Coronary Artery Flow Velocity Research Articles

Chronic myocardial hibernation in humans. From bedside to bench.

Since the pioneering work of Tennant and Wiggers,1 it has been known that total ischemia leads to a prompt cessation of contraction and eventually results in the appearance of cell damage and irreversible myocardial necrosis. Accordingly, in the minds of many cardiologists, the discovery of an abnormal regional contraction in a patient with coronary artery disease has long been equated with the presence of irreversible myocardial necrosis. With the advent of recanalization therapy, however, evidence progressively accumulated that prolonged regional “ischemic” dysfunction did not always arise from irreversible tissue damage and, to some extent, could be reversed by restoration of blood flow.2 3 4 5 These observations have led to the speculation that chronically hypoperfused myocardium, which is often referred to as “hibernating,”2 3 4 5 6 could maintain viability by simply reducing its metabolic demand to match the decreased supply for as long as myocardial perfusion was inadequate. The chronic impairment of contractile function in this setting has been regarded as a protective mechanism by which the heart spontaneously downgrades its myocardial function, minimizes its energy requirements, and prevents the appearance of irreversible tissue damage.2 4 5 The concept of chronic hibernation thus consists of two parts: a unique clinical observation that bears important implications for the management of patients with chronic coronary artery disease2 3 4 5 6 and a pathophysiological hypothesis, yet to be demonstrated, implying that the chronic dysfunction is due to a chronic reduction of resting MBF.4 5 Other aspects that were not included in the original description, ie, the rapidity of mechanical recovery after successful revascularization7 and the response of dysfunctional myocardium to inotropic stimulation, are now also considered to be integral parts of this condition. The purpose of this discussion is to review some of the …

Heart disease: functional evaluation with MR imaging.

Diagnosis of cardiovascular disease requires precise assessment of both morphology and function. Nearly all aspects of cardiovascular function can be quantified with fast magnetic resonance (MR) imaging techniques. Conventional and breath-hold cine MR imaging can provide precise and highly reproducible measurements of global and regional function of the left and right ventricles. Velocity-encoded cine (VEC) MR imaging provides measurements of blood flow in the heart and great vessels. Contrast-prepared fast gradient-echo sequences can be used to monitor the first-pass dynamics of contrast media, thus defining selective regional myocardial perfusion. Recently, the feasibility of using breath-hold VEC MR imaging to measure flow velocity in native coronary arteries and coronary revascularization conduits has been shown. This will most likely provide a noninvasive method for testing coronary vasodilator reserve and may emerge as a new method for detecting asymptomatic coronary artery disease.

Visualization and registration of coronary artery flow velocity by transthoracic 2D Doppler echocardiography: Preliminary observations: Folkert J. Ten Cate, Willem B. Vletter, Marcel M. Kofflard, P.M. Fioretti. Thoraxcenter, University Hospital and Erasmus University, Rotterdam, The Netherlands

Visualization and registration of coronary artery flow velocity by transthoracic 2D Doppler echocardiography: Preliminary observations: Folkert J. Ten Cate, Willem B. Vletter, Marcel M. Kofflard, P.M. Fioretti. Thoraxcenter, University Hospital and Erasmus University, Rotterdam, The Netherlands

Relation between symptoms and profiles of coronary artery blood flow velocities in patients with aortic valve stenosis: a study using transoesophageal Doppler echocardiography.

