Quantitative assessment of myocardial perfusion during graded coronary artery stenoses by intravenous myocardial contrast echocardiography

OBJECTIVES: The purpose of this study was to examine whether coronary stenoses of variable severity could be quantitatively assessed by analysis of myocardial perfusion as determined by intravenous (IV) myocardial contrast echocardiography. BACKGROUND: Recently, new contrast agents and imaging technology have been developed that may enable improved assessment of myocardial perfusion by IV contrast injection. METHODS: Variable obstruction of the left anterior descending (LAD) coronary artery in dogs was produced by a screw occluder. Coronary artery flow was measured with a transit time flowmeter during baseline, pharmacological vasodilation, a non-flow-limiting stenosis at rest in conjunction with vasodilation, a flow-limiting stenosis, and total occlusion. Myocardial contrast echocardiography was performed after IV injection of the contrast agent NC 100100. Time-intensity curves were obtained off-line for the LAD risk area and the adjacent left circumflex (LCx) territory, and peak background-subtracted video intensity was determined. Fluorescent microspheres were injected at each intervention for determination of regional myocardial blood flow. RESULTS: During non-flow-limiting stenosis, flow limiting stenosis and total occlusion, LAD/LCx ratios of peak myocardial videointensity and blood flow decreased proportionately. Both LAD/LCx ratios of video intensity and blood flow identified the non-flow-limiting and the flow-limiting stenoses as well as total occlusion of the LAD artery. A significant correlation between LAD/LCx video intensity and blood flow ratios was observed (r = 0.83, p < 0.0001). CONCLUSIONS: The degree of blood flow mismatch between ischemic and normal myocardial regions during graded coronary stenoses can be estimated in the dog by quantitative assessment of myocardial perfusion produced by IV myocardial contrast echocardiography.     

Minimal coronary stenoses and left ventricular blood flow during CPR.

STUDY OBJECTIVE: To assess the effect of a 33% coronary stenosis on myocardial blood flow during normal sinus rhythm and CPR. DESIGN: Prospective, before and after cardiac arrest and CPR; before and after creation of a 33% stenosis. SETTING: The University of Arizona Resuscitation Research Laboratory. SUBJECTS: Ten domestic closed-chest swine with patent coronary stenoses. INTERVENTIONS: A Teflon cylinder was placed in the mid-left anterior descending coronary artery to create a 33% stenosis. Myocardial blood flow was measured with colored microspheres both proximal and distal to the stenosis during normal sinus rhythm and during CPR. MEASUREMENTS AND MAIN RESULTS: During normal sinus rhythm, the stenosis did not alter the amount of myocardial blood flow distribution or quantity. Proximal to the stenosis the endocardial/epicardial flow ratio was 1.49 +/- 0.33, and distal to the stenosis it was 1.50 +/- 0.50. Likewise, during normal sinus rhythm, blood flow proximal and distal to the stenosis did not differ for either the epicardium (79 +/- 9 versus 66 +/- 13 mL/min/100 g) or the endocardium (111 +/- 27 versus 83 +/- 19 mL/min/100 g). However, the distribution of myocardial blood flow was markedly altered during CPR. The resultant endocardial/epicardial flow ratios were significantly less than during normal sinus rhythm, 0.49 +/- 0.11 (three minutes of CPR) and 0.74 +/- 0.07 (eight minutes of CPR) proximal to the stenosis and 0.39 +/- 0.15 (three minutes of CPR) and 0.49 +/- 0.14 (eight minutes of CPR) distal to the stenosis (P less than .05 versus normal sinus rhythm). In the presence of a 33% mid-left anterior descending coronary artery stenosis, endocardial blood flow at eight minutes of CPR was significantly lower distal to the stenosis compared with proximal to the stenosis (23 +/- 7 mL/min/100 g versus 74 +/- 18 mL/min/100 g; P less than .02). CONCLUSION: Minimal coronary lesions that do not diminish myocardial perfusion during normal physiologic conditions appear to significantly decrease subendocardial blood flow during cardiac arrest and CPR.     

