Ninety-minute exclusion of acute myocardial infarction by use of quantitative point-of-care testing of myoglobin and troponin I.

BACKGROUND: Diagnostic strategies with ECG and serum cardiac markers have been used to rule out acute myocardial infarction in 6 to 12 hours. The present study evaluated whether a multimarker strategy that used point-of-care measurement of myoglobin, creatine kinase (CK)-MB, and troponin I could exclude acute myocardial infarction in

The why and wherefore of fructosamine.

GH and FA are useful monitors in the care of diabetic patients. For most situations, GH is the preferred test and should be routinely monitored. FA should be reserved for exceptional situations in which blood glucose control over one to two weeks must be assessed or in patients with a hemoglobinopathy. Patients with diabetes should be advised of their present GH level and the preferred goal.

Biochemical diagnosis of myocardial infarction.

A rapid, sensitive, and specific marker for the diagnosis of acute myocardial infarction (MI) and the assessment of reperfusion following thrombolytic therapy has been sought by research workers for years. Creatine kinase-MB (CK-MB) is the best biochemical marker currently available to the cardiologist and the emergency room physician for the assessment of patients presenting with symptoms of acute MI. CK-MB is best measured using immunoassay techniques at 3- to 4-hour time intervals during the first 12 hours after onset of symptoms. Other currently available markers include lactate dehydrogenase and its isoenzymes and myoglobin. Future developments include assays for troponin, reported to be a true cardiac-specific marker, and myosin light chains which may have value in noninvasive infarct sizing.

An evaluation of cocaine-induced chest pain.

STUDY OBJECTIVE: To determine if enzymatic evidence of acute myocardial injury is present in patients complaining of chest pain after cocaine use when the ECG is normal or nondiagnostic. DESIGN: Serial ECG and creatinine kinase (CK) and CK isoenzymes (CK-ISO) determinations were performed at time of emergency department presentation and every six hours over 12 hours on individuals complaining of chest pain within six hours of last cocaine use. SETTING: ED of an urban tertiary care center. TYPE OF PARTICIPANTS: Forty-two individuals with a mean age of 28.5 years. INTERVENTIONS: Patients with positive CK-ISOs were admitted immediately to formally rule out myocardial infarction. Patients developing ECG changes during observation period also were admitted even if CK-ISOs were normal. Patients with unchanged ECGs and normal CK-ISOs were discharged after 12 hours of observation. RESULTS: Eight patients (19%) had elevated CK and CK-ISO values at presentation. Two of these patients had elevated values on three sequential determinations and were believed to have sustained acute myocardial infarction. Six patients had elevated CK and CK-ISOs at presentation only. ECGs remained normal or nondiagnostic in all patients. CONCLUSIONS: Enzymatic evidence of acute myocardial injury may occur in patients who develop chest pain after cocaine use and have normal or nondiagnostic ECGs. This injury may reflect acute infarction or transient ischemia. Single or serial normal or nondiagnostic ECGs do not rule out ischemia or injury in this group of patients.

Determination of non-enzymatically glycated apolipoprotein A1.

A procedure for the quantitation of non-enzymatically glycated apolipoprotein A1 (GApoA1) was developed and optimized. Glycated total protein was separated from plasma using m-aminophenyl-boronate affinity chromatography. Apolipoprotein A1 present in the glycated and non-glycated fractions of each sample was determined by rate nephelometry, and the percent glycated apo A1 calculated. The measuring range of the assay was 0.5-8.0% GApoA1. The within- and between-run CV's were less than 5.2 and 7.9%, respectively, and recoveries were greater than 92%. Free glucose did not affect the results. In a group of female non-insulin diabetic subjects the mean GApoA1 was 3.8 +/- 1.6% (mean +/- SD). In non-diabetic subjects the mean level of GApoA1 was 2.1 +/- 0.8% (mean +/- SD).

The effect of cardiopulmonary bypass resuscitation on cardiac arrest induced lactic acidosis in dogs.

