Original Contribution

Hemodynamic Effects of Standard Versus Larger-Capacity Intraaortic Balloon Counterpulsation Pumps

Navin K. Kapur, MD;  Vikram Paruchuri, MD;  Arjun Majithia, MD;  Michele Esposito, MD;  Henry Shih, MD;  Andrew Weintraub, MD;  Michael Kiernan, MD;  Duc Thinh Pham, MD;  David Denofrio, MD;  Carey Kimmelstiel, MD

Navin K. Kapur, MD;  Vikram Paruchuri, MD;  Arjun Majithia, MD;  Michele Esposito, MD;  Henry Shih, MD;  Andrew Weintraub, MD;  Michael Kiernan, MD;  Duc Thinh Pham, MD;  David Denofrio, MD;  Carey Kimmelstiel, MD

Abstract: Objective. Several recent trials have examined the clinical utility of intraaortic balloon counterpulsation pumps (IABPs) in cardiogenic shock and acute coronary syndromes. More recently, a larger-capacity 50 cc IABP was introduced into practice. No data comparing the hemodynamic effects of the 40 cc vs 50 cc IABP exist. Our aim was to explore the hemodynamic effects of the 50 cc IABP in real-world clinical practice. Methods. Demographic, hemodynamic, and laboratory data were retrospectively examined in 26 consecutive subjects treated with a 50 cc IABP and compared with 26 patients receiving a 40 cc IABP between 2012 and 2013. IABP tracings were analyzed within 24 hours of implantation in all patients. Pulmonary artery catheter data were available before and after IABP implantation in 20 subjects. Results. Baseline demographics, including body surface area, were similar between groups. Compared with the 40 cc IABP group, 50 cc IABP recipients showed higher augmented diastolic blood pressure, greater systolic unloading, and a larger reduction in pulmonary capillary occlusion pressure (PCOP). Percent diastolic augmentation was higher among 50 cc IABP recipients. Only 58% of subjects achieved <10 mm Hg of systolic unloading in the 40 cc group compared with 27% in the 50 cc group. For both the 40 cc and 50 cc IABPs, the magnitude of systolic unloading correlated inversely with PCOP and directly with the magnitude of diastolic augmentation. Conclusion. In real-world practice, greater systolic unloading and diastolic augmentation were observed among 50 cc vs 40 cc IABP recipients. Future trials evaluating the clinical utility of the 50 cc IABP are required.  

J INVASIVE CARDIOL 2015;27(4):182-188

Key words: intraaortic balloon pump, hemodynamics, coronary disease, heart failure, acute coronary syndrome


The demand for temporary circulatory support (TCS) options to stabilize patients with acutely decompensated heart failure and cardiogenic shock or during high-risk coronary and non-coronary interventions is growing. The intraaortic balloon counterpulsation pump (IABP) is the most widely used TCS.1-5 The IABP is a catheter-mounted balloon that augments pulsatile blood flow by inflating during diastole, which displaces blood volume in the descending aorta and increases mean aortic pressure, thereby potentially augmenting coronary perfusion. Upon deflation, during systole, the IABP generates a pressure sink, which is filled by ejecting blood from the heart. As a result, the net effect of reducing ventricular afterload with an IABP is an increase in mean arterial pressure and augmented ventricular stroke volume.6,7 The hemodynamic effect of an IABP can be directly measured using tracings obtained from the IABP console to determine the magnitude of systolic unloading and diastolic augmentation.

Over the past decade, several large clinical trials examined the utility of IABPs during high-risk PCI, acute myocardial infarction, or cardiogenic shock and failed to identify any significant improvement in in-hospital mortality or myocardial salvage.8-12 None of these trials examined the hemodynamic effect of IABP activation. Furthermore, larger-capacity IABPs were recently introduced into clinical practice with the goal of increasing volume displacement from 40 cc to 50 cc and were generally not included in these trials.13 No data comparing 50 cc vs 40 cc IABPs exist. The primary objective of this study was to examine the hemodynamic effects of the larger-capacity 50 cc IABP and standard-capacity 40 cc IABP in a real-world clinical practice. 


