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PubMed1980

Do patients in whom myocardial infarction has been ruled out have a better prognosis after hospitalization than those surviving infarction?

To determine the prognosis after hospitalization of patients hospitalized with acute chest pain in a coronary-care unit, we undertook a prospective study of 211 consecutive admissions to the Stanford Coronary Care Unit. On the basis of predetermined criteria, 16 patients were found to have noncardiac chest pain, and myocardial infarction was ruled out in 89, one of whom died in the hospital. Infarction was documented in 84 others, six of whom died in the hospital. Prospective follow-up after hospitalization was carried out in the 88 patients in whom infarction was ruled out and in the 78 patients who survived infarction. The rate of myocardial infarction or death was 8.0 per cent at six months and 21.6 per cent at a mean of 27.8 months of follow-up for patients who had infarction ruled out, as compared with 7.7 per cent at six months and 21.8 per cent at a mean of 27.8 months of follow-up for those who had a documented infarction during the initial hospitalization. Cardiomegaly, congestive heart failure, and angina after discharge from the hospital tended to increase the risk of morbidity and mortality in both groups. The patient hospitalized with acute ischemic chest pain without evolution of a myocardial infarction has a six to 24-month prognosis similar to that of the patient hospitalized with an acute infarction, and therefore requires similar diagnostic and therapeutic assessment.

Angina Pectoris↗
PubMed1993

Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction.

BACKGROUND: Acute inferior myocardial infarction frequently involves the right ventricle. We hypothesized that right ventricular involvement, as diagnosed by ST-segment elevation in the right precordial lead V4R, may affect the prognosis of patients with inferior myocardial infarctions. METHODS: In 200 consecutive patients admitted to the hospital with acute inferior myocardial infarctions, we assessed the prevalence and diagnostic accuracy of ST-segment elevation in lead V4R (as compared with four other diagnostic procedures) to identify right ventricular involvement and its prognostic implications for in-hospital and long-term outcomes. RESULTS: The in-hospital mortality after inferior myocardial infarction was 19 percent, and major complications occurred in 47 percent of the patients. The presence of ST-segment elevation in lead V4R in 107 patients (54 percent) was highly predictive of right ventricular infarction (sensitivity, 88 percent; specificity, 78 percent; diagnostic accuracy, 83 percent), as compared with the other diagnostic procedures. The patients with ST-segment elevation in lead V4R had a higher in-hospital mortality rate (31 percent vs. 6 percent, P < 0.001) and a higher incidence of major in-hospital complications (64 percent vs. 28 percent, P < 0.001) than did those without ST-elevation in V4R. Multiple logistic-regression analysis showed ST elevation in V4R to be independent of and superior to all other clinical variables available on admission for the prediction of in-hospital mortality (relative risk, 7.7; 95 percent confidence interval, 2.6 to 23) and major complications (relative risk, 4.7; 95 percent confidence interval, 2.4 to 9). The post-hospital course (follow-up, at least 1 year; mean follow-up, 37 months) was similar in patients with and in those without electrocardiographic evidence of right ventricular infarction. CONCLUSIONS: Right ventricular involvement during acute inferior myocardial infarction can be accurately diagnosed by the presence of ST-segment elevation in lead V4R, a finding that is a strong, independent predictor of major complications and in-hospital mortality. Electrocardiographic assessment of right ventricular infarction should be routinely performed in all patients with acute inferior myocardial infarctions.

Adult↗
PubMed1976

Effect of reperfusion on myocardial infarct, and the accuracy of estimating infarct size from serum creatine phosphokinase in the dog.

