Effects of pulsed external augmentation of diastolic pressure on coronary and systemic hemodynamics in patients with coronary artery disease

Effects of pulsed external augmentation of diastolic pressure on coronary and systemic hemodynamics in patients with coronary artery disease The purpose of this study was to define the effects of pulsed external diastolic pressure augmentation on coronary and systemic hemodynamics in 14 men with coronary artery disease and normal left ventricular function. Coronary sinus and great vein blood flow (thermodilution) and systemic hemodynamics were measured before, during, and after timed lower extremity compression, augmenting peak diastolic pressure to within 5 mm Hg of systolic pressure. Systolic and diastolic pressure-time indices were calculated from the high-fidelity micromanometer left ventricular-aortic recordings. External counterpulsation increased mean arterial pressure (108 +- 11 [l SD] to 114 +_ 12 mm Hg, p < 0.01) and the diastolic pressure-time index (440 ? 51 to 498 +_ 82 units, p < O.Ol), with no change in the systolic pressure-time index, absolute coronary sinus, or great cardiac vein blood flow. External diastolic pressure augmentation did not affect heart rate, right heart hemodynamics, cardiac output, or calculated myocardial oxygen consumption. An unanticipated finding was a 210% reduction in peak systolic pressure during external diastolic pressure augmentation in 8 of 14 patients. Despite minimal changes in absolute myocardial blood flow and oxygen consumption, the increase in the diastolic pressure-time/systolic pressure-time Index ratio suggests that subendocardial perfusion may be favorably influenced by diastolic pressure augmentation and may explain the previously reported clinical benefits of external counterpulsation in some patients with ischemic heart disease. (AM HEART J 110:727, 1985.)

Morton J. Kern, M.D., Rodney H. Henry, M.D., Nicholas Lembo, M.D., R. Conrad Park, M.D., Michael S. Lujan, B.A., David Ferry, M.D., and Robert A. O’Rourke, M.D. San Antonio, Texas

Although intra-aortic balloon counterpulsation is recognized as an effective treatment for certain complications of ischemic heart disease such as hypotension and refractory angina,1-5 successful and timely application may not be feasible in all patients6 The noninvasive external augmentation of diastolic pressure alone may improve coronary blood flow in some patients with severe coronary artery disease.7-13 Since the introduction of external diastolic pressure augmentation devices a decade ag~,‘~-~~ clinical studies have demonstrated improvement, to variable degrees, in patients with acute myocardial infarction,7-10 cardiogenic shock,16-1g and

From Audie L. Murphy University of Texas Health Received Reprint University

for publication requests: Morton Hospital, 1325

Veterans’ Science April

Administration Center.

23, 1985;

accepted

Hospital May

and

the

24, 1985.

J. Kern, M.D., Dept. of Cardiology, St. Louis So. Grand Avenue, St. Louis, MO 63104.

unstable angina. 2o However, there are conflicting data as to the effects of diastolic augmentation on coronary and systemic hemodynamics in patients with normal left ventricular function. In prior studies there is no consistent pattern of ‘change in cardiac output, myocardial blood flow, or left ventricular end-diastolic pressure in patients with cardiogenic shock, acute myocardial infarction, stable or unstable angina. 21-28There are no data on changes in myocardial contractility. The precise systemic and coronary hemodynamic responses during augmented diastolic pressure without simultaneous systolic pressure reduction have not been evaluated in patients with normal left ventricular function. Accordingly, the purpose of this study was to define the simultaneous coronary and systemic hemodynamic effects of externally augmented diastolic pressure in patients with stable angina pectoris with normal or minimally abnormal resting hemodynamits and left ventricular function. 727

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Fig. 1. External counterpulsation leg unit and control consoleposition in the catheterization laboratory. In contrast to earlier models,onlv the natients’ lensare enclosedwith the warm water-filled compression bags inside the plastic shell of the leg-unit. METHODS

