Marker For Acute Myocardial Infarction Research Articles

Evidence for infection with Helicobacter pylori in patients with acute myocardial infarction

Background: Anti- Helicobacter pylori (HP) IgA and IgG antibody titers were measured in patients with ischemic heart diseases. Methods: There were 60 healthy individuals that served as control subjects, and 21 patients with acute myocardial infarction (AMI), 34 with old myocardial infarctions (OMI), 35 with effort angina (AP) and 41 with vasospastic angina (VSA). Results: In the control group, the IgA and IgG anti-HP antibody titers were positively correlated with age. When the IgA and IgG antibody titers were compared among patient groups, IgG did not significantly differ between each patient group and the control group, whereas IgA was significantly higher in the AMI group (5.10±1.25 EV) than in the OMI ( p<0.01), AP, or the control ( p<0.05). Moreover, the positivity rate for IgA anti-HP antibody was the highest in the AMI group (90%), with an odds ratio to the age-matched control group of 4.09, whereas the positivity rate for IgG did not significantly differ between the groups when either the 10 or 55 U/ml cut-off value was used. Conclusions: These results suggest that an increased IgA antibody titer, which is an index of the active phase of HP infection, should be an etiological marker for acute myocardial infarction.

Circulating monocyte-platelet aggregates are an early marker of acute myocardial infarction

OBJECTIVESWe investigated whether elevated levels of circulating monocyte-platelet aggregates (MPA) can be used to identify patients with acute myocardial infarction (AMI).BACKGROUNDCommonly used blood markers of AMI reflect myocardial cell death, but do not reflect the earlier pathophysiologic processes of plaque rupture, platelet activation and resultant thrombus formation. Circulating MPA form after platelet activation.METHODSIn a single center between October 1998 and November 1999, we measured circulating MPA in a blinded fashion by whole blood flow cytometry in 211 consecutive patients who presented to the emergency department (ED) with chest pain and were admitted to rule out AMI. Acute myocardial infarction was diagnosed by a CK-MB fraction greater than three times control.RESULTSPatients with AMI (n = 61), as compared with those without AMI (n = 150), had significantly higher numbers of circulating MPA (11.6 ± 11.4 vs. 6.4 ± 3.6, mean ± SD, p < 0.0001). After controlling for age, the adjusted odds of developing AMI for patients in the 2nd, 3rd and 4th quartiles of MPA, in comparison with patients in the lowest quartile (odds ratio = 1.0), were 2.1 (95% confidence interval [CI]: 0.7, 6.8), 4.4 (95% CI: 1.5, 13.1) and 10.8 (95% CI: 3.6, 32.0), respectively. The number of circulating MPA in patients with AMI presenting within 4 h of symptom onset (14.4) was significantly greater than those presenting after 4 h (9.4) and after 8 h (7.0), (p < 0.001). Of the 61 patients with AMI, 35 (57%) had a normal creatine kinase isoenzyme ratio at the time of presentation to the ED, but had high levels of circulating MPA (13.3).CONCLUSIONSCirculating MPA are an early marker of AMI.

Dependency on Infarct Size Limits the Clinical Applicability of Non-Invasive Reperfusion Assessment by Biochemical Markers in Acute Myocardial Infarction

Background: Thrombolytic therapy often fails to obtain reperfusion in acute myocardial infarction (AMI). To allow further intervention, various methods for non-invasive reperfusion assessment, e.g. release kinetics of biochemical markers and ST segment recovery analysis on the ECG, have been proposed. Methods and Results: In 85 thrombolysed AMI patients <76 years with significant ST elevation on ECG and time delay ≤6 h, blood was drawn and ECGs recorded before and 90 min after the start of treatment. Myoglobin, creatine kinase-MB and troponin I were measured, and slopesand relative increases (RIs) of the markers were calculated. Moreover, the relative decrease in total sum of ST elevation (ST recovery_0–90) on the ECG was calculated. A slope_0–90 or RI_0–90 below previously validated threshold values or an ST recovery <25% was considered indicative of failed reperfusion. Final infarct size was determined as cumulative release of LD1. Patients were followed for 1 year to register deaths, re-infarctions, and coronary revascularisation. The various non-invasive reperfusion indexes showed poor agreement, and no significant prognostic information was obtained. A positive correlation between increase rates and infarct size probably reflected a direct, concentration-dependent enhancement of release of biochemical markers in blood. Thereby, high-risk patients with large, non-reperfused infarcts might have been overlooked while only low-risk patients with small non-reperfused infarcts were recognised. This could readily explain the lack of correlation with long-term outcome. Conclusions: Dependency on infarct size seems to limit the usefulness of biochemical markers for reperfusion assessment. Correction for expected infarct size might improve performance in the future. At present, routine use of biochemical markers for reperfusion assessment is not justified.

