The effect of previous coronary-artery bypass surgery on the prognosis of patients with diabetes who have acute myocardial infarction. Bypass Angioplasty Revascularization Investigation Investigators

BACKGROUND: Acute myocardial infarction in patients with diabetes is associated with high mortality. We studied whether previous revascularization by coronary-artery bypass grafting (CABG), as compared with percutaneous transluminal coronary angioplasty (PTCA), influences the prognosis in such patients. METHODS: We classified all patients eligible for the Bypass Angioplasty Revascularization Investigation who underwent coronary revascularization within three months after entry into the study according to whether they had diabetes and whether they had undergone CABG, either initially or after PTCA. The protective effect of CABG with regard to mortality in the presence and in the absence of subsequent spontaneous Q-wave myocardial infarction was estimated with the use of Cox regression models. RESULTS: Among the 641 patients with diabetes and the 2962 without diabetes, the cumulative five-year rates of death were 20 percent and 8 percent, respectively (P<0.001), and the five-year rates of spontaneous Q-wave myocardial infarction were 8 percent and 4 percent (P<0.001). CABG greatly reduced the risk of death after spontaneous Q-wave myocardial infarction in the patients with diabetes (relative risk, 0.09; 95 percent confidence interval, 0.03 to 0.29). Among patients with diabetes who had undergone CABG but did not have spontaneous Q-wave myocardial infarctions, the corresponding relative risk of death was 0.65 (95 percent confidence interval, 0.45 to 0.94). Among the patients without diabetes, no protective effect of CABG was evident. CONCLUSIONS: Among patients with diabetes, previous coronary bypass surgery, as compared with coronary angioplasty, has a highly favorable influence on prognosis after acute myocardial infarction and a smaller beneficial effect among patients who do not have infarction. These findings should influence the type of coronary revascularization procedure selected for patients with diabetes who have multivessel coronary artery disease.     

A randomized trial of intravenous tissue plasminogen activator for acute myocardial infarction with subsequent randomization to elective coronary angioplasty

Patients presenting within four hours of the onset of acute myocardial infarction were randomly assigned to receive 80 to 100 mg of recombinant human-tissue plasminogen activator (t-PA) intravenously over a period of three hours (n = 72) or placebo (n = 66). Administration of the study drug was followed by coronary arteriography, and candidates for percutaneous transluminal coronary angioplasty were randomly assigned either to undergo angioplasty on the third hospital day (n = 42) or not to undergo angioplasty during the 10-day study period (n = 43). The patency rates of the infarct-related arteries were 66 percent in the t-PA group and 24 percent in the placebo group. No fatal or intracerebral hemorrhages occurred, and episodes of bleeding requiring transfusion were observed in 7.6 percent of the placebo group and 9.8 percent of the t-PA group. As compared with the use of placebo, administration of t-PA was associated with a higher mean (+/- SEM) ejection fraction on the 10th hospital day (53.2 +/- 2.0 vs. 46.4 +/- 2.0 percent, P less than 0.02), an improved ejection fraction during the study period (+3.6 +/- 1.3 vs. -4.7 +/- 1.3 percentage points, P less than 0.0001), and a reduction in the prevalence of congestive heart failure from 33 to 14 percent (P less than 0.01). Angioplasty improved the response of the ejection fraction to exercise (+8.1 +/- 1.4 vs. +1.2 +/- 2.2 percentage points, P less than 0.02) and reduced the incidence of postinfarction angina from 19 to 5 percent (P less than 0.05), but did not influence the ejection fraction at rest. These data support an approach to the treatment of acute myocardial infarction that includes early intravenous administration of t-PA and deferred cardiac catheterization and coronary angioplasty.     

