN priming appears to be a necessary preamble to PMN sequestration in patients with major torso trauma. Upregulation of PMN function, accompanied by subsequent end organ sequestration, may represent an important early event in the pathogenesis of MOF after injury.     

Evaluation of acute mental status change in the nonhead injured trauma patient

Acute mental status change in the first 24 hours after trauma is uncommon in nonhead injured patients who initially present with a normal sensorium. Although arterial hypoxemia is the classic etiology for such a mental status change, three less common etiologies should always be considered: cerebral fat embolism, blunt carotid artery injury, and vertebrobasilar artery thrombosis. Prompt diagnosis and appropriate treatment can significantly improve patient morbidity and mortality. Three nonhead injured trauma patients are described illustrating cerebral fat embolism, blunt carotid artery injury, and vertebrobasilar artery thrombosis as causes of acute mental status change. Each patient initially presented with a clear sensorium, but subsequently developed neurological deficits within 24 hours after admission. All had a normal admission CT scan of the head. MRI or conventional arteriography was diagnostic in each case. Any patient who is initially lucid and subsequently develops a neurological deficit, or a patient whose neurological status does not correlate with brain CT findings should undergo immediate evaluation for possible cerebral fat embolism or cervical vessel injury. An algorithm for management of nonhead injured trauma patients with acute mental status deterioration is presented.     

MR and cerebrospinal fluid enzymes as sensitive indicators of subclinical cerebral injury after open-heart valve replacement surgery

PURPOSE: To evaluate MR imaging and lumbar cerebrospinal fluid enzymes as potential sensitive indicators of cerebral injury after open-heart valve replacement surgery. METHODS: Thirty-four patients with cardiac valvular disease were prospectively entered into this study and then underwent valve replacement or repair under cardiopulmonary bypass using a membrane oxygenator. In 26 patients, MR head images were obtained 12 to 24 hours before surgery; repeat MR images were obtained between 1 and 2 weeks after surgery. In 18 patients, lumbar puncture cerebrospinal fluid was analyzed 24 to 48 hours after surgery; the analyses included measurement of lactic dehydrogenase, creatine phosphokinase, adenylate kinase, and neuron-specific enolase. RESULTS: After surgery, MR imaging showed new ischemic lesions in 15 (58%) of 26 patients: 7 with deep white matter hyperintense lesions; 5 with brain stem, caudate, cerebellar, or thalamic/basal ganglia infarcts; 1 with intraparenchymal hemorrhage; 1 with a subdural hematoma and cortical infarct; and 1 with a corpus callosum lesion consistent with calcium or air. These new ischemic lesions seen on MR images were associated with a focal neurologic deficit in only 4 (27%) of the 15 patients. Neuron-specific enolase and lactic dehydrogenase were abnormally elevated after surgery in 5 (28%) of 18 patients. Adenylate kinase and creatine phosphokinase (brain isozymes) were elevated in one (67%) of the patients. Two (40%) of the five patients with abnormally high neuron-specific enolase or lactic dehydrogenase after surgery also showed a new focal neurologic deficit. CONCLUSIONS: MR imaging is a sensitive measure of subclinical cerebral ischemia after cardiac valve replacement under cardiopulmonary bypass. Cerebrospinal fluid neuron-specific enolase and lactic dehydrogenase are less sensitive than MR imaging for detecting subclinical cerebral ischemia, but these values were elevated after surgery more frequently than was adenylate kinase in our patients.     

A calpain inhibitor attenuates cortical cytoskeletal protein loss after experimental traumatic brain injury in the rat

The capacity of a calpain inhibitor to reduce losses of neurofilament 200-, neurofilament 68- and calpain 1-mediated spectrin breakdown products was examined following traumatic brain injury in the rat. Twenty-four hours after unilateral cortical impact injury, western blot analyses detected neurofilament 200 losses of 65% (ipsilateral) and 36% (contralateral) of levels observed in naive, uninjured rat cortices. Neurofilament 68 protein levels decreased only in the ipsilateral cortex by 35% relative to naive protein levels. Calpain inhibitor 2, administered 10 min after injury via continuous arterial infusion into the right external carotid artery for 24 h, significantly reduced neurofilament 200 losses to 17% and 3% relative to naive neurofilament 200 protein levels in the ipsilateral and contralateral cortices, respectively. Calpain inhibitor administration abolished neurofilament 68 loss in the ipsilateral cortex and was accompanied by a reduction of putative calpain-mediated neurofilament 68 breakdown products. Spectrin breakdown products mediated by calpain 1 activation were detectable in both hemispheres 24 h after traumatic brain injury and were substantially reduced in animals treated with calpain inhibitor 2 both ipsilaterally and contralaterally to the site of injury. Qualitative immunofluorescence studies of neurofilament 200 and neurofilament 68 confirmed western blot data, demonstrating morphological protection of neuronal structure throughout cortical regions of the traumatically injured brain. Morphological protection included preservation of dendritic structure and reduction of axonal retraction balls. In addition, histopathological studies employing hematoxylin and eosin staining indicated reduced extent of contusion at the injury site. These data indicate that calpain inhibitors could represent a viable strategy for preserving the cytoskeletal structure of injured neurons after experimental traumatic brain injury in vivo.     

