Original Article
Reduced Coronary Vasodilator Function in Infarcted and Normal Myocardium after Myocardial Infarction
N Engl J Med 1994; 331:222-227July 28, 1994
- Abstract
Background
The ability of the coronary vascular bed to dilate and thus increase blood flow to the myocardium may be impaired in coronary artery disease, even in regions of myocardium supplied by an angiographically normal coronary artery. If this kind of vasomotor dysfunction was present or accentuated after acute myocardial infarction, it might influence the extent of ischemia and necrosis in areas not directly injured by the infarction.
Methods
We studied 13 patients (mean [±SD] age, 62 ±11 years) with single-vessel coronary artery disease after they had received thrombolytic therapy for myocardial infarction. Using positron-emission tomography (PET) with oxygen-15-labeled water, we measured regional myocardial blood flow under basal conditions and after the intravenous administration of dipyridamole (0.5 mg per kg of body weight over a period of four minutes) 8 ±3 days after infarction in all 13 patients (1-week study) and 6 ±2 months after infarction in 9 of the 13 (6-month study). On both occasions we measured blood flow both in the infarcted region and in a region of myocardium that was remote from the infarcted region and supplied by a normal artery.
Results
At the one-week PET study, the coronary vasodilator response (the ratio of the myocardial blood flow after the administration of dipyridamole to basal blood flow) was 1.12 ±0.50 in the infarct-related artery and 1.53 ±0.36 in the remote region (P = 0.015). At the six-month study, the coronary vasodilator response was 1.42 ±0.37 in the infarcted region and 2.19 ±0.69 in the remote region (P = 0.004 for the comparison with the infarcted region; P = 0.011 for the comparison with the remote region at the one-week study). The value in remote myocardium remained lower than that in similar regions in 10 control patients, who had single-vessel coronary artery disease but no evidence of myocardial infarction (3.17 ±0.72; P = 0.009).
Conclusions
After acute myocardial infarction, there is a severe vasodilator abnormality involving not only resistance vessels in infarcted myocardium, but also those in myocardium perfused by normal coronary vessels. This dysfunction may affect the extent of myocardial ischemia and necrosis after coronary occlusion.
Media in This Article
Figure 1
Net Change in Regional Myocardial Blood Flow in the Infarcted Region and the Remote Region in Patients and the Remote Region in Controls.Figure 2
Mean (±SD) Coronary Vasodilator Response in the Infarcted Region and the Remote Region in Patients and the Remote Region in Controls.Article Activity
- Article
Several studies have shown that in patients with chronic stable angina due to single-vessel coronary artery disease, the coronary vasodilator response (defined as the ratio of maximal to basal coronary blood flow) is reduced not only in the region of myocardium perfused by the stenosed artery but also in the regions supplied by angiographically normal coronary arteries1-3. These observations suggest that in patients with stable coronary disease, there is a diffuse vasodilator abnormality of the coronary resistance vessels4,5.
After acute myocardial infarction, the coronary vasodilator response in the infarcted myocardial region remains severely impaired despite successful recanalization of the infarct-related artery by thrombolysis6-8; this impairment has been attributed to dysfunction of resistance vessels in the infarcted tissue9. The effect of myocardial infarction on the coronary vasodilator response in the myocardial regions perfused by angiographically normal arteries that are remote from the site of tissue necrosis is unknown, however.
Our main purpose was to investigate the effect of acute myocardial infarction on the coronary vasodilator response in regions of myocardium remote from the site of infarction. We used dynamic positron-emission tomography (PET) to measure regional myocardial blood flow in infarcted myocardium and in remote regions perfused by angiographically normal coronary arteries under basal conditions and after maximal vasodilation by dipyridamole approximately one week and six months after myocardial infarction. The responses in the patients with myocardial infarction were compared with those in controls who had stable single-vessel coronary disease and no evidence of myocardial infarction.