Diltiazem and reinfarction in patients with non-Q-wave myocardial infarction. Results of a double-blind, randomized, multicenter trial

We performed a multicenter, double-blind, randomized study to evaluate the effect of diltiazem on reinfarction after a non-Q-wave myocardial infarction. Nine centers enrolled 576 patients: 287 received diltiazem (90 mg every six hours) and 289 received placebo. Treatment was initiated 24 to 72 hours after the onset of infarction and continued for up to 14 days. The primary end point, reinfarction, was defined as an abnormal reelevation of MB creatine kinase in plasma within 14 days. Reinfarction occurred in 27 patients in the placebo group (9.3 percent) and in 15 in the diltiazem group (5.2 percent)--a 51.2 percent reduction in cumulative life-table incidence (P = 0.0297; 90 percent confidence interval, 7 to 67 percent). Diltiazem reduced the frequency of refractory postinfarction angina (a secondary end point) by 49.7 percent (P = 0.0345; 90 percent confidence interval, 6 to 73 percent). Mortality was similar in the two groups (3.1 and 3.8 percent, respectively, in the placebo and diltiazem groups), but adverse drug reactions (most of which were mild) were more common in the diltiazem group. Nevertheless, the drug was well tolerated, despite concurrent treatment with beta-blockers in 61 percent of the patients. We conclude that diltiazem was effective in preventing early reinfarction and severe angina after non-Q-wave infarction and that it was also safe and generally well tolerated.     

Anatomic variant of the posterior interventricular coronary artery: Implications for coronary angioplasty in acute myocardial infarction

Acute thrombotic occlusion of an infarct-related artery is frequently found in patients presenting with myocardial infarction. In a patient with acute inferior wall myocardial infarction complicated by continuous chest pain and hemodynamic instability, emergency diagnostic coronary arteriography demonstrated a patent, infarct-related, “pseudo” right coronary artery while, in fact, this vessel was a rare anatomic variant of the posterior interventricular branch with very early origin from the right coronary artery and the true right coronary artery was completely occluded by a thrombotic obstruction. Accurate anatomic-angiographic interpretation of the angiogram was crucial for successful performance of emergency recanalization and revascularization of the true right coronary artery with laser and balloon angioplasty. Once antegrade flow was restored another rare coronary variant was discovered, i.e., a sinoatrial node artery arising from the middle portion of the newly patent right coronary artery. Clin. Anat. 10:303–306, 1997. © 1997 Wiley-Liss, Inc.     

Platelet glycoprotein IIb/IIIa inhibition with coronary stenting for acute myocardial infarction.

BACKGROUND: When administered in conjunction with primary coronary stenting for the treatment of acute myocardial infarction, a platelet glycoprotein IIb/IIIa inhibitor may provide additional clinical benefit, but data on this combination therapy are limited. METHODS: We randomly assigned 300 patients with acute myocardial infarction in a double-blind fashion either to abciximab plus stenting (149 patients) or placebo plus stenting (151 patients) before they underwent coronary angiography. Clinical outcomes were evaluated 30 days and 6 months after the procedure. The angiographic patency of the infarct-related vessel and the left ventricular ejection fraction were evaluated at 24 hours and 6 months. RESULTS: At 30 days, the primary end point--a composite of death, reinfarction, or urgent revascularization of the target vessel--had occurred in 6.0 percent of the patients in the abciximab group, as compared with 14.6 percent of those in the placebo group (P=0.01); at 6 months, the corresponding figures were 7.4 percent and 15.9 percent (P=0.02). The better clinical outcomes in the abciximab group were related to the greater frequency of grade 3 coronary flow (according to the classification of the Thrombolysis in Myocardial Infarction trial) in this group than in the placebo group before the procedure (16.8 percent vs. 5.4 percent, P=0.01), immediately afterward (95.1 percent vs. 86.7 percent, P=0.04), and six months afterward (94.3 percent vs. 82.8 percent, P=0.04). One major bleeding event occurred in the abciximab group (0.7 percent); none occurred in the placebo group. CONCLUSIONS: As compared with placebo, early administration of abciximab in patients with acute myocardial infarction improves coronary patency before stenting, the success rate of the stenting procedure, the rate of coronary patency at six months, left ventricular function, and clinical outcomes.     

