A decision tree for the early diagnosis of acute myocardial infarction in nontraumatic chest pain patients at hospital admission.

STUDY OBJECTIVE: To find an accurate algorithm for the diagnosis of acute myocardial infarction in nontraumatic chest pain patients on presentation to the emergency department. DESIGN: In a prospective clinical study, we compared the diagnostic performances of clinical symptoms, presenting ECG, creatinine kinase, creatine kinase MB activity and mass concentration, myoglobin, and cardiac troponin T test results of hospital admission blood samples. By classification and regression trees, a decision tree for the diagnosis of acute myocardial infarction was developed. SETTING: Emergency room of a Department of Internal Medicine (University Hospital). PATIENTS: One hundred fourteen nontraumatic chest pain patients (median delay from onset of chest pain to hospital admission, 3 h; range, 0.33 to 22): 26 Q-wave and 19 non-Q-wave myocardial infarctions, 49 patients with unstable angina pectoris, and 20 patients with chest pain caused by other diseases. MEASUREMENTS AND RESULTS: Of each parameter taken by itself, the ECG was tendentiously most informative (areas under receiver operating characteristic plots: 0.87 +/- 0.04 [ECG], 0.80 +/- 0.08 [myoglobin], 0.80 +/- 0.04 [creatine kinase MB mass], 0.77 +/- 0.04 [creatine kinase activity], 0.69 +/- 0.06 [clinical symptoms] 0.67 +/- 0.06 [creatine kinase MB activity], 0.67 +/- 0.05 [troponin T]). In patients presenting 3 h or less after the onset of chest pain, ECG signs of acute transmural myocardial ischemia were the best discriminator between patients with and without myocardial infarction. In patients presenting more than 3 h, however, creatine kinase MB mass concentrations (discriminator value, 6.7 micrograms/L) were superior to the ECG, clinical symptoms, and all other biochemical markers tested. This algorithm for diagnosing acute myocardial infarction was superior to each parameter by itself and was characterized by 0.91 sensitivity, a 0.90 specificity, a 0.90 positive and negative predictive value, and a 0.90 efficiency. CONCLUSIONS: We found an algorithm that could accurately separate the myocardial infarction patients from the others on admission to the emergency department. Therefore, this classifier could be a valuable diagnostic aid for rapid confirmation of a suspected myocardial infarction.

Water intoxication in the course of an acute schizophrenic episode.

In the course of a schizophrenic episode a woman drank a large amount of tap water. She was found nearly unconscious in her room and was admitted to the clinic. Very low sodium and potassium values in the serum were indicative of water intoxication. During hospitalization she also suffered from several convulsive seizures. After replacement of electrolytes she recovered within 12 to 17 h. This case report demonstrates that water intoxication should also be considered in cases of suspected poisoning with other substances such as drugs. In all these cases an electrolyte status is indicated.

Different time courses of cardiac contractile proteins after acute myocardial infarction.

For the first time we have compared time courses of cardiac myosin light chain-1 (MLC-1), beta-type myosin heavy chain (MHC), troponin T (TnT), myoglobin, creatine kinase (CK) and CKMB in the same patients with acute myocardial infarction (AMI). Blood samples were serially collected in 23 patients with first-time AMI. All but 3 patients received intravenous thrombolytic treatment. TnT and MLC-1 time courses were biphasic in most patients and showed two distinct peaks in 13 and 8 patients, respectively. MHC time courses were usually monophasic. Only 1 patient showed a biphasic MHC time course with two distinct peak values. Although MHC and MLC were lower by about the fourth day after onset of AMI in early reperfused patients, reperfusion did not qualitatively alter MLC and MHC release (no significant influence on the first appearance in blood or on time to peak). MLC and MHC peaks correlated closely (r = 0.75, P = 0.0001), whereas TnT peaks were correlated less closely with MLC or MHC peaks (r = 0.58 each, P < 0.007). Peak values of all cardiac contractile proteins correlated closely and significantly with CKMB peaks (0.75 < or = r < or = 0.81, P < or = 0.0006). Myoglobin was the first marker to increase in blood after AMI and showed the earliest peaks, whereas MHC increased latest showing the latest peaks. TnT increased significantly (P = 0.0001) earlier than MLC and MHC. These results can be explained by the impact of the intracellular compartmentation of a cardiac protein on the rapidity with which it is released after AMI.