Methods
Patients
Thirteen consecutive patients, 11 men and 2 women (mean [±SD] age, 62 ±11 years; range, 40 to 77), with single-vessel coronary disease and otherwise angiographically normal coronary arteries were studied after myocardial infarction. Patients with multi-vessel disease and those who had recurrent myocardial ischemia at rest, who had acute heart failure, or who required inotropic support were excluded from the study. The infarct-related artery was the left anterior descending artery in nine patients, a dominant right coronary artery in three, and a dominant left circumflex artery in one. All 13 patients received 1.5 million units of intravenous streptokinase and 300 mg of aspirin 4.2 ±2.4 hours (range, 2.0 to 7.8) after the onset of chest pain (Table 1Table 1
Characteristics of the 13 Patients with Myocardial Infarction.). All patients had abnormal Q waves on 12-lead electrocardiography within 24 hours of the onset of chest pain (Table 1).We also studied a control group made up of 10 men (mean age, 52 ±9 years; range, 44 to 72) with chronic stable angina due to single-vessel coronary disease (in the left anterior descending artery) and normal left ventricular function.
Study Protocol
The protocol was approved by the Research Ethics Committee of Hammersmith Hospital, and all patients gave written informed consent.
None of the patients had been given either beta-blockers or calcium-channel antagonists after myocardial infarction. PET was performed 8 ±3 days (range, 4 to 13) after infarction (1-week study) and cardiac catheterization was performed 27 ±35 days (range, 7 to 122) after infarction. Nine of the 13 patients underwent repeat positron-emission tomography 6 ±2 months after infarction (6-month study); of the remainder, 1 died, 2 declined the procedure, and 1 had scanning performed outside the designated follow-up period of 12 months. Before the six-month examination, any antianginal medication (except sublingual nitroglycerin) was discontinued for at least 72 hours. No patient took nitroglycerin within two hours of any of the protocol examinations, and all abstained from drinking tea or coffee on the morning of the PET procedures. Treadmill exercise testing was performed according to the modified Bruce protocol.
The control group was made up of patients undergoing routine cardiac catheterization. Discontinuation of antianginal medication and abstinence from compounds containing theophylline were required, as for the study patients.
Cardiac Catheterization and Quantitative Coronary Arteriography
Coronary arteriograms were obtained by the Judkins technique and analyzed by a computerized, automated edge-contour detection system (Cardiovascular Angiographic Analysis System, Pie Medical Equipment, Maastricht, the Netherlands)10. The luminal diameters of the coronary artery in the projection showing maximal severity of stenosis and of the adjacent reference segments were measured at end diastole. Severity of stenosis was also expressed as the percent reduction in the estimated luminal diameter, interpolated from the diameter at the proximal and distal boundaries of the stenosis. Patency of the infarct-related artery was defined according to the Thrombolysis in Myocardial Infarction (TIMI) trial's system for grading recanalization after myocardial infarction11.
The global left ventricular ejection fraction was measured from the left ventricular cineangiogram obtained in the 30 degrees right anterior oblique projection, with an automated, hard-wired endocardial contour detector linked to a microcomputer12,13. The area affected by infarction was classified as one of five regions: anterobasal, anterolateral, apical, inferior, or posterobasal13. In patients with anterior or anterolateral infarction, the posterobasal and inferior regions were considered remote from the infarcted region; in patients with inferior infarction, the anterobasal and anterolateral regions were considered remote.
Measurement of Regional Myocardial Blood Flow with PET
All PET scans were obtained with an ECAT 931-08/12 camera (CTI, Knoxville, Tenn.). Regional myocardial blood flow (in milliliters per minute per gram) was measured in patients and controls using oxygen-15-labeled water as a flow tracer, with use of a previously validated technique for the inhalation of oxygen-15-labeled carbon dioxide (C15O2)14,15. Measurements were made at rest (basal blood flow) and two minutes after the intravenous administration of dipyridamole (0.5 mg per kilogram of body weight over a period of four minutes). The heart rate, systemic blood pressure, and a 12-lead electrocardiogram were recorded every minute during and after the infusion of dipyridamole.
