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[Worsening of heart failure during hospital course in myocardial infarction is a factor of poor prognosis. Apropos of a prospective cohort study of 2,507 patients hospitalized with myocardial infarction: the PRIMA study].

BACKGROUND: Worsening of heart failure in patients with myocardial infarction is seldom studied, elderly patients often are not included, and multivariate analysis is uncommon. AIMS: The prospective PRIMA study (Prise en charge de l'Infarctus du Myocarde Aigu; management of acute myocardial infarction) sought to determine the incidence of heart failure worsening, its risk factors, and its prognostic importance in patients with myocardial infarction, regardless of age and hospital facilities, in the "real world" in a region in France, using multivariate analysis. METHODS: Data were prospectively collected in all patients with myocardial infarction admitted in all hospitals in three departments in the Rhône-Alpes region in France between September 1, 1993 and January 31, 1995. RESULTS: Among 2,507 patients, 33% were in Killip classes II-IV at admission. Four hundred and sixteen patients (17%) had worsening of Killip class during the first five days. In-hospital mortality (overall: 14%) increased dramatically with Killip class at admission (9% in class I; 62% in class IV) and with worsening of Killip class during the first five days (36% vs 8% if no worsening). In multivariate analysis, older age, diabetes mellitus and anterior Q-wave myocardial infarction were significant predictors of Killip class at admission and of its worsening. The significant predictors of in-hospital mortality were older age, Killip class III at admission and worsening of Killip class during the first five days. CONCLUSION: This large, unselected cohort revealed that among patients with myocardial infarction, heart failure and its worsening are frequent, especially in the elderly, and dramatically worsen the in-hospital mortality.

Aged↗

Plasma cardiac troponin T closely correlates with infarct size in a mouse model of acute myocardial infarction.

BACKGROUND: Cardiac troponins replaced creatine kinase and lactate dehydrogenase isoenzymes as criterion standards for the laboratory diagnosis of myocardial damage. However, there are only few publications on correlations of cardiac troponin T (cTnT) with pathologically determined infarct size which are flawed by insufficient sample size. METHODS: In 38 anesthetized wildtype mice, the chest and pericardium were opened and the left descending artery was ligated. After sham operation, all mice recovered. Twenty-four hours after surgical induction of acute myocardial infarction heparinized blood samples were collected, the animals sacrificed and hearts harvested. Plasma cTnT was measured by a quantitative rapid assay using the Cardiac Reader (Roche Diagnostics). The hearts were cut into four transverse sections which were stained with 1.5% triphenyltetrazolium chloride for evaluation of necrosis by computerized planimetry. Pearson correlation coefficients were calculated between histological infarct size and cardiac markers. RESULTS: Infarct sizes ranged from 14% to 55% of left ventricle and cTnT concentrations from 3.9 to 14.1 microg/l. cTnT correlated closely with histological infarct size (r = 0.84, p < 0.001). CONCLUSIONS: This study for the first time demonstrates a close correlation of cTnT release with pathological infarct size in a suitable experimental model with a sufficient sample size.

Animals↗

Troponin I concentrations following primary percutaneous coronary intervention predict large infarct size and left ventricular dysfunction in patients with ST-segment elevation acute myocardial infarction.

