Angiographic occurrence and clinical correlates of intraluminal coronary artery thrombus: role of unstable angina

The importance of intraluminal coronary artery thrombus in acute myocardial infarction is now recognized. Coronary thrombi, however, may be important in ischemic syndromes other than infarction. The coronary angiograms of 268 consecutive patients undergoing diagnostic angiography were prospectively examined for intracoronary thrombus and form the basis of this study. Of these patients, 29 (11%) (25 men and 4 women) met the criteria for coronary artery thrombus. Of the 29 patients with thrombus, 24 (83%) had unstable angina before angiography. The five remaining patients with thrombus had had a transmural myocardial infarction 3 to 18 months before cardiac catheterization. In 21 patients, the thrombus was distal to a significant stenosis; in 8 it was proximal to or at the site of a significant stenosis. Coronary artery thrombus was identified in 24 (35%) of 67 patients with unstable angina compared with only 5 (2.5%) of 201 patients with stable angina (p less than 0.0001).     

Angiographic observations and clinical relevance of coronary thrombus in unstable angina pectoris

To assess the mechanisms of unstable angina, the coronary angiographic studies in 69 patients with severe unstable angina (prolonged pain or pain at rest) and in 20 patients with stable angina were blindly reviewed to assess the coronary morphologic changes in these syndromes. Coronary angiography was performed an average of 1.7 days from admission and an average of 24 hours from last symptoms of chest pain in patients with unstable angina. Angiographic studies were analyzed for evidence of coronary thrombus (intraluminal filling defects) at significant stenoses in patent vessels or thrombus at sites of total occlusion) and for coronary lesion morphology suggesting a complex or acute lesion (irregular or ill-defined margins, inhomogeneity, haziness or ulceration). Angiographic evidence of coronary thrombus was present in 40 of 69 patients (58%) with unstable angina: 31 (45%) had intraluminal filling defects and 9 (13%) had thrombotic total occlusion with well-developed collaterals present. Only 1 of 20 patients (5%) with stable angina had evidence of thrombus (p less than 0.001). Complex lesions were present in 18 other unstable patients (26%) and in 2 other patients (10%) with stable angina who did not have angiographic evidence of thrombus. Overall, 58 of 69 patients (84%) with unstable angina had morphologic findings suggesting an acute process (thrombus or complex lesion) compared with 3 of 20 patients (15%) with stable angina, p less than 0.0001. Thus, unstable angina is associated with a high prevalence of angiographic coronary thrombus and complex lesions suggesting an acute process, in contrast to stable angina.(ABSTRACT TRUNCATED AT 250 WORDS)     

Unstable angina: from physiopathology to therapeutics]

Unstable angina is a term which encompasses several clinical syndromes (crescendo angina, angina de novo, resting angina, postinfarction angina), intermediary between stable angina and myocardial infarction. The results of coronary angioscopy have allowed differentiation of accelerated effort angina which seems related to ulceration of an atheromatous plaque from resting angina, more commonly associated with intraluminal thrombosis. The diagnosis of unstable angina is clinical and justifies immediate hospital admission to a coronary care unit because of the risk of myocardial infarction and/or sudden death. Medical management comprises triple anti-ischemic therapy (nitrate derivatives, betablockers, calcium antagonists), anticoagulants and platelet antiagregants. Randomised therapeutic trials versus placebo have shown that this treatment decreases the incidence of refractory angina and myocardial infarction. Several studies are under way to assess the role of thrombolytic therapy in unstable angina. When unstable angina is refractory to maximal medical therapy, emergency coronary angiography should be performed. However the outcome is usually favourable and coronary angiography can be performed several days after the acute event. The coronary lesion responsible for unstable angina is often "complex", an eccentric, irregular, severe stenosis or appearances of thrombosis. Whenever possible, depending on the coronary lesion, myocardial revascularisation by coronary angioplasty or aorto-coronary bypass should be proposed. Surgical treatment has been shown to be more effective (symptomatic relief, improved survival) than medical therapy in patients with triple vessel disease. However, the results of studies comparing medical or surgical treatment with coronary angioplasty are not yet available.     