This study was designed to determine the effect of coronary reperfusion on (1) myocardial infarct size and (2) the accuracy of previously reported methods for estimation of infarct size serum creatine phosphokinase (CPK) values. Thirty mongrel dogs, chronically prepared, were studied in the awake state, and were divided into four groups according to the period or left circumflex coronary artery (LCCA) occlusion. Group 1: permanent occlusion (24 h) in nine dogs; group 2: 45 min occlusion (eight dogs); group 3: 1 h occlusion (five dogs); and group 4: 3 h occlusion (eight dogs). Serial blood samples were drawn for 24 h following the beginning of occlusion and were used to determine total and isoenzyme levels of CPK, and lactic dehydrogenase isoenzymes. All dogs were sacrified 24 h after the beginning of occlusion and were anatomically examined. The extent of anatomical myocardial infarction was determined and compared with the extent of myocardial infarction as estimated from serial serum CPK values. Total serum CPK increased significantly in all groups and was associated with the appearance of CPK-MB isoenzyme and an increase in LDH1,2 (LDH1 greater than LDH2) in most dogs. Total serum CPK increased within an hour after reperfusion and the mean values in groups 2, 3, and 4 were significantly high (P less than 0.05) than serum CPK values in group 1 in the period from 110 min to 4 after occlusion. These data demonstrate that reperfusion after 45 min to 3 h of coronary occlusion results in an earlier appearance of total serum CPK. The anatomical infarction in group 1 averaged 28% +/- 3% (SEM) of the total heart and was significantly larger than infarct size in all groups with reperfusion. In contrast, estimated infarction calculated from total CPK in group 1 was not significantly different from the reperfused groups. Although there was correlation between estimated and anatomical infarction, the data in each group showed that anatomical infarct size could not be accurately estimated from total serum CPK.

Animals↗
PubMed1990

Influence of reflow ventricular fibrillation and electrical defibrillation on infarct size in a canine preparation of myocardial infarction.

STUDY OBJECTIVE - The aim of the study was to investigate the influence of reflow ventricular fibrillation and electrical defibrillation on infarct size in a model of myocardial ischaemia. DESIGN - Myocardial ischaemia was induced in an open chest canine model by occluding the left coronary artery for 2 h. This was followed by 6 h reperfusion. The influence of reflow fibrillation and internal electric defibrillation on infarct size was investigated and compared to dogs which did not develop fibrillation. Infarct size and its major determinants, rate-pressure product (RPP), area at risk (AR), and collateral flow (MBF), were measured and their relationships studied in the two situations, using uni- and multilinear regression analysis. SUBJECTS - 21 adult mongrel dogs of either sex were used in the studies, which were done under pentobarbitone anaesthesia. Two were excluded because they developed ventricular fibrillation soon after coronary occlusion, and one did not survive reflow ventricular fibrillation. Of the remaining 18 dogs, six developed reflow ventricular fibrillation and were compared to the control group of 12 which did not develop fibrillation. MEASUREMENTS and RESULTS - A mean of 70.8(SEM 18.7) joules was required to revive the six dogs with reflow ventricular fibrillation. Difference in mean infarct size in the two groups did not reach significance [49.1(4.4) in fibrillation group v 38(6.2) in the controls]. The multiple linear regression model in the control group accounted for 91% of the variation in infarct size (IS): IS = -3.4 + 0.49 (AR) -21.8 (MBF) + 0.025 (RPP). The equation was not modified by including the reflow fibrillation dogs: IS = -3.1 + 0.52 (AR) - 19 (MBF) + 0.02 (RPP). Ischaemic determinants of infarct size in the reflow fibrillation dogs were computed in the control group equation to compare the infarct size predicted by the model to the measured infarct size in each individual dog in the reflow fibrillation group. There was no significant difference between the means: 12.9(2.9)% (predicted) v 14.9(2.5)% (measured). CONCLUSIONS - In this model of myocardial infarction, reflow ventricular fibrillation and low energy internal electric shocks do not damage the myocardium at risk significantly.

Animals↗
PubMed1986

Angina pectoris early after myocardial infarction: clinical experience of the multicentre post-infarction program.

