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Reperfusion therapy in patients with acute myocardial infarction and prior coronary artery bypass graft surgery (National Registry of Myocardial Infarction-2).

We reviewed data from the National Registry of Myocardial Infarction-2 to determine the differences in characteristics and outcomes in patients with acute myocardial infarction (AMI) who have undergone previous coronary artery bypass grafting (CABG), and those who have not, and between post-CABG patients who were treated with alteplase (recombinant tissue-type plasminogen activator [rt-PA]) and those who were treated with primary percutaneous transluminal coronary angioplasty (PTCA). Demographic, therapeutic, and outcome data from patients with AMI were collected at > 1,000 hospitals in the United States in collaboration with National Registry of Myocardial Infarction-2. Of the 45,925 patients receiving reperfusion therapy, 2,544 of the 39,574 treated with rt-PA (6.4%) had a history of CABG, and 375 of the 6,351 treated with primary PTCA (5.9%) had a history of CABG. Patients with a history of CABG were older, more likely to be men, and had more comorbidities, but prior CABG was still an independent predictor of mortality after multivariate regression analysis (odds ratio 1.23; 95% confidence interval 1.05 to 1.44). Among the post-CABG patients who received rT-PA or underwent PTCA, there was no significant difference in in-hospital mortality rate or the combined end point of death and nonfatal stroke. Thus, (1) prior CABG is an independent predictor of mortality, and (2) for post-CABG patients with AMI who are not in shock and who are lytic-eligible, reperfusion therapy with rt-PA and PTCA result in similar outcomes with regard to in-hospital mortality and the combined end point of death and nonfatal stroke.

Aged↗

Intracranial hemorrhage rates and effect of immediate beta-blocker use in patients with acute myocardial infarction treated with tissue plasminogen activator. Participants in the National Registry of Myocardial Infarction-2.

In acute myocardial infarction (AMI), immediate beta-blocker therapy reduces the incidence of reinfarction and recurrent chest pain in patients receiving tissue plasminogen activator (t-PA). Data from the Thrombolysis in Myocardial Infarction (TIMI)-2 trial also raises the possibility that such therapy may reduce the rate of intracranial hemorrhage (ICH). We reviewed data obtained from 60,329 patients treated with t-PA who were enrolled in the National Registry of Myocardial Infarction 2. Of the 60,329 in the study cohort, 23,749 patients (39.4%) were treated with immediate beta-blocker therapy and 542 patients (0.9%) developed an ICH. In a multivariate model that included all covariates known to be associated with the development of ICH, immediate beta-blocker therapy was associated with a 31% reduction in the ICH rate (odds ratio 0.69, 95% confidence intervals 0.57 to 0.84). Thus, in the present study, the use of immediate beta-blocker therapy in patients with AMI treated with t-PA was associated with a significant reduction in ICH. This finding supports the observations made in the TIMI 2 trial and serves to reinforce the recommendations made by the American College of Cardiology/American Heart Association task force that immediate beta-blocker therapy should be administered to all patients with AMI who do not have contraindications to this therapy.

Adrenergic beta-Antagonists↗

Value of rescue percutaneous transluminal coronary angioplasty following unsuccessful thrombolytic therapy in patients with acute myocardial infarction. Thrombolysis in Myocardial Infarction Investigators.

Rescue percutaneous transluminal coronary angioplasty (PTCA) has been advocated as a mechanical method to achieve reperfusion in instances where the myocardial infarct artery remains occluded after thrombolytic therapy. Most prior reports of rescue PTCA have been observational and analyses of value have been inconclusive. To evaluate the benefit of rescue PTCA, we studied 133 patients enrolled in the Thrombolysis in Myocardial Infarction Phase I Open Label and Phase II trials who had an occluded infarct-related artery after thrombolytic therapy. According to protocol, 100 consecutive patients had no rescue PTCA performed (no rescue group), and 33 consecutive patients underwent protocol-directed rescue PTCA (rescue group). The 2 cohorts were compared for clinical and angiographic outcome. Baseline characteristics of the 2 groups were similar. Rescue PTCA was attempted in each rescue group patient and was successful in 82%. At 21 days the mortality rate was 12% in the rescue group and 7% in the no rescue group (p = NS). Failed rescue PTCA was associated with a mortality of 33%. Reinfarction occurred in 6% of patients in the rescue group, and in 5% of those in the no rescue group (p = NS). At 21 days, mean left ventricular ejection fraction was 51 +/- 13% in the rescue group and 48 +/- 12% in the no rescue group (p = NS). We conclude that the routine use of rescue PTCA does not appear to offer significant benefit beyond that of contemporary medical therapy after thrombolytic failure.

