Intracoronary blood flow velocity and transstenotic pressure gradient using sensor-tip pressure and doppler guidewires: A new technology for the assessment of stenosis severity in the catheterization laboratory

In a patient undergoing percutaneous balloon angioplasty of a stenotic proximal right coronary artery the transstenotic pressure gradient was measured using a “0.018” guidewire with a distal optical microsensor. Blood flow velocity was measured proximal to the stenosis using a “0.018” Doppler guidewire. Transstenotic pressure gradient and blood flow velocity were measured in baseline conditions and after intracoronary injection of 12.5 mg of papaverine. Coronary blood flow was calculated from the measured blood flow velocity and the corresponding cross-sectional area. The measured pressure gradients were compared with the values derived from the stenosis geometry assessed with quantitative coronary angiography (automated edge detection measurements in two orthogonal views, assuming an elliptical cross-sectional area). The measured transstenotic pressure gradient was 15 mm Hg in baseline conditions and 42 mm Hg at the peak effect of the papaverine injection. A 50% flow velocity increase was observed at peak hyperemia (time-averaged maximal flow velocity = 30 cm/s before and 45 cm/s after papaverine). The transstenotic pressure gradient calculated from the measured stenosis geometry was 20 mm Hg and 42 mm Hg in baseline and hyperemic conditions, respectively. The combined use of a pressure and a Doppler guidewire provides a complete assessment of the transstenotic pressure/coronary flow velocity relation at rest and after pharmacologically induced hyperemia and allows the characterization of stenosis hemodynamics and functional severity. © 1993 Wiley-Liss, Inc.     

Comparative evaluation of coronary stenoses using fluid dynamic equations and standard quantitative coronary arteriography

Traditional quantitative coronary arteriographic measurements have largely ignored geometric variables, which may be important in determining the obstructive nature of coronary stenoses. To illustrate the relation between standard quantitative coronary arteriography and calculated transstenotic fluid dynamics, 25 patients with 1-vessel disease referred for coronary angioplasty were analyzed. Minimal lumen diameter and percent stenosis were measured and the values compared with calculations of pressure loss that used standard hydraulic formulas encompassing both frictional and separation components within the stenotic segments. Baseline flow velocity was assumed to equal 4 cm/s and normal hyperemic flow response was presumed to equal 5 times that of baseline. Fluid dynamic estimates suggested that initial translesional pressure gradients would develop at a minimal diameter of 0.6 mm (80% diameter), with an exponentially severe pressure differential beyond a minimal coronary diameter of 0.3 mm (92% diameter). Maximal velocities were calculated based upon an assumed normal hyperemic flow response of 5 times that of baseline, with the demonstration of early impairment of hyperemic flow reserve at minimal diameters of 1.2 mm (46% diameter). Furthermore, hyperemic flow reserve was completely abolished at a minimal diameter of 0.3 to 0.5 mm (89 to 92% diameter). Beyond a minimal diameter of 0.2 mm (93% diameter), resting hypoperfusion was anticipated with flow velocities below the initially assumed value (4 cm/s). Thus, it is feasible to estimate transstenotic pressure losses and maximal coronary flow velocity by applying Newtonian fluid dynamic equations to actual angiographic stenoses in man. These calculations generally correlate with traditional quantitative arteriographic estimates of stenosis severity, although other geometric parameters such as lesion length, "exit angle" and blood viscosity may alter transstenotic hemodynamics.     

Vasoconstriction of stenotic coronary arteries during dynamic exercise in patients with classic angina pectoris: reversibility by nitroglycerin

