Rapid progression of coronary stenosis in patients with unstable angina pectoris selected for coronary angioplasty

We studied the course of coronary stenosis in the first 62 patients (45 men and 17 women) referred for coronary angioplasty in the interval between the diagnostic arteriogram and the preangioplasty coronary arteriogram. In 42 patients, the stenosis was in the left anterior descending artery, in 17 patients in the right coronary artery, in one patient in the left circumflex, and in two patients in the vein graft. Twenty-six patients had stable angina pectoris, 34 patients had unstable angina, and two patients had no angina. The coronary stenosis did not change significantly in any patient with stable angina. Conversely, the stenosis progressed in nine of the 34 patients with unstable angina (26.5%). In five of the nine patients with progression, total occlusion ensued. In four of the five patients total occlusion occurred within the 45-day interval between the diagnostic and the preangioplasty coronary arteriogram. New or increased preexisting collaterals to the occluded vessel developed in all five patients with total occlusion. None of these patients had clinical or electrocardiographic evidence of myocardial infarction or significant changes in ventricular function. Angiographic evidence of thrombi was seen in ten of 34 patients with unstable angina (29%). We concluded that coronary artery stenosis in patients with unstable angina pectoris is progressive in a significant number after a short time. The cause of progression of coronary stenosis in patients with unstable angina is unknown. Since in a significant number of patients with unstable angina coronary thrombus was suggested by angiography, coronary thrombosis superimposed on coronary atherosclerosis may play a significant role in this syndrome. Further prospective studies are needed, including repeat coronary arteriograms to evaluate the cause of unstable angina, define the role of coronary thrombosis, and evaluate the cause of unstable angina, define the role of coronary thrombosis, and evaluate the efficacy of more aggressive treatment adding the use of prolong heparin and antiplatelet agents prior to coronary angioplasty.     

Unstable angina and evolving myocardial infarction following coronary bypass surgery: pathogenesis and treatment with interventional catheterization

Effective therapy for patients with unstable angina or evolving myocardial infarction following coronary bypass surgery requires accurate delineation of the pathoanatomy and prompt intervention. We therefore performed cardiac catheterization in 10 consecutive patients: four with acute myocardial infarction and six with refractory unstable angina (NYHA class IV). All patients with acute myocardial infarction were found to have completely thrombosed vein grafts supplying totally occluded native coronary arteries. In three patients with evolving myocardial infarction occurring within 4 weeks of coronary bypass surgery, graft thrombosis was caused by venous valves in two patients and a suboptimal anastomosis in a third. The fourth patient sustained a myocardial infarction 7 years after coronary bypass surgery with atherosclerotic plaque rupture causing vein graft thrombosis. Therapy with intragraft streptokinase resulted in complete clearing of thrombus, pain relief, and control of injury current in all four patients. Rest angina with concomitant ST and T wave changes occurred in six patients. In two patients symptoms occurred early (within 6 months), whereas angina developed 4 to 10 years after coronary bypass graft surgery in four patients. In the two patients with early recurrence of symptoms suboptimal anastomosis was found in one, while the other patient had a venous valve in the vein graft in conjunction with a stenosis in the native coronary artery. In three of four patients with late recurrence of angina, symptoms developed as a result of atherosclerotic stenosis in their vein grafts; in the fourth patient an occluded graft was found to supply a stenosed native coronary artery.(ABSTRACT TRUNCATED AT 250 WORDS)     

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).     

Morphologic features of unstable atherothrombotic plaques underlying acute coronary syndromes

Unstable angina appears to be a good clinical marker for rapidly progressing coronary artery disease. Pathologically, an unstable atherothrombotic coronary lesion, represented by a raised atherosclerotic plaque with ruptured surface causing variable degree of hemorrhage into the plaque and luminal thrombosis (rapid plaque progression), usually is present in patients at autopsy after a period of unstable angina. The thrombus at the rupture site may be mural and limited (just sealing the rupture) or occlusive, depending on the degree of preexisting atherosclerotic stenosis. An occlusive thrombus is seldom seen over ruptured plaques causing less than 75% stenosis (histologic cross-sectional area reduction), but it is found with increasing frequency when severity of stenosis increases beyond 75%. Most occlusive thrombi have a layered structure with thrombus material of differing age indicating an episodic growth by repeated mural deposits, and microemboli/microinfarcts are frequently found in the myocardium downstream to coronary thrombi, indicating intermittent thrombus fragmentation with peripheral embolization. Such a "dynamic thrombosis" (with or without a concomitant focal vasospastic phenomenon) at the site of an unstable (ruptured) atherosclerotic lesion obviously may lead to the other thrombus-related acute coronary events: myocardial infarction or sudden death. Accordingly, progression of unstable angina to myocardial infarction or sudden death should, in principle, be preventable by the correct timing of current available therapies aimed to prevent or eliminate (1) the chronic atherosclerotic obstruction, (2) the acute plaque disruption, (3) luminal thrombosis, and (4) vasospasm.     

