Beneficial effects of timolol on infarct size and late ventricular tachycardia in patients with acute myocardial infarction

This investigation was undertaken to study the effects of beta-adrenergic blockade with timolol on infarct size and on the incidence of late ventricular tachycardia in patients with acute myocardial infarction of less than 6 hr of evolution. Patients were assigned randomly either to a placebo-treated group (98 patients) or to a timolol-treated group (102 patients). The patients were treated with 5.5 mg iv timolol (or matched placebo) as a bolus divided into four doses during the first 2 hr followed by 10 mg orally twice daily for 1 month. Cumulative total creatine kinase (CK) release, which reflects the amount of myocardial necrosis was 1677 +/- 132 IU/liter in the placebo group (n = 83) and 1274 +/- 73 IU/liter in the timolol group (n = 81, p less than .01), a 24% reduction. Cumulative release of CK-MB was 138 +/- 8 IU/liter in the placebo group and 106 +/- 8 IU/liter in the timolol group (p less than .01), a 23% reduction. Twenty-four hour Holter electrocardiograms were obtained on days 7, 14, 21, and 28 after the onset of the acute myocardial infarction in 80 patients in the placebo group and 82 patients in the timolol group. The incidence of ventricular tachycardia was lower in the timolol than in the placebo group (7 vs 16 patients, p = .05). We conclude that early administration of intravenous timolol followed by oral treatment in patients with acute myocardial infarction reduces infarct size as assessed by CK and CK-MB serum activity, and decreases the occurrence of late ventricular tachycardia.     

Long-term prognosis after myocardial infarction in patients with previous coronary artery bypass surgery

A group of 205 patients hospitalized with myocardial infarction 2 to 162 months (mean 66) after bypass surgery and 205 control patients with myocardial infarction were compared and followed up for 34 +/- 25 months after hospital discharge. At baseline the postbypass group contained more men (p less than 0.03) and more patients with previous myocardial infarction (p less than 0.06), but the groups were otherwise comparable. Indexes of infarct size were lower in postbypass patients: sum of ST elevation, QRS score, peak serum creatine kinase (CK) (1,115 +/- 994 versus 1,780 +/- 1,647 IU/liter) and peak MB CK (all p less than or equal to 0.001). Postmyocardial infarction ejection fraction was 45 +/- 15% in the postbypass group and 43 +/- 15% in the control group (p = NS); in-hospital mortality rate was 4 and 5%, respectively (p = NS). When patent grafts were taken into account, the two groups were comparable in extent of coronary artery disease. At 5 years after discharge, cumulative mortality was similar in the postbypass and control groups (30 versus 25%, respectively, p = NS). However, postbypass patients had more reinfarctions (40 versus 23%, p = 0.007), more admissions for unstable angina (23 versus 18%, p = 0.04) and more revascularization procedures (34 versus 20%, p = 0.04) than did control patients. The total for these events at 5 years was 70% in the postbypass group and 49% in the control group (p = 0.001). Thus, although patients with previous bypass surgery who develop acute myocardial infarction have a smaller infarct, their subsequent survival is no better than that of other patients with acute myocardial infarction. They experience more reinfarctions and unstable angina. Previous bypass surgery is an important clinical marker for recurrent cardiac events after myocardial infarction.     

Prognostic significance of a low peak serum creatine kinase level in acute myocardial infarction