In the Multicenter Post Infarction Program, 33% of 867 patients had early angina pectoris, i.e. angina between 2 days and hospital discharge 17 +/- 9 days after infarction. Early post-infarction angina was not significantly associated with cardiac death during 2.5 years of follow-up whereas both ventricular arrhythmias and left ventricular dysfunction were strongly and independently related to subsequent mortality. After myocardial infarction, there is no significant association between early angina pectoris and either ventricular arrhythmias or systolic or diastolic dysfunction of the left ventricle. However, patients with early post-infarction angina were one-and-a-half times as likely to be rehospitalized and two-and-a-half times as likely to experience recurrent non-fatal myocardial infarction during the year after myocardial infarction. Exercise angina pectoris was associated with subsequent mortality but not with recurrent non-fatal myocardial infarction. ST segment depression greater than or equal to 1 mm or greater than or equal to 2 mm during exercise was not significantly associated with either subsequent death or non-fatal myocardial infarction.

Adrenergic beta-Antagonists↗
PubMed2006

Postmortem unenhanced magnetic resonance imaging of myocardial infarction in correlation to histological infarction age characterization.

AIMS: Postmortem magnetic resonance (MRI) imaging is currently evaluated as alternative to traditional autopsy and myocardial infarction plays a key role therein. The aim of this study is to determine the suitability of postmortem MRI in infarction age staging. METHODS AND RESULTS: In eight human forensic corpses presenting with a total of 11 myocardial infarcted areas, short-axis, transversal, and longitudinal long-axis images (T1, T2, stir, flair) were acquired in situ on a 1.5 T system. During subsequent autopsy, the section technique was adapted to short-axis images. Histological investigations were performed along the entire circumference of the left ventricle to correlate the signal alteration in MR to the histological appearance. Two peracute infarctions were not detected in MRI and autopsy. Four acute infarcted areas presented with decreased signal in necrotic centres and increased signal in marginal myocardial regions (T2-weighted). T1-weighted images showed local hyperintensities when intramyocardial haemorrhage occurred. Four cases showed subacute infarctions with hyperintense regions in T2-weighted images and no signal alteration in T1-weighted images. Four chronic myocardial infarctions showed distinctively decreased signals in all applied sequences. CONCLUSION: Postmortem MRI demonstrates myocardial infarction in situ and allows for an infarction age estimation based on the signal behaviour.

Acute Disease↗
PubMed1996

Differential effects of tissue plasminogen activator and streptokinase on infarct size and on rate of enzyme release: influence of early infarct related artery patency. The GUSTO Enzyme Substudy.

BACKGROUND: The recent international GUSTO trial of 41,021 patients with acute myocardial infarction demonstrated improved 90-min infarct related artery patency as well as reduced mortality in patients treated with an accelerated regimen of tissue plasminogen activator, compared to patients treated with streptokinase. A regimen combining tissue plasminogen activator and streptokinase yielded intermediate results. The present study investigated the effects of treatment on infarct size and enzyme release kinetics in a subgroup of these patients. METHODS: A total of 553 patients from 15 hospitals were enrolled in the study. Four thrombolytic strategies were compared: streptokinase with subcutaneous heparin, streptokinase with intravenous (i.v.) heparin, tissue plasminogen activator with i.v. heparin, and streptokinase plus tissue plasminogen activator with i.v. heparin. The activity of alpha-hydroxybutyrate dehydrogenase (HBDH) in plasma was centrally analysed and infarct size was defined as cumulative HBDH release per litre of plasma within 72 h of the first symptoms (Q(72)). Patency of the infarct-related vessel was determined by angiography in 159 patients, 90 min after treatment. RESULTS: Infarct size was 3.72 g-eq.1(-1) in patients with adequate coronary perfusion (TIMI-3) at the 90 min angiogram and larger in patients with TIMI-2 (4.35 g-eq.1(-1) or TIMI 0-1 (5.07 g-eq.1(-1) flow (P = 0.024). In this subset of the GUSTO angiographic study, early coronary patency rates (TIMI 2 + 3) were similar in the two streptokinase groups (53 and 46%). Higher, but similar, patency rates were observed in the tissue plasminogen activator and combination therapy groups (87 and 90%). Median infarct size for the four treatment groups, expressed in gram-equivalents (g-eq) of myocardium, was 4.4, 4.5, 3.9 and 3.9 g-eq per litre of plasma (P = 0.04 for streptokinase vs tissue plasminogen activator). Six hours after the first symptoms, respectively 5.3, 6.6, 14.0 and 13.6% of total HBDH release was complete (P < 0.0001 for streptokinase vs tissue plasminogen activator). CONCLUSIONS: Rapid and complete coronary reperfusion salvages myocardial tissue, resulting in limitation of infarct size and accelerated release of proteins from the myocardium. Treatment with tissue plasminogen activator, resulting in earlier reperfusion was more effective in reducing infarct size than the streptokinase regimens, which contributes to the differences in survival between treatment groups in the GUSTO trial.

