Comparison of platelet activation in unstable and stable angina pectoris and correlation with coronary angiographic findings.

We sought to investigate the relation between platelet activation and the angiographic evidence of ruptured plaque in patients presenting with unstable and stable angina pectoris. We prospectively enrolled 25 consecutive patients (5 women and 20 men, mean age 62 +/- 3 years), 17 with unstable angina and 8 with stable angina. Systemic venous blood samples were collected within 4 to 6 hours of admission for flow cytometry analysis. Activation-dependent epitope CD63 and glycoprotein IIb/IIIa on the platelet membrane were assayed. Fibrinogen levels were also measured. All patients with unstable angina underwent cardiac catheterization and had angiographic evidence of ruptured plaque. Of the patients with stable angina, 5 underwent coronary angiography with smooth noncomplex lesions and 3 had negative technetium-99m sestamibi stress tests. Patients with unstable angina were characterized by 39% higher levels of fibrinogen than patients with stable angina (423 +/- 304 vs 304 +/- 51 mg/dl, p = 0.004). The percentage of platelets positive for the activation-dependent epitope CD63 was 5 times higher in patients with unstable than stable angina (14.6 +/- 5.6% vs 2.75 +/- 1.6%, p = 0.0026). They also had a 15% higher expression of their glycoprotein IIb/IIIa (517 +/- 79 vs 449 +/- 50 mean fluorescence intensity, p = 0.038). Thus, this study establishes a direct relation between the morphology of ruptured plaque and platelet activation in patients with unstable angina. This may allow for further risk stratification. Patients with unstable complex lesions had a fivefold higher expression of the platelet activation epitope CD63 than patients with stable angina. Furthermore, they had 15% more glycoprotein IIb/IIIa aggregation sites expressed on their platelet membrane, thus indicating an intense thrombogenic potential.

Restoration of patency of left internal mammary artery graft with progression of the underlying left anterior descending coronary artery disease.

The use of the left internal mammary artery (LIMA) to graft a borderline lesion in the left anterior descending coronary artery (LAD) has been associated with distal narrowing and occlusion of the LIMA. We present a patient in whom the LIMA occluded 1 year after coronary artery bypass, but was found to be fully patent 4 years later, after progression of the native LAD disease.

Comparison of the histopathology of culprit lesions in chronic stable angina, unstable angina, and myocardial infarction.

BACKGROUND: The etiology of unstable angina (UA) and myocardial infarction (MI) both involve rupture of an atherosclerotic plaque in a coronary artery. It has been suggested that the two syndromes differ because MI results if a red occlusive permanent thrombus occurs and UA occurs only if a nonocclusive platelet (white) thrombus occurs. HYPOTHESIS: The purpose of this study was to determine the differences between coronary lesion pathology in MI and UA and compare them with lesions of chronic stable angina (CSA). METHODS: We reviewed the pathologic specimens of culprit lesions obtained by directional coronary atherectomy in 27 patients with MI, 29 patients with UA, and 16 patients with CSA. RESULTS: The incidence of ruptured plaque was high and identical in patients with MI (77.8%), and UA (75.8%), and significantly lower in patients with CSA (25.0%) (p < 0.001). Similarly, the incidence of red thrombus was the same in MI (92.6%) and UA (82.7%), and significantly less in CSA (p < 0.001). CONCLUSIONS: The underlying pathophysiology of both UA and MI appears to be the same, with red thrombus playing an important role in both syndromes. The only difference is in the degree of occlusiveness of the red thrombus on the ruptured plaque and whether the occlusion is transient (UA) or persistent (MI). The balance between thrombosis and endogenous clot lysis determines which syndrome occurs. Lytic therapy is not effective in UA, probably because the clot is not occlusive or because endogenous lysis has already achieved the degree of coronary opening that eventuates from tissue plasminogen activator or streptokinase administration. Prompt catheterization and revascularization may be as indicated in patients with MI if there remains viable myocardium as in patients with UA.

Hemoptysis and unilateral intra-alveolar hemorrhage complicating intravenous thrombolysis for myocardial infarction.

This report deals with a patient who developed hemoptysis due to unilateral intra-alveolar hemorrhage after receiving tissue-type plasminogen activator (TPA) for acute myocardial infarction; the patient had sustained an ipsilateral lung injury 2 years earlier.

Assessing myocardial viability: correlation of myocardial wall motion abnormalities and pathologic Q waves with technetium 99m sestamibi single photon emission computed tomography.