Markers of activated coagulation for early diagnosis of acute myocardial infarction.

Intracoronary thrombosis plays a key role in the pathogenesis of acute myocardial infarction (AMI), and the formation of an occlusive thrombus usually precedes the development of myocardial damage. Therefore we evaluated and compared the early sensitivities of thrombin-antithrombin III complex (TAT), D-dimer, myoglobin, creatine kinase (CK) MB mass concentration, and cardiac troponin T (cTnT) on admission to a coronary care unit (CCU) before heparin or thrombolytic therapy was started. We investigated 31 consecutive patients admitted to CCU for evolving AMI within 6 hours from the onset of infarct-related symptoms; the median delay from chest pain onset to CCU admission was 135 minutes. Of all biochemical markers tested TAT had the highest early sensitivity on admission to the CCU, and TAT was significantly more sensitive than cTnT, CKMB mass, myoglobin, and D-dimer. However, TAT increases give no information about the location of clot formation in the body, and the diagnosis of AMI must be subsequently verified by an increase in more cardiac specific proteins, such as troponins or CKMB.

Cardiac troponin I in the diagnosis of myocardial injury and infarction.

We used a cardiospecific enzymoimmunometric assay to measure cardiac troponin I (cTnI) in samples serially drawn from 78 patients with acute myocardial infarction (AMI), 7 patients with unstable angina (Braunwald class III), 22 multi-traumatized patients, and in 30 athletes after eccentric exercise, as well as in 101 non-traumatic chest pain patients on admission to the emergency department. cTnI assay crossreactivity with crude human skeletal muscle homogenates was < 0.1%. cTnI could not be detected in athletes or multi-traumatized patients except for 2 trauma patients with myocardial damage. Increased cTnI concentrations were found in 6 of 7 patients with unstable angina at rest and in all AMI patients. After AMI, cTnI increased about 3.5 h (median) after the onset of chest pain, reached peak values parallel to CKMB, and stayed increased for at least 4 days. Cardiac troponin T (cTnT) increased and mostly peaked parallel to cTnI. cTnT sensitivity on the 7th day after AMI was significantly higher than that of cTnI. In contrast to cTnI, cTnT mostly showed a second, usually smaller, peak about day 4 after AMI. During the first 4 h after the onset of chest pain and before thrombolytic therapy the sensitivities of myoglobin (0.43) and CKMB mass (0.56) were significantly higher than those of both troponins (cTnI, 0.29; cTnT, 0.25). Areas under receiver operator characteristic curves indicated only moderate diagnostic accuracies of bio-chemical markers for early AMI diagnosis in non-traumatic chest pain patients that cTnI is a highly sensitive and specific marker for myocardial damage which is suitable for early and late diagnosis.

Usefulness of a new rapid bedside troponin T assay in patients with chest pain.

We evaluated the usefulness of a rapid, qualitative, bedside immunoassay for cardiac-specific troponin T in patients with chest pain. A concordant result between quantitative troponin T and qualitative troponin T assay was observed in 183 (96%) tests. The sensitivity of the rapid troponin T assay for detecting acute myocardial infarction increased significantly according to the number of hours elapsed after onset of chest pain from 17% for patients presenting within 4 h to 71% for patients presenting in the time interval of greater than 8 h from onset of chest pain (P < 0.001). Specificity ranged from 83 to 93% in the three time intervals evaluated. A concordant result between CK-MB-measurement and rapid troponin T assay was observed in 159 (83%) tests. In 14/191 tests a positive rapid troponin T and a negative CK-MB assay was observed. In 9/14 (64%) cases this result was true positive for the rapid troponin T assay and in 5/14 (36%) cases false negative. As sensitivity and specificity of the rapid troponin T assay are comparable with CK-MB measurements, rapid troponin T assay is a simple and useful laboratory tool for the bedside triage in patients with chest pain.

Rapid accurate diagnosis of acute myocardial infarction in patients with non-traumatic chest pain within 1 h of admission.