To study the vasomotility of normal and diseased coronary arteries during dynamic exercise, symptom-limited supine bicycle exercise during cardiac catheterization was performed by 18 patients with classic angina pectoris. The cardiovascular response was assessed by hemodynamic measurements and computer-assisted determination of normal and stenotic coronary artery luminal areas from biplane coronary angiograms made before, during, and after exercise. After baseline measurements were recorded, 12 patients (group 1) performed bicycle exercise for 3.4 min (mean), reaching a maximum workload of 81 W (mean); at the end of exercise they received 1.6 mg sublingual nitroglycerin. After measurements at rest in six other patients (group 2), 0.1 mg intracoronary nitroglycerin was given, followed by exercise (3.8 min, 96 W; NS) and sublingual nitroglycerin as in group 1. During exercise in group 1, luminal area of the coronary stenosis decreased to 71% of resting levels (p less than .001), while area of the normal coronary artery increased to 123% of control (p less than .001). After sublingual nitroglycerin at the end of exercise, area of the normal vessel further increased to 140% of control (p less than .001), while luminal area of the stenosis dilated to 112% of resting levels (p less than .001 vs exercise, NS vs rest). Pretreatment with intracoronary nitroglycerin increased both normal (121%; p less than .05) and stenotic (122%; p less than .05) luminal areas, while preventing the previously observed narrowing of stenosis during exercise (114%; NS). Exercise resulted in a similar heart rate-systolic pressure product and caused angina pectoris in two-thirds of the patients in each group. However, patients pretreated with intracoronary nitroglycerin (group 2) had a lower mean pulmonary arterial pressure during maximum exercise (35 mm Hg) than those patients (group 1) not receiving pretreatment (47 mm Hg; p less than .001). Group 2 patients reached a percentage of their predicted work capacity (65%) that was about the same as that during previous upright bicycle exercise (71%; NS), while group 1 patients had a significantly lower work capacity (51% of predicted) than that before catheterization (82%; p less than .001). Hence, narrowing of coronary artery stenosis during dynamic exercise is attributable to active vasoconstriction due to its reversibility by preexercise intracoronary nitroglycerin. Patients who did not experience narrowing of stenosis during exercise (group 2) had less evidence of myocardial ischemia (lower mean pulmonary arterial pressure) and maintained their work capacity.(ABSTRACT TRUNCATED AT 400 WORDS)     

Effect of intracoronary nitroglycerin administration on phasic pattern and transmural distribution of flow during coronary artery stenosis.

BACKGROUND. Nitroglycerin is effective in relieving myocardial ischemia; however, intracoronary nitroglycerin often fails to relieve angina and has been reported to have deleterious effects on subendocardial blood flow. To understand the mechanisms involved, we evaluated the direct effect of nitroglycerin on coronary circulation of the ischemic hearts. METHODS AND RESULTS. We measured the phasic pattern of intramyocardial coronary arterial flow with an 80-channel, 20-MHz pulsed Doppler ultrasound flowmeter under moderate to severe coronary artery stenosis (distal perfusion pressure approximately 45 mm Hg group 1, n = 6) and transmyocardial blood flow distribution using radioactive microspheres while maintaining coronary pressure at a low constant level (40 mm Hg, group 2, n = 6). In anesthetized open-chest dogs, the left main coronary artery was perfused directly from the right carotid or femoral artery. In this bypass circuit, pressure was controlled with an occluder or a reservoir was connected to the circuit. In group 1, the systolic and diastolic pressures distal to the stenosis decreased significantly after intracoronary administration of nitroglycerin at maximal coronary flow from 66.5 +/- 18.5 to 56.5 +/- 13.8 mm Hg (p less than 0.01) and from 36.6 +/- 14.4 to 27.5 +/- 8.9 mm Hg (p less than 0.01), respectively. The phasic pattern of the septal artery flow was predominantly diastolic and was characterized by systolic reverse flow even in the absence of stenosis. Coronary stenosis increased systolic reverse flow. Nitroglycerin increased diastolic forward flow (p less than 0.05) but augmented systolic reverse flow markedly (p less than 0.001). In group 2, nitroglycerin increased subepicardial flow (p less than 0.05) but failed to increase subendocardial flow. With the administration of nitroglycerin, the subendocardial-to-subepicardial flow ratio decreased significantly from 0.73 +/- 0.19 to 0.32 +/- 0.14 (p less than 0.01). CONCLUSIONS. The increased systolic reverse flow after intracoronary administration of nitroglycerin may be closely related to failure of subendocardial blood flow to increase with increase subepicardial flow.     

Residual coronary stenoses and calculated transstenotic gradients after intravenous streptokinase versus tissue plasminogen activator.

To compare the relative success of intravenous streptokinase (STK) and tissue plasminogen activator (TPA) on the severity of residual infarct-related coronary stenoses, we evaluated 45 patients receiving thrombolytic therapy for acute myocardial infarction. Twenty-three patients (18 men and 5 women) received STK (1.5 million units), while 22 patients (18 men and 4 women) received TPA (100 mg) within 6 hours of chest discomfort. Cardiac catheterization was performed before hospital discharge (8 days) with quantitative coronary arteriography and estimation of transstenotic pressure gradients using fluid dynamic equations. Although angina pectoris was equally common (STK, 7 of 23 [30%] versus TPA, 5 of 22 [23%], p = NS), recurrent infarction (STK, 3 of 23 [13%] versus TPA, 7 of 22 [32%], p less than 0.05) and coronary angioplasty (STK, 2 of 23 [9%] versus TPA, 7 of 22 [32%], p less than 0.05) were more frequent in those receiving TPA. Infarct-related coronary patency was greater in TPA-treated subjects (STK, 15 of 23 [65%] versus TPA, 19 of 22 [86%], p less than 0.05), although minimum stenotic diameter (STK, 0.77 +/- 0.48 mm versus TPA, 0.57 +/- 0.38 mm, p less than 0.05), and calculated transstenotic pressure gradient (STK, 8.7 +/- 17.0 mm Hg versus TPA, 23.7 +/- 30.2 mm Hg, p less than 0.05) suggested severe residual stenosis. These effects were accentuated at elevated coronary flow velocities (8 to 20 cm/sec).(ABSTRACT TRUNCATED AT 250 WORDS)     

