Intracoronary Doppler Research Articles

Discrepancies Between Morphologic and Functional Changes in Cardiac Allograft Vasculopathy. Assessment by Serial Intracoronary Ultrasound and Doppler Studies

Discrepancies Between Morphologic and Functional Changes in Cardiac Allograft Vasculopathy. Assessment by Serial Intracoronary Ultrasound and Doppler Studies

Restenosis After Coronary Stenting Guided by Intracoronary Doppler Flow Velocity Reserve Measurements

Restenosis After Coronary Stenting Guided by Intracoronary Doppler Flow Velocity Reserve Measurements

Eventfree Survival Following Deferral of Coronary Interventions Based on Relative Flow Velocity Reserve Derived From Intracoronary Doppler Measurements

Eventfree Survival Following Deferral of Coronary Interventions Based on Relative Flow Velocity Reserve Derived From Intracoronary Doppler Measurements

Protected Left Main Angioplasty: Alterations of Intracoronary Doppler Flow Velocity

Coronary blood flow velocity measurements during protected left main coronary angioplasty have not been previously reported. In a patient undergoing angioplasty of left main and circumflex vessels with prior coronary artery bypass grafting, distal coronary flow velocity was measured before, during, and after angioplasty, and again after stenting of the circumflex stenosis. The data demonstrated preserved coronary flow during left main occlusion in this individual and provided new observations that highlight the limitations of our understanding of myocardial blood flow in complex circumstances of high risk angioplasty and interventions following bypass graft surgery.

Eventfree survival following deferral of coronary interventions based on relative flow velocity reserve derived from intracoronary doppler measurements

Eventfree survival following deferral of coronary interventions based on relative flow velocity reserve derived from intracoronary doppler measurements

Restenosis after coronary stenting guided by intracoronary doppler flow velocity reserve measurements

Restenosis after coronary stenting guided by intracoronary doppler flow velocity reserve measurements

Biphasic flow reaction after nitroglycerine provocation in patients with myocardial bridging demostrated by intracoronary doppler flow measurement

Biphasic flow reaction after nitroglycerine provocation in patients with myocardial bridging demostrated by intracoronary doppler flow measurement

Biphasic Flow Reaction After Nitroglycerine Provocation in Patients With Myocardial Bridging Demonstrated by Intracoronary Doppler Flow Measurement

Biphasic Flow Reaction After Nitroglycerine Provocation in Patients With Myocardial Bridging Demonstrated by Intracoronary Doppler Flow Measurement

Comparison of intracoronary Doppler guide wire and transesophageal echocardiography in measurement of flow velocity and coronary flow reserve in the left anterior descending coronary artery

Background The intracoronary Doppler tipped guide wire has been shown to be highly accurate in the measurement of coronary flow velocity (CFV). Recent studies have indicated that blood flow velocity in the left anterior descending coronary artery (LAD) can be determined by transesophageal echocardiography (TEE). The purpose of this study was to compare flow velocity recordings and coronary flow reserve measurements in the LAD by TEE with those obtained by Doppler guide wire. Methods and Results The study population consisted of 14 patients with chest pain and normal coronary arteriograms. After routine coronary arteriography was performed, a 0.014-inch Doppler guide wire was advanced into the proximal part of the LAD. After baseline measurement of coronary flow velocity (CFV) was obtained, 140 μg/kg/min adenosine was administered intravenously for 3 minutes, and the flow velocity was recorded. TEE was performed within 24 hours of the cardiac catheterization. After baseline measurements of CFV in the LAD, heart rate, and blood pressure were obtained, 140 μg/kg/min adenosine was administered intravenously, and the CFV was recorded. Coronary flow reserve was calculated as the ratio of the peak diastolic CFV during adenosine infusion to the peak diastolic CFV at baseline. A good correlation was found ( r = 0.91, p < 0.0001) between CFV by Doppler guide wire and that determined by TEE. A good correlation was also found between the coronary flow reserve assessed by Doppler guide wire and that determined by TEE ( r = 0.92, p < 0.0001). Conclusion Our data indicate that CFV and coronary flow reserve in the LAD can be accurately measured by transesophageal echocardiography. (Am Heart J 1998;135:38-42.)

