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Clinical and angiographic outcomes in patients with previous coronary artery bypass graft surgery treated with primary balloon angioplasty for acute myocardial infarction. Second Primary Angioplasty in Myocardial Infarction Trial (PAMI-2) Investigators.

OBJECTIVES: We sought to characterize the presenting characteristics of patients with previous coronary artery bypass graft surgery (CABG) and acute myocardial infarction (AMI) and to determine the angiographic success rate and clinical outcomes of a primary percutaneous transluminal coronary angioplasty (PTCA) strategy. BACKGROUND: Patients who have had previous CABG and AMI comprise a high risk group with decreased reperfusion success and increased mortality after thrombolytic therapy. Little is known about the efficacy of primary PTCA in AMI. METHODS: Early cardiac catheterization was performed in 1,100 patients within 12 h of onset of AMI at 34 centers in the prospective, controlled Second Primary Angioplasty in Myocardial Infarction trial (PAMI-2), followed by primary PTCA when appropriate. Data were collected by independent study monitors, end points were adjudicated and films were read at an independent core laboratory. RESULTS: Of 1,100 patients with AMI, 58 (5.3%) had undergone previous CABG. The infarct-related vessel in these patients was a bypass graft in 32 patients (55%) and a native coronary artery in 26 patients. Compared with patients without previous CABG, patients with previous CABG were older and more frequently had a previous myocardial infarction and triple-vessel disease. Coronary angioplasty was less likely to be performed when the infarct-related vessel was a bypass graft rather than a native coronary artery (71.9% vs. 89.8%, p = 0.001); Thrombolysis in Myocardial Infarction trial (TIMI) flow grade 3 was less frequently achieved (70.2% vs. 94.3%, p < 0.0001); and in-hospital mortality was increased (9.4% vs. 2.6%, p = 0.02). As a result, mortality at six months was 14.3% versus 4.1% in patients with versus without previous CABG (p = 0.001). By multivariate analysis, independent determinants of late mortality in the entire study group were advanced age, triple-vessel disease, Killip class and post-PTCA TIMI flow grade <3. CONCLUSIONS: Reperfusion success of a primary PTCA strategy in patients with previous CABG, although favorable with respect to historic control studies, is reduced as compared with that in patients without previous CABG. New approaches are required to treat patients with previous CABG and AMI, especially when the infarct-related vessel is a diseased saphenous vein graft.

Aged↗

Regional wall motion index for infarct and noninfarct regions after reperfusion in acute myocardial infarction: comparison with global wall motion index.

A regional wall motion index has been derived from two-dimensional echocardiograms by use of a 16-segment model that was subdivided into anterior (nine segments) and infero-postero-lateral (seven segments) regions. This new method is compared with the use of a previously described global wall motion index for the analysis of serial echocardiograms after reperfusion in 23 patients who had acute myocardial infarction. Mean global index improved from 1.84 +/- 0.46 to 1.56 +/- 0.37 at 24 hours (p less than 0.01) and to 1.50 +/- 0.29 after 3 days to 7 days (p less than 0.02), whereas mean regional index for infarct regions improved from 2.28 +/- 0.73 to 1.82 +/- 0.58 at 24 hours (p less than 0.01) and to 1.70 +/- 0.42 after 3 to 7 days (p less than 0.01), with no significant change in the noninfarct index (1.34 +/- 0.32 initially and 1.28 +/- 0.36 after 3 to 7 days). Although both global and regional indexes effectively demonstrate early recovery of left ventricular function, (within 24 hours in many patients), the regional index for infarct regions is higher than the global index and effectively distinguishes between infarct and noninfarct segments. An overlap index in which an additional apical segment is included in the anterior region (10 segments) for anterior infarctions and in the infero-postero-lateral region (eight segments) for inferior infarctions results in a greater differentiation between infarct and noninfarct regions, with the mean initial noninfarct overlap index (1.17 +/- 0.33) significantly less than the nonoverlap index.(ABSTRACT TRUNCATED AT 250 WORDS)

Echocardiography↗

Spatially and temporally different expression of osteonectin and osteopontin in the infarct zone of experimentally induced myocardial infarction in rats.