Development of a simple whole blood panel test for detection of human heart-type fatty acid-binding protein

Objective: For the diagnosis of acute myocardial infarction (AMI), we have developed a rapid and simple whole blood panel test for the detection of human heart-type fatty acid-binding protein (H-FABP) using one-step immunochromatography. Methods and Results: We have developed a whole blood panel test for rapid detection of human H-FABP using a one-step immunochromatography technique. The result of this panel test was not affected by the other contents of the blood such as bilirubin, hemoglobin and others. Furthermore, no cross-reactivity of the antibodies was found with other cardiac markers or other tissue-type FABPs. The result of this panel test was similar to the diagnostic cut-off value, 6.2 ng of H-FABP per mL of serum which was evaluated by the enzyme-linked immunosorbent assay (ELISA). Conclusion: We have developed a simple one-step immunochromatography technique to detect H-FABP in whole blood sample. Further studies are required to identify the value of this point-of-care testing (POCT) as a diagnostic marker for AMI.

Serum creatine kinase elevation in a medical department.

Serum creatine kinase (CK) levels are diagnostic markers for acute myocardial infarction. Many other causes however, including neuromuscular disorders, may induce serum CK elevation as well. Aim of the study was to investigate the prevalence of potential causes for serum CK elevation in a medical department. In particular we were interested in the recognition of patients in whom serum CK elevation was due to a neuromuscular disorder. Included in this prospective study were 100 consecutive patients in whom the CK level, determined at admission, was increased (> 70 IU/l in female, > 80 IU/l in male patients). After admission we looked for the presence of causes known to induce CK elevation. Patients with no potential cause for CK elevation were invited for follow-up investigations three months later. If no potential cause could be found and if CK was elevated again on this occasion, the patient was referred for a comprehensive neurological investigation. The prevalence of patients with CK elevation was 11.2%. The 100 patients (44 female, 56 male) were aged from 23 to 94 (mean 67) years. In 95% CK elevation was only up to 500 IU/l. The most frequent cause for serum CK elevation was acute myocardial infarction in 32%. Further frequent causes were drug intake (32%), fall (24%), haematoma (17%), intramuscular injection (16%) and malignancy (11%). In 61% of the cases at least two potential causes for serum CK elevation could be detected. Neuromuscular disorders were found in only 2%. This study shows that serum CK elevation occurs in 11% of patients admitted to a medical department and can be explained by acute myocardial infarction in only 32%. In almost two thirds of the patients, more than one potential cause for serum CK elevation can be found thus making CK elevation a rather unspecific finding. Neuromuscular disorders are rarely found as a cause of serum CK elevation in a medical department.

A genetically engineered fusion protein with horseradish peroxidase as a marker enzyme for use in competitive immunoassays.

Horseradish peroxidase is one of the most widely used marker enzymes in immunoassays. Several disadvantages are encountered upon chemical conjugation of peroxidase with antibodies or antigens, as are low reproducibility and undefined stoichiometry. We here describe for the first time the production of a recombinant fusion of a protein analyte with horseradish peroxidase in Escherichia coli, employing refolding of inclusion bodies and reconstitution with heme. The genetic fusion approach enables preparation of conjugates with 1:1 stoichiometry and defined structure. As a protein analyte, the human heart fatty acid binding protein (H-FABP) was chosen, which is a new and sensitive marker for acute myocardial infarction. The recombinant conjugate was fully active [650 U/mg with 2,2-azino-bis(3-ethyl-thiazoline-6-sulfonate) as substrate] and obtained in a yield of 12 mg/L of E. coli culture, which is better than that for recombinant peroxidase alone. The competitive immunoassay that was developed with the recombinant conjugate requires fewer incubation steps than the traditional sandwich ELISA format. It permitted the detection of H-FABP directly in plasma in the range of 10-1500 ng/mL which is the relevant range for clinical decision-making.