Angioplasty, Balloon, Coronary↗

Relations between Doppler tracings of pulmonary regurgitation and invasive hemodynamics in acute right ventricular infarction complicating inferior wall left ventricular infarction.

To test the hypothesis that flow characteristics from pulmonary regurgitation (PR) can predict right ventricular (RV) involvement in patients with inferior wall acute myocardial infarction, we prospectively recorded continuous-wave Doppler tracings and right-sided cardiac hemodynamics in 48 consecutive patients with inferior wall acute myocardial infarction and PR. Right heart hemodynamics enabled the identification of 29 patients with (group 1) and 19 without (group 2) RV involvement. In patients with RV involvement, the pulmonary regurgitant flow pattern was characterized by a rapid rise in flow velocity to a peak level followed by an abrupt deceleration in mid-diastole, whereas in patients without RV involvement, the deceleration in mid-diastole was gradual. The pressure half-time of PR (PHTPR) and the lowest mid-diastolic to peak early diastolic velocity ratio were significantly lower in group 1 than in group 2 (91 +/- 31 vs 214 +/- 57 ms [p < 0.001], 0.35 +/- 0.08 vs 0.59 +/- 0.13 [p < 0.001], respectively). The best diagnostic accuracy (95%) was obtained with cut-off values of PHTPR < or = 150 ms and the lowest mid-diastolic to peak early diastolic velocity ratio < or = 0.5: sensitivity 100%, specificity 89%, positive predictive value 94%, and negative predictive value 100%. Using multiple logistic regression analysis, we found that PHTPR was the strongest predictor of RV involvement. Thus, these parameters, derived from pulmonary regurgitant tracings, are useful in the noninvasive bedside diagnosis of RV infarction.

Aged↗

Q-wave regression unrelated to patency of infarct-related artery or left ventricular ejection fraction or volume after anterior wall acute myocardial infarction treated with or without reperfusion therapy.

We examined the relation of Q-wave regression to left ventricular (LV) indexes in acute anterior wall myocardial infarction (AMI) in relation to reperfusion therapy. A total of 94 patients with their first anterior wall AMI (segment 6 or 7 occlusion according to the American Heart Association classification) were examined. The follow-up period with 12-lead electrocardiograms ranged from 6 to 60 months (mean 24 +/- 18). An abnormal Q wave was defined as > 40 ms and > 25% of the R-wave amplitude. Q-wave regression was defined as Q-wave disappearance and r-wave regression > 0.1 mV in > or = 1 lead. Contingency tables with the chi-square test and analysis of variance were used for assessment of the relation between Q-wave regression and angiographic and clinical indexes. Q-wave regression in > or = 1 lead was found in 77% of the patients. The incidence of Q-wave regression in patients with patent infarct-related artery (81%) was not significantly different from that in those with an occluded lesion (67%). Q-wave regression appeared within 1 month in 60% of patients with a patent infarct-related artery but in 25% of those with an occluded lesion. No difference in the incidence of Q-wave regression was seen between patients with lesions at segments 6 (81%) and 7 (70%), or between those with (75%) and without (77%) collateral circulation. Q-wave regression did not correlate with LV ejection fraction, LV end-diastolic or end-systolic volumes, or regional wall motion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

CPK and CPK-MB in the early diagnosis of acute myocardial infarction and prediction of infarcted area.