To assess the prognostic significance of a low peak creatine kinase (CK) level, 723 consecutive patients admitted with acute myocardial infarction (AMI) within 16 hours after onset of symptoms were studied. Thrombolytic therapy was not attempted during the study. Patients were dichotomized according to their peak CK levels, determined from a cluster analysis of peak CK distribution among the population of patients who died within 3 years after hospital discharge. The 139 patients with low peak CK (less than or equal to 650 IU/liter) (group 1) were compared to the 584 patients with high peak CK (greater than 650 IU/liter) (group 2). Patients in group 1 were older and had a higher incidence of previous AMI, angina pectoris before AMI and non-Q-wave AMI. Despite a lower incidence of in-hospital complications and a nonsignificantly lower hospital mortality rate (4 vs 9%) the group 1 three-year posthospital mortality rate was higher (26 vs 17%; p less than 0.02), especially in the subgroup of patients with a Q-wave infarct (mortality 31% in group 1 vs 16% in group 2; p less than 0.001). Among the 491 patients who had a first Q-wave AMI, 55 had a peak CK less than or equal to 650 IU/liter. Compared to the 436 patients with a higher peak CK, these 55 patients had a higher incidence of early postinfarction angina (31 vs 14%; p less than 0.01), a similar hospital mortality (4 vs 7%) but a higher 3-year posthospital mortality (23 vs 12%; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Arteriographic predictors of spontaneous improvement in left ventricular function after myocardial infarction

To better characterize the changes in left ventricular ejection fraction after myocardial infarction, we compared radionuclide ventriculograms obtained acutely and 2 weeks after acute myocardial infarction in 40 patients. These patients underwent angiography within a mean of 4 hr and 20 min after the onset of symptoms of infarction and either received no therapy (32 patients who were control subjects in a thrombolysis trial) or did not experience reperfusion (eight patients) despite receiving streptokinase infusions. In all 40 patients, the change in left ventricular ejection fraction over 2 weeks was small (+2.6%). Patients were then grouped according to the presence or absence of residual flow on their angiograms. Residual flow was considered to be present in 21 patients, in 12 by virtue of subtotal occlusion of the artery supplying the area of infarct and in nine because of well-developed coronary collaterals to the distal infarct artery. Mean change in ejection fraction for patients with residual flow was +6.9 +/- 2.3% vs -2.2 +/- 1.7% for patients without residual flow (p less than .01). Fourteen of 21 (67%) patients with residual flow had a spontaneous rise in ejection fraction of greater than 5%, as compared with two of 19 (11%) patients without residual flow (p less than .01). Time to peak level of creatine kinase (CK) was significantly shorter in the residual flow group (15 vs 23 hr, p less than .01), while the peak level of CK was lower (1550 vs 2220 IU) in these patients. This latter difference did not reach statistical significance (p = .10).(ABSTRACT TRUNCATED AT 250 WORDS)     

Long-term outcome in patients with inferior myocardial infarction and complete atrioventricular block

Some studies have reported increased short-term mortality and higher incidence of multivessel coronary artery disease in patients with inferior myocardial infarction and complete heart block, but information is lacking on clinical outcome after hospital discharge. Therefore, data were obtained and analyzed in 749 patients who were admitted with inferior myocardial infarction to four different centers and followed up for 1 year. Six hundred fifty-four patients (Group 1) did not have complete heart block and 95 (Group 2) had complete heart block during their hospital stay (incidence rate 12.8%). Compared with Group 1, Group 2 patients were older (66 versus 61 years, p less than 0.01), more often had signs of left ventricular failure (p less than 0.001) and had higher peak creatine kinase values (1,840 versus 1,322 IU/liter, p less than 0.001). The in-hospital mortality rate was higher in Group 2 than in Group 1 (24.2 versus 6.3%, p less than 0.001). However, at discharge there was no difference between Group 1 and Group 2 in clinical characteristics, left ventricular ejection fraction (0.52 +/- 0.12 versus 0.52 +/- 0.11) or incidence of complex ventricular arrhythmias on ambulatory electrocardiographic monitoring. Furthermore, during the year after hospital discharge, patients in Groups 1 and 2 did not have significantly different mortality rates (6.4 versus 10.1%, p = NS). The incidence rate of reinfarction (4%) was the same in Groups 1 and 2. The incidence of coronary artery bypass surgery was slightly but not significantly higher in Group 1 compared with Group 2 (11 versus 4%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of spontaneous reperfusion on myocardial infarct size