Unstable angina: Relationship of clinical presentation,coronary artery pathology,and clinical outcome

Patients with unstable angina are heterogeneous with respect to presentation, coronary artery morphology, and clinical outcome. Subclassification of these patients based on clinical history has been proposed as a means of identifying individuals at increased cardiac risk. We applied such a classification system to 129 patients discharged from a coronary care unit with a diagnosis of acute myocardial ischemia. Patients were then assessed for cardiac events (recurrent angina requiring revascularization, myocardial infarction, death) 12 months following hospital discharge. Patients were classified as recent onset unstable angina preinfarction (n = 42), crescendo unstable angina preinfarction (n = 48), and unstable angina postinfarction (n = 39). Within each of these groups, the patients were further subclassified based on the occurrence of angina on effort, at rest, or both. No attempt was made to subset patients taking antiischemic drugs at the time of clinical presentation to the physician. Coronary angiographic pathology (morphology and number of vessels involved) was similar in the subgroups, but coronary artery thrombus was statistically more likely to be found in patients with crescendo rest angina preinfarction or with frequent anginal episodes at rest postinfarction. Mortality was significantly higher for patients with unstable angina postinfarction (7.7%) than preinfarction (1.1%). No statistical differences were noted between the subgroups with respect to the occurrence of myocardial infarction or recurrent unstable angina requiring revascularization. These data suggest that subclassification of unstable angina patients based on clinical characteristics at presentation is not useful to predict subsequent myocardial infarction or recurrent angina requiring revascularization. However, as one might expect, patients with recurrent angina postinfarction have a higher mortality rate than patients with unstable angina preinfarction, and patients with recurrent rest angina, either pre- or postinfarction, are more likely to have intracoronary thrombus than patients with new onset angina or crescendo effort angina; however, the presence of thrombus did not predict a poor clinical outcome.     

Coronary angiographic morphology in myocardial infarction: a link between the pathogenesis of unstable angina and myocardial infarction

It has previously been shown that analysis of coronary morphology can separate unstable from stable angina. An eccentric stenosis with a narrow neck or irregular borders, or both, is very common in patients who present with acute unstable angina, whereas it is rare in patients with stable angina. To extend these observations to myocardial infarction, the coronary morphology of 41 patients with acute or recent infarction and nontotally occluded infarct vessels was studied. For all patients, 27 (66%) of 41 infarct vessels contained this eccentric narrowing, whereas only 2 (11%) of 18 noninfarct vessels with narrowing of 50 to less than 100% had this lesion (p less than 0.001). In addition, a separate group of patients with acute myocardial infarction who underwent intracoronary streptokinase infusion were also analyzed in similar fashion. Fourteen (61%) of 23 infarct vessels contained this lesion after streptokinase infusion compared with 1 (9%) of 11 noninfarct vessels with narrowing of 50 to less than 100% (p less than 0.01). Therefore, an eccentric coronary stenosis with a narrow neck or irregular borders, or both, is the most common morphologic feature on angiography in both acute and recent infarction as well as unstable angina. This lesion probably represents either a disrupted atherosclerotic plaque or a partially occlusive or lysed thrombus, or both. The predominance of this morphology in both unstable angina and acute infarction suggests a possible link between these two conditions. Unstable angina and myocardial infarction may form a continuous spectrum with the clinical outcome dependent on the subsequent change in coronary supply relative to myocardial demand.     

Coronary angioplasty in unstable angina. Immediate and short-term results

We report the results of percutaneous transluminal coronary angioplasty (PTCA) in 67 consecutive patients with unstable angina. Twenty patients had new onset (less than 2 months) angina, 33 patients had crescendo angina and 14 had early postinfarction angina. Fifty-one patients had one-vessel disease, 12 patients had two-vessel disease and two patients had three-vessel disease; two patients had a stenosis of a venous graft. In cases with multivessel disease, we performed only the dilatation of the ischaemia-related vessel identified by morphologic features of coronary lesion and electrocardiographic changes during chest pain. The procedure was successful in 54 cases (80.6%). Seven patients (10.4%) had major complications. Emergency coronary artery bypass graft surgery was performed in 6 cases (8.9%) because of occlusion of the left anterior descending artery; despite emergency operation one patient died and two patients sustained a myocardial infarction. One patient had occlusion of the right coronary artery and inferior myocardial infarction. In all patients in whom angioplasty was successful unstable angina disappeared. At 6 months follow-up there were no infarctions or deaths but 14 of 42 patients (33%) had recurrent angina. Restenosis occurred in 16 of 33 patients (48%) who had repeat coronary angiography. Four patients with recurrence of unstable angina had repeat angioplasty; it was successful in 3 cases. One patient died of refractory cardiac arrest. The mortality rate of 71 procedures performed in 67 patients was 2.8% (2/71) and the overall myocardial infarction rate was 4.2% (3/71).(ABSTRACT TRUNCATED AT 250 WORDS)     

