title: High frequency QRS electrocardiography in the detection of reperfusion following thrombolytic therapy.
abstract: The hypothesis that an increase in the amplitude (root-mean-square voltage) of the high frequency (150-250 Hz) components of the QRS complex occurs with successful reperfusion following thrombolytic therapy in acute myocardial infarction (AMI) and fails to occur when thrombolysis fails was tested. Clinical markers for successful or failed reperfusion following thrombolytic therapy for AMI are notoriously insensitive. The amplitude of the high-frequency components of the QRS complex decreases during ischemia and returns to normal with resolution of ischemia, but neither the variability in measurement of these potentials nor their patterns of change during the course of AMI have been described. In 32 control subjects, the average coefficient of variation for the amplitude of the high-frequency QRS complex was 10% or 0.3 uV. Based on these data, for the acute infarction population a significant change in this measurement was therefore defined as a change in amplitude > 20% or 0.6 uV on two consecutive recordings. In 30 patients with AMI treated with a thrombolytic agent, either cardiac catheterization, serial serum myoglobin, or complete resolution of ST-segment elevation were used to define successful or failed reperfusion. High-frequency QRS electrocardiograms were obtained at the start of treatment with a thrombolytic agent and for 3 h thereafter using a signal-averaging technique and digital filtering. Standard 12-lead electrocardiograms were obtained at the same time. In patients who reperfused successfully, the high-frequency QRS amplitude increased significantly (1.2 +/- 0.9 uV above its nadir at 83 +/- 36 min after initiation of thrombolytic therapy) in 23 of 25 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Johns Hopkins Medical Institutions, Baltimore, Maryland.
authors.forename: T
authors.initials: T
authors.lastname: Aversano
authors.forename: B
authors.initials: B
authors.lastname: Rudikoff
authors.forename: A
authors.initials: A
authors.lastname: Washington
authors.forename: S
authors.initials: S
authors.lastname: Traill
authors.forename: V
authors.initials: V
authors.lastname: Coombs
authors.forename: J
authors.initials: J
authors.lastname: Raqueno
mesh_terms: D000328:Adult; D000787:Angina Pectoris / Q000503:physiopathology; D006328:Cardiac Catheterization; D003326:Coronary Circulation / Q000502:physiology*; D004562:Electrocardiography / Q000379:methods*; D006801:Humans; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000503:physiopathology* / Q000628:therapy*; D009211:Myoglobin / Q000097:blood; D013300:Streptokinase / Q000627:therapeutic use; D015912:Thrombolytic Therapy; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use; D014568:Urokinase-Type Plasminogen Activator / Q000627:therapeutic use; D014654:Vascular Patency
chemical_list: D009211:Myoglobin; D013300:Streptokinase; D010959:Tissue Plasminogen Activator; D014568:Urokinase-Type Plasminogen Activator