Coronary blood flow changes during atrioventricular sequential pacing with different atrioventricular delays in normal individuals.

This study examined the effects of different atrioventricular (AV) intervals, during AV sequential pacing, on hemodynamics and coronary blood flow in individuals with normal hearts. Left anterior descending artery blood flow velocity was measured, using intracoronary Doppler, in 17 normal individuals. Five pacing tests were applied in random order for 5 min, at 15 beats/min above the sinus rate. Four tests using AV sequential pacing with AV intervals of 175, 150, 100, and 50 ms, and one using atrial pacing were applied. Mean flow velocity was 21 +/- 9 cm/s, 20 +/- 9 cm/s, 17 +/- 7 cm/s, 17 +/- 7 cm/s, and 22 +/- 10 cm/s, respectively (F = 8.87, p = .00001). The hemodynamic effects of these 5 pacing tests were assessed in 8 different normal subjects. Isovolumic relaxation time constant and left ventricular systolic pressure decreased, whereas right atrial pressure increased during AV sequential pacing with short AV intervals. Thus, during short-term AV sequential pacing at rest, coronary blood flow in a normal left anterior descending artery decreases with short AV intervals.

Relation between Perfusion Status of Dysfunctional Myocardium and Coronary Flow Reserve in Acute Myocardial Infarction

Background：Dysfunction of microvasculature was frequently observed despite of successful revascularization with alteration of coronary flow dynamics in acute myocardial infarction(AMI. Reduction of coronary vasodilatory reserve was found in poorly perfused infarcted myocardium. The objectives of this study was to evaluate the vasodilatory reserve in infarcted myocardium and determined its relationship to perfusion status of myocardium in early recovery phase of acute myocardial infarction. Method：The study subjects consisted of 14 patients with anterior AMI and 6 controls with atypical chest pain and have normal coronary artery. The coronary flow pattern was assessed using intracoronary Doppler wire and vasodilatory reserve was measured after injection of 18μ g of adenosine to infarct-related artery after successful revascularization by percutaneous angioplasty at average 11days post-AMI. After measurement of coronary blood flow pattern, myocardial perfusion status was evaluated by myocardial contrast echocardiography(MCE. Perfusion status by MCE was analysed semiquantitatively and compared to various parameters of coronary flow and vasodilatory reserve of infarct-related artery. Results：After successful revascularization, perfusion defect by MCE was observed in 50%(n＝7 of patients. The vasodilatory reserve was lower in patients with perfusion defect by MCE than those of patients without perfusion defect(p<0.05 and contol(p<0.05. There was no difference in coronary

Magnetic resonance quantification of the myocardial perfusion reserve with a Fermi function model for constrained deconvolution.

The myocardial perfusion reserve, defined as the ratio of hyperemic and basal myocardial blood flow, is a useful indicator of the functional significance of a coronary artery lesion. Rapid magnetic resonance (MR) imaging for the noninvasive detection of a bolus-injected contrast agent as a MR tracer is applied to the measurement of regional tissue perfusion during rest and hyperemia, in patients with microvascular dysfunction. A Fermi function model for the distribution of tracer residence times in the myocardium is used to fit the MR signal curves. The myocardial perfusion reserve is calculated from the impulse response amplitudes for rest and hyperemia. The assumptions of the model are tested with Monte Carlo simulations, using a multiple path, axially distributed mathematical model of blood tissue exchange, which allows for systematic variation of blood flow, vascular volume, and capillary permeability. For a contrast-to-noise ratio of 6:1, and over a range of flows from 0.5 to 4.0 ml/min per g of tissue, the ratio of the impulse response amplitudes for hyperemic and basal flows is linearly proportional to the ratio of model blood flows, if the mean transit time of the input function is shorter than approximately 9 s. The uncertainty in the blood flow reserve estimates grows both at low (< 1.0 ml/min/g) and high (> 3-4 ml/min/g) flows. The predictions of the Monte Carlo simulations agree with the results of MR first pass studies in patients without significant coronary artery lesions and microvascular dysfunction, where the perfusion reserve in the territory of the left anterior descending coronary artery (LAD) correlates linearly with the intracoronary Doppler ultrasound flow reserve in the LAD (r = 0.84), in agreement with previous PET studies.

