Letter from the Editor

Your Patient Has Critical Left Main Stenosis. Do You Need an Intra-aortic Balloon Pump?

Morton Kern, MD
Morton Kern, MD

A 59-year-old man with high blood pressure has progressive angina over the last six weeks. The patient’s angina occurs while brushing his teeth as well as during easy walking. He is admitted for cardiac catheterization immediately after an office visit that morning. His EKG is normal. He had only intermittent brief chest pain in the preceding days. The patient is pain-free at the time of the cath procedure. The first coronary angiographic shot (Figure 1) showed a critical left main stenosis involving the distal trifurcation of the left anterior descending (LAD) artery, Ramus and circumflex arteries. There was no coronary catheter pressure damping. The right coronary artery (RCA) was irregular but widely patent. No other angiograms were obtained. No ventriculography was performed. From the cath lab, the patient was referred to our cardiovascular surgeon, who agreed to operate on the first available surgical slot. Does this patient need an intra-aortic balloon pump (IABP)?

Before the simple answer, consider the conventional wisdom. An IABP is used in patients with left main coronary stenosis, cardiogenic shock, refractory ischemia and mechanical complications of acute myocardial infarction (e.g., ruptured papillary muscle or ventricular septal defect). An IABP is thought to provide clinical benefit by increasing diastolic pressure (and diastolic flow) and reducing myocardial oxygen demand by afterload reduction. To review the physiology of an IABP, recall that by inflating the 40 cc intra-aortic balloon during diastole, blood is displaced both toward the head and heart as well as toward the feet. The inflated balloon augments diastolic pressure, creating a pressure wave increasing blood flow backward into the coronary arteries. Depending on stenosis severity, it can increase coronary flow across some coronary narrowings. This augmented diastolic pressure wave can also improve coronary collateral flow in certain circumstances.
The deflation of the balloon immediately before R wave of systole produces a negative space in the aorta and makes it easier for the ventricle to eject blood. Less left ventricle (LV) work means less LV oxygen demand. That is, reducing ventricular afterload reduces myocardial oxygen demand.
The coronary physiology of the IABP was previously described some 15 years ago from our laboratory where we measured pressure and flow with Doppler sensor angioplasty guidewires across critical stenoses.1,2 We learned that coronary flow velocity does not increase across very severe stenosis during intra-aortic balloon pumping and that after balloon angioplasty opening of the arteries, flow velocity was increased to levels seen in the normal arteries adjacent to the target vessels. Coronary perfusion pressure is still somewhat attenuated due to the diffuse disease that is present in many of these vessels, but coronary pressure it is markedly improved by opening the artery and IABP pressure transmission can be appreciated. Recently Yoshitani et al3 confirmed the fact that severe lesions do not transmit IABP pressure. By using pressure guidewires across significant stenoses, they found that in patients with these critical lesions, pressure could not be increased by IABP. The mechanism by which the degree of lumen narrowing impacts the pressure transmission appears to be that of a high pass filter reducing high frequency components of pressure waves as well as absolute pressure.4