Altered coronary flow responses to vasoactive drugs in the presence of coronary arterial stenosis in the dog

Recent in vitro observations of human coronary arteries have suggested that intraluminal pressure can be a determinant of the resistance to flow through the stenosis. This study examined whether similar pressure-dependent changes in stenotic resistance could be observed and analyzed in an open chest, anesthetized, animal model of coronary arterial stenosis. Without stenosis, intracoronary isoproterenol (1 μg) or nitroglycerin (10 μg) increased flow and decreased coronary resistance, whereas methoxamine (500 μg) or vasopressin (0.2 U) decreased flow and increased coronary resistance. After partial arterial constriction, administration of isoproterenol (1 μg) resulted in a decrease in coronary pressure from 61.2 ± 2.5 to 39.4 ± 2.7 mm Hg (p ≤ 0.05), a 23 percent derease in distal coronary resistance (p ≤ 0.05) and a 22 percent decrease in flow associated with an increase in stenotic resistance of 2.34 ± 0.97 (p ≤ 0.05). Similarly, nitroglycerin caused a decrease in coronary pressure from 55.7 ± 3.1 to 42.1 ± 3.6 mm Hg (p ≤ 0.05), a 29 percent increase in distal coronary resistance and only a 1 percent increase in flow associated with a 38 percent increase in stenotic resistance. Methoxamine caused an increase in coronary pressure from 62.8 ± 2.0 to 73.6 ± 3.4 mm Hg (p ≤ 0.05), an 18 percent increase in distal coronary resistance, an 8 percent decrease in flow and a 10 percent decrease in stenotic resistance. Vasopressin caused an increase in coronary pressure from 61.0 ± 1.5 to 99.2 ± 7.1 mm Hg (p ≤ 0.05), a 239 percent increase in distal coronary resistance but only a 45 percent decrease in flow associated with a decrease in stenotic resistance of 1.33 ± 0.91 (p ≤ 0.05).Passive changes in the stenotic area caused by coronary pressure changes are postulated as part of the mechanism for the observed changes in stenotic resistance. This hypothesis is strengthened by the changes in stenotic resistance and radiographic analysis obtained from an in vitro carotid arterial preparation. The pressure-dependency of stenotic resistance could be an additional factor in the treatment of patients with coronary artery disease.     

Acute outcome of directional coronary atherectomy vs standard balloon angioplasty in de novo left anterior descending stenoses.

To assess the immediate outcome of directional coronary atherectomy (DCA) versus standard balloon angioplasty (PTCA) in de novo left anterior descending coronary stenoses, 25 consecutive atherectomies (22 men, 3 women) performed at The Toronto Hospital, between July 1990 and March 1991 were compared with 25 (14 men, 11 women) temporally matched successful angioplasties. Coronary stenoses were analyzed by quantitative arteriography, using the Coronary Measurement System (Leiden, The Netherlands), with estimation of transstenotic hemodynamics by fluid dynamic equations. Before and after procedure qualitative blood flow (TIMI criteria) was also evaluated, as was intimal haziness and coronary dissection. In comparison to PTCA, coronary atherectomy produced less residual minimum stenotic diameter (DCA, 2.75 +/- 0.55 vs PTCA, 1.70 +/- 0.44 mm, p < 0.001), and relative percent diameter stenosis (DCA, 17.9 +/- 10.7 vs PTCA, 34.4 +/- 10.7 percent, p < 0.001), with less transstenotic obstructive gradient (DCA, 0.2 +/- 0.2 vs PTCA, 1.0 +/- 1.5 mm Hg, p < 0.05), and greater estimated stenotic flow reserve (DCA, 4.86 +/- 0.15 vs PTCA, 4.50 +/- 0.48 x baseline, p < 0.05). Coronary atherectomy "normalized" TIMI flow patterns in virtually all patients (DCA, 2.96 +/- 0.20 vs PTCA, 2.72 +/- 0.45, p < 0.05), while creating less intimal haziness (DCA, 10/25 [40 percent] vs PTCA, 23/25 [92 percent], p < 0.01), and coronary dissection (DCA, 6/25 [24 percent] vs PTCA, 16/25 [64 percent], p < 0.05). Therefore, when compared with standard balloon angioplasty, DCA produces less residual stenosis, better transstenotic hemodynamics, while decreasing the frequency of coronary artery damage, in de novo left anterior descending stenoses.     

