Denise Muncy

Intra-aortic balloon counterpulsation before primary percutaneous transluminal coronary angioplasty reduces catheterization laboratory events in high-risk patients with acute myocardial infarction

The benefit of intra-aortic balloon counterpulsation (IABC) before primary percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction in high-risk patients has not been well documented. Consecutive patients (n = 1,490) with acute myocardial infarction treated with primary PTCA from 1984 to 1997 were prospectively enrolled in an ongoing registry. Catheterization laboratory events occurred during or after intervention in 88 patients (5.9%), including ventricular fibrillation in 59 patients (4.0%), cardiopulmonary arrest in 46 patients (3.1%), and prolonged hypotension in 33 patients (2.2%). Cardiogenic shock was the strongest predictor of catheterization laboratory events (odds ratio [OR] 2.18, 95% confidence intervals [CI] 1.58 to 3.02) followed by low ejection fraction (<30%) (OR 1.51, 95% CI 1.06 to 2.15) and congestive heart failure (CHF) (OR 1.45, 95% CI 1.01 to 2.07). IABC used before intervention was associated with fewer catheterization laboratory events in patients with cardiogenic shock (n = 1 19) (14.5% vs. 35.1%, p = 0.009), in patients with CHF or low ejection fraction (n = 119) (0% vs. 14.6%, p = 0.10), and in all high-risk patients combined (n = 238) (1 1.5% vs. 21.9%, p = 0.05). IABC was a significant independent predictor of freedom from catheterization laboratory events (OR 0.48, 95% CI 0.29 to 0.79). These data support the use of IABC before primary PTCA for acute myocardial infarction in all patients with cardiogenic shock, and suggest that prophylactic IABC may also be beneficial in patients with CHF or depressed left ventricular function.

Timing and mechanism of death determined clinically after primary angioplasty for acute myocardial infarction.

We reviewed the timing and mechanism of death in 1,184 consecutive patients with acute myocardial infarction (AMI) treated with primary angioplasty from 1984 to 1995. Of 98 deaths, 48 (49%) occurred early on day 0 or 1. The mechanisms of death were pump failure in 60 patients (61%), reinfarction in 7 patients (7.1%), left ventricular rupture in 5 patients (5.1%), arrhythmia in 3 patients (3.1%), other cardiac causes in 5 patients (5.1%), stroke in 6 patients (6.1%), anoxic encephalopathy in 7 patients (7.1%), and procedure-related deaths in 5 patients (5.1%). The strongest predictors of mortality were cardiogenic shock and unsuccessful reperfusion. Our data indicate that mortality after primary angioplasty, like thrombolytic therapy, is highest in the early hours and is usually due to pump failure. In contrast to thrombolytic therapy, the incidence of death from myocardial rupture and bleeding complications is low. Future treatment strategies will need to focus on the large number of patients with early death due to pump failure, especially patients with cardiogenic shock.

Effect of treatment delay on outcomes in patients with acute myocardial infarction transferred from community hospitals for primary percutaneous coronary intervention

Outcomes were evaluated in 1,841 consecutive patients with acute myocardial infarction treated with primary percutaneous coronary intervention from 1984 to 2000 comparing patients transferred from community hospitals (n = 680) with patients presenting locally (n = 1,161). Baseline variables were similar except transferred patients had fewer prior infarctions (13% vs 21%, p <0.001) and underwent less prior bypass surgery (2.8% vs 6.0%, p = 0.002). Median times from symptom onset to emergency department arrival were similar, but door-to-balloon times and reperfusion times were approximately 1 hour longer in transferred patients (2.8 vs 1.9 hours [p <0.001] and 4.5 vs 3.5 hours [p <0.001], respectively). Despite longer treatment times, there were no significant differences between transferred and nontransferred patients in 30-day mortality (7.6% vs 8.1%, p = 0.73), reinfarction, urgent target vessel revascularization, stroke, and late mortality. After adjusting for differences in baseline variables, mortality remained similar between transferred and nontransferred patients (odds ratio 0.90, 95% confidence interval 0.59 to 1.36). Peak cardiac enzyme values were higher in transferred patients, but there were no differences in 6-month ejection fractions between groups. In conclusion, patients transferred from community hospitals for primary percutaneous coronary intervention have almost 1-hour additional treatment delay, but this does not appear to have a major adverse effect on clinical outcomes. These data should encourage further randomized trials to evaluate the role of transfer for mechanical reperfusion in patients presenting to community hospitals with acute myocardial infarction.

Benefit of late coronary reperfusion in patients with acute myocardial infarction and persistent ischemic chest pain

The benefit of thrombolytic therapy given late after the onset of acute myocardial infarction (AMI) has been controversial because of low reperfusion rates and limited myocardial salvage. Persistent chest pain has been used as a criteria for late intervention, but there is little documentation to validate this practice. Clinical outcomes and myocardial salvage were evaluated in 74 patients with AMI and persistent chest pain who underwent late reperfusion (> 6 hours) with direct coronary angioplasty, and these were compared with outcomes in 460 patients with early reperfusion (< or = 6 hours). Patients with late reperfusion had a high infarct artery patency rate (96%), a low hospital mortality rate (5.4%), and a low incidence of reinfarction (1.4%) and recurrent ischemia that were similar to patients with early reperfusion. Patients with late reperfusion had surprisingly good recovery of left ventricular function with improvement in ejection fraction from 50% to 60% at follow-up angiography. Patients with late reperfusion had a greater incidence of collateral flow (45% vs 22%, p < 0.001) and a lower value of peak creatine kinase (1,357 vs 2,057 U/liter, p < 0.001) than patients with early reperfusion. This study emphasizes the importance of persistent chest pain as a marker of continued myocardial viability in patients who present late after AMI. These data suggest that the probable mechanism of continued viability is preserved flow to the infarct zone. Patients with AMI and persistent chest pain may benefit from reperfusion therapy beyond 6 to 12 hours.