La troponina T como posible marcador del daño miocárdico menor. Su aplicación en el miocardio aturdido y en la isquemia silente

The need for more specific, more sensitive and earlier biochemical markers of acute myocardial infarction, has led to the development of alternative methods to CK-MB). The aim of this work is to assess the usefulness of TnT measurement, in comparison with other markers for detecting transitory ischemic processes without necrosis in some experimental models. The plasma levels of Troponine T, CK, CK-MB and adenosine were assessed as markers of ischemic myocardial injury. Two protocols were used: in Series I and II very brief (2 min ischemia with 3-min reperfusion) repeated (20 episodes) ischemias were induced, while Series III involved a single 15-min ischemia with a 60-min reperfusion. In Series I the coronary occlusor was placed close to the anterior descending coronary artery (AD); in Series II and III it was placed distally in the AD. Blood samples were taken from the peripheral vein (PVB) and corresponding coronary segment vein; in a basal situation, during ischemia, upon reperfusion, after 24 hours, and after 5 and 10 days. The plasma levels of adenosine, troponine T, CK and CK-MB as well as general and regional function parameters were measured. In Series I we observed hypokinesis that lasted 10 days, reaching its maximum on days 4-5. In Series II and III regional function was restored by 24 hours. CK and CK-MB showed similar behaviour; they rose significantly when the chest was opened (p < 0.05) reaching the highest value at 24 hours in all the series. Adenosine rose significantly only during reperfusion (p < 0.05). Troponine T increased after ischemia but not before, remained high for 5 days in all series (PVB). Troponine T rises in absence of necrosis, preferably when the ischemia is longer.

Leitsymptom Thoraxschmerz in der Notaufnahme - Nutzen kardialer Marker bei der Risikostratifizierung -

The acute coronary syndrome (ACS)--acute infarction or unstable angina pectoris--requires special monitoring and differentiated treatment. A prospective trial was undertaken to determine (1) clinical characteristics of patients with chest pain; (2) value of cardiac markers troponin T, myoglobin and CK-MB mass in differentiating cardiac and noncardiac chest pain; (3) the proportion of patients with ACS in whom these markers provided helpful additional information on admission and afterwards.233 consecutive patients (134 men, 99 women; aged 18-98 years), presenting in 1998 with nontraumatic chest pain at the emergency unit of the Lippe-Detmold Hospital were prospectively enrolled in the study. Levels of troponin T, myoglobin, CK-MB mass and activity and creatine kinase were measured on admission and after 2, 4 and 12-24 hours.ACS was ultimately diagnosed in 73 patients (31%). These were significantly older (p = 0.0015) and more often male (p = 0.046). 91% of patients with ACS but only 68% of those without described the chest pain as a sense of pressure or stabbing (p = 0.0002). Measurement of troponin T and myoglobin on admission was helpful in 39% of those with ACS, compared with 15% of those without. When the admission ECG was normal or nonspecific in patients with ACS, troponin T was elevated in 16%, CK-MB mass in 24%. In patients with unstable angina no single marker was associated with an increased risk (high rate of special supervision and intervention).In the assessment of patients with acute chest pain clinical judgement plays the predominant role. In the mostly elderly and male patients with ACS (31% of the cohort) feeling of pressure or stabbing chest pain were most prominent (91%). Cardiac markers troponin T, CK-MB mass and myoglobin were helpful in the differential diagnosis of chest pain, even when the ECG was unremarkable or nonspecific. At the time of admission myoglobin was the most significant marker for acute myocardial infarction or unstable angina.

El infarto sin onda Q en cirugía cardíaca valvular convencional. Diagnóstico mediante la troponina I cardíaca

Morbidity and mortality in elective valve surgery is still significant. The main cause of death in these patients is cardiogenic shock, of which the most frequent etiology is acute myocardial infarction (AMI) with Q wave in the ECG. However, there are patients with cardiogenic shock without Q wave in the ECG and with rises in CK-MB enzyme that makes us suspect non-Q wave AMI.To analyze the use of the determination of cardiac troponin-I, a more specific marker of AMI than CK-MB after cardiac surgery, to detect perioperative non-Q wave AMI, and to establish its clinical significance.A total of 147 patients without coronary artery disease scheduled for elective valve surgery were included. We used, based in anterior publications, ECG (presence or not of new Q wave) and cardiac troponin I to define perioperative AMI. Levels of cardiac troponin-I were analysed before surgery and 14 hours after. Non-Q wave AMI was diagnosed when troponin I was superior to 38.85 ng/ml and there was not a phatologic Q wave in ECG.One hundred twenty-three (83.67%) of patients did not have AMI, 9 (6.12%) suffered perioperative AMI with Q wave, and 15 (10.27%) carried out criteria of non-Q wave perioperative AMI. Morbidity and mortality in this last group was similar to that in the group with Q wave AMI. Morbidity and mortality were minimum in patients without AMI.This study suggest the possibility of in vivo identification of non-Q wave perioperative AMI, an entity with important morbidity and mortality in our series, with a simple determination of cardiac troponin I 14 hours after surgery.