However, despite the reports of no improvement in flow across critical lesions, IABP still is associated with clinical benefits, particularly in patients at high risk during angioplasty. Brigouri et al5 found that IABP placed at the time of intervention in high-risk individuals was better than a provisional IABP approach. In a subsequent paper6, his same group found that IABP during elective unprotected left main stenosis was better than no IABP, with lower complications as compared to historic controls of PCI for unprotected left main stenosis. Mishra et al7 also found better results using prophylactic IABP than rescue IABP for these high-risk individuals. However, in a recent work by Vijayalakshmi et al8, in high risk, non-shock patients, intra-aortic balloon pumping (17 patients with IABP were compared to the 16 patients who did not have an IABP) had no effect on TIMI flow grade, TIMI frame count, myocardial blush score or electrocardiographic and wall motion indices of myocardial ischemia, both at day 1 and 30 following PCI. The authors concluded that it was unclear whether IABP provided any benefit to non-shock patients and that if any, the potential benefit of IABP does not appear to be associated with early improvement in angiographically-determined coronary flow. These data are highly consistent with direct measurements of coronary flow velocity and pressure during intra-aortic balloon pumping.
Would an IABP improve flow across the left main coronary stenosis in our patient above? It seems to me unlikely, but an IABP does provide some degree of satisfaction for the operators that we are taking no chances. In reality, IABP does little in terms of increasing myocardial perfusion. Therefore, for ischemia, the IABP would work only through the reducing oxygen demand. However, an IABP might assist in maintaining perfusion pressure to other zones (none in this case, but other patients might have intermediate stenoses in the RCA). An IABP has a potential to increase collateral flow9 and has the potential to provide perfusion in distal arteries, which are not critically narrowed.
Some surgeons and anesthesiologists request an IABP as part of preoperative stabilization prior to induction of anesthesia for high-risk coronary surgery. Our patient might qualify under this request. However, before inserting the IABP for elective indications, it is worthwhile to quickly consider the contraindications, which include aortic dissection, aortic aneurysm, aortic insufficiency, coagulopathy, potential for sepsis and peripheral vascular disease.
Returning to our patient with the left main stenosis who was very stable, it was clear that an operation was needed soon. Since he likely had this narrowing for weeks beforehand, the patient could be urgently scheduled (as opposed to dire emergency). If the patient remains stable, he certainly can go to the operating room without an IABP and a decision to have one inserted made at the time of surgery, so that the induction of anesthesia (with the possibility of transient hypotension) will go smoothly. Others recognize the fact that the IABP will do nothing to improve perfusion and that careful induction of anesthesia and preparation prior to manipulation of heart at surgery is required.
In any patient with left main stenosis who is unstable, an IABP is indicated, barring any contraindications and that cardiogenic shock, hypotension, and arrhythmias should be treated with all measures to reduce ischemia and move to coronary artery bypass surgery emergently.
Our bottom line for the IABP is that it has the potential to increase flow across stenoses which are only moderately narrowed. Critical lesions do not really obtain benefit from diastolic pressure augmentation and these patients are improved through afterload reduction and potential collateral perfusion improvement rather than direct augmentation of flow. Our stable left main patient did not get an IABP. Surgery was uncomplicated and he is pain-free on his last clinic visit six weeks later.




1. Kern MJ, Aguirre F, Tatineni S, et al. Enhanced coronary blood flow velocity during intra-aortic balloon counterpulsation in critically ill patients. J Am Coll Cardiol 1993;21:359–368.
2. Kern MJ, Aguirre F, Bach R, et al. Augmentation of coronary blood flow by intra-aortic balloon pumping in patients after coronary angioplasty. Circulation 1993;87:500–511.
3. Yoshitani, et al. AHJ, effects of IABP on coronary pressure in patients stenotic coronary arteries. Am Heart J 2007;154:725–731.
4. Holmes D, Velappan P, Kern MJ. Coronary pressure notch: an early non-hyperemic visual indicator of the physiologic significance of a coronary artery stenosis. J Invasive Cardiol 2005;16:617–620.
5. Briguori C, Sarais C, Pagnotta P, et al. Elective versus provisional intra-aortic balloon pumping in high-risk percutaneous transluminal coronary angrioplasty. Am Heart J 2003;145:700–707.
6. Briguori C, Airoldi F, Chieffo A, et al. Elective versus provisional intraaortic balloon pumping in unprotected left main stenting. Am Heart J 2006;152:565–572.
7. Mishra S, Chu WW, Torguson R, et al. Role of prophylactic intra-aortic balloon pump in high-risk patients undergoing percutaneous coronary intervention. Am J Cardiol 2006;98:608–612.
8. Vijayalakshmi K, Kunadian B, Whittaker VJ, et al. Intra-aortic counterpulsation does not improve coronary flow early after PCI in a high-risk group of patients: Observations from a randomized trial to explore its mode of action. J Invasive Cardiol 2007;19:339–346.
9. Flynn MS, Kern MJ, Donohue TJ, et al. Alterations of coronary collateral blood flow velocity during intra-aortic balloon pumping in patients. Am J Cardiol 1993;71:1451–1454.