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Failure of intraaortic balloon counterpulsation to augment distal coronary perfusion pressure during percutaneous transluminal coronary angioplasty
February
Distribution of coronary stenoses in patients with one-vessel coronary artery disease: Of the 354 with lvessel CAD, the LAD was narrowed in 179 (51%), the right in 124 (35%) and the LC in 51 (14%) (Fig. 1). The LC was narrowed less frequently than the LAD or right (p
Failure of Intraaortic Balloon Counterpulsationto Augment Distal CoronaryPerfusion PressureDuring Percutaneous TransluminalCoronaryAngioplasty ROBERT G. MacDONALD, MD JAMES A. HILL, MD ROBERT L. FELDMAN, MD
I
ntraaortic balloon counterpulsation (IABP) has been used extensively in the management of patients with refractory myocardial ischemia and left ventricular failure. Specific clinical applications in which IABP has demonstrated success include unstable angina, acute myocardial infarction and cardiogenic shock. Recently, IABP has been used as adjunctive therapy during performance of percutaneous transluminal From the Division of Cardiology, Department of Medicine, University of Florida, and the Veterans Administration Hospital, Gainesville, Florida. Manuscript received May 27,1986; revised manuscript received August 18, 1986, accepted August 20, 1986.
1, 1997
THE AMERICAN
JOURNAL
OF CARDIOLOGY
Volume
59
359
(40%) right involvement and only 1 subject (4%) LC involvement. Thus, the relatively infrequent significant LC narrowing appears to occur in patients with symptomatic CAD and those who die of noncardiac causes. Alternatively, the relative infrequency of LC atherosclerotic involvement may reflect some degree of LC protection, possibly due to differences among the coronary arteries in turbulence of flow. Feit et al” speculated that the marked difference between right and LC involvement may be related to the difference of angle from which these arteries arise from the aorta and left main coronary artery, respectively. Although the LC arises at a 90° angle from the left main artery, the right arises directly from the aorta. The resultant differences in flow characteristics may cause a greater frequency of atherosclerosis in the right than in the LC. 1. Diethrich EB. Liddicoat JE, Kinard SA, Garrett HE, Lewis JM. DeBakey ME. Surgical significance of angiographic patterns in coronary arterial disease. Circulation 1967;35:suppI I:I-155-1-162. 2. Roberts WC, Jones AA. Quantitation of coronary arterial narrowing at necropsy in sudden coronary death. Analysis of 31 patients and comparison with 25 control subjects. Am J Cardiol 1979:44:39-45. 3. Roberts WC, Virmani R. Quantification of coronary arterial narrowing in clinically-isolated unstable angina pectoris. An analysis of 22 necropsy patients. Am J Med 1979;67:792-799. 4. Roberts WC, Jones AA. Quantification of coronary arterial narrowing at necropsy in acute transmural myocardial infarction. Analysis and comparison of findings in 27 patients and 22 controls. Circulation 1980:61:786-790. 5. Virmani R, Roberts WC. Quantification of coronary arterial narrowing and of left ventricular myocardial scarring in healed myocardial infarction with chronic. eventually fatal. congestive cardiac failure. Am J Med 1980;68:831838. 6. Feit A, Khan R, El-Sherif N. Reddy CVR. Nonrandom occurrence ofsinglevessel coronary artery disease. Am J Med 1984;77:683-684.