The aim of this study was to investigate the ability of troponin I (cTnI) levels to predict myocardial infarction size in patients with ST-segment elevation acute myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). In 87 patients with STEMI undergoing primary PCI, serial plasma concentrations of cTnI and alpha-hydroxybutyrate deshydrogenase (HBDH) were measured before PCI and over the following 72 h. Enzymatic infarct size was estimated by the cumulative release of HBDH during the 72 h following PCI (QHBDH72). Delayed radionuclide left ventricular ejection fraction (LVEF) was measured in 63 patients. While cTnI concentrations at admission did not correlate with QHBDH72 or with LVEF, from the 3rd to the 72nd h following PCI, they did correlated with QHBDH72 (P<0.001; R: 0.76-0.86) and with LVEF (P<0.001; R: -0.42 to -0.50). Receiver-operator characteristic (ROC) curve analysis showed that admission concentrations of cTnI could not predict either a large infarct size (i.e., QHBDH72>10 g-eq l(-1)) or a low LVEF (i.e., LVEF<40%). However, 6 h and up until 72 h after PTCA, cTnI concentrations were predictive of large enzymatic infarct size (sensitivity: 91 and 95%, specificity: 90 and 87%, respectively) and of LVEF under 40% (sensitivity: 75 and 77%, specificity: 90 and 78%, respectively). Thus, our study suggests that in contrast with admission cTnI concentration, cTnI levels following primary PCI represent a reliable tool for predicting large enzymatic infarct size and may help in selecting patients with a high risk of low LVEF at 1 month.

Aged↗

Impact of low level laser irradiation on infarct size in the rat following myocardial infarction.

Low energy level irradiation (LLLI) has been found to modulate biological processes. The effect of LLLI on the development of acute myocardial infarction (MI) was investigated following chronic ligation of the left anterior descending (LAD) coronary artery in laboratory rats. The hearts of 22 rats were laser irradiated (LI) using a diode laser (804 nm, 38 mW power output) through the intercostal muscles in the chest following MI and on day 3 post MI. In the control non laser irradiated (NLI) group (19 rats) MI was induced experimentally and laser irradiation was not applied. All rats were sacrificed 21 days post MI. Size, thickness and relative circumferential length of the infarct, as well as other parameters, were determined from histological sections stained with Masson's trichrome and hearts stained with triphenyl tetrazolium chloride (TTC) using histomorphometric methods. The infarct size (expressed as percent of total left ventricle area) of the LI rats was 10.1+/-5.8, which was significantly lower (65%; P<0.01) than the infarct size of NLI rats which was 28.7+/-9.6. Correlatively, the ratio of circumferential length of the infarcted area was significantly lower (2-fold; P<0.01) in the LI rats as compared to the NLI rats. LLLI of the infarcted area in the myocardium of experimentally induced MI rats, at the correct energy, duration and timing, markedly reduces the loss of myocardial tissue. This phenomenon may have an important beneficial effect on patients after acute MI or ischemic heart disease.

Animals↗

Temporal trends in the treatment of over 1.5 million patients with myocardial infarction in the US from 1990 through 1999: the National Registry of Myocardial Infarction 1, 2 and 3.

OBJECTIVES: We sought to determine trends in the treatment of myocardial infarction from 1990 through 1999 in the U.S. and to relate these trends to current guidelines. BACKGROUND: Limited data are available to show how recent clinical trials and clinical guidelines have impacted treatment of myocardial infarction. METHODS: Temporal trends in myocardial infarction treatment and outcome were assessed by using data from 1,514,292 patients in the National Registry of Myocardial Infarction (NRMI) 1, 2 and 3 from 1990 through 1999. RESULTS: During this interval, the use of intravenous thrombolytic therapy declined from 34.3% to 20.8%, but the use of primary angioplasty increased from 2.4% to 7.3% (both p = 0.0001). The median "door-to-drug" time among thrombolytic therapy recipients fell from 61.8 to 37.8 min (p = 0.0001), primarily owing to shorter "door-to-data" and "data-to-decision" times. The prevalence of non-Q wave infarctions increased from 45% in 1994 to 63% in 1999 (p = 0.0001). From 1994 through 1999, there was increased usage of beta-blockers, aspirin and angiotensin-converting inhibitors, both during the first 24 h after admission and on hospital discharge (all p = 0.0001). Between 1990 and 1999, the median duration of hospital stay fell from 8.3 to 4.3 days, and hospital mortality declined from 11.2% to 9.4% (both p = 0.0001). CONCLUSIONS: The NRMI data from 1990 through 1999 demonstrate that the recommendations of recent clinical trials and published guidelines are being implemented, resulting in more rapid administration of intravenous thrombolytic therapy, increasing use of primary angioplasty and more frequent use of adjunctive therapies known to reduce mortality, and may be contributing to the higher prevalence of non-Q wave infarctions, shorter hospital stays and lower hospital mortality.