In this retrospective study, we reviewed the records of 88 patients who received an IABP between January and December 2012 at Tufts Medical Center. A total of 88 IABPs were inserted during the study period. Thirty-six patients received either 34 cc pumps or had their IABP inserted via the axillary approach. These patients were excluded from further analysis. The remaining 52 patients represent consecutive IABP implants. The 50 cc IABP was introduced in July 2012. Data were collected for over 90% of patients in the 40 cc IABP group before July 2012, after which the 50 cc IABP became the primary IABP used at this center. Both the 40 cc and 50 cc IABPs require a minimum height of 162 cm. Indications for IABP insertion included: acute decompensated heart failure (ADHF), cardiogenic shock (CGS), acute coronary syndrome (ACS), or high-risk coronary intervention (HR-PCI). ADHF was defined as documentation of New York Heart Association (NYHA) class III or IV symptoms without hypotension at the time of IABP insertion. CGS was defined as ADHF with a systolic blood pressure <90 mm Hg at the time of IABP insertion. Subjects with aortic valve disorders and in whom the IABP was deployed via the axillary artery were excluded. All subjects received standard clinical care during their index hospitalization. The indications for device implantation were determined from available medical records. Demographic information, hemodynamic data, laboratory parameters, medication use, and outcome data were recorded. Thrombolysis in Myocardial Infarction (TIMI) major bleeding was defined as any intracranial bleeding (excluding microhemorrhages <10 mm evident only on gradient-echo magnetic resonance imaging), clinically overt signs of hemorrhage associated with a drop in hemoglobin of ≥5 g/dL, or fatal bleeding (bleeding that directly results in death within 7 days).14 The institutional review board approved this study. 

IABP tracings obtained within 24 hours of device activation were collected from the medical records and analyzed. As per standard clinical protocols, IABP tracings were acquired from the IABP console at a balloon to heart beat synchronization ratio of 1:2 (Figure 1). Non-augmented systolic and diastolic pressures, dicrotic notch pressure, augmented systolic and diastolic pressures, and reduced aortic end-diastolic pressure were measured manually for each patient by three blinded reviewers (VP, ME, HS). Systolic unloading was calculated as the difference between non-augmented and augmented systolic pressures. Diastolic augmentation was calculated as the difference between non-augmented and augmented diastolic pressures. Diastolic unloading was calculated as the difference between non-augmented diastolic pressure and reduced aortic end-diastolic pressure. The change in aortic pressure at balloon deflation (deflation pressure) was calculated as the difference between augmented diastolic pressure and reduced aortic end-diastolic pressure. The slope of the deflation pressure was calculated as the deflation pressure divided by time. Pulmonary artery (PA) catheter indices acquired immediately before and within 24 hours after device implantation were available in 20 out of 52 patients (40 cc IABP [n = 9]; 50 cc IABP [n = 11]). Cardiac filling pressures and cardiac output measured by the Fick method were analyzed.15 Clinical outcomes including in-hospital mortality and device-associated complications (defined as complications related to the IABP occurring during or within 24 hours of device implantation or removal) were recorded. 

Statistical analysis. Data are expressed as mean ± standard deviation for continuous variables. Differences between groups and conditions were compared by t-test for continuous variables and Fisher exact test for categorical variables. Specifically, comparisons were made between 40 cc and 50 cc IABP recipients; between baseline (pre-IABP) and post-IABP conditions in the total group, and between 40 cc  and 50 cc IABP recipients. For each variable in Table 2, all statistical analyses were performed using SigmaStat, Version 3.1 (Systat Software, Inc) and Statistical Package for the Social Sciences (SPSS, Version 16.0.1; SPSS, Inc). A P-value <.05 denoted significant differences. 


Patient population. Data from 52 consecutive subjects receiving either a 40 cc IABP (n = 26) or 50 cc IABP (n = 26) in the cardiac catheterization laboratory were studied. Baseline characteristics of the total study population are provided in Table 1. No significant differences in baseline characteristics or medication use were observed between 40 cc and 50 cc IABP cohorts. The number of vasoactive/inotropic agents used did not differ at baseline (Table 1) and did not significantly change within 24 hours after IABP implantation (Supplemental Table 1). A trend toward a higher incidence of diabetes was observed in the 50 cc IABP cohort. No difference in height, weight, or body surface area was noted between groups. Primary indications for IABP use included ADHF (33%; n = 17), ACS (33%, n = 17), CGS (23%, n = 12), and HR-PCI (12%, n = 6). ACS subjects included non-ST segment elevation myocardial infarction (6%; n = 3) and ST-elevation myocardial infarction (27%; n = 14) presentations. All ACS patients underwent successful revascularization. 