Aspirin and dipyridamole in the prevention of restenosis after percutaneous transluminal coronary angioplasty

To examine the role of antiplatelet therapy in the prevention of arterial restenosis after percutaneous transluminal coronary angioplasty (PTCA), we conducted a randomized, double-blind, placebo-controlled study in 376 patients. The active treatment consisted of an oral aspirin-dipyridamole combination (330 mg-75 mg) given three times daily, beginning 24 hours before PTCA. Eight hours before PTCA, the oral dipyridamole was replaced with intravenous dipyridamole at a dosage of 10 mg per hour for 24 hours, and oral aspirin was continued. Sixteen hours after PTCA, the initial combination was reinstituted. Treatment was continued in patients with a successfully dilated vessel until follow-up angiography four to seven months after PTCA--or earlier, if symptoms dictated. Of 249 patients who underwent follow-up angiography, 37.7 percent of patients receiving the active drug had restenosis in at least one segment, as compared with 38.6 percent of patients taking placebo (P not significant). The number of stenotic segments was virtually the same in the two groups. Among the 376 randomized patients, there were 16 periprocedural Q-wave myocardial infarctions--13 in the placebo group and 3 in the active-drug group (6.9 percent vs. 1.6 percent, P = 0.0113). Although the use of this antiplatelet regimen before and after PTCA did not reduce the six-month rate of restenosis after successful coronary angioplasty, it markedly reduced the incidence of transmural myocardial infarction during or soon after PTCA. Thus, the short-term use of antiplatelet agents in relation to PTCA can be recommended.     

Decreased incidence of ventricular late potentials after successful thrombolytic therapy for acute myocardial infarction

In some patients with acute myocardial infarction, low-amplitude potentials that prolong the QRS complex, termed "late potentials," can be recorded on a signal-averaged electrocardiogram. The presence of these late potentials is known to be associated with an increase in the risk of ventricular tachycardia and sudden death. Because patients with acute myocardial infarction who receive thrombolytic therapy have a reduced incidence of ventricular tachyarrhythmia and sudden death, we sought to determine whether such patients also have a decreased incidence of late potentials. We studied 106 patients less than 75 years of age who were admitted with a first myocardial infarction and in whom a signal-averaged electrocardiogram was recorded within 48 hours of admission. Within four hours of the onset of chest pain, tissue plasminogen activator (t-PA) was given to 44 patients, and 62 were treated conventionally. In the t-PA group, late potentials were recorded in 2 of 44 patients (5 percent), as compared with 14 of 62 (23 percent) in the conventionally treated group (P = 0.01). Furthermore, among the patients treated with t-PA, continued occlusion of the infarct-related artery was related to the presence of late potentials. In the t-PA group, late potentials were recorded within 24 hours of angiography in 2 of the 6 patients with an occluded infarct-related artery, as compared with none of the 38 patients with a patient infarct-related artery. Our data suggest that successful thrombolytic therapy is associated with a marked reduction in the incidence of late potentials on the signal-averaged electrocardiogram. Long-term follow-up will be required to determine whether this finding predicts a reduced incidence of subsequent ventricular tachyarrhythmia and sudden death.     

An association between collateral blood flow and myocardial viability in patients with recent myocardial infarction.