Angioplasty, Balloon, Coronary↗

Recovery of myocardial perfusion in acute myocardial infarction after successful balloon angioplasty and stent placement in the infarct-related coronary artery.

OBJECTIVES: This study sought to investigate changes in myocardial perfusion after direct percutaneous transluminal coronary angioplasty (PTCA) in acute myocardial infarction (MI). BACKGROUND: After initially successful recanalization of the infarct-related artery, coronary perfusion may deteriorate as a result of reocclusion, distal embolization of platelet aggregates formed at the dilated plaque or microvascular reperfusion injury. This change could offset the benefit from early intervention. METHODS: The study included 19 patients in whom the infarct-related artery was successfully recanalized by PTCA with Palmaz-Schatz stent placement within 24 h after the onset of pain. Basal and papaverine-induced coronary blood flow were assessed by Doppler flow velocity measurements and quantitative coronary angiography. In addition, basal and adenosine-induced myocardial blood flow were measured by nitrogen-13 ammonia positron emission tomography (PET). RESULTS: Immediately after completion of the intervention, the average coronary flow reserve (CR) in the recanalized vessel was 1.56 +/- 0.51; it increased to 2.04 +/- 0.65 at 1 h (p = 0.013) and to 2.66 +/- 0.72 at 2 weeks after reperfusion (p = 0.008, n = 16). PET studies in 12 patients revealed that perfusion defect size and CR in the infarct region (2.19 +/- 0.89 vs. 2.33 +/- 0.86) did not change significantly between day 2 after recanalization and 2 weeks. However, we found significant (p < 0.03) increases in basal (by 26%) and adenosine-induced (by 40%) blood flow in the infarct region. CONCLUSIONS: Despite the persistence of a perfusion defect after successful recanalization of the occluded artery in acute MI, CR of the infarct region improves in most patients within 1 h and further improves within 2 weeks.

Adult↗

The influence of gating on measurements of myocardium at risk and infarct size during acute myocardial infarction by tomographic technetium 99m-labeled sestamibi imaging.

BACKGROUND: Serial perfusion imaging with 99mTc-labeled sestamibi has been useful in the assessment of myocardial salvage from reperfusion therapy during acute myocardial infarction. Studies in animal models have shown that discernible perfusion defects can be created by left ventricular asynergy from partial volume effects in the setting of homogenous perfusion tracer distribution. The purpose of this study was to examine the influence of gating on serial perfusion images during acute myocardial infarction to determine the magnitude of potential partial volume effects. METHODS AND RESULTS: 99mTc-labeled sestamibi was injected into 18 patients during acute myocardial infarction and 29 patients 5 to 8 days after myocardial infarction. Tomographic imaging was acquired in gated format (16 frames per R-R cycle of the electrocardiogram) for each set of images. All frames were summed to produce ungated images. Tomographic images were quantified on three different thresholds to define the perfusion defect: 50%, 60%, and 70% of maximal counts. Severity of perfusion defects was calculated as the lowest ratio of minimum/maximum counts on five short-axis slices. Regional wall motion was assessed subjectively on the gated images by cine-loop display. Radionuclide ventriculography was performed at 6 weeks. There was a close correlation between perfusion defect size on ungated images and end-diastolic and end-systolic images independent of the quantitative threshold used (r = 0.90 to 0.93; p < 0.0001 for all correlations). Gated images provided consistently significantly greater estimates of perfusion defect size and severity by a small increment (3% to 9% of the left ventricle; p < 0.05 for all comparisons) independently of the quantitative threshold used or the time of imaging (acute or late). Ungated images provided slightly better correlations with left ventricular ejection fraction at 6 weeks independently of the quantitative threshold used and despite significant wall motion abnormalities present on both the acute and final studies. CONCLUSIONS: The differences between perfusion defect size for gated and ungated images were highly significant as a group, but the magnitude of difference was small and not clinically relevant. The larger estimates provided by end-diastolic gated images are opposite the difference expected if partial volume effects were significantly influencing perfusion defect size. Partial volume effects appear to have minimal impact on clinical tomographic imaging during acute myocardial infarction for the quantification of myocardium at risk and infarct size.

