The heart in fatal unstable angina pectoris

Compared to patients with sudden coronary death and acute myocardial infarction, relatively little morphologic data has been reported in patients with unstable angina pectoris. This article reviews necropsy data collected from one laboratory on unstable angina pectoris. From these data, several observations are appropriate: (1) Patients with unstable angina as a group have more coronary narrowing by atherosclerotic plaque than do patients with sudden coronary death or acute or healed myocardial infarction. (2) Patients with unstable angina have a much higher frequency of severe narrowing of the left main coronary artery than do patients in other coronary subsets. (3) The coronary atherosclerotic plaques in unstable angina consist primarily of fibrous tissue, and they are more similar to those found in patients with sudden coronary death than in patients with acute myocardial infarction. (4) The frequency of acute coronary lesions (thrombi, plaque rupture, and plaque hemorrhage) is similar to that observed in patients with sudden coronary death and significantly less than that observed in acute myocardial infarction. (5) The frequency of multiluminal channels throughout the major coronary arteries is significantly higher in unstable angina compared to sudden coronary death or acute myocardial infarction. (6) The major epicardial arteries and the heart are smaller in patients with unstable angina than in patients with sudden coronary death or acute myocardial infarction. (7) The left ventricular cavity is usually of normal size in patients with unstable angina and therefore left ventricular function is usually normal.     

Coronary anatomy and arteriography in patients with unstable angina pectoris.

A prospective series of 188 patients with the syndrome of unstable angina pectoris undergoing coronary arteriography was reviewed to determine the spectrum of anatomic coronary artery disease, suitability for coronary revascularization and in-hospital morbidity and mortality. Thirty-two patients demonstrated normal to moderately diseased coronary arteries. None of these patients sustained myocardial infarction or died. Twenty patients (10.6 percent) had normal coronary arteriograms. Of the 156 patients having severe coronary artery disease (greater than 70 percent stenosis), 20 patients (13 percent) had left main coronary artery disease. One hundred forty-two patients (91 percent) were potential candidates for coronary surgery; 14 were not candidates because of distal vessel disease or poor left ventricular function. During cardiac angiography or in the subsequent hospital period 12 patients sustained a myocardial infarction and 7 of these died. Of these seven, six had left main coronary artery disease and one had three vessel disease. In three patients who died (1.9 percent of those with severe coronary artery disease) the death may have been related to cardiac catheterization because evidence of myocardial necrosis began within 24 hours of study. Thus, patients with the syndrome of unstable angina pectoris usually presented with severe coronary artery disease and were candidates for coronary revascularization. The anatomic severity of coronary artery disease appeared to be the most important factor contributing to myocardlal infarction or death after cardiac catheterization. Mortality after catheterization was primarily associated with left main coronary artery disease.     

Pitfalls in the prediction of coronary artery disease from the electrocardiogram or vectorcardiogram

Seventy-eight patients with inferior, lateral and dorsal myocardial infarction patterns on electrocardiogram and vectorcardiogram had coronary cineangiographic studies. Of 41 cases with inferior infarction patterns 11 (27%) had entirely normal coronary arteries on cineangiography. Six of these had rheumatic heart disease, 2 had primary myocardial disease and 3 with angina pectoris had no demonstrable abnormality. Of 16 cases with lateral wall infarction patterns 4 (25%) had normal coronary arteries on cineangiography. Three of these had primary myocardial disease and one had idiopathic hypertrophic subaortic stenosis. With revised and stringent criteria for isolated dorsal wall infarction 21 cases were analyzed. Six of 21 (29%) were free of coronary artery disease. Five of these had angina pectoris but no demonstrable disease and 1 had rheumatic heart disease. When coronary artery disease was found in the overall group of 78 patients, double and triple vessel involvement occurred in 75% of the cases.Thus, patients with infarction patterns on electrocardiogram and vectorcardiogram frequently slow complete absence of coronary artery obstruction when studied by the technique of selective coronary arteriography. When such patients are found to have diseased coronary arteries, the disease, is frequently widespread and involves multiple vessels.     