Osteonectin and osteopontin, two secreted matricellular proteins, have a variety of functions that are exerted through interaction with matrix components. These proteins appear in response to tissue injury. To test our hypothesis that osteopontin and osteonectin are expressed with spatially and temporally different patterns in myocardial infarct tissue, we investigated osteonectin and osteopontin expression in experimentally induced myocardial infarction in rats, in comparison with Type I collagen expression. Northern blotting demonstrated that osteonectin mRNA did not markedly increase on Day 2 after the infarction, but it increased on Days 7 and 14 by 1.7+/-0.12- and 1.8+/-0.01-fold compared to that in preligation hearts. In contrast, osteopontin mRNA was increased on Day 1 (41.9+/-11.3-fold increase) and on Day 2 (58.3+/-7.6-fold increase), and then it declined on Days 7 and 14 (24.8+/-9.0- and 13.5+/-4.7-fold increase, respectively). In situ hybridization revealed that osteonectin mRNA signals were observed in fibroblasts, myofibroblasts and macrophages around infarct necrotic tissue on Days 7 and 14. Osteopontin mRNA signals were observed in macrophages in the infarct marginal zone on Day 2. Immunopositive staining for both osteonectin and osteopontin showed the same pattern as that obtained by in situ hybridization. The time course of osteonectin mRNA was almost parallel with that of Type I collagen mRNA, while that of osteopontin was not. These results demonstrated spatially and temporally different expression patterns of osteonectin and osteopontin in myocardial infarction and suggest that osteonectin appears to be involved in the pathological course in the late phase after infarction concomitantly with Type I collagen, while osteopontin may play a role in the early phase.

Animals↗

Adenoviral-delivered angiopoietin-1 reduces the infarction and attenuates the progression of cardiac dysfunction in the rat model of acute myocardial infarction.

In acute myocardial infarction (AMI), prognosis and mortality rate are closely related to the infarct size and the progression of postinfarction cardiac failure. Angiogenic gene therapy has presented a new approach for the treatment of AMI. Angiopoietin-1 (Ang1) is a critical angiogenic factor for vascular maturation and enhances vascular endothelial growth factor (VEGF)-induced angiogenesis in a complementary manner. We hypothesized that gene therapy using Ang1 for AMI might promote angiogenesis cooperatively with intrinsic VEGF, since high concentrations of circulating VEGF have been reported in AMI. To evaluate our hypothesis, we employed a rat AMI model and adenoviral Ang1 (HGMW-approved gene symbol ANGPT1) gene transfer to the heart. A significant increase in capillary density and reduction in infarct sizes were noted in the infarcted hearts with adenoviral Ang1 gene treatment compared with control infarcted hearts treated with saline or adenoviral vector containing the beta-galactosidase gene. Furthermore, the Ang1 group showed significantly higher cardiac performance in echocardiography (55.0% of ejection fraction, P < 0.05 vs control) than the saline or adenoviral controls (36.0 or 40.5%, respectively) 4 weeks after myocardial infarction. The adenoviral delivery of Ang1 during the acute phase of myocardial infarction would be feasible to attenuate the progression of cardiac dysfunction in the rat model.

Adenoviridae↗

Eating fish may reduce infarct size and the occurrence of Q wave infarcts.