Comparison of quantitative angiographically derived and measured translesion pressure and flow velocity in coronary artery disease

Although quantitative coronary angiography (QCA) has been used to determine lesion severity, angiographically derived parameters of translesional physiology have not been compared with those directly measured in the same patients. Thus, the aim of this study was to correlate QCA-derived translesional pressure and flow data with directly measured data in patients. QCA (DCI-ACA program), translesional pressure gradient (2.2Fr fluid-filled tracking catheter), and intracoronary Doppler flow velocity (0.018-inch FloWire ^™ measurements were simultaneously performed in 28 arteries (25 patients). Mean diameter stenosis was 51 ± 2.3% (range 29 to 73). No patient had left ventricular hypertrophy or valvular heart disease. The arteries studied were left anterior descending in 14, circumflex in 8, and right coronary in 6 patients. Stenotic flow reserve and baseline and maximal gradients were calculated by the DCI program. Coronary flow reserve and baseline and maximal hyperemic gradients were also directly measured distal to the stenosis after administration of intracoronary adenosine (12 to 18 μg). QCA-derived pressure gradients did not correlate with the measured gradients at baseline (r² = 0.005; p = 0.73) or at maximal hyperemia (r² = 0.1; p = 0.13). No correlation was found between the QCA-predicted flow reserve and the coronary flow reserve measured distal to the stenosis (r² = 0.02; p = 0.46). Furthermore, stenotic flow reserve and measured gradient were not significantly correlated (r² = 0.1; p = 0.16). In this range of stenoses of intermediate severity, there was no correlation between the measured pressure gradient or coronary flow reserve and lesion diameter or cross-sectional area by QCA. These results indicate that due to inherent limitations of angiography and theoretical assumptions of the physiologic state, QCA-derived parameters of translesional physiology, particularly relevant for intermediately severe lesions, do not correlate with directly measured pressure and flow beyond the stenosis. Given these limitations, caution should be applied in utilizing these parameters for clinical decision-making. QCA-derived parameters may benefit from further refinement in determining the hemodynamic significance of coronary stenoses.     

Effect of abruptly increased intrathoracic pressure on coronary blood flow velocity in patients

To assess the effects of abruptly increased intrathoracic pressure on coronary blood flow, arterial pressure, heart rate, and intracoronary Doppler blood flow velocity were measured continuously during cough(s) and again during the four phases of the Valsalva maneuver in 14 patients. Coughing significantly increased the systolic pressure (137 +/- 25 to 176 +/- 30 mm Hg), diastolic pressure (72 +/- 10 to 84 +/- 18 mm Hg), and arterial pulse pressure (65 +/- 27 to 92 +/- 35 mm Hg), with no change in heart rate. The mean coronary flow velocity decreased (17 +/- 10 to 14 +/- 12 cm/sec, p less than 0.03). During the Valsalva maneuver, despite marked reduction in the mean arterial pressure during phase III (96 +/- 12 to 68 +/- 14 mm Hg, p less than 0.05), the reduction of coronary blood flow velocity did not achieve statistical significance. These data demonstrate that neither type of abrupt physiologic increase in intrathoracic pressure enhances coronary blood flow. Coughing does not improve coronary perfusion pressures or flow velocity, despite marked increases in arterial diastolic pressure. The Valsalva maneuver, for the most part, does not significantly alter coronary blood flow velocity.     

Measurement of coronary flow velocity with Doppler catheter: evaluation of coronary flow reserve in successful angioplasty