Injury panorama and medical consequences for 1158 persons assaulted in the central part of Stockholm, Sweden

This retrospective study describes assaults, type of trauma, injury panorama, the abbreviated injury scale score and medical consequences for 1158 assaulted persons. All patients were examined by surgeons at the Emergency Department, Sabbatsberg's Hospital, Stockholm, Sweden, which is open around the clock. The police were not notified. The study group included all assaulted patients who attended and were examined at the Emergency Department from 1 April 1992 to 31 March 1993: 84% men and 16% women. Their median age was 25 years (range 13-86 years). Sixty-eight percent arrived at the Emergency Department between 11 p.m. and 4 a.m. In 44% the hospital staff registered in the case notes that the victims were drunk. Blunt trauma of low-energy type predominated, 44% were hit by fists and 30% by kicks. Penetrating trauma occurred in 10% of the assaults (knife 8%), and a combination of blunt and/or cutting trauma (bottle/ glass) in 10%. Eighty-two percent of the victims suffered an injury to the head, resulting in concussion in 116 cases, 4 skull fractures, 1 intracerebral contusion, 74 fractures of nose bones, 17 fractures of other face bones, and 6 mandible fractures. Two persons died because of knifestab wounds. Eighty-two percent of the victims had minor injuries, and 16% had moderate injuries according to the score on the Abbreviated Injury Scale (AIS). The present study shows that assault in the central part of Stockholm, Sweden, is mainly a problem involving young men, especially late in the evening, and that many of the victims are drunk. Injuries to the head due to low-energy trauma are the most common (hit by fists and kicks), but severe injuries seldom occur.     

Control of gene expression in Plasmodium falciparum

Myocardial contusion is an infrequent, but sometimes serious complication in patients who experienced deceleration (blunt) trauma. We investigated the assessment of the new cardiac markers troponin I (cTnI) and troponin T (cTnT) in relation to the conventional CKMB-activity, the CKMB-activity/CK-total ratio, CKMB-mass and the CKMB-mass/CK-total ratio for the detection of myocardial contusion in 89 patients with blunt trauma (38 patients with thoracic injuries and 51 patients without thoracic injuries). All parameters were analysed at admission (t1) and 24 h after admission (t2). For the patients with thoracic injuries, at t1 cTnI was elevated in three, and cTnT in four patients; at t2 both cTnI and cTnT were elevated in nine patients. At t1, eighteen to thirty patients had increased levels of the conventional parameters; at t2 this was true for six to thirty-five patients. For the patients without thoracic injuries all cTnI and cTnT levels were within the reference ranges at t1. At t2 one patient, who experienced an acute myocardial infarction, had elevated cTnI and cTnT levels. At t1, five to thirty-five patients had increased levels of the conventional parameters; at t2 this was true for four to forty-two patients. From this study we conclude that the conventional parameters are not useful for the detection of myocardial contusion in patients experiencing blunt trauma. The parameters cTnI and cTnT are equally accurate and more reliable for the selection of patients who require intensive cardiac monitoring. If at admission the cTnI or the cTnT levels are within the reference ranges, a second analysis after admission is necessary to reach a reliable conclusion concerning myocardial contusion as a result of trauma on basis of the troponin levels.     

Use of adrenocorticotrophic hormone analog to minimize brain injury

STUDY OBJECTIVES: To investigate the effects of a vasoactive analog of adrenocorticotrophic hormone (GMM2) on time-dependent disturbances in regional cerebral blood flow, permeability-capillary surface area products, and intracranial pressure in a rat model of moderate concussion/brain injury. SETTING AND DESIGN: Regional permeability-capillary surface area products and cerebral blood flow were measured at two hours after trauma. Intracranial pressure was monitored for 120 hours after trauma. SUBJECTS: Male Wistar rats (330 to 430 g) (regional cerebral blood flow studies, n = 35; permeability-capillary surface area product studies, n = 36; intracranial pressure studies, n = 32). INTERVENTIONS: Post-traumatic subcutaneous administration of nanomolar concentrations of GMM2 (31 nmol per rat). MEASUREMENTS AND MAIN RESULTS: Untreated trauma acutely increased average brain permeability-capillary surface area products for sucrose and decreased average brain cerebral blood flow. Moreover, it produced marked and prolonged increases in intracranial pressure. Post-traumatic subcutaneous administration of nanomolar concentrations of GMM2 effectively reduced the early hypoperfusion, blood-brain barrier leakiness, and pathologic elevation of intracranial pressure. CONCLUSION: Post-traumatic administration of GMM2, in nanomolar amounts, can prevent or reverse significantly the serious cerebrovascular sequelae of moderate head injury in this animal model. In view of its potency, low toxicity, and other neuroprotective properties, in both rats and human beings, these data suggest that GMM2 may have considerable clinical benefits in the treatment of central nervous system trauma.     

