Eur J Cardiothorac Surg 2005;28:711-716
© 2005 Elsevier Science NL
Phasic coronary blood flow pattern during a continuous flow left ventricular assist support
Yoshio Ootaki,
Keiji Kamohara,
Masatoshi Akiyama,
Firas Zahr,
Michael W. Kopcak, Jr.,
Raymond Dessoffy,
Kiyotaka Fukamachi
*
Department of Biomedical Engineering, Lerner Research Institute, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA
Received 5 July 2005;
accepted 9 August 2005.
* Corresponding author. Tel.: +1 216 445 9344; fax: +1 216 444 9198. (Email: fukamak{at}ccf.org).
 |
Abstract
|
|---|
Objective: Continuous flow left ventricular assist devices (LVADs) have been introduced and tested as a bridge to heart transplantation, bridge to recovery, and destination therapy, and several studies have been conducted to assess the physiologic effects of continuous flow LVADs. However, the effect of reduced pulsatility on the phasic coronary blood flow pattern is unknown. The aim of this study was to investigate the phasic coronary blood flow patterns during continuous flow LVAD support. Methods: Phasic coronary blood flow patterns and hemodynamic data were analyzed using three flow probes placed around the left anterior descending coronary artery (LAD), left circumflex coronary artery (LCX), and the right coronary artery (RCA) in 16 pigs before and after initiating the LVAD support with or without creating LAD stenosis. Results: The total coronary blood flow (TCBF, 112.8 ± 31.4 mL/min) gradually decreased when the continuous flow LVAD support increased to 2.0 L/min (110.7 ± 29.0 mL/min, P
= 0.571), 2.5 L/min (103.7 ± 26.1 mL/min, P
= 0.079), and 3.0 L/min (101.5 ± 27.2 mL/min, P
= 0.027) because of decreases in LAD flow and LCX flow. LVAD support caused decrease in systolic and peak systolic LAD flow, LCX flow, and RCA flow, whereas diastolic RCA flow increased. In the presence of LAD stenosis, the TCBF (97.7 ± 36.1 mL/min) decreased when the continuous flow LVAD support increased to 2.0 L/min (83.9 ± 22.1 mL/min, P
= 0.029), 2.5 L/min (83.2 ± 25.2 mL/min, P
= 0.012), and 3.0 L/min (87.6 ± 23.4 mL/min, P
= 0.005) because of decreases in LCX flow. Conclusion: Use of a continuous flow LVAD decreased TCBF, LAD flow, and LCX flow secondary to reduced systolic LAD flow and LCX flow, and decreased TCBF and LCX flow in the presence of LAD stenosis. These findings are potentially relevant to understanding the physiology of myocardial blood perfusion during continuous flow LVAD support especially in patients with coronary artery disease.
Key Words: Circulatory assistance Left ventricular assist device Perfusion
 |
1. Introduction
|
|---|
The left ventricular assist device (LVAD) field has experienced a number of striking technical breakthroughs over the past 40 years. The initial clinical experience with implantable, pulsatile LVADs was directed at patients with end-stage heart failure as a bridge to heart transplantation. Recently, a controlled study was undertaken to compare medical treatments and LVAD treatments as destination therapy (REMATCH trial), and it yielded statistically favorable results for recipients of the HeartMate® (Thoratec Corp., Pleasanton, CA) LVAD [1]. Pulsatile LVADs also serve another equally important role as a bridge to recovery. Commercially available, pulsatile LVADs are being used in the United States to provide these therapeutic options.
Recently, continuous flow LVADs, including axial flow and radial (centrifugal) flow pumps, have been introduced and tested [24]. The primary characteristics of the continuous flow LVADs are their small size, diminished pulsatility, and absence of a compliance chamber and prosthetic valves. Several studies have been conducted to assess the physiologic effects of pulsatile and continuous flow LVADs as related to hemodynamics [5], cardiac function [6], autonomic nervous system [7], immune system [8], coagulopathy [9], digestive system [10], cerebral metabolism [11], and morphological change in the aortic wall [12]. However, the effect of reduced pulsatility on the phasic coronary blood flow pattern is unknown. Since LVAD utilization in patients with ischemic cardiomyopathy has increased [1] and the limited supply of donor hearts encourages bridge to recovery use [13,14], assessment of the coronary flow characteristics under reduced pulsatility is required to achieve the best results for bridge to recovery use. The objective of this study was to investigate the phasic coronary blood flow pattern during continuous flow LVAD support.
 |
2. Materials and method
|
|---|
2.1 Animal model
Sixteen pigs weighing 42.961.6 kg (48.5 ± 4.9 kg) were used in this study. This study was approved by the Cleveland Clinic's Institutional Animal Care and Use Committee, and all animals received humane care in accordance with the Guide for the Care and Use of Laboratory Animals published by the National Institutes of Health (National Institutes of Health publication 85-23, revised 1985).