Morphologic comparison of frequency and types of acute lesions in the major epicardial coronary arteries in unstable angina pectoris, sudden coronary death and acute myocardial infarction

The frequency and type of acute lesions in the four major (right, left main, left anterior descending, left circumflex) epicardial coronary arteries were examined at necropsy in 14 patients with unstable angina pectoris, 21 patients with sudden coronary death and 32 patients with a fatal first acute myocardial infarction. None of the 67 patients had a grossly visible left ventricular scar (healed myocardial infarct) and only the group with acute myocardial infarction had left ventricular myocardial necrosis. Although the frequency of intraluminal thrombus was similar in patients with unstable angina (29%) and sudden death (29%) and significantly lower than in those with acute infarction (69%) (p = 0.02), the thrombus in the patients with unstable angina and sudden death consisted almost entirely of platelets and was nonocclusive, whereas the thrombus in the group with acute infarction consisted almost entirely of fibrin and was occlusive. The frequency of plaque rupture was insignificantly different in the groups with unstable angina (36%) and sudden death (19%), and was significantly lower than in the group with acute infarction (75%) (p = 0.02). The frequency of plaque hemorrhage was insignificantly different in the groups with unstable angina (64%) and sudden death (38%) and was significantly lower than in the group with acute infarction (90%) (p = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)     

Angiographic morphology of coronary lesions in various syndromes of ischemic cardiopathy

The angiographic morphology of coronary lesions is often completely ignored in the prognostic and decision-making process related to patients with coronary disease. We performed this study to evaluate the possibility of identifying complex or complicated atherosclerotic lesions by means of routine diagnostic coronary arteriography, and to assess their prevalence in the different syndromes of ischaemic heart disease. From an overall group of 200 successive cases studied using coronary angiography, 111 patients with significant coronary artery disease in whom a "culprit lesion" could be identified were retrospectively selected. The angiographic morphology of coronary lesions was defined according to an original classification as: 1) simple stenosis, 2) complex lesion, 3) thrombosis. Of the 111 patients, 36 had been studied for stable angina, 31 for unstable angina, 10 for a non-Q wave myocardial infarction, 34 for transmural infarction. The clinical groups did not show any significant differences when compared on the basis of number of vessels involved and degree of narrowing of the ischaemia-producing artery. Significant differences were found when angiographic morphology was analyzed. In stable angina 78% of ischaemia producing lesions appeared as simple stenoses, while 92% of the unstable or more severely ischaemic patients exhibited complicated lesions (p less than 0.001). In unstable angina and non-Q infarction a complex lesion was present respectively in 71% and 60% of the cases; clear-cut intraluminal thrombosis was demonstrated in 23% of unstable angina, in 30% of non-Q wave infarction and in 39% of transmural infarction (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Differential progression of complex culprit stenoses in patients with stable and unstable angina pectoris

Objectives. This study sought to compare the evolution of complex culprit stenoses in patients with stable and those with unstable angina pectoris.Background. Complex coronary stenoses are associated with adverse clinical and angiographic outcomes. However, it is not known whether the evolution of complex stenoses differs in unstable angina versus stable angina pectoris.Methods. We prospectively assessed stenosis progression in 95 patients with unstable angina whose angina stabilized with medical therapy (Group 1) and 200 patients presenting with stable angina (Group 2). After diagnostic angiography, all patients were placed on a waiting list for coronary angioplasty and restudied at 8 ± 4 (mean ± SD) months later. In each patient the presumed culprit stenosis was identified and classified as complex (irregular borders, overhanging edges or thrombus) or smooth (absence of complex features). Stenosis progression, as assessed by computerized angiography, was defined as ⩾20% diameter reduction or new total occlusion.Results. At the first angiogram, 364 stenoses ⩾50% and 383 stenoses <50% were identified. At restudy, 36 (15%) of 236 stenoses progressed in 29 Group 1 patients and 36 (7%) of 502 stenoses in 31 Group 2 patients (p = 0.001). Forty-five (88%) of 51 stenoses ⩾50% and 6 (29%) of 21 stenoses <50% that nitrogeressed developed to total coronary occlusion (p = 0.001). More culprit stenoses progressed in Group 1 than in Group 2 (p = 0.006), whereas progression of nonculprit stenoses was not significantly different in both groups. Culprit complex stenoses progressed more frequently in Group 1 than in Group 2 (p = 0.01). During follow-up, 3 patients died (myocardial infarction), and 51 had a nonfatal coronary event. Culprit steenoses progressed in 15 (54%) of the 28 patients with a nonfatal coronary event in Group 1 and in 9 (39%) of 23 patients in Group 2 (p = NS). Complex morphology (p < 0.001) and unstable angina at initial presentation (p < 0.01) were predictive factors for progression of culprit stenoses.Conclusions. A larges proportion of culprit complex stenoses progress in unstable angina than stable angina, and this is frequently associated with recurrence of coronary events.     