Characterization of the functional significance of subcritical coronary stenoses with H(2)15O and positron-emission tomography

We have previously developed a method employing cardiac positron-emission tomography (PET) with 15O (half-life 2.1 min)-labeled water (H2(15)O) and blood pool subtraction with C15O for assessment of myocardial perfusion. This study was performed to determine whether the method developed permits detection of the differences in blood flow, induced by vasodilator stress, indicative of functionally significant subcritical coronary stenosis despite normal perfusion at rest. Coronary stenoses were induced with a small Teflon cylinder placed in the left anterior descending coronary artery of the closed-chest dog. Regional myocardial blood flow was assessed tomographically with H(2)15O given intravenously and C15O given inhalation. Blood flow distal to the stenoses was normal under conditions of rest. However, significant reductions in the hyperemic response to dipyridamole were detected consistently in regions distal to 50% to 70% diameter stenoses. Flow distal to stenoses more than doubled in absolute terms in response to dipyridamole but was only 43 +/- 9% of the increased flow in normal regions in the same dogs or in corresponding anterior regions in normal dogs. Relative myocardial blood flow measured noninvasively with PET correlated closely with the distribution of radiolabeled microspheres measured in vitro (r = .88). Thus, assessment of myocardial blood flow with H(2)15O and PET in dogs at rest and during vasodilator-induced stress permits detection of physiologically significant coronary stenoses. The procedure should therefore prove useful diagnostically for the detection of coronary insufficiency in patients as well as for the assessment of clinical interventions designed to augment regional perfusion.     

Measuring blood flow velocity in the coronary sinus with Doppler catheters]

Measurements of the coronary sinus blood flow velocity with Doppler catheters (Medtronic Floscan; Millar DC201) were performed to assess coronary flow reserve and significance of coronary artery stenosis. In seven patients with normal coronary angiogram coronary sinus blood flow velocity (Doppler catheters) and coronary sinus blood flow volume (thermodilution) were simultaneously recorded. Coronary flow reserve was calculated as the quotient of the peak flow velocity (peak flow volume) and resting flow velocity (resting flow volume) after infusion of 0.5 mg/kg dipyridamole intravenously. The correlation coefficient was r = 0.88. Coronary sinus blood flow velocity was measured in 31 patients at resting conditions and after injection of contrast media during coronary angiography. At resting conditions blood flow velocity was 3.6 +/- 1.5 cm/s (n = 31), 3.5 +/- 1.8 cm/s (n = 9; controls), and 3.6 +/- 1.1 cm/s (n = 9; significant stenosis of the left anterior descending; not significant). After injection of contrast media flow velocity amounted to 2.2-fold resting flow in controls and to 1.5-fold resting flow in patients with stenoses of the left anterior descending artery (p less than 0.01). Measurement of coronary sinus blood flow velocity with Doppler catheters is a valuable adjunct for determination of coronary flow reserve and for assessment of stenosis severity of the left anterior descending artery. Continuous on-line monitoring of phasic flow velocity provides important information of the myocardial perfusion, e.g., during angioplasty.     

Homogeneous distribution and pressure dependent reduction of coronary blood flow in right ventricular free wall during coronary hypoperfusion in anaesthetised open chest dogs

Relationship of coronary perfusion pressure with total and regional myocardial blood flow in right ventricular free wall was studied in 10 anaesthetised open chest dogs. The right coronary artery was perfused by an autoperfusion system from the carotid artery. Total coronary blood flow into the perfused area was measured by an extracorporeal electromagnetic flow probe. Critical perfusion pressure of the right coronary artery, defined as the lowest pressure level below which the regional wall motion deteriorated, was 39(SEM1) mm Hg. Reactive hyperaemia was noted at 60(2) mm Hg, a level well above the critical perfusion pressure. There was an inverse linear relation between the level of reactive hyperaemia and perfusion pressure. Regional myocardial blood flow was measured by a tracer microsphere technique at control condition, just above and below the critical perfusion pressures and during coronary occlusion. This correlated closely with values obtained by an electromagnetic flow probe (r = 0.94, p less than 0.001) and both values were dependent on the level of perfusion pressure. Endocardial to epicardial flow ratio remained at unity at any level of coronary perfusion pressure. Thus the level of coronary perfusion pressure was a major determinant of the regional myocardial blood flow into the right coronary artery, and autoregulation of the regional myocardial blood flow was not apparent across the wall, despite the presence of a reactive hyperaemia.     

