Influence of electrocardiographic findings on admission decisions in patients with acute chest pain

This study prospectively evaluated the influence of current electrocardiograms obtained at the time of emergency department presentation, as well as that of previous comparison electrocardiograms, on decision-making regarding coronary care unit admission of patients presenting with a chief complaint of chest pain or chest pain equivalent. Emergency department physicians were asked to commit themselves to recommending either coronary care unit admission or some other disposition, both before and after evaluating current comparison electrocardiographic findings. They were also asked, prior to reviewing these results, whether they thought information gained from the electrocardiograms would have any affect on their decision. Despite wide expectation that electrocardiographic findings would in fact affect decision-making, neither current nor comparison electrocardiograms virtually ever altered the ultimate decision of whether or not to admit. Faculty and house officers performed similarly in all regards, except insofar as attending physicians were less likely to expect electrocardiographic findings to help them in patients who were ultimately discharged. Emergency department nurses, who were asked whether they believed these patients needed admission to a coronary care unit on the basis of only a brief initial triage history, performed very similarly to the physicians. Thus, electrocardiographic findings are rarely if ever helpful in determining the need for admission to a coronary care unit in patients presenting to the emergency department with chest pain, and seem to have particularly little value in patients in whom myocardial infarction is considered clinically unlikely. Although physicians at all levels of training often feel a need to rely on electrocardiograms in patients they ultimately admit, greater experience allows more senior physicians to be comfortable in correctly discharging patients with no clinical evidence of disease without obtaining an electrocardiogram. Routine ordering of electrocardiograms in patients with chest pain in whom likelihood of significant acute ischemic pain is clinically low should be reconsidered.     

Peak creatine kinase as a measure of effectiveness of thrombolytic therapy in acute myocardial infarction

As part of the National Heart, Lung, and Blood Institute multicenter Thrombolysis in Myocardial Infarction Trial, the time to peak plasma creatine kinase (CK) activity as a marker of reperfusion in 272 patients with validated acute myocardial infarction was analyzed. Patients were treated with either tissue-type plasminogen activator or streptokinase by intravenous administration. All patients underwent acute coronary angiography. The infarct-related artery was identified and thrombolytic therapy administered. Reperfusion at 90 minutes was documented by angiography. CK was determined before institution of therapy and every 4 hours thereafter for the first 24 hours. Patients were classified into 3 groups for comparative purposes: group 1--occlusion with no reperfusion (n = 119); group 2--occlusion with reperfusion (n = 98); and group 3--subtotal occlusion (n = 55). Early (within 4 hours after treatment) and late (more than 16 hours after treatment) peaking of CK differentiated patients with drug-induced perfusion from those without reperfusion. Although peak CK between 5 and 11 hours after drug treatment did suggest perfusion through the infarct-related artery, it did not differentiate between drug-induced and spontaneous reperfusion. Clinically, early peak CK is a useful noninvasive means of assessing coronary artery patency. However, in clinical trials assessing drug therapy, the use of peak CK may overestimate drug effectiveness by including patients with spontaneous reperfusion.     

Time of onset of chest pain in acute myocardial infarction

We studied the time of onset of chest pain in 1099 patients admitted to a coronary care unit with myocardial infarction using a statistical model. Statistical analysis demonstrated an excess of infarcts with time of onset of chest pain at 0700 hours (14%) and at midnight (11%), with the remaining infarct population (75%) forming a background distribution over the 24 hr.     

Usefulness of intravenous thrombolytic therapy with pro-urokinase in acute myocardial infarction

Treatment of acute myocardial infarction (AMI) with plasminogen activators reduces infarct size and mortality rate.¹ This therapy has been attended by significant problems. Both urokinase and streptokinase lack clot selectivity and promote generalized fibrinogenolysis, at times resulting in severe bleeding.² Tissuetype plasminogen activator and pro-urokinase are more fibrin specific.^3,4 Although tissue-type plasminogen activator has been more extensively studied, only 1 clinical report is available for pro-urokinase.⁵ This study determines whether intravenously administered pro-urokinase could be confirmed to be an effective and clot-selective fibrinolytic agent and reports information about the minimal dose required for effective coronary thrombolysis in patients with AMI.     