BACKGROUND. We hypothesized that successful reperfusion of an occluded infarct-related coronary artery even late after acute myocardial infarction would result in improved regional wall motion and that such improvement might be related to the presence of collateral blood flow within the infarct bed. METHODS. We assessed regional wall motion by two-dimensional echocardiography at base line and one month after angioplasty was attempted in the occluded infarct-related artery in 43 patients who had had a myocardial infarction two days to five weeks earlier. A wall-motion score was assigned to each patient on a five-point scale (from 1 [normal function] to 5 [dyskinesia]). The percentage of the infarct bed perfused by collateral flow was assessed with myocardial contrast echocardiography. RESULTS. In the 41 patients who had abnormal wall motion at base line, improvement in function was noted in 25 (78 percent) of the 32 in whom angioplasty was successful, as compared with only 1 (11 percent) of the 9 in whom it was unsuccessful (P < 0.001). The percentage of the infarct bed supplied by collateral flow at base line was directly correlated with wall function and inversely correlated with the wall-motion score one month after successful angioplasty (r = -0.64, P < 0.001). Among the patients in whom angioplasty was successful, the 23 in whom > 50 percent of the infarct bed was supplied by collateral flow had better wall motion (P < 0.001) and greater improvement in wall motion at one month (P = 0.004) than the 9 in whom < or = 50 percent of the bed was supplied by collateral flow. The degree of improvement in function was not influenced by the length of time between the infarction and the attempted angioplasty. CONCLUSIONS. The myocardium remains viable for a prolonged period in many patients with acute infarction and an occluded infarct-related artery. Viability appears to be associated with the presence of collateral blood flow within the infarct bed.     

Detection of early myocardial infarction in formalin-fixed, paraffin-embedded tissue

Whether the early infarct area in formalin-fixed, paraffin-embedded tissue could be delineated by the immunohistochemical method using myoglobin-antibody was studied in 23 pig hearts without collateral circulation. Five hearts were examined at 20 minutes, 2 hours, 4 hours, and 6 hours after occlusion of the distal one third of the left anterior descending coronary artery, respectively. Three pigs were killed 24 hours after occlusion. Heart rate and aortic pressure before and after occlusion did not change in any groups. The subepicardial and subendocardial regional blood flows were reduced to almost zero in all hearts after occlusion (0.88 +/- 0.10 to 0.02 +/- 0.02 mL/g/min). Slight myoglobin defects in the ischemic tissue were noted in the five pigs examined 2 hours after occlusion and definite myoglobin defects were detected in all pigs examined at 4, 6, and 24 hours after occlusion. Nitrotetrazorium blue stain of myocardial tissue before formalin fixation showed slight demarcation of the ischemic area at 4 hours after occlusion and definite demarcation at 6 and 24 hours after occlusion. Slight demarcation was noted at 2 hours after occlusion in Masson trichrome stain and 4 hours after occlusion in the hematoxylin-eosin stain. However, definite demarcation of the ischemic area was seen in Masson trichrome stain only at 24 hours after occlusion and was not noted in hematoxylin-eosin stain even at 24 hours after occlusion. Our previous electron microscopic study revealed that, in the pig heart, irreversible cellular damage was transmurally seen at two hours after occlusion of the coronary artery. Therefore, a definite myoglobin defect reflects irreversible cellular damage such as infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intermittent coronary occlusion in acute myocardial infarction. Value of combined thrombolytic and vasodilator therapy

We performed continuous electrocardiographic ST-segment monitoring and serial coronary arteriography in 45 consecutive patients presenting in the early stages of acute myocardial infarction. During cardiac catheterization, 28 episodes of arteriographically confirmed coronary reopening and subsequent reocclusion were observed in 16 patients before (3 episodes) and during (25 episodes) continuous intracoronary infusion of streptokinase. In addition, ST-segment monitoring demonstrated 12 episodes of spontaneous transient return of the ST segment to the base line in eight patients between the time of admission and the performance of coronary arteriography. During arteriographically documented reocclusion, intracoronary isosorbide dinitrate (2 mg) reestablished the patency of the coronary artery within one to two minutes in 14 of 28 episodes that occurred in 11 of 16 patients. After streptokinase infusion, intracoronary administration of isosorbide dinitrate was followed by dilatation of the infarct-related stenosis from a mean value (+/- SD) of 1.12 +/- 0.3 mm (58.1 +/- 12.1 percent) to 1.33 +/- 0.4 mm (51.6 +/- 12.9 percent; P = 0.004). Spontaneous intermittent coronary recanalization and reocclusion resulting from a variable combination of thrombosis and vasoconstriction are frequent during the early phase of acute myocardial infarction. We propose that the combination of intracoronary streptokinase and isosorbide dinitrate may increase the rate of stable coronary recanalization.     