This study was carried out on patients of a coronary unit to evaluate the diagnostic efficiency of total CPK and CPK-MB by using different analytical techniques: catalytic, immunoassisted, cellulose acetate electrophoresis, radioimmunoassay and immunoradiometric assay. The behaviour of the enzyme was studied in all patients with reference to the localization and extent of the infarct. In all cases a diagnostic algorithm was followed based on the combined use of CPK and its MB isoenzyme; the activity was measured twice, at three-hour intervals after admission. In this way the utilization of total CPK and MB isoenzyme allows almost complete diagnostic efficiency within the first 9 hours from onset of chest pain, together with the possibility of calculating the slope of the curve of MB isoenzyme release useful for calculating infarct size. Maximum diagnostic efficiency is also obtained in cases of small infarcts, with silent ECG, and those difficult to classify clinically.

Creatine Kinase↗

Calcium antagonists and evolving myocardial infarction: studies of the effects of nifedipine on tissue ATP, collateral flow and infarct size in the closed chest dog.

In previous studies nifedipine has been shown to limit infarct size during 24 h of regional ischemia in the dog. Using a closed chest embolization procedure, autoradiographic (141-cerium at onset of ischemia) microsphere risk zone analysis and tetrazolium staining, the ability of nifedipine to influence collateral flow, energy metabolism and infarct size over 48 h was assessed in the dog. A second microsphere (46-scandium), which did not interfere with the autoradiography, was given after 48 h of ischemia to allow temporal changes in flow to be assessed. Transmural biopsies, taken after 48 h from non-ischemic tissue, ischemic tissue which had become necrotic and ischemic tissue which had survived (tetrazolium-positive tissue within the risk zone) were assayed for flow, adenosine triphosphate (ATP) and creatine phosphate (CP). The results indicate: nifedipine may still afford some small degree of protection up to 48 h of elapsed ischemia, (infarct size as a percent of risk zone size was 86.1 +/- 3.0 in control vs 70.4 +/- 4.5 in drug group (p less than 0.025 n = 9 in each group), 'salvage' in both the control and the nifedipine-treated groups was predominantly subepicardial and in the transmural plane. The extent and location of salvage and necrosis was determined by the epicardial to endocardial distribution of collateral flow. In tissue which was destined to necrosis (mainly in the subendocardium) collateral flow at the onset of ischemia (7.2 +/- 1.2% relative to surrounding non-ischemic tissue) did not increase over 48 h (8.0 +/- 1.4) whereas in tissue which was 'salvaged' (mainly in the subepicardium) flow was greater (27.4 +/- 3.2%) at onset of ischemia) and increased substantially (to 64.6 +/- 5.9%) over 48 h; nifedipine does not increase the amount of flow per g of tissue in salvaged tissue but rather it may increase the amount of tissue receiving sufficient flow to promote salvage; it follows that in nifedipine-treated animals more flow is delivered to the ischemic zone; tissue ATP and CP parallel flow and the results support the concept of a critical threshold of flow (approx. 25% at onset of ischemia) below which tissue eventually deteriorates to necrosis and above which tissue is likely to amenable to salvage. However, for sustained survival this flow level must eventually increase to above 40-50%. In conclusion, while nifedipine can achieve a substantial delay in the onset of tissue necrosis, for sustained salvage there must be early and substantial reflow to the tissue.

Adenosine Triphosphate↗

Association of plasma levels of activated protein C with recanalization of the infarct-related coronary artery after thrombolytic therapy in acute myocardial infarction.

