Original Article
Angioscopic Evaluation of Coronary-Artery Thrombi in Acute Coronary Syndromes
N Engl J Med 1992; 326:287-291January 30, 1992
- Abstract
- Abstract
Background.
Disruption of an atherosclerotic plaque in a coronary artery followed by the formation of a thrombus is believed to be the cause of both unstable angina and acute myocardial infarction. Although thrombolytic therapy is efficacious in patients with acute myocardial infarction, for unknown reasons it is far less effective in patients with unstable angina. We postulated that there might be differences in the composition of the coronary-artery thrombi in unstable angina and acute myocardial infarction.
Methods.
To investigate the appearance of coronary-artery thrombi, we performed percutaneous transluminal coronary angioscopy in 15 patients with unstable angina and 16 with acute myocardial infarction. Angioscopy was performed within 48 hours after an episode of pain at rest in the patients with unstable angina and within 8 hours of onset in those with acute myocardial infarction.
Results.
Angioscopy revealed coronary thrombi in all but two patients (one in each group). Of the 29 patients with thrombi, those with unstable angina were frequently observed to have grayish-white thrombi (10 of 14, 71 percent), but none were seen in the 15 patients with acute myocardial infarction (P<0.01). By contrast, reddish thrombi were observed in all 15 patients with acute myocardial infarction who had thrombi, but in only 4 of the 14 patients with unstable angina and thrombi (P<0.01). As assessed by coronary angiography, occlusive thrombi occurred frequently in patients with acute myocardial infarction (13 of 16 patients) but were not seen in any of the 15 patients with unstable angina (P<0.01).
Conclusions.
Coronary-artery thrombi play an important part in the pathogenesis of unstable angina and acute myocardial infarction. However, the appearance of the thrombi is different in the two conditions, possibly reflecting differences in the composition or age of the thrombi or the presence or absence of blood flow in the artery. This difference may account for the contrasting results of thrombolytic therapy. (N Engl J Med 1992;326: 287–91.)
Media in This Article
Figure 1
Arteriogram (Panel A) and Angioscopic Image (Panel B) of the Left Coronary Artery of a Patient with Unstable Angina.Figure 2
Arteriogram (Panel A) and Angioscopic Image (Panel B) of the Left Coronary Artery of a Patient with Acute Myocardial Infarction.Article Activity
- Article
A THROMBUS overlying a disruption in the fibrous cap of an atherosclerotic plaque in a coronary artery is considered to be the cause of both unstable angina and acute myocardial infarction.1 2 3 4 5 Recently, the administration of antiplatelet agents, heparin, or both has been found to prevent nonfatal myocardial infarction or cardiac death in patients with unstable angina.6 7 8 9 Although neither of these agents is fibrinolytic, their presumed mechanism of action is to prevent the extension or recurrence of thrombus formation by decreasing platelet aggregation, the formation of fibrin, or both processes. On the basis of these studies and given such pathogenetic mechanisms, it was assumed that thrombolytic therapy, theoretically a potent means of reducing thrombotic obstruction, might be effective in patients with unstable angina. However, several trials assessing changes in the severity of coronary stenosis or the extent of clinical improvement after the administration of thrombolytic agents have yielded conflicting results.10 11 12 13 14 15 16 By contrast, thrombolytic therapy is clearly efficacious in patients with acute myocardial infarction. Several mechanisms have been suggested for the lack of efficacy of thrombolytic agents in unstable angina,17 although there are no confirmed differences in the composition of the thrombi in these two syndromes.
Percutaneous transluminal coronary angioscopy allows the direct visualization of the intracoronary lumen during cardiac catheterization. Angioscopy can be used to assess the histologic appearance of the thrombus2 and can distinguish the thrombus from the vessel wall even if the clot is very small.5 , 18 19 20 The purpose of this study was to investigate the visual characteristics of intraluminal thrombi in patients with unstable angina and to compare them with thrombi seen in patients with acute myocardial infarctions.
Methods
Patients
Between January 1989 and September 1990, percutaneous transluminal coronary angioscopy was performed in 18 consecutive patients with unstable angina and 20 consecutive patients with acute myocardial infarction. These patients were anatomically suitable for angioscopy. Written informed consent for coronary angioscopy was obtained from all patients, and the project was approved by the institutional review board of the National Defense Medical College. Patients with proximal lesions (>50 percent reduction in arterial diameter) of the major coronary arteries were considered appropriate candidates for angioscopy. Angioscopy was not performed in cases of disease affecting the left main coronary artery or an artery supplying an equivalent amount of myocardium, in vessels with less than 50 percent stenosis, or when the affected arteries were considered too small to allow the passage of the angioscope. Three patients with unstable angina and 4 with acute myocardial infarction were excluded from the study because adequate angioscopic pictures could not be obtained; thus, 15 patients with unstable angina and 16 with acute myocardial infarction (Q-wave infarction in 15 and a non-Q-wave infarction in 1) were studied.