The effect of perfusion of the infarct artery on myocardial infarct size was studied in 39 patients who had not received interventive therapy. At predischarge coronary angiography, 19 patients had subtotal and 20 total occlusion of the infarct artery. The early ST-segment elevation recorded on a 12-lead electrocardiogram was used as an index of the amount of initially jeopardized myocardium. Infarct size was estimated by peak serum creatine kinase and, at discharge, by a QRS score, sigma Q and sigma R on a 12-lead electrocardiogram, and by radionuclide global and infarct segment left ventricular ejection fraction. Despite a similar degree of initial ischemia (sigma ST), infarct size was smaller in the 11 patients with anterior infarction and subtotal occlusion than in the 9 patients with anterior infarction and total occlusion when measured by peak serum creatine kinase (2114 +/- 1192 U/l vs. 3653 +/- 1059 U/l, p less than 0.02), QRS score (5.0 +/- 2.7 vs. 9.6 +/- 3.5, p less than 0.01), sigma Q (3.25 +/- 2.74 mV vs. 5.92 +/- 3.56 mV, p less than 0.10), sigma R (4.36 +/- 1.25 mV vs. 2.16 +/- 0.91 mV, p less than 0.001), global left ventricular ejection fraction (45.0 +/- 12.2% vs. 33.4 +/- 6.7%, p less than 0.05), and infarct segment ejection fraction (40.4 +/- 8.2% vs. 30.3 +/- 5.4%, p less than 0.05). In the inferior infarct patients, both the degree of initial ischemia and final infarct size were similar in the 8 patients with subtotal and in the 11 patients with total occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical and prognostic importance of persistent precordial (V1-V4) electrocardiographic ST segment depression in patients with inferior transmural myocardial infarction

Forty-three consecutive patients with acute inferior transmural myocardial infarction but no history or electrocardiographic evidence of prior myocardial infarction were evaluated prospectively to assess the clinical and prognostic importance of persistent precordial (V1-V4) ST segment depression. Patients were evaluated within 24 hr of admission by history, physical examination, cardiac enzyme levels, right heart catheterization, and radionuclide angiography; all were followed for 1 year. Ten of the 43 patients (group I) had persistent anterior precordial ST segment depression, defined as 1 mm or greater in one or more precordial leads (V1-V4) 24 hr after admission to the coronary care unit, and 33 patients (group II) did not. Clinical variables that differed between groups I and II, respectively, included mean age (67 +/- 9 [+/- 1 SD] vs 59 +/- 8 years; p less than .01), incidence of Killip class II to IV (100% vs 33%; p less than .001), and average peak creatine kinase concentration (2878 +/- 1139 vs 1511 +/- 1034 IU/liter; p less than .001). Hemodynamic differences between groups I and II included a higher pulmonary arterial wedge pressure (19 +/- 4 vs 11 +/- 5 mm Hg; p less than .001) and a lower cardiac index (2.0 +/- 0.5 vs 2.6 +/- 0.7 liters/min/m2; p less than .05). An evaluation of left ventricular ejection fraction and wall motion index by radionuclide angiography showed that group I had a lower ejection fraction (44 +/- 11% vs 53 +/- 10%; p less than .05) and higher wall motion index (1.7 +/- 0.4 vs 1.4 +/- 0.3; p less than .05) compared with group II.(ABSTRACT TRUNCATED AT 250 WORDS)     

Higher Gensini score of coronary arteries in acute inferior myocardial infarction with precordial ST-segment depression.