Protein C is one of the most important antithrombotic components. After activation by the thrombin-thrombomodulin complex on endothelial cells, activated protein C (APC) inactivates factors Va and VIIIa, which leads to the inhibition of thrombin formation. We examined the association of plasma levels of APC with the responsiveness to coronary thrombolytic therapy of the infarct-related coronary artery in patients with acute myocardial infarction (AMI). Plasma levels of APC, thrombin-antithrombin III complex (TAT), and plasminogen activator inhibitor (PAI) activity were measured in 32 consecutive AMI patients who underwent coronary angiography followed by thrombolytic therapy, and compared to the measurements in 23 control subjects. On admission, APC levels (ng/mL) were significantly elevated in patients with AMI, as compared with controls (2.5+/-0.4 vs. 1.2+/-0.2, 1.3+/-0.2, respectively, p<0.01). At discharge, plasma levels in AMI patients decline to values not significantly different from those in controls. (1.2+/-0.2, 1.3+/-0.2, respectively). TAT levels (ng/mL) were different among the groups in a fashion similar to that of APC (14.1+/-3.1 on admission vs. 3.3+/-0.4 at discharge, 1.8+/-0.1 in the control subjects, respectively, p<0.01). PAI activity levels (IU/mL) were higher on admission than at discharge and higher than the control subjects (19.7+/-1.8 vs. 10.5+/-1.0, 5.4 +/- 0.7, respectively, p<0.01). Thirty-two patients with AMI were classified into two groups according to the results of thrombolysis: the success group (24 patients) and the failure group (eight patients). APC levels were higher in the failure group than in the success group (5.1+/-0.7 vs. 1.6+/-0.2, p<0.01). TAT levels were also higher in the failure group than in the success group (30.8+/-9.6 vs. 8.6+/-1.7, p<0.01). PAI activity levels (IU/mL) were lower in the failure group than in the success group (13.5+/-3.1 vs. 21.7+/-2.1, p<0.05). There were correlations between APC and TAT levels both on admission (r=0.75, p<0.0001) and at discharge (r=0.71, p<0.0001). Elevated APC was thought to correlate with increased thrombin generation in patients with AMI. This study demonstrated that there was a significant relation between plasma APC level and the responsiveness to thrombolytic therapy of the infarct artery. This study may also indicate that increased thrombin generation is a cause of the resistance to thrombolytic therapy.

Acute Disease↗

Clinical value of 12-lead electrocardiogram after successful reperfusion therapy for acute myocardial infarction. Zwolle Myocardial infarction Study Group.

BACKGROUND: A simple clinical method to stratify risk for patients who have had successful reperfusion therapy after myocardial infarction is attractive since it facilitates the tailoring of therapy. METHODS: We investigated the clinical value of the 12-lead electrocardiogram (ECG), in 403 patients after successful reperfusion therapy by primary coronary angioplasty, in relation to infarct size measured by enzyme activity, left-ventricular function, and clinical outcome. ECGs were analysed to find the extent of the ST-segment-elevation resolution 1 h after reperfusion therapy. FINDINGS: A normalised ST segment was seen in 51% of patients, a partly normalised ST segment in 34%, and 15% had no ST-segment-elevation resolution. Enzymatic infarct size and ejection fraction were related to the extent of the early resolution of the ST segment. The relative risk of death among patients with no resolution compared with patients with a normalised ST segment was 8.7 (95% CI 3.7-20.1), and that among patients with partial resolution compared with patients with a normalised ST segment was 3.6 (1.6-8.3). INTERPRETATION: Our findings suggest that ECG patterns reflect the effectiveness of myocardial reperfusion. Patients for whom reperfusion therapy by primary angioplasty was successful and who had normalised ST segments had limited damage to the myocardium and an excellent outlook during follow-up. Patients with persistent ST elevation after reperfusion therapy may need additional interventions since they have more extensive myocardial damage and have a higher mortality rate.

Aged↗

Baroreflex sensitivity and heart-rate variability in prediction of total cardiac mortality after myocardial infarction. ATRAMI (Autonomic Tone and Reflexes After Myocardial Infarction) Investigators.