Downstream resistance effects of intracoronary thrombosis in the stenosed canine coronary artery.

OBJECTIVE: The presence is well established in unstable angina of intracoronary thrombosis in a stenosed epicardial coronary artery. The effects of the thrombus formation on the distal microcirculation are however still unclear. METHODS: We adapted the Folts canine model of left circumflex coronary arterial stenosis and intracoronary thrombosis by the insertion of a pressure catheter distal to the stenosis and by the use of 15 microns radioactive microspheres for measurement of regional myocardial blood flow. This permitted measurement during circumflex artery occlusion of collateral flow, downstream vascular resistance and collateral resistance. RESULTS: Distal circumflex resistance, obtained by dividing the distal circumflex coronary pressure gradient by the collateral flow, significantly increased with thrombosis (94.47 +/- 35.72 to 120.06 +/- 34.47; p = 0.0018) mmHg/ml/min/g. Changes in collateral flow and resistance in the presence of thrombosis, during maximum ischaemic vasodilatation, were inconsistent. CONCLUSION: Thrombosis causes increased vascular resistance in the microcirculation distal to the site of injury. This may be of clinical relevance in unstable angina, characterised by episodes of thrombus growth and embolization, in which ischaemic episodes may be worsened by generalised downstream vascular changes.     

Effects of thrombolytic therapy in unstable angina: clinical and angiographic results

The incidence of intracoronary thrombus and the effects of thrombolytic therapy were studied in 41 patients with unstable angina. All patients underwent coronary angiography 2 to 69 h (mean 19) after their last attack of chest pain. Immediately after angiography, 21 patients received intracoronary streptokinase (250,000 IU in 45 min) and were retrospectively analyzed. Twenty patients received intravenous recombinant tissue-type plasminogen activator (rt-PA) (100 mg in 3 h) and were involved in a prospective study. Eleven of the 21 patients from the streptokinase group and 11 of the 20 patients from the rt-PA group showed a decrease in the severity of the coronary stenosis on repeat angiography 1 day later. A decrease in coronary obstruction was primarily observed in 10 of 13 patients with a complete stenosis and in 6 of 9 patients with a subtotal stenosis and markedly diminished coronary flow. Improvement in coronary anatomy was not determined by the clinical characteristics of the patients. Twenty-eight of the 41 patients had angiographic evidence of intracoronary thrombus formation before and 16 had such evidence after thrombolytic treatment. Nine patients developed a small increase in serum cardiac enzymes before or during treatment. Ischemic symptoms and the incidence of surgical or angioplastic intervention were not different in patients with or without a reduction in coronary artery stenosis after fibrinolytic therapy. These observations suggest a high incidence of coronary thrombosis in patients with unstable angina. The data do not permit assessment of the clinical therapeutic efficacy of thrombolytic therapy. Better risk stratification and placebo-controlled prospective studies are required to obtain information on the risk/benefit ratio of such therapy in unstable angina.     

Prediction of coronary artery disease by left ventricular regional wall motion abnormalities in patients with stenosis of the aortic valve