OBJECTIVE: The present investigation was carried out to see whether intake of fish could influence infarct size as assessed by peak enzyme levels (CKmax and LDmax) as well as the occurrence of Q wave infarcts. DESIGN: The investigation was a prospectively planned cohort study. SETTING: The investigation was carried out at Ullevål University Hospital, Department of Cardiology and Department of Pharmacotherapeutics, University of Oslo, Oslo, and in four other Hospitals in Oslo and Lillehammer. SUBJECTS: Seven hundred and forty-five patients (median age 70 y, 64% males) admitted with proven acute myocardial infarction. RESULTS: Crude effects showed that the regression lines between the number of fish meals/week (FM/week) and CKmax in all patients and in the restricted cohorts of patients receiving/not receiving thrombolytic treatment were: y = 2086-157.x(2P = 0.004); y = 2807-156.x (2P = 0.110) and y = 1260-54.x (2P = 0.230); the corresponding results regarding LDmax were: y = 1329-76.x (2P = 0.009); y = 1556-73.x (2P = 0.120) and y = 1047-39 x (2P = 0.230). Odds ratio (OR) for developing Q wave infarcts in patients consuming > 1.0 FM/week was 0.52, 95% confidence interval (CI) 0.34-0.79; 2P = 0.001. For the adjusted effects, the coefficients of FM/week for log (peak enzyme levels) in all three groups of patients (all patients, and the restricted cohorts of patients receiving/not receiving thrombolytic treatment) were negative with 2P values of 0.014, 0.033 and 0.165 (CKmax), and 0.006, 0.033 and 0.158 (LDmax). OR for developing Q wave infarcts in patients consuming > 1.0 FM/week was 0.59, 95% CI 0.38-0.92; 2P = 0.022. CONCLUSIONS: The results indicate that consuming fish may reduce infarct size as assessed by CKmax and LDmax as well as the occurrence of Q wave infarcts.

Aged↗

Trends in the treatment of patients with myocardial infarction and coronary revascularization procedures in Finland during 1986-92: the FINMONICA Myocardial Infarction Register Study.

OBJECTIVES: To investigate changes in the medical treatment of patients with myocardial infarction and the trends in revascularization procedures in Finland. DESIGN: A population-based myocardial infarction (MI) register study. SETTING: Populations, aged 25-64 years, of the three geographical areas of Finland, provinces of North Karelia and Kuopio in eastern Finland and the Turku-Loimaa area in south-western Finland. MAIN OUTCOME MEASURES: Medical treatment administered prior to the coronary event, during the hospitalization and at discharge from hospital to all patients hospitalized due to suspected myocardial infarction and all CAD deaths occurring during three separate 4-month periods in 1986, 1989 and 1992. Data on coronary bypass surgery and percutaneous coronary angioplasty in the study areas for 1986-92. RESULTS: The most marked change in the medical treatment of hospitalized myocardial infarction patients was the significant increase in the use of thrombolytic treatment (5% of patients in 1986 and 24% in 1992, P < 0.001 for trend). The use of antiplatelet agents increased from 1986 to 1992 prior to the coronary event, during the hospitalization and at discharge. The use of beta-blockers and intravenous nitrates increased and the use of calcium-channel blockers declined significantly in hospitalized patients during the study period. Hospitalized male myocardial infarction patients were treated more often with beta-blockers, nitrates, antiplatelet agents and thrombolytic agents than female patients, suggesting less intensive medical treatment in women. CONCLUSION: The results of the large clinical trials regarding the medical treatment of myocardial infarction patients were adopted in the clinical practice rapidly and the treatment of myocardial infarction patients and the number of revascularization procedures changed markedly from 1986 to 1992 in Finland. These changes may in part explain the favourable changes in mortality from CAD in Finland.

Adult↗

The predischarge electrocardiographic pattern in anterior acute myocardial infarction: relation between evolutionary ST segment and T-wave configuration and prediction of myocardial infarct size and left ventricular systolic function by the QRS Selvester score.

