Coronary bypass surgery improves global and regional left ventricular function following thrombolytic therapy for acute myocardial infarction. TAMI Study Group

Coronary bypass surgery was performed prior to hospital discharge in 303 (22%) of 1387 consecutive patients enrolled in the TAMI 1 to 3 and 5 trials of intravenous thrombolytic therapy for acute myocardial infarction. Bypass surgery was of emergency nature (less than 24 hours from treatment with intravenous thrombolytic therapy) in 36 (2.6%) and was deferred (greater than 24 hours) in 267 (19.3%) patients. The indications for bypass surgery included failed angioplasty (12%); left main or equivalent coronary disease (9%); complex or multivessel coronary disease (62%); recurrent postinfarction angina (13%); and refractory pump dysfunction, mitral regurgitation, ventricular septal rupture or abnormal predischarge functional test (1% each). Although patients having bypass surgery were older (59.5 +/- 9.8 versus 56.0 +/- 10.2 years, (p less than 0.0001), had more extensive coronary artery disease (46% with three-vessel disease versus 11%, (p less than 0.0001), had more frequent diabetes mellitus (19% versus 15%, (p = 0.048), had more prior infarctions (p less than 0.0001), had more severe initial depression in global left ventricular ejection fraction (48.0 +/- 11.9% versus 51.8 +/- 11.9%, p = 0.0002), and regional infarct zone (-2.7 +/- 0.94 versus -2.5 +/- 1.1 SD/chord, p = 0.02) and noninfarct zone function (-0.36 +/- 1.8 versus 0.43 +/- 1.6 SD/chord, p less than 0.0001) than patients not having coronary bypass surgery, no difference in the incidence of death in hospital (7% surgical versus 6% nonsurgical) or death at long-term follow-up of hospital survivors (7% surgical versus 6% nonsurgical) was noted between groups. Surgical patients demonstrated a greater degree of recovery in left ventricular ejection fraction (3.4 +/- 9.8% versus 0.16 +/- 8.5%, p = 0.036) and infarct zone regional function (0.71 +/- 1.1 versus 0.34 +/- 0.99 SD/chord, p = 0.001) when immediate (90 minutes following initiation of thrombolytic therapy) and predischarge (7 to 14 days after treatment) contrast left ventriculograms were compared than did patients who received only intravenous thrombolytic therapy with or without coronary angioplasty. These data suggest a beneficial influence of coronary bypass surgery on left ventricular function and possibly on the clinical outcome of patients initially treated with intravenous thrombolytic therapy for acute myocardial infarction.     

Results of coronary surgery after failed elective coronary angioplasty in patients with prior coronary surgery

The results of coronary artery bypass surgery after failed elective coronary angioplasty in patients who have undergone prior coronary surgery are unknown. Coronary angioplasty may be performed to relieve angina after surgery either to the native coronary vessels or to grafts. Failure of attempted coronary angioplasty may mandate repeat coronary surgery, often in the setting of acute ischemia. From 1980 to 1989, 1,263 patients with prior coronary bypass surgery underwent angioplasty; of these patients, 46 (3.6%) underwent reoperation for failed angioplasty during the same hospital stay. Of the 46 patients who underwent reoperation, 33 had and 13 did not have acute ischemia. In the group with ischemia, 3 patients (9.1%) died and 14 (42.4%) died or had a Q wave myocardial infarction in the hospital compared with no deaths (p = NS) and no deaths or Q wave myocardial infarction (p = 0.005) in the group without ischemia. At 3 years, the actuarial survival rate was 88 +/- 6% in the group with ischemia, whereas there were no deaths in the group without ischemia (p = NS), and freedom from death or myocardial infarction was 51 +/- 10% in the group with ischemia, versus no events in the group without ischemia (p = 0.006). In most patients with prior coronary bypass surgery, coronary angioplasty was performed without the need for repeat coronary bypass surgery. Should coronary angioplasty fail, reoperation in patients without acute ischemia can be performed with overall patient survival comparable to that of elective reoperative coronary bypass without coronary angioplasty.(ABSTRACT TRUNCATED AT 250 WORDS)     

Favorable early and long-term prognosis following coronary bypass surgery therapy for myocardial infarction: results of a multicenter trial. TAMI Study Group