To analyse profiles of coronary artery flow velocity at rest in patients with aortic stenosis and to determine whether changes of the coronary artery flow velocities are related to symptoms in patients with aortic stenosis. A prospective study investigating the significance of aortic valve area, pressure gradient across the aortic valve, systolic left ventricular wall stress index, ejection fraction, and left ventricular mass index in the coronary flow velocity profile of aortic stenosis; and comparing flow velocity profiles between symptomatic and asymptomatic patients with aortic stenosis using transoesophageal Doppler echocardiography to obtain coronary artery flow velocities of the left anterior descending coronary artery. Tertiary referral cardiac centre. Fifty eight patients with aortic stenosis and 15 controls with normal coronary arteries. Adequate recordings of the profile of coronary artery flow velocities were obtained in 46 patients (79%). Left ventricular wall stress was the only significant haemodynamic variable for determining peak systolic velocity (r = -0.83, F = 88.5, P < 0.001). The pressure gradient across the aortic valve was the only contributor for explaining peak diastolic velocity (r = 0.56, F = 20.9, P < 0.001). Controls and asymptomatic patients with aortic stenosis (n = 12) did not differ for peak systolic velocity [32.8 (SEM 9.7) v 27.0 (8.7) cm/s, NS] and peak diastolic velocity [58.3 (18.7) v 61.9 (13.5) cm/s, NS]. In contrast, patients with angina (n = 12) or syncope (n = 8) had lower peak systolic velocities and higher peak diastolic velocities than asymptomatic patients (P < 0.01). Peak systolic and diastolic velocities were -7.7 (22.5) cm/s and 81.7 (17.6) cm/s for patients with angina, and -19.5 (22.3) cm/s and 94.0 (20.9) cm/s for patients with syncope. Asymptomatic patients and patients with dyspnoea (n = 14) did not differ. Increased pressure gradient across the aortic valve and enhanced systolic wall stress result in characteristic changes of the profile of coronary flow velocities in patients with aortic stenosis. Decreased or reversed systolic flow velocities are compensated by enhanced diastolic flow velocities, particularly in patients with angina and syncope. This characteristic pattern of the profile of coronary artery flow velocities in patients with angina or syncope may be useful for differentiating those patients from asymptomatic patients.

Effect of percutaneous cardiopulmonary support on coronary artery flow velocity

Effect of percutaneous cardiopulmonary support on coronary artery flow velocity

Effect of various atrio-ventricular intervals on coronary artery flow velocity profiles in dual chamber pacemakers

Effect of various atrio-ventricular intervals on coronary artery flow velocity profiles in dual chamber pacemakers

Coronary Arterial Flow-Velocity Dynamics in Children With Angiographically Normal Coronary Arteries

There have been few reports about coronary hemodynamics in children during the process of growth. In the present study, to assess the characteristics of coronary flow dynamics in children, we examined the phasic coronary flow-velocity (CFV) patterns at rest and during peak hyperemic responses in children with angiographically normal coronary arteries. Spectral Doppler phasic coronary flow velocity was recorded with a 0.018-in intracoronary Doppler guidewire at rest and during peak responses after intracoronary bolus injection of ATP in 30 patients with Kawasaki's disease (age, 8.2 +/- 5.1 years; 24 boys and 6 girls) without angiographic coronary lesions. Average peak velocity (APV), maximum peak velocity (MPV), and diastolic-to-systolic velocity ratio (DSVR) were evaluated in the left anterior descending coronary artery (LAD), left circumflex artery (LCx), and right coronary artery (RCA). Coronary vasodilator reserve (coronary flow reserve [CFR]) was calculated as the ratio of ATP-induced hyperemic to baseline APV. Flow-velocity parameters in RCA were significantly lower than those in the LAD and LCx in both proximal and distal portions. Although the distal LCx had significantly lower values of APV and MPV than did the proximal LCx, there was no significant difference between the proximal and distal portions of the LAD and RCA for APV and MPV. All three coronary vessels showed a diastolic dominant flow pattern in each segment. This coronary flow pattern was less marked in the RCA than in the LCA. All three coronary vessels showed a significant increase in APV and a significantly decrease in DSVR after ATP administration. CFR was significantly lower in the LCx than in the LAD or RCA (P < .01: 1.93 +/- 0.34 in LCx versus 2.32 +/- 0.42 in LAD and 2.37 +/- 0.44 in RCA). From the view of aging, it was revealed that APV values in three vessels were higher in the younger group than in the older group. CFR values in the LAD and LCx were significantly lower in the younger group than in the older group (P < .001 in LAD: 2.01 +/- 0.28 in the younger versus 2.53 +/- 0.37 in the older; P < .01 in LCx: 1.61 +/- 0.15 in the younger versus 2.06 +/- 0.31 in the older). In addition, intracoronary injection of ATP did not increase the absolute angiographic coronary luminal diameter. With the use of an intracoronary Doppler guidewire, we demonstrated that there are some characteristic findings in CFV dynamics in childhood. These physiological characteristics in CFV dynamics that occur with aging and occur in each vessel must be taken into consideration in the study of the coronary circulation in children.