Hemodynamic variables after IABP activation. To explore the hemodynamic impact of displacing 40 cc vs 50 cc of blood volume using IABPs, we analyzed hemodynamic variables derived from IABP tracings (Table 2). No differences in non-augmented diastolic pressure (A) or systolic pressure (B) were observed between groups. Peak augmented diastolic pressure (D) and the magnitude of diastolic augmentation (D-A) were significantly higher among 50 cc IABP recipients. No differences were observed in augmented systolic pressure, reduced aortic end-diastolic pressure, or diastolic unloading between groups. The magnitude of systolic unloading was greater in the 50 cc IABP group (Figure 2). The slope and magnitude of deflation pressure from peak augmented diastolic pressure to reduced aortic end-diastolic pressure were greater in the 50 cc IABP group (Table 2). 

Next, we examined PA catheter data before and after 40 cc or 50 cc IABP activation (Table 3). Cardiac filling pressures, cardiac output, cardiac index, and PA oxygen saturation were similar between 40 cc and 50 cc IABP groups before device activation. Within 24 hours after device activation, PA catheter variables did not significantly change among the 40 cc IABP recipients. In contrast, PA diastolic pressure and PA occlusion pressure were reduced, while cardiac output, cardiac index, and PA oxygen saturation were increased after 50 cc IABP activation. No statistically significant differences were observed for any hemodynamic variable between the 40 cc and 50 cc IABP groups after device activation. The absolute change in cardiac output before and after device activation was 0.7 ± 0.9 in the 40 cc IABP group and 1.4 ± 1.0 in the 50 cc IABP group (P=.08). Relative to baseline values for cardiac output, the percent increase was 18% vs 40% for the 40 cc and 50 cc IABP groups, respectively. Only the 50 cc IABP group achieved a statistically significant increase in cardiac output when compared with baseline values (Table 3). Among all 20 subjects with available PA catheter data, PA occlusion pressure after device activation correlated inversely with the magnitude of systolic unloading (R=0.48; P=.03).

 We then examined how many individuals in each group “responded” to IABP therapy, as defined by a reduction in assisted systolic pressure ≥10 mm Hg or an increase in augmented diastolic pressure ≥40 mm Hg compared with non-augmented values based on prior reports showing a correlation between systolic unloading and augmented diastolic pressure with myocardial oxygen consumption6,16,17 and coronary blood flow.1,2,18,19 Among the total group of 52 patients, 44% (n = 23) and 13% (n = 7) did not achieve a reduced systolic pressure ≥10 mm Hg or an augmented diastolic pressure ≥40 mm Hg, respectively. Compared with the 40 cc IABP group, significantly more patients achieved a reduction in systolic pressure ≥10 mm Hg in the 50 cc IABP group (42% for 40 cc IABP vs 69% for 50 cc IABP; P=.03). Augmented diastolic pressures >40 mm Hg were observed in 81% and 92% of patients in the 40 cc and 50 cc IABP groups, respectively (Figure 3). Among all 52 subjects, the magnitude of diastolic augmentation correlated directly with the magnitude of systolic unloading (R = 0.73; P<.01). A significant correlation was observed between the magnitude of systolic unloading and augmented diastolic pressure among both the 50 cc and 40 cc IABP groups (Figure 4). 

Clinical outcomes after IABP implantation. In-hospital mortality was 23% among all study subjects. In-hospital mortality was 27% (n = 7) and 19% (n = 5) in the 40 cc and 50 cc IABP groups, respectively (P=NS). In both groups, 19% (n = 5) of IABP recipients went on to require surgical left ventricular assist device (LVAD) implantation. No subject in this study required initiation of a percutaneous LVAD or veno-arterial extracorporeal membrane oxygenation (VA-ECMO). TIMI major bleeding was observed in 15% (n = 8) of all subjects. No difference in TIMI major bleeding was observed between groups (19% for the 40 cc IABP group [n = 5] vs 12% for the 50 cc IABP group [n = 3]; P=.80). Among all subjects, 1 patient experienced an intracranial hemorrhage while on support with a 50 cc IABP. No vascular perforation or dissection was reported in any subject. No differences were observed in baseline laboratory parameters between the 40 cc and 50 cc IABP groups (Table 4). Platelet counts after device activation were decreased in both groups, but were significantly decreased in the 50 cc IABP group only (Table 4). 