The creatine kinase curve area and peak creatine kinase after acute myocardial infarction: Usefulness and limitations

We determined creatine kinase (CK) curve areas in 112 patients with acute myocardial infarction. Two-hour sampling was performed for the first 24 hours or until peak CK was reached, and a gamma density function was used to calculate curve areas from all available samples. Attempts to predict CK curve area by means of the portion of the curve prior to peak CK proved to be inaccurate; not until values 2 hours or more beyond peak CK were utilized did predicted and actual CK areas agree well. A good correlation (r = 0.93) was found between CK area and peak CK. To establish an approach for detecting peak CK in the clinical setting, a range of sampling intervals (4 to 24 hours) was assessed; 4-and 6-hour sampling intervals for 48 hours produced maximum CK values at or above 85% of true peak CK in 90% and 89% of patients, respectively, and average maximum CK at both sampling intervals exceeded 94% of that obtained with 2-hour samplings. We conclude that this simplified approach can provide a basis for estimating infarct severity in the individual patient.     

Usefulness of a rapid initial increase in plasma creatine kinase activity as a marker of reperfusion during thrombolytic therapy for acute myocardial infarction

This study evaluates a new nonangiographic marker of reperfusion--a rapid initial increase in plasma creatine kinase (CK) and CK-MB activity--in 50 patients receiving intracoronary streptokinase. Blood for CK and CK-MB activity was sampled at 30-minute intervals and angiography performed at 15-minute intervals or earlier if there were clinical signs suggestive of reperfusion. An absolute first-hour increase in CK activity of 480 +/- 345 IU/liter (range 54 to 1,440 IU/liter), or a relative first-hour increase of 34 +/- 18% (range 13 to 67% of the peak rise), or an absolute first-hour increase in CK-MB activity of 48 +/- 36 IU/liter (range 10 to 144 IU/liter) or a relative first-hour increase of 27 +/- 13% (range 13 to 57%) was found in patients immediately after reperfusion with Thrombolysis In Myocardial Infarction (TIMI) grade 3 perfusion of the artery of infarction. The onset of rapid increase in CK and CK-MB activity closely reflected the time of angiographic documentation of reperfusion. In contrast, in the absence of reperfusion, the absolute rate of increase in CK activity measured in the last hour of the 2 1/2-hour period beginning with the start of treatment was only 15 +/- 9 IU/liter on the average (range 2 to 30 IU/liter) and the relative rate of rise was 3 +/- 2% on the average (range 1 to 6%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Usefulness of the presenting electrocardiogram in predicting myocardial salvage with thrombolytic therapy in patients with a first acute myocardial infarction.

AIMS: Patients with Q waves and T-wave inversion are generally at a later stage of the infarction process than patients without these changes. Our aim was to investigate whether a single assessment of electrocardiographic parameters at presentation would predict the proportion of myocardium salvageable by thrombolytic therapy. METHODS AND RESULTS: Electrocardiographic algorithms to calculate the potential and final infarct size have been developed and allow the proportion of myocardium salvageable with therapy to be calculated. This was measured in 146 patients with acute myocardial infarction who had angiography at a median of 91 min after streptokinase. The relationship between myocardial salvage and the electrocardiographic parameters at presentation (Q waves, T-wave inversion, quantitative ST segment changes, and the initial QRS score), was examined together with the 90-min angiographic parameters (TIMI flow grade and collateral grade), clinical parameters (haemodynamics and age), and time to therapy. Parameters that correlated with myocardial salvage included the initial QRS score (r=-0.56, P<0.0001), Q wave grade (r=-0.36, P<0.0001), number of leads with ST depression (r=0.28, P<0.001), maximum ST depression (r=0.27, P<0.01), T-inversion grade (r=-0.26, P<0.01), and TIMI flow grade at 90 min (r=0.21, P<0.02). The time from symptom onset to thrombolytic therapy did not correlate with salvage (r=-0.09). On multivariate analysis, only the initial QRS score and T-inversion grade on the initial electrocardiogram were independent predictors of salvage (multivariate r using both variables combined=0.57, P<0.001). CONCLUSIONS: The QRS score and T-wave inversion grade on the presenting electrocardiogram provide important information in predicting myocardial salvage. These parameters may help triage patients to appropriate therapies.     