A comparison between heparin and low-dose aspirin as adjunctive therapy with tissue plasminogen activator for acute myocardial infarction. Heparin-Aspirin Reperfusion Trial (HART) Investigators

BACKGROUND. We report the results of the Heparin-Aspirin Reperfusion Trial, a collaborative study comparing early intravenous heparin with oral aspirin as adjunctive treatment when recombinant tissue plasminogen activator (rt-PA) is used for coronary thrombolysis during acute myocardial infarction. METHODS. Two hundred five patients were randomly assigned to receive either immediate and then continuous intravenous heparin (starting with a 5000-unit bolus; n = 106) or immediate and then daily oral aspirin (80 mg; n = 99) together with rt-PA (100 mg intravenously over a six-hour period) initiated within six hours of the onset of symptoms. We evaluated the patency of the infarct-related artery by angiography 7 to 24 hours after beginning rt-PA infusion, the frequency of reocclusion of the artery by repeat angiography on day 7, and ischemic or hemorrhagic complications during the hospital stay. RESULTS. At the time of the first angiogram, 82 percent of the infarct-related arteries in the patients assigned to heparin were patent, as compared with only 52 percent in the aspirin group (P less than 0.0001). Of the initially patent vessels, 88 percent remained patent after seven days in the heparin group, as compared with 95 percent in the aspirin group (P not significant). The numbers of hemorrhagic events (18 in the heparin and 15 in the aspirin group) and recurrent ischemic events (8 in the heparin and 2 in the aspirin group) were similar in the two groups. CONCLUSIONS. Coronary patency rates associated with rt-PA are higher with early concomitant systemic heparin treatment than with concomitant low-dose oral aspirin. This observation has important implications for clinical practice and should be considered in the design and interpretation of clinical trials involving coronary thrombolytic therapy.     

Intravenous thrombolytic treatment for acute myocardial infarction. Effects of early intervention and early examination

Intravenous thrombolytic treatment (streptokinase or anisoylated plasminogen streptokinase activator complex (APSAC) was given to 50 consecutive patients within 3 hours after onset of symptoms of acute myocardial infarction. Left heart catheterisation with coronary angiography and simultaneous double view left ventriculography were performed approximately 4 hours after start of thrombolytic treatment. This examination showed that the acute infarct-related coronary artery was open in 36 patients (72%) and closed in 14 patients (28%). A higher left ventricular ejection fraction was found among patients with open, than among patients with closed infarct-related artery (58.8% vs. 48.4%, p = 0.05). The group with open artery also had a lower score of regional left ventricular dysfunction (1.7 vs. 2.4, p less than 0.05, on a scale from 0-3). Single, double and triple vessel coronary heart disease was found in 22, 14 and 13 patients respectively. Mean age was lower in the group with single vessel disease as compared to double and triple vessel disease (48.4 years vs. 53.4 and 55.4 years, p less than 0.05 and p less than 0.005). Independently of whether the infarct-related artery was open or closed, there tended to be an inverse correlation between number of diseased vessels and preservation of left ventricular function (statistical significance only for single vessel versus triple vessel disease with respect to score of regional left ventricular dysfunction, 1.8 vs. 2.4, p less than 0.05). These findings suggest that early thrombolytic treatment within 3 hours of onset of symptoms may preserve myocardial tissue during the evolution of acute infarction. Furthermore, a presumably better collateralisation from adjacent coronary arteries without stenoses may be important for myocardial preservation. Finally, early angiographic examination can be performed safely and is a good support for determination of further treatment, which in the actual patients was coronary bypass surgery in 8 cases, transluminal angioplasty, PTCA, in 20 cases, and medical treatment alone in 22 cases.     