This is the first report to compare the hemodynamic effects of intraaortic balloon counterpulsation using 40 cc vs 50 cc of volume displacement in clinical practice. The central finding of this report is that the larger-capacity 50 cc IABPs provides greater diastolic augmentation and systolic unloading compared with the 40 cc IABP. Specifically, we identified that: (1) recipients of the 50 cc IABP achieved a greater reduction in cardiac filling pressures and increased cardiac output compared with the 40 cc group; (2) compared with the 40 cc IABP group, a greater number of patients achieved a reduction in systolic pressure >10 mm Hg in the 50 cc IABP group; and (3) the magnitude of systolic unloading correlates directly with the magnitude of diastolic augmentation and inversely with pulmonary artery occlusion pressure. Taken together, these observations suggest that the 50 cc IABP may achieve a greater hemodynamic effect compared with the standard 40 cc IABP. 

Nearly 160,000 patients are supported with an IABP worldwide each year.20 Since the device was introduced in 1953, IABPs have become a relatively low-cost, standard treatment option for patients with decompensated heart failure, cardiogenicshock, and impaired coronary flow.21 The overall goals of temporary circulatory support systems are to: (1) increase vital organ perfusion; (2) augment coronary perfusion; and (3) reduce ventricular volume and filling pressures, thereby reducing wall stress, stroke work, and myocardial oxygen consumption. IABP therapy achieves these objectives by displacing blood volume during diastole to augment coronary blood flow and to reduce left ventricular afterload during systole.21 The pioneering work of Kantrowitz, Weber, Janicki, Sarnoff, Schreuder, Kern1,2,6,7,17,19,23,24 and many others has established that the hemodynamic impact of balloon counterpulsation is primarily determined by four factors: (1) the magnitude of diastolic pressure augmentation; (2) the magnitude of reduced systolic pressure; (3) the magnitude of volume displacement; and (4) the timing of balloon inflation and deflation. In this study, we identified that an incremental displacement volume of 10 cc generates a greater reduction in systolic unloading and diastolic pressure augmentation. In the absence of aortic valve disease, prior studies have shown that balloon deflation reduces systolic pressure and increases left ventricular stroke volume, resulting in less myocardial wall tension and oxygen consumption.6,17,24 Further study confirming the clinical benefit of increased volume displacement is required.

 Registry data have historically supported the use of IABPs;4,5,25,26 however, recent studies attempting to identify optimal candidates for IABP support in HR-PCI, acute MI, or cardiogenic shock have shown no significant benefit associated with elective IABP insertion. The CRISP-AMI (Counterpulsation Reduces Infarct Size Acute Myocardial Infarction) trial12 showed that IABP implantation immediately prior to revascularization for an anterior ST-elevation myocardial infarction did not reduce infarct size or improve short-term survival. The IABP-SHOCK II study11 suggested that not all patients presenting with an ACS with marginal blood pressures and clinical evidence of hypoperfusion benefit from IABP activation. In HR-PCI patients, the PROTECT II study27 showed no difference in major adverse cardiovascular events between IABP and the Impella 2.5 axial flow catheter. The BCIS-1 (Balloon Pump Assisted Coronary Intervention Study) also showed no reduction in short-term 

mortality with IABP insertion prior to HR-PCI; however, follow-up data suggested a possible long-term benefit up to 5 years after PCI.8,9 Based on our findings, the number of patients achieving optimal hemodynamic benefit from IABP activation may be <50% with standard 40 cc IABPs. These observations suggest that future clinical trials employing 50 cc IABPs may demonstrate better clinical outcomes than studies predominantly using the 40 cc IABP. Since these devices are designed to “unload” the heart of excess volume congestion and pressure overload, measuring hemodynamic variables prior to device deployment may identify optimal candidates for IABP therapy vs another TCS option. 

Since the majority of patients with acute decompensated heart failure present with elevated vascular resistance and low cardiac output,28,29 the magnitude of systolic pressure reduction achieved by IABP therapy may be a primary determinant of clinical benefit in this population. The net result of the larger-capacity IABPs is a significant reduction in cardiac filling pressures and augmentation in cardiac output. Based on our findings, the larger-capacity 50 cc IABP may yield better clinical outcomes than the standard 40 cc IABP in patients requiring temporary circulatory support. The dynamics of volume displacement and counterpulsation therapy are of particular importance as emerging technologies have now begun to focus on extraaortic volume displacement, aortic root counterpulsation, and long-term, implantable systems for chronic heart failure.30 The clinical effect of IABP therapy in patients with non-ischemic heart failure remains largely unexplored.