To assess the therapeutic effect of percutaneous transluminal coronary angioplasty (PTCA) on coronary flow reserve, coronary flow velocity (CFV) was measured with a Doppler catheter before and immediately after PTCA in 11 patients, who underwent elective PTCA for critical stenosis in proximal or mid portion of the left anterior descending artery (LAD). A Doppler catheter was positioned at the proximal portion of the LAD and the CFV was measured at rest and after intracoronary injection of 6 ml of contrast material (Iopamidol), 6 ml of saline or 3 mg of Isosorbide Dinitrate (ISDN). Peak to resting velocity ratio (PRVR) was calculated as an estimate of coronary flow reserve. Percent diameter stenosis (%S) was measured from cineangiogram. A translesional pressure gradient was obtained with an angioplasty catheter. These parameters measured in PTCA candidates were compared with those in 11 patients whose LAD had no critical stenosis. After PTCA, %S was decreased (94.2 +/- 1.4 vs 34.1 +/- 5.1%; mean +/- SEM). Pressure gradient was also decreased (59.5 +/- 4.9 vs. 25.1 +/- 3.3 mmHg). There was no difference between mean CFV at rest in patients before PTCA and that in patients without stenosis (4.52 +/- 0.63 vs. 5.46 +/- 0.61 cm/sec). By successful PTCA, CFV at rest was increased (7.39 +/- 1.32, p less than 0.05 vs. before PTCA). PRVRs in patients before PTCA were smaller than those in patients without stenosis (1.5 +/- 0.1, 1.4 +/- 0.1, 1.6 +/- 0.2 vs. 2.8 +/- 0.1, 2.5 +/- 0.2, 2.8 +/- 0.2, p less than 0.01; by contrast material, saline, ISDN, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Variable effects of intracoronary nitroglycerin on myocardial blood flow and segmental shortening according to dose and degree of coronary occlusion

The effects of intracoronary nitroglycerin were determined in 21 open-chest dogs. Six dogs with severe stenosis (25 mm Hg diastolic perfusion pressure) and nine dogs with moderate stenosis (40 mm Hg) received a 12 micrograms bolus followed by 44 micrograms/min intracoronary nitroglycerin. In addition, six dogs with moderate stenosis (40 mm Hg) received 5 micrograms followed by 5 micrograms/min nitroglycerin. Myocardial blood flow was measured with radioactive microspheres and segment shortening with ultrasonic crystals. At 40 mm Hg, high-dose but not low-dose nitroglycerin raised epicardial blood flow, while at 25 mm Hg nitroglycerin had no effect. Subendocardial blood flow was not affected in any group. Partial occlusion resulted in a decrease in segment shortening in the 25 mm Hg group but not at 40 mm Hg. High-dose nitroglycerin had no effect on shortening at either level of occlusion. Thus, in the presence of coronary vascular reserve, high-dose nitroglycerin may overcome coronary autoregulation. A dose equivalent to one that simulates the amount of nitroglycerin delivered to the coronary circulation by a systemic infusion did not affect myocardial blood flow. In addition, even a large dose of nitroglycerin did not affect segment shortening.     

Coronary wedge pressure: a predictor of restenosis after coronary balloon angioplasty

Coronary wedge pressure is the pressure recorded distal to a stenosis while the inflated balloon occludes the coronary artery during angioplasty. This pressure has been shown to reflect actual (visible) and potential (recruitable) collateral flow to the stenosed artery, distal to the angioplasty site. In 100 consecutive vessels (91 patients) for which coronary wedge pressure had been measured at the time of angioplasty, the long-term (7 +/- 3 months) angiographic results was evaluated. The overall angiographic restenosis rate was 37%. It was 52% (25 of 48) in arteries with a coronary wedge pressure greater than or equal to 30 mm Hg and 23% (12 of 52) in arteries with a coronary wedge pressure less than 30 mm Hg (p less than 0.01). The mean coronary wedge pressure was 30 +/- 10 mm Hg for vessels with restenosis and 26 +/- 9 mm Hg for those without restenosis (p less than 0.01). The prevalence of angiographically visible collateral flow was 42% and 29%, respectively (p = NS). Neither age, sex, presence of unstable angina, left ventricular function, number of diseased vessels nor initial and final transstenotic pressure gradient and degree of stenosis were significantly associated with the long-term outcome after angioplasty. Restenosis rate is significantly increased when coronary wedge pressure measured at the time of angioplasty is high (greater than or equal to 30 mm Hg). This suggests a negative influence of competitive collateral flow on long-term results of angioplasty.     

Abnormal endothelium-dependent coronary vasomotion in hypertensive patients.

