Luigi Casella

Pathophysiology and prognostic significance of holter-detected ST segment depression after myocardial infarction☆

OBJECTIVESnWe performed Holter monitoring on days 4 and 7 after acute myocardial infarction in 109 patients to assess whether ST segment shift would identify those with more severe coronary artery disease, left ventricular dysfunction and unfavorable prognosis.nnnBACKGROUNDnSilent myocardial ischemia is a frequent and prognostically significant event after acute myocardial infarction. However, the specific pathophysiologic mechanisms and the impact of thrombolytic therapy are uncertain.nnnMETHODSnIn addition to Holter monitoring, patients underwent exercise testing, radionuclide angiography on days 1 and 9 and quantitative coronary angiography on day 9.nnnRESULTSnThirty-five patients (32%) had ST segment depression and had similar recombinant tissue-type plasminogen activator (rt-PA) treatment assignment and a reduced cross-sectional area of the infarct-related artery (0.59 +/- 0.57 vs. 1.04 +/- 1.26 mm2, p < 0.05). Global left ventricular function improved from day 1 to day 9 in patients without (4% +/- 11%, p < 0.001) but not in those with (0% +/- 7%) ST segment depression. In-hospital event rates were similar; however, follow-up 18 +/- 11 months after hospital discharge revealed a greater frequency of death and recurrent myocardial infarction in patients with compared with those without ST segment depression (27% vs. 6%, p = 0.03).nnnCONCLUSIONSnAfter acute myocardial infarction, approximately one third of patients have ST segment depression on Holter monitoring, independent of the use of thrombolytic therapy. The unfavorable prognosis observed in these patients may be related to greater lumen obstruction in the infarct-related artery and lack of improvement in left ventricular function.

Importance of ST-segment depression as a determinant of ventricular premature complex frequency after thrombolysis for acute myocardial infarction

Ventricular premature complexes (VPCs) after acute myocardial infarction (AMI) remain important determinants of survival in the post-thrombolytic era. The role of thrombolysis, left ventricular function, and Holter ST-segment depression in modulating VPC frequency is unclear. In a placebo-controlled, randomized study of tissue-type plasminogen activator (t-PA) in 103 patients with AMI (Tissue Plasminogen Activator: Toronto study), VPC frequency and ST depression on Holter monitoring (day 7), ejection fraction by radionuclide scan (day 9), and infarct artery patency and cross-sectional area on day 1 (n = 42) were assessed. After administering t-PA, VPC frequency was 10 +/- 58/hour (mean +/- SD), similar to that after placebo (23.5 +/- 91.7, p = NS). However, patients with ST depression had greater VPC frequency (56 +/- 140/hour) than those without it (1.3 +/- 2.6/hour, p = 0.05). Ejection fraction was negatively correlated with VPC frequency (r = -0.33, p < 0.001). By multivariate analysis, ejection fraction (F = 7.0, p < 0.01) and ST depression (F = 5.8, p < 0.02) were the only independent predictors of VPC frequency. In this placebo-controlled study, VPC frequency after AMI was not related to thrombolytic administration but was associated with ST depression and ejection fraction. This suggests that the underlying extent of both infarcted and ischemic myocardium is important in modulating ventricular arrhythmias after AMI.