The adequacy of end organ blood flow following a cardiac arrest varies depending on the artificial reperfusion technique utilized and may critically affect patient outcome. Both oxygen consumption (VO2) and arterial lactate values have previously been used to assess tissue perfusion. Cardiopulmonary bypass resuscitation (CPB) is a reperfusion technique capable of providing near normal end organ blood flow. The purpose of this investigation was to study the effect of femoro-femoral veno-arterial CPB resuscitation compared to standard CPR on VO2 and arterial lactic acid values after a prolonged cardiac arrest. Ten mongrel dogs were electrically fibrillated and left in cardiopulmonary arrest without therapy for 12 min. Resuscitation was attempted according to a standardized protocol utilizing either CPB (n = 5) or standard external CPR (n = 5). Oxygen consumption values and arterial lactic acid samples were obtained at baseline, at timed intervals throughout resuscitation and after return of spontaneous circulation in successfully resuscitated dogs. Baseline hemodynamic and biochemical measurements were similar in both treatment groups (P greater than 0.05). Oxygen consumption (440 +/- 50 ml/min/M2) and mean arterial lactic acid values (7.44 +/- 2.25 mmol/l) were significantly higher at 1 min of resuscitation in CPB-treated dogs compared to dogs treated with CPR (60 +/- 10 ml/min/M2) (3.16 +/- 0.69 mmol/l) respectively (P less than 0.05). Mean arterial lactic acid values rose significantly at each sampling interval during CPR (P less than 0.05) but began to decrease after 5 min of resuscitation in the CPB animals and were not significantly different than baseline after 60 min of bypass (P greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Lactic acidosis during closed-chest CPR in dogs.

Survival after out-of-hospital cardiac arrest is intimately related to the time from cardiovascular collapse to the initiation of CPR, or downtime. Furthermore, the reperfusion technique that optimizes coronary and cerebral blood flow after cardiac arrest may also be dependent on downtime. Peak blood lactate levels have been shown to be unchanged throughout resuscitation and predictive of downtime in dogs subjected to cardiopulmonary arrest and open cardiac massage. The purpose of this study was to determine the course of arterial lactate levels in dogs subjected to a fibrillatory cardiopulmonary arrest and conventional closed-chest CPR (CCPR). Fourteen dogs were subjected to five minutes of cardiopulmonary arrest and 30 minutes of CCPR. Resuscitation was performed according to a standardized protocol. Arterial lactic acid samples were collected at timed intervals throughout the experiment. Mean arterial lactic acid levels increased significantly with each sampling interval during 30 minutes of CCPR (overall P less than .05). In nine dogs successfully resuscitated, there were no significant differences in mean arterial lactic acid levels after the return of spontaneous circulation (ROSC). Open-chest resuscitation after five minutes of ventricular fibrillation in dogs results in peak lactic acid levels that do not change significantly once internal cardiac massage is initiated. In contrast, CCPR in similarly arrested dogs does not appear to provide adequate tissue oxygenation and/or perfusion to prevent continuous lactic acid accumulation.

Hyperkalemia during cardiac arrest and resuscitation in the canine model.

Although recent clinical reports have noted hypokalemia after resuscitation from cardiac arrest, extensive animal work indicates that potassium is released from cells during ischemia. This study was undertaken to define the changes that occur in serum potassium ion during cardiac arrest and resuscitation in a canine model. Fourteen dogs were subjected to 5 min of cardiac arrest followed by 30 min of closed-chest CPR (CCPR). Resuscitation was performed according to a standardized protocol. Serum potassium increased significantly (p less than .001) from baseline, remained elevated 5 min after return of spontaneous circulation (ROSC), but declined to baseline levels at 15 min post-ROSC. Increases in interstitial potassium would be expected to be even greater due to the poor exchange between interstitial and intravascular compartments during CCPR. Interstitial hyperkalemia may play a role in the genesis of wide-complex electromechanical dissociation and may explain the reported success of calcium chloride in treating this problem.

Ionized calcium during CPR in the canine model.

The purpose of our study was to determine ionized calcium levels during cardiopulmonary resuscitation (CPR). Following placement of ascending aortic catheters in 15 adult mongrel dogs, ventricular fibrillation was induced electrically. After five minutes without therapy, mechanical external CPR was instituted. Animals received either standard CPR (S-CPR, n = 8) or simultaneous compression and ventilation CPR (SCV-CPR, n = 7) for 30 minutes. Ionized calcium levels were obtained prior to fibrillation and every five minutes during CPR. Mean ionized calcium levels during CPR (1.27 +/- 0.06 mmol/L) did not differ significantly from prearrest levels (1.27 +/- 0.07 mmol/L) at any point during CPR. This was true when the dogs were analyzed together (P = 0.1293) and when the animals receiving S-CPR (P = 0.4465) and SCV-CPR (P = 0.5470) were analyzed by groups. Defibrillation was attempted in all animals and resulted in electromechanical dissociation in three. None of these dogs was hypocalcemic either prior to arrest or during CPR, and none developed an effective rhythm with the administration of calcium. Furthermore, three of the four animals receiving calcium developed markedly elevated ionized calcium levels. Hypocalcemia apparently does not occur during CPR. The beneficial effect of calcium in reported cases cannot be explained routinely by correction of hypocalcemia. Further studies are needed to define the role of calcium administration, if any, in CPR.