Cardiac troponin I and CK-MB mass after cardiac surgery with cardiopulmonary bypass

Cardiac troponin I (cTnI) assay is used in the diagnosis of myocardial infarction after cardiac surgery. Variations in the cut-off value have been reported even with the same assay method. The aim of this work is to investigate the release profile of cTnI and CK-MB mass after cardiac surgery and to determine the cut-off value of cTnI and CK-MB mass allowing the diagnosis of perioperative myocardial infarction. In patients without postoperative cardiac complication, the cTnI peak was observed 24 hours after surgery both in coronary artery bypass grafting and in valve replacement. Moreover, the amount of cTnI released within the three hours after surgery is 2.5 fold higher in valve replacement than in coronary artery bypass grafting. The CK-MB peak was observed 3 hours after surgery in the two surgical procedures. In these patients, cTnI and CK-MB concentrations increased with the cross clamp time duration. In patients with postoperative myocardial infarction, the cTnI and CK-MB peaks were observed 24 hours after surgery. Diagnosis of perioperative myocardial infarction can be performed with a sensitivity of 100% at 24 hours with cut-off values of 32 and 7 microg/L for CK-MB and cTnI, respectively, both with Stratus (Dade Behring) and Immulite (DPC) analysers.     

Dosierung der intrakoronaren Urokinase-Infusion beim akuten Myokardinfarkt

Summary In 11 patients with acute myocardial infarction (mean age 52±6 years) coronary angiography was performed 4.5±3.6 h after the onset of symptoms. The infarct-related artery was in 7 cases the right coronary artery and in 4 cases the left anterior descending branch of the left coronary artery. The infarct-related artery showed total or subtotal occlusion and no perfusion (Thrombolysis in Myocardial Infarction trial (TIMI) grade 0 or 1). In 7 cases Urokinase was infused intracoronarily at a dosage of 250 000 IU over 30 min, but in only 1 case partial reperfusion was achieved. However, all patients treated with 500 000 IU Urokinase over 30 min or 1 Mill IU over 60 min had successful reperfusion (TIMI grade 2 or 3). Thus, it appears that 500 000 IU up to 1 Mill IU of Urokinase over a period of 30 to 60 min is adequate for intracoronary thrombolysis in patients with acute myocardial infarction.

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Abkürzungsverzeichnis TIMI Thrombolysis in Myocardial Infarction trial - PTCA Perkutane transluminale Koronarangioplastie - RCA rechte Koronararterie - RIVA Ramus interventrikularis anterior - IE Internationale Einheiten - min Minuten     

Myocardial infarction in dogs with acute and gradual occlusion of the circumflex or right coronary arteries

This study was designed to quantitate and describe the incidence and magnitude of myocardial infarction in the canine heart following acute and gradual occlusion of the circumflex or right coronary arteries. In animals with acute occlusion, the circumflex artery was ligated just distal to the bifurcation of the left coronary artery for 4 hr (seven dogs). Gradual occlusion was produced by placing an Ameroid occluder on the circumflex artery for 1 month (nine dogs), 3 months (nine dogs), and 5 months (eight dogs) and on the right coronary artery for 3 months (nine dogs). Ten dogs served as controls. At the end of the experiments the dogs were sacrificed, and identification of myocardial infarction was made with an enzyme-mapping technique in dogs with acute occlusion and with histological methods in dogs with gradual occlusion. The volume of ventricular infarction was determined with the use of an Apple II Computer and graphics tablet. After 3 months, gradual occlusion of the right coronary artery produced a 22% incidence of infarction which was significantly less (P <.01, X²) than the 67% incidence observed with 3 months of gradual circumflex occlusion. The average infarct volume produced by gradual right coronary occlusion was 0.94 + 0.69%. The average volume of left ventricular infarction in animals with circumflex acute occlusion was 15.6% + 6.6 and the incidence of infarction was 100%. With gradual occlusion of the circumflex artery for 1, 3, and 5 months, average left ventricular infarction was 2.02 ± 1.01%, 3.13 ± 1.53%, and 2.96 ± 1.35%, respectively. There were no significant differences in the amount of damage observed among the three groups with gradual occlusion, and the average incidence of infarction for these three groups was 76%. In the 1-, 3- or 5- month animals with circumflex occlusion, no additional areas of necrosis subsequent to the original damage were found, indicating that infarction is a single event in this model of gradual occlusion. These results suggest that infarct size is determined primarily by factors at the time of total occlusion and that gradual occlusion allows sufficient time for collateral growth, thereby limiting the extent of myocardial injury.     