Fourteen men were selected from patients with exertional or atypical angina pectoris scheduled for cardiac catheterization for routine clinical indications at the Audie L. Murphy Veterans’ Administration Hospital. The protocol was approved by the Human Subjects ResearchCommittee of the Institutional Review Board of the University of Texas Health ScienceCenter at San Antonio and the Audie L. Murphy Veterans’ Administration Hospital. Patients were not asked to participate if any of the following were present: X50% left main coronary artery stenosis,congestive heart failure, significant valvular heart disease, gastrointestinal, renal or hepatic disease,myocardial infarction within 3 weeks of the study, unstable angina, significant cardiac arrhythmias, or unsuitable (amputation or congenital deformity) lower extremity anatomy. Patients with a history of thromboembolic or severe peripheral vascular disease involving the lower extremities were not studied. No routine precatheterization medications were given. Hemodynamic methodology. A diagnostic catheterization including coronary angiography and left cineventriculography wasperformed from the brachial approach. After completion of the diagnostic study, a triple thermistor coronary sinus thermodilution catheter (Wilton Webster Laboratory Inc., Altadena, Calif.) was positioned via an antecubital vein under fluoroscopic guidance. The catheter position was maintained constant throughout the study and wasverified by periodic fluoroscopy. A balloontipped pulmonary artery catheter waspositioned to measure right atrial, phasic, and mean pulmonary artery pressure and cardiac output (thermodilution). Simultaneous high-fidelity left ventricular and aortic pressures were measuredwith a dual micromanometer transducertipped catheter (Millar Instruments, Houston, Texas). The first derivative of left ventricular pressure (dP/dt) Study

population.

was obtained electronically. In addition to the pressure and coronary flow signals, the wave forms of a finger plethysmograph, leg compressionpressure,and counterpulsation synchronizing signal were also recorded for event timing. All signalswere recorded on an Electronics for Medicine VR-16 optical strip-chart recorder (White Plains, N. Y.). Diastolic pressure augmentation device. The counterpulsation device (Cardiassist Inc., Austin, Texas) is an external circulatory assist system designed to compress the lower extremities during diastole, producing a diastolic pressurepulsenearly equivalent to that of peak systolic pressure.The system is comprised of two major pieces,a consoleand a leg unit. Controls on the consoleregulate the enclosed subsystems: system control program, monitor oscilloscope,ECG amplifier, pulse amplifier, strip-chart recorder, and the hydraulic, water heater, and fluid delivery systems. The leg unit, connected to the console by covered umbilicus cable, consists of a plastic shell base and separatecover and leg compressionbags.The leg bags within the sealedleg unit are filled with warmedwater and are then compressedduring the counterpulsation cycles. The device and componentsare shown in Fig. 1. The counterpulsation compression is timed with the patient’s cardiac cycle by meansof either an ECG signalor finger plethysmograph. For the majority of our patients, the onset of external compressionbegan 240 msec after the Q wave of the simultaneousECG, with a compression duration of 340 msec. The time to onset and duration of compressionwas adjusted to produce maximal diastolic pressure augmentation. Measurements of hemodynamic variables and coronary blood flow were reported for the maximal augmented diastolic pressure attained during counterpulsation. Doppler blood flow velocity profiles. Doppler echocardiographic velocity profiles of blood flow in the femoral

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2. A, Doppler velocity profiles of femoral artery flow during and after termination of external counterpulsation. The transducer is directed caudally. Reversal of femoral arterial flow away from the foot can be seen during the first two beats with external counterpulsation. B, Doppler velocity profiles of ascendingaortic flow. C, Superior vena caval flow during and after external counterpulsation does not demonstrate alteration in flow .velocity patterns in these regions. Fig.

artery, ascending aorta, and superior vena cava were obtained in several normal volunteers before and during counterpulsation to evaluate changesin the direction of blood flow during counterpulsation. Reversal of flow in the femoral artery during external counterpulsation was demonstrated. External counterpulsation did not alter ascendingaortic or central venous flow velocity patterns. Figs. 2 A, B, and C are representative examples of the Doppler velocity profiles. Protocol. Coronary blood flow data, systemic hemodynamics, and transmyocardial oxygen contents were obtained at least 20 minutes after angiographic contrast material for four conditions: (1) at rest, (2) at rest following application of the external counterpulsation device with the compressionbagsfilled but not active, (3) after 10 to 15 minutes of leg compressionby counterpulsation, and (4) 5 minutes after termination of external counterpulsation with the compressionbagsemptied. Data analysis. Total and regional coronary blood flow data were calculated by the method of Ganz et alzg and Pepine et al.3” Coronary vascular resistance was determined as the mean arterial pressuredivided by coronary blood flow. Myocardial oxygen consumption was calcu-