BACKGROUND: Experimental evidence suggests that autonomic markers such as heart-rate variability and baroreflex sensitivity (BRS) may contribute to postinfarction risk stratification. There are clinical data to support this concept for heart-rate variability. The main objective of the ATRAMI study was to provide prospective data on the additional and independent prognostic value for cardiac mortality of heart-rate variability and BRS in patients after myocardial infarction in whom left-ventricular ejection fraction (LVEF) and ventricular arrhythmias were known. METHODS: This multicentre international prospective study enrolled 1284 patients with a recent (<28 days) myocardial infarction. 24 h Holter recording was done to quantify heart-rate variability (measured as standard deviation of normal to normal RR intervals [SDNN]) and ventricular arrhythmias. BRS was calculated from measurement of the rate-pressure response to intravenous phenylephrine. FINDINGS: During 21 (SD 8) months of follow-up, the primary endpoint, cardiac mortality, included 44 cardiac deaths and five non-fatal cardiac arrests. Low values of either heart-rate variability (SDNN <70 ms) or BRS (<3.0 ms per mm Hg) carried a significant multivariate risk of cardiac mortality (3.2 [95% CI 1.42-7.36] and 2.8 [1.24-6.16], respectively). The association of low SDNN and BRS further increased risk; the 2-year mortality was 17% when both were below the cut-offs and 2% (p<0.0001) when both were well preserved (SDNN >105 ms, BRS >6.1 ms per mm Hg). The association of low SDNN or BRS with LVEF below 35% carried a relative risk of 6.7 (3.1-14.6) or 8.7 (4.3-17.6), respectively, compared with patients with LVEF above 35% and less compromised SDNN (> or = 70 ms) and BRS (> or = 3 ms per mm Hg). INTERPRETATION: ATRAMI provides clinical evidence that after myocardial infarction the analysis of vagal reflexes has significant prognostic value independently of LVEF and of ventricular arrhythmias and that it significantly adds to the prognostic value of heart-rate variability.

Aged↗

Factors associated with the occurrence of cardiac arrest during hospitalization for acute myocardial infarction in the second national registry of myocardial infarction in the US.

Cardiac arrest can occur as a complication of acute myocardial infarction (AMI). To date, few studies have described factors associated with cardiac arrest occurrence and survival during hospitalization for treatment of AMI. We used data from a large national registry of hospitalized AMI patients to identify these factors. Data were collected from 1073 participating institutions, representing 14.4% of US hospitals. Hospital site coordinators conducted periodic chart reviews for AMI patients and data were submitted to an independent center for periodic review. Univariate analysis and multivariate logistic regression were used to identify factors associated with cardiac arrest. We found that cardiac arrest occurred in 4.8% (14,725/305,812) of hospitalized AMI patients. The survival rate to hospital discharge for these individuals was 29.4%. Sustained ventricular tachycardia or fibrillation (VT/VF) was present in 34.7% and was associated with a higher rate of survival to hospital discharge compared to cardiac arrest patients without a ventricular tachyarrhythmia (47.5 vs. 19.8%, P < 0.00001). Hypotension (initial systolic BP < 90 mmHg), q-wave AMI, old age, heart failure and initial heart rate abnormalities (bradycardia or tachycardia) were associated with a higher prevalence of cardiac arrest. A higher percentage of women compared to men experienced cardiac arrest (6.0 vs. 4.41%, P < 0.0001). Cardiac arrest prevalence was lower in patients with inferior wall infarction than in other types of ST-elevation infarction. Use of reperfusion therapy (PTCA or tPA) was associated with improved survival compared to hospitalized AMI patients who did not receive such therapy.

Age Distribution↗

Relationship between transcardiac extraction of aldosterone and left ventricular remodeling in patients with first acute myocardial infarction: extracting aldosterone through the heart promotes ventricular remodeling after acute myocardial infarction.

