Precordial ST segment depression predicts a worse prognosis in inferior infarction despite reperfusion therapy. The Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) Study Group.

The impact of associated precordial ST segment depression in inferior myocardial infarction on angiographic and clinical outcomes after thrombolytic therapy and selective coronary angioplasty was studied in 583 patients with acute myocardial infarction. Anterior infarction (Group I), inferior infarction with precordial ST segment depression (Group II) and inferior infarction without precordial ST segment depression (Group III) were present in 289, 135 and 159 patients, respectively. Precordial ST segment depression was more frequent in circumflex than right coronary infarct-related arteries (44 [71%] of 62 versus 91 [40%] of 230; p = 0.000). Although acute patency rates were not statistically different, there was a trend toward different patency rates at day 7 (Group I 88%, Group II 84%, Group III 80%; p = 0.089) partly because of insignificantly higher reocclusion rates in inferior infarction without precordial ST segment depression (Group I 11%, Group II 10%, Group III 18%, p = 0.104). Infarct zone regional wall motion (standard deviations/chord) in inferior infarction was lower with precordial ST segment depression, both acutely (Group I -2.8 +/- 0.9, Group II -2.5 +/- 1.2, Group III 2.0 +/- 1.1; p = 0.000) and at day 7 (Group I -2.2 +/- 1.1, Group II -2.3 +/- 1.1, Group III -1.9 +/- 1.3; p = 0.011). Precordial ST segment depression was associated with a lower ejection fraction in inferior infarction both acutely (Group I 47 +/- 11%, Group II 53 +/- 11%, Group III 58 +/- 9%; p = 0.000) and at day 7 (Group I 49 +/- 12%, Group II 53 +/- 10%, Group III 58 +/- 8%; p = 0.000). Complication rates tended to be higher in inferior infarction when precordial ST segment depression was present. Mortality rates for Groups I, II and III were 8%, 6% and 5%, respectively. These results suggest that precordial ST segment depression in inferior infarction predicts a worse ventriculographic and clinical outcome despite reperfusion therapy.

Two-year outcome after angiographically documented myocardial reperfusion for acute coronary occlusion. Thrombolysis and Angioplasty Study Group.

Reperfusion therapy has been clearly shown to decrease the early mortality after acute myocardial infarction, but the impact of this therapy on long-term survival has been less extensively evaluated. This study reports the extended follow-up of a large cohort of 810 patients treated with intravenous thrombolytic therapy combined, when considered necessary to maintain or augment infarct vessel patency, with mechanical reperfusion therapies. Each patient underwent coronary angiography within 2 hours of the initiation of the thrombolytic infusion. Coronary angioplasty was performed in 62% of the patients before hospital discharge and 21% underwent coronary artery bypass graft surgery. Follow-up was obtained in 96% to a mean of 18.8 months (range, 1.5 to 48 months). All-cause mortality over this period was 3.3%; 2.1% died from cardiac causes. Nonfatal reinfarction occurred in 5.1%. Although the low event rate limits the validity of statistical comparisons, the patients who survived the follow-up period tended to be younger (56 +/- 10 vs 65 +/- 7 years), to have better predischarge left ventricular function (left ventricular ejection fraction, 52 +/- 11 vs 46 +/- 13%) and to have a lower prevalence of multivessel coronary artery disease (45 vs 67%). This excellent long-term survival may, in part, reflect the exclusion of high-risk patients from enrollment in the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) studies. It may also be attributable, however, to the frequent use of combined thrombolysis and mechanical revascularization in this population.

One-year outcome after therapy with tissue plasminogen activator: report from the Thrombolysis and Angioplasty in Myocardial Infarction trial.

To evaluate the long-term effects of reperfusion with tissue plasminogen activator (t-PA) and an aggressive strategy of revascularization with angioplasty and coronary artery bypass grafting, we obtained 1-year follow-up results from 386 consecutive patients enrolled in the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI I) trial. All patients were treated with 100 to 150 mg of t-PA intravenously over 6 to 8 hours, and coronary angiography was performed within 90 minutes of initiation of therapy. In 197 patients with suitable anatomic characteristics, angioplasty was either performed immediately or was deferred for 7 to 10 days on a randomized basis. The remainder of the patients were treated as considered clinically appropriate. The in-hospital mortality rate was 7%, and only 1.9% of patients died in the first year after discharge from the hospital; three patients died of cardiac events and four died of noncardiac causes. Ninety-four percent of patients discharged alive from the hospital remained alive and had no myocardial infarctions during the first 12 posthospital months. Revascularization procedures after discharge from the hospital included angioplasty in 8% of patients and coronary artery bypass grafting in 5%. The high survival rates were evident in high-risk groups defined by age, ejection fraction, and extent of coronary artery disease. At 1-year follow-up 64% of patients less than 65 years of age were employed and only 10% reported that they were disabled; 94% of patients were in Canadian Heart Association class I or II. These low rates of follow-up events suggest a change in the "natural history" of the first year after acute myocardial infarction.