Chest pain as a predictor of coronary artery disease in patients with obstructive aortic valve disease

To clarify the association between chest pain and significant coronary artery disease in patients who have aortic valve disease, 76 consecutive candidates for aortic valve replacement were evaluated prospectively with use of a historical questionnaire and coronary arteriography. Of the 76 patients, 19 (25 percent) had no chest pain, 21 (28 percent) had chest pain that was not-typical of angina pectoris and 36 (47 percent) had chest pain typical of angina pectoris. In 18 of 19 patients the absence of chest pain correlated with the absence of coronary artery disease. The single patient without chest pain who had coronary artery disease had evidence of an inferior myocardial infarction in the electrocardiogram. Thus, absence of chest pain and the absence of electrocardiographic evidence of infarction predicted the absence of coronary disease in all cases.

The presence of chest pain did not predict the presence of coronary artery disease, but the more typical the pain of angina pectoris the more likely were patients to have significant coronary artery disease. Of the 21 patients with atypical chest pain, 6 (29 percent) had coronary artery disease, but of the 36 patients with typical angina pectoris 23 (64 percent) had significant coronary artery disease. In addition, when patients with chest pain not typical of angina pectoris also had coronary artery disease, the diseased vessels usually supplied smaller areas of the left ventricle than when the pain was typical of angina pectoris. In 21 of 23 patients (91 percent) with typical angina pectoris and significant coronary artery disease, lesions were present in the left coronary artery. There was no systolic pressure gradient across the aortic valve that excluded the presence of coronary artery disease, although all patients with a calculated aortic valve area of less than 0.4 cm² were free of coronary artery disease. Patients with severe left ventricular dysfunction were more likely to have normal coronary arteries.     

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)     

Qualitative and quantitative comparison of amounts of narrowing by atherosclerotic plaques in the major epicardial coronary arteries at necropsy in sudden coronary death, transmural acute myocardial infarction, transmural healed myocardial infarction and unstable angina pectoris

The amounts of narrowing of the 4 major (left main, left anterior descending, left circumflex and right) epicardial coronary arteries by atherosclerotic plaques were compared in 4 subsets of coronary patients. Of the 129 patients studied at necropsy, an average of 2.7 of the 4 arteries was narrowed greater than 75% in cross-sectional area at some point (0.7/4 in controls), and the group with unstable angina pectoris (3.2/4) had more narrowing than did the groups with sudden coronary death (2.8/4), acute myocardial infarction (2.7/4) and healed myocardial infarction (2.3/4). Each of the 4 major epicardial coronary arteries was divided into 5-mm long segments and a histologic section was prepared and stained by the Movat method of each of the 6,461 segments in the 129 patients and in the 1,849 segments in the 40 control subjects. In the 129 patients, 35% of the 5-mm segments were narrowed 75 to 100% in cross-sectional area (3% in controls) and the group with unstable angina had the highest percent (48%) of segments severely narrowed compared to the groups with sudden coronary death (36%), acute myocardial infarction (34%) and healed myocardial infarction (31%). Thus, of the 4 subsets of patients with fatal coronary artery disease studied at necropsy, those with unstable angina pectoris had the most severe and extensive coronary atherosclerosis.     

Candidates for transluminal coronary angioplasty

An analysis was made of clinical and electrocardiographic prognostic determinants of multiple vessel disease in 100 men, aged under 45 years, who survived a myocardial infarction. All patients underwent selective coronary arteriography within 1 year after sustaining a myocardial infarction. Multivessel disease was present in 64 patients; 33 patients had single vessel disease and 3 had either normal coronary arteries or minimal lesions. Exercise stress testing, electrocardiographic location of the infarction, total serum cholesterol and clinical features including body build, arterial blood pressure, smoking habits, family history of coronary artery disease and the presence of angina pectoris either before or after the acute event proved to be poor predictors of multiple vessel disease. Only 74 percent of the patients were correctly classified by a discriminant function analysis. Thus, for prognostic reasons, coronary arteriography seems warranted in young patients after acute myocardial infarction, even in the absence of residual angina or multiple risk factors.     

Amounts of coronary arterial narrowing by atherosclerotic plaque at necropsy in patients with lower extremity amputation.