In our analysis, the images of extravascular volume and washout of C15O2 were used to delineate four myocardial regions (anterior, lateral, inferoposterior, and septal) over five to seven transaxial planes, and data were averaged before myocardial perfusion was modeled. The regions of interest were superimposed on the kinetic time frames recorded during the inhalation and washout of C15O2 to give values for regional myocardial blood flow14. With this method of analysis, measurements of flow depend on the amount of perfused tissue but are independent of the size of the region and ventricular-wall thickness16. The anterior region was drawn from the intersection of the right ventricular free wall with the septum. The demarcation between the lateral and inferoposterior regions was drawn at the level of the posterior papillary muscle. In patients in whom the left anterior descending artery was the infarct-related artery, the anterior region was designated the infarcted region, and the inferoposterior region the remote region, thus avoiding transition between the two regions. In patients in whom the right coronary or left circumflex artery was the infarct-related artery, the converse procedure was used.
The coronary vasodilator response was defined as the ratio of peak myocardial blood flow after the administration of dipyridamole to the myocardial blood flow under basal conditions. In the controls, the inferoposterior region was defined as the remote region, since all 10 controls had disease only in the left anterior descending artery. To exclude the effect of changes in systemic hemodynamics on coronary blood flow, the total coronary resistance in the region was calculated from the mean arterial pressure divided by the myocardial blood flow under basal conditions and after the administration of dipyridamole. Scores for the change from basal to peak myocardial blood flow were also derived by subtracting basal flow from hyperemic flow in each region of interest.
Statistical Analysis
All data are expressed as means ±SD. Two-tailed paired and unpaired Student's t-tests were used to compare group means. The simultaneous comparison of more than two mean values was performed with one-way analysis of variance, and Fisher's least-significant-difference method was subsequently applied to identify the source of the difference17. Correlations between measurements were examined with simple linear regression. A P value of less than 0.05 was considered to indicate statistical significance.
Results
Quantitative Coronary Arteriography and Regional Left Ventriculography
Eleven of the 13 patients underwent successful recanalization of the infarct-related artery (TIMI grade 3 in 10 of the 11 patients), with a residual stenosis of 76.3 ±13.8 percent of the diameter (a minimal luminal diameter of 0.72 ±0.37 mm), equivalent to an area stenosis of 92.2 ±6.9 percent (a cross-sectional area of 0.60 ±0.54 mm2). On left ventriculography, the mean left ventricular end-diastolic pressure was 17 ±4 mm Hg, which was not significantly different from the pressure in the controls (13 ±3 mm Hg). The mean global left ventricular ejection fraction was 56.1 ±9.8 percent. In the four patients with inferior infarction, the mean percent contribution of the inferior and posterobasal segments to global wall motion was 18.3 ±4.2 percent (normal range, 26.3 to 43.6 percent), and the mean percent contribution of the anterobasal and anterolateral segments was 38.0 ±1.2 percent (normal range, 24.5 to 42.7 percent). In the nine patients with anterior or anterolateral infarction, the mean percent contribution to global wall motion was 30.2 ±9.2 percent in the inferior and posterobasal segments and 23.7 ±10.4 percent in the anterobasal and anterolateral segments.