OBJECTIVES: The purpose of this study was to evaluate whether plasma aldosterone (ALD) is extracted or produced through the heart in patients with acute myocardial infarction (AMI) and to determine the relationship between transcardiac extraction of plasma ALD and left ventricular (LV) remodeling. BACKGROUND: Although we demonstrated that circulating ALD was extracted through the failing heart and that transcardiac extraction of ALD correlated with LV end-diastolic volume index (LVEDVI) in patients with congestive heart failure, the existence and increase of ALD synthase in the hearts of infarct rats were reported, suggesting cardiac production of ALD in patients with AMI. METHODS: We measured plasma ALD in the aortic root (Ao) and coronary sinus (CS) in 57 consecutive patients who received successful revascularization and enalapril, with first AMI at acute phase and after one month. We also measured plasma procollagen type III aminoterminal peptide (PIIINP) in the CS. RESULTS: Plasma ALD was significantly lower in the CS than it was in the Ao at the acute phase (84.7 +/- 6.3 pg/ml vs. 105.5 +/- 8.0 pg/ml, p < 0.0001). Significant positive correlations exist between the transcardiac gradient of ALD at the acute phase and the LVEDVI at one month. Moreover, the transcardiac gradient of plasma ALD at the acute phase has a significant correlation with plasma PIIINP, a biochemical marker of fibrosis, after one month. Stepwise multivariate analysis showed that transcardiac extraction of plasma ALD at the acute phase had an independent and significant positive relationship with a large LVEDVI after one month. CONCLUSIONS: These results indicate that plasma ALD is extracted through the heart in patients with AMI at the acute phase and that the extracted ALD plays an important role in modulating post-infarct LV remodeling.

Acute Disease↗

Eptifibatide and low-dose tissue plasminogen activator in acute myocardial infarction: the integrilin and low-dose thrombolysis in acute myocardial infarction (INTRO AMI) trial.

OBJECTIVES: This study was designed to test the hypothesis that eptifibatide and reduced-dose tissue plasminogen activator (t-PA) will enhance infarct artery patency at 60 min in patients with acute myocardial infarction (AMI). BACKGROUND: Combination fibrin and platelet lysis improves epicardial and myocardial reperfusion in AMI. METHODS: Patients were enrolled in a dose finding (Phase A, n = 344) followed by a dose confirmation (Phase B, n = 305) protocol. All patients received aspirin and weight-adjusted heparin and underwent angiography at 60 and 90 min. In Phase A, eptifibatide in a single or double bolus (30 min apart) of 180, 180/90 or 180/180 microg/kg followed by an infusion of 1.33 or 2.0 microg/kg per min was sequentially added to 25 or 50 mg of t-PA. In Phase B, patients were randomized to: 1) double-bolus eptifibatide 180/90 (30 min apart) and 1.33 microg/kg per min infusion with 50 mg t-PA (Group I); 2) 180/90 (10 min apart) and 2.0 g/kg per min with 50 mg t-PA (Group II); or 3) full-dose, weight-adjusted t-PA (Group III). RESULTS: In Phase A, the best rate of Thrombolysis In Myocardial Infarction (TIMI) flow grade 3 was achieved using 180/90/1.33 microg/kg per min eptifibatide with 50 mg t-PA: 65% and 78% at 60 and 90 min, respectively. In Phase B, the incidence of TIMI flow grade 3 at 60 min was 42%, 56% and 40%, for Groups I through III, respectively (p = 0.04, Group II vs. Group III). The median corrected TIMI frame count was 38, 33 and 50, respectively (p = 0.02). TIMI major bleeding was reported in 8%, 11% and 6%, respectively; intracranial hemorrhage occurred in 1%, 3% and 2% of patients (p > 0.5 for both). The incidences of death (4%, 5% and 7%), reinfarction or revascularization at 30 days were similar among the three treatment groups. CONCLUSIONS: In comparison with standard t-PA regimen, double-bolus eptifibatide (10 min apart) with a 48-h infusion and half-dose t-PA (Group II) is associated with improved quality and speed of reperfusion. The safety profile of this therapy is similar to that of other combination regimens.

Adult↗

Evaluation of the time saved by prehospital initiation of reteplase for ST-elevation myocardial infarction: results of The Early Retavase-Thrombolysis in Myocardial Infarction (ER-TIMI) 19 trial.