BACKGROUND: Accurate diagnosis of impending acute myocardial infarction (AMI) in patients presenting at an emergency department with acute chest pain is essential for proper triage and treatment. We have developed an algorithm for the early diagnosis of AMI. METHODS: The diagnostic performances of ECG, creatine kinase (CK) and creatine kinase isoenzyme MB (CKMB) activities, CKMB mass, myoglobin, and cardiac troponin T (cTnT) were compared for early diagnosis of AMI in 60 non-traumatic chest pain patients (22 AMI, 29 unstable angina, nine other diseases) on presentation to an internal medicine emergency department and 1 h thereafter. The classification and regression trees method was used for data analysis and revealed the following results. RESULTS: In patients with electrocardographic signs of acute transmural myocardial ischaemia on admission (mostly regional ST-segment elevations), biochemical markers could not improve the diagnostic accuracy either on admission or 1 h later. By contrast, in patients with non-diagnostic ECG, CKMB mass concentration measured 1h after admission was the best discriminator between AMI and non-AMI patients (discriminator value 5.8 micrograms/l) and was superior to ECG and all other biochemical markers tested. This algorithm for diagnosing AMI is characterized by 96% sensitivity, 90% specificity, 84% positive predictive value, 97% negative predictive value, 92% accuracy, 0.05 negative likelihood ratio, and 9.1 positive likelihood ratio. CONCLUSION: The classification procedure obtained allows accurate rapid and early diagnosis of AMI and could therefore be a valuable diagnostic aid to physicians of emergency medicine.

Concentration time courses of troponin and myosin subunits after acute myocardial infarction.

BACKGROUND: As a result of the limited sensitivity and specificity of creatine kinase and lactate dehydrogenase (LDH) as well as their isoenzymes, there is increasing interest in the use of cardiac contractile proteins for the diagnosis of acute myocardial infarction (AMI) and myocardial damage. METHODS: This study compared the release of creatine kinase, creatine kinase MB, myoglobin, cardiac troponin I (cTnI), cardiac troponin T (cTnT), cardiac myosin light chain-1 (cMLC-1), and beta-type myosin heavy chains (bMHC) in serial blood samples from 13 patients (10 men, three women; median age 54 years, range 40-74 years) with first-time AMI (11 Q-wave, two non-Q-wave AMI; three anterior and 10 inferior wall AMI). All but one patient received intravenous thrombolytic treatment. RESULTS: Myoglobin was the first marker to increase in blood after AMI and showed the earliest peak levels, whereas bMHC increased latest, showing the latest peak levels. cTnI and cTnT increased significantly earlier than cMLC-1 and bMHC. cTnI and cTnT increased and reached peak levels parallel to each other, but the latter tended to stay increased longer. cTnT time courses were biphasic in the majority of AMI patients, unlike cTnI time courses. cMLC-1 release was mostly biphasic. cMLC-1 allows diagnosis during the acute phase as well as several days after the onset of AMI. The time courses of bMHC were usually monophasic. Its delayed appearance makes it useful for the diagnosis of remote infarction. In contrast to cTnI and cTnT, cMLC-1 and bMHC time courses were not significantly influenced by early reperfusion. CONCLUSION: Our results demonstrate the impact of the intracellular compartmentation of an intramyocardial protein (cytosolic, structurally bound, or structurally bound with soluble pool) on its concentration time course after AMI, particularly on the rapidity of its release.

Cardiac troponin T release in acute myocardial infarction is associated with scintigraphic estimates of myocardial scar.

BACKGROUND: This study compared clinical-chemical estimates of infarct size with scintigraphic estimates of myocardial scar in patients with first-time acute myocardial infarction (AMI). METHODS: Levels of the cardiac isoform of the contractile protein troponin T (TnT), of creatine kinase (CK), and of the isoenzyme MB of CK (CK MB) were tested in serially drawn blood samples from 21 patients (two females and 19 males; median age, 55 years). Of these 21 patients, five had anterior- and 16 had inferior-wall AMI; all patients received intravenous thrombolytic therapy. Single-photon emission computed tomography (SPECT) with technetium-99m-isonitrile (Tc-sestamibi) was performed at rest after the onset of AMI (median time, 5 weeks). Scintigraphic defects were calculated using "bull's-eye" polar coordinate maps. All patients had an uncomplicated course between discharge and myocardial scintigraphy. RESULTS: Scintigraphic defect sizes ranged from 3.2% to 47.8% of the left ventricle (median, 27.3%). Cardiac TnT and CK MB release correlated closely with each other and with scintigraphic estimates of myocardial scar. Significant correlates were found between cardiac TnT and CK MB peak values (r = 0.87, P = 0.0001), CK MB peaks and Tc-sestamibi defect sizes (r = 0.73, P = 0.0014), and TnT peaks and scintigraphic defect sizes (r = 0.73, P = 0.0011). CONCLUSIONS: Because animal studies have already shown a very close correlation between histologic infarct size and SPECT Tc-sestamibi defect size, our results indicate that cardiac TnT is a useful marker to assess infarct size noninvasively in man.