lated from the product of the arterial-coronary sinus oxygen content difference and coronary sinus blood flow. Paired simultaneouslycollected coronary sinusand arterial blood oxygen contents were analyzed by reflectance oximetry (Instrumentation Laboratories, Waltham, Mass., IL 282 co-oximeter). A diastolic pressure-timeindex was calculated from the planimetered diastolic area defined by the simultaneous measured high-fidelity left ventricular-aortic diastolic pressure tracings.31A modified systolic pressure-time index was calculated in a similar manner using the area defined during systole from the opening of the aortic valve to the dicrotic notch. The index was normalized for heart rate by dividing the area by the time from the dicrotic notch to the opening of the aortic valve (Fig. 3). Statistical analysis. Comparisons of hemodynamic variables for the four study conditions (rest, external counterpulsation application [control], external counterpulsation pump on, and external counterpulsation pump off) were determined by analysis of variance. When this analysis indicated a significant contribution of a particular variable, subsequentcomparisonsusing a paired t test with the probability value corrected for multiple compar-

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Fig. 3. Examples of simultaneous high-fidelity left ventricular-aortic pressure recordings with the control (solid line) and external counterpulsation (dotted lines) superimposed.The diastolic pressuretime index is shown by the cross-hatched area, the systolic pressure-time index is the striped area. Recording paper speed (100 mm/set) indicated by the l-second time marks on the horizontal axis.

isons(Bonferroni transformation) was used. A significant probability (p) was defined
The clinical and angiographic data for the 14 patients are summarized in Table I. All beta-blocking and calcium channel entry blocking drugs were continued to the time of study. Ten of 14 patients were receiving beta-blocking drugs: seven were receiving propranolol, two were receiving metopro101, and one was receiving nadolol. Nine of 14 were on maintenance therapy with either nifedipine or diltiazem. All patients were receiving either betablocking or calcium channel blocking drugs; five of them received both types. The cineangiographic left

ventriculographic ejection fraction averaged 64%, with abnormal wall motion demonstrated in 8 of 14 patients. Significant coronary artery disease was defined as greater than 60% reduction in angiographic lumen diameter. Five patients had insignificant or no coronary artery disease. One patient was studied while in atrial fibrillation with a moderate ventricular response; the remaining patients were in normal sinus rhythm. No patient required termination of external counterpulsation because of angina, leg discomfort, dyspnea, or other complaints. Hemodynamic data. Systemic and coronary hemodynamic data are summarized in Table II. Heart rate, right heart hemodynamics, cardiac output, and systemic vascular resistance were unchanged during external counterpulsation. External counterpulsa-

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I. Clinical and angiographic data in 14 men with coronary artery diseaseundergoing external counterpulsation ---- - -____ --..

Table

BB (mgl24 hr)

Patient

NO.

Medication

4%

1

41

2

64

3 4 5 6 7 8 9 10

41

11

51

12 13

50 59

14 Totals

!%I 52

59 46 59 56 62 40 51

DI PR RP IS CA PR CA CA PR PR MT CA NA CA

CA DI IS CA PR DI IS NA

CA CA DI -

CA (mgf24 hr)

40 160 160 0 320 160 0 80 10

IS CA IS

IS -

240 100 0 80 0

120 40 360 80 0 240 120 0 0 60 60 0 80

(f?,

WM

n8 70 56 41 7.i 51 69 63 72 74 60 7x 61 48 64 + 11

HYP HYP WNL DYS WNL WNL WNL HYP DYS WNL HYP WNL HYP HYP

LfK’