Effect of Chronic Dynamic Cardiomyoplasty on Coronary Arterial Blood Flow Velocity

Effect of Chronic Dynamic Cardiomyoplasty on Coronary Arterial Blood Flow Velocity

Impairment of flow-dependent coronary dilation in hypertensive patients: Demonstration by cold pressor test induced flow velocity increase

In normal coronary arteries, increased flow velocity induces endothelium-dependent dilation, and dilation in response to sympathetic stimulation evoked by the cold pressor test is partly due to increased flow velocity. In arterial hypertension, angiographically normal coronary arteries were constricted by acetylcholine, an endothelium-dependent vasodilator. To assess the epicardial coronary artery response to the increase blood flow velocity induced by the cold pressor test in hypertensive patients with angiographically normal coronary arteries, coronary artery diameters and flow velocity were measured during cold pressor test in 12 untreated hypertensive patients and in 10 control subjects. Diameters were determined by quantitative angiography on proximal and distal segments of the left anterior descending coronary artery, and flow velocity measurements were made by Doppler testing in the distal segment. In control subjects, the proximal and distal segments dilated during cold pressor test by 12.0 +/- 4.5% and 13.9 +/- 6.5%, respectively (both P < .001), when flow velocity increased by 46.7 +/- 26.1% (P > .05). In hypertensive patients, segments were constricted, respectively, by 10.3 +/- 8.5% (P < .001) and 7.9 +/- 8.6% (P < .01), when the flow velocity was increased by 68.3 +/- 48.2% (P < .001). Intracoronary injection of an endothelium-independent dilator resulted in similar dilation in control subjects (proximal: +30.0 +/- 12.9%; distal: +32.4 +/- 15.2%) and in hypertensive patients (proximal: +22.3 +/- 7.5%; distal: +28.8 +/- 15.4%). In conclusion, in hypertensive patients with angiographically normal coronary arteries and without any other coronary risk factors, endothelium-dependent flow-mediated coronary dilation evoked by the cold pressor test is impaired.(ABSTRACT TRUNCATED AT 250 WORDS)

983-31 A New Coronary Artery Autoperfusion Dilatation Catheter

Standard coronary balloon angioplasty (SBA) is limited by the development of myocardial ischemia during balloon inflation. We describe a new autoperfusion dilatation catheter (GAP catheter) where blood flow occurs around the angioplasty balloon. Arterial morphology changes following GAP angioplasty were assessed in a swine atherosclerotic plaque model and compared to SBA (N = 5). In order to assess coronary flow and the development of significant ischemia during GAP angioplasty, arterial pressure (BP). heart rate (HR), ECG and distal average peak coronary artery flow velocity(APV) (Doppler flow wire, Cardiometrics, Inc.) were determined in 7 dogs during 15 seconds of SBA and 60 minutes of continuous GAP angioplasty in 12 vessel segments, using 3.0–3.5 mm balloons, inflated to 6 atmospheres pressure. Distal flow dropped to zero during SBA in all animals. Results during GAP angioplasty are as follows:Empty CellMinutes of Perfusion Angioplasty with GAP510204060HR*103 ± 4101 ± 5103 ± 598 ± 5100 ± 4Systolic BP*96 ± 797 ± 798 ± 7103 ± 6101 ± 6APV*69 ± 771 ± 876 ± 783 ± 876 ± 7*data expressed as percent of baseline data expressed as percent of baseline There were no arrhythmias during GAP angioplasty. Similar morphologic changes in the dilated plaque occurred following GAP and SBA. Hemodynamic stability and maintenance of distal coronary flow velocity between 69% and 83% of baseline occur during a 60 minute inflation with a new autoperfusion angioplasty catheter. The absence of arrhythmias and stable hemodynamics suggest that significant ischemia during angioplasty is prevented with this new device. Histopathologic analysis following GAP angioplasty shows no differences compared to SBA. The GAP design can be adapted to any standard balloon catheter.

Role of Adenosine in Postischemic Dysfunction of Coronary Innervation

We sought to determine the role of adenosine in the sustained but reversible decrease in cardiac neurotransmission that occurs after brief ischemia. Adult mongrel dogs were anesthetized and instrumented for measurements of heart rate, arterial pressure, and left anterior descending coronary artery (LAD) and left circumflex coronary artery (LCX) flow velocities. Changes in coronary vascular resistance were measured during bilateral stimulation of the stellate ganglia. After beta-adrenergic blockade and bilateral vagotomy, stellate stimulation increased coronary vascular resistance in the LAD and LCX beds 28 +/- 2% and 30 +/- 3%, respectively. After a 15-minute infusion of adenosine into the LAD, the peak increase in LAD resistance was significantly reduced (18 +/- 2%) compared with LCX (34 +/- 5%) and control (P < .05, n = 6) resistance. The LAD response after infusion of the vasodilator papaverine was unchanged (n = 6). Intracoronary infusion of adenosine deaminase (n = 10) but not vehicle (n = 5) into the LAD during a 15-minute LAD occlusion prevented the attenuation in constriction to stellate stimulation. We conclude that adenosine, exogenously infused or endogenously produced, is capable of reducing cardiac neurotransmission.

