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PubMed1988

Relation between infarct size and left ventricular performance assessed in patients with first acute myocardial infarction randomized to intracoronary thrombolytic therapy or to conventional treatment.

Reperfusion of ischemic myocardium has been reported to increase the cumulative creatine kinase activity in plasma per gram of infarcted myocardium as assessed with the method of Shell et al. In an attempt to find out whether infarct size assessment using the method of Witteveen et al was affected by reperfusion, the relation between enzymatic infarct size was analyzed using Witteveen's method and left ventricular (LV) function parameters in 266 patients with first acute myocardial infarction randomized to intracoronary thrombolysis (n = 134) or conventional therapy (n = 132). Compared with patients allocated to conventional therapy, patients allocated to intracoronary thrombolysis had smaller enzymatic infarct size by 29% (p less than 0.001), smaller LV end-diastolic and end-systolic volume indexes by 10% (p less than 0.05) and 20% (p less than 0.005), respectively, and higher LV ejection fraction (55 +/- 1% vs 49 +/- 1%; p less than 0.001). The beneficial effects of thrombolytic therapy on LV performance were closely associated with thrombolysis-induced limitation of infarct size. The dependence from infarct size of LV end-diastolic volume, LV end-systolic volume, and ejection fraction was not different in the 2 therapy groups. It was concluded that Witteveen's method of infarct size assessment is not influenced by the presence of reperfusion. Therefore, this method was recommended for trials on recanalization in patients with acute myocardial infarction.

Angiography↗
PubMed1990

Sensitivity of a set of myocardial infarction screening criteria in patients with anatomically documented single and multiple infarcts.

A subset of 3 screening criteria (Q wave greater than or equal to 30 ms in lead aVF, any Q or R wave less than or equal to 10 ms and less than or equal to 0.1 mV in lead V2, and R wave greater than or equal to 40 ms in V1) has been proposed to identify single nonacute myocardial infarcts. Cumulatively, these 3 criteria achieved 95% specificity, and 84 and 77% sensitivities for inferior and anterior myocardial infarcts, respectively, among patients identified by coronary angiography and left ventriculography. This study establishes the true sensitivities of the set of screening criteria in 71 patients with anatomically proven single myocardial infarcts and 32 patients with multiple myocardial infarcts. In the single inferior infarct group, the aVF criterion was 90% sensitive. The V2 criterion (any Q or R wave less than or equal to 10 ms and less than or equal to 0.1 mV) was 67% sensitive in the single anterior infarct group. No single criterion proved sensitive in identifying a posterolateral infarct. The set of screening criteria performed just as well for multiple infarcts as it did for single infarcts, with a cumulative sensitivity of 72%. The overall sensitivity of the screening set in the 103 patients in all groups was 71%.

Adult↗
PubMed1992

Influence of collateral filling of the occluded infarct-related coronary artery on prognosis after acute myocardial infarction.

Previous studies showed that long-term morbidity and mortality after acute myocardial infarction (AMI) are influenced by the presence or absence of anterograde flow in the infarct artery. In comparison with patients with anterograde flow, those whose infarct artery remains occluded are more likely to have unstable angina, recurrent AMI, congestive heart failure and sudden death. This study was performed to assess the influence of collateral filling of the infarct artery on long-term morbidity and mortality in surviving patients of initial AMI in whom the infarct artery was occluded. Over a 12.5-year period, 146 subjects (108 men and 38 women, aged 25 to 76 years) with AMI, no anterograde flow in the infarct artery, and no disease of other coronary arteries were medically treated and followed for 42 +/- 28 (mean +/- standard deviation) months. Of these subjects, 120 had angiographic evidence of collateral filling of the infarct artery (group I), whereas the remaining 26 did not (group II). The groups were similar in age, sex, cardioactive medications, left ventricular performance and infarct artery. They were also similar in incidence of unstable angina (19% of group I, 31% of group II; p = not significant [NS]), recurrent AMI (12% of group I, 8% of group II; p = NS), congestive heart failure (16% of group I, 12% of group II; p = NS) and cardiac death (16% of group I, 19% of group II; p = NS). Thus, angiographic evidence of collateral filling of the infarct artery in surviving patients of AMI exerts no demonstrable influence (beneficial or detrimental) on long-term morbidity or mortality.