Using troponin T to diagnose acute coronary syndromes.

Elevated troponin T is a useful marker for acute myocardial infarction: it is more specific than is elevated creatine kinase MB isoenzyme, and it remains elevated for many days after creatine kinase levels have returned to normal, providing a useful indicator for late presentations. Nevertheless, creatine kinase MB still has many important roles, including providing estimates of infarct size and diagnosing acute myocardial infarction in patients with renal failure. Often, measuring both markers provides additional information. This article provides a diagnostic algorithm for using both markers.

Clinical utility of CKMB isoform determinations in patients who present to the Emergency Department with continuous or resolved chest pain

The object of this investigation was to demonstrate that the enhanced sensitivity of the diagnosis of acute myocardial infarction (AMI) using a more-inclusive criterion of CKMB Isoforms may detect earlier stages of AMI (designated Isoform Type 2) than the currently accepted marker for AMI by CKMB Isoform (designated Isoform Type 1) in a busy, urban Emergency Department (ED). Two features characterized the study of CKMB Isoforms in a prospective cohort of 223 ED patients: first, nontraumatic chest pain within 12 h before presentation, thought to be of ischemic etiology; and second, normal or nondiagnostic electrocardiogram (EKG). Patients were further divided into two groups characterized as either recent but resolved chest pain at ED visit, or ongoing or staccato chest pain. Sensitivity (S), specificity (SP), positive (PPV) and negative (NPV) predictive values, and 95% confidence intervals (CI) for AMI diagnosis were determined. Two criteria for AMI diagnosis by CKMB Isoforms were tested. The first and currently recommended criterion was identified as Isoform Type 1. An AMI diagnosis by Type 1 criterion requires both CKMB2≥2.6 IU/L and CKMB2/CKMB1≥1.7. The second criterion for AMI diagnosis was identified as Isoform Type 2, which is defined as either CKMB2≥2.6 IU/L or CKMB2/CKMB1≥1.7. Both Isoform types are predictive of AMI by the gold standard, and addition of EKG changes results in a small improvement. Type 1 demonstrates SP 0.94 (CI 0.90, 0.97) and NPV 0.90 (CI 0.86, 0.94), and Type 2 demonstrates S 0.90 (CI 0.80, 0.97) and NPV 0.97 (CI 0.93, 0.99) for AMI diagnosis. Type 2 criteria can confidently exclude the immediate risk of AMI in patients with resolved chest pain whereas in patients with continuous chest pain, Type 1 criteria may identify those at high risk for AMI.

Is apoptosis a diagnostic marker of acute myocardial infarction?

To investigate and quantify the presence of apoptosis in early myocardial ischemia in humans. Histologic sections from the left and right ventricles of 16 hearts with impending myocardial infarction were stained with terminal deoxynucleotidyl transferase-mediated deoxyuridine 5-triphosphate nick end labeling (TUNEL) method and with antibodies to p53, bcl-2, cpp32, FAS, FAS-L, and bax. DNA electrophoretic analysis was also performed. According to the inclusion criteria, all 16 cases showed morphologic changes consistent with ischemia and/or reperfusion. TUNEL results were positive in 14 of the 16 ischemic areas. Unexpectedly, they were also positive in "remote from ischemia" myocardium of both the left and right ventricles. DNA electrophoretic analysis confirmed the results of TUNEL. Immunohistochemistry was uniformly negative, probably because of autolysis phenomena. We showed that apoptosis precedes necrosis in humans, but the detection of apoptosis cannot be used as a diagnostic tool, since it can also be triggered by nonischemic events.