Left ventricular systolic function, determined mainly by final infarct size, has a major influence on prognosis after acute myocardial infarction (MI). It was found that infarct size and left ventricular ejection fraction can be predicted using the Selvester QRS-score in patients not receiving reperfusion therapy. We assessed whether the predischarge QRS-score can be used for estimating infarct size and left ventricular ejection fraction in 51 patients with a first anterior MI who had received reperfusion therapy and whether considering the configuration of the ST-segments and T-waves will increase the accuracy of these predictions. All patients had received reperfusion therapy and had predischarge resting 99mTc-sestamibi scan. We determined the Selvester QRS score using the electrocardiograms performed on the same day of the scan. In addition, we divided the patients into 3 groups: A: isoelectric ST and negative T-waves (n = 12); B: ST elevation (> or =0.1 mV) and negative T-waves (n = 23); and C: ST elevation (> or =0.1 mV) and positive T-waves (n = 16). The myocardial perfusion defect extent increased from group A to C (28.5+/-16.4%, 39.4+/-14.8%, and 45.3+/-15.8% in groups A, B, and C. respectively; P = .022). Similarly, the left ventricular ejection fraction decreased (41.7+/-11.6%, 38.4+/-8.1%, and 32.0+/-9.7%, respectively; P = .042) from group A to C. Overall, the correlation between the QRS-score and the myocardial perfusion defect extent (Rho = 0.249; P = .08), and ejection fraction (Rho = -0.229; P = .11) was not good. A statistically significant correlation between the myocardial perfusion defect size and the QRS-score was found only in group A (Rho = 0.599, P = .04). In patients with a first anterior myocardial infarction who underwent reperfusion therapy, the predischarge QRS-score is predictive of infarct size only in those in whom ST elevation resolved completely. In patients with residual ST elevation the Selvester QRS-score is inaccurate in predicting infarct size and left ventricular ejection fraction upon discharge.

Electrocardiography↗

Outcomes in patients with acute non-Q-wave myocardial infarction randomly assigned to an invasive as compared with a conservative management strategy. Veterans Affairs Non-Q-Wave Infarction Strategies in Hospital (VANQWISH) Trial Investigators.

BACKGROUND: Non-Q-wave myocardial infarction is usually managed according to an "invasive" strategy (i.e., one of routine coronary angiography followed by myocardial revascularization). METHODS: We randomly assigned 920 patients to either "invasive" management (462 patients) or "conservative" management, defined as medical therapy and noninvasive testing, with subsequent invasive management if indicated by the development of spontaneous or inducible ischemia (458 patients), within 72 hours of the onset of a non-Q-wave infarction. Death or nonfatal infarction made up the combined primary end point. RESULTS: During an average follow-up of 23 months, 152 events (80 deaths and 72 nonfatal infarctions) occurred in 138 patients who had been randomly assigned to the invasive strategy, and 139 events (59 deaths and 80 nonfatal infarctions) in 123 patients assigned to the conservative strategy (P=0.35). Patients assigned to the invasive strategy had worse clinical outcomes during the first year of follow-up. The number of patients with one of the components of the primary end point (death or nonfatal myocardial infarction) and the number who died were significantly higher in the invasive-strategy group at hospital discharge (36 vs. 15 patients, P=0.004, for the primary end point; 21 vs. 6, P=0.007, for death), at one month (48 vs. 26, P=0.012; 23 vs. 9, P=0.021), and at one year (111 vs. 85, P=0.05; 58 vs. 36, P= 0.025). Overall mortality during follow-up did not differ significantly between patients assigned to the conservative-strategy group and those assigned to the invasive-strategy group (hazard ratio, 0.72; 95 percent confidence interval, 0.51 to 1.01). CONCLUSIONS: Most patients with non-Q-wave myocardial infarction do not benefit from routine, early invasive management consisting of coronary angiography and revascularization. A conservative, ischemia-guided initial approach is both safe and effective.

Angioplasty, Balloon, Coronary↗

Cardiac troponin I and T alterations in dog hearts with myocardial infarction: correlation with infarct size.

We studied the distribution of cardiac troponins I (cTnI) and T (cTnT) in ischemic left ventricular (LV) tissue in 7 infarct zones, 7 remote nonischemic LV areas, and 7 nonischemic areas each from the right ventricle and circumflex in an acute coronary artery occlusion dog model to correlate myocardial loss of troponins with infarct size 3 weeks after the infarction and to determine whether the decrease of troponins in ischemic myocardium can be used to assess the infarct size in dogs after coronary occlusion. The serum profiles for time vs mean cTnI and cTnT concentrations in 6 dogs after occlusion showed peak concentrations at 1 day and 5 days, respectively. The concentrations of troponins were similar in all nonischemic zones. However, cTnI and cTnT decreased significantly in the LV ischemic tissues. Loss of cTnT, but not cTnI, in ischemic LV tissues correlated significantly with infarct size 3 weeks after the infarction. Biochemical alterations suggest that the increases in serum troponins after the infarction parallel the decreases in tissue concentrations of troponins.