The clinical benefit of coronary revascularization depends largely on the viability of the myocardium that is perfused. To determine if the combination of electrocardiogram and left ventriculography findings could be used to predict viability, the presence of pathologic Q waves and wall motion abnormalities on contrast left ventriculography were correlated with findings on stress sestamibi scanning in 201 patients. Wall motion was abnormal in 51.5% of 103 Q regions; 30 (56.6%) of these had fixed sestamibi defects, and 22.6% had fully or partially reversible sestamibi defects. Q waves were associated with 43.4% of 122 regions with wall motion abnormality; 67.9% of these areas had fixed or partially fixed sestamibi defects. Wall motion abnormalities were present in 46.1% of 104 areas with fixed sestamibi defects. Although there was a statistically significant correlation among Q waves, left ventricular wall motion abnormalities, and stress sestamibi uptake (and various combinations of these data), the relatively large number (53.8%) of discordant findings (e.g., normal ventricular wall motion in the presence of fixed sestamibi defects) suggests that nonviability cannot be assumed without at least assessing both contractile left ventricular motion and metabolic (e.g., sestamibi scanning) function.

Correlation of atherectomy specimen histology with coronary arteriographic lesion morphologic appearance in patients with stable and unstable angina.

Complex lesions on coronary arteriography are seen commonly in patients with unstable angina and have been considered to be evidence of ruptured plaque with or without thrombus. To investigate the cause of complex lesions the histologic findings in atherectomy-derived specimens in 111 patients were correlated with lesion morphologic appearance on coronary arteriography. Among 91 patients with complex lesions, 81.3% had thrombus and 57.1% had evidence of plaque rupture. Of 20 patients with smooth lesions, 15% had thrombus and 10% had plaque rupture on histologic evaluation (p < 0.01). On clinical correlation in 86 (83.3%) patients unstable angina was associated with thrombus, or plaque rupture (63.3%), or both on histologic evaluation (p < 0.001 compared with stable angina). Complex lesions not associated with thrombus or plaque rupture occurred mainly (83.3%) in patients with stable angina. Our findings support the concept that complex lesions are usually due to recent thrombus, plaque rupture, or both in patients with unstable coronary syndromes but may be due to remote plaque disruption in patients with stable angina.

The value of tilt table testing with isoproterenol in determining therapy in adults with syncope and presyncope of unexplained origin.

BACKGROUND: Previous studies have shown the effectiveness of tilt table testing in establishing the diagnosis of neurocardiogenic syncope and in dictating therapy in patients with syncope of unknown origin. Most studies have been limited by small numbers of patients and brief follow-up. Tilt table testing was performed with and without isoproterenol hydrochloride in 94 patients, and therapy was determined by the test findings. The patients were followed up for at least 10 months (mean, 17.8 months). METHODS: The 80 degrees tilt table test was performed in 94 consecutive patients who presented with syncope (n = 74) or presyncope (n = 20) and in whom neurologic and cardiac causes were ruled out. Therapy was determined by the tilt test findings. Sixty-seven patients were followed up for 17.8 +/- 5.3 months (mean +/- SD) (range, 10 to 27 months). RESULTS: Forty-nine patients had positive results of tilt studies and received therapy. Of these 49 patients, 36 returned for second tilt studies while they were taking medication, and 30 had negative results. Six patients had medication changes and had negative results of follow-up tilt studies. No symptoms were noted on follow-up in the 24 patients who presented with syncope and who had positive results of tilt tests that responded to therapy. Of these 35 patients presenting with syncope who had negative results of initial tilt studies and who did not receive any therapy, syncope recurred in four patients. Three of 10 patients contacted who presented with presyncope and had negative results of tilt studies reported symptoms. CONCLUSIONS: Tilt table testing is an excellent tool for diagnosing neurocardiogenic syncope in adults and in determining effective therapy in patients presenting with syncope of unknown origin.

Catheter ablation of the slow AV nodal pathway in AV nodal re-entry tachycardia.

AV node re-entry tachycardia has been managed with medical therapy to suppress AV node conduction. Radiofrequency ablation of the slow AV nodal pathway can eliminate recurrent spontaneous AVNRT, while preserving AV node conduction intact.

Temporal relationship of complications after coronary artery bypass graft surgery: scheduling for safe discharge.

The postoperative courses of 224 patients who left the operating room alive after coronary bypass surgery were followed to determine the time of onset of complications to determine when discharge is safe. A total of 155 complications occurred in 103 patients including 59 with supraventricular tachycardia, 17 with fever, and 9 to 11 with ventricular arrhythmias, cerebrovascular accidents, wound infection, or deep vein thrombosis. Pneumonia occurred in seven patients, and other complications occurred in five or fewer patients. Most initial complications (77.6%) occurred by day 5, and 89.3% of the patients with complications had their initial event before day 8. Hence it appears that it is safe to discharge patients on day 8 after coronary artery bypass graft surgery if they have not had a postoperative complication.

Comparison of the natural history of irregular and smooth coronary lesions: insights into the pathogenesis, progression, and prognosis of coronary atherosclerosis.