2.2 Anesthesia and surgical preparation
Each animal was anesthetized with an intramuscular injection of ketamine (20 mg/kg), and after intubation, the animal was ventilated through an endotracheal tube with a respirator. Anesthesia was maintained with isoflurane (0.52.5%). ECG leads were attached to the extremities to monitor cardiac vital signs. A venous catheter was placed in a peripheral vein to administer fluids. The respirator settings were adjusted as required based on the results of the arterial blood gas measurement.
The animal was placed on the surgical table in the supine position. A continuous infusion of lidocaine was started at the rate of 1 mg/kg/min before neck incision. A right lateral neck incision was made to isolate the right carotid artery and the jugular vein. An arterial pressure monitoring line was inserted into the right carotid artery, and a venous infusion line and right atrial pressure monitoring line were inserted through the right jugular vein. Pulsatility was quantified by pulse pressure and pulsatility index (pulse pressure/mean arterial pressure) [15]. A median sternotomy was performed, and the infusion rate of lidocaine was increased to 2 mg/kg/min when the pericardium was opened. A left atrial pressure monitoring line was inserted from the left atrial appendage into the left atrium. The pulmonary artery was isolated for placement of a flow probe (16 mm, Transonic Systems, Inc., Ithaca, NY) in order to assess the cardiac output. The right coronary artery (RCA), left anterior descending coronary artery (LAD), and left circumflex coronary artery (LCX) were also isolated for placement of flow probes (SB: 3.0 mm for LAD and LCX, SS: 2.5 mm for RCA, Transonic Systems, Inc.) in order to assess the coronary blood flow pattern during LVAD support. The flow probes measured the cardiac output, LAD flow (LADF), LCX flow (LCXF), and RCA flow (RCAF). We obtained the total coronary blood flow (TCBF) by summing the three coronary flow values. A vascular tourniquet was placed immediately distal to the flow probe of the LAD. A micromanometer-tipped pressure catheter (SPC 350, Millar Instruments, Inc., Houston, TX) was inserted through the left atrium into the left ventricle (LV). The maximum rate of change of LV pressure (LV dp/dt
max) was determined as the first derivative of the LV pressure.
After acquiring data for baseline without stenosis and with stenosis in the LAD, an outflow cannula (20 Fr. arterial cannula, Medtronic Perfusion Systems, Minneapolis, MN) was inserted into the ascending aorta through purse-string sutures. An inflow cannula (32 Fr. venous cannula, Medtronic Perfusion Systems, Minneapolis, MN) was inserted into the LV apex through purse-string sutures. Adequate anticoagulation was confirmed. The inflow and outflow cannulae were connected to the Medtronic centrifugal blood pump (Bio-Pump, Medtronic Perfusion Systems, Minneapolis, MN). A Transonic flow probe was placed around the outflow cannula to monitor the pump output, and the initial pump flow rate was adjusted to deliver 2.0 L/min.
2.3 Intraoperative hemodynamic assessment
Hemodynamic data were taken at baseline, 2.0, 2.5, and 3.0 L/min pump flow without LAD stenosis and with LAD stenosis. The conditions with LAD stenosis were induced by a 50% reduction in mean LADF resulting in a partial stenosis of the LAD. After at least 1 min of hemodynamic stabilization, hemodynamic data were measured in each condition.
2.4 Phasic coronary blood flow pattern
Systolic coronary flow was defined as the flow occurring in the period between the onset of rapid acceleration of TCBF associated with ventricular contraction and the onset of rapid acceleration of TCBF associated with ventricular relaxation. From the time-domain flow signal, the peak flow of the systolic and diastolic flow components was obtained. The time-flow integrals of the systolic and the diastolic flow components were also measured by the time-domain flow signal. Values for each parameter were obtained by averaging measurements from 7 to 10 consecutive cardiac cycles (Fig. 1
).