Adult↗

High-risk clinical features predict increased post-infarction myocardial apoptosis and the benefits as a result of an open infarct-related artery.

BACKGROUND: Infarct-related artery (IRA) patency after acute myocardial infarction (AMI) is associated with a more favourable clinical course, in particular in patients with high-risk features. As it has been recently reported that IRA patency is associated with a reduced postinfarction apoptotic rate (AR), the aim of our study was to assess whether IRA status late after AMI had a different impact on AR in high- vs. low-risk patients. METHODS AND RESULTS: Co-localization of TUNEL and caspase-3 was used to calculate the AR at the site of infarction at the time of death in 30 subjects. The Norris coronary prognostic index (NI) was calculated (computing age, presence of pulmonary congestion, heart size and history of previous additional AMI) in order to define the patients' individual risk at the time of hospitalization. According to the NI (< or =7 vs. >7), subjects were divided into low and high risk, as NI >7 carries an approximate threefold higher risk of death. The NI was significantly correlated with the AR at the time of death both in infarct and remote areas. Twenty subjects had IRA occlusion at the time of death, and in these patients AR was significantly higher both in infarct and remote areas (P<0.001 and P=0.009 vs. the others, respectively). However the impact of IRA occlusion on AR was significantly different comparing high- vs. low-risk subjects. In particular, AR at the infarct site was 10-fold higher in the high-risk subjects with IRA occlusion (26.1%[20.4-28.7%]) vs. those with open IRA (2.3%[0.6-3.5%]; P=0.002) and was nonsignificantly different in the low-risk subjects vs. those without IRA occlusion (8.2%[2.5-17.5%] vs. 5.4%[1.5-7.9%]; P=0.48). Similarly, in the high-risk subjects, AR in remote areas was significantly greater in cases with occluded vs. open IRA (0.7%[0.4-0.9%] vs. 0.3%[0.3-0.32%]; P=0.009). CONCLUSION: A significantly higher AR is associated with IRA occlusion late post AMI in subjects with high-risk clinical features, and not in low-risk patients. The diverse impact of IRA occlusion on AR in subjects with different risk profiles may explain the greater benefit associated with coronary reperfusion in high-risk subjects. The overall lower AR in low-risk subjects, independently from the IRA status, may be correlated with the better long-term prognosis after AMI in this case.

Aged↗

The 60 Minutes Myocardial Infarction Project. Characteristics on admission and clinical outcome in patients with reinfarction compared to patients with a first infarction.

PURPOSE: The purpose of the study was to evaluate parameters that characterize patients with myocardial reinfarction as compared to patients with a first infarction in clinical practice, and possibly to determine their clinical outcome. METHODS: The 60 minutes Myocardial Project is a German multicentre prospective observational study in which 136 hospitals are participating. Fourteen thousand, nine hundred and eighty consecutive patients with acute Q wave myocardial infarction were included from July 1992 to September 1994. RESULTS: Out of these 14,980 patients, there were 2854 (19%) with reinfarction and 12,126 (81%) with a first infarction. Patients with a reinfarction arrived at the hospital 24 min earlier than patients with a first infarction (pre-hospital delay 156 vs 180 min; P < 0.001); the door-to-needle time with reinfarction was longer (38 vs 30 min; P < 0.001); however, patients with reinfarction were older (69 vs 66 years; P < 0.001), had a lower rate of a diagnostic first ECG (54 vs 71%; P < 0.001) and received thrombolytic therapy less frequently than patients with a first infarction (46 vs 52%; P < 0.001). A low number of patients received primary PTCA ( n = 205) since only a few hospitals offered a primary PTCA service at the time the study was performed. In patients with reinfarction, there were more reasons as to why thrombolytic therapy was not given (24 vs 21%; P < 0.001). Left bundle branch block occurred more frequently in patients with reinfarction (15 vs 8%; P < 0.001). The intra-hospital course in patients with reinfarction was associated with an increase of complications and intra-hospital death (23 vs 15%; P < 0.001. CONCLUSIONS: Although reinfarction patients arrived earlier at hospital than patients with a first infarction, the former received thrombolytic therapy less frequently than the latter. Patients with reinfarction were older, more frequently had a non-diagnostic ECG on admission and had a higher rate of contraindications against thrombolytic therapy.