Adult↗
PubMed1994

Isolated mid-anterior myocardial infarction: a special electrocardiographic sub-type of acute myocardial infarction consisting of ST-elevation in non-consecutive leads and two different morphologic types of ST-depression.

UNLABELLED: We describe eight patients with a distinct electrocardiographic pattern of anterior wall myocardial infarction characterized by three main features: (1) a pattern of 'transmural ischemia' (ST-elevation with positive T-wave) in non-consecutive leads: a VL and V2, and two different types of ST-depression; (2) a pattern of 'true reciprocal changes' (ST-depression and negative T-wave) in III and a VF; (3) a pattern of 'sub-endocardial ischemia' (ST-depression with positive T-wave) in V4-5, while ST in V3 was either isoelectric or depressed. We characterize the electrocardiographic features and correlate them with the echocardiographic, radionuclide, and angiographic data. All patients admitted to the coronary care unit from January 1990 to April 1992 with evolving acute myocardial infarction were evaluated prospectively. Patients whose admission electrocardiogram met the description above were included. The electrocardiographic evolution, echocardiographic, Technetium MIBI tomography, and coronary angiography are described. Of 471 patients with acute anterior wall myocardial infarction, admitted to the coronary care unit during the study period, eight patients met the inclusion criteria (1.7% of acute anterior wall myocardial infarction). Echocardiographic studies revealed mid-anterior hypokinesis in two patients, anterior and apical hypokinesis in one, and no wall motion abnormality in four patients. Technetium MIBI tomography, done in five patients, was consistent with mid-anterior or midanterolateral infarction without involvement of the septum or apex. Coronary angiography, performed in seven patients, demonstrated significant obstruction of the first diagonal branch in all of the patients. In four patients, the diagonal occlusion was the only significant coronary lesion in the left coronary artery. CONCLUSION: Most of the anterior myocardial infarctions also involve the septal and apical regions. Anterior wall myocardial infarctions limited to the mid-anterior or mid-anterolateral wall, without apical or septal wall involvement are relatively rare. This study describes a special electrocardiographic form of anterior wall acute myocardial infarction. This distinct electrocardiographic pattern represents true mid-anterior wall myocardial infarction, caused by occlusion of a first diagonal branch of the left anterior descending coronary artery. The septal and apical regions are not involved because the blood supply via the left anterior descending artery is not interrupted.

Coronary Angiography↗
PubMed1989

Medical and surgical management of early Q wave myocardial infarction. I. Effects of surgical reperfusion on survival, recurrent myocardial infarction, sudden death and functional class at 10 or more years of follow-up.