coronary angioplasty (PTCA) in unstable patients or in the management of acute coronary occlusion complicating PTCA.1-5 Mechanisms through which IABP provides clinical benefit are incompletely understood. Studies consistently show reduction in indexes of myocardial oxygen demand through a decrease in afterload and preload. Whether IABP improves regional coronary blood flow, either directly or through collateral perfusion, remains uncertain because results of different studies are contradictory.3-6 We report 3 patients in whom IABP was used during PTCA. Patient 2: Patient 1 was a 57-year-old man with crescendo angina and severe coronary artery disease involving the right (lOO%), left circumflex (LC, 90%) and anterior descending (LAD, 99%) coronary arteries. Several hours after diagnostic catheterization, chest pain, anterior ST-segment elevation (leads I, aVL and VI-Vs) and hypotension occurred secondary to acute LAD occlusion. An intraaortic balloon was inserted and emergency PTCA planned while awaiting coronary bypass surgery. With the onset of IABP, there was prompt clinical improvement manifested by reduction in angina and a decrease in ST elevation. PTCA restored LAD patency. The transstenotic pressure gradient was reduced from 45 to 20 mm Hg. During PTCA, despite excellent augmentation of the aor-
360
BRIEF REPORTS
tic and proximal coronary diastolic pressures with IABP, no increase in coronary diastolic pressure distal to the stenosis occurred with the PTCA balloon either deflated or inflated (Fig. 1 and 4. Patient 2: Patient 2 was a %-year-old woman undergoing elective PTCA of the LAD and LC. Acute LC occlusion occurred complicated by ischemia [ST elevation in leads II, III and aVF) and hypotension. An intraaortic balloon pump was inserted, which lead to
mm Hg loo 00 00 40 26
I
mm Hg
I3 41
4 1 sac I
I
I I
I
I
1
..~
clinical improvement evidenced by return of systemic arterial pressure to normal and decreased chest pain. The LC occlusion was successfully recrossed (mean transstenotic gradient 30 mm Hg ] and redilated. Distal coronary pressure with and without the PTCA balloon inflated showed no important diastolic augmentation. Patient 3: A %-year-old man with severe left ventricular dysfunction and postinfarction angina had stenosis of the LAD (lOO%), LC (90%) and right (20%) coronary arteries. IABP was used prophylactically to reduce procedural risk during PTCA of the LC. Despite excellent aortic and proximal coronary diastolic pressure augmentation, there was no distal coronary pressure augmentation until the initial large transstenotic pressure gradient was essentially obliterated. PTCA was well tolerated. Pressure values from the 3 patients are shown in Table I. Pressure waveforms were assessed at 3 times. First, with the PTCA balloon catheter positioned proximal to the stenosis, similar waveforms were noted and diastolic augmentation was easily appreciated in each patient (Fig. 1A). Coronary pressure waveforms in this location reflect resistance to flow across the proximal epicardial coronary artery. Second, with the PTCA balloon across the stenosis and deflated, only minimal distal coronary diastolic augmentation was noted with IABP (Fig. 1B) compared with distal coronary pressure without IABP (Fig. IC). Coronary pressure waveforms in this position reflect resistance to anterograde flow across the stenosis-PTCA balloon obstruction and are not indicative of collateral function. Only minimal diastolic augmentation of distal coronary pressure was noted with IABP, suggesting mini-
2 FIGURE 1. Patient 1. Phasic and mean pressures recorded through the angioplasiy guide and balloon catheters and pulmonary artery catheter. A, paper speed of 10 mm/s, with the angloplasty guide in the left main coronary artery, the angioplasty balloon catheter in the coronary artery proximal to the stenosis and with intraaortlc balloon counterpulsation. A small difference in the frequency response of the 2 catheters was noted, but augmentation of diastolic pressure recorded from the angioplasty balloon catheter was readily appreciated and mean pressures were equal. 6, paper speed of 25 mm/s. With the angioplasty balloon catheter across the stenosis and wlth intraaortic balloon counterpulsation there was a marked increase in aortic diastolic pressure as measured in the left main coronary artery by the guide catheter. The coronary pressure waveform was augmented only slightly; there was a minimal Increase in coronary diastolic pressure. The mean transstenotic gradient was similar (18 mm Hg) to the gradient without intraaortlc balloon counterpulsatlon (C). The diastolic gradient was conslderably increased because of considerable augmentation of the aortic but not coronary diastolic pressures. C, paper speed of 25 mm/s. With the angloplasty balloon catheter across the steno& In the same location as In 6 and without intraaortlc balloon counterpulsation, normal pressure waveforms were noted. The mean transstenotlc gradient was 19 mm Hg.
V5 mm Hg 100 60 60
40 20 0 FIGURE 2. Paper speed of 10 mm/s. Phasic pressures recorded through the angioplasty guide and balloon catheters during balloon occlusion of the coronary artery. (The pressure measured from the angioplasty balloon catheter, therefore, reflects collateral perfusion pressure.) lntraaortic balloon counterpulsatlon was interrupted by a ventricular ectopic beat, and although a slight dtfference in collateral pressure waveform with and without lntraaortic balloon counterpulsation was noted, there was little difference In the pressure magnitude.