Is apoptosis a diagnostic marker of acute myocardial infarction? An autopsy study comparing histologic, immunohistochemical, tunel, and DNA electrophoresis evidence

Abstract Objective.—To investigate and quantify the presence of apoptosis in early myocardial ischemia in humans. Methods.—Histologic sections from the left and right ventricles of 16 hearts with impending myocardial infarction were stained with terminal deoxynucleotidyl transferase–mediated deoxyuridine 5-triphosphate nick end labeling (TUNEL) method and with antibodies to p53, bcl-2, cpp32, FAS, FAS-L, and bax. DNA electrophoretic analysis was also performed. Results.—According to the inclusion criteria, all 16 cases showed morphologic changes consistent with ischemia and/or reperfusion. TUNEL results were positive in 14 of the 16 ischemic areas. Unexpectedly, they were also positive in “remote from ischemia” myocardium of both the left and right ventricles. DNA electrophoretic analysis confirmed the results of TUNEL. Immunohistochemistry was uniformly negative, probably because of autolysis phenomena. Conclusions.—We showed that apoptosis precedes necrosis in humans, but the detection of apoptosis cann...

T102C polymorphism of the serotonin (5-HT) 2A receptor gene in patients with non-fatal acute myocardial infarction

Serotonin (5-HT), released from activated platelets, has been implicated in the pathogenesis of acute myocardial infarction (AMI). 5-HT induces platelet aggregation and vascular contraction through 5-HT2A receptor activation at sites of coronary atherosclerosis, leading to thrombus formation. Recently, a 5-HT2A receptor gene T102C polymorphism has been reported to be associated with clinical response to 5-HT2A receptor antagonist in patients with schizophrenia, suggesting this polymorphism of the gene affects the 5-HT2A receptor function. To investigate the relationship between the T102C polymorphism and AMI, we conducted a case-control study of 255 non-fatal AMI patients and 255 control subjects. Among the patients, the prevalence of TT genotype was significantly higher than in controls (32.5 vs. 24.3%; P<0.05). In male patients ( n=216), the prevalence was much higher than in control subjects (33.8 vs. 24.1%, P<0.03). In multiple logistic regression models, odds ratio of TT genotype was 1.45 (95% CI 0.96–2.20) in all and 1.61 (95% CI 1.03–2.53) ( P<0.05) in males. The association of T102C polymorphism of the 5-HT2A receptor gene with non-fatal AMI was statistically significant and independent of other risk factors in males. The TT genotype of the 5-HT2A receptor gene may enhance susceptibility to AMI. Our observations suggest that the T102C polymorphism of the 5-HT2A receptor gene can serve as a new genetic marker for AMI.

Very early diagnosis and risk stratification of patients admitted with suspected acute myocardial infarction by the combined evaluation of a single serum value of cardiac troponin-T, myoglobin, and creatine kinase MB(mass)

The diagnostic and prognostic capacity of biochemical markers of acute myocardial infarction in the emergency department were evaluated in consecutive patients (n=155) with suspected acute myocardial infarction. Serum myoglobin >/=110 microg. l(-1)and creatine kinase MB(mass)>/=5 microg. l(-1)had a high accuracy (0.77-0.85) (ns) for acute myocardial infarction diagnosis in patients presenting >2 h after symptom onset. Troponin-T (>/=0.10 microg. l(-1)) had a lower accuracy (0.53-0.70) for acute myocardial infarction diagnosis, but was the most important 1-year prognostic marker (cardiac death or non-fatal acute myocardial infarction). In patients without ST elevation, combined analysis of two biochemical tests would accurately identify an additional 20% of acute myocardial infarction patients (predictive value of a positive test=0.82) and also identify those without acute myocardial infarction (predictive value of a negative test=0.80). One-year event-free survival was excellent (96%) for patients with two negative biochemical tests, intermediate (74%) for those with discordant tests, and only 53% for patients with two positive biochemical tests. Analysis of biochemical tests in the emergency department prior to hospital admission could accurately identify approximately 20% additional acute myocardial infarction patients. The prognosis of these patients is poor, and they may be a target for primary PTCA or new early initiated aggressive medical therapies.