To define the outcome of patients given medical or surgical therapy for Q wave myocardial infarction, 387 patients were followed up for 10 to 13 years (mean 11.4). On study entry the groups had similar distributions for variables such as mean age, gender, previous myocardial infarction, abnormal creatine kinase activity, area of infarction, number of vessels diseased and clinical classification. The hospital mortality rate of the medical versus surgical group was 11.5% (23 of 200) versus 5.8% (11 of 187) (p = 0.07). Early reperfusion (that is, less than or equal to 6 h) resulted in a lower mortality rate than did medical therapy--2% (2 of 100) versus 11.5% (23 of 200) (p less than 0.05)--whereas the hospital mortality rate with late reperfusion was 10.3% (9 of 87). The long-term mortality rate of the medical and surgical groups was 41% (82 of 200) versus 27% (51 of 187) (p = 0.0007) with use of an adjusted Cox proportional hazards model. In the survivors, the differences between medical and surgical groups in recurrent myocardial infarction, mortality associated with reinfarction and sudden death were prospectively followed and evaluated by the life table method. Recurrent myocardial infarction was not prevented by surgical reperfusion or medical therapy (23% in both groups), however, the mortality rate in patients with recurrent infarction was higher in the medical therapy group--36.6% (15 of 41) versus 17.5% (7 of 40) (p = 0.04). The mortality difference did not depend on early or late surgical reperfusion. In the in-hospital survivors, the incidence of sudden death was 17.5% in the medical (31 of 177) versus 7.4% (13 of 176) in the surgical group (p = 0.01). This difference was much more pronounced in the early reperfusion group. Functional class was significantly lower than that for medical therapy in the early reperfusion but not the late reperfusion group. Thus, in comparable groups given medical and surgical therapy for acute myocardial infarction and followed up for greater than or equal to 10 years, surgical reperfusion appears to offer improved longevity in selected cases (when implemented early) but does not prevent recurrent myocardial infarction. The associated mortality with recurrent myocardial infarction is less as is the incidence of sudden death. Finally, lower functional class occurs most often in patients given early reperfusion.

Acute Disease↗
PubMed1989

Quantitative radionuclide assessment of regional ventricular function after thrombolytic therapy for acute myocardial infarction: results of phase I Thrombolysis in Myocardial Infarction (TIMI) trial.

In Thrombolysis in Myocardial Infarction (TIMI) Phase I,290 patients with acute myocardial infarction were randomized to either intravenous recombinant tissue-type plasminogen activator (rt-PA) or intravenous streptokinase. Two hundred twenty-nine patients had radionuclide ventriculograms at discharge for assessment of global and regional left ventricular ejection fraction. Among these 229 patients 185 had totally occluded infarct-related arteries, and angiographic reperfusion of the infarct-related artery occurred in 69% of patients treated with rt-PA and 28% of patients treated with streptokinase (p less than 0.001). Mean global left ventricular ejection fraction was not different for rt-PA-treated patients compared with streptokinase-treated patients (0.46 versus 0.45). However, the average regional ejection fraction of the regions subtended by the infarct-related artery showed a trend toward better average infarct region ejection fraction in patients treated with rt-PA than in patients treated with streptokinase (0.40 versus 0.36; 0.05 less than p less than 0.06). Analysis of data according to perfusion status of the infarct-related artery showed no difference in mean global left ventricular ejection fraction between patients with sustained versus nonsustained reperfusion (0.47 versus 0.44). However, there was better average regional ejection fraction of the region subtended by the infarct-related artery in patients with sustained reperfusion (0.40 versus 0.36; p less than 0.01). Thus, quantitation of regional left ventricular function by radionuclide techniques provides a noninvasive means for evaluating the effects of thrombolysis. This study suggests a direct relation between improvement of regional left ventricular function and the greater infarct-related artery patency rate achieved by rt-PA compared with streptokinase.

Aged↗
PubMed1995

ST segment tracking for rapid determination of patency of the infarct-related artery in acute myocardial infarction.