In 26 patients (mean age at death 68 +/- 9 years) who had undergone amputation (at mean age 63 +/- 12 years) of 1 or both lower extremities due to severe peripheral arterial atherosclerosis, the amounts of narrowing at necropsy in the 4 major (left main, left anterior descending, left circumflex, and right) epicardial coronary arteries were determined. During life, 15 of the 26 patients (58%) had symptoms of myocardial ischemia: angina pectoris alone in 1, acute myocardial infarction alone in 5, and angina and/or infarction plus congestive heart failure or sudden coronary death in 9. Twelve of the 26 patients (42%) died from consequences of myocardial ischemia: acute myocardial infarction in 5, sudden coronary death in 3, chronic congestive heart failure in 3, and shortly after coronary bypass surgery in 1. Grossly visible left ventricular necrosis or fibrosis, or both, was present in 21 patients (81%). Of the 26 patients, 24 (92%) had narrowing 76 to 100% in cross-sectional area of 1 or more major coronary arteries by atherosclerotic plaque. The mean number of coronary arteries per patient severely (> 75%) narrowed was 2.3 +/- 1.0/4.0. Of the 104 major coronary arteries in the 26 patients, 60 (58%) were narrowed > 75% in cross-sectional area by plaque. The 4 major coronary arteries in the 26 patients were divided into 5-mm segments and a histologic section, stained by the Movat method, was prepared from each segment.(ABSTRACT TRUNCATED AT 250 WORDS)     

Role of coronary artery spasm in ischemic heart disease. Therapeutic implications

The term coronary artery spasm should not be used interchangeably with the specific clinical syndrome "variant angina" since it does occur in other acute and chronic ischemic heart disease syndromes. The term coronary artery spasm should not be applied to patients with ischemic heart disease unless there is clinical, angiographic, and physiologic evidence of its presence. The diagnosis of coronary artery spasm is confirmed by angiography, i.e. change in caliber of the coronary arteries plus evidence of ischemia. Probable diagnosis is in patients who have the syndrome of variant angina, i.e. rest angina associated with ST segment elevation on the electrocardiogram. One can be highly suspicious that the spasm is at work in patients who have rest angina, especially those with unstable angina. One can be suspicious of patients who have variable effort angina or walk-through angina. Coronary artery spasm is a possibility in patients with an acute myocardial infarction or acute re-infarction and is also possible that sudden death in patients with normal coronary arteries can be related to coronary artery spasm. Coronary artery spasm is the usual cause of myocardial ischemia in patients with rest angina without effort angina. This has also commonly been documented in patients with rest and effort angina. There are isolated reports suggesting that patients with effort angina pectoris also develop coronary artery spasm. Coronary artery spasm has been documented to occur in association with acute myocardial infarction. Whether coronary artery spasm is the cause or the result of myocardial infarction has not been determined at this time. However, the recent combined use of intracoronary nitroglycerin and intracoronary streptokinase in patients with acute myocardial infarction has shown reversal of totally obstructed arteries and suggests the relationship between coronary artery disease, coronary artery spasm, and in situ coronary thrombosis. The incidence of sudden death in patients with documented coronary artery spasm is unknown. But, since complete heart block and/or ventricular tachycardia occur during episodes of coronary artery spasm, it is not unreasonable to assume that some patients have died as a result of these rhythm disturbances. The prognosis of patients with coronary artery spasm seems to depend on the presence or absence of severe coronary atherosclerosis, i.e. those with severe disease have a worse prognosis. Current therapy of patients with coronary artery spasm involves the use of nitrates and calcium antagonists.(ABSTRACT TRUNCATED AT 400 WORDS)     