Comparison of serial S-100 and NSE serum measurements after severe head injury

We investigated the time course of neuron specific enolase (NSE) and S-100 protein after severe head injury in correlation to outcome. We included 30 patients (GCS < 9), who had been admitted within 5 hours after injury, in a prospective study. Blood samples were taken on admission, 6, 12, and 24 hours and every 24 hours up to the fifth day after injury. The outcome was estimated on discharge using the Glasgow Outcome Scale. 70% reached a good outcome. All concentrations of NSE and 83% of the S-100 samples were elevated concerning the first probe (30.2 micrograms/l NSE mean and 2.6 micrograms/l S-100 mean). Patients with bad outcome had an NSE concentration of 38 micrograms/l (mean) compared with 26.9 micrograms/l (mean) in patients with good outcome. Patients with bad outcome had an S-100 concentration of 4.9 micrograms/l (mean) compared with 1.7 micrograms/l (mean) in patients with good outcome (p < 0.05). The mean values of NSE and S-100 decreased during the first 5 days. Four patients with increasing intracranial pressure showed a quick increasing concentration of NSE, in two patients the S-100 level showed a slower rise. The NSE serum levels did not correlate with intracranial pressure values. Our results show that the first serum concentration of S-100 seems to be predictive for outcome after severe head injury.     

Biological dynamics and distribution of 3-hydroxy fatty acids in the yeast Dipodascopsis uninucleata as investigated by immunofluorescence microscopy. Evidence for a putative regulatory role in the sexual reproductive cycle

PURPOSE: This study investigated the pathologic characteristics and some related factors of cerebral damage associated with maxillofacial high-velocity missile wounds. MATERIALS AND METHODS: Sixty dogs, divided into two groups, were wounded randomly by steel spheres weighting 1.03 g at impact velocities of 1,400 m/s (46 dogs) and 800 m/s (14 dogs). Six dogs served as controls. The maxillofacial wounds and cerebral injuries were examined grossly. The distance between the center of wound and the base of skull and the largest diameter of the wound were measured, and the incidence of the brain injury in the two groups was compared. The cerebral specimens, dissected at 1 and 6 hours after trauma, were observed by light and electron microscopy. RESULTS: Cerebral hyperemia, contusion, spotty hemorrhage, and intracerebral hematoma were found in some of the dogs. In the 1,400 m/s velocity missile wound group, the incidence of the brain injury was 71.7% (33 of 46), and in the 800 m/s group it was 7.1% (1 of 14) on macroscopic examination. Microscopic observation showed intracerebral microhemotomas and degeneration and necrosis of the nervous cells. CONCLUSION: High-velocity projectile maxillofacial wounds can induce associated brain injury.     

Analytical evaluation and comparison of Dupont aca lactate dehydrogenase-1 (LD1) isoenzyme assay diagnostic efficiency for acute myocardial infarction detection with other LD1 methods and aca CK-MB. A two-site study

The purpose of this study was to examine the analytical characteristics of a rapid new assay for lactate dehydrogenase 1 (LD1) isoenzyme on the Dupont aca analyzer and the diagnostic efficiency of LD1 for detection of acute myocardial infarction (AMI) when used alone and with creatine kinase MB (CKMB). Total aca LD1 assay precision, with percent coefficients of variation (%CVs) of less than 3.2% from 56 U/L to 469 U/L LD1, across fifty assay days was excellent. Linearity was confirmed from 0 to 332 U/L and no detectable calibration drift was noted from 5 to 489 U/L over a ninety-day period. The aca LD1 results compared well with Roche Isomune-LD1, Abbott Spectrum A-Gent, Helena electrophoresis, and Beckman electrophoresis LD1 methods, giving r's from 0.987 to 0.994, slopes from 0.94 to 1.65, and y-intercepts from -2.95 to 6.94 U/L. Examination of 450 ambulatory subjects, about equally distributed by sex, yielded a 43 +/- 14 U/L aca LD1 patient reference interval. Serum samples from 159 consecutive patients at the University of Tennessee Memorial Hospital and 96 patients at Allentown Hospital, submitted for AMI detection assistance, were assayed in a single-blind study for LD1 and ion-exchange CKMB by Dupont aca methods, which provide automated results in ten minutes whenever needed. The aca LD1 assay yielded a clinical sensitivity of 89% and specificity of 95% for AMI with a decision threshold of 120 U/L. The diagnostic efficiency of the aca LD1 assay was 94% at 120 U/L, which equaled or exceeded that of the three comparative LD1 methods. The predictive value of positive (PV+) and negative (PV-) results on the first sample collected were 80% and 85% for aca LD1, 65% and 90% for aca ion-exchange CKMB, and 83% and 90% when both tests were combined. Significantly, the PV+ and PV- results when two or more samples were assayed was improved to 88% and 95% for aca LD1, relatively constant at 65% and 97% for aca ion-exchange CKMB, and dramatically improved to 95% and 100% when both CKMB and LD1 tests were combined. The results from these two medical centers show that the aca LD1 assay provides useful clinical information for AMI diagnosis when employed alone or in combination with aca CKMB. These results also suggest that LD1 should be included in biochemical evaluations for AMI to attain optimal predictive values of results.