title: Higher T-wave amplitude associated with better prognosis in patients receiving thrombolytic therapy for acute myocardial infarction (a GUSTO-I substudy). Global Utilization of Streptokinase and Tissue plasminogen Activator for Occluded Coronary Arteries.
abstract: Increased T-wave amplitude is one of the earliest electrocardiographic (ECG) changes following coronary artery occlusion. Therefore, higher T waves in the presenting electrocardiogram should represent earlier time to treatment and thus be associated with lower mortality following thrombolytic therapy. However, T-wave amplitude has never been evaluated as a prognostic marker in this setting. We examined clinical outcomes in 3,317 patients with acute myocardial infarction (AMI) who underwent thrombolysis in the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO-I) Study. Patients were classified as either those with high T waves or those with low T waves. Higher T waves were defined as those >98th percentile of the upper limit of normal. T-wave amplitude was also evaluated as a continuous variable according to infarct location (maximum T-wave amplitude) and as the amount of excess T-wave amplitude above normal (excess T-wave amplitude). Patients with higher T waves had lower 30-day mortality than those without (5.2% vs 8.6%, p = 0.001) and were less likely to develop congestive heart failure (15% vs 24%, p <0.001) or cardiogenic shock (6.1% vs 8.6%, p = 0.023). Higher maximum T-wave amplitude and excess T-wave amplitude were predictive of lower 30-day mortality (chi-square = 67, p <0.001 and chi-square = 33, p <0.001, respectively). These differences remain significant after controlling for other prognostic baseline ECG variables. In addition, T-wave amplitude added prognostic significance after controlling for time to treatment. T-wave amplitude, an often-overlooked component of the electrocardiogram, can add significant prognostic information in initial evaluation of patients with AMI.
authors.affiliation: Department of Medicine, Duke University Medical Center, Durham, North Carolina 27705, USA.
authors.forename: J
authors.initials: J
authors.lastname: Hochrein
authors.forename: F
authors.initials: F
authors.lastname: Sun
authors.forename: K S
authors.initials: KS
authors.lastname: Pieper
authors.forename: K L
authors.initials: KL
authors.lastname: Lee
authors.forename: K B
authors.initials: KB
authors.lastname: Gates
authors.forename: P W
authors.initials: PW
authors.lastname: Armstrong
authors.forename: W D
authors.initials: WD
authors.lastname: Weaver
authors.forename: S G
authors.initials: SG
authors.lastname: Goodman
authors.forename: E J
authors.initials: EJ
authors.lastname: Topol
authors.forename: R M
authors.initials: RM
authors.lastname: Califf
authors.forename: C B
authors.initials: CB
authors.lastname: Granger
authors.forename: G S
authors.initials: GS
authors.lastname: Wagner
mesh_terms: D000368:Aged; D004562:Electrocardiography; D005260:Female; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015337:Multicenter Studies as Topic; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology*; D011379:Prognosis; D016032:Randomized Controlled Trials as Topic; D015912:Thrombolytic Therapy