Intracoronary thrombus in syndromes of unstable myocardial ischemia

The association of coronary thrombosis and transmural myocardial infarction is well documented. We have recently observed apparent intracoronary thrombl in patients with unstable myocardial ischemia without transmural infarction. To assess the frequency and angiographic characteristics of intracoronary defects consistent with thrombi, we reviewed the angiograms of all patients undergoing catheterization within 1 month of the onset of unstable angina or the intermediate coronary syndrome. Of 129 such patients, eight (6.2%) had nonoccluding, hazy, or nonopacified intracoronary filling defects consistent with thrombus in angiographically well-opacified vessels. All defects were just distal to a significant (80% to 99%) coronary stenosis. In each instance the thrombus-involved vessel supplied a myocardial segment referable to the electrocardiographically defined area of ischemia. Support for the theory that the intracoronary defects were thrombi includes three patients with enlargement of the filling defects, who underwent repeat angiography within 7 days, and two patients with embolization of defect fragments. Furthermore these defects were angiographically similar to poststenotic intraluminal defects seen transiently in some patients after partial intracoronary streptokinase recanalization. In conclusion, we have observed, angiographically, intracoronary filling defects consistent with thrombus in some patients with unstable myocardial ischemia.     

Coronary spasm-induced acute myocardial infarction associated with intracoronary thrombosis]

A 63-year-old man was admitted with an acute anteroseptal myocardial infarction. Coronary angiography performed 3 hours after the onset of chest pain revealed 99% stenosis of the proximal left anterior descending coronary artery (LAD) with delayed filling and intraluminal thrombus distal to the stenosis. After the intracoronary injection of isosorbide dinitrate, the delayed filling disappeared and a subsequent intracoronary urokinase partially dissolved the thrombus. Repeat coronary angiography in the chronic phase disclosed 75% stenosis of the LAD and disappearance of the thrombus. Intracoronary acetylcholine provoked a coronary spasm at the stenotic site of the LAD, concomitantly with chest pain and ST-segment elevation in the anterior leads. The present case demonstrated that coronary spasm plays an important role in thrombus formation and acute myocardial infarction. To date, the concept has been postulated that a dynamic interaction between atherosclerosis, platelet aggregation and spasm may work to cause coronary thrombosis and subsequently lead to acute myocardial infarction. Our report shed light on the importance of coronary spasm in the pathogenesis of myocardial infarction.     

Angiographic coronary artery lesion morphology and pathogenetic mechanisms of myocardial ischemia in stable and unstable coronary artery disease syndromes.

The angiographic morphology of coronary artery stenoses was studied in 160 patients referred for diagnostic coronary arteriography. Three groups of patients were studied: 60 patients with stable angina, 78 patients with unstable angina and 22 patients with a recent myocardial infarction. Complex lesions were more frequently observed in patients with unstable angina (59%, p less than 0.001) and in patients with a recent myocardial infarction (54%, p less than 0.05) then in patients with stable angina (25%). Angiographic signs suggestive for the presence of intravascular thrombi were almost exclusively observed in the patients with unstable angina (34%, p less than 0.001) and in the patients with a recent myocardial infarction (27%, P less than 0.001) and were almost completely absent in the patients with stable angina (1.5%). The high prevalence of complex coronary artery lesion morphology and of intravascular thrombi observed in patients with unstable angina or with a recent myocardial infarction emphasizes the important role of intima disruption and of subsequent thrombosis in the pathogenesis of myocardial ischemia in those unstable syndromes of ischemic heart disease.     