Localized intracoronary gamma-radiation therapy to inhibit the recurrence of restenosis after stenting

BACKGROUND: Although the frequency of restenosis after coronary angioplasty is reduced by stenting, when restenosis develops within a stent, the risk of subsequent restenosis is greater than 50 percent. We report on a multicenter, double-blind, randomized trial of intracoronary radiation therapy for the treatment of in-stent restenosis. METHODS: Of 252 eligible patients in whom in-stent restenosis had developed, 131 were randomly assigned to receive an indwelling intracoronary ribbon containing a sealed source of iridium-192, and 121 were assigned to receive a similar-appearing nonradioactive ribbon (placebo). RESULTS: The primary end point, a composite of death, myocardial infarction, and the need for repeated revascularization of the target lesion during nine months of follow-up, occurred in 53 patients assigned to placebo (43.8 percent) and 37 patients assigned to iridium-192 (28.2 percent, P=0.02). However, the reduction in the incidence of major adverse cardiac events was determined solely by a diminished need for revascularization of the target lesion, not by reductions in the incidence of death or myocardial infarction. Late thrombosis occurred in 5.3 percent of the iridium-192 group, as compared with 0.8 percent of the placebo group (P=0.07), resulting in more late myocardial infarctions in the iridium-192 group (9.9 percent vs. 4.1 percent, P=0.09). Late thrombosis occurred in irradiated patients only after the discontinuation of oral antiplatelet therapy (with ticlopidine or clopidogrel) and only in patients who had received new stents at the time of radiation treatment. CONCLUSIONS: Intracoronary irradiation with iridium-192 resulted in lower rates of clinical and angiographic restenosis, although it was also associated with a higher rate of late thrombosis, resulting in an increased risk of myocardial infarction. If the problem of late thrombosis within the stent can be overcome, intracoronary irradiation with iridium-192 may become a useful approach to the treatment of in-stent restenosis.     

The effect of warfarin on mortality and reinfarction after myocardial infarction

BACKGROUND AND METHODS. The use of oral anticoagulation in the long-term treatment of survivors of acute myocardial infarction has been highly controversial. We therefore randomly assigned 1214 patients who had recovered from acute myocardial infarction (mean interval from the onset of symptoms to randomization, 27 days) to treatment with warfarin (607 patients) or placebo (607 patients) for an average of 37 months (range, 24 to 63). RESULTS. At the end of the treatment period, there had been 123 deaths in the placebo group and 94 in the warfarin group--a reduction in risk of 24 percent (95 percent confidence interval, 4 to 44 percent; P = 0.027). A total of 124 patients in the placebo group had reinfarctions, as compared with 82 in the warfarin group--a reduction of 34 percent (95 percent confidence interval, 19 to 54 percent; P = 0.0007). Furthermore, we observed a reduction of 55 percent (95 percent confidence interval, 30 to 77 percent) in the number of total cerebrovascular accidents in the warfarin group as compared with the placebo group (44 vs. 20; P = 0.0015). Serious bleeding was noted in 0.6 percent of the warfarin-treated patients per year. CONCLUSIONS. Long-term therapy with warfarin has an important beneficial effect after myocardial infarction and can be recommended in the treatment of patients who survive the acute phase.     