Humans↗
PubMed1996

Evaluation of post-myocardial infarction regional and global left ventricular function by monoplane ventriculography: superiority of right versus left anterior oblique projection at any infarct location.

OBJECTIVES: To study the significance of serial quantitative regional wall motion analysis, volumes, and ejection fraction findings as well as their prognostic implications derived from cineventriculography in 30 degrees right anterior oblique (RAO) projection in comparison with 60 degrees left anterior oblique (LAO) projection in post-myocardial infarction patients. Ventriculographic left ventricular parameters are accepted surrogates of mortality in myocardial infarction. Nowadays, in contrast to a biplanar approach in most institutions and clinical trials, the investigation is reduced to monoplanar ventriculography. However, it is not known whether the relevance of the two established projections might differ in different infarct topographies. DESIGN AND METHODS: Two hundred and six consecutive patients with acute myocardial infarction (infarct duration < 6 h) were treated with streptokinase (group I, n = 103) and allocated randomly additional percutaneous transluminal coronary angioplasty (group II, n = 103). Biplanar cineventriculography studies were performed at the acute stage, before discharge, and 6 months after discharge from hospital. RESULTS: Regional wall motion analysis (using an algorithm of fixed radiants) documented larger hypokinetic areas and intensities on RAO than it did on LAO projections, whereby infarct size and its improvement (stunned myocardium) was displayed more comprehensively, and a higher predictive power for survival (P = 0.0002 versus NS) was shown in anterior and inferior infarcts. No advantage of the LAO projection could be detected for evaluation of lateral infarcts due to circumflex coronary artery thrombosis either. The predictive power of the global function (ejection fraction; the algorithm of disc summation method) established by RAO projection (P = 0.007) was superior to that of LAO projection (P = 0.03). Enlargement of volumes (left ventricular remodeling) could be documented significantly only by the RAO projection; the LAO projection failed to do so. Groups I and II did not differ in any respect. CONCLUSIONS: The RAO projection has excellent diagnostic and predictive power at any infarct location. In contrast, additional LAO projection provides little information that cannot be obtained reliably from the RAO projection.

Angioplasty, Balloon, Coronary↗
PubMed1992

Large striatocapsular infarcts: clinical presentation and pathogenesis in comparison with lacunar and cortical infarcts.

In a well-defined prospective series of 247 patients with a first-ever supratentorial brain infarct, 15 patients (6%; 95% confidence interval 3-9%) had a large striatocapsular infarct. Twelve (80%) had signs of cortical dysfunction, whereas risk factor profile, frequency of significant carotid stenosis, and frequency of potential cardioembolic sources did not differ between patients with striatocapsular and those with cortical infarction. However, patients with striatocapsular infarction more frequently had potential cardioembolic source and significant carotid stenosis than patients with lacunar infarction. Our findings show that large striatocapsular infarcts differ from lacunar infarcts with regard to both presenting signs and symptoms, and pathogenesis, whereas they resemble infarcts involving the cortex. Such patients should therefore be managed and treated as patients with cortical infarction.

Aged↗
PubMed1979

Evaluation of praecordial ST segment mapping as an index of infarct size in patients with acute myocardial infarction.