Effects of intraaortic balloon counterpulsation on flow velocity in stenotic left main coronary arteries from transesophageal echocardiography

Effects of intraaortic balloon counterpulsation on flow velocity in stenotic left main coronary arteries from transesophageal echocardiography

Effect of dynamic cardiomyoplasty on phasic coronary arterial flow velocity in canine hearts

The usefulness of dynamic cardiomyoplasty has been demonstrated repeatedly, both experimentally and clinically. Although clinical applications of dynamic cardiomyoplasty to ischemic heart disease have been reported, its effect on the coronary blood flow has never been discussed. Therefore, we tested the hypothesis that dynamic cardiomyoplasty might adversely affect coronary arterial blood flow through compression of the coronary arteries during systolic skeletal muscular contraction and incomplete relaxation of the skeletal muscle flap during diastole. Dynamic cardiomyoplasty was performed in seven mongrel dogs with the use of a left latissimus dorsi muscle flap, paced synchronously with the R wave of the electrocardiogram. A 3F Doppler catheter was placed in the left main trunk of the coronary artery to assess the instantaneous changes of coronary flow velocity by fast Fourier transformation analysis. We compared systolic and diastolic properties during assisted versus unassisted cardiac cycles by calculating the peak velocity and the time-velocity integral. During assisted cardiac cycles, a significant enhancement of coronary arterial blood flow velocity was demonstrated by significant increases in both systolic and diastolic peak velocity (26.9% ± 6.5%, p < 0.005; 4.0% ± 1.6%, p < 0.05, respectively) and time-velocity integral (20.9% ± 4.8%, p < 0.05; 10.0% ± 4.6%, p < 0.05, respectively). Enhancement of coronary arterial blood flow velocity was associated with an increase in mean aortic pressure (16.4% ± 1.3%, p < 0.005) and descending aortic flow (67.5% ± 5.3%, p < 0.005). Also, the improved systolic coronary arterial blood flow velocity was consistent with an increase in systolic aortic pressure (15.8% ± 1.5%, p < 0.005), and enhancement of diastolic coronary arterial blood flow velocity was associated with an increase in diastolic aortic pressure (8.6% ± 2.3%, p < 0.01). We concluded that coronary arterial blood flow velocity was increased by the enhancement of cardiac function as a result of dynamic cardiomyoplasty, leading to an increase of coronary perfusion pressure and cardiac output. (J THORAC CARDIOVASC SURG 1994;108:609-15)

Doppler flow velocity measurements during coronary angioplasty.

In addition to further studies using Doppler catheters to assess blood flow velocity during coronary angioplasty this study intends to evaluate the functional significance of coronary stenoses and to estimate their hemodynamic relevance prior to and after percutaneous transluminal coronary angioplasty (PTCA). Diameters of coronary artery stenoses were quantified by means of the cardiovascular angiographic analysis system (CAAS) both prior to and following successful PTCA in 37 patients. During coronary artery angioplasty a 12 M:Hz 0.018-in. Doppler-tipped guidewire was used to measure prestenotic and poststenotic parameters of coronary artery flow velocity both prior to and following PTCA. The minimal stenosis diameter was raised from 1.01 +/- 0.58 to 1.76 +/- 0.73 mm (P < 0.0001), the percent diameter stenosis decreased from 63 +/- 11 to 35 +/- 6% (P < 0.0001). Prestenotic average (APV) and maximum peak velocity (MPV), peak velocity integral (PVI), average systolic (ASPV) and diastolic (ADPV) peak velocity, systolic (SPVI) and diastolic (DPVI) peak velocity integral, and diastolic/systolic velocity ratio showed--in contrast to further studies--a considerably significant difference (P < 0.05), whereas poststenotic Doppler data (APV, MPV, PVI, ASPV, DSPV, SPVI, DPVI, DSVR) differed highly significantly (P < 0.0001) prior to and following PTCA. Prestenotic and poststenotic measurements of coronary artery flow velocity differed significantly before and after PTCA and offer the potential for estimating both the hemodynamic relevance of coronary artery stenoses and success of PTCA.