February
TABLE I Aortic Counterpulsation
and
Distal
Coronary
Pressures
1, 1967
With
THE AMERICAN
and
Without
Distal
Aortic
Patient 1 IABPoff IABP on Patient 2 IABP on Patient 3$ IABP off IABP on
Pressures
(mm Hg)
Balloon
JOURNAL
lntraaortlc
Coronary
Pressures
PTCA Deflated’
OF CARDIOLOGY
Volume
59
361
Balloon
(mm Hg) PTCA Balloon lnflatedt
PSP
ADP
EDP
Mean
PSP
ADP
EDP
Mean
PSP
ADP
EDP
Mean
92 76
100
73 52
79 75
75 67
54
53 47
60 57
20
MIN
12
16
85
130
60
85
70
50
45
55
20
MIN
14
17
102 91
114
66 76
85 97
59 59
38
36 36
50 50
40
MIN
20
28
*Reflects anterograde perfusion; treflects collateral perfusion; Sobtained before transstenotic gradient was maximally reduced. ADP = augmented diastolic pressure: EDP = enddiastolic pressure; IABP = intraaortic balloon counterpulsation; MIN = minimal; PSP = peak systolic pressure; PTCA = percutaneous transluminal coronary angioplasty.
ma1 change in anterograde perfusion pressure or flow. Third, with the PTCA balloon inflated, and again only minimal augmentation of the distal coronary occlusion, pressure was noted with IABP (Fig. 2). Distal coronary pressure during proximal PTCA balloon coronary occlusion reflects collateral perfusion pressure.7
These cases illustrate that although clinical benefit was derived from IABP, considerable augmentation of distal coronary perfusion pressure did not occur. Reduction or prevention of ischemia by IABP in these patients, therefore, most likely occurred predominantly through reduction of myocardial oxygen demand.
The reason for failure of distal coronary pressure to increase with IABP is not clear. The observed residual transstenotic pressure gradients suggest that the obstruction caused by the combination of the residual coronary stenosis and the deflated balloon catheter must have been functionally equivalent to a moderately severe stenosis. During coronary occlusion caused by PTCA balloon inflation, the distal coronary pressure was low in each of these patients in keeping with poorly developed collateral vessels. Therefore, when a functionally severe stenosis is present and collateral vessels are not developed, the augmented pressure that is transmitted to proximal unobstructed coronary arteries is usually not transmitted to the coronary artery distal to the stenosis either anterograde or through poorly developed collateral vessels. In patients with less severe stenoses, or others with well developed collateral vessels, important diastolic augmentation of coronary pressure might occur.
1. Fuchs RM, Brin KP, Brinker JA. C&man PA, Heuser RR, Yin FC. Augmentation of regional coronary blood flow by intra-aortic balloon counterpulsation in patients with unstable angina. Circulation 1983;68:117-123. 2. Williams DO, Kerr 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;66:593-597. 3. Part SC, Pate1 S, Schmidt DH. Effects of intraaartic balloon counterpulsation on myocardial blood flow in patients with severe coronary artery disease. JACC 1984;3:1367-1374. 4. Alcan KE. Stertzer SH. Wallsh E, DePasquale NP, Bruno MS. The role of intro-aortic balloon counterpulsation in patients undergoing percutaneous transluminal coronary angioplasty. Am Heart J 1983;105:527-530. 5. Margolis JR. The role of the percutaneous intra-aortic balloon in emergency situations following percutaneous transluminal coronary angioplasty. In: Kaltenbach M, Grontzig A, Rentrop K, Bussman WD. eds. Transluminal Coronary Angioplasty and Intracoronary Thrombolysis. Berlin: Springer Verlag. 1982: 145-150. 6. Gewirtz H, Ohley W, Williams DO, Sun Y, Most AS. Effect of intraaortic balloon counterpulsation on regional myocardial blood flow and oxygen consumption in the presence of coronary artery stenosis: observation in an awake animal model. Am J Cardiol 1982;50:829-837. 7. Gregg DE, Thornton JJ, Mautz FR. The magnitude, adequacy and source of the collateral blood flow and pressure in chronically occluded coronary arteries. Am J Physiol 1939;127:161-175.