We evaluated the usefulness and limitations of praecordial ST segment mapping as a clinical means of assessing the size of acute myocardial infarction in 14 patients with anterior myocardial infarction and 13 patients with inferior myocardial infarction. sigma ST, the sum of ST segment elevations, and nST, the number of leads showing ST segment elevation, were obtained from serial electrocardiograms recorded through 39 praecordial leads. The infarct size and period of the evolution of myocardial infarction were estimated respectively from the total creatine kinase (CK) released and the serial changes of the CK releasing rate. sigma ST and nST obtained at the time when the CK release had ceased correlated closely with the total CK released. Peak sigma ST and nST, and values 48 hours after the onset of myocardial infarction, also correlated well with the total CK released; but those on admission or 12 hours after the onset correlated poorly. These results suggest that sigma ST and nST at the end of evolution of myocardial infarction or 48 hours after the onset may be two useful indices for the assessment of infarct size in patients with either anterior or inferior myocardial infarction.

Adult↗
PubMed1995

Nitrates in myocardial infarction: influence on infarct size, reperfusion, and ventricular remodelling.

OBJECTIVE: To assess the possible benefits of intravenous isosorbide dinitrate in acute myocardial infarction and oral isosorbide mononitrate in subacute myocardial infarction. METHODS: 316 patients presenting with acute myocardial infarction were entered into double blind placebo controlled clinical trials assessing infarct size by enzyme release, ventricular size and function by echocardiography, reperfusion by continuous 12 lead ST segment monitoring and late potentials by high resolution electrocardiography. RESULTS: 301 patients, of whom 292 (97%) received thrombolytic treatment, were randomised on admission to intravenous isosorbide dinitrate or placebo. Overall, there was no significant effect of treatment on infarct size, ST segment resolution, ventricular remodelling, or late potentials at day 3. A trend was observed towards a reduction in infarct size in patients with non-Q wave infarction treated with isosorbide dinitrate. Heterogeneity of nitrate effect was observed in relation to the degree of ST segment elevation on presentation with a clear benefit of isosorbide dinitrate in patients with moderate ST segment elevation (472 U/l v 704 U/l, P = 0.003) and a trend towards a deleterious effect in patients with marked ST segment elevation (1152 U/l v 1058 U/l, P = 0.2). ST segment re-elevation was more common among patients receiving nitrate treatment than in those assigned to placebo (29 v 16, P < 0.05). Some 160 patients underwent a further randomisation to sustained release isosorbide mononitrate or placebo on day 3. Echocardiographic volumes after 6 weeks of treatment were similar in the two groups. CONCLUSIONS: No benefit was observed with administration of nitrates in the treatment groups as a whole for either acute or subacute infarction. There was, however, evidence of heterogeneity of effect in the different subgroups of acute infarction, and the possibility that nitrates may have differing actions in different groups of patients should be considered.

Aged↗
PubMed2000

High cardiac angiotensin-II-forming activity in infarcted and non-infarcted human myocardium.

The aims of this study were to compare human cardiac angiotensin-II-forming activity (AIIFA) between the intact area of control autopsy hearts without cardiac disease (n = 10) and the infarcted or non-infarcted area of autopsy hearts with myocardial infarction (MI, n = 7) and to determine responsible angiotensin-II-forming enzymes. Cardiac total and chymase-dependent AIIFAs were significantly higher in the infarcted and non-infarcted myocardium than those in non-MI heart, while angiotensin-converting enzyme-dependent AIIFA increased only in the infarcted myocardium. The density of chymase antibody-positive mast cells in the non-infarcted area of MI heart correlated positively with total or chymase-dependent AIIFA. Augmented AIIFA was also detected in the left atrium of post-MI hearts. Our results indicated that cardiac angiotensin II formation could be activated in the infarcted as well as in non-infarcted myocardium of the post-MI human heart.

Adult↗
PubMed1999

Relationship of elevated 23Na magnetic resonance image intensity to infarct size after acute reperfused myocardial infarction.

