- Email: [email protected]
Pressure and flow across severe stenoses: Does the intra-aortic balloon pump do its job?
Pressure and flow across severe stenoses: Does the intra-aortic balloon pump do its job? Morton J. Kern, MD, FSCAI, FAHA, FACC Orange, CA
Intra-aortic balloon counterpulsation displaces blood during diastole augmenting diastolic pressure. This augmented pressure wave carries blood to the coronary arteries and can increase coronary flow across some coronary narrowings and, in some circumstances, even improve collateral flow. Immediately before systole, the deflation of the counterpulsation balloon creates a negative space, reversing aortic flow and reducing ventricular afterload and, hence, myocardial oxygen demand. Yoshitani et al1 used an angioplasty sensor-tipped pressure guidewire to describe the effects of intra-aortic balloon counterpulsation on coronary pressure in patients with stenotic coronary arteries. Aortic and poststenotic coronary pressures were measured in 16 patients undergoing intra-aortic balloon pump (IABP) support. Intraaortic balloon pump significantly increased diastolic aortic pressure (80-98 mm Hg), decreased systolic mean pressure (96 to 84 mm Hg), and intracoronary pressure (76-68 mm Hg). Intra-aortic balloon pump (IABP) increased diastolic pressure (72-87 mm Hg) in unobstructed coronary arteries but not across stenotic arteries (43 vs 44 mm Hg). The percent diameter stenosis using quantitative coronary angiography correlated with the change in distal pressure after IABP; the more severe the stenosis is, the less is the augmentation of translesional pressure. The investigators concluded that intra-aortic balloon pumping does not increase diastolic pressure distal to severe coronary stenosis, and thus, the major benefit of IABP in such patients with coronary artery disease is the reduction of myocardial oxygen demand. This article confirms previous observations of the mechanisms of IABP when translesional flow velocities were directly measured with sensor-tipped Doppler angioplasty guidewires2,3 some 15 years ago. When blood travels across stenosis, the resistance to flow extracts heat energy from turbulence, friction, and separation forces, resulting in pressure loss distal to the stenosis. The pressure loss is curvilinearly related to flow with exponentially increasing loss as flow increases.4 In addition, the degree of lumen narrowing impacts the phasic wave form From the Division of Cardiology, University of California, Orange, CA. Submitted June 12, 2007; accepted June 15, 2007. Reprint requests: Morton J. Kern, MD, FSCAI, FAHA, FACC, Division of Cardiology, University of California, Irvine Bldg 53, Rt 81, Room 100, 101 The City Drive, Orange, CA 92868-4080. E-mail: [email protected] Am Heart J 2007;154:615-6. 0002-8703/$ - see front matter © 2007, Mosby, Inc. All rights reserved. doi:10.1016/j.ahj.2007.06.011
and pressure transmission. The stenosis acts as a high-pass filter, reducing the high-frequency components of a pressure waves as well as the absolute pressure.5 The more severe the stenosis is, the more pressure loss occurs. The pressure loss is coupled and corresponds to loss of flow velocity signals as identified previously.2,3 What Yoshitani et al1 did not provide is the association between the exact physiologic degree of stenosis and the degree of diminished IABP pressure augmentation. Using a fractional flow reserve, a measure of the percent of normal flow across a stenosis derived from translesional pressure at hyperemia, rather than a quantitative coronary angiography, the authors could have been able to identify which lesions might permit better pressure transmission and, hence, flow. The limitations of angiography to determine which lesions are significant have been strongly linked to the disparity of clinical responses.6 Does intra-aortic balloon pumping have a potential to paradoxically reduce coronary perfusion? In theory, an increase in aortic pressure without corresponding increase in poststenotic pressure might calculate as a more severe transstenotic pressure gradient with less perfusion pressure, but this response is balanced by ventricular unloading and reduction of myocardial oxygen demand. An infrequently discussed mechanism of potential IABP benefit is that of improved collateral flow. The effect of intra-aortic balloon pumping on collateral flow is a function of not only the severity of lesions but also the type of collateral supply to the poststenotic regions. Although the study is small,7 those beds with the largest epicardial collateral had evidence of IABP flow augmentation. In beds supplied by intraseptal or acute recruited collateral, no augmentation was seen. The issue with regard to collateral flow is certainly important and was not addressed in this particular study. The data would be available if the investigators had continued to make their measurements during coronary angioplasty balloon occlusion. A collateral flow index during intra-aortic balloon pumping has not been previously reported. However, the limitations of using epicardial flow or pressure to determine the degree of collateral supplied should be recognized.8,9 This investigation was confirmatory for directly measured flow across severe stenoses and provided refined pressure data because the measurements of pressure at the time of our flow velocity determinations could be made only with a balloon or tracking catheter, both about 1 mm in diameter.2,3 The use of transthoracic Doppler echo of the left anterior descending coronary artery demonstrating improved coronary flow distal to critical
616 Kern
stenosis suggested that a pressure-measuring guidewire may have contributed to some reduction in lumen area and flow.10 This is certainly possible, but given the wide range of stenosis investigated, the observations regarding critical stenoses are still valid. In the end, given the uncertainty of stenosis severity, intra-aortic balloon pumping certainly has the ability to increase coronary flow across some of the many lesions, especially those of an intermediate severity. Yoshitani et al1 should be complimented for an excellent study. In the future, using sensor guidewires, similar research would permit us to appreciate IABP influences on the collateral flow index, determinations of fractional flow, and responses of the microcirculation under a variety of different clinical scenarios.