Coronary bypass surgery was performed before hospital discharge on 82 (21%) of 386 consecutive patients enrolled in the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) multicenter trial of intravenous tissue plasminogen activator and coronary angioplasty for acute myocardial infarction. Time from infarct symptom onset to coronary bypass surgery was 7.3 +/- 1.9 hours for 24 patients operated upon on an emergency basis and 9.3 +/- 5.2 days for 58 patients having late in-hospital surgery. There were no operative deaths and five in-hospital deaths in the surgical group, all of which occurred in patients with preoperative cardiogenic shock. Although patients in the surgical group were older (59.7 +/- 10.4 years versus 54.9 +/- 10.2 years; p = 0.03), had more extensive coronary artery disease (42% three-vessel disease versus 11%; p = 0.001), and had a higher incidence of anterior wall myocardial infarction (48% versus 39%; p = 0.02), in-hospital mortality for the surgical group (6%) was similar to that in 301 patients not undergoing surgery (7%) in this trial. For patients discharged from the hospital, mortality at 1 year was 2.5% in the surgical group and 1.8% in patients not having coronary bypass surgery before hospital discharge. At a 1 year follow-up, there were no significant differences in the frequency of cardiac or noncardiac-related hospitalizations or in event-free survival between surgical and nonsurgical groups. The majority of patients in both groups considered themselves to be in excellent or good condition. Coronary bypass surgery can be performed with low morbidity and mortality rates in close temporal association to acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Angiographic findings after myocardial infarction in patients with previous bypass surgery: explanations for smaller infarcts in this group compared with control patients

The incidence of previous coronary artery bypass surgery (CABS) in patients with acute myocardial infarction admitted to our hospital has risen from 2.3% to 11.2% in 6 years. We compared infarct size and the angiographically determined cause of infarction in 52 control patients and in 52 consecutive patients with acute myocardial infarction at least 2 months after they had undergone CABS. Baseline characteristics were similar in both groups except for a higher incidence of preexisting Q waves in the post-CABS group (22 vs 10; p less than .05). Indexes of myocardial infarct size were smaller in the post-CABS group compared with those in control patients: peak creatine kinease (CK) level (IU/liter) 1113 +/- 1094 (mean +/- SD) vs 1824 +/- 1932 (p less than .01), peak CK-MB level (IU/liter) 173 +/- 230 vs 272 +/- 332 (p less than .02), peak summed ST segment elevation (mm) 3.5 +/- 4.8 vs 8.2 +/- 9.9 (p less than .005), and QRS score on days 7 to 10, 1.9 +/- 3.0 vs 4.3 +/- 3.4 (p less than .001). Postinfarction left ventricular ejection fraction was higher in the post-CABS group (53 +/- 13%) compared with that in control patients (47 +/- 12%; p less than .05). The incidence of total occlusion of the artery to the infarct zone was similar in the post-CABS and control patients (33 vs 27), as was the incidence of one-, two-, and three-vessel disease (artery plus graft). Collateral blood flow to the infarct zone was found in 27 post-CABS patients and in 23 control patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Myocardial viability in patients with Q wave myocardial infarction and no residual ischemia.

BACKGROUND. Coronary revascularization in patients with persistent angina after myocardial infarction reduces the incidence of recurrent angina pectoris and myocardial infarction and improves left ventricular function. The results of revascularization after a Q wave myocardial infarction when there is no residual ischemia may depend on myocardial viability. METHODS AND RESULTS. To determine whether there was viable myocardium in the infarct area in the absence of clinical and scintigraphic evidence of myocardial ischemia, 15 asymptomatic patients with a Q wave myocardial infarction, no redistribution on stress 201Tl test, and single-vessel disease (greater than 70% stenosis) with persistent anterograde blood flow were randomized to percutaneous transluminal coronary artery angioplasty (PTCA) or conservative medical treatment. After 2 months of follow-up, mean coronary blood flow measured by Doppler catheter in the infarct-related artery was higher in the PTCA treatment group (33 +/- 6 ml/min, n = 8) than in the conservative treatment group (16 +/- 4 ml/min, n = 7; p less than 0.05 between groups). The 201Tl pathological-to-normal ratios measured on postexercise images did not change in patients treated conservatively during the follow-up period (delta = +1.1 +/- 2.2%; NS from baseline) but increased significantly in patients treated by PTCA (delta = +8.5 +/- 2.3%; p less than 0.01 from baseline; p less than 0.05 between groups). Segmental wall motion improved on left ventricular angiography 2 months after PTCA (delta = +11.5 +/- 2.2%; p less than 0.001 from baseline) significantly more than in the conservative treatment group (delta = +4.1 +/- 1.4%; p less than 0.05 between both groups). Improvements of 201Tl ratios and segmental wall motion indexes correlated significantly (r = 0.73, p = 0.002). The mild improvement of global left ventricular ejection fraction measured in the PTCA treatment group did not differ significantly from changes in the conservative treatment group. CONCLUSIONS. Successful angioplasty of the stenotic infarct artery in patients with a Q wave myocardial infarction and no residual ischemia improved coronary flow, 201Tl uptake in the infarct area, and regional wall motion. Therefore, myocardial viability may last several weeks, as long as residual blood flow persists in the infarct-related artery. Optimal assessment of viability by imaging techniques should identify patients who are most likely to benefit from revascularization.     