The occurrence of angiographically detected intracoronary thrombus in patients with unstable angina pectoris

To examine the role of intracoronary thrombus (ICT) in unstable angina, we reviewed the coronary arteriograms of 83 patients with unstable angina (group I) and 37 patients with stable angina (group II) for angiographic evidence of ICT. Group I and group II patients were similar with respect to mean age, presence of single and multiple vessel disease, and past history of myocardial infarction. Group I patients had no ECG or creatine kinase enzyme evidence of acute myocardial infarction. The angiographic criteria for ICT included an intracoronary filling defect, intraluminal staining, and total coronary artery occlusion with convex dye outline. ICT was found in 10 of 83 patients in group I (12.0%) vs 0 of 37 patients in group II (p less than 0.05). These findings suggest that in some patients coronary artery thrombosis plays an important role in the pathogenesis of unstable angina.     

Transient ischaemia refractory to conventional medical treatment in unstable angina: angiographic correlates and prognostic implications.

Complex stenosis morphology is frequently seen in patients with unstable angina. However, its relation to transient myocardial ischaemia and clinical outcome has not been adequately elucidated. We studied 86 patients admitted to the Coronary Care Unit for unstable angina; all patients underwent ECG Holter monitoring during the first 2-4 days, while receiving intensive triple drug treatment. Coronary angiography and subsequent analysis of the ischaemia-related artery were performed within 12 days of admission. Patients were grouped according to their angiographic features: 45 showed complex coronary morphology (CM: 29 eccentric stenosis with irregular borders or overhanging edges; 16 intracoronary thrombus), 11 had documented coronary spasm as well as moderate atherosclerosis (CS), seven had left main coronary artery disease, and the remaining 23 patients showed regular and smooth morphology of coronary stenosis (RM). At admission, transient myocardial ischaemia (TMI) was greater in patients with CM (85 +/- 60 min .24 h-1) than in those with RM or CS (33 +/- 26 min .24 h-1; P less than 0.005). After 3 days of full medical treatment TMI decreased in all groups, but 34/45 patients with CM and 9/34 with RM or CS still showed residual ischaemia (greater than 0 min .24 h-1): 76% vs 26%, P less than 0.02. Follow-up was obtained at hospital discharge and after 1 year in all patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

冠状动脉心肌桥的临床意义

目的:探讨冠状动脉心肌桥的临床意义。方法:回顾分析接受选择性冠状动脉造影的756例病人中检出的82例(10.8%)有心肌桥患者的资料。结果:82例心肌桥患者临床表现为稳定型心绞痛者10例(12.2%),不稳定型心绞痛者33例(40.2%),不明原因的胸痛者34例(41.5%),急性心肌梗塞者3例(3.7%),肥厚型心肌病者2例(2.4%);心肌桥近端存在冠状动脉狭窄者23例(28.0%),心肌桥远端存在冠状动脉狭窄者3例(3.7%),孤立性心肌桥(无冠脉狭窄)者46例(56.1%)。结论:心肌桥的发生率高,可导致心肌缺血,引起心绞痛;对临床疑诊心绞痛的病人应尽早常规行冠状动脉造影检查。     

Short term results of percutaneous transluminal coronary angioplasty with the monorail technique: experience in the first 1000 patients

The monorail technique allows monitoring of all steps of the coronary angioplasty procedure by high quality coronary angiography; easy, rapid, and safe recrossing and redilatation of the lesion if necessary; and stepwise dilatation of a stenosis with sequential increase of size of balloons. Transstenotic pressure differences cannot, however, be measured through the narrow shaft of the standard monorail balloon catheter. The monorail technique was used in 1014 patients (820 men, 194 women; mean age 57.8 years (range 24 to 84]. The indication for coronary angioplasty was stable angina in 52%, unstable angina in 40%, and acute myocardial infarction in 8%. Single vessel coronary angioplasty was attempted in 78%, multilesion coronary angioplasty in 11%, and multivessel coronary angioplasty in 11%. Angiographic success (reduction of stenosis to less than 50% of the luminal diameter) of all attempted lesions was achieved in 93%. The technique was clinically successful--that is, angiographic success of all attempted lesions, no occurrence of a major complication (death, myocardial infarction, acute bypass surgery), and improvement of symptoms--in 92% and partially successful in 1.3%. The clinical success rates were similar for stable angina (91%) and unstable angina (94%), but were somewhat lower for acute myocardial infarction (88%). Failure without major complication occurred in 3.4% of the patients. Failure with a major complication occurred in 3.3% (death 0.3%, myocardial infarction 2.4%, and acute bypass surgery 2.3%). The total major complication rate was higher in unstable angina (4.2%) than in stable angina (3.0%). These results indicate that the monorail technique can be applied safely and effectively for coronary angioplasty of patients with stable angina, unstable angina, and acute myocardial infarction.     