Hemodynamic Measurements on PET Scanning
In the one-week and six-month PET scans, there was a significant increase in heart rate and systolic blood pressure and thus in the rate-pressure product from basal values to peak values after the receipt of dipyridamole (Table 2Table 2
Hemodynamic Values on PET Scanning in Patients and Controls, under Basal Conditions and after the Infusion of Dipyridamole (Peak Values).). There were no significant differences in any hemodynamic measures between the control group and the patients at the one-week and six-month PET studies. However, among the nine patients who underwent repeat study at six months, although there were no significant differences in basal values, the systolic blood pressure and mean arterial pressure after the administration of dipyridamole were lower at the one-week study than at six months.Regional Myocardial Blood Flow and Coronary Vascular Resistance
Regional myocardial blood flow in the controls and in the patients with myocardial infarction at the one-week and six-week PET examinations is shown in Figure 1Figure 1
Net Change in Regional Myocardial Blood Flow in the Infarcted Region and the Remote Region in Patients and the Remote Region in Controls., and data on the patients are shown in Table 3Table 3
Regional Myocardial Blood Flow and Coronary Vascular Resistance in the Patients with Myocardial Infarction.. In the control group, basal flow was 1.00 ±0.16 ml per minute per gram of perfusable tissue, and peak flow was 3.08 ±0.53 ml per minute per gram (P<0.001 for the comparison with the remote region in the patients at one week and P = 0.027 for the comparison with the remote region in the patients at six months). The mean coronary vasodilator response in the remote region was lower in the patients than in the controls, in whom this value was 3.17 ±0.72 (P<0.001 for the comparison with the patients at one week and P = 0.009 for the comparison with the patients at six months) (Figure 2Figure 2Mean (±SD) Coronary Vasodilator Response in the Infarcted Region and the Remote Region in Patients and the Remote Region in Controls.). In the infarcted regions, there was no improvement between the two PET studies in basal flow, which remained lower than flow in the remote regions, but there was a small improvement in peak flow. In the remote regions in the patients, peak flow was higher at six months than at one week, but there was no significant change in the basal flow. Despite this improvement, the peak myocardial blood flow, and thus the coronary vasodilator response in the remote regions at the six-month study, remained lower than in the controls.Regional coronary resistance in the patients at the one-week and six-month PET studies is shown in Table 3. As compared with the value in the remote regions in the patients, total coronary resistance in the controls was 90.4 ±6.7 mm Hg • min • g per milliliter at base line (P = 0.025 for the one-week study and P<0.001 for the six-month study) and 30.4 ±6.9 mm Hg • min • g per milliliter after the administration of dipyridamole (P = 0.001 for the one-week study and P = 0.026 for the six-month study).
Correlates of the Coronary Vasodilator Response
In the infarcted region, there was no relation between the absolute severity of coronary-artery stenosis or its severity expressed as a percentage of the luminal diameter, on the one hand, and basal myocardial blood flow, peak myocardial blood flow, or the coronary vasodilator response, on the other. There was also no relation between peak flow or the coronary vasodilator response in the infarcted region and peak flow or coronary vasodilator response in the remote region, peak creatine kinase level, or the length of time from the onset of symptoms to thrombolysis, nor between the peak creatine kinase level and either the coronary vasodilator response or the reduction in total coronary resistance in the remote region.
Discussion
Our findings show that in patients with acute myocardial infarction the coronary vasodilator response is significantly impaired even in areas of myocardium not directly supplied by the infarct-related artery, as compared with similar regions in patients with chronic stable coronary disease. These results may point to a novel mechanism of impaired myocardial perfusion, which could affect the extension of myocardial ischemia at the periphery of the vascular bed of the infarct-related artery, and may open up new avenues for research into an additional component of ischemia after myocardial infarction.
We confirmed that basal myocardial blood flow per gram of perfusable tissue18 was lower in the infarcted regions than in regions remote from the infarct, and we found a marked reduction in the vasodilator response to dipyridamole, not only in the infarcted regions but also in the remote regions perfused by angiographically normal arteries. After an average of six months, the basal flow in the infarcted regions remained unchanged, with a small increase in peak flow; in the remote regions, basal flow was also unchanged, and although the coronary vasodilator response increased significantly, it still remained lower than that in the remote regions of myocardium in the control patients. The mechanisms responsible for the reduced flow in regions of the myocardium remote from infarcted myocardium, which are supplied by nondiseased arteries, are still speculative, but these mechanisms may have important clinical implications.