I‘ ,4! ) i,

(‘FX (‘,I

INF INF WNL ANT WNL WNI. WNL API API WNL ANT WNL AN’1 INF

Abbreviations: BB = dose of beta blocker; CA = dose of calcium channel blocker; CFX = left circumflex coronary artery: EF := cineangiograpbic ventricular ejection fraction; LAD = left anterior descending coronary artery; HYP = hypokinesis; DYS = dyskinesis; WNL = within normal INF = inferior: ANT = anterior; API = apical; RCA = right coronary artery; WM = left ventricular wall motion abnormality: l,OC = location Medications: DT = diuretic; CA = calcium channel blocker; IS = isosorbide din&rate; MT = metoprolol; NA = nadolol; PR = propranolol.

tion decreased pulmonary vascular resistance and significantly increased mean arterial pressure (108 +- 10 to 113 f 11 mm Hg, p < 0.01) and the diastolic pressure-time index (440 -t 51 to 498 f 82 U, p < 0.05). Neither coronary sinus nor great vein blood flow or resistance was affected by external counterpulsation. External counterpulsation did not alter calculated myocardial oxygen consumption nor transmyocardial oxygen extraction. In eight of 14 patients, peak systolic pressure was reduced 10 to 15 mm Hg during external counterpulsation. A representative example of the reduction in systolic pressure during external counterpulsation is illustrated in Fig. 4, A and B. The data from three subgroups of patients-eight in whom external counterpulsation decreased peak systolic pressure ~10%~ seven with greater than 60% left anterior descend.ing coronary artery disease, or nine with greater than 10 mm Hg increase in mean arterial pressure-did not reveal significant subgroup differences. There was no correlation between any hemodynamic variable or coronary blood flow measurement with the duration, onset, or absolute pressure of lower extremity compression. DISCUSSION

Autoregulation of coronary blood flow may be attenuated in patients with coronary artery stenosis in hypoperfused and potentially ischemic regions. In these patients, coronary perfusion is directly related to diastolic pressure. The results of this study suggest that diastolic pressure augmentation in

RCA (“0

left limits; of WM.

patients with and without coronary artery disease and normal left ventricular function does not overcome autoregulation, and thus no increase in total or regional coronary blood flow is observed. The small and insignificant changes in heart rate, cardiac output, and other hemodynamic variables also imply that diastolic augmentation interferes little with normal systemic hemodynamic homeostasis. The increase in the diastolic pressure-time index/systolic pressure-time index ratio, however, does suggest that under circumstances of myocardial ischemia during which coronary reserve may be abolished, external diastolic pressure augmentation in a manner similar to intra-aortic counterpulsation might be beneficial in some patients in whom invasive intraaortic counterpulsation is not immediately available or technically feasible. Effects of counterpulsation

on systemic

hemodynam-

Although external counterpulsation has been shown to reduce left ventricular work,7-15 the precise mechanisms of improvement and effects on systemic and coronary hemodynamics have not been fully defined. Hemodynamic studies83 I2 have suggested that the beneficial effects may result from increased diastolic perfusion pressure, ratio of mean diastolic pressure to systolic pressure, coronary blood flow or coronary collateral flow, or favorable modification of the pulse pressure distribution in the aorta. From our results, heart rate and cardiac output during external counterpulsation are unchanged, suggesting that stroke volume per unit of work is unaffected. Although mean and peak diastolic pressure were elevated, there was no significant change in calcuits.

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Table

II. Hemodynamic data in the 14 patients during the four phasesof the study

American

Rest CSF GVF

ml/min mllmin

CSR

mmHg/min ml-’

GVR MAP SYS DIA LVEDP PAS PAD RAP HR dP/dt MVOt co SVR PVR A-O, csoz

mm Hg/min mm Hg mm Hg mm Hg mm Hg mm Hg mm Hg mm Hg bpm mm Hghec ml/min L/min U U ml/d1 ml/d1 ml/d1 U U

A-CSO, DPTI SPTI

104 f 78 f 1.15 + 1.65 f 105 k 143 f 79 k 15 k 27 r 12 k 5k2 67 2 1758 12.1 k 5.1 + 1560 226 18.8 f 6.6 * 12.2 zk -

. ml-’

Control 41 37 0.41 0.81 11 16 10 7 6 3

118 83 1.07 1.50 108 147 82 18 30 15 6 68 1675 13.6 5.1 1664 239 18.1 6.73 12.1 440 724