Effect of reperfusion on electrocardiographic and enzymatic infarct size: results of a randomized multicenter study of intravenous anisoylated plasminogen streptokinase activator complex (APSAC) versus intracoronary streptokinase in acute myocardial infarction

The effect of early coronary artery reperfusion on ECG and enzymatic parameters was examined in 240 patients with acute myocardial infarction. These patients had participated in a randomized trial comparing intravenous anisoylated plasminogen streptokinase activator complex (APSAC) (n = 123) and intracoronary streptokinase (n = 117) therapy. Reperfusion occurred in 59 of 115 (51%) patients receiving APSAC and 67 of 111 (60%) patients receiving streptokinase (p = NS). There was greater early resolution of ST segment elevation in the reperfused than in the nonreperfused patients (p less than or equal to 0.003) and more rapid Q wave evolution (p less than or equal to 0.03). Sigma Q was lower in reperfused than in nonreperfused patients at 8 hours (1.41 +/- 1.18 versus 2.11 +/- 2.10 mV; p less than or equal to 0.05) and at 24 hours (1.43 +/- 1.25 mV versus 2.08 +/- 1.88 mV; p less than or equal to 0.02). Time to peak level was shorter in the reperfused patients for creatine kinase (CK) (10.7 +/- 5.5 hours versus 14.9 +/- 5.9 hours; p less than 0.0001) and lactic acid dehydrogenase (LDH) (29.6 +/- 13.6 hours versus 34.4 +/- 10.5 hours; less than or equal to 0.03) enzymes. Peak LDH-1 was lower in the reperfused group (274 +/- 149 U/L versus 341 +/- 173 U/L; p less than or equal to 0.04). Reperfusion at a mean of 3.9 hours after the onset of infarction was associated with more rapid resolution of ST segment elevation, faster Q wave evolution, smaller ECG infarct size, earlier cardiac enzyme release, and smaller enzymatic infarct size than later or no reperfusion.     

Fascicular conduction disturbances and ischemic heart disease: adverse prognosis despite coronary revascularization

In patients with ischemic heart disease, fascicular conduction disturbances are associated with increased mortality. This study reveals that increased mortality also exists for certain types of fascicular conduction disturbances after myocardial revascularization. In 227 consecutive patients undergoing bypass surgery, 24 had preoperative and an additional 52 developed at surgery a fascicular conduction disturbance. At 66 +/- 14 months of follow-up, 6 (4%) of 148 control patients without pre- or postoperative fascicular conduction disturbances had died from cardiac causes. Although right bundle branch block and left hemifascicular block were the most common form of fascicular conduction disturbance, only 1 of 55 of these patients died (p = NS). Mortality rates were much higher for patients with left bundle branch block or an intraventricular conduction defect; 8 (38%) of 21 died from cardiac causes (p less than 0.05). A high risk subgroup was identified by comparing 14 consecutive patients with left bundle branch block or an intraventricular conduction defect who survived more than 1 year postoperatively with 21 consecutive patients with these same conduction defects who died within 1 year of surgery. The following variables were significantly (p less than 0.05) different (survivors versus nonsurvivors): age (58 +/- 7 versus 65 +/- 9 years); class IV angina (2 of 14 versus 16 of 21), prior myocardial infarction (9 of 14 versus 21 of 21), left ventricular ejection fraction (53 +/- 18 versus 41 +/- 15%), three vessel disease (9 of 14 versus 20 of 21) and left ventricular aneurysm (2 of 14 versus 13 of 21).(ABSTRACT TRUNCATED AT 250 WORDS)     

Myocardial infarction after coronary bypass surgery. Associated factors and prognosis

This paper studies the factors associated with perioperative myocardial infarction after coronary bypass surgery and assesses the medium-term prognosis of these patients. Four hundred and seventy patients underwent coronary bypass surgery between January 1983 and December 1986. The appearance and persistence of pathological Q waves, absent on the preoperative ECG, was the unique criterion of perioperative infarction. This complication was observed in 36 patients (7.65%). A comparison of these patients with a random group of 144 of teh 434 patients without perioperative infarction showed that they had a higher incidence of crescendo angina (55% vs 21%; p less than 0.001), ST-T wave changes on the resting ECG (78% vs 46%; p less than 0.001) and poor distal left anterior descending network (33% vs 13%; p less than 0.001): in addition, the group with infarction had a lower left ventricular ejection fraction (0.58 vs 0.64, p less than 0.01), incomplete myocardial revascularisation procedures (58% vs 32%; p less than 0.01), longer cardiopulmonary bypass times (86 mn vs 69 mn; p less than 0.001) and longer aortic clamping times (44.5 mn vs 37.4 mn p less than 0.05). The acute phase of the perioperative infarct was characterised by a higher incidence of major cardiac complications such as low output states (30.5% vs 2.02%; p less than 0.001). The hospital mortality was higher in the infarct group (8.3% vs 2.01%) but this was not statistically significant. After an average follow-up of 44 +/- 3 months, the 5 year survival rate was 95.4 +/- 2.1 per cent in patients without infarction and 76.5 +/- 6.9 per cent in those with perioperative infarction (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of coronary collateral vessels on myocardial infarct size in humans. Results of phase I thrombolysis in myocardial infarction (TIMI) trial. The TIMI Investigators