Adverse effects of circumflex coronary artery occlusion on blood flow to remote myocardium supplied by a stenosed left anterior descending coronary artery in anesthetized open-chest dogs

Left anterior descending coronary artery occlusion in open-chest dogs causes a decrease in endocardial blood flow to the remote posterior bed supplied by a stenosed left circumflex coronary artery. To determine if "remote" myocardial ischemia also occurred in the anterior bed after circumflex occlusion, myocardial blood flow (radiolabeled microspheres) and hemodynamics were measured before and after circumflex occlusion in the presence of a stenosed left anterior descending artery (gradient: 28 +/- 2 mm Hg) in 10 open-chest dogs. Aortic pressure fell from 108 +/- 3 to 100 +/- 3 mm Hg (p = 0.02) and mean distal left anterior descending coronary artery pressure fell from 81 +/- 4 to 69 +/- 5 mm Hg (p = 0.02) after circumflex occlusion. Transmural flow to normal myocardium supplied by unstenosed and unoccluded coronary arteries increased from 0.69 +/- 0.04 to 0.84 +/- 0.04 ml/min/gm (p less than 0.0001) after circumflex occlusion. Although epicardial flow to the remote anterior bed supplied by the stenosed left anterior descending coronary artery increased after left circumflex occlusion (0.61 +/- 0.03 to 0.73 +/- 0.04 ml/min/gm, p = 0.004), remote anterior bed endocardial flow did not increase, and the remote bed endocardial:epicardial blood flow ratio decreased from 0.98 +/- 0.06 to 0.78 +/- 0.10 (p less than 0.05). Therefore, in this model, remote anterior bed ischemia, relative to the normal myocardial flow response, developed when the left circumflex coronary artery was occluded in the presence of the stenosed left anterior descending coronary artery.     

Intermittent coronary sinus occlusion after coronary arterial ligation results in venous retroperfusion

Coronary sinus occlusion retards necrosis of ischemic myocardium. To test the hypothesis that coronary sinus occlusion induces retrograde venoarterial flow, the coronary arteriovenous pressure gradient and the coronary arterial oxygen saturation were measured distal to a left anterior descending coronary artery ligature in dogs. In parallel, we constructed a mathematical model of known coronary physiology to characterize pressure and flow patterns during coronary sinus occlusion. In dogs, coronary sinus occlusion produced a systolic pressure gradient between the coronary artery and the coronary sinus of -20 +/- 9 mm Hg (higher venous pressure, p less than 0.0001) and a positive diastolic gradient of 3 +/- 5 mm Hg (lower venous pressure p less than 0.01). An average reduction in the oxygen saturation in the ligated coronary artery of 20 +/- 13% was also observed (p less than 0.005) consequent to admixture of venous (desaturated) blood. By graded inflation of the coronary sinus balloon, it was demonstrated that desaturation of arterial blood typically occurs above a coronary sinus systolic pressure of 40-50 mm Hg. The mathematical model indicates the possibility of venoarterial pressure gradients and reversal of flow at the microcirculatory level during coronary sinus occlusion. These studies provide evidence that retrograde flow into the ischemic zone occurs in association with intermittent coronary sinus occlusion. Thus, alternating flow over the ischemic territory may be the mechanism of myocardial salvage during intermittent coronary sinus occlusion.     

Tachycardia induced reduction in coronary blood flow distal to a stenosis

Clinical and experimental data indicate that some coronary stenoses can rapidly change shape thereby influencing the hemodynamic severity of the stenosis. In 7 closed chest dogs, we examined the effects of distal coronary arteriolar vasomotor tone and myocardial oxygen demands on a coronary stenosis created by partial intraluminal occlusion, using a small balloon catheter. Myocardial blood flow (ml/g per min) was measured with 15-microns radioactive microspheres. Stenotic resistance was calculated as the mean pressure gradient across the stenosis divided by the mean blood flow through the stenosis. The mean pressure gradient was calculated as the ascending aortic pressure minus the left anterior descending coronary artery pressure distal to the stenosis. Coronary arteriolar vasodilation induced by pacing (170 beats/min) increased stenotic resistance (1.64 +/- 0.27 to 26.48 +/- 13.77 mmHg/ml per min, P less than 0.05) and decreased myocardial blood flow (endocardial 0.42 +/- 0.04 to 0.17 +/- 0.04, P less than 0.05, midcardial 0.35 +/- 0.03 to 0.13 +/- 0.04, P less than 0.05; epicardial 0.22 +/- 0.05 to 0.15 +/- 0.05). Five dogs fibrillated within 10 min of continuous tachycardia and partial arterial occlusion. The change in arteriolar vasomotor tone and decreased aortic pressure induced by pacing altered the severity of the stenosis and resulted in a reduction of blood flow to the myocardium.     