OBJECTIVES: This study was designed to test the hypothesis that monitoring the ST segment on a single electrocardiographic (ECG) lead reflecting activity in the infarct zone provides sensitive and specific recognition of reperfusion within 60 min of initiation of therapy in acute myocardial infarction. BACKGROUND: Infarct-related arteries that fail to recanalize early may benefit from immediate rescue angioplasty. Hence, detection of reperfusion has important practical clinical implications. METHODS: Of 41 patients with acute myocardial infarction who had ambulatory ECG (Holter) monitors placed, 38 had adequate ST segment monitoring for 3 h; 35 of the 38 were treated with thrombolytic agents and 3 with primary angioplasty. All patients underwent early coronary angiography and were classified into two groups: Group P (22 patients) had angiographic patency (Thrombolysis in Myocardial Infarction [TIMI] grade 2 or 3 flow), the Group O (16 patients) had persistent occlusion (TIMI grade 0 or 1 flow) of the infarct-related vessel at 60 min from initiation of therapy. The initial ST segment level was defined as the first ST segment level recorded; the peak ST segment level was defined as the highest ST segment level measured during the 1st 60 min. To assess the optimal ST segment recovery criteria for reperfusion, the presence or absence of a > or = 75%, > or = 50% and > or = 25% decrement from initial and peak ST segment levels, sampled and analyzed at 2.5-, 5-, 10-, 15-and 20-min intervals, was correlated with patency of the infarct-related artery at 60 min. RESULTS: ST segment recovery of > or = 50% reduction from peak ST segment levels with sampling rates at < or = 10-min intervals provided the optimal criterion for recognizing coronary artery patency at 60 min (sensitivity 96%, 95% confidence interval [CI] 77% to 99%; specificity 94%, 95% CI 69% to 99%, p < 0.0001). The subgroup of 13 patients in Group P with TIMI grade 3 reperfusion flow all met this criterion (sensitivity 100%, 95% CI 75% to 100%). The use of the initial ST segment level as the baseline for determining the presence of a > or = 50% reduction in ST segment levels within 60 min was less sensitive. Prediction of coronary reperfusion within 60 min of therapy on the basis of a > or = 75% decrement from peak ST segment levels was less sensitive, and the use of a > or = 25% decrement was less specific. CONCLUSIONS: ST segment monitoring of a single lead reflecting the infarct zone provides a reliable method for assessing reperfusion within 60 min of acute myocardial infarction. Optimal criteria for ECG reperfusion include a > or = 50% decrease from peak ST segment levels, with ST segment measurements recorded continuously or at least every 10 min.

Anistreplase↗
PubMed1995

One-year results of the Thrombolysis in Myocardial Infarction (TIMI) IIIB clinical trial. A randomized comparison of tissue-type plasminogen activator versus placebo and early invasive versus early conservative strategies in unstable angina and non-Q wave myocardial infarction.

OBJECTIVES: We report mortality, infarction, revascularization and repeat hospital admission events for 1 year after enrollment and randomization in the Thrombolysis in Myocardial Ischemia (TIMI) IIIB clinical trial. BACKGROUND: The purpose of this trial was to investigate the role of a thrombolytic agent added to conventional medical therapies and to compare an early invasive management strategy to a more conservative early strategy in patients with unstable angina and non-Q wave myocardial infarction. METHODS: There were 1,473 patients enrolled, and they received conventional anti-ischemic medical therapies. They were randomized to therapy with either tissue-type plasminogen activator (t-PA) or placebo and also to an early invasive management strategy with coronary arteriography at 18 to 48 h, followed by revascularization as soon as possible if appropriate, or, alternatively, to an early conservative strategy with arteriography and revascularization reserved for failure of initial therapy to prevent recurrent ischemia. The primary end point was a composite outcome variable and was assessed at 42 days. Patients were then managed entirely at the discretion of their treating physician. Follow-up contacts were made at 1 year. RESULTS: The incidence of death or nonfatal infarction for the t-PA- and placebo-treated groups was similar after 1 year (12.4% vs. 10.6%, p = 0.24). The incidence of death or nonfatal infarction was also similar after 1 year for the early invasive and early conservative strategies (10.8% vs. 12.2%, p = 0.42). A trial of this size should be able to detect differences in relative risk for death or infarction > or = 1.81 with a power of 80% at a significance level (alpha) of 0.01. Revascularization by 1 year was common, but was slightly more common with the early invasive than the early conservative strategy (64% vs. 58%, p < 0.001). This result was related entirely to a small difference in angioplasty rates (39% vs. 32%, p < 0.001) inasmuch as rates of bypass grafting by 1 year were equivalent (30% in each group, p = 0.50). The high rate of revascularization in both strategies was accompanied by comparable clinical status at the 1-year follow-up contact. CONCLUSIONS: In this large study of unstable angina and non-Q wave myocardial infarction, the incidence of death and nonfatal infarction or reinfarction was low but not trivial after 1 year (4.3% mortality, 8.8% nonfatal infarction). An early invasive management strategy was associated with slightly more coronary angioplasty procedures but equivalent numbers of bypass surgery procedures than a more conservative early strategy of catheterization and revascularization only for signs of recurrent ischemia. The incidence of death or nonfatal infarction, or both, did not differ after 1 year by strategy assignment, but fewer patients in the early invasive strategy group underwent later repeat hospital admission (26% vs. 33%, p < 0.001). Either strategy is appropriate for patient management; differences in hospital admissions and revascularization procedures, with their attendant costs, are likely to be minimal.