Coronary vasomotion is abnormal in hypertensive patients, as evidenced by reduced coronary vasodilator reserve, but endothelium-dependent coronary vasomotion in hypertensive patients has not been studied. To assess the integrity of endothelium-dependent vasodilation, the response of coronary arteries to acetylcholine (an endothelium-dependent vasodilator) and nitroglycerin (an endothelium-independent vasodilator) was studied in 14 patients undergoing cardiac catheterization. Eight patients with essential hypertension were compared with six normotensive patients. None had obstructive disease detectable by coronary arteriography. Coronary artery diameter was measured with digital-subtracted arteriography and coronary blood flow velocity with a Doppler flow velocity catheter. At baseline, coronary artery diameter was similar in the hypertensive and the normotensive control patients (2.4 +/- 0.3 vs. 2.8 +/- 0.7 mm). During intracoronary acetylcholine infusion (30 micrograms/min), coronary artery diameter decreased to 1.3 +/- 0.7 mm in the hypertensive patients (p less than 0.005), but was unchanged (2.7 +/- 0.8 mm) in the normotensive patients. With intracoronary nitroglycerin (200 micrograms), coronary artery diameter increased significantly in both groups. Calculated coronary blood flow decreased during acetylcholine infusion by 59 +/- 31% in the hypertensive patients but increased by 3 +/- 3% in the normotensive group (p less than 0.005). There was a significant negative correlation between the percent change in estimated coronary blood flow during acetylcholine infusion and mean arterial pressure measured at baseline (r = 0.67, p less than 0.02). Therefore, these hypertensive patients exhibited marked coronary vasoconstriction in response to intracoronary acetylcholine but normal vasodilation in response to nitroglycerin, suggesting abnormal endothelium-dependent vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Exercise-induced decrease in flow through stenotic coronary arteries in the dog

In the presence of a coronary stenosis, it is generally believed that exercise-induced ischemia is caused by an inadequate increase in coronary blood flow. This study was carried out to test the hypothesis that, in the presence of a critical coronary stenosis, exercise would result in a decrease in flow across the stenosis. Five dogs were chronically instrumented with a flow probe and a wire snare occluder on the circumflex coronary artery and with catheters in the left atrium, left ventricle, and aorta. Four dogs also had a catheter in the circumflex coronary artery distal to the occluder. Measurements were recorded with the animals resting quietly and then during moderate exercise.

In the absence of a stenosis, circumflex flow increased with exercise. In 13 experiments in which a severe stenosis was produced in the circumflex coronary artery, the changes from rest to exercise were as follows: heart rate from 102 ± 7 to 151 ± 12 beats/min (p < 0.001 ), mean aortic pressure from 103 ± 4 to 107 ± 3 mm Hg (difference not significant), distal circumflex pressure from 71 ± 5 to 36 ± 2 mm Hg (p < 0.001), the pressure gradient across the stenosis from 32 ± 4 to 71 ± 3 mm Hg (p < 0.001), stenosis resistance from 2.3 × 0.7 to 13.9 ± 3.9 units (p < 0.01), and flow through the stenotic artery from 29 ± 4 to 10 ± 3 ml/min (p < 0.001). Left ventricular filling pressure increased from 9 ± 1 to 15 ± 1 mm Hg (p < 0.01). The decrease in intraluminal pressure distal to the stenosis and thus in the stenosis itself may have resulted in passive narrowing of the stenotic segment, which may have caused the decrease in flow. Exercise, therefore, may result in a decrease in flow through a stenotic coronary artery.     

Prevention of coronary vasoconstriction by diltiazem during dynamic exercise in patients with coronary artery disease

Whether exercise-induced vasoconstriction of coronary artery stenoses is modified by the administration of calcium antagonists was examined in 14 patients with classic angina pectoris. In this group the effect of intracoronary diltiazem (2 to 3 mg) on luminal area was evaluated in normal and stenotic segments of epicardial coronary arteries during symptom-limited supine exercise. The luminal area of a normal and a stenotic coronary artery segment was determined by quantitative coronary arteriography with a computer-assisted system. Patients were studied at rest, 6 min after 2 to 3 mg of intracoronary diltiazem, during supine bicycle exercise (96 W) and 5 min after sublingual administration of 1.6 mg nitroglycerin. Heart rate, mean pulmonary and aortic pressure as well as the percent change of both normal and stenotic luminal area were determined. Intracoronary administration of diltiazem was associated with mild dilation of both normal (19%, p less than 0.01) and stenotic coronary luminal area (11%, p less than 0.05). During subsequent exercise, luminal area of the stenotic vessel segment increased by 23% (p less than 0.001) and that of the normal vessel segment by 24% (p less than 0.001), whereas in a previously reported control group, luminal area of the stenotic vessel segment decreased by 29% during exercise. After sublingual administration of nitroglycerin, the luminal area of both the normal and the stenotic vessel segment increased further by 19% (p less than 0.01) and 22% (p less than 0.01), respectively, compared with the values after intracoronary administration of diltiazem.(ABSTRACT TRUNCATED AT 250 WORDS)     