In the infarcted region, the lower values for basal flow, with no improvement after six months, may be due to reduced oxygen consumption in the residual myocardium, caused in turn by reduced myocardial contractility. The partial improvement in the vasodilator response may occur as a result of the recovery of function of resistance vessels in some of the areas of viable myocardium within the infarcted region.
In remote myocardium perfused by nondiseased arteries, the reduced flow in response to dipyridamole may be explained by several possible mechanisms, some of which can reasonably be ruled out, whereas others should be explored. Our findings cannot be explained by increased total coronary resistance due to elevated left ventricular diastolic pressure19-21. Elevated end-diastolic wall tension, which could increase myocardial oxygen demand22 and thus blood flow,23 is unlikely, because end-diastolic pressures measured by ventriculography and basal flow in remote myocardium were not increased, in contrast to the changes observed in experiments in animals24,25. Structural changes in remote myocardium after infarction due to fiber slippage26 or to altered systolic regional geometry27,28 are also unlikely to have caused the reduced flow response in our patients, since remote regions were selected on the side opposite the site of infarction and there were no signs of regional hypercontractility.
The most likely explanation for the reduced vasodilator response in myocardium remote from the site of infarction is an accentuation of the impaired coronary vasodilatation observed in myocardial regions supplied by nondiseased coronary arteries in patients with chronic coronary disease1-3. Impaired endothelium-dependent dilatation in response both to increased blood flow and to acetylcholine may occur before obstructive coronary artery disease develops4,5,29-32. The generalized increase in neurohormonal sympathetic activity33,34 could lead to an impairment of vasodilator responsiveness in the remote regions35,36 for several days after infarction. However, the failure of the coronary vasodilator response to return to normal after six months suggests a persistent resistance-vessel abnormality, because systemic diastolic blood pressure and heart rate were similar at the time of the two PET studies.
If an abnormal vasomotor response were also present during the development of infarction, inappropriate constriction of resistance vessels distal to the site of coronary thrombosis could influence the development of myocardial necrosis. Mural thrombi are frequent in unstable angina, and coronary occlusion is often intermittent in myocardial infarction37. Vasoconstrictor substances released by coronary thrombi (such as thromboxane A2, serotonin, and thrombin) can constrict the vascular smooth muscle surrounding the site of a thrombus when the artery is sufficiently compliant, but they can also constrict distal vessels, as suggested by the effects of the intracoronary infusion of serotonin38. In the vascular territory of the infarct-related artery, an enhanced response of resistance vessels to substances released by platelets would cause blood-flow stasis, which, in the presence of mural thrombi, could lead to the formation of an occlusive thrombus. In the vascular bed of the non-infarct-related arteries, an enhanced response of resistance vessels to systemic and local neurohormonal constrictor stimuli could increase the extent of ischemia at the periphery of the infarcted area and reduce collateral flow to the infarct-related arterial bed, thus contributing to the acute impairment of ventricular function and to the extension of necrosis.
This inappropriate constriction of resistance vessels may not respond to nitrates or calcium antagonists because the local stimulus and vasoconstrictor response may be too intense to be prevented by the blood levels achieved with the doses currently used, or because the vessels involved have a limited response to such drugs. The development of a rational strategy to counteract this abnormal vasomotor response requires a better understanding of the underlying mechanisms.
Drs. Uren and Lefroy are the recipients of Junior Fellowships from the British Heart Foundation.
Source Information
From the Division of Cardiology (N.G.U., T.C., D.C.L., G.J.D., A.M.) and the Medical Research Council Cyclotron Unit, Hammersmith Hospital, London (R.S.).
Address reprint requests to Dr. Uren at the Department of Cardiology, Glenfield General Hospital, Groby Rd., Leicester LE3 9QF, United Kingdom.
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