Adult↗
PubMed1996

Importance of infarct-related artery patency for recovery of left ventricular function and late survival after primary angioplasty for acute myocardial infarction.

OBJECTIVES: The purpose of this study was to evaluate the importance of late infarct-related artery patency for recovery of left ventricular function and late survival after primary angio-plasty for acute myocardial infarction. BACKGROUND: Infarct-related artery patency is thought to improve late survival by its effect on preservation of left ventricular function. Patency may also enhance late survival by preventing left ventricular dilation and reducing arrhythmias, independent of myocardial salvage. However, most studies have not shown patency to be an independent predictor of survival when late left ventricular function is taken into account. METHODS: We followed up 576 hospital survivors of acute myocardial infarction treated with primary angioplasty for 5.3 years. Ejection fraction and infarct-related artery patency were determined at follow-up catheterization at 6 months. Predictors of late cardiac survival were determined using Cox regression models. RESULTS: Patients with patent arteries had more improvement and a better late ejection fraction than patients with occluded arteries (56.3% vs. 47.9%, p = 0.001). In patients with acute ejection fraction < 45%, late survival was better in those with patent versus occluded arteries (89% vs. 44%, p = 0.003), but patency was not a significant predictor after improvement in ejection fraction was taken into account. In patients with a large anterior infarction, patency was a significant independent predictor of late survival. CONCLUSIONS: Infarct-related artery patency is important for recovery of left ventricular function, and in patients with acute ejection fraction < 45%, patency is important for late survival. Our data are consistent with the hypothesis that the survival benefit is due primarily to the effect of patency on recovery of left ventricular function. In patients with a large anterior infarction, patency appears to provide an additional late survival benefit independent of myocardial salvage. These observations support the need for additional clinical trials of late reperfusion in patients with a large anterior infarction.

Angioplasty, Balloon, Coronary↗
PubMed2006

Cardiac troponin T at 96 hours after acute myocardial infarction correlates with infarct size and cardiac function.

OBJECTIVES: In clinical practice, myocardial infarct size can be estimated non-invasively by nuclear imaging techniques or contrast-enhanced magnetic resonance imaging (CE-MRI). Due to limited availability and high costs, serologic tests are frequently used as an alternative. BACKGROUND: We examined the ability of a single value of cardiac troponin T (cTnT) 96 h after onset of ST-/non-ST-segment elevation myocardial infarction (STEMI/NSTEMI) to estimate absolute infarct mass. METHODS: Functional and CE-MRI were conducted on a 1.5-T whole-body system 4 days after STEMI/NSTEMI using gadolinium (0.2 mmol/kg/bw). Infarct sizes were measured employing a specified software (Philips Medical Systems, Best, the Netherlands) and correlated with TnT measurements 96 h after onset of STEMI/NSTEMI. RESULTS: We enrolled 23 STEMI and 21 NSTEMI patients. Median time delay from onset of symptoms to balloon angioplasty was 6.25 and 9.9 h for STEMI/NSTEMI patients, respectively. Contrast-enhanced magnetic resonance imaging (median 4 days) revealed an absolute mean infarct size of 16.2 g (7.7 to 30.1 g) with a mean ejection fraction of 58% (53% to 63%) and mean stroke volume of 84 ml (75 to 107 ml). Absolute infarct sizes and median cTnT values were larger in STEMI than in NSTEMI (29.3 g [interquartile range (IQR) 16.0 to 53.0] and 1.88 microg/l [IQR 0.7 to 2.57] vs. 8.8 g [IQR 3.3 to 16.4] and 0.83 microg/l [IQR 0.4 to 1.3], both p < 0.02). Linear regression analysis was excellent for STEMI (r = 0.910) and moderate albeit still significant for NSTEMI (r = 0.575). CONCLUSIONS: A single 96-h cTnT value provides an accurate estimate of absolute infarct mass in myocardial infarction. The ability to quantify and the potential to distinguish effects of novel drug regimens on infarct size make cTnT attractive for routine practice and as a clinical end point.