Adult↗

[Cine-MRT in the functional and morphological diagnosis of the heart after a myocardial infarct/ A comparison with angiocardiography, 2-dimensional echocardiography, intracardiac scintigraphy and enzymatic infarct size estimation].

PURPOSE: The aim of the study was to test the reliability of cine magnetic resonance imaging (cine-MRI) on the infarction heart with its altered geometry. MATERIAL AND METHODS: 61 patients (17 women, 44 men, 36-83 years, 32 with anterior, 29 with posterior wall infarction) received Cine-MRI in the true long and short axis of the heart and two-dimensional echocardiography one and 4 weeks post infarction. Two-level angiocardiography (ACG) and radionuclide ventriculography (RNV) were performed 4 weeks p.i. The size of myocardial infarction was determined enzymatically with the CK integral method. Left ventricular volume indices (EDVI, ESVI, SVI), ejection fraction (EF) and infarction weight (IW) were compared. RESULTS: Excellent correlations existed between cine-MRI in the long and short axis for the volume indices and EF. Between cine-MRI in the short axis and ACG all correlations were excellent as well. They were significantly less satisfactory between cine-MRI and 2DE due to the inhomogeneity of echo quality. Cine-MRI and RNV produced similar EF results (r = 0.884), and a comparison of IW in cine-MRI and CK integral method also showed a good correspondence (r = 0.967). CONCLUSION: Cine-MRI is a reliable method for the morphological and functional examination of post-myocardial infarction.

Adult↗

A prospective trial of intravenous streptokinase in acute myocardial infarction (I.S.A.M.). Mortality, morbidity, and infarct size at 21 days.

Within six hours after the onset of symptoms of myocardial infarction, we randomly assigned 1741 patients up to 75 years of age to a one-hour intravenous infusion of 1.5 million IU of streptokinase or placebo. At 21 days mortality was 6.3 percent in the streptokinase group and 7.1 percent in the placebo group. Of those treated within three hours of the onset of symptoms, 5.2 percent died in the streptokinase group (n = 477), as compared with 6.5 percent in the placebo group (n = 463). These differences were not significant. The time to peak serum levels of creatine kinase of myocardial origin (CK-MB) after the onset of symptoms was significantly shorter (13.9 vs. 19.2 hours), and the integrated area under the CK-MB curve (CK-MB infarct size) was significantly smaller, in the streptokinase group (P less than 0.02). Angiograms obtained in 848 patients three to four weeks after infarction revealed that the streptokinase group had higher global ejection fractions (56.8 vs. 53.9 percent, P less than 0.005) and regional ejection fractions (all patients in group, P less than 0.005; patients with anterior or inferior infarctions, P less than 0.05). We conclude that beginning intravenous streptokinase infusion early after the onset of myocardial infarction limits the size of the infarct regardless of its localization. There was, however, only a trend toward reduced mortality at 21 days.

Aged↗

Tea consumption and infarct-related ventricular arrhythmias: the determinants of myocardial infarction onset study.