BACKGROUND. The influence of coronary collateral vessels on infarct size in humans remains controversial, partly because no previous study has examined the impact of collaterals present at the onset of acute myocardial infarction on infarct size. METHODS AND RESULTS. The present study used the data base of the Thrombolysis in Myocardial Infarction (TIMI) Phase I trial to correlate the presence or absence of angiographically documented collaterals in the initial hours of myocardial infarct evolution with the size of the infarct as assessed by serial measurements of serum creatine kinase (CK). To avoid the confounding effects of reperfusion on enzymatic estimates of infarct size, this report is limited to those 125 patients who failed to recanalize at 90 minutes after administration of tissue plasminogen activator or streptokinase. Patients with angiographically documented collaterals (group A, n = 51) had significantly lower values of peak serum CK than patients without collaterals (group B, n = 74) (1,877 +/- 216 versus 2,661 +/- 212 IU/l, respectively [mean +/- SEM], p = 0.004). Similarly, CK-derived infarct size estimates were significantly lower in group A than in group B (20.6 +/- 2.5 versus 31.4 +/- 2.8 CK gram equivalents, p = 0.001). The infarct size observed in patients with collaterals was less for anterior infarctions as well as for infarctions of other locations; thus, the beneficial effects of collaterals were independent of the site of the infarct. In 65 of the 125 patients who failed to reperfuse, left ventricular ejection fraction (LVEF) was assessed by contrast ventriculography both at initial cardiac catheterization (before thrombolytic therapy) and at hospital discharge. Among the patients who had both studies, global LVEF tended to increase from pretreatment to hospital discharge in group A (from 50.6 +/- 1.8% to 53.4 +/- 1.8%, p = 0.10) but decreased in group B patients (from 50.3 +/- 1.8% to 47.8 +/- 1.7%, p = 0.02). At hospital discharge, global LVEF was greater in patients with coronary collaterals (53.5 +/- 1.7% versus 49.6 +/- 1.7%, p = 0.01). CONCLUSIONS. The results demonstrate that, in patients in whom thrombolytic therapy fails to induce reperfusion, the presence of coronary collateral vessels at the onset of myocardial infarction is associated with limitation of infarct size as assessed enzymatically and with improved ventricular function on discharge as assessed by LVEF.     

Diabetes mellitus prevents ischemic preconditioning in patients with a first acute anterior wall myocardial infarction

OBJECTIVES: This study was undertaken to assess whether prodromal angina could have beneficial effects in diabetic patients with acute myocardial infarction (AMI). BACKGROUND: Prodromal angina occurring shortly before the onset of AMI is associated with favorable outcomes by the mechanism of ischemic preconditioning. However, little is known about the impact of diabetes on ischemic preconditioning. METHODS: We studied 611 patients with a first anterior wall AMI who underwent emergency catheterization within 12 h after the onset of chest pain: 490 patients without diabetes and 121 patients with non-insulin treated diabetes. Prodromal angina was defined as angina episode(s) occurring within 24 h before the onset of AMI. Serial contrast left ventriculograms were obtained in 424 patients at the time of acute and predischarge catheterization. RESULTS: In non-diabetic patients, prodromal angina was associated with lower peak creatine kinase (CK) value (3,068 +/- 2,647 IU/l vs. 3,601 +/- 2,462 IU/l, p = 0.037), larger increase in left ventricular ejection fraction (LVEF) (10.1 +/- 13.0% vs. 5.8 +/- 13.4%, p = 0.004) and lower in-hospital mortality (3.4% vs. 9.3%, p = 0.015). On the contrary, in diabetic patients, there was no significant difference in peak CK value (3,382 +/- 2,520 IU/l vs. 3,233 +/- 2,412 IU/l, p = NS), the change in LVEF (6.7 +/- 13.8% vs. 7.1 +/- 12.4%, p = NS) and in-hospital mortality (8.8% vs. 11.0%, p = NS) between patients with and patients without prodromal angina. CONCLUSIONS: Prodromal angina limited infarct size, enhanced recovery of LV function and improved survival in non-diabetic patients with AMI. However, such beneficial effects of prodromal angina were not observed in diabetic patients, suggesting that diabetes might prevent ischemic preconditioning.     