Flow velocity quantification in human coronary arteries with fast, breath-hold MR angiography.

Measurement of coronary artery flow velocities has, until now, largely required the use of invasive technologies. The authors have implemented a breath-hold magnetic resonance (MR) angiography technique for depicting the coronary arteries and for quantifying flow velocities. The method was tested in flow phantoms and then applied to a series of subjects: 11 subjects were studied at rest, and four were studied before and during pharmacologic stress induced by intravenous adenosine. Flow velocities at rest in the midportion of the right coronary artery were 9.9 cm/sec +/- 3.5 (n = 12); in the proximal left anterior descending coronary artery, they were significantly higher, measuring 20.5 cm/sec +/- 5.2 (n = 6). With adenosine, flow velocities typically increased at least fourfold. The authors conclude that noninvasive measurement of coronary artery flow velocities is feasible with MR angiography; this method may prove useful for determining the physiologic significance of coronary artery stenosis.

Decreased mid-to-late diastolic decay of diastolic coronary artery flow velocity in pressure-overloaded left ventricular hypertrophy.

This study was carried out to investigate the characteristics of coronary arterial flow in left ventricular hypertrophy secondary to systemic hypertension. The blood velocities in the left anterior descending coronary artery (LAD) were measured by a No. 3F 20 MHz Doppler catheter in 23 hypertensive patients with left ventricular hypertrophy (systolic/diastolic pressure: 181 +/- 15/100 +/- 4 mmHg) and 13 patients with atypical chest pain, but without left ventricular hypertrophy and any abnormal hemodynamic findings. All patients had normal coronary arteriograms. The LAD blood velocity waveforms in pressure overloaded left ventricular hypertrophy were characterized by both a decreased mid-to-late diastolic deceleration rate (delta V/delta T) and a normalized value of delta V/delta T by peak diastolic velocity [delta V/(delta T.Vpeak)], as well as delayed early diastolic inflow (time for diastolic rise; TDR). The values of the delta V/(delta T.Vpeak) in the patients with hypertensive left ventricular hypertrophy and in the normotensive controls were 1.26 +/- 0.61 and 3.03 +/- 1.18/s, respectively (P < 0.001). The TDR was 145 +/- 56 and 66 +/- 15 ms (P < 0.001). In patients with hypertensive left ventricular hypertrophy, the delta V/(delta T.Vpeak) correlated well with the degree of hypertrophy (r = 0.75, P < 0.01) and with the TDR (r = 0.82, P < 0.01). The coronary flow reserve, calculated from the ratio of the diastolic mean velocity after intracoronary injection of papaverine to the resting flow velocity increased with the delta V/(delta T.Vpeak) (r = 0.68, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Alterations of coronary collateral blood flow velocity during intraaortic balloon pumping

Controversy exists regarding the ability of intraaortic balloon pumping to increase coronary blood flow either directly or through collateral perfusion. 1–4 In patients, directly measured coronary flow velocity by intracoronary Doppler guidewire technique distal to severe coronary stenoses is minimal and unaffected by intraaortic balloon pumping. 5 After coronary angioplasty, intraaortic balloon pumping increases both proximal and, more importantly, distal coronary artery flow velocity. 5 Whether collateral flow is altered during intraaortic balloon pumping has not been adequately studied in humans because of a lack of quantitative means to assess collateral blood flow. 6 With the use of a Doppler-tipped angioplasty guidewire, retrograde collateral flow velocity can be directly measured, and thus quantitate the effects of interventions altering collateral blood flow responses. 7 While performing angioplasty with the Doppler guidewire, we quantitated intracoronary collateral blood flow alterations during intraaortic balloon pumping in 3 patients: 2 with acute myocardial infarction and 1 with unstable angina. These observations using flow velocity techniques to evaluate perturbations of collateral flow are the first physiologic demonstrations in patients of one of the unique hypothesized beneficial antiischemic mechanisms of intraaortic balloon pumping.

Response of collateral-dependent myocardium to vasopressin release during prolonged intense exercise.