Intracoronary temperature in patients with coronary artery disease

OBJECTIVES: Measurements of changes in plaque temperature may predict plaque rupture. The present study investigated variations in temperature within the atherosclerotic coronary artery using a pressure guide wire with thermal sensor (dual sensor guide wire). METHODS AND RESULTS: Seventy-seven patients (78 lesions), who had no significant lesion at the orifice of the culprit coronary artery, were studied. The patients had acute myocardial infarction (22 patients), unstable angina pectoris (20 patients), and stable angina pectoris (35 patients). The thermal sensor was calibrated at the orifice of the coronary artery, and then inserted into the culprit coronary artery. deltaT was defined as the difference between the intracoronary temperature at the position of the pressure gradient and at the orifice. deltaT was higher in patients with acute myocardial infarction and unstable angina pectoris than in patients with stable angina pectoris (0.09 +/- 0.07 and 0.07 +/- 0.07 vs 0.03 +/- 0.04 degrees C, p < 0.001, p = 0.02, respectively). There was no significant difference in deltaT between patients with acute myocardial infarction and unstable angina pectoris (p = 0.48). Patients with acute myocardial infarction and unstable angina pectoris showed a significant relationship between deltaT and C-reactive protein (r = 0.59, p = 0.0004). CONCLUSIONS: The variations in intracoronary temperature of the culprit coronary arteries in patients with acute coronary syndrome were higher than those in patients with stable angina pectoris. These variations may be related to inflammation of vulnerable plaque.     

冠心病患者血浆血栓调节蛋白水平的测定及其临床意义

目的　测定冠心病患者血浆血栓调节蛋白 ( throm bom odulin,TM)水平并探讨其临床意义。方法　急性心肌梗死、不稳定型心绞痛、稳定型心绞痛三组患者及正常对照组 ,抽取血浆并用酶联免疫吸附试验测量其血浆 TM水平。结果　急性心肌梗死组、不稳定型心绞痛组、稳定型心绞痛组血浆 TM水平均高于正常对照组 ( P<0 .0 5 ) ;急性心肌梗死组与不稳定型心绞痛组间患者血浆 TM水平没有显著性差异 ( P>0 .0 5 ) ,但均高于稳定型心绞痛组和正常对照组 ( P<0 .0 5 )。结论　血浆可溶性 TM水平是反映冠心病患者内皮细胞损伤程度和范围的良好标志 ,对急性心肌梗死、不稳定型心绞痛、稳定型心绞痛的鉴别有一定的临床指导意义     

Long-term prognosis of “variant” angina with medical treatment

One hundred thirty-eight patients with “variant angina” were followed up for periods of 2 to 8 years. All patients had a history of angina at rest, and 42 percent also had exertional angina. Normal coronary arteries were found in 9 of the 107 patients who underwent coronary arteriography; the remainder had stenosis greater than 50 percent in diameter of at least one major vessel. Coronary vasospasm was demonstrated in all 37 patients studied with coronary arteriography during angina at rest. Twenty-eight patients had acute myocardial infarction and five patients died within 1 month of admission to hospital. Of the 133 surviving patients, 120 were treated medically and 13 underwent coronary arterial surgery. In the medically treated group, only seven patients died and only four had acute myocardial infarction during the remainder of the follow-up period. Symptoms became less frequent and less severe; approximately 50 percent of the patients remained completely asymptomatic for at least 12 months by the end of the 4th year. Death, acute myocardial infarction and persistence of symptoms were more frequent in those patients with more severe coronary atherosclerotic disease although, even in this group, the overall incidence of death and acute myocardial infarction was small. It is concluded that the prognosis of patients with “variant” angina receiving appropriate medical therapy is reasonably good after the acute phase, even in the presence of severe coronary atherosclerosis.     

Myocardial lesions of progressive systemic sclerosis. A cause of cardiac dysfunction.

The nature, prevalence, functional significance, and indeed existence of myocardial disease in progressive systemic sclerosis (PSS) has been debated. In this study the clinical and pathological features of 52 autopsied patients were analyzed in an attempt to resolve these questions. A distinctive focal myocardial lesion ranging from contraction band necrosis to replacement fibrosis throughout both ventricular walls was present in 23 patients who had widely patent extramural coronary arteries. There were no morphologic abnormalities of the intramyocardial coronary arteries to account for these lesions. Comparing those patients having severe (13), mild (10), or no (24) PSS myocardial lesions, and patent extramural coronary arteries, there were no major differences in age, sex, frequency and severity of pulmonary, renal or hypertensive disease which could account for the myocardial necrosis and fibrosis. The three groups did differ, however, with regard to clinical cardiac abnormalities: ventricular arrhythmias and conduction disturbances were six and two times as frequent, respectively, in those with severe myocardial PSS compared to the other two groups. A pattern of primary myocardial disease with intractable congestive heart failure resulted from severe myocardial PSS in four patients, angina pectoris with normal coronary arteries was associated with the severe myocardial lesion in three patients, and sudden death in five. The occurrence of contraction band necrosis suggests that the myocardial damage in PSS might be due to intermittent vascular spasm of the type recognized in the digits and possibly kidneys and lungs, i.e., an intramyocardial Raynaud's phenomenon. The findings in our patients clearly show that myocardial progressive systemic sclerosis is a distinct entity with relatively frequent occurrence which may lead to arrhythmias, congestive heart failure, angina pectoris with normal coronary arteries and sudden death.     

