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COMMENTARY: Cardiogenic Shock — The Role of Revascularization after Failed Thrombolysis

*Pranab Das, MD, §Aravinda Nanjundappa, MD, 1Robert S. Dieter, MD
May 2007
Technological advancements have revolutionized the field of interventional cardiology by introducing newer devices and better pharmacological agents. The incidence of cardiogenic shock (CS) complicating acute myocardial infarction (AMI) remains the major cause of death among hospitalized patients with AMI with mortality up to 60% and this has remained constant over last 25 years.1,2 The SHOCK Trial (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock)3,4 demonstrated a nonsignificant 9% absolute reduction in 30-day mortality and 13% significant absolute reduction in one year mortality among patients with early revascularization compared to initial medical stabilization, a trend that was sustained even at 6 years of follow up, with 13% absolute and 67% relative improvement in 6-year survival.5 Current American College of Cardiology guidelines carry a class I indication for primary percutaneous coronary intervention (PCI) in cardiogenic shock for patients < 75 years of age and class IIa for patients > 75 years of age.6 Current guidelines also recommend direct or expeditious transfer of patients with cardiogenic shock to hospitals with primary PCI capabilities and favoring primary PCI over fibrinolytic therapy for CS patients. In spite of these strong recommendations by the guideline committee, there remain a significant number of patients with ST elevation MI with cardiogenic shock who are treated by fibrinolytic therapy primarily as either immediate transfer to a PCI-capable facility may not be achieved within the recommended 90 minute door-to-balloon time or the shock state is not clinically recognized. Fibrinolytic therapy can successfully restore TIMI 3 flow in only up to 60% of patients by 90 minutes. Delay in restoration of normal flow is a strong predictor of short- and long-term mortality following an AMI. ACC guidelines therefore recommend rescue PCI among patients with cardiogenic shock complicating AMI (class I for age < 75 years and class IIa for > 75 years).

In this issue of the journal, Kunadian et al has reported the outcome of their retrospective study comparing rescue PCI to primary PCI among patients with cardiogenic shock. The study included patients undergoing PCI between 1994 and 2005, with 65 patients with primary PCI and 59 patients with rescue PCI. Patients undergoing rescue PCI had longer door to balloon time (298 minutes versus 130 minutes for PPCI; p < 0.01), and fewer glycoprotein IIb/IIIa inhibitors use (20% versus 42%; p = 0.01). Patients undergoing rescue PCI had lower TIMI III flow rate (56% versus 74% with primary PCI; p = 0.04) and higher 1-year mortality (71% versus 49% with primary PCI; p = 0.01). The study also reported one year mortality of above 80% in the event of unsuccessful PCI and mortality of 100% for patients > 70 years of age undergoing rescue PCI as compared to 70% for patients undergoing primary PCI.

This study further enriches our knowledge of acute management of patients with cardiogenic shock complicating acute ST elevation MI. But the small sample size, longer span over 11 years, and retrospective nature remain as important limitations. Nevertheless, the study further proves to us that time is myocardium and time is the key to better survival. Expeditious transfer of these moribund patients to the skilled catheterization laboratory with cardiothoracic surgery backup for primary PCI continues to remain the most definitive way of improving their chances of survival even if it means not meeting the guideline recommendations of 90 minutes of door-to-balloon time. As we have seen in this study, unlike in uncomplicated STEMI where early fibrinolysis is quite effective in successful reperfusion, cardiogenic shock poses a far bigger challenge. Delaying transfer for immediate fibrinolysis and then rescue PCI for failed thrombolysis carries a much higher risk of death even with successful PCI. Two recent studies have also shown that revascularization of an occluded infarct-related artery in the subacute phase (3 to 28 days after infarction) does not improve clinical outcomes (death, MI, or heart failure or ejection fraction), rather there may be a chance for harm.8,9

In summary, early and prompt recognition of cardiogenic shock or impending cardiogenic shock among patients presenting with acute ST elevation MI is the most crucial step in managing these critically ill patients. Once properly diagnosed, these patients can be immediately transferred to a PCI capable skilled catheterization laboratory for primary PCI. Patients with cardiogenic shock who undergo fibrinolysis or rescue PCI for failed fibrinolysis remain at substantial risk for cardiovascular morbidty and mortality.

 

References

  1. Babaev A, Frederick OD, Pasta DJ, et al. NRMI investigators. Trend in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock. JAMA 2005;294:448–454.
  2. Goldberg RJ, Samad NA, Yarzebski J, et al. Temporal trends in cardiogenic shock complicating acute myocardial infarction. N Engl J Med 1999;340:1162–1168.
  3. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. N Engl J Med 1999;341:625–634.
  4. Hochman JS, Sleeper LA, White HD, et al. SHOCK Investigators. One year survival following early revascularization for cardiogenic shock. JAMA 2001;285:190–192.
  5. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization and long term survival in cardiogenic shock complicating acute myocardial infarction. JAMA 2006;295:2511–2515.
  6. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA Guidelines for the management of patients with ST-elevation myocardial infarction. J Am Coll Cardiol 2004;44:671–719.
  7. The Gusto Angiographic Investigators. The effects of tissue plasminogen activator, streptokinase, or both on coronary artery patency, ventricular function, and survival after acute myocardial infarction. N Engl J Med 1993;329:1615–1622.
  8. Hochman JS, Lamas GA, Buller CE, et al. Coronary intervention for persistent occlusion after myocardial infarction. N Engl J Med 2006;355:2395–2407.
  9. Dzavik V, Buller CE, Lamas GA, et al. Randomized trial of percutaneous coronary intervention for subacute infarct-related coronary artery occlusion to achieve long-term patency and improve ventricular function: The Total Occlusion Study of Canada (TOSCA)-2 trial. Circulation 2006;114:2449–2457.

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