BACKGROUND: Tea consumption is associated with lower post-infarct mortality among patients with acute myocardial infarction. We previously found preliminary evidence that tea consumption may also be associated with lower risk of infarct-related ventricular arrhythmias. METHODS: Between 1989 and 1996, 3882 subjects with AMI were enrolled in the two phases of the Determinants of Myocardial Infarction Onset Study a median of four days after admission. Trained interviewers assessed self-reported usual tea and coffee consumption during the year prior to infarction with a standardized questionnaire. We examined the prevalence of ventricular arrhythmias in the two phases of the study separately and together. RESULTS: Among the 1912 patients with complete information in the first phase, the prevalence of ventricular arrhythmias was 16% among abstainers from tea, 11% among moderate tea drinkers (<14 cups per week), and 14% among heavier tea drinkers (> or =14 cups per week) (p homogeneity = 0.03). Among the 1791 patients with comparable information in the second phase, the corresponding prevalence rates were 11%, 8%, and 8%, respectively (p = 0.06). When the phases were combined, the adjusted odds ratios for VA were 0.7 (95% confidence interval, 0.6-0.9) among moderate tea drinkers and 0.9 (95% confidence interval, 0.7-1.2) among heavier tea drinkers. The findings were of similar direction for both ventricular tachycardia and fibrillation. In contrast, there was higher risk of VA with increasing coffee intake (odds ratio for >14 cups per week 1.3; 95% confidence interval, 1.0-1.7; p trend 0.02). CONCLUSIONS: Moderate tea intake is associated with a lower prevalence, and higher coffee intake with a slightly higher prevalence, of ventricular arrhythmias among patients hospitalized with acute myocardial infarction. If the association with tea intake is confirmed, it may suggest new approaches to prevention of ischemia-related arrhythmias.

Analysis of Variance↗

More non-Q-wave myocardial infarctions but similar infarct sizes in patients with hypertension.

Of 350 consecutive patients without previous symptoms of coronary artery disease, admitted to hospital with an acute myocardial infarction, 109 of them (31%) reported a history of previous hypertension. Hypertensive patients were older than their normotensive counterparts, more of them were females, and thrombolytic treatment was administered to significantly fewer. Blood pressure values at admission to hospital were higher in hypertensive patients; this difference was significant in hypertensive males. Altogether 44 out of 49 female (90%) and 42 out of 60 male hypertensive patients (70%) reported using antihypertensive medication. A previous history of hypertension did not change infarct size as assessed by peak enzyme levels, neither in the bivariate nor in the multivariate analysis. In contrast to this, the adjusted odds ratio for developing a non-Q-wave infarct was 2.51 (p=0.003), i.e. the chance of developing a non-Q-wave infarct in hypertensives was increased by 151%. Thus, in spite of similar infarct size in normotensive and hypertensive patients, a relative smaller proportion of the probably hypertrophied left ventricular wall developed necrosis in the hypertensive population. The propensity towards non-Q-wave infarctions may contribute to the observed less use of fibrinolytic drug treatment in the presently observed patients with hypertension.

Aged↗

Left ventricular function and infarct size 20 months after primary angioplasty for acute myocardial infarction.

OBJECTIVE: To study changes in left ventricular function and infarct size during long-term follow-up after acute myocardial infarction treated with primary angioplasty. DESIGN: From 1996 to 1998, 100 consecutive patients were treated with primary angioplasty for acute ST-elevation myocardial infarction. Angioplasty was successful in 95% of the patients. Global left ventricular ejection fraction (LVEF) was determined by radionuclide ventriculography before discharge, after 6 weeks and after a mean follow-up time of 20 months. Infarct size was assessed by technetium 99m-tetrofosmin myocardial perfusion tomography (SPECT) at rest, performed at the same time intervals. RESULTS: Mean LVEF was 56% at discharge, 55% after 6 weeks and 57% after 20 months of follow-up. No significant improvement in LVEF was observed. Only 8% of the patients at follow-up had LVEF lower than 40%. After 1 week, a mean perfusion defect of 19% was measured by SPECT. After 6 weeks and 20 months of follow-up, the mean perfusion defects were reduced to 14% (p < 0.001) and 15%, respectively. CONCLUSION: Left ventricular function was well preserved with a mean LVEF of 57% 20 months after primary angioplasty for acute myocardial infarction. No significant change in LVEF was observed from 1 week after angioplasty to follow-up. Infarct sizes as assessed by SPECT imaging with tetrofosmin were reduced from 1 to 6 weeks, but did not change further during long-term follow-up. The reduction in the perfusion defects over time was probably due to gradual relief of stunning.