BACKGROUND: Elevated 23Na MR image intensity after acute myocardial infarction has previously been shown to correspond to high tissue [Na+] and loss of myocardial viability. In this study, we explored the potential of in vivo 23Na MRI to assess infarct size and investigated possible mechanisms for elevated 23Na image intensity. METHODS AND RESULTS: Thirteen dogs and 8 rabbits underwent in situ coronary artery occlusion and reperfusion and were imaged by 23Na MRI. For anatomically matched left ventricular short-axis cross sections (n=46), infarct size measured by in vivo 23Na MRI correlated well with triphenyltetrazolium chloride staining (r=0.87, y=0.92x+3.37, P<0.001). Elevated 23Na image intensity was observed in infarcted myocardium (206+/-37% of remote in dogs, P<0.001; 215+/-58% in rabbits, P<0.002) but was not observed after severe but reversible ischemic injury (101+/-11% of baseline, P=NS). High-resolution ex vivo imaging revealed that regions of elevated 23Na image intensity appeared to be identical to those of infarcted regions (r=0.97, y=0.92x+1.52, P<0.001). In infarcted regions, total tissue [Na+] was elevated (89+/-12 versus 37+/-9 mmol/L in control tissue, 156+/-60% increase, P<0.001) and was associated with increased intracellular sodium (254+/-68% of control, P<0.005) and an increased intracellular sodium/potassium ratio (868+/-512% of control, P<0.002). Morphometric analysis demonstrated only a minor increase in extracellular volume (17+/-8% versus 14+/-5%, P<0.05) in the infarcted territory. CONCLUSIONS: Elevated 23Na MR image intensity in vivo measures infarct size after reperfused infarction in both a large and a small animal model. The mechanism of elevated 23Na image intensity is probably intracellular sodium accumulation secondary to loss of myocyte ionic homeostasis.

Animals↗
PubMed1986

Abrupt withdrawal of beta-blockade therapy in patients with myocardial infarction: effects on infarct size, left ventricular function, and hospital course.

The effects of abrupt withdrawal or continuation of beta-blockade therapy during acute myocardial infarction were evaluated in 326 patients participating in the Multicenter Investigation of the Limitation of Infarct Size (MILIS). Thirty-nine patients previously receiving a beta-blocker and randomly selected for withdrawal of beta-blockers and placebo treatment during infarction (group 1) were compared with 272 patients previously untreated with beta-blockers who were also randomly assigned to placebo therapy (group 2). There were no significant differences between the two groups in MB creatine kinase isoenzyme (15.8 +/- 10.9 vs 18.2 +/- 14.4 g-eq/m2, respectively) estimates of infarct size, radionuclide-determined left ventricular ejection fractions within 18 hr of infarction (0.44 +/- 0.15 vs 0.47 +/- 0.16) or 10 days later (0.42 +/- 0.14 vs 0.47 +/- 0.16), creatine kinase-determined incidence of infarct extension (13% vs 6%), congestive heart failure (43% vs 37%), nonfatal ventricular fibrillation (5% vs 7%), or in-hospital mortality (13% vs 9%). Patients in group 1 had more recurrent ischemic chest pain (p = .002) within the first 24 hr after infarction, but not thereafter. However, this did not appear to be related to a rebound increase in systolic blood pressure, heart rate, or double product. In a separate analysis, 20 propranolol-eligible group 1 patients randomly selected for withdrawal of beta-blockade (group 3) were compared with 15 patients randomly selected for continuation of prior beta-blockade therapy (group 4). This comparison yielded similar results. These data indicate that the beta-blockade withdrawal phenomenon is not a major clinical problem in patients with acute myocardial infarction. beta-Blockade therapy can be discontinued abruptly during acute myocardial infarction if clinically indicated.

Aged↗
PubMed1993

Late reperfusion for acute myocardial infarction limits the dilatation of left ventricle without the reduction of infarct size.