PTCA at first sight: angioplasty based on video only

The results of 326 coronary angioplasties (PTCAs) performed during a first diagnostic angiography and based on video images only (PTCA at first sight, Group I) are compared with those of 756 PTCAs done during the same time period in patients with a previous cine-film and therefore a known or predictable coronary anatomy (Group II). Group I patients had more single vessel disease (74% versus 58%, p less than 0.001), single vessel PTCA (93% versus 84%, p<0.001), unstable angina (54% versus 28%, p less than 0.001), recent myocardial infarction (66% versus 37%, p less than 0.001), and total occlusion PTCA (29% versus 19%, p<0.01). On the other hand, they had less severe stable angina (mean New York Heart Association class 1.3+/-1.2 versus 1.8+/-1.4, p less than 0.001), less advanced disease (average of 1.3+/-0.5 versus 1.5+/-0.7 diseased vessels, p less than 0.001) and worse left ventricular ejection fraction (61+/-12% versus 63+/-12%, p less than 0.01). The angiographic and clinical success rates were 90% and 84% in Group I and 92% and 87% in Group II respectively, (p=NS). Complication rates were not statistically different between the groups (Q-wave myocardial infarction 2% versus 3%, non Q-wave myocardial infarction 4% in both groups, emergency surgery 0.3% versus 0.8% and inhospital mortality 0.9% for both groups). In selected patients, coronary angioplasty can be performed safely and effectively during a first coronary angiography based on video images exclusively.     

Significance of preinfarction angina for preservation of left ventricular function in acute myocardial infarction.

The effect of preinfarction angina on the preservation of left ventricular function was evaluated with the use of cineventriculography in 37 patients who had either total or subtotal occlusion of the proximal left anterior descending coronary artery during the convalescent period of myocardial infarction. In 15 patients who had preinfarction angina more than 1 week before the onset of acute myocardial infarction (group A), the global left ventricular ejection fraction was 54 +/- 3% (SEM) and regional wall motion in the infarct area was 10 +/- 3%. In 10 patients who had preinfarction angina occurred within 1 week before the onset of acute myocardial infarction (group B), the left ventricular ejection fraction and regional wall motion in the infarct area were 42 +/- 3% and 1 +/- 2%, respectively. In 12 patients without preinfarction angina (group C), the left ventricular ejection fraction and regional wall motion in the infarct area were 38 +/- 3% and -1 +/- 2%, respectively. In groups B and C, both the left ventricular ejection fraction and regional wall motion in the infarct area were lower than those in group A (p less than 0.05). The collateral circulation at the onset of acute myocardial infarction was better in group A compared with groups B and C (p less than 0.05). Thus the collateral circulation, promoted by repetitive anginal episodes indicative of myocardial ischemia, causes the preservation of myocardial function.     

Effectiveness of excimer laser coronary angioplasty in acute myocardial infarction or in unstable angina pectoris

This study was conducted to evaluate the feasibility, safety, and acute results of percutaneous excimer laser coronary angioplasty (ELCA) in acute coronary syndromes. Fifty-nine patients were treated with ELCA (308 nm), including 33 patients with unstable angina pectoris (UAP) (35 vessels with 39 lesions) and 26 patients with acute myocardial infarction (AMI) (26 vessels with 29 lesions). In each patient the target lesion had a complex morphology. Overall, 71% of the patients had contraindications for pharmacologic thrombolytic agents or glycoprotein IIb/IIIa receptor antagonists. All patients received adjunct balloon dilation followed by stent implantation in 88% of patients with AMI versus 76% of patients with UAP (p = NS). Quantitative angiography was performed at an independent core laboratory; 86% laser success and 100% procedural success was achieved in the AMI group versus 87% laser success and 97% procedural success in the UAP group (p = NS). In the AMI group, the minimal luminal diameter increased from 0.77 +/- 0.56 to 1.44 +/- 0.47 mm after lasing to a final 2.65 +/- 0.47 mm versus 0.77 +/- 0.38 to 1.35 +/- 0.4 mm after lasing to 2.66 +/- 0.5 mm final in the UAP group. A prelaser percent stenosis of 76 +/- 17% for the AMI group versus 70 +/- 16% for the UAP group (p = NS) was decreased after lasing to 52 +/- 16% for the AMI group versus 51 +/- 14% for the UAP group (p = NS) and to a final stenosis of 15 +/- 17% for the AMI group versus 12 +/- 15% for the UAP group (p = NS). A 96% laser-induced reduction of thrombus burden area was achieved in the AMI group versus 97% in the UAP group (p = NS). Preprocedure Thrombolysis In Myocardial Infarction flow of 1.3 +/- 0.9 in the AMI group versus 2.3 +/- 1.2 for the UAP group (p = 0.01) increased to a final flow of 3.0 +/- 0 for the AMI group versus 3.0 +/- 0 for the UAP group (p = NS). There were no deaths, cerebrovascular accident, emergency bypass surgery, acute closure, major perforation or major dissection, distal embolization, or bleeding complications in either group. One patient with AMI had localized perforation (caused by guidewire) without sequelae and 1 patient with UAP had an abnormal increase in creatine kinase levels. All 59 patients survived the laser procedure, improved clinically, and were discharged. Thus, early experience in patients with acute coronary syndromes suggest that percutaneous ELCA is feasible and safe.     