The coronary arteriograms of 255 patients who had two to four arteriograms within 2.6 +/- 1.7 years were reviewed. Two hundred three patients had lesions on at least one arteriogram; among the 167 patients without coronary surgery, there were 48 complex irregular lesions (suggesting a ruptured plaque and/or thrombosis) and 141 smooth lesions with follow-up, and 73 irregular and 164 smooth lesions with preceding arteriograms available. Severe irregular lesions (> or = 90% diameter occlusion) progressed to total occlusion (46%) more often than did severe smooth lesions (11.5%) (p < 0.01). Less severe lesions usually did not progress, with no difference in incidence of progression between irregular and smooth lesions (27.8% vs 23.9%). Irregular lesions > or = 80% usually occurred as a result of progression in less severe smooth lesion or occurred in areas that were minimally diseased or appeared normal, whereas smooth lesions > or = 80% had usually not changed since the previous arteriogram. Irregular lesions very rarely became smooth. A study of lesions in 36 patients with surgery was confirmatory. We conclude that plaque rupture is a common mechanism for progression of coronary disease but is not a common pathway for the growth of smooth lesions; irregular lesions remain irregular for years. There is no relationship between the severity of smooth plaques and their likelihood to rupture. Progression of coronary disease can occur by either of two modes: (1) gradual growth of a smooth-walled plaque or (2) plaque rupture with marked progression to a severe irregular lesion. Because most smooth and most irregular lesions remain stable for years, except possibly for > or = 90% irregular lesions, there is no anatomic finding that justifies urgent revascularization. Instability is a clinical diagnosis.

Are reciprocal changes a consequence of "ischemia at a distance" or merely a benign electric phenomenon? A PTCA study.

The significance of reciprocal ST-segment depression during acute occlusion of an epicardial coronary artery is still actively debated. "Ischemia at a distance" has been implicated in numerous reports. To determine the prevalence and mechanism of reciprocal changes, we recorded 12-lead electrocardiograms (ECG) during balloon inflation in 66 patients undergoing 79 coronary angioplasty (PTCA) procedures. The 38 men and 28 women had a mean age of 59 +/- 12 years. Twenty nine PTCAs were of the dominant right coronary artery (RCA), 24 were of the proximal left anterior descending artery (LAD), 24 of the left circumflex artery (LCF), and 2 of the diagonal branch of the LAD. Primary ST elevation (> or = 1 mm) occurred in 56 (71%) PTCAs, 49 (88%) of which showed reciprocal (> or = 1 mm) ST depression. Reciprocal changes occurred in 15 of 21, 19 of 20, and 14 of 14 PTCAs of the LAD, RCA, and LCF, respectively (p value not significant [NS]) and were common in patients with collateral vessels supplying the arterial bed distal to the site of balloon occlusion (60%). They were equally prevalent in PTCAs of patients with single-vessel disease and patients with multivessel disease (90% vs 82%, p = NS). We conclude that reciprocal changes occur in the majority regardless of the vessel involved or the extent of coronary artery disease, that they usually represent electric phenomena and not remote ischemia, and that "ischemia at a distance" is not a diagnosis that can be made by ECG.

Chest pain secondary to membranous subaortic stenosis in a young woman.

Left ventricular outflow obstruction can be divided into three distinct categories: valvular aortic stenosis, the most common form; supravalvular aortic stenosis, which is often seen in early childhood; and subvalvular stenosis, which can be further subdivided into muscular, tunnel, and fibromembranous subtypes. All may be found in a patient seen with symptoms of angina, syncope, or heart failure as a precursor to sudden death. Prompt clinical recognition is essential as is a high degree of suspicion when these signs are associated with a systolic ejection murmur on clinical examination. Echocardiography and a meticulous Doppler examination are very useful in the diagnosis of these disorders as well as in further distinguishing among the different subtypes. The authors describe the case of a 40-year-old woman with chest pain refractory to medical therapy and a long systolic ejection murmur.

Coronary angioplasty in patients eighty years of age or older.

Percutaneous transluminal coronary angioplasty (PTCA) was performed on 58 lesions in 53 patients 80 years of age or older with unstable angina. Most patients had previous myocardial infarction, abnormal left ventricular contraction patterns, and multivessel coronary disease. In most (48) patients only one vessel was dilated. PTCA was successful in 48 (82.8%) lesions, but complications were frequent. Eight patients died, six after anatomically successful PTCA (three with cardiac complications, two with noncardiac complications, and one with both cardiac and noncardiac complications). Two patients died after unsuccessful PTCA (one of cardiac complications and one of noncardiac complications), and 11 patients with PTCA were alive with significant complications (all noncardiac). Twenty-nine patients had successful PTCA with no complications; 40 (74.5%) patients were discharged with clinically successful PTCA. It is concluded that PTCA is feasible in patients 80 years of age or older but that both cardiac and noncardiac complications are common in this group of very fragile patients.