BACKGROUND: While previous clinical studies have shown a possible beneficial effect of the reperfusion performed at a relatively late phase of acute myocardial infarction ("late reperfusion") in preventing left ventricular enlargement, the mechanism has not been clarified. METHODS AND RESULTS: Of 89 patients with an initial anterior myocardial infarction, reperfusion was successful in 69. These 69 were divided into three groups according to the time required to achieve reperfusion after the onset of symptoms: early-reperfused (< 3 hours from the onset to reperfusion; n = 22), intermediate-reperfused (3 to 6 hours from the onset to reperfusion; n = 28), and late-reperfused (> 6 hours from the onset to reperfusion; n = 19). The 20 patients whose infarct-related artery were occluded in the acute phase as well as 1 month later was classified as nonreperfused. Infarct size, evaluated as defect volume by 201Tl single-photon emission computed tomography 1 month after the onset, was 1593 +/- 652 units (mean +/- SD) in the late-reperfused group, significantly larger (P < .05) than that of the intermediate-reperfused (1066 +/- 546 U) or the early-reperfused groups (372 +/- 453 U) but not different from that of the nonreperfused group (1736 +/- 562 U). Wall motion abnormality index as well as global ejection fraction evaluated by left ventriculography 1 month after the onset showed that late reperfusion did not preserve the left ventricular wall motion and function. These results indicate that the earlier reperfusion decreased the size of the infarction and preserved left ventricular function, whereas late reperfusion (> 6 hours after onset) did not limit infarct size or preserve left ventricular function. In contrast, the end-diastolic volume index did not differ significantly among the early-reperfused (50 +/- 15 mL/m2), intermediate-reperfused (54 +/- 14 mL/m2), and late-reperfused (53 +/- 19 mL/m2) groups; those were significantly smaller than that of the nonreperfused group (68 +/- 12 mL/m2; P < .05). Left ventriculographic data obtained in both the acute and chronic phase in 39 patients showed that left ventricular volumes increased significantly during the course of myocardial infarction only in the nonreperfused group. CONCLUSIONS: Late reperfusion appeared to prevent ventricular dilatation acute myocardial infarction independent of the limitation of infarct size.

Adult↗
PubMed1995

Infarct salvage with liposomal prostaglandin E1 administered by intravenous bolus immediately before reperfusion in a canine infarction-reperfusion model.

BACKGROUND: Prostaglandin E1 (PGE1) inhibits leukocyte and platelet function and reduces infarct size during left atrial infusion. Intravenous liposomal PGE1 (TLC C-53) accelerates thrombolysis and prevents reocclusion in canine coronary thrombosis. We tested the hypothesis that intravenous TLC C-53 would attenuate reperfusion injury in a canine infarction-reperfusion model. METHODS AND RESULTS: Twenty-one open-chest dogs were randomized to receive a 10-minute intravenous infusion of either liposome diluent (placebo), free PGE1 (2 micrograms/kg), or TLC C-53 (2 micrograms/kg PGE1) after 2 hours of left anterior descending (LAD) occlusion just before reperfusion. Hemodynamic assessment, regional myocardial blood flow determination with radioactive microspheres, myocardial leukocyte infiltration by myeloperoxidase assay, and estimation of infarct size using triphenyl tetrazolium chloride staining were performed. Regional fractional shortening was measured with sonomicrometer crystals implanted in the midmyocardium. Infarct size as a percentage of the risk region was significantly reduced (P < .05) with TLC C-53 (37.9 +/- 17.4%) compared with PGE1 (56.7 +/- 13.9%) or placebo (58.0 +/- 9.9%) infusion. Infarct salvage with TLC C-53 was independent of collateral blood flow by ANCOVA. There was a dramatic reduction in myeloperoxidase activity in the infarct, risk, and border regions of dogs treated with TLC C-53 compared with placebo. Enzyme activity was also significantly reduced (P < .05) in the infarct zone with TLC C-53 (0.11 +/- 0.1 U/100 mg) treatment compared with PGE1 (0.38 +/- 0.3 U/100 mg). No significant differences in regional myocardial blood flow or myocardial function among treatment groups were identified, although there was a trend toward improved function in the TLC C-53 dogs. CONCLUSIONS: Bolus intravenous administration of TLC C-53 immediately before reperfusion results in reduced leukocyte infiltration and substantial infarct salvage. TLC C-53 mah be useful in limiting reperfusion injury during treatment of acute myocardial infarction.