Distribution of coronary stenoses in patients with one-vessel coronary artery disease: Of the 354 with lvessel CAD, the LAD was narrowed in 179 (51%), the right in 124 (35%) and the LC in 51 (14%) (Fig. 1). The LC was narrowed less frequently than the LAD or right (p
Failure of Intraaortic Balloon Counterpulsationto Augment Distal CoronaryPerfusion PressureDuring Percutaneous TransluminalCoronaryAngioplasty ROBERT G. MacDONALD, MD JAMES A. HILL, MD ROBERT L. FELDMAN, MD
I
ntraaortic balloon counterpulsation (IABP) has been used extensively in the management of patients with refractory myocardial ischemia and left ventricular failure. Specific clinical applications in which IABP has demonstrated success include unstable angina, acute myocardial infarction and cardiogenic shock. Recently, IABP has been used as adjunctive therapy during performance of percutaneous transluminal From the Division of Cardiology, Department of Medicine, University of Florida, and the Veterans Administration Hospital, Gainesville, Florida. Manuscript received May 27,1986; revised manuscript received August 18, 1986, accepted August 20, 1986.
1, 1997
THE AMERICAN
JOURNAL
OF CARDIOLOGY
Volume
59
359
(40%) right involvement and only 1 subject (4%) LC involvement. Thus, the relatively infrequent significant LC narrowing appears to occur in patients with symptomatic CAD and those who die of noncardiac causes. Alternatively, the relative infrequency of LC atherosclerotic involvement may reflect some degree of LC protection, possibly due to differences among the coronary arteries in turbulence of flow. Feit et al” speculated that the marked difference between right and LC involvement may be related to the difference of angle from which these arteries arise from the aorta and left main coronary artery, respectively. Although the LC arises at a 90° angle from the left main artery, the right arises directly from the aorta. The resultant differences in flow characteristics may cause a greater frequency of atherosclerosis in the right than in the LC. 1. Diethrich EB. Liddicoat JE, Kinard SA, Garrett HE, Lewis JM. DeBakey ME. Surgical significance of angiographic patterns in coronary arterial disease. Circulation 1967;35:suppI I:I-155-1-162. 2. Roberts WC, Jones AA. Quantitation of coronary arterial narrowing at necropsy in sudden coronary death. Analysis of 31 patients and comparison with 25 control subjects. Am J Cardiol 1979:44:39-45. 3. Roberts WC, Virmani R. Quantification of coronary arterial narrowing in clinically-isolated unstable angina pectoris. An analysis of 22 necropsy patients. Am J Med 1979;67:792-799. 4. Roberts WC, Jones AA. Quantification of coronary arterial narrowing at necropsy in acute transmural myocardial infarction. Analysis and comparison of findings in 27 patients and 22 controls. Circulation 1980:61:786-790. 5. Virmani R, Roberts WC. Quantification of coronary arterial narrowing and of left ventricular myocardial scarring in healed myocardial infarction with chronic. eventually fatal. congestive cardiac failure. Am J Med 1980;68:831838. 6. Feit A, Khan R, El-Sherif N. Reddy CVR. Nonrandom occurrence ofsinglevessel coronary artery disease. Am J Med 1984;77:683-684.