To investigate the significance of precordial ST-segment depression in acute inferior myocardial infarction, we compared the Gensini score of coronary artery stenosis between 2 groups of patients with and without precordial ST-segment depression. Group I consisted of 28 patients who showed ST-segment depression on admission (greater than or equal to 1 mm in V2-V6) and Group II (n = 16) those without ST-segment depression (less than 1 mm). The Gensini score of the coronary arteries (56 +/- 29 vs. 28 +/- 18; p less than 0.001), the partial score of the infarction-related artery (29 +/- 16 vs. 17 +/- 11; p less than 0.01) and of the infarction-nonrelated artery (27 +/- 24 vs. 11 +/- 12; p less than 0.02) were significantly higher in Group I than in Group II. The Killip score (greater than or equal to II) (34% vs. 6%; p less than 0.05), frequency of arrhythmias (75% vs. 38%; p less than 0.02) and peak CK value (3,676 +/- 2,290 vs. 1,818 +/- 1,153 IU/L; p less than 0.005) were higher in Group I than in Group II. Four patients in Group I died following admission, while no patient died in Group II (N.S.). Autopsy findings from the 4 Group I patients revealed fresh extensive inferior infarction and healed diffuse subendocardial infarction which could not be predicted from electrocardiograms. All patients who survived the acute stage performed treadmill exercise testing and 22 patients underwent exercise thallium-201 single photon emission computer tomography (SPECT). On treadmill exercise test, there was no significant difference between the 2 groups in the frequency of angina pectoris and ST-segment depression. On SPECT, the perfusion defect area under 55% of maximum uptake at the redistribution phase was 45.8 +/- 19.6 cm2 in Group I (n = 14) and 34.7 +/- 21.3 cm2 in Group II (n = 8; N.S.). In conclusion, precordial ST-segment depression in acute inferior myocardial infarction suggested advanced atherosclerosis in both the infarction-related and nonrelated coronary arteries, indicating a larger infarct size.     

Effectiveness of intravenous streptokinase on infarct size and left ventricular function in acute myocardial infarction. Prospective and randomized study

Within 3 h after the onset of symptoms of myocardial infarction, 64 patients were randomly assigned to receive either a 1-h intravenous infusion of 1,500,000 IU of streptokinase (SK) or a conventional therapy. Infarct size was estimated in CK gram equivalent (CKg) by measurement of CK-MB every 3 hours during a 48-h period. Enzymatic study revealed that myocardial infarction of the SK group was significantly smaller (61.4 +/- 45 vs. 89.4 +/- 56 CKg, p less than .05). Angiograms were performed at early stage and five weeks after myocardial infarction. At first coronary angiogram, the infarct-related vessel was open in 82% in the SK group versus 12% in controls. The SK group had higher global ejection fraction at second angiogram (57 +/- 11% vs. 49 +/- 11%, p less than .02), but differences in regional wall motion were not significant. By analysis according to patency or occlusion of infarct-related vessel, global and regional ejection fractions were significantly better at first and at second angiograms in all patients and in anterior infarctions with a patent infarct-related coronary artery. There was no significant difference for inferior infarction. We conclude that intravenous streptokinase infusion early after the onset of myocardial infarction reduces infarct size and improves left ventricular function, chiefly in anterior infarction. This benefit appears to be closely correlated to patency of infarct-related vessels.     

Clinical and prognostic significance of lung thallium uptake on rest imaging in acute myocardial infarction

Exercise-induced pulmonary uptake of thallium-201 in patients with ischemic heart disease is probably due to transient pulmonary edema and left ventricular failure induced by exercise. The significance of increased lung uptake of thallium-201 at rest after acute myocardial infarction (AMI) has not been described. Ninety-six patients admitted with chest pain for suspected AMI or unstable angina underwent thallium-201 imaging at rest. Using conventional diagnostic criteria, 62 had AMI, 12 had unstable angina and 22 had neither. Increased lung uptake of thallium-201 was present in 24 of the total 96 (25%) patients, 20 of the 62 (32%) patients with AMI and 4 of 34 (13%) patients with no evidence of infarction. In the AMI group, those with increased lung thallium-201 uptake had a higher mean +/- standard deviation segmental thallium-201 defect score (22 +/- 7 vs 12 +/- 8, p less than 0.0001), lower ejection fraction (35 +/- 14 vs 49 +/- 14%, p less than 0.002), higher peak creatine kinase levels (2,410 +/- 1,247 vs 1,496 +/- 1,228 IU/liter, p less than 0.01), higher wall motion abnormality score (25 +/- 13 vs 13 +/- 12, p less than 0.0001), increased incidence of clinical in-hospital heart failure (15 of 20 vs 7 of 42, p less than 0.0001) and higher short-term mortality (4 of 20 vs 1 of 42, p less than 0.02) compared to those without increased lung thallium-201 uptake.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemodynamic profile of patients with acute myocardial infarction at risk of infarct expansion