Alprostadil↗
PubMed1995

Triggering of acute myocardial infarction onset by episodes of anger. Determinants of Myocardial Infarction Onset Study Investigators.

BACKGROUND: Many anecdotes and several uncontrolled case series have suggested that emotionally stressful events, and more specifically, anger, immediately precede and appear to trigger the onset of acute myocardial infarction. However, controlled studies to determine the relative risk of myocardial infarction after episodes of anger have not been reported. METHODS AND RESULTS: We interviewed 1623 patients (501 women) an average of 4 days after myocardial infarction. The interview identified the time, place, and quality of myocardial infarction pain and other symptoms, the estimated usual frequency of anger during the previous year, and the intensity and timing of anger and other potentially triggering factors during the 26 hours before the onset of myocardial infarction. Anger was assessed by the onset anger scale, a single-item, seven-level, self-report scale, and the state anger subscale of the State-Trait Personality Inventory. Occurrence of anger in the 2 hours preceding the onset of myocardial infarction was compared with its expected frequency using two types of self-matched control data based on the case-crossover study design. The onset anger scale identified 39 patients with episodes of anger in the 2 hours before the onset of myocardial infarction. The relative risk of myocardial infarction in the 2 hours after an episode of anger was 2.3 (95% confidence interval, 1.7 to 3.2). The state anger subscale corroborated these findings with a relative risk of 1.9 (95% confidence interval, 1.3 to 2.7). Regular users of aspirin had a significantly lower relative risk (1.4; 95% confidence interval, 0.8 to 2.6) than nonusers (2.9; 95% confidence interval, 2.0 to 4.1) (P < .05). CONCLUSIONS: Episodes of anger are capable of triggering the onset of acute myocardial infarction, but aspirin may reduce this risk. A better understanding of the manner in which external events trigger the onset of acute cardiovascular events may lead to innovative preventive strategies aimed at severing the link between these external stressors and their pathological consequences.

Adrenergic beta-Antagonists↗
PubMed1995

Measurement of infarct size using MRI predicts prognosis in middle cerebral artery infarction.

BACKGROUND AND PURPOSE: An accurate measure of the severity of ischemic insult and the resulting prognosis is needed to assess the effectiveness of new treatments for acute stroke. We studied the reproducibility and accuracy of measurements of infarct volume with MRI and correlated the measurements with outcome. METHODS: Infarct volume was measured on T2-weighted images with the Analyze image analysis software. This technique was found to be highly accurate and reproducible. RESULTS: Measurements of infarct volume were found to be highly accurate and reproducible. Twenty-one patients (mean age, 66.5 years; range, 28 to 90 years) with cortical middle cerebral artery territory infarcts in whom adequate data could be obtained were studied within 72 hours from onset (mean delay to MRI, 27.5 hours; range, 5 to 72 hours). The Scandinavian Stroke Scale was used to calculate a prognostic score, and clinical outcome was assessed at 3 months. Infarct volume was found to significantly predict outcome. Mean infarct volume in the independent patients was 35.7 +/- 29.7 cm3 compared with 88.3 +/- 71.3 cm3 in dependent patients and 166.5 +/- 65.9 cm3 in dead patients (F = 10.52, P < .001). Patients with an initial infarct volume less than 80 cm3 were found to have a better outcome than those with larger infarct volumes. Secondary hemorrhage visible on MRI also predicted a poor outcome. In contrast, the Scandinavian Stroke Scale did not significantly predict outcome. CONCLUSIONS: The results demonstrate that measurement of the size of middle cerebral artery infarction with MRI is a useful tool in assessing prognosis and will have a valuable role in assessing new therapeutic agents.

Adult↗