coronary angioplasty (PTCA) in unstable patients or in the management of acute coronary occlusion complicating PTCA.1-5 Mechanisms through which IABP provides clinical benefit are incompletely understood. Studies consistently show reduction in indexes of myocardial oxygen demand through a decrease in afterload and preload. Whether IABP improves regional coronary blood flow, either directly or through collateral perfusion, remains uncertain because results of different studies are contradictory.3-6 We report 3 patients in whom IABP was used during PTCA. Patient 2: Patient 1 was a 57-year-old man with crescendo angina and severe coronary artery disease involving the right (lOO%), left circumflex (LC, 90%) and anterior descending (LAD, 99%) coronary arteries. Several hours after diagnostic catheterization, chest pain, anterior ST-segment elevation (leads I, aVL and VI-Vs) and hypotension occurred secondary to acute LAD occlusion. An intraaortic balloon was inserted and emergency PTCA planned while awaiting coronary bypass surgery. With the onset of IABP, there was prompt clinical improvement manifested by reduction in angina and a decrease in ST elevation. PTCA restored LAD patency. The transstenotic pressure gradient was reduced from 45 to 20 mm Hg. During PTCA, despite excellent augmentation of the aor-
360
BRIEF REPORTS
tic and proximal coronary diastolic pressures with IABP, no increase in coronary diastolic pressure distal to the stenosis occurred with the PTCA balloon either deflated or inflated (Fig. 1 and 4. Patient 2: Patient 2 was a %-year-old woman undergoing elective PTCA of the LAD and LC. Acute LC occlusion occurred complicated by ischemia [ST elevation in leads II, III and aVF) and hypotension. An intraaortic balloon pump was inserted, which lead to
mm Hg loo 00 00 40 26
I
mm Hg
I3 41
4 1 sac I
I
I I
I
I
1
..~
clinical improvement evidenced by return of systemic arterial pressure to normal and decreased chest pain. The LC occlusion was successfully recrossed (mean transstenotic gradient 30 mm Hg ] and redilated. Distal coronary pressure with and without the PTCA balloon inflated showed no important diastolic augmentation. Patient 3: A %-year-old man with severe left ventricular dysfunction and postinfarction angina had stenosis of the LAD (lOO%), LC (90%) and right (20%) coronary arteries. IABP was used prophylactically to reduce procedural risk during PTCA of the LC. Despite excellent aortic and proximal coronary diastolic pressure augmentation, there was no distal coronary pressure augmentation until the initial large transstenotic pressure gradient was essentially obliterated. PTCA was well tolerated. Pressure values from the 3 patients are shown in Table I. Pressure waveforms were assessed at 3 times. First, with the PTCA balloon catheter positioned proximal to the stenosis, similar waveforms were noted and diastolic augmentation was easily appreciated in each patient (Fig. 1A). Coronary pressure waveforms in this location reflect resistance to flow across the proximal epicardial coronary artery. Second, with the PTCA balloon across the stenosis and deflated, only minimal distal coronary diastolic augmentation was noted with IABP (Fig. 1B) compared with distal coronary pressure without IABP (Fig. IC). Coronary pressure waveforms in this position reflect resistance to anterograde flow across the stenosis-PTCA balloon obstruction and are not indicative of collateral function. Only minimal diastolic augmentation of distal coronary pressure was noted with IABP, suggesting mini-
2 FIGURE 1. Patient 1. Phasic and mean pressures recorded through the angioplasiy guide and balloon catheters and pulmonary artery catheter. A, paper speed of 10 mm/s, with the angloplasty guide in the left main coronary artery, the angioplasty balloon catheter in the coronary artery proximal to the stenosis and with intraaortlc balloon counterpulsation. A small difference in the frequency response of the 2 catheters was noted, but augmentation of diastolic pressure recorded from the angioplasty balloon catheter was readily appreciated and mean pressures were equal. 6, paper speed of 25 mm/s. With the angioplasty balloon catheter across the stenosis and wlth intraaortic balloon counterpulsation there was a marked increase in aortic diastolic pressure as measured in the left main coronary artery by the guide catheter. The coronary pressure waveform was augmented only slightly; there was a minimal Increase in coronary diastolic pressure. The mean transstenotic gradient was similar (18 mm Hg) to the gradient without intraaortlc balloon counterpulsatlon (C). The diastolic gradient was conslderably increased because of considerable augmentation of the aortic but not coronary diastolic pressures. C, paper speed of 25 mm/s. With the angloplasty balloon catheter across the steno& In the same location as In 6 and without intraaortlc balloon counterpulsation, normal pressure waveforms were noted. The mean transstenotlc gradient was 19 mm Hg.
V5 mm Hg 100 60 60
40 20 0 FIGURE 2. Paper speed of 10 mm/s. Phasic pressures recorded through the angioplasty guide and balloon catheters during balloon occlusion of the coronary artery. (The pressure measured from the angioplasty balloon catheter, therefore, reflects collateral perfusion pressure.) lntraaortic balloon counterpulsatlon was interrupted by a ventricular ectopic beat, and although a slight dtfference in collateral pressure waveform with and without lntraaortic balloon counterpulsation was noted, there was little difference In the pressure magnitude.