Bidirectional crossover and late outcome after coronary angioplasty and bypass surgery: 8 to 11 year follow-up

Between March 1978 and July 1981, 217 symptomatic patients underwent coronary angioplasty as an alternative to coronary bypass surgery. Angioplasty was successful in 143 patients (66%), unsuccessful but uncomplicated in 65 (30%) and complicated in 9 (4%) by one or more of the following criteria: Q wave myocardial infarction (2%), emergency surgery (4%) or death (0.5%). Late follow-up evaluation was obtained in 213 patients at a mean of 9 +/- 1 years. Of patients in whom angioplasty was successful, 59 (42%) of 140 required another revascularization procedure (repeat angioplasty in 26% and bypass surgery in 16%). The actuarial survival rate at 5, 9 and 10 years after successful angioplasty was 98%, 93% and 92%, respectively. Of the 65 patients with unsuccessful and uncomplicated angioplasty (usually as a result of technical factors), 58 underwent elective bypass surgery within 2 months and 56 survived. These 56 surgical patients were compared with the 140 patients with successful angioplasty. Univariate analysis of prognostic factors did not reveal significant differences between these two groups. At late follow-up study, the successful angioplasty and the successful surgical groups had similar rates of survival (93% versus 95%, p = NS) and of death or infarction, or both (11% versus 12.5%, p = NS). Repeat revascularization was required more frequently after successful angioplasty than after surgery (42% versus 18%, p less than 0.001). Crossover from angioplasty to surgery occurred slightly more often than from surgery to angioplasty (16% versus 12.5%, p = NS). The time to crossover from angioplasty to surgery occurred earlier than from surgery to angioplasty (mean 21 versus 76 months, p less than 0.001).     

Multicenter trial of intravenous anisoylated plasminogen streptokinase activator complex (APSAC) in acute myocardial infarction: effects on infarct size and left ventricular function

Two hundred thirty-one patients with a first acute myocardial infarction were randomly allocated within 5 h after the onset of symptoms either to treatment with anisoylated plasminogen streptokinase activator complex (APSAC), 30 U over 5 min, or to conventional heparin therapy, 5,000 IU in a bolus injection. Heparin was reintroduced in both groups 4 h after initial therapy at a dosage of 500 IU/kg per day. One hundred twelve patients received APSAC and 119 received heparin within a mean period of 188 +/- 62 min after the onset of symptoms. Both groups were similar in age, location of the acute myocardial infarction, Killip functional class and time of randomization. Elective coronary arteriography was performed on an average of 4 +/- 1.2 days after initial therapy. Follow-up radionuclide angiography and thallium-201 single photon emission computed tomography were performed before hospital discharge. Infarct size was estimated from single photon emission computed tomography and expressed as a percent of total myocardial volume. The patency rate of the infarct-related artery was 77% in the APSAC group and 36% in the heparin group (p less than 0.001). Left ventricular ejection fraction determined from contrast angiography was significantly higher in the APSAC group than in the heparin group. This was true for the entire study group (0.53 +/- 0.13 versus 0.47 +/- 0.12; p = 0.002) as well as for the subgroups of patients with anterior and inferior wall infarction (0.47 +/- 0.13 versus 0.40 +/- 0.11; p = 0.04 and 0.56 +/- 0.10 versus 0.51 +/- 0.11; p = 0.02, respectively). At 3 weeks, the difference remained significant for the anterior myocardial infarction subgroup. A significant 31% reduction in infarct size was found in the APSAC group (33% for the anterior infarction subgroup [p less than 0.05] and 16% for the inferior infarction subgroup [p = NS]). A close inverse relation was found between the values of left ventricular ejection fraction and infarct size (r = -0.73, p less than 0.01). By the end of a 3 week follow-up period, seven APSAC-treated patients and six heparin-treated patients had died. In conclusion, the early infusion of APSAC in acute myocardial infarction produced a high early patency rate, significant limitation of infarct size and significant preservation of left ventricular systolic function, mainly in anterior wall infarction.     