12 6.5 0.8

1.1 0.94 1.3

* * k f + 2 k 2 f 2 + _t

53 34 43 65 10 13 9 7 8 4 27 23

k 5.3 + 1.2

+ 1.0 f 1.0 f 1.3 f 51 of: 88

Pump on 105 rt 48 75 + 29 1.28 +- 54 1.69 +- 64 113 rt 11t 145 * 15 83 + 10 17 -c 10 28 + 7 13 k 5 6k2 67 t 23 1733 11.7 k 6.3 5.2 k 1.0 1662 206t 19.0 +- 1.1 6.7 k 1.1 12.3 k 1.0 498 + 82* 748 -t 100

fimp 106 68 1.24 1.94 108 145 81 15 26 11 5 65 1552 11.3 4.8 1734 207 18.7 6.5 12.3

1995

Heart

Journal

n = n = n = n = n = n = n = n = n=9 n=9

10 12 10 12 14 14 14 11

off f t + + rt -rk k k -t * zk

63 30 50 1.0 12t 18 12 9t 7 4 27 lit

* 5.3 + 0.9

k 0.73 -r- 0.85 + 0.87

n=9 n = n = n=6 n=9 n=9 n=9 n=9 n=9 n=9 n= n =

14 10

11 11

Abbreviations: CSF = coronary sinus blood flow; GVF = great cardiac vein flow; R = resistance; MAP = mean arterial pressure; SYS = systolic; DIA = diastolic; LVEDP = left ventricular end-diastolic pressure; PAS = pulmonary artery systolic pressure; PAD = pulmonary artery diastolic pressure; RAP = right atria1 pressure; HR = heart rate; dP/dt = rate of rise in ventricular pressure; MVO, = myocardial oxygen consumption (CSF x A-CSO,); CO = cardiac output; SVR = systemic vascular resistance; PVR = pulmonary vascular resistance; A-O, = arterial oxygen content; CSO, = coronary sinus oxygen content; A-CSO, = arterial CSO, content difference; DPTI = diastolic pressure-time index; SPTI = systolic pressure-time index (mm Hg/ set min); *p < 0.5; tp < 0.01 as compared to previous value.

lated myocardial oxygen consumption or dP/dt as an index of contractility. Unlike an earlier study,B our data did not demonstrate either an increase in cardiac output or a significant reduction in left ventricular pressure or the modified systolic pressure-time index. Increases in left ventricular enddiastolic pressure in patients during external counterpulsation have been reported.22’ 23 The hemodynamic effects of external counterpulsation with and without systolic afterload reduction using intravenous nitroprusside were studied in patients with acute myocardial infarction.‘-’ As in our patients, external counterpulsation alone increased both peak diastolic pressure and mean diastolic pressure. However, the 14% increase in cardiac index reported by Parmley et aLs was not observed in our patients without ischemia. Parmley et aLB suggested that the increased cardiac output during counterpulsation may have been due to increased venous return without increased left ventricular filling pressures. External counterpulsation in our patients did not significantly alter either right or left ventricular filling pressures. Effects of counterpulsation flow. Although intra-aortic

on

myocardial

counterpulsation

blood

has

been demonstrated to reduce cardiac afterload and myocardial work in patients with unstable angina and coronary artery disease,‘4s24-2g the effects of counterpulsation on coronary blood flow to normal as well as to regions supplied by collateral vessels or to regions to distal critical coronary artery stenosis are controversial. Increased coronary blood flow during counterpulsation has been suggested to correlate with the increased diastolic pressure,11*24 but the precise contribution of coexistent hemodynamic changes, especially those relating to afterload reduction, can not be separated as contributory factors. Counterpulsation techniques in this study and in been unable other investigations 9, 10, 1% 17,22, ‘Z-28 have to demonstrate consistent increases in myocardial blood flow during counterpulsation in patients with severe coronary artery disease. Clinical studies. As in initial studies of intra-aortic counterpulsation, application of external counterpulsation has been associated with improved survival in some patient subgroups with cardiogenic shock, unstable angina, and acute myocardial infarction.7-*0, 16-18In patients with acute myocardial infarction and mild left ventricular dysfunction studied in a prospective randomized trial of 258 patients from