References 1. Yoshitani, et al. AHJ, effects of IABP on coronary pressure in patients with stenotic coronary arteries. Am Heart J 2007;154:725-31. 2. 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;21:359-68.
American Heart Journal October 2007
3. 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;87:500-11. 4. Hoffman JIE, Spaan JAE. Pressure-flow relations in coronary circulation. Physiol Rev 1990;70:331-90. 5. Holmes D, Velappan P, Kern MJ. Coronary pressure notch: an early non-hyperemic visual indictor of the physiologic significance of a coronary artery stenosis. J Invasive Cardiol 2005;16:617-20. 6. Topol EJ, Nissen SE. Our preoccupation with coronary luminology. The dissociation between clinical and angiographic findings in ischemic heart disease. Circulation 1995;92:2333-42. 7. 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;71:1451-4. 8. Pijls NHJ, Bech GJW, el Gamal MIH, et al. Quantification of recruitable coronary collateral blood flow in conscious humans and its potential to predict future ischemic events. J Am Coll Cardiol 1995; 25:1522-8. 9. Piek JJ, van Liebergen RAM, Koch KT, et al. Clinical, angiographic and hemodynamic predictors of recruitable collateral flow assessed during balloon angioplasty coronary occlusion. J Am Coll Cardiol 1997;29:275-82. 10. Takeuchi M, Nohtomi Y, Yoshitani H, et al. Enhanced coronary flow velocity during intra-aortic balloon pumping assessed by transthoracic Doppler echocardiography. J Am Coll Cardiol 2004;43: 368-76.
Intra-aortic balloon counterpulsation displaces blood during diastole augmenting diastolic pressure. This augmented pressure wave carries blood to the coronary arteries and can increase coronary flow across some coronary narrowings and, in some circumstances, even improve collateral flow. Immediately before systole, the deflation of the counterpulsation balloon creates a negative space, reversing aortic flow and reducing ventricular afterload and, hence, myocardial oxygen demand. Yoshitani et al1 used an angioplasty sensor-tipped pressure guidewire to describe the effects of intra-aortic balloon counterpulsation on coronary pressure in patients with stenotic coronary arteries. Aortic and poststenotic coronary pressures were measured in 16 patients undergoing intra-aortic balloon pump (IABP) support. Intraaortic balloon pump significantly increased diastolic aortic pressure (80-98 mm Hg), decreased systolic mean pressure (96 to 84 mm Hg), and intracoronary pressure (76-68 mm Hg). Intra-aortic balloon pump (IABP) increased diastolic pressure (72-87 mm Hg) in unobstructed coronary arteries but not across stenotic arteries (43 vs 44 mm Hg). The percent diameter stenosis using quantitative coronary angiography correlated with the change in distal pressure after IABP; the more severe the stenosis is, the less is the augmentation of translesional pressure. The investigators concluded that intra-aortic balloon pumping does not increase diastolic pressure distal to severe coronary stenosis, and thus, the major benefit of IABP in such patients with coronary artery disease is the reduction of myocardial oxygen demand. This article confirms previous observations of the mechanisms of IABP when translesional flow velocities were directly measured with sensor-tipped Doppler angioplasty guidewires2,3 some 15 years ago. When blood travels across stenosis, the resistance to flow extracts heat energy from turbulence, friction, and separation forces, resulting in pressure loss distal to the stenosis. The pressure loss is curvilinearly related to flow with exponentially increasing loss as flow increases.4 In addition, the degree of lumen narrowing impacts the phasic wave form From the Division of Cardiology, University of California, Orange, CA. Submitted June 12, 2007; accepted June 15, 2007. Reprint requests: Morton J. Kern, MD, FSCAI, FAHA, FACC, Division of Cardiology, University of California, Irvine Bldg 53, Rt 81, Room 100, 101 The City Drive, Orange, CA 92868-4080. E-mail: [email protected] Am Heart J 2007;154:615-6. 0002-8703/$ - see front matter © 2007, Mosby, Inc. All rights reserved. doi:10.1016/j.ahj.2007.06.011