Clinical and angiographic features and prognostic significance of early postinfarction angina with and without electrocardiographic signs of transient ischemia

PURPOSE: The goal of the study was to characterize the clinical and angiographic characteristics and the prognostic significance of early postinfarction angina associated or unassociated with ST-T changes. PATIENTS AND METHODS: Four hundred forty-nine consecutive patients surviving an acute myocardial infarction and catheterized before hospital discharge were included. They were closely monitored in the coronary care unit and a 12-lead electrocardiogram (ECG) was promptly obtained before the administration of nitroglycerin whenever chest pain suggestive of ischemia occurred. Complete follow-up information was obtained for all patients a mean of 14 +/- 8 months after the qualifying infarction. RESULTS: Early postinfarction angina occurred in 164 patients. Transient ST-T changes were documented during pain in 79 patients and were absent in 85. Compared with patients without postinfarction angina, patients with angina without ST-T changes were older and had a more frequent past history of angina (42% versus 28%, p = 0.01). They also more often had a non-Q-wave myocardial infarction with lower peak creatine kinase blood level elevation. At angiography, patients with angina had more extensive coronary artery disease (1.9 +/- 0.8 diseased vessels per patient versus 1.6 +/- 0.8, p less than 0.05) and more left ventricular segments at jeopardy by a significant coronary artery stenosis (1.5 +/- 1.1 versus 1.2 +/- 1.1, p less than 0.05). The presence of ST-T changes during chest pain was associated with a further increase in the severity of coronary artery disease (2.1 +/- 0.8 diseased vessels per patient, p less than 0.05) and with a less well-developed collateral circulation (18% versus 34% of patients, p = 0.01) that was more often compromised by a coronary artery stenosis (22% versus 8% of patients, p = 0.008). In-hospital infarct extension occurred in 2% of patients without angina, 3.5% of patients with angina without ECG changes, and 28% of patients with angina and ST-T changes (p less than 0.01). The 2-year survival was similar in the first two groups (90% and 96%), and poorer (83%, p = 0.02) in patients with ST-T changes. Survival rates without myocardial infarction were respectively 80%, 78%, and 67% (p less than 0.004). CONCLUSION: A gradient in the severity of coronary artery disease and in the extent of myocardium at jeopardy exists from patients with no postinfarction angina to patients with angina and to patients with angina accompanied by ECG signs of ischemia. The presence of ST-T changes during pain indicates a much less favorable clinical outcome.     

Influence of partial sympathetic denervation on the results of myocardial revascularization in variant angina

Poor results of the aortocoronary bypass graft operation in the treatment of variant angina have been ascribed to recurrent vasospastic activity due to autonomic imbalance. Cardiac sympathetic denervation (plexectomy) may represent a rational approach in the prevention of vasospasm. To test the value of plexectomy in the treatment of variant angina, 31 patients were studied, 17 of whom (Group 1) underwent conventional coronary artery grafting whereas the remaining 14 (Group 2) underwent cardiac sympathetic denervation also. The 2 groups were similar with respect to age (54 +/- 8 versus 50 +/- 7 years), sex distribution (male/female ratio 12/5 versus 9/5), prevalence of coexisting effort angina (10 versus 12 patients), previous myocardial infarction (7 versus 4 patients), and duration of variant angina (3.3 +/- 5.4 versus 2.4 +/- 2.7 months). The left ventricular ejection fraction was comparable in both groups (60 +/- 11 versus 60 +/- 4%) as were left ventricular end-diastolic pressure (15 +/- 4 versus 13 +/- 5 mm Hg) and extent of coronary artery disease (65 versus 71% prevalence of multivessel disease). The average duration of follow-up was 23 +/- 15 months in Group 1 and 22 +/- 18 months in Group 2 (p = not significant [NS]). There were no operative deaths. Four patients, 2 in each group, had a perioperative myocardial infarction. Seven patients in Group 1 and 1 patient in Group 2 had recurrent variant angina. There was sudden death and 2 infarcts in Group 1. Actuarial curves showed the cumulative probability of recurrent variant angina to be significantly lower (p less than 0.05 and p less than 0.001 at 6 and 10 months, respectively) in Group 2. This study suggests that cardiac sympathetic denervation may prevent recurrent vasospastic activity in variant angina.     

Influence of collateral filling of the occluded infarct-related coronary artery on prognosis after acute myocardial infarction.