View larger version (24K):
[in this window]
[in a new window]
|
Fig. 1. Sample cardiovascular data. (ECG: electrocardiogram; CO: cardiac output; LADF: left anterior descending coronary artery flow; LCXF: left circumflex coronary artery flow; RCAF: right coronary artery flow; TCBF: total coronary blood flow.)
|
|
2.5 Statistical analysis
Hemodynamic data were evaluated for each data point. The hemodynamic variables were obtained using a PowerLab data acquisition system (AD Instruments, Inc., Mountain View, CA) and analyzed using a custom-made visual basic program on Excel software (Excel 2000, Microsoft Corporation, CA). All values were expressed as mean ± standard deviation. A paired Student's t test was used to assess the differences between the baseline value and each pump flow condition. Differences were considered significant at P<0.05.
 |
3. Results
|
|---|
All experiments were successfully completed without surgical or device complications. Table 1
shows the hemodynamic data without stenosis in the LAD. Mean right atrial pressure, mean arterial pressure, and cardiac output had no significant differences after initiating the LVAD support. Left atrial pressure, systolic left ventricular pressure, end-diastolic left ventricular pressure, dp/dt
max, systolic arterial pressure, and pulsatility index were significantly lower than baseline values after initiating the LVAD support. Diastolic arterial pressure increased after initiating the LVAD support.
Table 2
shows the hemodynamic data with stenosis in the LAD. Heart rate, mean right atrial pressure, mean arterial pressure, and cardiac output had no significant differences after initiating the LVAD support. Left atrial pressure, systolic left ventricular pressure, end-diastolic left ventricular pressure, dp/dt
max, systolic arterial pressure, and pulsatility index were significantly lower than baseline values after initiating the LVAD support. Diastolic arterial pressure increased after initiating the LVAD support.
Table 3
shows the coronary blood flow data in the conditions without LAD stenosis. The TCBF (112.8 ± 31.4 mL/min) gradually decreased when the pump flow increased to 2.0 L/min (110.7 ± 29.0 mL/min, P
= 0.571), 2.5 L/min (103.7 ± 26.1 mL/min, P
= 0.079), and 3.0 L/min (101.5 ± 27.2 mL/min, P
= 0.027). The mean LADF and LCXF at baseline (34.5 ± 10.2 mL/min; 30.4 ± 17.4 mL/min) gradually decreased after increasing the LVAD flow to 3.0 L/min (27.3 ± 10.3 mL/min, P<0.001; 25.7 ± 13.3 mL/min, P
= 0.023), whereas the mean RCAF had no significant change between baseline (48.0 ± 17.8 mL/min) and 3.0 L/min LVAD support (48.5 ± 16.2 mL/min) (Fig. 2
). The systolic and peak systolic LADF, LCXF, and RCAF significantly decreased after initiating the LVAD (Fig. 3
). The diastolic LADF and LCXF experienced no significant change after initiating the LVAD, whereas the diastolic RCAF significantly increased. The peak diastolic LADF significantly decreased after initiating the LVAD.

View larger version (19K):
[in this window]
[in a new window]
|
Fig. 2. Mean coronary blood flow before and after initiating LVAD support without LAD stenosis. *P<0.05 vs. baseline.
|
|

View larger version (16K):
[in this window]
[in a new window]
|
Fig. 3. Systolic coronary blood flow before and after initiating LVAD support without LAD stenosis. *P<0.05 vs. baseline.
|
|
Table 4
shows the coronary blood flow data in the conditions with LAD stenosis. After creating stenosis in the LAD, peak systolic LADF, peak diastolic LADF, and diastolic LADF decreased, whereas these values were constant after initiating the LVAD support. The TCBF (97.7 ± 36.1 mL/min) decreased when the pump flow increased to 2.0 L/min (83.9 ± 22.1 mL/min, P
= 0.029), 2.5 L/min (83.2 ± 25.2 mL/min, P
= 0.012), and 3.0 L/min (87.6 ± 23.4 mL/min, P
= 0.005). The mean LCXF at the baseline (32.7 ± 21.2 mL/min) gradually decreased after increasing the LVAD flow to 3.0 L/min (23.0 ± 12.1 mL/min, P
= 0.013), whereas the mean RCAF had no significant change between the baseline (47.4 ± 19.7 mL/min) and 3.0 L/min LVAD support (47.1 ± 13.6 mL/min). The systolic and peak systolic LCXF and RCAF significantly decreased after initiating the LVAD (Fig. 4
). The systolic LADF significantly decreased after initiating the LVAD, whereas peak systolic LADF had no significant change. The diastolic LADF and LCXF had no significant change after initiating the LVAD, whereas the diastolic RCAF significantly increased. The peak diastolic LCXF significantly decreased after initiating the LVAD.