Usefulness of QTc interval on the discharge electrocardiogram for predicting survival after acute myocardial infarction

The corrected QT (QTc) interval was measured on the discharge electrocardiogram of 457 consecutive patients who had survived the first 28 days after a first acute myocardial infarction (AMI). The patients were followed for 4 years. The QTc interval was not related to long-term survival after the acute phase of AMI. Sixteen percent of the patients had a QTc interval above the normal upper limit of 440 ms. Of them, 71% survived 4 years and 77% with a shorter QTc interval survived (p = 0.31). When mortality per 100 patient-years was calculated for different QTc intervals, with 10 ms accuracy, no consistent relation between the 2 variables was seen. Results that indicate a strong relation between QTc-interval prolongation and sudden death after AMI should be reevaluated. The QTc interval is not a useful prognostic tool after AMI.     

Outcome in suspected acute myocardial infarction with normal or minimally abnormal admission electrocardiographic findings

Seven hundred seventy-five consecutive patients with symptoms suggestive of acute myocardial infarction (AMI) who were admitted to the cardiac care unit from the emergency room were studied; 107 had normal electrocardiographic findings and 73 had only minimal nonspecific changes. AMI subsequently evolved in 11 patients (10%) with normal electrocardiographic findings and in 6 (8%) with minimal changes, compared with 245 (41%) with frankly abnormal emergency room findings. Only 1 (1%; 95% confidence limits 0.02 to 5%) and 4 (6%; 95% confidence limits 2 to 15%) of those with normal and nonspecific initial electrocardiographic findings, respectively, had a complication for which they potentially benefited from intensive care unit intervention, although many patients received prophylactic therapy. Thus, the initial emergency room electrocardiogram can effectively separate patients into high- and low-risk groups for AMI and serious complications. Admission to a monitored intermediate care ward may be an acceptable practice in patients with chest pain and a normal or minimally changed initial electrocardiogram.     

Myoglobin and creatine kinase in acute myocardial infarction

Serum myoglobin concentration and creatine kinase activity were measured serially in 70 consecutive patients presenting within four hours of the onset of symptoms of suspected acute myocardial infarction. Of 36 patients with definite or possible myocardial infarction (WHO criteria), the serum myoglobin concentration was raised (greater than 85 micrograms/l) one hour after the onset of symptoms in 25% and at four hours in 89%. Creatine kinase activity was raised (greater than 140 U/l) one hour after the onset in 25% and at four hours in only 56%. Within 12 hours of the onset of symptoms the myoglobin concentration reached a peak in 83% and the creatine kinase a peak in only 14%. Within 36 hours the myoglobin concentration fell to normal values in 67% while creatine kinase activity fell to normal values in only 3%. Four hours after the onset of symptoms the serum myoglobin concentration distinguished easily those patients with myocardial infarction from those without, whereas when creatine kinase values were used the sensitivity was poor but the specificity high. From the combined results of the two studies and using a single measurement of serum myoglobin concentration at six hours from the onset of symptoms to predict the diagnosis in 114 patients with suspected infarction, the sensitivity was 93% and specificity 89%.     

Circadian variation in the frequency of onset of chest pain in acute myocardial infarction

The time of onset of chest pain was studied prospectively in 1154 consecutive patients admitted to a coronary care unit with myocardial infarction during a five year period. Statistical analysis confirmed a previous finding in a retrospective study of a bimodal frequency distribution with peaks in the time of onset of chest pain between 2330 and 0030 hours and between 0630 and 0830 hours.     

