Systematic review: Intra-aortic balloon counterpulsation pump therapy: a critical appraisal of the evidence for patients with acute myocardial infarction

Abstract

Intra-aortic balloon counterpulsation pump (IABP) therapy has been used in several clinical situations, predominantly in critically ill patients, since 1968 [1]. In acute myocardial infarction (AMI) patients who are experiencing continued ischemia, IABP therapy may be used in an attempt to improve patency of an infarct-related coronary artery (IRA) and reduce the rates of recurrent myocardial ischemia and its sequelae. The mechanism for this benefit is thought to be a combination of reduced oxygen demand [2], increased coronary artery blood flow velocity [3], and augmentation of diastolic arterial pressure enhancing thrombolysis, leading to faster reperfusion [4]. IABP therapy may also be used in patients with ventricular septal rupture, severe mitral regurgitation, and cardiogenic shock. The technique for IABP therapy involves insertion of an 8 or 9.5 Fr helium-filled balloon via the femoral artery into the descending aorta. The device is preferably inserted through an existing vascular access site in an attempt to reduce the rate of vascular and hemorrhagic complications. It is crucial that the tip be positioned distal to the left subclavian artery, but proximal to the renal arteries. The balloon is synchronized to deflate during early systole, thus decreasing left ventricular (LV) afterload. In turn, LV ejection fraction (EF) and stroke volume (SV) are enhanced, leading to reduced myocardial oxygen consumption. The balloon inflates during early diastole, thus increasing coronary blood flow and peripheral perfusion. The IABP is usually commenced at a rate of 1 : 1. Once the benefit of IABP therapy is thought to be concluded, patients are usually gradually weaned from the pump at rates of 1 : 2 to 1 : 3 over 6-12 h. Following the procedure, one must ensure that the patient has adequate radial artery pulses, suggesting no IABP interference with the subclavian arteries. A chest roentgenogram should be inspected for the location of the IABP marker, which should be 1-2 cm below the aortic arch knuckle. The patient's serum creatinine and urine output should be followed for evidence of IABP interference with the renal arteries. When used to prevent recurrent ischemia post-AMI, all patients who receive IABP therapy should also be prescribed daily aspirin and systemic heparinization with 1000-2000 U/h infused for at least 48 h to maintain activated partial thromboplastin time (aPTT) between 50 and 84 s. Contraindications to IABP use include severe peripheral vascular disease (PVD), defined as diminished femoral pulses or absent pedal pulses; aortic valve regurgitation (AVR); aortic dissection; tortuous or aneurysmal descending thoracic or abdominal aorta; and patients unable to be systemically heparinized. IABP therapy does not prohibit the use of other medications often used in AMI patients, including aspirin, systemic heparinization, angiotensin-converting enzyme inhibitors, intravenous nitroglycerine, and beta blockers. Complications of IABP therapy may include limb ischemia and hemorrhage to the femoral access site. A recently developed technique of sheathless insertion may reduce the rate of limb ischemia [5].