To identify patients at risk of cardiac expansion during hospital stay for a first acute myocardial infarction (AMI), 41 patients underwent right-sided cardiac catheterization soon after admission and serial 2-dimensional echocardiography on days 1, 3 or 4 and between days 7 and 10. Infarct expansion was recognized by echocardiography in 11 patients (27%), most often on the second recording (day 3 or 4). Age, sex, time from onset of pain to catheterization, peak levels of creatine kinase and creatine kinase-MB isoenzyme, heart rate, mean pulmonary artery wedge pressure and left ventricular stroke work index were similar in the 2 groups. Patients in whom infarct expansion developed had a higher incidence of previous systemic hypertension (73% vs 27%, p less than 0.01) and anterior AMI (91% vs 30%, p less than 0.001) and a higher mortality rate at 1 year (73 vs 7%, p less than 0.001) than those who did not. They also had higher systolic (139 +/- 24 vs 126 +/- 18 mm Hg, p less than 0.05) and diastolic (91 +/- 14 vs 75 +/- 13 mm Hg, p less than 0.001) arterial pressures, lower stroke volume index (31 +/- 10 vs 40 +/- 10 ml/m2, p less than 0.01) and much higher systemic vascular resistance (SVR) values (1,713 +/- 380 vs 1,253 +/- 264 dynes s cm-5, p less than 0.0001). In the subgroups of patients with anterior AMI, differences were significant for diastolic arterial pressure, stroke volume index, SVR and mortality.(ABSTRACT TRUNCATED AT 250 WORDS)     

Transient left ventricular filling abnormalities (diastolic stunning) after acute myocardial infarction

A variety of experimental studies suggest that diastolic left ventricular (LV) function changes after acute myocardial infarction (AMI), but limited data exist on these changes in humans. To assess diastolic filling after AMI, 60 patients underwent Doppler echocardiographic examination within 24 hours of AMI. Of 54 patients who also underwent catheterization, 45 (83%) were successfully reperfused. A subgroup of 17 patients underwent a follow-up Doppler examination at 7 days after infarction, whereas 15 patients with stable exertional angina served as control subjects. There was no significant difference in age, gender, incidence of systemic hypertension or diabetes mellitus, heart rate, mean arterial pressure or severity of coronary artery disease between the infarct and control groups. The infarct group had a lower velocity time integral total (9.9 +/- 0.4 cm vs 12.0 +/- 0.9 cm, p less than 0.001), a lower velocity time integral E (5.8 +/- 0.3 cm vs 6.8 +/- 0.5 cm, p less than 0.01) and a lower velocity time integral 0.333 (3.5 +/- 0.4 cm vs 6.1 +/- 0.5 cm, p less than 0.01) than the control group. In addition, velocity time integral A/total was significantly greater in the infarction group (0.44 +/- 0.03 vs 0.35 +/- 0.04, p less than 0.01) compared to the control group. The follow-up subgroup showed an increase in velocity time integral total (p less than 0.01), velocity time integral E (p less than 0.05) and velocity time integral 0.333/total (p less than 0.05) over the first 7 days after infarction. The final recovery values at 7 days were not significantly different from those of the coronary artery disease group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Short- and long-term prognostic importance of complete bundle-branch block complicating acute myocardial infarction

Among 1013 consecutive patients with acute myocardial infarction (AMI), 104 (10%) developed complete bundle-branch block (BBB). The clinical characteristics and the short- and long-term prognosis were similar in the 53 patients with right and the 51 patients with left BBB. Compared to the 909 patients without this conduction disturbance, these 104 patients were older (64 +/- 9 vs. 58 +/- 10 years, p less than 0.001), more frequently women (26 vs. 17%, p less than 0.05), had a larger infarct (peak CK 1672 +/- 1124 vs. 1356 +/- 1089 IU/l, p less than 0.001), more frequently anterior (60 vs. 37%, p less than 0.001). They had a higher incidence of Killip class greater than 1 (63 vs. 38%, p less than 0.001), pericarditis (40 vs. 23%, p less than 0.001), atrial fibrillation or flutter (22 vs. 12%, p less than 0.01), ventricular fibrillation (15 vs. 9%, p less than 0.05), and atrioventricular block (23 vs. 11%, p less than 0.001). Both hospital mortality (32 vs 10%, p less than 0.001) and 3-year posthospital mortality (37 vs. 18%, p less than 0.001) were much higher among patients with complete BBB. Transient BBB had the same deleterious prognosis as BBB persistent at discharge (mortality 33 vs. 39%, NS). The prognostic importance of BBB was more prominent during the first 6 months after infarction (mortality between 6 and 36 months: 18% with BBB vs. 11% without BBB, NS).     