Effect of intravenous metoprolol before hospital admission on chest pain in suspected acute myocardial infarction

BACKGROUND: The aim of this study was to describe the effect of intravenous metoprolol on the intensity of chest pain before hospital admission in patients with suspected acute myocardial infarction AMI). METHODS AND RESULTS: Two hundred sixty-two patients with acute chest pain and suspected AMI were randomly assigned before hospital admission to either 5 mg morphine plus metoprolol 5 mg x 3 intravenously or 5 mg morphine plus intravenous placebo. Chest pain was evaluated on a 10-grade scale before and for 60 minutes after intravenous injection. One hundred thirty-four patients were randomly assigned to metoprolol and 128 to placebo. Among all patients randomized to metoprolol, the mean chest pain score was reduced by 3.0 +/- 1.9 arbitrary units AU) from before to after intravenous injection compared with 2.6 +/- 2.1 AU for placebo not significant). Among patients with an initially confirmed or strong suspicion of AMI, the corresponding figures were 3.1 +/- 1.8 AU for metoprolol and 2.2 +/- 1.6 AU for placebo P =.02). Among patients with only a vague or moderate suspicion of AMI, there was no difference. The treatment was well tolerated. CONCLUSIONS: When all patients were included in the analyses, there was no significant difference with regard to reduction of chest pain in the patients randomly assigned to metoprolol compared with placebo. A retrospective subgroup analysis indicated a beneficial effect of metoprolol among patients with an initially strong suspicion of or confirmed AMI. Further investigations are warranted to confirm this finding.     

Usefulness of the chest x-ray for predicting abnormal left ventricular function after acute myocardial infarction

We evaluated 229 patients discharged after a definite acute myocardial infarction. Pulmonary venous congestion determined from chest x-ray films during the hospitalization and at discharge and the cardiothoracic ratio at discharge were compared to the left ventricular ejection fraction measured at discharge by a gated radionuclide technique. During hospitalization, pulmonary venous congestion was found on at least one x-ray frame in 94 patients (41%). At discharge 134 patients (59%) had abnormal ejection fraction (less than 0.51) and 35 had pulmonary venous congestion (15%). The sensitivity of the x-ray for detecting an abnormal ejection fraction was 20% when pulmonary venous congestion was observed on the discharge x-ray film (specificity 92% and predictive value 77%), 52% if pulmonary venous congestion was present on any x-ray film during the hospitalization (specificity 74% and predictive value 73%), and 47% if the cardiothoracic ratio was abnormal (greater than or equal to 0.50) on the discharge x-ray film (specificity and predictive value 66%). We conclude that an abnormal x-ray film at discharge or during the hospitalization will identify approximately one-half of the abnormal ejection fractions at the time of hospital discharge. Therefore, to reliably assess left ventricular function, either for prognostic or therapeutic purposes in the individual patient, a more direct measure of left ventricular function such as radionuclide angiography must be obtained.     

Optimised function for determining time to peak creatine kinase and creatine kinase-MB as non-invasive reperfusion indicators after thrombolytic therapy in acute myocardial infarction

STUDY OBJECTIVE--The aim of the study was to investigate the use of an optimised function to approximate and interpolate the time course of serum creatine kinase and creatine kinase-MB values after thrombolytic therapy in acute myocardial infarction. DESIGN--A three parameter interpolating function was developed which approximates the time course of serum enzyme levels. In the proposed function, time to peak creatine kinase and maximum of creatine kinase determined from raw data were used as starting parameters of the non-linear interpolation routine, thus providing ideal starting conditions for the iteration. The efficacy of the function was compared with that of three other functions cited in published reports (log-normal distribution function, modified gamma density function, three compartment function). SUBJECTS--Serum enzyme data from 20 patients with acute myocardial infarction were used in the comparisons. The patients have all been treated with anisoylated plasminogen streptokinase activator complex. RESULTS--In comparison with the other models, deviations of the experimental model function from the raw data were minimal. The fit remained stable for time intervals between blood samples of up to 6 h. CONCLUSIONS - Due to its numerical stability, the function outlined in this study is suitable for large clinical reperfusion trials. In the case of uncomplicated infarctions without thrombolytic therapy, the area under the creatine kinase activity curve could be directly calculated in terms of maximum activity and time to peak.     