Which Variable of Stenosis Severity Best Describes the Significance of an Isolated Left Anterior Descending Coronary Artery Lesion?: Correlation Between Quantitative Coronary Angiography,Intracoronary Doppler Measurements and High Dose Dipyridamole Echocardiography

Objectives. This study sought to investigate the angiographic or intracoronary Doppler variables of stenosis severity that best correlate with the results of dipyridamole echocardiography.Background. Quantitative coronary angiography and intracoronary Doppler flow velocity assessments are the commonly used techniques for the objective identification of significant coronary artery stenosis.Methods. Thirty patients with an isolated lesion of the left anterior descending coronary artery (LAD) were studied by means of on-line quantitative coronary arteriography, intracoronary Doppler flow velocity measurements and dipyridamole echocardiography 6 months after percutaneous transluminal coronary angioplasty. The quantitative arteriographic analyses were performed on-line; post-stenotic Doppler flow velocities were measured at baseline and after adenosine infusion. Angiographic and Doppler measurements were compared with the corresponding dipyridamole echocardiographic data and analyzed by discriminant analysis.Results. The dipyridamole echocardiographic response was positive in 11 patients (37%). The best cutoff values for predicting an abnormal echocardiographic response were 1) stenotic flow reserve of 2.8 (p = 0.0001); 2) 59% diameter stenosis (p = 0.0001); 3) minimal lumen diameter of 1.35 mm (p = 0.001); 4) coronary flow reserve of 2.0 (p = 0.0002); and 5) maximal peak velocity of 60 cm/s during hyperemia (p = 0.04). Multivariate analysis identified stenotic flow reserve as the only independent predictor of ischemia during dipyridamole echocardiography.Conclusions. Stenotic flow reserve is the variable that best describes the functional significance of an isolated LAD lesion, and a value of 2.8 is the best predictor of a positive dipyridamole echocardiographic response. Furthermore, angiographic variables of stenosis severity relate to echocardiographic test results better than intracoronary Doppler variables.     

Is the residual translesional pressure gradient useful to predict regional myocardial perfusion after percutaneous transluminal coronary angioplasty?

Routine assessment of the severity of a coronary artery lesion with coronary cineangiography is limited by its variability and poor correlation with blood flow and postmortem findings. In this investigation, we compared the usefulness of the final coronary artery translesional pressure gradient and the final angiographic coronary percent stenosis to assess immediate percutaneous transluminal coronary angioplasty (PTCA) success. To accomplish this, pressure gradients and percent stenoses were compared to stress thallium-201 regional myocardial perfusion before and after 56 uncomplicated PTCAs in 51 patients with single-vessel coronary artery disease. There were 39 men and 12 women; their mean age was 59 +/- 12 years. No patient had evidence of myocardial infarction. A new quantitative method to assess regional myocardial perfusion was used. Patients exercised for 433 +/- 130 seconds before PTCA and for 545 +/- 126 seconds after PTCA (p less than 0.001). Group coronary stenosis and translesional pressure gradient decreased from 77 +/- 11% and 48 +/- 5 mm Hg, respectively, before PTCA, to 25 +/- 11% and 9 +/- 5 mm Hg, respectively, after PTCA (p less than 0.001). Regional myocardial perfusion in the segment of the diseased (dilated) coronary artery increased after PTCA from 77 +/- 17% to 94 +/- 9% (p less than 0.001). Although a significant relationship was noted between regional myocardial perfusion and percent stenosis and translesional pressure gradient, a large individual scatter was present (r values lower than 0.55). We conclude that the final translesional pressure gradient during PTCA is not a better measure of immediate PTCA success than the angiographic percent stenosis.     

Coronary artery distensibility in diabetic patients with simultaneous measurements of luminal area and intracoronary pressure: evidence of impaired reactivity to nitroglycerin.