Can myocardial contrast echo determine coronary flow reserve?

OBJECTIVE: The aim was to evaluate the applicability of myocardial contrast echocardiography in the measurement of coronary flow reserve. METHODS: Eleven anaesthetised open chest pigs were studied, in which coronary atherosclerosis had been induced by abrasion of the left anterior descending coronary artery at one month, followed by an atherogenic diet for eight months. Coronary flow reserve was determined by electromagnetic flow measurement and contrast echocardiography before and after partial occlusion of the left anterior descending coronary artery, using papaverine as a coronary vasodilator. Coronary blood flow was reduced by tightening a clamp placed around the coronary artery. Systemic haemodynamics and myocardial wall thickness (epicardial ultrasound 5 MHz transducer) were recorded simultaneously. Echocardiograms were recorded on VHS tape and analysed by digitised videodensitometry off line for construction of the time v videointensity curve (time-intensity curves). From these curves washout time (T50), area under the curve, peak contrast intensity, and time to peak intensity were calculated. RESULTS: Following papaverine, coronary blood flow increased significantly from 47 (SD 23) ml.min-1 at baseline to 88(39) ml.min-1 (p less than 0.05). During the stenosis, flow decreased to 19(16) ml.min-1 (p less than 0.01), and increased to 38(29) ml.min-1 (p less than 0.05 v stenosis) after administration of papaverine. Correlations between coronary blood flow and indices calculated from the quantitative videodensitometric analysis were poor, varying between r = 0.03 for area at control flow to r = 0.62 for T50 during stenosis. The same was true for coronary flow reserve: r = 0.09 for peak to r = 0.75 (p less than 0.05) for time to peak without the stenosis. CONCLUSIONS: Current limitations in injection, imaging, and analysis techniques cause variability in data from time-intensity curves, which precludes accurate quantification of coronary flow (reserve) by myocardial contrast echocardiography.     

Absence of coronary vascular reserve in myocardium distal to a fixed coronary stenosis

In a study to test the hypothesis that vascular reserve is exhausted in the setting of a resting blood flow deficit, the left anterior descending or circumflex artery was cannulated and perfused from the left carotid artery. After reactive hyperaemia had been assessed a stenosis was produced with a screw clamp. In the first experiment a moderate stenosis (diastolic perfusion pressure 40 mmHg) was produced in the left anterior descending artery (three dogs) or left circumflex artery (three dogs). Blood pressure was held constant with aortic constriction during intracoronary adenosine infusion (6 mumol.min-1). The stenosis was then adjusted to the preadenosine perfusion pressure. In the second experiment the anterior interventricular coronary vein was also isolated and segment length crystals were placed in the ischaemic and non-ischaemic zones. Severe stenosis (flow reduction of at least 50% and evidence of decreased segmental shortening) was produced in the cannulated left anterior descending artery (eight dogs). Intracoronary adenosine was given with aortic pressure held constant by transfusion and coronary venous drainage. In the first experiment resting coronary flow (ml.min-1) decreased from 41(3) to 29(6) (p less than 0.05) with stenosis. Coronary flow increased from 29(6) to 34(7) (p less than 0.05) with adenosine and to 50(10) (p less than 0.05) with stenosis adjustment. Subendocardial flow (ml.g-1.min-1) decreased from 0.89(0.26) to 0.78(0.23) (p less than 0.05) with adenosine and then increased from 0.94(0.49) with perfusion pressure adjustment. Subepicardial flow tended to increase with adenosine, and increased further with stenosis adjustment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Role of ATP-sensitive potassium channels in coronary microvascular autoregulatory responses