Angioplasty, Balloon, Coronary↗

Infarct-related artery occlusion, tissue markers of ischaemia, and increased apoptosis in the peri-infarct viable myocardium.

AIMS: Unfavourable cardiac remodelling often complicates acute myocardial infarction (AMI) as a result of increased cardiomyocyte apoptosis. It is currently unclear whether ongoing or recurrent ischaemia is an independent determinant for increased apoptosis in peri-infarct viable myocardium. METHODS AND RESULTS: In order to assess the link between infarct-related artery (IRA) occlusion, ischaemia, and apoptosis, 30 subjects dying 7-120 days after AMI (16 with IRA occlusion and 14 with patent IRA) and five control subjects were selected at autopsy. Cardiomyocytes were defined as apoptotic if co-expressing TUNEL and activated caspase-3. Expression of both hypoxia-inducible factor-1 and cyclo-oxygenase-2 was assessed in the peri-infarct myocardium and considered as tissue markers of ischaemia. Evidence of ischaemia was significantly more frequent in cases with IRA occlusion (53%) than in cases with patent IRA (15%) or control hearts (0%, P=0.026). The finding of IRA occlusion and markers of ischaemia identified cases with higher apoptotic rates (ARs) in the peri-infarct viable myocardium [12.2% (8.2-14.0), P<0.001 vs. others], whereas IRA occlusion without ischaemia was associated with lower AR, not significantly different from patent IRA [3.0% (1.0-7.9) vs. 2.2% (1.0-5.8), respectively, P=0.42] CONCLUSION: Ischaemia in the peri-infarct viable myocardium is present in over 50% of subjects dying late after AMI with IRA occlusion, and it is associated with increased apoptosis. Relief of ischaemia after AMI may prove of benefit in preventing apoptosis and its consequences.

Actins↗

Association between toenail selenium and risk of acute myocardial infarction in European men. The EURAMIC Study. European Antioxidant Myocardial Infarction and Breast Cancer.

The association between selenium status and risk of acute myocardial infarction was examined in a multicenter case-control study in 10 centers from Europe and Israel in 1991-1992. Selenium in toenails was assessed for 683 nonfatal male cases with first acute myocardial infarction and 729 controls less than 70 years of age. Median toenail selenium content was 0.553 microgram/g for cases and 0.590 microgram/g for controls. After adjustment for age, center, and smoking, the odds ratio for myocardial infarction in the highest quintile of selenium as compared with the lowest was 0.63 (95 percent confidence interval 0.37-1.07, p for trend = 0.08). The observed inverse trend was somewhat stronger when the authors adjusted for vitamin E status (p = 0.05). Analysis stratified for smoking habits showed an inverse association in former smokers (odds ratio for the 75th-25th percentile contrast = 0.63 (95 percent confidence interval 0.43-0.94)), but not in current smokers (odds ratio = 0.97 (0.71-1.32)) or in those who had never smoked (odds ratio = 1.55 (0.87-2.76)). Analysis stratified by center showed a significant inverse association between selenium levels and risk of myocardial infarction for Germany (Berlin) only (75th to 25th percentile odds ratio = 0.62 (95 percent confidence interval 0.42-0.91)), which was the center with the lowest selenium levels. It appears that the increased risk of acute myocardial infarction at low levels of selenium intake is largely explained by cigarette smoking; selenium status does not appear to be an important determinant of risk of myocardial infarction at the levels observed in a large part of Europe.