Direct intracoronary evidence of collateral steal in humans.

Coronary steal is defined as a fall in blood flow toward a certain vascular region in favor of another area during arteriolar vasodilatation, ie, a coronary flow velocity reserve (CFVR) <1. The purpose of this study was to determine the frequency of steal in patients with a wide range of collateral supply to a vascular area of interest and to assess whether steal is associated with the amount of collateral flow. One hundred patients 57+/-9 years old with a coronary artery stenosis to be dilated were examined with intracoronary (IC) Doppler guidewires. IC adenosine-induced CFVR<1 obtained distal to the stenosis was defined as steal. An index for collateral flow was determined by positioning the Doppler guidewire in the collateral-dependent vessel distal to the stenosis and measuring the flow velocity time integral during (Vi(occl), cm) and after (Vi(ø-occl)) balloon occlusion. Vi(occl)/Vi(ø-occl) was determined without and with intravenous adenosine (140 microg x kg(-1) x min(-1)). Coronary steal occurred in 10 of 100 patients. Patients with steal showed superior collaterals compared with those without steal: Vi(occl)/Vi(ø-occl)=0.65+/-0.24 in patients with steal versus 0.29+/-0.18 in those without steal (P=.0001). In all patients with steal, there was a reduction in collateral flow during intravenous adenosine-induced hyperemia, whereas in the majority (70%) of patients without steal, collateral flow increased or remained unchanged during hyperemia. Coronary steal assessed by intracoronary Doppler flow velocity measurements occurs in 10% of patients with a wide range of coronary collaterals to the vascular area from which blood flow is redistributed. There is a direct association between the presence of steal away from and the amount of collateral flow toward the region under investigation. Collateral flow to the vascular region studied decreases during adenosine-induced hyperemia, which indicates a mechanism of steal via the extensive collaterals.

Coronary endothelial dysfunction in humans is associated with myocardial perfusion defects.

Coronary endothelial dysfunction may occur in patients with minimally obstructive coronary artery disease and angina, and potentially may cause myocardial ischemia. Coronary endothelium-dependent vasodilation was examined in patients with angina and <50% coronary artery diameter (CAD) stenosis by selectively infusing acetylcholine (10(-6) mol/L to 10(-4) mol/L) into the left anterior descending coronary artery (LAD). Percent change in CAD (%deltaCAD) was measured by quantitative coronary angiography, and percent change in coronary blood flow (%deltaCBF) was calculated using intracoronary flow Doppler. Coronary endothelium-independent vasodilation was examined using intracoronary adenosine and nitroglycerin. 99mTc sestamibi was injected intravenously just prior to the infusion of the highest dose of acetylcholine. Patients were divided blindly into three groups: Perfusion defects in non-LAD territory (group 1, n=6), no perfusion defects (group 2, n=7), and perfusion defects in the LAD territory (group 3, n=7). All patients had intact endothelium-independent vasodilation. In group 1, perfusion defects outside the LAD territory reflected an increase in %deltaCAD and %deltaCBF by 24+/-5% and 241+/-46% in the LAD. In group 2, %deltaCAD decreased by 26+/-5%, but %deltaCBF increased by 54+/-17%. In group 3, perfusion defects were within the LAD territory, reflecting a decrease in %deltaCAD and %deltaCBF by 35+/-5% and 51+/-14%, respectively. This study demonstrates that coronary endothelial dysfunction in humans may be temporally associated with myocardial perfusion defects and supports a role for the coronary epicardial and microcirculation endothelium in regulating myocardial perfusion. Myocardial ischemia may occur in humans with impaired endothelium-dependent coronary flow reserve of the coronary epicardial and microcirculation.