Unstable angina pectoris was defined as either an exacerbation of angina that was previously stable, such that angina now occurred at rest, or the new onset of chest pain occurring at rest. No patient had an elevation in the level of creatine kinase to more than twice the normal level. The diagnosis of acute myocardial infarction was documented by a characteristic history of prolonged chest pain, diagnostic electrocardiographs changes, and an elevation of serum cardiac enzymes.
Coronary arteriography and coronary angioscopy were performed within 48 hours of an episode of chest pain at rest in patients with unstable angina and within 8 hours of the onset of acute myocardial infarction. No thrombolytic therapy was administered before angioscopy was performed. A continuous intravenous infusion of heparin (500 to 1000 units per hour) that lasted 9 to 21 hours was administered before angioscopy in three patients with unstable angina. Chest pain was present from the onset of acute myocardial infarction until angioscopy in all but one patient with acute myocardial infarction; none received a continuous infusion of heparin before undergoing angioscopy.
Angioscopy
Coronary angioscopy was performed with an angioscope (Mitsubishi Cable) that incorporates a balloon at the distal tip and an angulation mechanism that was developed in our institution. Immediately before the angioscopic examination, all patients received a bolus intravenous injection of heparin (3000 to 5000 units). Details of the coronary angioscope and angioscopic procedures have been reported previously.21 Although our angioscope was advanced over an angioplasty guide wire, we did not pass the guide wire through the lesion to avoid disrupting the thrombus. The guide wire was withdrawn into the angioscope while the catheter was flushed with physiologic saline in order to observe the entire thrombus. We adjusted the balance of the white and black tones of the images before each coronary angioscopic procedure. Color was adjusted by projecting control colors of red, green, and blue on the cathode-ray-tube display. Halation (the formation of halos) was avoided by adjusting the intensity of the light.
Several factors were considered in determining the site of coronary angioscopy. In cases of single-vessel disease, the target vessel was considered to be an ischemia- or infarct-related artery, and the most severely stenosed lesion was selected. In patients with multivessel disease, the target artery was designated by the occluded or significantly stenotic vessel that corresponded most closely to the ischemic area determined by changes in the ST-T segment during pain at rest.
Thrombi were defined as masses of red or white or of both colors that adhered to the intima and protruded into the lumen. The surface of the thrombus undulated during the infusion of the clear viewing solution (physiologic saline) in most cases but was not dislodged. Coronary thrombi could be readily categorized according to color: those that were grayish white with a minimum (if any) of red were termed grayish-white thrombi, and those that were all red or mixed red and white were termed reddish thrombi.
The angioscopic results were reviewed separately by two physicians, each of whom was unaware of the clinical data and arteriographic findings. In all cases, both observers were in agreement about the categorization of the thrombus. The angioscopist, however, was not blinded to the patients' diagnoses.
In all cases, the angioscopic procedure was completed within eight minutes after the advancement of the guiding catheter and was well tolerated by all patients.
Coronary arteriography was performed immediately before and after coronary angioscopy. After the last injection of contrast material before angioscopy was performed, we decided whether or not an artery was totally occluded. During the same catheterization procedure, percutaneous transluminal coronary angioplasty was performed in 17 patients in whom it was indicated.
Statistical Analysis
Differences between groups were compared by the chi-square test for discrete variables and an independent Student's t-test for continuous variables. Fisher's exact test was used when the expected value for a cell was less than 5. All P values were two-tailed. A P value of less than 0.05 was considered to indicate statistical significance.
Results
The base-line characteristics of the patients in the two groups are shown in Table 1Table 1
Base-Line Characteristics and Frequency of Thrombus Formation in Patients with Unstable Angina and Acute Myocardial Infarction.*. The length of time from the onset of episodes of chest pain to coronary angioscopy was significantly longer in patients with unstable angina than in those with acute myocardial infarction (mean [±SD], 19.2±16.0 vs. 4.7±1.9 hours; P<0.01). A complete occlusion was observed in one patient with unstable angina during the first injection of contrast material, but it was not apparent after the second injection. Among the ischemia- or infarct-related lesions, the frequency of complete occlusion was significantly greater in patients with acute myocardial infarction than in those with unstable angina (13 of 16 vs. 0 of 15, P<0.01). There were no significant differences between the two groups with respect to other clinical and angiographic characteristics.Angioscopy revealed coronary thrombi in all but two patients (one patient in each group). However, the appearance of the thrombi differed between the two groups (Table 1). In the 29 patients with thrombi, grayish-white thrombi (Fig. 1Figure 1
Arteriogram (Panel A) and Angioscopic Image (Panel B) of the Left Coronary Artery of a Patient with Unstable Angina.) were observed in 10 of 14 patients with unstable angina (71 percent) but in none of 15 patients with acute myocardial infarction. On the other hand, reddish thrombi (Fig. 2Figure 2Arteriogram (Panel A) and Angioscopic Image (Panel B) of the Left Coronary Artery of a Patient with Acute Myocardial Infarction.) were observed in all 15 patients with acute myocardial infarction and thrombi but in only 4 of the 14 patients with unstable angina and thrombi (Table 1). Differences between groups with respect to the appearance of the thrombi were statistically significant (P<0.01).Since angioscopy was performed within eight hours of the onset of chest pain in patients with acute myocardial infarction, we divided the patients with unstable angina into an early-angioscopy group (those who had coronary angioscopy less than eight hours after the onset of pain at rest) and a late-angioscopy group (those who had coronary angioscopy eight or more hours after the onset of pain at rest), and the frequency and type of thrombus were compared in the two groups. The frequency of thrombi was not significantly different between the two groups: six of six patients (100 percent) in the early-angioscopy group as compared with eight of nine patients (89 percent) in the late-angioscopy group. Grayish-white thrombi were observed in four of six patients (67 percent) in the early-angioscopy group and in six of nine patients (67 percent) in the late-angioscopy group. Reddish thrombi were observed in two of six patients (33 percent) in the early-angioscopy group and in two of nine patients (22 percent) in the late-angioscopy group. There were no significant differences between the two groups. Finally, there were no major complications during angioscopy in either group.