Coronary angiography and left ventriculography in survivors of transmural and nontransmural myocardial infarction

Recent studies have suggested a similar prognosis for patients with transmural myocardial infarction and nontransmural myocardial infarction despite a smaller infarct size in the latter patients estimated by creatine phosphokinase (CPK). Thirty-one patients with transmural myocardial infarction and 17 patients with nontransmural myocardial infarction as defined by electrocardiographic criteria underwent coronary angiography and left ventriculography from 10 to 24 days after they had an acute myocardial infarction. Forty-three of these 48 patients were asymptomatic following their myocardial infarction. When compared to patients with nontransmural myocardial infarction, those with transmural myocardial infarction had greater peak CPK levels, 1,090 +/- 210 versus 290 +/- 60 IU (p less than 0.01). There was no difference in prevalence of single, double or triple vessel coronary artery disease, mean number of coronary arteries 50 per cent narrowed (2.0 +/- 0.2 versus 2.0 +/- 0.2), near total or total occlusions, coronary score (Friesinger) (7.9 +/- 0.6 versus 8.2 +/- 0.7), left ventricular ejection fraction (48 +/- 2 versus 53 +/- 4), or per cent of akinetic-dyskinetic myocardial segments (66 of 242 [27 per cent] versus 32 of 132 [24 per cent]) between two groups. The similar extent of coronary artery narrowing and degree of left ventricular dysfunction may explain the similar prognosis for patients with transmural myocardial infarction and those with nontransmural myocardial infarction despite differences in enzymatically estimated acute infarct size.     

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 intracoronary adenosine infusion during coronary intervention on myocardial reperfusion injury in patients with acute myocardial infarction

Despite early recanalization of an occluded infarct artery, up to 33% of patients with acute myocardial infarction do not obtain complete myocardial reperfusion due to a process of reperfusion injury. This study assessed whether adjunctive therapy with adenosine might prevent or attenuate the phenomenon of myocardial reperfusion injury. Myocardial reperfusion was assessed in 79 consecutive patients receiving a 20-minute intracoronary infusion of adenosine during percutaneous coronary intervention (PCI) and in a historical cohort of 200 patients with acute myocardial infarction who were treated with PCI (controls). Myocardial reperfusion injury was defined as persistent (> or =50% of initial value) ST-segment elevation after successful recanalization. Its effect on infarct size was evaluated by calculating the Selvester QRS score before intervention and at follow-up. Myocardial reperfusion injury was present in 19% of patients receiving adenosine versus 35% of control patients (p = 0.004). Evaluation of infarct expansion over time showed almost no change in the QRS score in patients receiving adenosine (3.4 +/- 3.0 before PCI; 3.5 +/- 3.1 at follow-up). In contrast, infarct QRS score in the control group worsened from 3.1 +/- 2.7 before PCI to 4.5 +/- 3.2 at follow-up (p = 0.003 treatment with adenosine vs control). Multivariate analysis identified adjunctive therapy with adenosine as an independent protective determinant of myocardial reperfusion injury and of infarct expansion. The rate of major adverse cardiac events (death and myocardial infarction) at 1 month tended to be lower in patients receiving adenosine (4% vs 6.5%, p = 0.7) and was mainly observed in patients with evidence of myocardial reperfusion injury (cardiac event rate 2% in patients with ST-segment elevation of <50% vs 14% in patients with ST-segment elevation > or =50%, p = 0.003). Thus, impaired myocardial reperfusion is the most important determinant of clinical outcome in patients with acute myocardial infarction treated with PCI. Adjunctive therapy with intracoronary infusion of adenosine during PCI prevents the occurrence of severe myocardial reperfusion injury and is associated with less infarct expansion.     