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Fig. 4. A, Simultaneous high-fidelity left ventricular-aortic pressure recordings demonstrating reduction in systolic pressure and diastolic augmentation during external counterpulsation. A0 = aortic pressure; FP = finger plethysomograph tracing; LP = leg (pants) compression pressure; ECG = electrocardiogram; LV = left ventricular pressure; SYNC = counterpulsation synchronizing signal. Pressure scale, 0 to 200 mm Hg. B, Simultaneous left ventricular-aortic pressure and coronary sinus and great cardiac vein A0 = mean and phasic aortic thermodilution signals before and during external counterpulsation. pressures; CSF = coronary sinus flow; GVF = great vein flow. Although systolic pressure is reduced and diastolic pressure is augmented, there is no significant change in either CSF or GVF. institutions,7 the in-hospital mortality was reduced in groups receiving 4 or more hours of external counterpulsation within the first 24 hours compared to control groups. The results were similar in several smaller trials of external counterpulsation.16-1g Although improved left ventricular function was postulated as the mechanism of improved survival in the treatment group, many of the clinical studies were severely compromised by inadequate experimental design and data complicating the interpretation of the clinical trials. Myocardial blood flow techniques. Coronary SinUS thermodilution blood flow values may vary widely 25

between patients but, in any individual with stable catheter position, coronary sinus blood flow determinations are reliable indicators of relative changes in blood flow during interventions. Coronary sinus thermodilution blood flow techniques, as well as radioisotope measurements in man cannot determine transmural myocardial blood flow. An increased flow to the subendocardium may be present and yet may not detect regional blood flow differences. Several methods have been proposed to predict the transmural distribution of left ventricular myocardial blood flow in man?1-36 However, Hoffman and Buckberg note that the diastolic

October.

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pressure-time index is limited as a predictor of myocardial oxygen supply, excluding considerations such as coronary flow inertia, blood viscosity, or coronary capacitance, while the systolic pressuretime index is insensitive to acute changes in contractility and to chronic changes in left ventricular wall stress which determine myocardial oxygen consumption. The diastolic pressure-time index/systolic pressure-time index ratio is thus an oversimplification of factors affecting myocardial oxygen supply and demand.35 However, given that measured changes in contractility, myocardial oxygen consumption, and systolic tension-time index remained stable during the study periods, the diastolic pressure-time index and diastolic pressure-time index/ systolic pressure-time index ratio may be a crude but adequate approximation of the effect of the intervention on transmural left ventricular perfusion. Patient characteristics. External counterpulsation significantly augmented diastolic pressure in 11 of 14 patients. A reduction in peak systolic pressure occurred in 8 of 14 patients in our study. Although the mechanism of systolic pressure reduction during external counterpulsation is unclear, studies in animalsg and in patient+ l”pz3 have yielded similar observations. The variation in degree of diastolic augmentation and systolic reduction may be related to body habitus, lower extremity blood volume, and systemic arterial compliance. The optimal hemodynamic effects of counterpulsation may vary depending on heart rate and compression cycle timing and duration. Peripheral vascular disease, history of lower extremity thromboembolic disease, and atypical anatomy may preclude the use of counterpulsation in some patients. external Although clinical benefits of external counterpulsation were suggested in early studies, difficulties with data interpretation as well as with device application and removal and patient discomfort during counterpulsation significantly impaired wide acceptance. In our study the external counterpulsation device was easily applied and was well tolerated by all patients during the brief study period. Several patients were studied over longer periods without discomfort. Future technical improvements3’j may permit wider application of external counterpulsation. Because of the duration of the study following diagnostic examination, a lo- to 15-minute equilibration period of counterpulsation was selected. Longer counterpulsation duration and active myocardial ischemia may possibly alter the current findings. Conclusions. External augmentation of diastolic pressure may be advantageous in patients in whom