OBJECTIVES: This study investigated whether noninsulin dependent diabetes mellitus (NIDDM) adversely affects the elastic properties of the coronary arteries in patients with coronary artery disease (CAD) and NIDDM. BACKGROUND: Attenuated vascular smooth muscle dilation to exogenous donors of nitric oxide, such as nitroglycerin, has been observed with forearm blood flow studies in patients with NIDDM. METHODS: Twenty patients with CAD and NIDDM (diabetics), and 20 patients with only CAD (nondiabetics) were evaluated. Intracoronary ultrasound (ICUS) imaging with simultaneous intracoronary pressure (P2) recordings were performed at the imaging site with 0.014 in fiber-optic high fidelity pressure monitoring wire. The same wire was used as guide wire for the ICUS catheter. Sites with less than 50% luminal stenosis by ICUS were studied. Recordings were done before and after 300 microg of intracoronary nitroglycerin (IC-NTG). Electrocardiographic tracings recorded simultaneously with ICUS images were used for timing. Systolic and diastolic cross-sectional lumen area (CSLA) and coronary artery distensibility (C-DIST) were measured, C-DIST = [(systolic CSLA-diastolic CSLA)/[(intracoronary pulse pressure) x (diastolic CSLA)]] x 1,000. RESULTS: Diabetics had smaller CSLA (diabetics = 8.6 +/- 0.6 mm2, nondiabetics = 11.5 +/- 0.5 mm2, p < 0.01). Although C-DIST was similar before IC-NTG in the two groups, it became significantly lower in diabetics after IC-NTG (diabetics C-DIST = 3.02 +/- 0.14 mm Hg(-1), nondiabetics C-DIST = 4.21 +/- 0.15 mm Hg(-1), p < 0.01). Degrees of circumference involved, total plaque burden and composition were similar in both groups. CONCLUSIONS: Noninsulin dependent diabetes mellitus reduces C-DIST after IC-NTG administration.     

Coronary microcirculatory vasoconstriction during ischemia in patients with unstable angina

OBJECTIVE: To verify the behavior of coronary microvascular tone during spontaneous ischemia in patients with unstable angina (UA). BACKGROUND: In UA, the pathogenetic role of vasoconstriction is classically confined at the stenotic coronary segment. However, microcirculatory vasoconstriction has been also suggested by previous experimental and clinical studies. METHODS: The study included 10 patients with UA (recent worsening of anginal threshold and appearance of angina at rest) and single-vessel CAD. Blood flow velocity was monitored by a Doppler catheter in the diseased artery. Transstenotic pressure gradient was monitored by aortic and distal coronary pressure monitoring. Stenosis resistance was calculated as the ratio between pressure gradient and blood flow, microvascular resistance as the ratio between distal pressure and blood flow. Measurements were obtained at baseline, following intracoronary adenosine (2 mg) and during transient ischemia. Aortic and distal coronary pressures were also measured during balloon coronary occlusion. RESULTS: Adenosine did not affect stenosis resistance, while it decreased (p < 0.05) microvascular resistance to 52 +/- 22% of baseline. Angina and ischemic ST segment shift were associated with transient angiographic coronary occlusion in 7 of 10 patients; however, in no case was ischemia associated with interruption of flow. Despite markedly different flow values, distal coronary pressure was similar during adenosine and during spontaneous ischemia (48 +/- 15 vs. 46 +/- 20 mm Hg, respectively, NS). During ischemia, a marked increase in the resistance of both coronary stenosis and coronary microcirculation was observed (to 1,233% +/- 1,298% and 671% +/- 652% of baseline, respectively, p < 0.05). Distal coronary pressure was markedly reduced during balloon coronary occlusion (14 +/- 7 mm Hg, p < 0.05 vs. both adenosine and ischemia), suggesting the absence of significant collateral circulation. CONCLUSIONS: In patients with UA, transient myocardial ischemia is associated with vasoconstriction of both stenotic arterial segment and downstream microcirculation.     

Phase variations in the left coronary transstenotic pressure gradient before and after dilatation by percutaneous coronary angioplasty

The concept of significant coronary stenosis may be approached by studying the effects of the narrowing not in absolute values of pressure and flow but by studying the mode of blood flow across the stenosis. Ten patients with isolated stenosis of the LAD were studied for phasic variations of the transstenotic pressure gradient before and after dilatation. The material used was a ST 3.7 catheter with a 0.12 inch guide. Instantaneous pressure recording throughout the cardiac cycle were obtained using a computer. After dilatation, the area of the stenosis minus the area of transverse section of the dilating catheter increased from 0.5 +/- 0.3 to 2.2 +/- 0.3 mm2, the average gradient between the aorta and the post stenotic LAD decreased from 75 +/- 10 to 12 +/- 8 mmHg, and the ratio between the mean diastolic gradient and mean gradient increased from 75 +/- 7 to 245 +/- 30% (p less than 0.01 for the 3 parameters, paired t test). These results show that the LAD transstenotic pressure gradient is not phasic in severe stenosis. It becomes phasic, only in diastole, after dilatation of the stenosis (slight residual stenosis due to the catheter). This difference may be due to the type of flow, continuous and dependent on the stenosis before dilatation, or phasic dependent on the distal coronary circulation after dilatation. Analysis of the phasic changes of coronary flow may be useful for the evaluation of the severity of left coronary stenosis in the absence of pressure measurements.