View larger version (17K):
[in this window]
[in a new window]
|
Fig. 4. Systolic coronary blood flow before and after initiating LVAD support with LAD stenosis. * P<0.05 vs. baseline.
|
|
 |
4. Comment
|
|---|
Analysis of the phasic coronary blood flow pattern revealed that (1) the decreased TCBF observed during continuous flow LVAD support resulted from decreases in LADF and LCXF, (2) continuous flow LVAD support decreased systolic and peak systolic LADF, LCXF, and RCAF, (3) continuous flow LVAD support increased diastolic RCAF, and (4) continuous flow LVAD support decreased TCBF and LCXF in the presence of LAD stenosis.
There are only a few studies that measured the flows of the LAD, LCX, and RCA simultaneously using three flow probes [16,17]. Grundeman and associates reported the effect of vertical displacement on the beating heart using three flow probes placed around LAD, LCX, and RCA [16]. Ross and Mulder reported the effects of right and left cardiosympathetic nerve stimulation on blood flow in the major coronary arteries using three flow probes in 1969 [17]. However, these measurements did not include an analysis of the phasic coronary blood flow patterns. Our report was the first to analyze the phasic coronary blood flow patterns of all three coronary arteries simultaneously during continuous flow LVAD support in our literature search.
Some reports measured only mean coronary blood flows of the LAD or LCX during continuous flow LVAD support. Tuzun and associates reported that the coronary blood flow of the LAD measured by an ultrasonic flow probe gradually decreased below baseline levels when the Jarvik 2000 axial pump flow increased [18]. Their microsphere study assessing the myocardial tissue blood flow yielded the same result. Merhige and associates reported that LCXF decreased during Hemopump® LVAD support [19]. Pêgo-Fernandes and associates also reported that the Biopump reduced the LCXF [20]. The decreases in the TCBF, LADF, and LCXF during continuous flow LVAD support that we observed in this study were consistent with these reports. The mechanism for these decreased coronary blood flows appeared to be related to effective unloading of the left ventricle and reduced energy demand of the healthy myocardium secondary to decreased LV wall tension, as was previously shown in these studies [1820]. The analysis of the phasic coronary blood flow pattern revealed that systolic LADF and LCXF was reduced and diastolic LADF and LCXF was maintained during continuous flow LVAD support. These analyses suggest that the continuous flow LVAD reduced systolic LADF and LCXF secondary to the diminished pulsatility of the aortic flow, and the diastolic LADF and LCXF was constant since these arteries did not require compensation for the decreased systolic coronary blood flow due to reduced energy demand. On the other hand, the continuous flow LVAD reduced the systolic RCAF secondary to the diminished pulsatility of the aortic flow, and the diastolic RCAF increased to compensate for the decrease during the systolic phase.
Compared with baseline without LAD stenosis, the baseline with LAD stenosis demonstrated a reduction in peak systolic flow, peak diastolic flow, and percentage of LADF during systole, as other investigators have been reported [21,22]. During continuous flow LVAD support in the presence of LAD stenosis, the mean LADF, diastolic LADF, peak systolic LADF, and peak diastolic flow were constant, whereas the systolic LADF was diminished. During systole, distal vascular resistance is high due to myocardial compression and the stenotic resistance is less important. On the other hand, distal vascular resistance is low so that stenotic resistance may limit blood flow during diastole. Kimura and associates reported that intraaortic balloon pumping failed to increase diastolic inflow to the myocardium in the presence of severe coronary artery stenosis [21]. Pulsatility of the inflow may not affect the coronary blood flow in a severely stenotic region.
There are few studies to assess and compare the coronary blood flow with pulsatile and nonpulsatile LVAD support. Nakata and associates reported that mean coronary blood flow and tissue myocardial perfusion had no significant differences between pulsatile and nonpulsatile circulation [23]. However, there is a possible disadvantage of nonpulsatile circulation relative to pulsatile circulation that could become very significant if the devices are used as a destination therapy or a bridge to recovery. Koster and associates reported that the axial flow LVAD strongly influenced the systems of contact activation and fibrinolysis [24]. Cao and Rittgers reported that stagnation in immediate downstream locations of stenotic region might cause platelet adherence and eventual thrombus formation [25]. Reduced peak systolic and diastolic flow in the stenotic region due to continuous flow LVAD might also promote these phenomena. It is likely that the number of the LVAD implantations for patients with ischemic heart disease might increase based upon results of the REMATCH study, in which the average patient age was 67 years and the percentage of heart failure due to ischemic causes was about 78% [1]. Further studies will be needed to compare the effect of a pulsatile LVAD and continuous flow LVAD on phasic coronary blood flow patterns.