Discussion
Angiographic,22 23 24 25 26 27 angioscopic,5 , 18 pathological,28 and biochemical29 30 31 data have implicated the formation of thrombus in the pathogenesis of unstable angina. Although thrombolytic therapy is efficacious in patients with acute myocardial infarction, its benefit in patients with unstable angina remains controversial in spite of the frequent presence of coronary-artery thrombus in such patients.17 Several possible explanations have been proposed for the lack of efficacy of thrombolytic therapy in unstable angina. One explanation is that perhaps not all patients have intracoronary thrombus at the time of the administration of thrombolytic therapy.16 , 17 However, the present study revealed that thrombi were present in most patients with unstable angina regardless of the timing of coronary angioscopy. Since angiography has been shown to be less sensitive than angioscopy for the detection of thrombus,5 , 18 19 20 this finding is not surprising.
In the present study, coronary angioscopy showed that the thrombi observed in unstable angina differed from those observed in acute myocardial infarction. Most patients with unstable angina had grayish-white thrombi, whereas reddish thrombi predominated in patients with acute myocardial infarction. These differences in color probably reflect differences in the composition of the thrombus, perhaps related in part to the different ages of the thrombi or to the presence or absence of blood flow in the artery. Whereas red thrombi tend to form under conditions of stasis (as in an occluded vessel), white thrombi tend to form when blood flow has not been completely interrupted. Pathological studies of coronary thrombi showed that white thrombi were platelet-rich, whereas red thrombi contained an abundance of fibrin mixed with erythrocytes and platelets.32 In addition, when observed after thrombolysis, white thrombi were found to be older than red thrombi and had a tight fibrin network.33 Because we did not perform histologic examinations of the coronary thrombi observed in our study, we cannot be certain that the composition of the grayish-white and red thrombi in fact differed from one another in the same way as they did in the pathological studies.
Angioscopy performed percutaneously cannot be used to examine the entire lesion, since the angioscope cannot be passed through the obstructed lesion. Therefore, the portion of the lesion that is visualized may not contain the entire thrombus. In an artery that is totally occluded by a thrombus composed of fibrin and red cells, a red thrombus will be seen on angioscopy. However, in a less than totally occluded artery, it is conceivable that a component of the thrombus that was situated downstream might be missed, since this portion would be beyond the range of the angioscope. Thrombi forming in an area of altered blood flow distal to a severe stenosis are rich in fibrin.4 , 34 These thrombi, seen angiographically as filling defects distal to a lesion, are sometimes found in unstable angina but are more common after myocardial infarction. In the presence of unstable angina, such red thrombi would be missed by this angioscopic approach. Although retrograde angioscopy has been performed at the time of bypass surgery and is capable of visualizing the downstream thrombus,18 this procedure is obviously limited by patient selection. In addition, we cannot exclude the possibility that the differences we observed in the composition of thrombi in the two syndromes may solely reflect the fact that thrombi were occlusive in myocardial infarction but were not occlusive in unstable angina. To answer this question more patients will need to be studied. Finally, although the results of angioscopy were reviewed by two physicians who had no knowledge of the patients' diagnoses, the angioscopy itself was not performed in a blinded fashion, leaving open the possibility of bias.
In conclusion, thrombus formation has an important role in the pathogenesis of unstable angina and myocardial infarction. However, the appearance of the thrombus as determined angioscopically differs in these two syndromes. This difference may account for the contrasting results of thrombolytic therapy in the two syndromes.
Source Information
From the First Department of Internal Medicine (K.M., K.S., A.M., K.A., T.S., A.K., H.N.) and the Department of Medical Engineering (T.A.), National Defense Medical College, Saitama, Japan, and the Department of Medicine, Division of Cardiology, Mount Sinai Medical Center, New York (J.A.A.). Address reprint requests to Dr. Mizuno at the First Department of Internal Medicine, National Defense Medical College, 3–2, Namiki, Tokorozawa, Saitama 359, Japan.
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