Lactic acidosis as a predictor of downtime during cardiopulmonary arrest in dogs.

Studies have shown that over 50% of cardiovascular deaths occur before hospitalization. A major factor associated with survival in cases of out-of-hospital cardiac arrest is the time from cardiovascular collapse to the initiation of cardiopulmonary resuscitation (CPR) or "downtime." The purpose of this study was to determine whether blood lactate levels could be used to predict downtime in the canine cardiac arrest model. Femoral arterial and Swan-Ganz catheters were placed in 22 mongrel dogs, and ventricular fibrillation was electrically induced. The dogs remained in ventricular fibrillation without ventilation for 5, 10, 15, 30, or 60 minutes. After the predetermined fibrillation time, a left anterolateral thoracotomy was performed, and open-chest cardiac massage was begun. Arterial and mixed venous lactate levels were determined for every 5 minutes during 30 minutes of cardiopulmonary resuscitation. The correlation coefficient between the mixed venous and arterial lactate levels was 0.96 or greater during all stages of resuscitation. Peak serum lactate level increased linearly in relation to downtime. The increase in lactate level was not evident until after CPR was begun, and it remained at peak levels or decreased insignificantly, despite optimal open-chest CPR. Linear regression analysis revealed that 84% of the variability in serum lactate levels could be explained by downtime differences. In this model, blood lactate level is a reliable and objective measure of downtime and may be a useful indicator of the adequacy of CPR if levels decrease or remain stable. The clinical implications of this study lie with the use of blood lactate levels in the emergency department to guide the aggressiveness of resuscitative efforts.

Automated creatine kinase-MB estimation by immuno-inhibition: a clinical evaluation.

We detected the presence of creatine kinase (EC 2.7.3.2) MB isoenzyme (CK-MB) in serum by using an immunoinhibition technique to inactivate the creatine kinase isoenzyme of muscle origin (CK-MM). The GEMSAEC centrifugal analyzer is ideally suited for this procedure because it rapidly mixes reagents and has a throughput of 60 samples/h. The within-run CV was acceptable when the CK-MB value was 7.5 U/L or more. CK-MM was totally inactivated up to 5000 U/L, a value well above that usually seen in myocardial-infarct patients. We assessed the predictability of the assay for detecting myocardial infarction among 120 coronary-care patients when 2% of total CK activity was considered diagnostic and compared the results with those obtained with an electrophoresis technique. The positive predictive value of the immunoinhibition assay was 97.8%, as compared to 92% with the CK electrophoresis technique, when lactate dehydrogenase (EC 1.1.1.27) isoenzyme results were included in both cases. The optimal negative predictive value was 95.1% with the immunoinhibition assay vs 98.2% with electrophoresis. We conclude that the immunoinhibition technique for estimating CK-MB can be automated to assess myocardial status rapidly, precisely, inexpensively, and sensitively.

Performance of the Du Pont aca ammonia method.

We evaluated the performance of the Du Pont aca ammonia procedure with regard to (a) linearity, (b) precision, (c) interferences, and (d) effect of anticoagulants. Linearity extends to 2,000 mumol/L. The SD of the method was essentially constant (2 to 3 mumol/L) and independent of the NH3 concentration. Hemoglobin, bilirubin, and lipemia do not interfere. Either EDTA or heparin is suitable as anticoagulant. Recovery of NH3 added to plasma samples averaged 102% (range: 97--107%). We established normal values by measuring NH3 in 188 plasma samples from apparently healthy individuals. The 95% confidence range is from 10 to 35 mumol/L. The aca ammonia method compares very well with that of Kingsley and Tager but correlates less strongly with that of Reinhold and Chung. We describe a protein-based solution with stable NH3 concentration that is suitable as a control material.