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invasive intra-aortic counterpulsation is unavailable or technically not feasible. External pulsatile augmentation of diastolic pressure in patients with coronary artery disease, stable angina pectoris, and normal ventricular function does not interfere with systemic or coronary autoregulation, producing only minimal changes in systemic hemodynamics and coronary blood flow. The increase in diastolic pressure-time index suggests that under conditions of myocardial ischemia in which autoregulation may be abolished, diastolic pressure augmentation may improve subendocardial perfusion and may explain previously reported clinical benefits with this intervention. The authors wish to acknowledge the following contributions: Dr. K.L. Richards for the Doppler velocity profiles; the catherization team of Evelyn Saunders-Webb, David Foster, and Charles Sandefur for their superb technical assistance; Peggy Nicholson and Sally Byrd for manuscript preparation; and Cardiassist Inc., for technical support. REFERENCES

1. Marcus ML: Intraaortic balloon counterpulsation. In: The coronary circulation in health and disease. New York, 1983, McGraw-Hill Book Company, Inc, p 390. 2. Gold HK, Leinbach RC, Sanders CA, Buckley MJ, Mundth ED, Austin WG: Intraaortic balloon pumping for control of recurrent myocardial ischemia. Circulation 42:1197, 1973. 3. Weintraub RM, Voukydis PC, Aroesty JM, Cohen SI, Ford P, Kurland GS, LaRaia PJ, Morkin E, Paulin S: Treatment of preinfarction angina with intraaortic balloon counterpulsation and surgery: Am J Cardiol 34:809, 1974. 4. Gill GC. Wechsler AS. Newman GE. Oldham HN Jr.: Auementation and redistribution of myocardial blood flow during acute ischemia by intraaortic balloon pumping. Ann Thorac Surg 16:445, 1977. 5. Saini VK. Hood WB Jr. Hechtman HB. Bereer RL: Nutrient myocardial blood flow in experimental myocardial ischemia: Effects of intraaortic balloon pumping and coronary reperfusion. Circulation 52:1086, 1975. 6. Gottlieb SO, Brinker JA, Borkon M, Kallman CH, Potter A, Gott VL, Baughman KL: Identification of patients at high risk for complications of intra-aortic balloon counterpulsation: A multivariate risk factor analysis. Am J Cardiol 53:1135, 1984. I. Amsterdam EA, Banas J, Criley JM, Loeb HS, Mueller H, Willerson JT, Mason DT: Clinical assessment of external pressure circulatory assistance in acute myocardial infarction. Am J Cardiol 45:349, 1980. 8. Parmley WW, Chatterjee K, Charuzi Y, Swan HJC: Hemodynamic effects of noninvasive systolic unloading (nitroprusside) and diastolic augmentation (external counterpulsation) in patients with acute myocardial infarction. Am J Cardiol 33:819, 1974. 9. Soroff HS, Birtwell WC, Norton RL, Cloutier CT, Katoka K, Giron F: Experimental and clinical studies in assisted circulation. Transplantation Proc 3:1485, 1971. 10. Mueller H, Ayres SM, Grace WJ: Hemodynamic and myocardial metabolic response to external counterpulsation in acute myocardial infarction in man (abstr). Am J Cardiol 31:149, 1973. 11. Kataoka K, Birtwell WC, Norton RL, Soroff HS: Experimental evaluation of coronary collateral enhancement by external counterpulsation. Trans Am Sot Artif Intern Organs 19:408, 1973. 12. Watson JT, Platt MR, Rogers DE, Sugg WL, Willerson JT: Similarities in coronary flow between external counterpulsaY

Volume Number

13.

14.

15.

16.

17.

18.

19.

20.

21.

22.

23.

24.