Impact of thromboischemic reentry mechanism of coronary thrombosis and microembolism in acute myocardial infarction.

It has been suggested that the thromboischemic reentry mechanism (TRM) is responsible for washing platelet aggregates out of the coronary vessels during the early phase of acute myocardial infarction (AMI). This might account for the observation of Schwartz, who reported the presence of multiple microthrombi in the subendocardial blood vessels following AMI but found only a few thrombotic occlusions in the main coronary arteries. This washing-out of the vessel (due to reperfusion waves) intermittently releases myoglobin into the serum and is responsible for the "staccato phenomenon." We examined a group of 177 patients with a mean age of 66.1 years, whose sudden death was definitely of cardiac origin. Infarction was confirmed in 84.7% of the subjects (fresh infarct: 23.7%; fresh infarct with scarring: 25.9%; scarring alone: 35.0%; no change in myocardium: 15.2%). In other words, 49.7% of all postmortem subjects (88 cases) showed fresh infarction. Opening the coronary arteries longitudinally revealed only 7 thrombi in these 88 cases, i.e., 7.9% of all fresh infarcts. These observations confirm those of Roberts (8.5%) and Friedmann (4%).

New perspectives on the function of coronary artery spasm in acute myocardial infarction: the thromboischemic reentry mechanism. A review of 10 years research on the pathophysiology of AMI.

Research during the last ten years into the pathophysiology of acute myocardial infarction (AMI) has made it gradually clearer that this is a phasic event. A number of independent authors have made this conclusion quite obvious. The authors of this review suggest that the alternating sequence of coronary spasm and dilatation should be described as the "thromboischemic reentry mechanism," which itself leads to waves of reperfusion, producing characteristic episodic changes in some of the parameters of AMI. The spasms are brought about by substances let loose from aggregating platelets. Metabolites released during the concomitant ischemia lead the vessel from spasm to dilatation. Following thrombolytic treatment, the 'staccato' signs of myoglobinemia disappear, because of the withdrawal of the spasmogenic products of the platelets. It could also be shown that the concentration of myoglobin in the serum as a result of the dilating effect of calcium antagonists is twice the mean maximum value that the myoglobin time curve would show without such treatment.

[Does myocardial damage arise as a result of administration of tocolytic drugs? (author's transl)]. / Myokardschäden unter Tokolyse?

Fifty pregnant women admitted consecutively on account of threatened abortion or premature labour and treated with Ritodrine and Verapamil intravenously in the usual dosage were investigated with respect to creatine kinase activity and, in the event of a raised level, its isoenzyme creatine kinase--MB. Determinations were carried out before treatment and, in accordance with expected peak values in case of myocardial necrosis, after 6 and 12 hours. Three pathological values were recorded and these are discussed individually. Furthermore, statistical evaluation of the recorded values showed no significant differences.

[Does myocardial damage arise as a result of administration of tocolytic drugs? (author's transl)]. / Myokardschäden unter Tokolyse?

Fifty pregnant women admitted consecutively on account of threatened abortion or premature labour and treated with Ritodrine and Verapamil intravenously in the usual dosage were investigated with respect to creatine kinase activity and, in the event of a raised level, its isoenzyme creatine kinase--MB. Determinations were carried out before treatment and, in accordance with expected peak values in case of myocardial necrosis, after 6 and 12 hours. Three pathological values were recorded and these are discussed individually. Furthermore, statistical evaluation of the recorded values showed no significant differences.

[Complete occlusion of the aortic arch in an adult (author's transl)]. / Kompletter Verschluss des Aortenbogens beim Erwachsenen.

This paper reports the case of a 55-year-old patient with complete obstruction of the aorta between the left common carotid artery and the left subclavian artery. The arterial blood supply to the lower half of the body is provided by extensive collateral networks in the region of the right hemithorax, the neck and the base of the brain. Only 10 similar cases appear to have been described in the literature; our patient seems to be the oldest so far.