Nuclear magnetic resonance and radionuclide angiographic assessment of acute myocardial infarction in a randomized trial of intravenous streptokinase

Sixty-six patients presenting with their first evolving transmural acute myocardial infarction (AMI) were randomized to receive either streptokinase (n = 41) or placebo therapies (n = 25) within 6 hours of the onset of chest pain. These patients then underwent supine rest, exercise and after-nitroglycerin radionuclide angiography 3 weeks after AMI. Nuclear magnetic resonance (NMR) imaging was performed at 3 weeks as a more direct estimate of AMI size. Although peak creatine kinase values were comparably elevated between groups (2,367 +/- 1,486 IU/liter for streptokinase vs 2,637 +/- 1,305 IU/liter for placebo), there was a significant reduction in NMR-measured AMI size in the streptokinase group (3 +/- 2% of left ventricular volume vs 10 +/- 4% in the placebo group, p less than 0.05). This occurred despite comparable resting (54 +/- 11 vs 47 +/- 10% and exercise (53 +/- 12 vs 49 +/- 11%) global ejection fractions. However, following nitroglycerin, there was an improvement in global ejection fraction in the streptokinase-treated group that was not observed with placebo (61 +/- 13 vs 48 +/- 10%, p less than 0.05). A similar pattern was also observed with regional functional analysis. Thus, streptokinase therapy leads to a significant reduction in NMR-measured AMI size and to a greater degree of reversible left ventricular dysfunction.     

Comparison of clinical features of non-Q wave and Q wave myocardial infarction

The clinical spectrum and outcome of 119 patients with acute non-Q wave myocardial infarction (NQMI) were studied, in comparison with those of 354 patients with acute Q wave myocardial infarction (QMI). The patients with NQMI had a significantly higher incidence of preinfarction angina (73% vs 63%), previous myocardial infarction (43% vs 22%), multivessel disease (73% vs 51%), postinfarction angina (55% vs 21%), and recurrent myocardial infarction during follow-up for an average of 25 months (17% vs 8%). NQMI patients also had a lower rate of complication of pump failure and smaller infarct size estimated by peak creating phosphokinase (CPK) levels (1361 +/- 1243 vs 2711 +/- 1684 IU/L) than those with QMI. There was no difference in in-hospital mortality between the two groups (17% vs 17%). However, death due to cardiac rupture was exclusively noted in the QMI group. The present study suggests that NQMI is more unstable than QMI in the clinical course.     

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)     

Intravenous treatment with streptokinase of acute myocardial infarction. II. Effect of patency of the artery supplying the infarction area on the infarction size and post-infarction impairement of left-ventricular function

153 patients with a first acute myocardial infarction underwent the study. 90 of them received 1.000.000 units of streptokinase intravenously, followed by intravenous heparin administration for 5-7 days. The control group consisted of 63 remaining. In all patients serum CK-MB activity was determined every 4 hours for 72 hours: the infarct mass was calculated from the obtained curves. In 118 patients selective coronarography and left ventriculography was performed in the 2-nd or 3-rd week of hospitalisation. Left ventricular ejection fraction (E.F.) and dyssynergy index were calculated from ventriculographic data. Coronarography revealed a patent infarct-related artery in 76.7% of patients treated with streptokinase and in 44.4% of the control group (p less than 0.001). Among patients with a patent infarct-related artery an early peak of serum CK-MB activity (suggesting early recanalisation) occurred in 72.2% of streptokinase patients but in only 42.1% of the control group. Patients with a patent infarct-related artery had a significantly lower infarct mass (45 +/- 28 g vs 56 +/- 30 g), a lower left ventricular dyssynergy index (229 +/- 243 vs 348 +/- 247) and a significantly higher E.F. (63 +/- 12% vs 54 +/- 15%) compared with patients with an occluded artery.