For several reasons, the results in this study do not directly contribute to human clinical applications. An obvious limitation of this study is the duration of support after implantation of the continuous flow LVAD. Nishimura and associates reported that prolonged nonpulsatile left heart bypass diminished the constrictive function of the vascular system [7]. In addition, our model was not one of the chronic ischemic heart diseases but rather acute ischemic heart disease. The second limitation of this study is that we did not measure oxygen consumption of the heart before and after initiating an LVAD support. The coronary blood flow decreased probably due to reduced energy demand; however, clinicians have to consider that reduced pulsatility might be a cause of stagnation, especially in the stenotic region [25]. Further studies measuring oxygen consumption will be needed to clarify the phasic coronary blood flow patterns during long-time continuous flow LVAD support using a chronic ischemic heart disease model. The further studies will also provide clinicians with better LVAD selection criteria and identify the optimal methods to support patients who receive continuous flow LVADs in bridge to recovery applications as well as in bridge to transplant and in destination therapy.
In conclusion, use of a continuous flow LVAD decreased the TCBF, LADF, and LCXF secondary to reduced systolic LADF and LCXF, and it decreased TCBF and LCXF in the presence of LAD stenosis. These findings are potentially relevant to understanding the physiology of myocardial blood perfusion during continuous flow LVAD support, especially in patients with coronary artery disease.
 |
References
|
|---|
- Rose EA, Gelijns AC, Moskowitz AJ, Heitjan DF, Stevenson LW, Dembitsky W, Long JW, Ascheim DD, Tierney AR, Levitan RG, Watson JT, Meier P, Ronan NS, Shapiro PA, Lazar RM, Miller LW, Gupta L, Frazier OH, Desvigne-Nickens P, Oz MC, Poirier VL. Long-term mechanical left ventricular assistance for end-stage heart failure. N Engl J Med 2001;345:1435-1443.[Abstract/Free Full Text]
- Wieselthaler GM, Schima H, Hiesmayr M, Pacher R, Laufer G, Noon GP, DeBakey M, Wolner E. First clinical experience with the DeBakey VAD continuous-axial-flow pump for bridge to transplantation. Circulation 2000;101:356-359.[Abstract/Free Full Text]
- Frazier OH, Myers TJ, Gregoric ID, Khan T, Delgado R, Croitoru M, Miller K, Jarvik R, Westaby S. Initial clinical experience with the Jarvik 2000 implantable axial-flow left ventricular assist system. Circulation 2002;105:2855-2860.[Abstract/Free Full Text]
- Saito S, Westaby S, Piggott D, Katsumata T, Dudnikov S, Robson D, Catarino P, Nojiri C. Reliable long-term non-pulsatile circulatory support without anticoagulation. Eur J Cardiothorac Surg 2001;19:678-683.[Abstract/Free Full Text]
- Tominaga R, Smith W, Massiello A, Harasaki H, Golding LA. Chronic nonpulsatile blood flow. II. Hemodynamic responses to progressive exercise in calves with chronic nonpulsatile biventricular bypass. J Thorac Cardiovasc Surg 1996;111:857-882.
- Kono S, Nishimura K, Nishina T, Yuasa S, Ueyama K, Hamada C, Akamatsu T, Komeda M. Autosynchronized systolic unloading during left ventricular assist with a centrifugal pump. J Thorac Cardiovasc Surg 2003;125:353-360.[Abstract/Free Full Text]
- Nishimura T, Tatsumi E, Nishinaka T, Taenaka Y, Masuzawa T, Nakata M, Takano H. Diminished vasoconstrictive function caused by long-term nonpulsatile left heart bypass. Artif Organs 1999;23:722-726.