We hypothesized that vasopressin concentrations during exercise attenuate the increase in collateral-dependent blood flow leading to left ventricular dysfunction in Ameroid-occluded miniswine. An Ameroid occluder was placed around the proximal left circumflex coronary artery (LCX) of 19 miniswine. Ten weeks later V1 receptor blockade with the use of [d(CH2)5Tyr-(Me)]arginine vasopressin (10-12 micrograms/kg iv) increased resting transmural flow (radioactive microspheres) in the LCX region, indicating the presence of V1 receptors. Neither injection of lysine vasopressin (125 pmol/kg) after V1 receptor blockade nor injection of two specific V2 receptor agonists caused changes in mean arterial pressure, heart rate, or left anterior descending coronary arterial flow velocity, indicating that V2 receptors mediate no appreciable vasodilation in the swine coronary circulation. Next the ratio of collateral to noncollateral flow and regional systolic wall thickening (sonomicrometer dimension gauges) were measured at rest and after 20 min of prolonged, intense treadmill exercise (85-90% of heart rate reserve) in the presence and absence of V1 receptor antagonism. This degree of exertion increased plasma lysine vasopressin from 6.2 +/- 1.0 at rest to 21.0 +/- 7.0 pg/ml (P < 0.05) during the unblocked run. However, the decrease in transmural blood flow ratio (collateral to noncollateral flow) from rest was similar during exercise before and after V1 receptor blockade (0.78 +/- 0.07 and 0.80 +/- 0.05, respectively; P < 0.05 vs. rest). Likewise, percent systolic wall thickening in the collateral-dependent region decreased from rest to exercise in the absence and presence of V1 receptor antagonism (35.9 +/- 4.5 and 39.5 +/- 3.8%, respectively; P < 0.05 vs. rest).(ABSTRACT TRUNCATED AT 250 WORDS)

Origin of the left main coronary artery from the right aortic sinus with retroaortic course of the anomalistically arising artery

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Alterations of phasic coronary artery flow velocity humans during percutaneous coronary angioplasty

Background and Objectives. Studies using Doppler catheters to assess blood flow velocity and vasodilator reserve in proximal coronary arteries have failed to demonstrate significant improvement immediately after coronary angioplasty. Measurement of blood flow velocity, flow reserve and phasic diastolic/systolic velocity ratio performed distal to a coronary stenosis may provide important information concerning the physiologic significance of coronary artery stenosis. This study was designed to measure these blood flow velocity variables both proximal and distal to a significant coronary artery stenosis in patients undergoing coronary angioplasty.Methods. A low profile (0.018-in.) (0.046-cm) Doppler angioplasty guide wire capable of providing spectral flow velocity data was used to measure blood flow velocity, flow reserve and diastolic/systolic velocity ratio both proximal and distal to left anterior descending or left circumflex coronary artery stenosis. These measurements were made in 38 patients undergoing coronary angioplasty and in 12 patients without significant coronary artery disease.Results. Significant improvement in mean time average peak velocity was noted in distal coronary arteries after angioplasty (before 19 ± 12 cm/s; after 35 ± 16 cm/s; p < 0.01). Increases in proximal average peak velocity after angioplasty were less remarkable (before 34 ± 18 cm/s; after 41 ± 14 cm/s; p = 0.04). Mean flow reserve remained unchanged after angioplasty both proximal (1.5 ± 0.5 vs. 1.6 ± 1; p > 0.10) and distal (1.6 ± 1 vs. 1.5 ± 0.8; p > 0.10) to a coronary stenosis. Before angioplasty, mean diastolic/systolic velocity ratio measured distal to a significant stenosis was decreased compared with that in normal vessels (1.3 ± 0.5 vs. 1.8 ± 0.5; p < 0.01). After angioplasty, distal abnormal phasic velocity patterns generally returned to normal, with a significant increase in mean diastolic/systolic velocity ratio (1.3 ± 0.5 vs. 1.9 ± 0.6; p < 0.01). Phasic velocity patterns and mean diastolic/systolic velocity ratio measured proximal to a coronary stenosis ware not statistically different from values in normal vessels (1.8 ± 0.8 vs. 1.8 ± 0.5; p > 0.10) and did not change significantly after angioplasty (1.8 ± 0.8 vs. 2.13 ± 0.9; p > 0.10).Conclusions. Flow velocity measurements may be performed distal to a coronary stenosis with the Doppler guide wire. Phasic velocity measurements made proximal to a coronary stenosis differed from those in the distal coronary artery. Both proximal and distal flow reserve measurements made immediately after angioplasty were of limited utility. Changes in distal flow velocity patterns and diastolic/systolic velocity ratio appeared to be more relevant than the hyperemic response in assessing the immediate physiologic outcome of coronary angioplasty.