Animals↗

Evolution of vectorcardiographic QRS changes during myocardial infarction in dogs and their relation to infarct size.

The ability of vectorcardiographic QRS changes to quantify myocardial ischaemia and necrosis in dogs was studied. Myocardial infarction was produced in 21 anaesthetised dogs by inflating a balloon inserted into the right, left anterior descending, or left circumflex coronary artery. A Frank vectorcardiogram was recorded before and every 15-30 minutes for 10 hours after the occlusion. ST vector magnitude (ST-VM), QRS summation vectors, and QRS integral differences (QRS-VD) between the preocclusion recording and subsequent recordings were computed. Twenty four hours after occlusion two vectorcardiograms were obtained, the hearts removed, and the infarcts cut out and weighed. Four dogs were excluded from the study because of persistent arrhythmias, major conduction defects, or sudden death. In the remaining 17 dogs the QRS summation vectors rotated maximally towards the site of infarction 7 minutes after occlusion corresponding to a median minimum QRS-VD of -19 (range -2 to -29) microVs. This coincided with the maximum ST-VM, median 0.43 (range 0.12-0.68) mV. The QRS summation vectors subsequently rotated away from the infarct producing a median maximum QRS-VD of 20 (range 6-28) microVs. The maximum QRS-VD correlated significantly with the percentage of infarcted myocardium (r = 0.82). The correlation between the early minimum QRS-VD and the maximum ST-VM was r = 0.83. The QRS-VD was recomputed with a reference taken 2 or 4 hours after occlusion. The relation between maximum QRS-VD and infarct percentage was not significantly changed with the reference at 2 hours, but with the reference at 4 hours the ability to predict infarct size was lost.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Myocardial enzyme depletion in infarcted human hearts: infarct size and equivalent tissue mass.

Myocardial activities of several enzymes were measured in infarcted and non-infarcted areas of heart sections obtained from eight patients who died after acute myocardial infarction. Similar data were obtained from four patients with cardiovascular disorders who died from causes other than myocardial infarction and from six patients without previously known heart disease. It was found that both non-infarcted and infarcted tissue samples contained considerably altered enzyme activities. This finding explains the low correlations between enzymatic and histological estimates of infarct size previously reported. However, when the residual myocardial activities of different enzymes were compared with each other, a close correlation was found between creatine kinase, alpha-hydroxybutyrate dehydrogenase, and aspartate aminotransferase. It appears that the pathological changes in the myocardial activities of these enzymes may be explained by the phenomenon of diluted myocardium. This indicates that myocardial injury, as estimated from plasma enzyme activities, may still be expressed meaningfully in gram equivalents of healthy myocardium.

Adult↗

Ventricular fibrillation threshold in acute myocardial infarction and its relation to myocardial infarct size.

The effect of myocardial infarct size on ventricular fibrillation threshold (VFT) was evaluated by determining changes in VFT during acute myocardial infarction and relating those changes to infarct size. Infarct size was estimated from gross measurement and from serial changes in serum CPK activity in 25 dogs. VFT reduction correlated well with gross infarct size (r=0.92). This suggests that the severity of electrical instability during AMI is related to the size of the developing infarct, and that appropriate therapeutic interventions to reduce infarct size during this time may also render the heart more electrically stable.

Animals↗

Functional role of microvascular integrity in patients with infarct-related artery patency after acute myocardial infarction.