Previous studies showed that long-term morbidity and mortality after acute myocardial infarction (AMI) are influenced by the presence or absence of anterograde flow in the infarct artery. In comparison with patients with anterograde flow, those whose infarct artery remains occluded are more likely to have unstable angina, recurrent AMI, congestive heart failure and sudden death. This study was performed to assess the influence of collateral filling of the infarct artery on long-term morbidity and mortality in surviving patients of initial AMI in whom the infarct artery was occluded. Over a 12.5-year period, 146 subjects (108 men and 38 women, aged 25 to 76 years) with AMI, no anterograde flow in the infarct artery, and no disease of other coronary arteries were medically treated and followed for 42 +/- 28 (mean +/- standard deviation) months. Of these subjects, 120 had angiographic evidence of collateral filling of the infarct artery (group I), whereas the remaining 26 did not (group II). The groups were similar in age, sex, cardioactive medications, left ventricular performance and infarct artery. They were also similar in incidence of unstable angina (19% of group I, 31% of group II; p = not significant [NS]), recurrent AMI (12% of group I, 8% of group II; p = NS), congestive heart failure (16% of group I, 12% of group II; p = NS) and cardiac death (16% of group I, 19% of group II; p = NS). Thus, angiographic evidence of collateral filling of the infarct artery in surviving patients of AMI exerts no demonstrable influence (beneficial or detrimental) on long-term morbidity or mortality.     

A Randomized Trial of Intravenous Streptokinase Versus Tissue Plasminogen Activator for the Treatment of Acute Myocardial Infarction: Results Using an Aggressive Approach

Seventy-six patients presenting within 6 hours of the onset of an acute myocardial infarction were randomized to either treatment with 1.5 million units of Streptokinase or 100 mg of recombinant tissue plasminogen activator intravenously. Patients not demonstrating clinical reperfusion within 1 hour were taken emergently for “salvage” angioplasty or coronary bypass surgery. Those patients demonstrating clinical reperfusion underwent early (12 to 72 hours) elective angiography and either elective angioplasty or bypass surgery. The mean time from pain onset to treatment was 149 minutes in the Streptokinase group and 134 minutes in the recombinant tissue plasminogen activator group (P = NS). There were no statistical differences between groups with regard to prior myocardial infarction, infarct location, prior coronary bypass surgery and Killip classification. Clinical reperfusion was demonstrated in 56% of the Streptokinase group and 53% of the recombinant tissue plasminogen activator group (P - NS). Angiographic patency was demonstrated in 70% of the Streptokinase group and 66% of the recombinant tissue plasminogen activator group (P = NS). Left ventricular ejection fraction at discharge was no different: 47% in the Streptokinase group and 43% in the recombinant tissue plasminogen activator group (P = NS). Recurrent ischemic events were found more often in the recombinant tissue plasminogen activator group, 18%, versus the Streptokinase group 3% (P = 0.05). Treatment outcomes did not differ between groups. There was one (3%) death in the Streptokinase group versus two (6%) deaths in the recombinant tissue plasminogen activator group (P = NS). There was a trend toward a greater need for emergent coronary bypass surgery after attempted angioplasty in the recombinant tissue plasminogen activator group, four of 18 patients (22%) versus one of 23 patients (4%) in the Streptokinase group (P = 0.14). In summary, in the setting of acute myocardial infarction treated by thrombolysis, those patients treated with recombinant tissue plasminogen activator experienced significantly more recurrent ischemic events and required emergent coronary bypass surgery more frequently for failed angioplasty compared to those treated with Streptokinase. The results suggest there may be agent specific increases in complications dependent upon the thrombolytic agent of choice when salvage or early coronary angioplasty is used.     

Comparison of radionuclide and enzymatic estimate of infarct size in patients with acute myocardial infarction

A comparison was made of the estimated size of the myocardial infarction occurring in 26 patients with a first infarction using creatine kinase (CK) enzyme release between radionuclide gated blood pool measurement of total and regional ventricular function and thallium-201 scintigraphic measurement of myocardial perfusion defects. Creatine kinase estimates of infarct size (enzymatic infarct size) correlated closely with the percent of abnormal contracting regions, left ventricular ejection fraction and thallium-201 estimates of percent of abnormal perfusion area (r = 0.78, 0.69 and 0.74, respectively, p less than 0.01). A close correlation also existed between percent abnormal perfusion area and percent of abnormal contracting regions (r = 0.81, p less than 0.01) and left ventricular ejection fraction (r = 0.69, p less than 0.01). Enzymatic infarct size was larger in anterior (116 +/- 37 CK-g-Eq) than inferior (52 +/- 29 CK-g-Eq) myocardial infarction (p less than 0.01) and was associated with significantly more left ventricular functional impairment as determined by left ventricular ejection fraction (33 +/- 7 versus 60 +/- 10%) (p less than 0.01) and percent abnormal perfusion area (58 +/- 14 versus 13 +/- 12) (p less than 0.01). No significant correlation was observed between enzymatic infarct size and right ventricular ejection fraction. These different methods of estimating infarct size correlated closely with each other in these patients with a first uncomplicated myocardial infarction.