Experimental study on size-limitation of myocardial infarct in swine produced by a coronary balloon-catheterization. I. Preliminary report; morphometry of infarct size

Experimental myocardial infarction was produced in 15 subject swine using a balloon catheter to occlude the left anterior descending coronary artery (LAD). After 30 minutes obstruction, the LAD was reperfused, and then the animals were sacrificed at 3 hours, 6 hours, 24 hours, and 48 hours after the onset of coronary occlusion, respectively. During and after the experiment they were investigated physiologically and pathomorphologically to measure the size of myocardial infarct, and the obtained results are as follows; Experimentally produced myocardial infarcts could be detected histopathologically by routine gross and light-microscopical means in the group which had suffered from ischemia for over 24 hours till sacrifice. Ischemic areas could not be distinguished from normal areas of the myocardium by routine techniques, but could be identified enzyme-histochemically in the groups observed for less than 6 hours. The mean weight ratio of infarcted myocardium to total ventricular myocardium was 25 +/- 3.6%. This method was useful for measuring infarct size.     

Prevention of myocardial damage in acute myocardial ischemia by early treatment with intravenous streptokinase

We evaluated the effectiveness of early intravenous administration of 750,000 units of streptokinase in 53 patients with acute myocardial ischemia treated by a mobile-care unit at home (9 patients) or in the hospital (44 patients). Treatment was begun an average (+/- S.D.) of 1.7 +/- 0.8 hours from the onset of pain. Non-Q-wave infarctions developed subsequently in eight patients, whereas all the others had typical Q-wave infarct patterns. In 81 per cent of the patients the infarct-related artery was patent at angiography performed four to nine days after admission. Vessel patency was independent of the time of treatment, but residual left ventricular function was time dependent. Patients treated less than 1.5 hours after the onset of pain had a significantly higher ejection fraction (56 +/- 15 vs. 47 +/- 14 per cent; P less than 0.05) and infarct-related regional ejection fraction (51 +/- 19 vs. 34 +/- 20 per cent; P less than 0.01) and a lower QRS score (5.6 +/- 4.9 vs. 8.6 +/- 5.5; P less than 0.01) than patients receiving treatment between 1.5 and 4 hours after the onset of pain. Patients treated earlier by the mobile-care unit also had better-preserved left ventricular function than patients treated in the hospital. We conclude that thrombolytic therapy with streptokinase is most effective if given within the first 1.5 hours after the onset of symptoms of acute myocardial infarction.     

Clinical first myocardial infarction: coronary artery disease and old infarcts in 53 consecutive fatal cases from a coronary care unit

The frequency and size of previous unrecognized myocardial infarction in patients with first clinical diagnosed acute myocardial infarction are unknown. In this study, 53 consecutive patients with clinical first acute myocardial infarction which proved fatal were studied postmortem. All showed acute infarction (inclusion criterium). Acute coronary thrombosis was found in 51 (96%). One-, two-, and three-vessel disease diagnosed by postmortem coronary angiography (diameter stenosis greater than or equal to 75%) was present in 17 (32%), 22 (42%), and 14 (26%), respectively. One or more old infarcts were found in 24 of the cases (45%) despite no history of previous myocardial infarction. Old infarcts were found in 86% of the hearts with three-vessel disease and in 55% of the hearts with two-vessel disease, but none were found in the hearts with one-vessel disease. The median weight of the old infarcts was 4 grams (range: 0.5 to 25 grams) corresponding to 5% (0.5 to 14%) of the ventricular myocardium. Thus, two- or three-vessel coronary artery disease and old infarcts are often present in patients dying from their clinical first acute myocardial infarction.