The origin and fate of complex coronary lesions.

Complex irregular coronary artery stenoses, representing plaque rupture/thrombosis, are associated with the acute coronary syndromes. However, the natural history (origin and fate) of these lesions is not known. To examine this issue we studied 255 patients who had had two to four arteriograms within a mean interval of 2.6 +/- 1.7 years. Of 53 irregular lesions that had progressed on a later arteriogram, 35 (66%) originated from areas that were smooth and less than 50% in stenosis diameter. Of 44 irregular lesions on an earlier study, 10 (23%) became totally occluded, five (11%) progressed in severity (all remained irregular), 25 (57%) showed no change in severity (all remained irregular), and four (9%) regressed (two became smooth). Nine of the 10 lesions progressing to occlusion were greater than or equal to 95% stenosed on the earlier study. Only 2 of 44 lesions (5%) showed smoothing. These findings are in agreement with the concept that irregular lesions represent ruptured atherosclerotic plaques and demonstrate that they usually originate from mildly occlusive smooth plaques. Markedly narrowed irregular lesions (greater than or equal to 95% stenosis) frequently progress to occlusion. Irregular lesions less than 90% narrowed commonly remain angiographically stable, and irregular over several years. They were found rarely to evolve into smooth-walled plaques.

Effect of severe pulmonary hypertension on the calculation of mitral valve area in patients with mitral stenosis.

We studied 50 consecutive patients with mitral valve stenosis (MS) by cardiac catheterization and Doppler echocardiography to assess whether the presence of severe pulmonary hypertension affected the calculation of valve area by Doppler pressure half-time method and by the Gorlin formula using pulmonary capillary wedge pressure as an index of left atrial pressure. Patients with severe mitral regurgitation were excluded. In patients with pulmonary artery systolic pressure (PAS) less than 70 mm Hg (n = 33), there was good correlation between the mitral valve area derived from Doppler echocardiography and from cardiac catheterization (r = 0.85). However, in patients with PAS greater than or equal to 70 mm Hg (n = 17), this correlation was not as good (r = 0.57). In these 17 patients, the Gorlin formula tended to underestimate the valve orifice area (mean valve area 0.85 +/- 0.49 and 1.06 +/- 0.46 cm2 by catheterization and by Doppler respectively, p = NS). Direct measurement of the valve area by two-dimensional echocardiography was possible in 12 of the 17 patients and correlated well with Doppler values (r = 0.91). Hence in the presence of severe pulmonary hypertension, Doppler pressure half-time estimation of mitral valve area is more accurate than is catheterization-derived valve area, using the wedge pressure and the Gorlin formula.

Correlation of cross-linked fibrin degradation products (D-dimer) with coronary angiographic lesion morphology.

We tested the hypothesis that complex irregular coronary lesions are "active" lesions and thus associated with ongoing fibrinolysis by measuring the degradation products of cross-linked fibrin (D-dimer) in 136 patients undergoing coronary arteriography. Blood samples obtained before catheterization were assayed by an enzyme linked immunosorbent assay (ELISA) using specific monoclonal antibodies for D-dimer particles. In the four groups with complex coronary morphologies (filling defects, extrinsic lesions with irregular borders and total occlusions with or without staining) the majority of patients (64%) had normal D-dimer levels. The incidence of abnormal D-dimer levels was not significantly higher in any of these four groups than in the two groups with normal coronaries or with smooth lesions. In the same patients, however, the clinical diagnosis was predictive of the presence of elevated D-dimer levels. These findings suggest that complex coronary lesions are often not associated with ongoing fibrinolysis and that endogenous fibrinolysis frequently ceases in the presence of persistent clot.

Coronary angioplasty in symptomatic patients after bypass surgery.

With the availability of percutaneous transluminal coronary angioplasty (PTCA), the management of patients who present with recurrent angina following coronary artery bypass surgery (CABG) has changed. From January 1987 to December 1988, 149 symptomatic post CABG patients underwent coronary angiography at our institution. Ninety were treated with medical antianginal therapy, 14 had repeat surgery, and 45 underwent PTCA. Complications of repeat CABG included one death, two perioperative myocardial infarctions, and four patients with postoperative supraventricular arrhythmia. PTCA was performed on 42 lesions in 37 native vessels (88% success rate), and on 24 lesions in 23 vein grafts (91.7% success rate). Complications included acute reocclusion (one patient), peripheral artery occlusion (one patient), hematoma formation (one patient), and periprocedure myocardial infarction (one patient). No deaths occurred. At a mean follow-up of 5.9 +/- 3.8 months, 10 patients had recurrent symptoms, six of whom were found to have restenosis. Repeat PTCA was successfully accomplished in four patients; the other two were treated medically. It is concluded that PTCA is a feasible alternative to repeat CABG in selected patients and can be achieved with a high success rate and minimal complications.