OBJECTIVES: The Early Retavase-Thrombolysis In Myocardial Infarction (ER-TIMI) 19 trial tested the feasibility of prehospital initiation of the bolus fibrinolytic reteplase (rPA) and determined the time saved by prehospital rPA in the setting of contemporary emergency cardiac care. BACKGROUND: Newer bolus fibrinolytics have undergone only limited evaluation for prehospital administration. In addition, as door-to-drug times have decreased, the relevance of findings from prior trials of prehospital fibrinolysis has become less certain. METHODS: Patients (n = 315) with ST-elevation myocardial infarction (STEMI) were enrolled in 20 emergency medical systems in North America. The time from emergency medical service (EMS) arrival to administration of a fibrinolytic was compared between study patients receiving prehospital rPA and sequential control patients from 6 to 12 months before the study who received a fibrinolytic in the hospital. RESULTS: Acute myocardial infarction was confirmed in 98%. The median time from EMS arrival to initiation of rPA was 31 min (25th to 75th percentile, 24 min to 37 min). The time from EMS arrival to in-hospital fibrinolytic for 630 control patients was 63 min (25th to 75th percentile, 48 min to 89 min), resulting in a time saved of 32 min (p < 0.0001). By 30 min after first medical contact, 49% of study patients had received the first bolus of fibrinolytic compared with only 5% of controls (p < 0.0001). In-hospital mortality was 4.7%. Intracranial hemorrhage occurred in 1.0%. CONCLUSIONS: Prehospital administration of rPA is a feasible approach to accelerating reperfusion in patients with STEMI. Valuable time savings can be achieved in the setting of contemporary transport and door-to-drug times and may translate into an improvement in clinical outcomes.

Emergency Medical Services↗

Myocardial infarction with minimal coronary atherosclerosis in the era of thrombolytic reperfusion. The Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) Study Group.

The incidence of minimal residual atherosclerotic coronary obstruction after successful intravenous thrombolytic therapy was evaluated in 799 patients with acute myocardial infarction. Minimal residual coronary obstruction (less than or equal to 50%) was observed on selective coronary angiography performed 90 min after initiation of thrombolytic therapy in 43 patients (5.5%). In 42 other patients (5.4%), a greater than 50% but less than 100% residual stenosis noted at 90 min demonstrated further resolution of obstruction to less than 50% at an angiographic follow-up study 7 to 10 days later. Patients with minimal residual coronary obstruction were significantly younger (52 +/- 10.7 versus 56.7 +/- 10 years; p = 0.002) and had less multivessel coronary disease (p less than 0.001), better initial left ventricular ejection fraction (54 +/- 12% versus 50.2 +/- 11.4%; p = 0.006) and a lower in-hospital mortality rate (1% versus 7%; p = 0.04) than did patients who had a significant (greater than 50%) residual coronary obstruction after intravenous thrombolysis. Long-term follow-up study of patients with a minimal coronary lesion (average 1.5 +/- 0.6 years) and those with significant residual stenosis (average 1.6 +/- 0.7 years) demonstrated that the incidence of death (2.4% in patients with minimal stenosis versus 3.5% in those with significant stenosis) and recurrent myocardial infarction (5% each) were similar in both groups. New strategies are needed to prevent coronary rethrombosis in patients with minimal atherosclerosis after thrombolytic therapy for acute myocardial infarction.

Coronary Angiography↗

Nonfatal cardiac events and recurrent infarction in the year after acute myocardial infarction.

The occurrence and importance of nonfatal cardiac events in the year after an acute myocardial infarction were studied in 866 patients who were enrolled by nine hospitals with a broad geographic distribution. The extensive clinical data acquired on each patient included special tests, such as radionuclide-determined ejection fraction, 24 hour ambulatory electrocardiogram and a low level exercise tolerance test. Recurrent events were frequent in the first 5 months, and certain events were significant indicators of a poor prognosis. An ejection fraction less than 40% and angina after discharge from the coronary care unit predicted patients at high risk of rehospitalization. Recurrent infarction was similarly predicted by angina, but not by any features of an exercise test. This study demonstrates the considerable morbidity that occurs after an acute myocardial infarction and its relation to and role in subsequent mortality.