Lack of evidence for improvement in internal mammary graft flow by occlusion of side branch

Coronary steal due to unligated side branches of an internal mammary artery graft has been reported previously [1-3]. Embolization of these side branches has been shown to result in symptomatic improvement, but objective evidence of improved flow to the coronary artery has been lacking. We studied intracoronary Doppler flow in a patient presenting with symptoms thought to be due to a large unligated side branch of mammary graft. There was no significant change in the mammary flow after balloon occlusion of the side branch. More objective data may be required to routinely prescribe side branch embolization for symptomatic patients with unligated side branches of a mammary graft. Cathet. Cardiovasc. Diagn. 42:291–293, 1997. © 1997 Wiley-Liss, Inc.

Acute effects of conjugated estrogens on coronary blood flow response to acetylcholine in men

Estrogen therapy is associated with a 50% reduction in the clinical manifestations of coronary artery disease in postmenopausal women. Attenuation of coronary vasomotor dysfunction may contribute to estrogen's cardioprotective effects. We hypothesized that conjugated estrogens, which contain several vasoactive estrogenic compounds, may favorably influence the vasomotor response to acetylcholine in men. Twenty men, 56 ± 5 years of age, referred for clinically indicated coronary angiography, participated in this study. Acetylcholine-induced changes in coronary flow were measured by quantitative coronary angiography and intracoronary Doppler ultrasonography before and 15 minutes after intravenous administration of conjugated estrogens (0.625 mg) in 12 men and placebo in 8 men. Initial acetylcholine infusion resulted in no significant increase in coronary blood flow. However, 15 minutes after estrogen administration repeat acetylcholine infusion caused a mean 32% increase in coronary blood flow from 41 ± 5 to 54 ± 8 ml/min (p = 0.02). Acetylcholine-induced change in flow after estrogen was significantly different from that before estrogen (p = 0.03). Placebo administration did not affect acetylcholine-induced changes in coronary flow. Thus, intravenous conjugated estrogens favorably modulate acetylcholine-induced changes in coronary hemodynamics in men. This suggests that novel nonfeminizing estrogenic compounds may have anti-ischemic effects in men.

Evaluation of successful PTCA by transstenotic flow velocity ratios.

Doppler probes mounted on the tip of a guidewire allow the measurement of coronary blood flow velocities, not only proximal but also distal to stenoses eligible for percutaneous transluminal coronary angioplasty (PTCA). The objective of this study was to determine the improvement of transstenotic Doppler flow velocity ratios following PTCA and to investigate the possible impact on restenosis during follow-up control angiography three months later. Doppler flow velocity measurements were performed in 29 patients with 29 stenoses eligible for PTCA. Results of PTCA were morphologically evaluated by computer-assisted quantitative coronary angiography (QCA) and measured hemodynamically by determining transstenotic Doppler flow velocity ratios. Successful PTCA according to QCA was present in all cases with a reduction of mean diameter stenosis from 66 +/- 8% to 35 +/- 7%. Resting spectral peak velocities and velocity integrals were markedly reduced distal to lesions (all P < 0.001), resulting in mean transstenotic flow velocity and velocity integral ratios of less than 0.60 prior to PTCA. Owing to endoluminal enlargement, significant improvement of transstenotic Doppler ratios was observed in mean ratios greater than 0.90 (all P < 0.0001). In patients with restenosis, transstenotic ratios following PTCA demonstrated a tendency to be smaller than in patients without restenosis. Transstenotic Doppler flow velocity ratios are diminished in severe coronary stenoses. Improvement of these ratios provides information on hemodynamic success of interventional procedures. Thus, the determination of intracoronary Doppler flow velocity ratios contributes, in addition to angiographic estimation, to the evaluation of stenoses severity and success of interventional procedures.

Assessment of stenosis severity using a novel method to estimate spatial and temporal variations of blood flow velocity in biplane coronarography