AIMS: The study was set up to evaluate the functional role of post-infarct preserved microvascular integrity. Low dose dobutamine echocardiography and myocardial contrast echocardiography were used to study patients before hospital discharge who had suffered a recent myocardial infarction and had a patent infarct-related artery (TIMI flow grade 3). METHOD: In the dysfunctioning infarct area, the wall motion score index was calculated at baseline, during the dobutamine infusion and at the 3 month follow-up echocardiogram; contrast echocardiography was performed at the time of coronary angiography, before hospital discharge. RESULTS: In patients with more than 50% of the dysfunctioning infarct area opacified at contrast echocardiography (group A), regional wall motion score index decreased, compared to baseline, during the dobutamine infusion (1.97 +/- 0.78 vs 2.5 +/- 0.35 at baseline; P < 0.001) and at follow-up echocardiography (1.83 +/- 0.63 vs 2.5 +/- 0.35 at baseline; P < 0.001). In patients with less extensive microvascular integrity as revealed by contrast echocardiography (group B), regional wall motion score index did not decrease from baseline during either the dobutamine infusion (2.73 +/- 0.21 vs 2.81 +/- 0.20 at baseline; P = ns), or at follow-up (2.81 +/- 0.20 vs 2.81 +/- 0.20 at baseline; P = ns). CONCLUSION: In patients with post-infarct dysfunctioning myocardium but a patent infarct-related artery, microvascular integrity, as assessed by myocardial contrast echocardiography, is an indicator of myocardial viability in terms of preserved contractile reserve, as demonstrated by dobutamine infusion and functional recovery at follow-up.

Cardiotonic Agents↗

A sex difference in short-term survival after initial acute myocardial infarction. The MONICA-Bremen Acute Myocardial Infarction Register, 1985-1990.

AIMS: To assess the difference between men and women as regards fatality shortly after acute myocardial infarction, and the relationship of patient characteristics. METHODS AND RESULTS: One thousand seven hundred and ten male and 563 female patients, 25-69 years of age and hospitalized with a first acute myocardial infarction occurring from 1985 to 1990, were included in the population-based World Health Organization MONICA-Bremen Acute Myocardial Infarction Register. Patient information, including short-term survival status, was obtained from the medical records of the seven Bremen hospitals with internal medicine departments and municipal death certificate files. The unadjusted 28-day fatality rate after acute myocardial infarction was higher among women than among men (23.1% vs 16.1% respectively: P < 0.001). Adjusting for the older age of women did not eliminate the difference completely (females; 20.9%, males: 16.8%; P = 0.041). Controlling for previous use of inotropic medicine and diuretics, during-the-event receipt of thrombolysis and platelet inhibitors, and age in logistic regression analyses resulted in a similar 28-day mortality risk after acute myocardial infarction for both sexes (female/male odds ratio = 1.13, 95% confidence interval = 0.86 1.50; P = 0.389). CONCLUSIONS: Sex was not an independent predictor of early acute myocardial infarction fatality. Our data suggest that the excess mortality risk in women can be explained by sex differences in age, pre-infarction cardiac impairment, and treatment during the coronary event.

Adult↗

Comparison based on age of baseline electrocardiographic abnormalities in non-Q-wave myocardial infarction. VANQWISH Trial Research Investigators. Veterans Affairs Non-Q-Wave Infarction Strategies In-Hospital.

OBJECTIVE: To compare the incidence of electrocardiographic abnormalities between older (age > or = 70 years) and younger patients presenting with acute non-Q-wave myocardial infarction. DESIGN: Retrospective review of qualifying electrocardiograms in 918 patients enrolled in the multicenter Veterans Affairs Non-Q-Wave Infarction Strategies In-Hospital (VANQWISH) study. SETTING: Seventeen Department of Veterans Affairs medical centers. PARTICIPANTS: A total of 918 patients (224 > or = 70 years old) with acute non-Q-wave myocardial infarction. MEASUREMENTS: Comparison of electrocardiograms in patients aged > or = 70 years and younger patients for presence of left ventriculary hypertrophy, widened QRS complex, ST and T wave abnormalities, rhythm other than sinus, heart rate > or = 80 beats/minute, and location of acute non-Q-wave myocardial infarction. RESULTS: Left ventricular hypertrophy and ST depression > or = 1 mm were significantly more frequent in older than in younger patients. CONCLUSIONS: Older patients presenting with non-Q-wave myocardial infarction have a greater incidence of left ventricular hypertrophy and ST depression on their electrocardiograms than younger patients. Both of these electrocardiographic findings have previously been associated with increased risk of death and recurrent myocardial infarction and may help account for the worse prognosis of non-Q-wave myocardial infarction in older patients.