To identify predictive factors for coronary artery disease in patients with stenosis of the aortic valve the clinical histories, haemodynamic measurements, biplane contrast left ventriculograms, and coronary angiograms of 83 consecutively catheterised patients with valvar aortic stenosis were examined retrospectively. The mean (SD) age was 66.4 (9.1) years and 78% were men. Fifty five patients had significant coronary artery disease (greater than or equal to 50% diameter narrowing). Forty five (82%) of 55 patients with and 23 (82%) of 28 patients without coronary disease had angina. Heart failure occurred in a third of the patients; these patients were on average older, were more likely to be female, and had lower ejection fractions and cardiac outputs than patients in whom failure did not occur. Calculated valve area, transvalvar gradient, and left ventricular end diastolic pressure did not discriminate between patients with and without coronary disease. Syncope was less common than angina and heart failure and was associated with significantly lower valve areas and higher gradients than those found in patients without syncope. Left ventricular regional wall motion abnormalities were equally common in the groups with and without angina and predicted coronary artery disease with 94% accuracy. The absence of regional wall motion abnormality was an insensitive marker of normal coronary arteries as 45% of such patients had coronary disease. Five of the 83 patients had significant coronary disease without angina or regional wall motion abnormality. In patients with aortic stenosis angina did not predict the presence of coronary artery disease; therefore, it is advisable to have the results of coronary angiography before aortic valve replacement in a population such as this. Two of the patients with heart failure and severe aortic stenosis had regional wall motion abnormality with normal coronary arteries. Thus in some patients left ventricular failure produced by increased afterload may itself be a cause of left ventricular regional wall motion abnormality.     

Prediction of coronary artery disease by left ventricular regional wall motion abnormalities in patients with stenosis of the aortic valve.

To identify predictive factors for coronary artery disease in patients with stenosis of the aortic valve the clinical histories, haemodynamic measurements, biplane contrast left ventriculograms, and coronary angiograms of 83 consecutively catheterised patients with valvar aortic stenosis were examined retrospectively. The mean (SD) age was 66.4 (9.1) years and 78% were men. Fifty five patients had significant coronary artery disease (greater than or equal to 50% diameter narrowing). Forty five (82%) of 55 patients with and 23 (82%) of 28 patients without coronary disease had angina. Heart failure occurred in a third of the patients; these patients were on average older, were more likely to be female, and had lower ejection fractions and cardiac outputs than patients in whom failure did not occur. Calculated valve area, transvalvar gradient, and left ventricular end diastolic pressure did not discriminate between patients with and without coronary disease. Syncope was less common than angina and heart failure and was associated with significantly lower valve areas and higher gradients than those found in patients without syncope. Left ventricular regional wall motion abnormalities were equally common in the groups with and without angina and predicted coronary artery disease with 94% accuracy. The absence of regional wall motion abnormality was an insensitive marker of normal coronary arteries as 45% of such patients had coronary disease. Five of the 83 patients had significant coronary disease without angina or regional wall motion abnormality. In patients with aortic stenosis angina did not predict the presence of coronary artery disease; therefore, it is advisable to have the results of coronary angiography before aortic valve replacement in a population such as this. Two of the patients with heart failure and severe aortic stenosis had regional wall motion abnormality with normal coronary arteries. Thus in some patients left ventricular failure produced by increased afterload may itself be a cause of left ventricular regional wall motion abnormality.     

Unstable angina pectoris and the progression to acute myocardial infarction. Role of platelets and platelet-derived mediators

The conversion from stable to unstable angina and the further progression to myocardial infarction are usually associated with atherosclerotic plaque fissuring or ulceration at sites of coronary artery stenosis and subsequent development of a thrombus. This thrombus formation is initiated by platelet adhesion and aggregation; these, in turn, are promoted by the local release and accumulation of thromboxane A(2) and serotonin. This accumulation and the resulting platelet aggregation at sites of endothelial injury cause dynamic vasoconstriction. With time, the platelet-initiated thrombus expands to include white and red blood cells in a fibrin mesh. Thus, a fully occlusive coronary thrombus may develop and cause the progression from unstable angina to acute myocardial infarction, often Q-wave myocardial infarction. We believe that the connection between unstable angina and acute myocardial infarction is a continuum relative to the processes of coronary artery thrombosis and vasoconstriction. When the period of platelet aggregation or dynamic vasoconstriction at sites of endothelial injury and coronary stenosis lasts only a few minutes and is repetitive, unstable angina or non-Q wave myocardial infarction occurs. However, when complete coronary artery occlusion lasts for longer than 4 hours, a transmural or Q-wave myocardial infarction results. Recently, in experimental animal models with mechanically induced coronary artery stenoses and endothelial injury, we have found that other mediators, including adenosine diphosphate and thrombin, also contribute to coronary artery thrombosis. Moreover, in humans with limiting angina, we have identified spontaneous coronary blood flow variations in a pattern similar to the variations caused by alternating platelet attachment and dislodgement in experimental canine modes. In this review, we add information to our previous observations in order to present the possible mechanisms of conversion from chronic to acute coronary heart disease syndromes.     