Angiographic morphology in unstable angina and its relation to transient myocardial ischemia and hospital outcome

Complex stenosis morphology frequently occurs in patients with unstable angina pectoris. However, its relation to transient myocardial ischemia and hospital outcome has not been ascertained. To address this issue, 88 patients with significant (greater than or equal to 50%) coronary artery disease presenting with angina--new onset (n = 38), worsening (n = 20) or at rest (n = 30)-were studied. Patients with left main artery disease, normal coronary arteries or occlusion of the ischemia-related arteries were not included in the study. Continuous electrocardiographic recordings were obtained during the first 24 hours. Angiography was performed within 1 week from admission. Complex morphology was defined as any stenosis with irregular borders, overhanging edges or intracoronary thrombus. Only data referring to the in-hospital outcome were considered in this study. Adverse end points were sudden death, myocardial infarction and emergency revascularization. Analysis of the angiograms revealed a complex morphology in 58 patients (group 1). The remaining 30 patients served as control subjects (group 2). Thirty-two of the 58 group 1 patients had an unfavorable clinical outcome (positive predictive value, 55%). A similar outcome occurred in only 2 of the 30 group 2 patients (negative predictive value, 93%). Of the 32 group 1 patients who had an unfavorable clinical outcome, 29 had a cumulative duration of transient myocardial ischemia of greater than or equal to 60 minutes per 24 hours. A similar duration of ischemia, however, was observed in another 6 group 1 and in 8 group 2 patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Holmium laser-assisted coronary angioplasty in acute ischemic syndromes

Background and hypothesis: Initial studies have shown holmium laser to be effective in ablation of coronary atheromam, and small studies suggest that it may be helpful in ablation of thrombotic stenoses. Therefore, holmium laser-assisted coronary angioplasty was studied in 85 consecutive patients with acute ischemia syndromes. Methods: Indications for therapy were acute myocardial infarction (MI) in 7 patients (8%), post-MI ischemic in 32 patients (38%), and crescendo angina pectoris in 46 patients (54%). Coronary morphology characteristics by multivessel angioplasty prognosis group criteria were Type A in 9 (10%), Type B1 in 15 (18%), Type B2 in 44 (52%), Type C in 17 patients (20%). Results: Angiographic evidence of thrombus was seen in 37 (44%) of patients. The laser successfully crossed the total length of the coronary narrowing in 76 patients (89%). Procedure/clinical success was 92% for the total study population, 100% for patients with acute MI, 94% for post-MI ischemia patients, and 89% for patients with crescendo angina. Lesions with and without thrombus had identical procedure succes rates. Major complication rate was 3.5%, (deaths 0%, Q-wave MI 0%, and emergent bypass surgery 3.5%). Six-month angiographic restenosis rate (>50% stenosis) was 45%. Conclusion: Holmium laser-assisted balloon angioplasty appears promising in the treatment of acute ischemic syndromes and thrombotic coronary lesions.     

Silent myocardial ischemia in unstable angina and acute myocardial infarction. Prospective clinical study

To establish the prevalence and characteristics of silent myocardial ischemia in patients with unstable angina and acute myocardial infarction and its possible correlation with coronary artery lesions; two groups patients were studied, fifteen with unstable angina and fifteen with acute myocardial infarction. In all patients a continuous 24 hours ECG recording was made with a solid state microprocessor for ST variation analysis, and all underwent coronary arteriography and ventriculography, the severity of coronary heart disease was determined by Gensini scoring system and the coronary angiography morphology was studied. In 86% patients with unstable angina ischemic ST changes were found, 90% of these episodes were silent. There were 66% of the patients with acute myocardial infarction and ST ischemic changes of these 75% were silent. There was no correlation with the ischemic myocardium score index, nor with the angiographic morphology or the heart rate. Therefore it can be said that myocardial ischemia is a result not only of anatomic factors but of many others such as vasoconstriction, endothelial, myocardial, systemic and hemorheological alterations.