Coronary Artery Bypass↗

Reverse redistribution of thallium-201: a sign of nontransmural myocardial infarction with patency of the infarct-related coronary artery.

The pattern of reverse redistribution on the day 10 poststreptokinase resting thallium-201 myocardial scintigrams is a common finding in patients who have undergone streptokinase therapy in evolving myocardial infarction. To investigate this phenomenon, 67 patients who underwent streptokinase therapy were studied pre- and 10 days poststreptokinase therapy resting thallium-201 studies, poststreptokinase therapy resting radionuclide ventriculography and coronary arteriography (60 of the 67 patients). Of the 67 patients, 50 (75%) showed the reverse redistribution pattern on the day 10 thallium-201 study (Group I), 9 (13%) had a nonreversible defect (Group II) and the remaining 8 (12%) had a normal study or showed a reversible defect (Group III). The reverse redistribution pattern was associated with patency of the infarct-related artery (100%), quantitative improvement in resting thallium-201 defect size from day 1 to day 10 study (94%) and normal or near normal wall motion on day 10 radionuclide ventriculography (80% of segments with marked and 54% of those with mild reverse redistribution). In contrast, nonreversible defects were associated with significantly less frequent patency of the infarct-related artery (67%, p = 0.01), improvement in defect size (11%, p less than 0.001) and normal or near normal wall motion (21%, p less than 0.05). Group III patients were similar to Group I with respect to these variables. The quantitated thallium-201 percent washout was higher in the regions with the reverse redistribution pattern (49 +/- 15%) compared with the contralateral normal zone (24 +/- 15%, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Relevance of increased lung thallium uptake on stress imaging in patients with unstable angina and non-Q wave myocardial infarction: results of the Thrombolysis in Myocardial Infarction (TIMI)-IIIB Study.

OBJECTIVES: This study sought to determine the significance of abnormal thallium-201 (Tl-201) lung uptake on stress imaging in the absence of perfusion abnormalities. BACKGROUND: Abnormal Tl-201 lung uptake, represented by an increased lung/heart ratio (LHR), on stress imaging is a marker of stress-induced left ventricular dysfunction and poor prognosis in patients with coronary artery disease. METHODS: We evaluate 1,271 patients from the Thrombolysis in Myocardial Infarction (TIMI)-IIIB trial (86% of TIMI-IIIB cohort) with unstable angina or non-Q wave myocardial infarction, who underwent predischarge exercise (92%) or dipyridamole stress (8%) Tl-201 imaging. An increased LHR (> or = 0.50) was related to perfusion abnormalities and adverse cardiac events at 1 year. RESULTS: Of 1,271 patients, there were 762 (60%) with and 509 (40%) without perfusion abnormalities. An increased LHR was seen in 227 patients (18%) (173 [23%] with, 54 [11%] without perfusion abnormalities). Patients with an increased LHR had a lower left ventricular ejection fraction, higher body weight, lower exercise capacity and a higher prevalence of angina on exercise than patients with a normal LHR. In the two groups with increased LHR, there was no difference in age, hypertension, previous myocardial infarction, total exercise time, frequency of angina and ST segment depression on exercise. However, the group with an increased LHR and normal myocardial perfusion had a preponderance of women (65% vs. 30%, p < 0.001). At 1-year follow-up, patients with an increased LHR had a higher cardiac event rate than those with a normal LHR (18% vs. 10%, respectively, p = 0.001) despite a higher revascularization rate (28% vs. 15%, p < 0.001). An increased LHR was associated with increased adverse cardiac events, irrespective of the presence or absence of perfusion abnormalities. CONCLUSIONS: An increased LHR continues to be associated with higher adverse cardiac events in the current era of aggressive interventional management of coronary artery disease. An increased LHR in the absence of myocardial perfusion abnormality is seen mostly in women and overweight patients. However, despite the apparent absence of perfusion abnormalities, an increased LHR in this group is also associated with a higher rate of adverse cardiac events.

Angina, Unstable↗