[Myoglobin increase during tocolysis (author's transl)]. / Myoglobinanstieg unter Tokolyse.

The serum myoglobin level was performed before as well as two and four hours following the beginning of intravenous tocolysis in 22 pregnant patients who were treated with the betasympathicomimetic agent, hexoprenalin because of premature labour. In six of the patients a rise of 26--140% in myoglobin was observed in comparison with the basal level. One of the patients even produced a twenty-fold rise. The value of serum myoglobin determination in the diagnosis of myocardial necroses is discussed with respect to the literature and the presented material.

[Incidence and presentation of myocardial infarction in Tyrol, Austria; (WHO ischaemic heart disease register Innsbruck 1971/72) (author's transl)]. / Der akute Myokardinfarkt in der Tiroler Bevölkerung (WHO Infarktregister Innsbruck 1971/72)

In 1971 a population-based Ischaemic Heart Disease (IHD) Register was established in the Innsbruck area as part of the WHO international collaborative study. Demographic and geographic data covering the area, as well as the locally-applied methods are described. One hundred and seventy four cases (133 males and 41 females) of acute myocardial infarction (AMI) were registered in the age group 20-64 years. This corresponds to an annual incidence rate of 1.9(0/00) in men and 0.6(0/00) in women. These results confirm indications from the national mortality statistics that Innsbruck belongs to the group of areas in Europe with a relatively low incidence of AMI. The epidemiology of AMI in Europe is discussed. The frequency distribution of AMI according to month of the year, day of the week and hour of the day is reported for this area.

[Differential diagnosis between skeletal muscle lesions and myocardial damage in multiple injury by determination of myocardial-specific creatine phosphokinase (CK-MB) (author's transl)]. / Differentialdiagnose von Skelettmuskel- und Herzmuskeltrauma bei polytraumatischen Verletzungen durch Bestimmung der herzspezifischen Kreatinphosphokinase (CKMB).

The serum level of the myocardial-specific isoenzyme of creatine phosphokinase, CK-MB was determined in 50 patients with severe multiple injuries or following extensive surgery. It is concluded that whenever the proportion of CK-MB exceeds 10% of the total creatine phosphokinase activity myocardial damage has occurred, especially since equivalent ECG changes were registered in this group of patients.

[Type, number and mode of distribution of cases of poisoning at the University Department of Internal Medicine, Innsbruck]. / Art, Zahl und Verteilungsmodus von Intoxikationsfällen an de Universtiätsklinik für Innere Medizin, Innsbruck.

In the course of one year 357 patients were treated in our department for poisoning, nearly always with suicidal intent. Altogether 249 patients were admitted to the wards for 24 hours or longer, and 108 of these (44.6%) were taken into the intensive care unit. Apart from myocardial infarction (276 patients/year), poisoning is the most common reason for admission to the intensive care unit. The age distribution showed a maximum between 15 and 20 years. Only one case proved fatal, representing a mortality rate of 0.3%.

[Anesthesia for cardioversion. A comparison of propofol and etomidate]. / Anesthésie pour cardioversion. Comparaison du propofol et de l'étomidate.

Anaesthesia for elective direct current cardioversion (DCC) was induced with propofol (Diprivan) 1.2 mg/kg in 28 patients and with 0.2 mg/kg etomidate (Hypnomidate) in 20 patients. These mostly high risk patients (NYHA class II to III) were successfully treated with defibrillation. Blood pressure and heart rate were recorded before and after induction and at 2 minutes intervals up to 20 minutes after DCC. Both anaesthetic agents caused mild hypotension. Heart rate did not change significantly after induction but fell significantly after DCC from the mean value of 124 +/- 26 bpm and 122 +/- 37 bpm to 94 +/- 19 bpm and to 91 +/- 19 bpm in propofol and etomidate treated patients respectively. Four patients became apnoeic necessitating assisted ventilation for approximately four minutes. All propofol treated patients had rapid recovery times and opened eyes on command within 5.6 +/- 1.9 minutes after induction, and were fully orientated about 4 minutes later also. Complete amnesia was observed in all patients in this group. In contrast etomidate induced anaesthesia did not cause respiratory depression, but the recovery time was longer. Four patients of this group complained of recall of DCC. In 7 patients due to involuntary movements or myoclonus, after induction with etomidate reliable EKG monitoring appeared to be difficult.