Reappraising the role of immediate intervention following thrombolytic recanalization in acute myocardial infarction

Early studies indicated that after successful thrombolytic recanalization, adjunctive percutaneous transluminal coronary angioplasty (PTCA) was not appropriate, even when a significant residual stenosis was present. The aim of this study was to assess in-hospital clinical outcomes of patients with acute myocardial infarction (AMI) who underwent successful recanalization after thrombolytic therapy. The relation between repeat AMI/unstable angina and the severity of the stenosis, as well as other angiographic and clinical features was also examined. One hundred patients with AMI of <10 hours underwent coronary angiography 2 hours after receiving thrombolytic therapy. Salvage PTCA +/- stenting was performed if recanalization was unsuccessful (Thrombolysis In Myocardial Infarction [TIMI] trial grade 0 to 2), and no PTCA was undertaken if there was brisk anterograde flow (TIMI 3). Angiographic analysis was performed to assess the severity of the residual lesion, as well as the presence or absence of thrombus. Forty patients had unsuccessful recanalization, and of these, 36 underwent attempted PTCA. Of the 60 patients with TIMI 3 flow, 15 required repeat angiography and PTCA after repeat AMI (n = 13) or unstable angina (n = 2) within 5 days. Receiver-operating characteristic analysis indicated an optimum percent diameter stenosis predictor of 85% for repeat AMI/unstable angina. There was no additional relation to age, gender, time to thrombolysis, the infarct-related artery, or the presence of culprit lesion thrombus. After recanalization, a high-grade stenosis >85% is common (n = 25, 42.4%). This is associated with a 54% repeat AMI/unstable angina risk-a ninefold increase in the incidence of such events than in patients with lesions <85%. Thus, patients with narrowings >85% may benefit from early intervention rather than a conservative approach. Narrowings <85% have a 94% probability of no repeat AMI/unstable angina and do not require early intervention.     

Thrombolytic therapy reduces the incidence of left ventricular thrombus after anterior myocardial infarction: Relationship to vessel patency and infarct size

BACKGROUND: Controversial evidence exists as to whether thrombolytic therapyreduces the incidence of left ventricular thrombus in acutemyocardial infarction and, if so, how this relates to successfulreperfusion. METHODS: Four hundred and eighteen consecutive patients underwent echocardiographyand coronary angiography within 3 weeks of an acute myocardialinfarction. A dyssynergic score was calculated by analysingregional wall motion in 18 left ventricular segments. The infarct-relatedartery was considered patent if TIMI grade 2 or 3 flow and lessthan 90% stenosis were present. Retrograde perfusion by Rentrop'sgrade 2 or 3 collaterals was considered significant. RESULTS: Large anterior myocardial infarctions were associated with thehighest prevalence (39%) of left ventricular thrombosis. Thrombuswas also very frequent if the left anterior descending coronaryartery was occluded and no collaterals to the infarct area wereseen (75%). Anticoagulant therapy reduced the prevalence ofleft ventricular thrombus, regardless of whether the infarct-relatedvessel was patent or not. Conversely, in patients undergoingthrombolysis the incidence of left ventricular thrombosis waslower when the left anterior descending coronary artery waspatent, and especially when an early creatine kinase peak, suggestiveof reperfusion, was recorded (7%). Finally, the presence ofleft ventricular thrombosis was inversely related to the asynergyscore. CONCLUSION: These observations suggest that the presence of left ventricularthrombus is related to the extent of myocardial damage. Thrombolytictherapy reduces thrombus probably by salvaging myocardium atrisk. (Eur Heart J 1996; 17: 421–428)     

The role of intracoronary thrombus in unstable angina: angiographic assessment and thrombolytic therapy during ongoing anginal attacks