The purpose of the present study was to test the hypothesis that ATP-sensitive potassium channels mediate autoregulatory vasodilatation of coronary arterioles in vivo. Experiments were performed in 23 open-chest anesthetized dogs. Coronary arterial microvascular diameters were directly measured with fluorescence microangiography using an intravital microscope and stroboscopic epi-illumination synchronized to the cardiac cycle. A mild coronary stenosis (perfusion pressure = 60 mm Hg), a critical coronary stenosis (perfusion pressure = 40 mm Hg), and complete coronary artery occlusion were produced with an occluder around the left anterior descending coronary artery in the presence or absence of glibenclamide (10(-5) M, topically), which inhibits ATP-sensitive potassium channels, or of vehicle. During topical application of vehicle (0.01% dimethyl sulfoxide), there was dilatation of small (less than 100 microns diameter) arterioles during reductions in perfusion pressure (percent change in diameter: 6.7 +/- 1.5%, 11.7 +/- 3.5%, and 10.4 +/- 5.1% during mild stenosis, critical stenosis, and complete occlusion, respectively). In the presence of glibenclamide, arteriolar dilatations during coronary stenoses and occlusions were abolished. Glibenclamide did not affect responses of arterioles greater than 100 microns. Glibenclamide did not alter microvascular responses to nitroprusside. These data suggest that ATP-sensitive potassium channels play an important role in determining the coronary microvascular response to reductions in perfusion pressure.     

Mechanism of remote myocardial ischaemia after coronary occlusion in open chest dogs

To determine whether or not the fall in coronary perfusion pressure after coronary occlusion is the cause of remote myocardial ischaemia, regional myocardial blood flow was measured using radiolabelled microspheres before and after left anterior descending (LAD) occlusion in the presence of a left circumflex artery stenosis in 22 anaesthetised dogs. Aortic pressure was maintained constant at the time of left anterior descending artery occlusion in 13 dogs (group 1) and proximal left circumflex artery pressure was held constant by a servocontrolled pump in nine dogs with a carotid artery-left circumflex artery shunt (group 2). Despite the maintenance of constant mean aortic pressure in group 1, remote posterior bed mean(SEM) endocardial flow fell from 0.69(0.05) to 0.43(0.07) ml.min-1.g-1 (p less than 0.05). In the dogs in which left atrial pressure rose to less than or equal to 9 mmHg after left anterior descending artery occlusion, remote bed endocardial flow did not fall significantly (0.66(0.07) to 0.56(0.11) ml.min-1.g-1; NS). In contrast, remote bed endocardial flow fell from 0.73(0.07) to 0.28(0.06) ml.min-1.g-1 (p less than 0.0001) after left anterior descending artery occlusion in the dogs in which left atrial pressure rose to greater than 9 mmHg. The fall in remote bed endocardial flow was prevented in group 2 dogs by maintaining proximal left circumflex artery pressure constant (0.95(0.08) to 0.86(0.09) ml.min-1.g-1; NS). An important mechanism for the development of remote myocardial ischaemia appears to be the fall in proximal coronary perfusion pressure at the time of coronary occlusion.     

Collateral conductance changes during a brief coronary occlusion in awake dogs

Function of the coronary collateral circulation during the course of a single abrupt coronary occlusion was evaluated in awake dogs instrumented over the long term. Studies were performed approximately 2 weeks after collateral development had been stimulated in the dogs by partial stenosis of the proximal left circumflex coronary artery. The pressure drop from the central aorta to the distal circumflex coronary artery was measured continuously. Under control conditions and at 30 sec and 4 min of a single abrupt complete circumflex occlusion, myocardial blood flow was determined by a radioactive microsphere technique. Coronary collateral conductance was calculated as mean collateral blood flow divided by the mean drop in pressure. The following was noted in dogs that developed collateral vessels: during the coronary occlusion, mean distal circumflex coronary pressure increased from 42 +/- 9 to 49 +/- 10 mm Hg (p less than or equal to .01); mean collateral flow increased from 0.78 +/- 0.30 to 0.84 +/- 0.33 ml/min/g (p less than or equal to .05); the endocardial/epicardial flow ratio increased from 0.77 +/- 0.36 to 1.04 +/- 0.25 (p less than or equal to .01); and the coronary collateral conductance increased significantly from 0.017 +/- 0.017 to 0.021 +/- 0.021 (ml/min/g)/mm Hg (p less than or equal to .005). These data suggest that during a brief occlusion of a major coronary artery, immature coronary collateral channels do not reach maximal function immediately after the occlusion. Rather, coronary collateral conductance increases with time and may be associated with improved transmural perfusion of the myocardium.     