Study limitations. Limitations of the present study exist. A small number of patients were studied, which limited our statistical power to perform multiple subgroup analyses. We were also unable to retrospectively determine timing intervals used for IABP activation in either group. Finally, due to the retrospective nature of the study, operator bias may have influenced IABP selection. 


As experience with TCS devices grows, the role of IABP therapy in the armamentarium of mechanical therapy for heart failure, ACS, and HR-PCI will depend less on the technical ability to place the device, and more on improved algorithms for patient selection, monitoring, and weaning protocols. Findings from this analysis may inform future device designs and the development of prospective clinical studies to evaluate the role of IABP therapy. 


  1. Kern MJ, Aguirre F, Bach R, Donohue T, Siegel R, Segal J. Augmentation of coronary blood flow by intra-aortic balloon pumping in patients after coronary angioplasty. Circulation. 1993;87(2):500-511.
  2. Kern MJ, Aguirre FV, Tatineni S, et al. Enhanced coronary blood flow velocity during intraaortic balloon counterpulsation in critically ill patients. J Am Coll Cardiol. 1993;21(2):359-368.
  3. Williams DO, Korr KS, Gewirtz H, Most AS. The effect of intraaortic balloon counterpulsation on regional myocardial blood flow and oxygen consumption in the presence of coronary artery stenosis in patients with unstable angina. Circulation. 1982;66(3):593-597.
  4. Stone GW, Ohman EM, Miller MF, et al. Contemporary utilization and outcomes of intraaortic balloon counterpulsation in acute myocardial infarction: the benchmark registry. J Am Coll Cardiol. 2003;41(11):1940-1945.
  5. Cohen M, Urban P, Christenson JT, et al. Intra-aortic balloon counterpulsation in US and non-US centres: results of the Benchmark Registry. Eur Heart J. 2003;24(19):1763-1770.
  6. Schreuder JJ, Maisano F, Donelli A, et al. Beat-to-beat effects of intraaortic balloon pump timing on left ventricular performance in patients with low ejection fraction. Ann Thorac Surg. 2005;79(3):872-880.
  7. Schreuder JJ, Castiglioni A, Donelli A, et al. Automatic intraaortic balloon pump timing using an intrabeat dicrotic notch prediction algorithm. Ann Thorac Surg. 2005;79(3):1017-1022.
  8. Perera D, Stables R, Thomas M, et al. Elective intraaortic balloon counterpulsation during high-risk percutaneous coronary intervention: a randomized controlled trial. JAMA. 2010;304(8):867-874.
  9. Perera D, Stables R, Clayton T, et al. Long-term mortality data from the balloon pump-assisted coronary intervention study (BCIS-1): a randomized, controlled trial of elective balloon counterpulsation during high-risk percutaneous coronary intervention. Circulation. 2013;127(2):207-212.
  10. Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J Med. 2012;367(14):1287-1296.
  11. Thiele H, Schuler G, Neumann FJ, et al. Intraaortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock: design and rationale of the Intraaortic Balloon Pump in Cardiogenic Shock II (IABP-SHOCK II) trial. Am Heart J. 2012;163(6):938-945.
  12. Patel MR, Smalling RW, Thiele H, et al. Intraaortic balloon counterpulsation and infarct size in patients with acute anterior myocardial infarction without shock: the CRISP AMI randomized trial. JAMA. 2011;306(12):1329-1337.
  13. Nair PK, Scolieri S, Lee AB. Improvement in hemodynamics with a new, larger-volume (50 cc) intraaortic balloon for high-risk percutaneous coronary intervention. J Invasive Cardiol. 2011;23(4):162-166.
  14. Mehta SK, Frutkin AD, Lindsey JB, et al; National Cardiovascular Data Registry. Bleeding in patients undergoing percutaneous coronary intervention: the development of a clinical risk algorithm from the National Cardiovascular Data Registry. Circ Cardiovasc Interv. 2009;2(3):222-229. Epub 2009 May 8.