Case-Control Studies↗

Thrombolytic therapy reduces the incidence of left ventricular thrombus after anterior myocardial infarction. Relationship to vessel patency and infarct size.

BACKGROUND: Controversial evidence exists as to whether thrombolytic therapy reduces the incidence of left ventricular thrombus in acute myocardial infarction and, if so, how this relates to successful reperfusion. METHODS: Four hundred and eighteen consecutive patients underwent echocardiography and coronary angiography within 3 weeks of an acute myocardial infarction. A dyssynergic score was calculated by analysing regional wall motion in 18 left ventricular segments. The infarct-related artery was considered patent if TIMI grade 2 or 3 flow and less than 90% stenosis were present. Retrograde perfusion by Rentrop's grade 2 or 3 collaterals was considered significant. RESULTS: Large anterior myocardial infarctions were associated with the highest prevalence (39%) of left ventricular thrombosis. Thrombus was also very frequent if the left anterior descending coronary artery was occluded and no collaterals to the infarct area were seen (75%). Anticoagulant therapy reduced the prevalence of left ventricular thrombus, regardless of whether the infarct-related vessel was patent or not. Conversely, in patients undergoing thrombolysis the incidence of left ventricular thrombosis was lower when the left anterior descending coronary artery was patent, and especially when an early creatine kinase peak, suggestive of reperfusion, was recorded (7%). Finally, the presence of left ventricular thrombosis was inversely related to the asynergy score. CONCLUSION: These observations suggest that the presence of left ventricular thrombus is related to the extent of myocardial damage. Thrombolytic therapy reduces thrombus probably by salvaging myocardium at risk.

Adult↗

Intravenous streptokinase in acute myocardial infarction (I.S.A.M.): assessment of left ventricular function 1 and 7 months after infarction by radionuclide ventriculography.

I.S.A.M. was a prospective, placebo-controlled, double-blind multicentre trial of high-dose short-term intravenous streptokinase in acute myocardial infarction (AMI) within 6 h of the onset of symptoms. Determination of left ventricular ejection fraction (LVEF) by radionuclide ventriculography was performed 1 and 7 months after AMI in a subset of 192 patients at rest and, in 140 of them, also during exercise. Regional myocardial function was analysed in all 145 patients with neither a history of a previous myocardial infarction nor revascularization procedures or reinfarction within the 7-month follow-up period. One month after AMI, mean LVEF was higher in the streptokinase group in patients with anterior AMI (50 +/- 15% vs 42 +/- 16%, P = 0.013). This difference was more marked in the subgroup treated within 3 h (53 +/- 14% vs 42 +/- 15%, P = 0.004), whereas patients treated 3-6 h after the onset of symptoms did not differ from respective controls (41 +/- 16% vs 41 +/- 18%). In patients with inferior AMI, the difference in mean LVEF was small (57 +/- 11% vs 55 +/- 12%, P = 0.47). After anterior AMI benefit due to streptokinase therapy was preserved up to 7 months (52 +/- 14% vs 44 +/- 17%, P = 0.013). During exercise, the increase of mean LVEF was greater in the streptokinase group at both dates, especially 7 months after AMI (4.1 +/- 6.1% vs 1.2 +/- 6.3%, P = 0.015). In streptokinase-treated patients with anterior AMI, regional LVEF at rest was higher at both dates compared with controls, within the infarct zone as well as in remote myocardium. No treatment-control differences were demonstrable in patients with inferior AMI. During exercise, regional contractile reserve was better in the streptokinase group within the infarct zone as well as in remote myocardium, irrespective of the site of infarction. Thus, intravenous streptokinase within 3 h after the onset of AMI preserves global left ventricular function in anterior AMI over a period of at least 7 months. Intravenous streptokinase improves regional myocardial function within the infarct zone as well as in remote areas. In inferior AMI investigation solely at rest may underestimate the benefit of streptokinase therapy.

Aged↗