Oxygen consumption and coronary reactivity in postischemic myocardium

Coronary vascular responses in regions of reversible postischemic myocardial contractile dysfunction (stunned myocardium) were examined in chronically instrumented, awake dogs. Left anterior descending coronary artery blood flow and oxygen extraction, aortic and left ventricular pressures, and regional myocardial segment shortening were determined. Regional myocardial blood flow was measured with microspheres. Coronary reactive hyperemia and vasodilator reserve, and regional myocardial oxygen consumption were determined. Three sequential 10-minute left anterior descending coronary artery occlusions separated by 30-minute reperfusion periods resulted in progressive postischemic dysfunction so that 1 hour after the final coronary artery occlusion, myocardial segment shortening was reduced to 37% of baseline. Despite this decrease in contractile function, left anterior descending artery flow (19.6 +/- 2.6 vs. 18.4 +/- 3.0 ml/min), myocardial blood flow and the transmural distribution of flow measured with microspheres, and regional myocardial oxygen consumption were unchanged. Although the coronary vasodilator reserve in response to adenosine was unaltered (63 +/- 9 vs. 70 +/- 15 ml/min), the reactive hyperemia response to a 10-second coronary occlusion was decreased in intensity (debt repayment ratio = 474 +/- 78% vs. 322 +/- 74%; p less than 0.05) and duration (57 +/- 9.1 vs. 35 +/- 4.5 seconds; p less than 0.05), while the peak flow response was unchanged (57 +/- 6.8 vs. 60 +/- 7.1 ml/min). Thus, in the intact awake animal postischemic myocardial contractile dysfunction was not associated with decreased myocardial oxygen consumption and did not impair the normal relation between coronary blood flow and myocardial oxygen utilization. Although coronary vessels showed a normal ability to vasodilate in response to adenosine, coronary reactive hyperemia was reduced.     

Coronary hemodynamics and subendocardial perfusion distal to stenoses

We compared distal coronary hemodynamics and regional myocardial perfusion in anesthetized dogs in the presence of a single or two coronary artery stenoses in series. After application of either a single or two stenoses on the left anterior descending coronary artery, regional myocardial blood flow was measured with radioactive microspheres. Moderate degrees of single-vessel stenosis (no change in resting coronary blood flow but reduction in reactive hyperemic response of 70%) resulted in no significant change in regional myocardial perfusion at rest despite a pressure drop across the stenosis of 24 +/- 3 mm Hg. When two such stenoses were applied in series, there was a 91% decrease in reactive hyperemia, a significant reduction in resting diastolic coronary blood flow and a 51 +/- 7 mm Hg pressure drop across the two stenoses. Alone, each stenosis produced no change in regional myocardial perfusion; however, together the two stenoses resulted in a significant decrease in subendocardial blood flow and a redistribution of transmural perfusion within the ischemic zone favoring the subepicardium (endo/epi from 0.95 +/- 0.03 to 0.72 +/- 0.03). The results indicate that whereas resting subendocardial perfusion is not significantly affected by moderate degrees of a single coronary artery stenosis, multiple stenoses of the same severity may dramatically reduce subendocardial perfusion.     

Evaluation of "ischemia at a distance": effects of coronary occlusion on a remote area of left ventricle

The effect of coronary occlusion on blood flow and function in a remote zone of the left ventricle was studied in 21 open-chest dogs. Group A consisted of 6 dogs not undergoing left circumflex (LC) coronary artery cannulation. The other 15 dogs underwent cannulation of the LC artery followed by partial occlusion to 40 mm Hg diastolic perfusion pressure. Of these dogs, 7 with constant perfusion pressure (group B) were separately evaluated from 8 with declining perfusion pressure (group C). Sequentially more proximal left anterior descending (LAD) occlusions were performed in each group. Blood flow in the LC zone remained unchanged in group A after sequential LAD occlusions, whereas in groups B and C distal and proximal LAD occlusions caused progressive reduction in LC flow. Although in group A segment shortening improved in the LC zone after distal LAD occlusion, in groups B and C progressive impairment in segmental shortening was observed in the LC zone after distal and proximal LAD occlusions. Thus, in the setting of critical coronary stenosis in a zone, total occlusion in another coronary artery can initiate a series of events leading to decreased blood flow in the territory of the stenotic coronary artery, resulting in ischemia and impaired segmental function.     

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.     