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tion and intra-aortic balloon pumping. Am J Physiol 230:1616, 1976. Silverstein DM, Hamilton GW, Hammermeister KE: The effect of external pressure diastolic augmentation on regional myocardial perfusion in experimental myocardial infarction. Cardiology 60:329, 1975. Hirsch LJ, Lluch S, Katz LN: Counterpulsation effects of coronary blood flow and cardiac oxygen utilization. Circ Res 19:1031, 1966. Spontnitz HM, Cove11 .JW, Ross J, Braunwald E: Left ventricular mechanics and oxygen consumption during arterial counterpulsation. Am J Physiol 217:1352, 1969. Soroff HS, Cloutier CT, Birtwell WC, Begley LA, Messer JV: External counterpulsation: Management of cardiogenic shock after myocardial infarction. JAMA 229:1441, 1974. Dennis C, Moreno JR, Hall DP, Gross C, Ross SM, Wesolowski SA, Senning A: Studies on external counterpulsation as potential measure for acute left heart failure. Trans Am Sot Artif Intern Organs 9:186, 1963. Soroff HS, Birtwell WC, Giron F, Collins SA, Deterling RA: Support of systemic circulation and left ventricular assist by synchronous pulsation of extramural pressure. Surg Form 16:148, 1965. Wright PW: External counterpulsation for cardiogenic shock following cardiopulmonary bypass surgery. AM HEART J 90:231, 1975. Mueller H, Ayres S, Grace W, et al: External counterpulsation-a noninvasive method to protect ischemic myocardium in man? (abstr), Circulation 46:11-195, 1972. Soroff HS, Giron F, Ruiz U, Birtwell WC, Hirsch LJ, Det.erling RA: Medical progress: Physiologic support of heart action. N Engl J Med 280:693, 1964. Ryan TJ, Flessa A, Connelly G, Crooker C, Birtwell W, Giron F, Soroff H: The hemodynamic evaluation of external counterpulsation in man. Circulation 42:111-77, 1970. Beckman CB, Dietzman RH, Romero LH, Shatney CH, Nicoloff DM. Lillehei RC: Hemodvnamic evaluation of external counterpulsation in surgical”patients. Surgery 74:846, 1974. Fuchs RM, Brin KP, Brinker JA, Guzman PA, Heuser RR, Yin FC: Augmentation of regional coronary blood flow by intra-aortic balloon counterpulsation in patients with unstable angina. Circulation 68:117. 1983.

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25. Weber KT, Janicki JS: Intra-aortic balloon counterpulsation. Ann Thorac Surg 17:602, 1974. 26. Port SC, Pate1 S, Schmidt DH: Effects of intraaortic balloon counterpulsation on myocardial blood flow in patients with severe coronary artery disease. JACC 3:1367, 1984. 27. Leinbach RC, Buckley MJ, Austen WC, Petscheck HE, Kantrowitz AR, Sanders CA: Effects of intraaortic balloon pumping on coronary flow and metabolism in man. Circulation 43 and 44(suppl 1):77, 1971. 28. Powell WJ, Daggett WM, Margo AE, Bianco JA, Buckley MJ, Sanders CA, Kantrowitz AR, Austen WG: Effects of intraaortic balloon counterpulsation on cardiac performance, oxygen consumption, and coronary blood flow in dogs. Circ Res 26:753, 1970. 29. Ganz W, Tamura K, Marcus HS, Conoso R, Yoshida S, Swan HJC: Measurement of coronary sinus blood flow by continuous thermodilution in man. Circulation 44:181, 1971. 30. Pepine CJ, Mehta J, Webster WW Jr, Nichols WW: In vivo validation of a thermodilution method to determine regional left ventricular blood flow in patients with coronary disease. Circulation 58:795, 1978. 31. Brazier J, Cooper N, Buckberg GD: The adequacy of subendocardial oxygen delivery: The interaction of determinants of flow, arterial oxygen content and myocardial oxygen need. Circulation 49:968, 1974. 32. Buckberg GD, Fixler DE, Archie JP, Hoffman JIE: Experimental subendocardial ischemia in dogs with normal coronary arteries. Circ Res 30:67, 1972. 33. Lueptow RM, Karlen JM, Kamm RD, Shapiro AH: Circulatory model studies of external cardiac assist by counterpulsation. Cardiovas Res 15:443, 1981. 34. Hoffman JIE, Buckberg GD: Transmural variations in mgocardial perfusion. In YuPH, Goodwin JF, editors: Progress in cardioloev. Philadelnhia. 1976. Lea & Febizer. D 37. 35. Rouleau-J, Boerboom LE, Surjadhana A, Hoffman JIE: The role of autoregulation and tissue diastolic pressures in the transmural distribution of left ventricular hlood flow in anesthetized dogs. Circ Res 45:804, 1979. 36. Cohen LS, Mullins CB, Mitchell JH, Alsobrook HD: Sequenced external counterpulsation and intraaortic balloon pumping in cardiogenic shock. Am d Cardiol 32:656, 1973.