Age Distribution↗

Infarct zone viability influences ventricular remodelling after late recanalisation of an occluded infarct related artery.

OBJECTIVE: To investigate the influence of infarct zone viability on remodelling after late recanalisation of an occluded infarct related artery. METHODS: A subgroup of 26 volunteers from TOAT (the open artery trial) underwent dobutamine stress cardiovascular magnetic resonance at baseline to assess the amount of viable myocardium present with follow up to assess remodelling at one year. TOAT studied patients with left ventricular dysfunction after anterior myocardial infarction (MI) associated with isolated proximal occlusion of the left anterior descending coronary artery with randomisation to percutaneous coronary intervention (PCI) with stent at 3.6 weeks after MI (PCI group) or to medical treatment alone (medical group). RESULTS: In the PCI group there was a significant relation between the number of viable segments within the infarct zone and improvement in end systolic volume index (-7.7 ml/m2, p = 0.02) and increased ejection fraction (4.1%, p = 0.03). The relation between viability and improvements in end diastolic volume index (-8.8 ml/m2, p = 0.08) and mass index (-6.3 g/m2, p = 0.01) did not reach significance (p = 0.27 and p = 0.8, respectively). In the medical group, there was no significant relation between the number of viable segments in the infarct zone and the subsequent changes in end diastolic (p = 0.84) and end systolic volume indices (p = 0.34), ejection fraction (p = 0.1), and mass index (p = 0.24). CONCLUSION: The extent of viable myocardium in the infarct zone is related to improvements in left ventricular remodelling in patients who undergo late recanalisation of an occluded infarct related artery.

Adult↗

Myocardial infarct size and cardiac performance at exercise soon after myocardial infarction.

Infarct size was estimated from serial serum CK MB measurements in a series of 101 patients admitted less than 15 hours after the first acute myocardial infarction. A maximal symptom limited exercise test comprising impedance measurements for the estimation of stroke volume at rest and at different levels of exercise was performed early after admission by 26 patients. There was a slight, though not significant, negative correlation between infarct size and physical capability as measured by the duration of work. The rise in systolic blood pressure during exercise showed a significantly negative and the increase in heart a significantly positive correlation to infarct size. This suggests that the rise in blood pressure, which is less in patients with the larger infarcts, is compensated by an increase in heart rate, so that the same maximum of cardiac performance and myocardial oxygen consumption is reached. The increase in cardiac stroke volume during exercise was negatively correlated with infarct size. Stroke volume only increased during lower levels of exercise; the increase in cardiac output at higher levels of exercise was achieved entirely by an increase in heart rate. The magnitude of ST segment elevation during exercise showed a significantly positive correlation with infarct size, whereas the occurrence of arrhythmias during exercise was independent of it.

Aged↗

Improved detection of myocardial infarction by emission computed tomography with thallium-201. Relation to infarct size.

Emission computed tomography with thallium-201 was compared with planar imaging in its ability to detect myocardial infarctions of various sizes four weeks after the onset. Tomography was performed after planar imaging at rest in 160 patients with a first myocardial infarction, in whom infarct size was prospectively estimated by the peak value of creatine kinase activity at the time of the acute episode and in 39 patients without infarction. The planar images and the transaxial, short axial, and long axial tomograms were interpreted qualitatively. Tomography was significantly more sensitive than planar imaging in detecting anterior (87% v 96%), inferior (73% v 97%), and non-transmural (47% v 87%) infarcts. The increased sensitivity was confined to detecting small infarcts as assessed by the peak creatine kinase value (44% v 89% when peak creatine kinase activity was less than or equal to 1000 IU/l). The overall sensitivity was 96% for tomography and 78% for planar imaging. The specificity was similar (92%) with the two techniques. Thus emission computed tomography can improve the detection rate of small infarcts that cannot be identified on planar images, by showing the three dimensional distribution of thallium-201, and increases the diagnostic value of thallium-201 scintigraphy.

Adult↗