Details of coronary stenosis morphology influence its hemodynamic severity and distal flow reserve

Differences in coronary flow reserve with anatomically similar coronary artery stenoses have been attributed to 1) nonstandard physiologic conditions, 2) inadequacies of measurements of coronary artery stenosis dimension and/or coronary blood flow, and 3) inadequate hyperemic stimulus. Our study tested the hypothesis that details of coronary artery stenosis geometry, which may or may not be apparent on coronary angiograms, also may contribute importantly to such differences. A simple and complex coronary artery stenosis, each of which reduced vessel cross-sectional area by 84%, was introduced in random order into the left anterior descending coronary artery of nine closed-chest, sedated swine. The simple stenosis had a single lumen while the complex stenosis had five small lumena whose combined area equaled that of the single lumen stenosis. Measurements of hemodynamics and regional myocardial blood flow (microspheres) were made at control and after 10 minutes of adenosine infused at 400 micrograms/min and then at 800 micrograms/min distal to each stenosis. Both heart rate and aortic mean pressure were controlled and thus did not change versus initial baseline (129 +/- 4 minutes and 120 +/- 10 mm Hg, mean +/- SD, respectively) during the study. Baseline total flow (ml/sec) distal to the stenosis was similar at each control (1.05 +/- 0.35 vs. 0.92 +/- 0.34, simple versus complex, respectively; p = NS). At maximal adenosine, total flow with the simple stenosis was 3.44 +/- 0.92 versus 2.77 +/- 0.51 for complex (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of acute coronary occlusion on hemodynamics in an adjacent coronary artery in dogs

The effects of acute occlusion of 1 coronary artery on flow responses in another were studied in 24 open-chest dogs. Left circumflex (LC) flow was measured with and without LC stenoses before and during reactive hyperemia. In 19 dogs the left anterior descending artery (LAD) was occluded and measurements were repeated after 1 hour (group 1). Four dogs had measurements before and after 1 hour without LAD occlusion (group 2). In group 2 no systemic, left ventricular (LV) or coronary hemodynamic changes were observed after 1 hour. In group 1, an hour after LAD occlusion, heart rate and aortic pressure had not changed but stroke volume decreased slightly (-8 +/- 7%, mean +/- SD, p = not significant) and LV end-diastolic pressure had increased (2 +/- 3 mm Hg, p less than 0.05). Basal LC flow was not changed by less than 90% LC stenosis. Ninety percent LC stenosis decreased LC flow both before and after LAD occlusion. During reactive hyperemia without LC stenosis, LC flow decreased after LAD occlusion in 15 of 19 dogs (from 154 +/- 80 to 141 +/- 75 ml/min, p less than 0.05). With 60 and 80% LC stenoses, LC flow during reactive hyperemia decreased before LAD occlusion (110 +/- 62 and 74 +/- 40 ml/min, respectively), but decreased further (both p less than 0.05) after LAD occlusion (98 +/- 54 and 63 +/- 43 ml/min).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of percutaneous coronary intervention on coronary blood flow at rest in myocardial sites remote from the intervention site in patients with stable angina pectoris

Little is known about changes in myocardial perfusion of myocardial regions supplied by angiographically normal or near-normal coronary arteries after percutaneous coronary intervention (PCI) of the target lesion. The purpose of this study was to assess the effect of PCI on coronary blood flow at rest in sites remote from the PCI. We studied 85 patients who underwent successful elective PCI for stable angina. We used the Thrombolysis In Myocardial Infarction frame count to provide a simple continuous index of coronary flow and myocardial perfusion in the target and nontarget arteries. Coronary artery diameters of nontarget vessels did not significantly differ before and after PCI and at 6 months' follow-up. At baseline, the greater the percent diameter stenosis in the target artery, the slower the flow in the target (r = 0.22, p <0.01) and nontarget arteries (r = 0.28, p <0.01). Relief of stenosis using PCI did not account for simultaneous changes in epicardial coronary blood flow of the nontarget artery. After 6 months, coronary blood flow improved in both the target (p <0.05) and nontarget arteries (p = 0.007). In conclusion, this study provided evidence of a functional link between coronary blood flow in diseased and nondiseased arteries. Relief of a significant stenosis using PCI globally improved regional and global myocardial blood flow at rest in patients with stable angina. Flow improvement was not apparent at the time of revascularization, but at 6 months' follow-up. Late upturn of the microcirculation may account for delayed recovery of myocardial perfusion.