  15. Wagner HR, Gamble WJ, Albers WH, Hugenholtz PG. Fiberoptic-dye dilution method for measurement of cardiac output. Comparison with the direct Fick and the angiocardiographic methods. Circulation. 1968;37(5):694-708.
  16. Cheung A, Savino J, Weiss S. Beat-to-beat augmentation of left ventricular function by intraaortic balloon counterpulsation. Anesthesiology. 1996;84(3):545-554.
  17. Sarnoff SJ, Braunwald E, Welch GH, Case RB, Stainsby WN, Macruz R. Hemodynamic determinants of oxygen consumption of the heart with special reference to the tension-time index. Am J Physiol. 1958;192(1):148-156. 
  18. Zehetgruber M, Mundigler G, Christ G, et al. Relation of hemodynamic variables to augmentation of left anterior descending coronary flow by intraaortic balloon pulsation in coronary artery disease. Am J Cardiol. 1997;80(7):951-955.
  19. Braunwald E, Sarnoff SJ, Case RB, Stainsby WN, Welch GH. Hemodynamic determinants of coronary flow: effect of changes in aortic pressure and cardiac output on the relationship between myocardial oxygen consumption and coronary flow. Am J Physiol. 1958;192(1):157-163.
  20. Trost J, Hillis D. Intraaortic balloon counterpulsation. Am J Cardiol. 2006;97(9):1391-1398. Epub 2006 Mar 20.
  21. Kantrowitz A, Tjønneland S, Freed PS, Phillips SJ, Butner AN, Sherman JL Jr. Initial clinical experience with intraaortic balloon pumping in cardiogenic shock. JAMA. 1968;203(2):113-118. 
  22. Papaioannou TG, Stefanadis C. Basic principles of the intraaortic balloon pump and mechanisms affecting its performance. ASAIO J. 2005;51(3):296-300.
  23. Weber KT, Janicki JS. Coronary collateral flow and intraaortic ballooncounterpulsation. Trans Am Soc Artif Intern Organs. 1973;19:395-401.
  24. Weber KT, Janicki JS. Intraaortic balloon counterpulsation. A review of physiological principles, clinical results, and device safety. Ann Thorac Surg. 1974;17(6):602-636.
  25. Abdel-Wahab M, Saad M, Kynast J, et al. Comparison of hospital mortality with intraaortic balloon counterpulsation insertion before versus after primary percutaneous coronary intervention for cardiogenic shock complicating acute myocardial infarction. Am J Cardiol. 2010;105(7):967-971. Epub 2010 Feb 13.
  26. Curtis JP, Rathore SS, Wang Y, Chen J, Nallamothu BK, Krumholz HM. Use and effectiveness of intra-aortic balloon pumps among patients undergoing high-risk percutaneous coronary intervention: insights from the National Cardiovascular Data Registry. Circ Cardiovasc Qual Outcomes. 2012;5(1):21-30. Epub 2011 Dec 6.
  27. O’Neill WW, Kleiman NS, Moses J, et al. A prospective, randomized clinical trial of hemodynamic support with Impella 2.5 versus intraaortic balloon pump in patients undergoing high-risk percutaneous coronary intervention: the PROTECT II study. Circulation. 2012;126(14):1717-1727. Epub 2012 Aug 30.
  28. Gheorghiade M, Pang PS. Acute heart failure syndromes. J Am Coll Cardiol. 2009;53(7):557-573.
  29. Styron JF, Jois-Bilowich P, Starling R, et al. Initial emergency department systolic blood pressure predicts left ventricular systolic function in acute decompensated heart failure. Congest Heart Fail. 2009;15(1):9-13.
  30. Solanki P. Aortic counterpulsation: C-Pulse and other devices for cardiac support. J Cardiovasc Transl Res. 2014;7(3):292-300. Epub 2014 Feb 20.


From the Division of Cardiology, Tufts University School of Medicine, Boston, Massachusetts. 

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Kapur reports grants from Maquet; grants and consultant/speaker honoraria from Abiomed and CardiacAssist; and consultant/speaker honoraria from Thoratec. The remaining authors report no disclosures.

Manuscript submitted June 17, 2014, provisional acceptance given August 11, 2014, final version accepted September 4, 2014.

Address for correspondence: Navin K. Kapur, MD, Tufts University School of Medicine, Division of Cardiology, Boston, MA. Email: nkapur@tuftsmedicalcenter.org