Intracoronary thrombus is regarded as a potentially important factor in the etiology of unstable angina, but the incidence of intracoronary thrombus in unstable angina has not been clearly defined. To determine the occurrence of intracoronary thrombus during ongoing angina pectoris, coronary angiography was performed during spontaneous ischemic attacks in 37 patients with prolonged rest angina. All patients exhibited significant (greater than 50%) stenoses of at least one major coronary artery. Of the 37 patients, 21 (57%) had intracoronary thrombus in major coronary arteries, whereas 14 (38%) had fixed narrowings without evidence of intracoronary thrombus and two exhibited coronary spasm. ST segment elevation was observed in 16 of 21 patients with thrombus and in all of the patients with coronary spasm, but all the patients with organic stable obstruction showed ST segment depression. Twenty of the 21 patients with thrombus improved after thrombolytic therapy with intracoronary injection of urokinase; obstructed arteries were reopened, or narrowings were attenuated, with relief of ischemic symptoms. In patients with fixed obstructions, the rate-pressure product during active symptoms was significantly higher than during an asymptomatic period, indicating that a transient increase in myocardial oxygen demand may contribute to the ischemic attack in these patients. A high incidence (71%) of recurrent symptoms was observed in patients with intracoronary thrombus even after successful thrombolysis, in contrast to a much lower incidence (36%) in those without intracoronary thrombus. Myocardial infarction within 4 weeks after catheterization was observed more frequently in patients with intracoronary thrombus (24%) than in those without thrombus (7%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Subacute coronary stent thrombosis in a patient developing clopidogrel associated thrombotic thrombocytopenic purpura

Clopidogrel, in combination with aspirin, is commonly used for the prevention of thrombosis in patients who have received coronary artery stents. As a rare but critical complication, clopidogrel associated thrombotic thrombocytopenic purpura (TTP) has previously been described. A 78 year old man presented with unstable angina and filiform subtotal stenosis of the left anterior descending artery. He was treated with balloon angioplasty and stent implantation. After four days the patient again had angina caused by stent thrombosis, which was treated with balloon angioplasty. During hospital stay the typical course of clopidogrel associated TTP was observed with thrombocytopenia and petechial purpura occurring 14 days after drug initiation and prompt response to therapeutic plasma exchanges. These findings strongly suggest that clopidogrel may have increased platelet activation and aggregation in this immunologically susceptible patient, ultimately leading to a stent thrombosis.     

Spontaneous coronary artery dissection causing myocardial infarction and left ventricular aneurysm.

Spontaneous coronary artery dissection (SCAD) is a rare cause of myocardial infarction (MI). A 66-year-old Japanese man, who had had an anterior wall MI caused by SCAD of the left anterior descending coronary artery, developed left ventricular aneurysm 5 years later, with depressed left ventricular function and thrombus observed on echocardiography. Left endoventricular circular patch plasty according to Dor's technique was performed without coronary artery bypass grafting, because of the absense of significant coronary artery stenosis on the preoperative coronary angiogram. The clinical course of SCAD in the late phase is generally favorable, but because the prognosis of SCAD is uncertain, patients with SCAD should be carefully followed.     

Specific platelet mediators and unstable coronary artery lesions. Experimental evidence and potential clinical implications

We have speculated previously that the abrupt conversion from chronic stable to unstable angina and the continuum to acute myocardial infarction may result from myocardial ischemia caused by progressive platelet aggregation and dynamic vasoconstriction themselves caused by local increases in thromboxane and serotonin at sites of coronary artery stenosis and endothelial injury. Platelet aggregation and dynamic coronary artery vasoconstriction probably result from the local accumulation of thromboxane and serotonin and also relative decreases in the local concentrations of endothelially derived vasodilators and inhibitors of platelet aggregation, such as endothelium-derived relaxing factor (EDRF) and prostacyclin. With severe reductions in coronary blood flow caused by these mechanisms, platelet aggregates may increase, and an occlusive thrombus composed of platelets and white and red blood cells in a fibrin mesh may develop. When coronary arteries are occluded or narrowed for a sufficient period of time by these mechanisms, myocardial necrosis, electrical instability, or sudden death may occur. We believe that unstable angina and acute myocardial infarction are a continuum in relation to the process of coronary artery thrombosis and vasoconstriction. When the period of platelet aggregation or dynamic vasoconstriction at sites of endothelial injury and coronary artery stenosis is brief, unstable angina or non-Q wave infarction may occur. However, when the coronary artery obstruction by these mechanisms is prolonged for several hours, Q wave myocardial infarction results. Chronic endothelial injury and coronary artery stenosis are probably associated with the accumulation of platelets, white and red blood cells, and a fibrin mesh at the site of stenosis and endothelial injury.     