and pressure transmission. The stenosis acts as a high-pass filter, reducing the high-frequency components of a pressure waves as well as the absolute pressure.5 The more severe the stenosis is, the more pressure loss occurs. The pressure loss is coupled and corresponds to loss of flow velocity signals as identified previously.2,3 What Yoshitani et al1 did not provide is the association between the exact physiologic degree of stenosis and the degree of diminished IABP pressure augmentation. Using a fractional flow reserve, a measure of the percent of normal flow across a stenosis derived from translesional pressure at hyperemia, rather than a quantitative coronary angiography, the authors could have been able to identify which lesions might permit better pressure transmission and, hence, flow. The limitations of angiography to determine which lesions are significant have been strongly linked to the disparity of clinical responses.6 Does intra-aortic balloon pumping have a potential to paradoxically reduce coronary perfusion? In theory, an increase in aortic pressure without corresponding increase in poststenotic pressure might calculate as a more severe transstenotic pressure gradient with less perfusion pressure, but this response is balanced by ventricular unloading and reduction of myocardial oxygen demand. An infrequently discussed mechanism of potential IABP benefit is that of improved collateral flow. The effect of intra-aortic balloon pumping on collateral flow is a function of not only the severity of lesions but also the type of collateral supply to the poststenotic regions. Although the study is small,7 those beds with the largest epicardial collateral had evidence of IABP flow augmentation. In beds supplied by intraseptal or acute recruited collateral, no augmentation was seen. The issue with regard to collateral flow is certainly important and was not addressed in this particular study. The data would be available if the investigators had continued to make their measurements during coronary angioplasty balloon occlusion. A collateral flow index during intra-aortic balloon pumping has not been previously reported. However, the limitations of using epicardial flow or pressure to determine the degree of collateral supplied should be recognized.8,9 This investigation was confirmatory for directly measured flow across severe stenoses and provided refined pressure data because the measurements of pressure at the time of our flow velocity determinations could be made only with a balloon or tracking catheter, both about 1 mm in diameter.2,3 The use of transthoracic Doppler echo of the left anterior descending coronary artery demonstrating improved coronary flow distal to critical
616 Kern
stenosis suggested that a pressure-measuring guidewire may have contributed to some reduction in lumen area and flow.10 This is certainly possible, but given the wide range of stenosis investigated, the observations regarding critical stenoses are still valid. In the end, given the uncertainty of stenosis severity, intra-aortic balloon pumping certainly has the ability to increase coronary flow across some of the many lesions, especially those of an intermediate severity. Yoshitani et al1 should be complimented for an excellent study. In the future, using sensor guidewires, similar research would permit us to appreciate IABP influences on the collateral flow index, determinations of fractional flow, and responses of the microcirculation under a variety of different clinical scenarios.
References 1. Yoshitani, et al. AHJ, effects of IABP on coronary pressure in patients with stenotic coronary arteries. Am Heart J 2007;154:725-31. 2. 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;21:359-68.
American Heart Journal October 2007
3. 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;87:500-11. 4. Hoffman JIE, Spaan JAE. Pressure-flow relations in coronary circulation. Physiol Rev 1990;70:331-90. 5. Holmes D, Velappan P, Kern MJ. Coronary pressure notch: an early non-hyperemic visual indictor of the physiologic significance of a coronary artery stenosis. J Invasive Cardiol 2005;16:617-20. 6. Topol EJ, Nissen SE. Our preoccupation with coronary luminology. The dissociation between clinical and angiographic findings in ischemic heart disease. Circulation 1995;92:2333-42. 7. 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;71:1451-4. 8. Pijls NHJ, Bech GJW, el Gamal MIH, et al. Quantification of recruitable coronary collateral blood flow in conscious humans and its potential to predict future ischemic events. J Am Coll Cardiol 1995; 25:1522-8. 9. Piek JJ, van Liebergen RAM, Koch KT, et al. Clinical, angiographic and hemodynamic predictors of recruitable collateral flow assessed during balloon angioplasty coronary occlusion. J Am Coll Cardiol 1997;29:275-82. 10. Takeuchi M, Nohtomi Y, Yoshitani H, et al. Enhanced coronary flow velocity during intra-aortic balloon pumping assessed by transthoracic Doppler echocardiography. J Am Coll Cardiol 2004;43: 368-76.