The authors present a novel method to estimate absolute blood flow velocity in coronary arteries from biplane angiograms. Spatial and temporal velocity variations are derived giving simultaneously a direct geometric and an indirect functional index of stenosis severity, stenosis ratio and coronary flow reserve. No prior assumption concerning stenosis geometry is made. Deformable models are used to track a coronary artery segment dynamically in three dimensions. A densitometric map is obtained by summing densities across sections at every position along the previously calculated path and at every time of the cardiac cycle. An advection relationship between density and velocity is observed. The spatiotemporal velocity map is a solution of a nonlinear least-squares scheme. A simulation protocol based on simple geometric conformations and blood flow properties is used to assess numerical stability and immunity towards noise. Predicted results for temporal velocity variations are compared with the intracoronary Doppler recordings to test the model assumptions for basal state and hyperaemia examinations of the same patient. The stenosis ratio was accurate to within 3% for a simulated additive Gaussian noise with a standard deviation of 0.14. The limits of agreement between angiographic and Doppler velocities were -11.4 and for a peak value of (basal state) and -16.8 and for a peak value of (hyperaemia), corresponding to 18 and 3.5% errors on the average peak values and a 16% error on the coronary flow reserve. To summarize, the advection model derivation and its solution are presented. Simulated and experimental results corroborate the validity of the numerical schemes and support clinical applicability.

Bradykinin-Induced Vasodilation of Human Coronary Arteries In Vivo: Role of Nitric Oxide and Angiotensin-Converting Enzyme

Objectives. The present study aimed to determine the role of nitric oxide (NO) and angiotensin-converting enzyme (ACE) in bradykinin (BK)-induced dilation of human coronary arteries in vivo.Background. BK, produced by way of the kinin-kallikrein system, causes endothelium-dependent vasodilation. However, little is known about the mechanism of BK-induced dilation of coronary arteries in humans in vivo.Methods. The effects of an inhibitor of NO synthesis and of an ACE inhibitor on BK-induced coronary vasodilation were examined in 20 patients who had no significant atherosclerotic stenosis in the artery under study. Lumen diameters of the large epicardial coronary arteries and coronary blood flow (CBF) were measured by quantitative coronary arteriography and intracoronary Doppler technique.Results. Intracoronary infusion of BK (0.6 and 2.0 μg/min) increased coronary artery diameter and CBF with no change in arterial pressure or heart rate. The BK-induced increases in coronary artery diameter and CBF were significantly reduced (p < 0.01) after pretreatment with NG-monomethyl-l-arginine (200 μmol) and were significantly increased (p < 0.01) after pretreatment with enalaprilat (50 μg).Conclusions. BK-induced dilation of human large epicardial and resistance coronary arteries is mediated by NO and increased by prior ACE inhibition.(J Am Coll Cardiol 1997;30:108–12)

Isolated Defect of Adenosine-Mediated Coronary Vasodilation: Functional Evidence for a New Microangiopathic Entity

Objectives. The present study describes an isolated defect of the coronary vasodilation in response to adenosine in five patients examined for clinically suspected coronary microangiopathy.Background. Coronary microangiopathies can be defined functionally as dysregulation of the microcirculatory vasomotion.Methods. The five patients were compared with 24 control subjects. Coronary flow velocity was measured with an intracoronary Doppler guide wire (0.018 in. [0.046 cm], 12 MHz) at rest and during intracoronary administration of adenosine (80 μg/min and 160 μg/min over 3 min each), papaverine (10-mg bolus) and acetylcholine (30 μg/min over 5 min). Diameters of the epicardial coronary arteries were measured by quantitative coronary angiography.Results. All subjects (patients and control) exhibited angiographically normal epicardial coronary arteries and normal and comparable endothelium-independent and -dependent vasomotion, as assessed with papaverine (mean [± SD] relative coronary flow reserve 2.62 ± 0.66 vs. 2.97 ± 0.88, p = 0.32) and acetylcholine (volumetric coronary flow reserve 2.61 ± 0.27 vs. 2.91 ± 0.67, p = 0.58), respectively. Affected patients were identified by an isolated complete defect of the adenosine-mediated vasodilation compared with control subjects (relative coronary flow reserve in response to 80 μg/min of adenosine 1.08 ± 0.17 vs. 2.45 ± 0.74 [p < 0.001] and 160 μg/min of adenosine 1.03 ± 0.15 vs. 2.89 ± 0.65 [p < 0.001]).Conclusions. These findings are consistent with functional evidence for a new entity of a coronary microangiopathy affecting a subtype of the endothelium-independent vasomotion.(J Am Coll Cardiol 1997;30:103–7)