Acute left main occlusion during percutaneous coronary intervention associated with heparin induced thrombocytopenia with thrombosis syndrome

A 76-year-old male was admitted with Braunwald IIIB unstable angina and treated with intravenous heparin. Coronary angiography 20 days later revealed a severe stenosis in the left circumflex artery. During coronary angioplasty thrombus developed in the circumflex artery, extended in the left main and lead to its occlusion. Normal left coronary artery patency and flow were achieved after intracoronary and intravenous administration of abciximab, and multiple stenting. Platelet-count decrease and an ELISA assay documented the presence of heparin-induced thrombocytopenia with thrombosis syndrome (HITTS). HITTS should be suspected after acute thrombus formation during coronary angioplasty.     

Staged thrombolysis and percutaneous transluminal coronary angioplasty for unstable and postinfarction angina

The precise timing of intravenous thrombolysis and coronary angioplasty continues to be evaluated for patients who have coronary thrombosis and unstable angina or postinfarction angina. Coronary angioplasty is effective for these patients but is associated with thromboembolic coronary occlusion in 24% to 29% of cases. After adjunctive intravenous thrombolysis and oral antiplatelet therapy to improve the success rate and to decrease the risk of acute occlusion, deferred angioplasty was successful in three patients with intracoronary thrombus and unstable angina or postinfarction angina. Staged thrombolysis and deferred angioplasty is feasible for selected patients with these acute coronary syndromes.     

Cardiac multidetector-row computed tomography in patients with unstable angina

Ideally, information on coronary artery stenosis and left ventricular (LV) function is obtained in patients who have unstable angina to allow optimal risk stratification. The value of multidetector-row computed tomography (MDCT) was evaluated for a simultaneous assessment of coronary artery disease and global/regional LV function using a single acquisition. Twenty-five patients who had unstable angina underwent a single multidetector-row computed tomographic acquisition using a 4-slice multidetector-row computed tomographic system. Based on retrospective electrocardiographic gating, images and cine movies were reconstructed, which allowed 2 independent observers to analyze the 9 major coronary artery segments and global/regional LV function. Conventional angiography (with quantitative analysis) and echocardiography served as standards of reference, which were performed /=50%) coronary artery stenosis was detected with sensitivities, specificities, and positive and negative predictive values of 95%, 91%, 85%, and 97% for observer 1 and 89%, 87%, 79%, and 94% for observer 2, respectively; the interobserver kappa value was 0.73. MDCT showed excellent agreement with echocardiography for regional wall motion (90%; kappa = 0.88) and LV ejection fraction (correlation 0.95%, mean difference 0.7 +/- 3.9). Thus, MDCT can simultaneously assess coronary artery disease and LV function in patients who have unstable angina. High accuracies in excluding significant coronary artery disease and in confirming normal LV function were observed, suggesting potential clinical use for screening of patients who present with symptoms of unstable angina.     

Effect of coronary angioplasty on electrocardiographic changes in patients with unstable angina secondary to left anterior descending coronary artery disease

The effect of semiemergent percutaneous transluminal coronary angioplasty on clinical and electrocardiographic (ECG) variables was assessed in 76 patients with unstable angina secondary to an isolated severe proximal left anterior descending coronary artery stenosis. All patients manifested symmetric T wave inversion in two or more anterior ECG leads. Wall motion abnormalities were present in 37 patients on ventriculography before dilation. Angioplasty was successful in 70 patients (92%), resulting in a reduction in luminal diameter stenosis from 91 +/- 8% to 21 +/- 6%, with no major acute procedure-related complications observed. The other six patients underwent semiurgent (less than 48 h) coronary artery bypass surgery and three patients experienced a myocardial infarction (before bypass surgery in two). Serial ECGs revealed complete resolution of ST-T wave changes in 51% of patients at 14 weeks and in 90% at 28 weeks. In contrast, prolongation of the corrected QT interval, which was present in 16 patients (8%), normalized within 48 h of successful angioplasty. Twelve of these 16 patients with a prolonged QT interval had nonocclusive thrombus formation and poor collateral circulation on angiography. Patients were followed up for 6 to 43 months (mean 23 +/- 10). Angiographic evidence of restenosis was present in 34% of patients, all of whom underwent a successful second or third procedure. One death occurred at 8 months after successful angioplasty. Wall motion abnormalities had completely resolved in 13 of 15 patients who underwent repeat ventriculography, at which time 10 had a normal ECG. This study demonstrates that ECG changes may persist for up to 7 months in patients who undergo successful angioplasty for severe left anterior descending coronary artery disease and unstable angina. Semiemergent angioplasty was associated with a high initial success rate and excellent long-term outcome.