National Academy of Clinical Biochemistry Standards of Laboratory Practice: Recommendations for the Use of Cardiac Markers in Coronary Artery Diseases

The Sixth Conference on the "Standards of Laboratory Practice Series", sponsored by the National Academy of Clinical Biochemistry (NACB), was held on August 4-5, 1998, at the Annual Meeting of the American Association for Clinical Chemistry, in Chicago, IL. An expert committee was assembled to write recommendations on the use of cardiac markers in coronary artery diseases. The NACB Committee prepared a preliminary draft of the guidelines, made them available on the World Wide Web (www.nacb.org), and distributed them before the presentations. The recommendations were divided into four areas: the use of markers in the triage of patients with chest pain, acute coronary syndromes, clinical applications other than acute myocardial infarction and research, and assay platforms and markers of acute myocardial infarction. The recommendations were revised and subsequently re-presented in part at the "Biomarkers in Acute Cardiac Syndromes Conference", sponsored by the Jewish Hospital Heart and Lung Institute, Louisville KY, on October 16-17, 1998. This report lists each recommendation, its scientific justification, and a summary of discussions from conference participants and reviewers. Approximately 100 individuals responded to various versions of these recommendations via direct correspondences, telephone calls to Committee members, electronic mail correspondence to the Committee Chairman, or oral questions and comments raised during one of the two conference presentations. Some of the recommendations were changed to reflect the consensus opinion. In cases in which there was no consensus, the Committee included pertinent discussion without necessarily changing the original recommendations. At times, the Committee members felt that although a particular recommendation might not be the current standard of care today, they anticipate that it likely will be adopted in the near future.

A New Principle for Rapid Immunoassay of Proteins Based on In Situ Precipitate-Enhanced Ellipsometry

A new technique is presented that allows measurement of protein concentrations in the picomolar range with an assay time of only 10–20 min. The method is an enzyme-linked immunosorbent assay (ELISA), but uses in-situ ellipsometric measurement of a precipitating enzyme product instead of the usual colorimetric detection of accumulating enzyme product in solution. Quantitative validation was obtained by use of annexin V, a protein with high binding affinity for phosphatidylserine-containing phospholipid membranes, resulting in a transport-limited adsorption rate. This property was exploited to obtain a range of low surface concentrations of annexin V by timed exposures of phospholipid bilayers to known concentrations of annexin V. Using polyvinylchloride (PVC)-coated and silanized silicon slides, various versions of this technique were used for the rapid assay of fatty acid-binding protein (FABP), a recently introduced early marker for acute myocardial infarction with a normal plasma concentration below 1 nmol/l, interleukin 6 (IL-6), a cytokine with normal plasma concentrations below 1 pmol/l, and again, annexin V. A possible future application of the method in the development of a one-step ELISA is discussed.

Multicenter evaluation of an amperometric immunosensor for plasma fatty acid-binding protein:: An early marker for acute myocardial infarction

Multicenter evaluation of an amperometric immunosensor for plasma fatty acid-binding protein:: An early marker for acute myocardial infarction

Blood Ketone Body As a Stress Marker in Acute Myocardial Infarction.

Blood Ketone Body As a Stress Marker in Acute Myocardial Infarction.

QT Dispersion as a Noninvasive Arrhythmiogenic Marker in Acute Myocardial Infarction

Backround: Prolongation of QT dispersion (QTD), defined as the difference between maximum and minimum QT intervals on surface ECG, has been proposed as a noninvasive arrythmogenic marker. The aim of this study was to estimate the value of QTD in identifing patients susceptible to ventricular fibrillation or ventricular tachycardia (VF/VT) after an acute myocardial infarction (AMI) and to evaluate the behavior of QTD in relation to the thrombolytic therapy.Methods: We studied 108 consecutive patients with AMI. All patients had a 12‐lead surface ECG recorded upon admission and a second ECG 24 hours later. QT interval was measured from the onset of Q to the end of T in each of 12 standard ECG leads. QTD was the difference between the longest and shortest values of QT. All QTD measurements were corrected for heart rate (QTcD) using QTc values according to Bazzet formula.Results: Fifteen patients (13.8%) developed VF/VT in the first week after AMI (group 1A) and 93 patients (86.2%) did not have VF/NT (group 1B). QTD and QTcD values were significantly greater in group 1A in comparison to group 1B on admission and 24 hours later. Sixty‐five patients (60%) received intravenous thrombolysis in the acute phase of AMI (group 2A) and 43 patients (40%) did not (group 2B). No significant difference in QTD and QTcD was observed in the first ECG on admission between the two groups. Conversely, QTD and QTcD were lower in group 2A patients in the second ECG 24 hours after admission.Conclusions: These results provide evidence that increased values of QTD are correlated well with occurrence of malignant ventricular arrhythmias after acute myocardial infarction while lower values associated with the thrombolytic therapy. A.N.E. 1999;4(1):35–38