February
TABLE I Aortic Counterpulsation
and
Distal
Coronary
Pressures
1, 1967
With
THE AMERICAN
and
Without
Distal
Aortic
Patient 1 IABPoff IABP on Patient 2 IABP on Patient 3$ IABP off IABP on
Pressures
(mm Hg)
Balloon
JOURNAL
lntraaortlc
Coronary
Pressures
PTCA Deflated’
OF CARDIOLOGY
Volume
59
361
Balloon
(mm Hg) PTCA Balloon lnflatedt
PSP
ADP
EDP
Mean
PSP
ADP
EDP
Mean
PSP
ADP
EDP
Mean
92 76
100
73 52
79 75
75 67
54
53 47
60 57
20
MIN
12
16
85
130
60
85
70
50
45
55
20
MIN
14
17
102 91
114
66 76
85 97
59 59
38
36 36
50 50
40
MIN
20
28
*Reflects anterograde perfusion; treflects collateral perfusion; Sobtained before transstenotic gradient was maximally reduced. ADP = augmented diastolic pressure: EDP = enddiastolic pressure; IABP = intraaortic balloon counterpulsation; MIN = minimal; PSP = peak systolic pressure; PTCA = percutaneous transluminal coronary angioplasty.
ma1 change in anterograde perfusion pressure or flow. Third, with the PTCA balloon inflated, and again only minimal augmentation of the distal coronary occlusion, pressure was noted with IABP (Fig. 2). Distal coronary pressure during proximal PTCA balloon coronary occlusion reflects collateral perfusion pressure.7
These cases illustrate that although clinical benefit was derived from IABP, considerable augmentation of distal coronary perfusion pressure did not occur. Reduction or prevention of ischemia by IABP in these patients, therefore, most likely occurred predominantly through reduction of myocardial oxygen demand.
The reason for failure of distal coronary pressure to increase with IABP is not clear. The observed residual transstenotic pressure gradients suggest that the obstruction caused by the combination of the residual coronary stenosis and the deflated balloon catheter must have been functionally equivalent to a moderately severe stenosis. During coronary occlusion caused by PTCA balloon inflation, the distal coronary pressure was low in each of these patients in keeping with poorly developed collateral vessels. Therefore, when a functionally severe stenosis is present and collateral vessels are not developed, the augmented pressure that is transmitted to proximal unobstructed coronary arteries is usually not transmitted to the coronary artery distal to the stenosis either anterograde or through poorly developed collateral vessels. In patients with less severe stenoses, or others with well developed collateral vessels, important diastolic augmentation of coronary pressure might occur.
1. Fuchs RM, Brin KP, Brinker JA. C&man PA, Heuser RR, Yin FC. Augmentation of regional coronary blood flow by intra-aortic balloon counterpulsation in patients with unstable angina. Circulation 1983;68:117-123. 2. Williams DO, Kerr 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;66:593-597. 3. Part SC, Pate1 S, Schmidt DH. Effects of intraaartic balloon counterpulsation on myocardial blood flow in patients with severe coronary artery disease. JACC 1984;3:1367-1374. 4. Alcan KE. Stertzer SH. Wallsh E, DePasquale NP, Bruno MS. The role of intro-aortic balloon counterpulsation in patients undergoing percutaneous transluminal coronary angioplasty. Am Heart J 1983;105:527-530. 5. Margolis JR. The role of the percutaneous intra-aortic balloon in emergency situations following percutaneous transluminal coronary angioplasty. In: Kaltenbach M, Grontzig A, Rentrop K, Bussman WD. eds. Transluminal Coronary Angioplasty and Intracoronary Thrombolysis. Berlin: Springer Verlag. 1982: 145-150. 6. Gewirtz H, Ohley W, Williams DO, Sun Y, Most AS. Effect of intraaortic balloon counterpulsation on regional myocardial blood flow and oxygen consumption in the presence of coronary artery stenosis: observation in an awake animal model. Am J Cardiol 1982;50:829-837. 7. Gregg DE, Thornton JJ, Mautz FR. The magnitude, adequacy and source of the collateral blood flow and pressure in chronically occluded coronary arteries. Am J Physiol 1939;127:161-175.