Usefulness of early positive technetium-99m stannous pyrophosphate scan in predicting reperfusion after thrombolytic therapy for acute myocardial infarction

To test the hypothesis that scans with technetium-99m pyrophosphate (Tc-99m-PPi) are positive when performed early after successful thrombolytic therapy for acute myocardial infarction (AMI), 16 consecutive patients with AMI who received thrombolytic therapy within 5 hours after the onset of chest pain were studied. Patients were included if chest pain lasted for greater than 30 minutes, was unresponsive to sublingual nitroglycerin and was associated with at least 0.2 mV ST-segment elevation in at least 2 contiguous electrocardiographic leads. All patients received 1.5 million IU of streptokinase intravenously, a mean of 195 +/- 99 minutes after onset of chest pain. Tc-99m-PPi scans and coronary cineangiograms were recorded 491 +/- 156 minutes and 518 +/- 202 minutes, respectively, after the onset of symptoms. Effective reperfusion was present in 10 patients, 6 of whom had positive Tc-99m-PPi scans (sensitivity of 60% to detect reperfusion). Of the 6 patients without effective reperfusion, 3 had positive Tc-99m-PPi scans (specificity of 50%, p greater than 0.05). Analysis of the data using various definitions of effective reperfusion or artery patency yielded similar results. Thus, our findings indicate that early AMI scanning with Tc-99m-PPi does not accurately detect the presence or absence of reperfusion in patients with AMI after treatment with intravenous streptokinase. At this time, coronary cineangiography is the only reliable method to detect reperfusion promptly after thrombolytic therapy.     

Diagnostic changes in plasma creatine kinase isoforms early after the onset of acute myocardial infarction

Conventional plasma isoenzyme and enzyme values usually are normal during the first few hours of acute myocardial infarction. Thus definitive diagnosis may be delayed. We have shown recently that infarction in dogs can be detected within 1 hr after coronary occlusion by analysis of relative activities of MM creatine kinase (CK) isoforms in plasma. Isoforms of MM CK evolve through posttranslational modifications in plasma of the form released from tissue (MMA) to MMB and MMC. In this study we quantified changes in isoform profiles in the first available plasma samples from patients with evolving myocardial infarction, from patients with angina, and from normal subjects. In the 26 control subjects, the ratio of MMA to MMC was 1.09 +/- 0.4 (SE) (range 0.31 to 3.1; upper limit of normal [defined as the mean plus 2 SD] 2.5). In the seven control patients with coronary artery disease, the ratio of MMA to MMC was 1.3 +/- 0.3 with a range of 0.5 to 2.5. In contrast, among the 28 patients with acute myocardial infarction, the ratio of MMA to MMC in the first available plasma sample averaged 14.6 +/- 4.5 (p less than .01 compared with both control groups). First available samples were obtained 3.9 +/- 0.4 hr after the onset of pain. In 24 of 28 patients (86%) the ratio of MMA to MMC was greater than 2.5.(ABSTRACT TRUNCATED AT 250 WORDS)     

Circadian variation in the frequency of onset of chest pain in acute myocardial infarction.

The time of onset of chest pain was studied prospectively in 1154 consecutive patients admitted to a coronary care unit with myocardial infarction during a five year period. Statistical analysis confirmed a previous finding in a retrospective study of a bimodal frequency distribution with peaks in the time of onset of chest pain between 2330 and 0030 hours and between 0630 and 0830 hours.