- Loebe M, Koster A, Sanger S, Potapov EV, Kuppe H, Noon GP, Hetzer R. Inflammatory response after implantation of a left ventricular assist device: comparison between the axial flow MicroMed DeBakey VAD and the pulsatile Novacor device. ASAIO J 2001;47:272-274.[CrossRef][Medline]
- Koster A, Loebe M, Hansen R, Potapov EV, Noon GP, Kuppe H, Hetzer R. Alterations in coagulation after implantation of a pulsatile Novacor LVAD and the axial flow MicroMed DeBakey LVAD. Ann Thorac Surg 2000;70:533-537.[Abstract/Free Full Text]
- Hamulu A, Atay Y, Yagdi T, Discigil B, Bakalim T, Buket S, Bilkay O. Effects of flow types in cardiopulmonary bypass on gastric intramucosal pH. Perfusion 1998;13:129-135.[Abstract/Free Full Text]
- Nishinaka T, Tatsumi E, Nishimura T, Taenaka Y, Imada K, Takano H, Koyanagi H. Effects of reduced pulse pressure to the cerebral metabolism during prolonged nonpulsatile left heart bypass. Artif Organs 2000;24:676-679.[CrossRef][Medline]
- Nishimura T, Tatsumi E, Takaichi S, Taenaka Y, Wakisaka Y, Nakatani T, Masuzawa T, Takewa Y, Nakamura M, Endo S, Nakata M, Takano H. Prolonged nonpulsatile left heart bypass with reduced systemic pulse pressure causes morphological changes in the aortic wall. Artif Organs 1998;22:405-410.[CrossRef][Medline]
- Stevenson LW, Rose EA. Left ventricular assist devices: bridges to transplantation, recovery, and destination for whom?. Circulation 2003;108:3059-3063.[Free Full Text]
- Frazier OH, Delgado RM. Mechanical circulatory support for advanced heart failure: where does it stand in 2003? Circulation 2003;108:3064-3068..
- Kihara S, Litwak KN, Nichols L, Litwak P, Kameneva MV, Wu Z, Kormos RL, Griffith BP. Smooth muscle cell hypertrophy of renal cortex arteries with chronic continuous flow left ventricular assist. Ann Thorac Surg 2003;75(178-183):183.[Free Full Text]
- Grundeman PF, Borst C, van Herwaarden JA, Verlaan CW, Jansen EW. Vertical displacement of the beating heart by the octopus tissue stabilizer: influence on coronary flow. Ann Thorac Surg 1998;65:1348-1352.[Abstract/Free Full Text]
- Ross G, Mulder DG. Effects of right and left cardiosympathetic nerve stimulation on blood flow in the major coronary arteries of the anaesthetized dog. Cardiovasc Res 1969;3:22-29.[Abstract/Free Full Text]
- Tuzun E, Eya K, Chee HK, Conger JL, Bruno NK, Frazier OH, Kadipasaoglu KA. Myocardial hemodynamics, physiology, and perfusion with an axial flow left ventricular assist device in the calf. ASAIO J 2004;50:47-53.[CrossRef][Medline]
- Merhige ME, Smalling RW, Cassidy D, Barrett R, Wise G, Short J, Wampler RK. Effect of the hemopump left ventricular assist device on regional myocardial perfusion and function. Reduction of ischemia during coronary occlusion. Circulation 1989;80:III158-III166.
- Pêgo-Fernandes PM, Stolf NA, Moreira LF, Fabri HA, Leirner AA, Oliveira SA, Jatene AD. Influence of biopump with and without intraaortic balloon on the coronary and carotid flow. Ann Thorac Surg 2000;69:536-540.[Abstract/Free Full Text]
- Kimura A, Toyota E, Lu S, Goto M, Yada T, Chiba Y, Ebata J, Tachibana H, Ogasawara Y, Tsujioka K, Kajiya F. Effects of intraaortic balloon pumping on septal arterial blood flow velocity waveform during severe left main coronary artery stenosis. J Am Coll Cardiol 1996;27:810-816.[Abstract]
- Crowley JJ, Shapiro LM. Analysis of phasic flow velocity dynamics in the left anterior descending coronary artery before and after angioplasty using transthoracic echocardiography in patients with stable angina pectoris. Am J Cardiol 1997;80:614-617.[CrossRef][Medline]
- Nakata K, Shiono M, Orime Y, Hata M, Sezai A, Saitoh T, Sezai Y. Effect of pulsatile and nonpulsatile assist on heart and kidney microcirculation with cardiogenic shock. Artif Organs 1996;20:681-684.[Medline]
- Koster A, Loebe M, Hansen R, Potapov EV, Noon GP, Kuppe H, Hetzer R. Alterations in coagulation after implantation of a pulsatile Novacor LVAD and the axial flow MicroMed DeBakey LVAD. Ann Thorac Surg 2000;70:533-537.[Abstract/Free Full Text]
- Cao J, Rittgers SE. Particle motion within in vitro models of stenosed internal carotid and left anterior descending coronary arteries. Ann Biomed Eng 1998;26:190-199.[CrossRef][Medline]