Percutaneous transluminal coronary angioplasty in acute myocardial infarction

Percutaneous transluminal coronary angioplasty (PTCA) has, in general, been restricted to therapy for patients with angina pectoris. Thrombolytic therapy and guide wire recanalization have been used to recanalize coronary arteries in patients with evolving myocardial infarction. Recently we and others have examined the use of PTCA to recanalize the acutely occluded artery associated with the early evolving phase of myocardial infarction. PTCA was performed as definitive therapy in eight patients with acute myocardial infarction. Seven of these had totally occluded arteries to the region of infarct. The infarct-related artery was open within 20 minutes in each of these cases. PTCA recanalization resulted in evidence for reperfusion in each case. Residual stenoses either were not present or were minimal. The procedure was well tolerated. These preliminary results suggest that PTCA may be a reasonable alternative to intracoronary thrombolytic therapy in certain patients with acute evolving myocardial infarction.     

Coronary artery spasm induced by 5-fluorouracil

The frequently used chemotherapeutic drug 5-fluorouracil (5-FU) is known to cause angina pectoris and arrhythmias; myocardial infarction and sudden cardiac death could occur. Potential reasons for these phenomena range from toxic/metabolic disturbances to coronary artery spasms. This report shows angiographically proven spasmophilia of the coronary arteries and contributes to the understanding of angina pectoris occurring during treatment with 5-FU. Thus, verapamil type calcium antagonists as well as nitrates should be administered primarily in patients with coronary artery disease and in all patients who had been symptomatic during 5-FU administration in order to prevent further episodes.     

Degrees of coronary arterial narrowing at necropsy in men with large fusiform abdominal aortic aneurysm.

In 27 patients (mean age at death 72 +/- 9 years) with abdominal aortic aneurysm (AAA) > or = 5.0 cm in its widest transverse diameter, the amounts of narrowing at necropsy in the 4 major (left main, left anterior descending, left circumflex, and right) epicardial coronary arteries were determined. During life, 12 of the 27 patients (44%) had symptoms of myocardial ischemia: angina pectoris alone in 2, acute myocardial infarction alone in 3, angina pectoris and acute myocardial infarction in 5, and sudden coronary death in 2. Ten of the 27 patients (37%) died from consequences of myocardial ischemia. Six (22%) died from rupture of the AAA. Grossly visible left ventricular necrosis or fibrosis, or both, was present in 15 patients (56%). Of the 27 patients, 23 (85%) had narrowing 76 to 100% in cross-sectional area of 1 or more major coronary arteries by atherosclerotic plaque. The mean number of coronary arteries per patient severely (> 75%) narrowed was 2.0 +/- 1.3/4.0. Of the 108 major coronary arteries in the 27 patients, 55 (51%) were narrowed > 75% in cross-sectional area by plaque. The 4 major coronary arteries in the 27 patients were divided into 5-mm segments and a histologic section, stained by the Movat method, was prepared from each segment. The mean percentages of the resulting 1,475 five-mm segments narrowed in cross-sectional area 0 to 25%, 26 to 50%, 51 to 75%, 76 to 95% and 96 to 100% were 17, 37, 28, 15 and 3%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Disabling angina pectoris with normal coronary arteries in patients undergoing long-term hemodialysis

Reports of patients undergoing long-term hemodialysis presenting with angina pectoris have usually shown severe coronary atherosclerosis. we studied a series of nine patients undergoing regular maintenance dialysis referred for incapacitating angina. Of them, four had strictly normal coronary angiograms.The patients with normal angiograms were all females who were significantly younger (p < 0.05) and had more severe hypertension and higher left ventricular wall stress than patients showing coronary artery lesions.Anemia and increased myocardial oxygen consumption due to high blood pressure may explain the syndrome of angina pectoris in the presence of long-term dialysis in patients with normal coronary arteries. The prevalence of this association cannot be ascertained unless prospective studies are conducted. However, our data suggest that it might not be an uncommon finding.     

Cardiac pain at rest. Management and follow-up of 100 consecutive cases.

One hundred consecutive patients, admitted to the coronary care unit with cardiac pain at rest but no evidence of recent myocardial infarction have been followed up for nine to 26 (mean 14) months. They were treated initially with bed rest, beta-adrenergic blockade, and nitrates. In 54 patients pain subsided within 24 hours. Coronary angiography was carried out in 46. Thirty-five had coronary artery lesions and three had spasm in normal coronary arteries. One had hypertrophic cardiomyopathy and seven had normal findings. Seventeen patients with previous angina and severe coronary disease were operated on, with one death and one perioperative infarction; two died late, 12 were symptom free, and two had angina. Seven of 18 patients treated medically had recurrent angina and underwent operation. Of the 11 unoperated patients, one died, three had angina, and seven were symptom free. Two of the eight patients who were not catheterised developed infarction, four had angina, and three were symptom free. Recurrent pain continued for more than 24 hours in 46 patients, and all underwent angiography. Forty-three had coronary artery disease and 34 underwent early bypass surgery; there were two operative deaths and three perioperative infarctions. Twenty-six symptom free at follow-up. Of the nine unoperated patients with coronary disease, four developed infarction, two were operated on for recurrent angina, two were symptom free, and one had mild angina. Optimal management of patients with pain at rest can be determined only with knowledge of the coronary artery anatomy and of left ventricular function. Many respond initially to intensive medical treatment and coronary angiography can be performed electively. In those with continuing pain, urgent angiography is required and can be done safely.     

Anomalous origin of right coronary artery from left coronary sinus

Anomalous aortic origin of the coronary arteries is uncommon but clinically significant. Manifestations vary from asymptomatic patients to those who present with angina pectoris, myocardial infarction, heart failure, syncope, arrhythmias, and sudden death. We describe 4 patients, aged 34 to 59 years, who were diagnosed with right coronary artery arising from the left sinus of Valsalva, confirmed by coronary angiography, which was surgically repaired. Three patients presented dyspnea and angina, and one with acute myocardial infarction. At operation, the right coronary artery was dissected at the take-off from the intramural course, and reimplanted into the right sinus of Valsalva. There was no mortality. One patient had associated coronary artery disease that required stent placement postoperatively. This reimplantation technique provides a good physiological and anatomical repair, eliminates a slit-like ostium, avoids compression of the coronary artery between the aorta and the pulmonary artery, and gives superior results to coronary artery bypass grafting or the unroofing technique.     

Fibrinopeptide A and beta thromboglobulin in patients with angina pectoris and acute myocardial infarction

The purpose of this study was to investigate the degree of platelet activation and thrombin generation in 40 patients with stable angina pectoris and in 20 patients with acute myocardial infarction (AMI) by determining the plasma beta thromboglobulin (BTG) and fibrinopeptide A (FPA) concentrations. In patients with angina pectoris increased platelet activation correlated with extensive coronary pathology; the activation, however, was not influenced by a previous myocardial infarction, use of oral anticoagulants, beta-blocking agents, or hyperlipidemia. The plasma beta thromboglobulin concentration predicted more accurately the extent of the coronary artery disease than the functional angina pectoris classification. Thrombin generation was within the normal range. In patients with acute myocardial infarction increased platelet activation and enhanced thrombin generation were found, which were not related to the infarct localization, infarct size, or the presence of complications. Consequently, in these patients determination of plasma beta thromboglobulin and fibrinopeptide A concentrations is useless for the diagnosis of venous thromboembolism.