Aged↗
PubMed2002

Infarct restraint attenuates remodeling and reduces chronic ischemic mitral regurgitation after postero-lateral infarction.

BACKGROUND: Chronic ischemic mitral regurgitation (IMR) is produced by adverse postinfarction ventricular remodeling. We hypothesize that restraining infarct expansion reduces left-ventricular (LV) dilatation and the severity of mitral regurgitation. METHODS: Two groups of 6 sheep had coronary snares placed around the second and third obtuse marginal coronary arteries and four piezoelectric transducers sutured within myocardium across the mid short axis of the LV. In one group, a patch of Marlex mesh was precisely fitted and lightly sutured to myocardium destined for infarction (determined by temporary snare occlusion). Two weeks after instrumentation, coronary snares were tied tight to infarct approximately 24% of the posterolateral LV mass. Transdiaphragmatic echocardiograms were obtained in all animals at baseline, and 30 minutes, and 2, 5, and 8 weeks after infarction. RESULTS: Echocardiograms confirmed similar infarct sizes and locations in both groups. Eight weeks after infarction, IMR grade averaged 3.6+ (scale: 0, no MR; 4, severe MR) in control sheep and 1.9+ in mesh-restrained animals (p = 0.0001). LV end-diastolic and end-systolic volumes at the eighth week were less in mesh-treated sheep (87 +/- 11.3 vs 113 +/- 18.3; 61 +/- 10.6 vs 77 +/- 14.1, respectively), but differences were not significant. Data from mid short axis piezoelectric transducers indicated significantly less strain in the infarcted myocardium in mesh-restrained sheep than in control. CONCLUSIONS: Early restraint of postero-lateral infarct expansion attenuates the severity of ischemic mitral regurgitation and slows ventricular dilatation. However, the remodeling process is not arrested 8 weeks after infarction.

Animals↗
PubMed1984

Relation between the location of the infarcted area in body surface isopotential mapping and the location of myocardial infarction in vectorcardiography.

In order to examine whether our method of determining the location of the infarcted area in body surface isopotential mapping (MAP) is adequate for clinical use, a comparison was made between the location of the infarcted area using MAP and the location of myocardial infarction using vectorcardiography (VCG). The percentage of agreement between MAP and VCG in the retrospective study was 91.7% in the anterior wall, 76.7% in the lateral wall, 93.3% in the inferior wall and 73.3% in the posterior wall. The reason for the disagreement between these two methods was investigated, and criteria for determining the infarcted area using MAP and vectorcardiographic criteria for myocardial infarction were partly corrected in anterior, lateral and (high) posterior infarction to increase the clinical accuracy of both methods. Consequently, the percentage of agreement in the four walls ranged from 83.7% to 87.9%, and the diagnostic value of MAP for the infarcted area was not inferior but was more sensitive than that of VCG except in anterior infarction. In the prospective study, the same result was obtained. Secondly, in order to establish the superiority of MAP or VCG, the sensitivity and specificity of MAP and VCG to SCG (thallium-201) were calculated. Except in the anterior wall, the sensitivity of MAP to SCG was higher than that of VCG to SCG, especially in the lateral and posterior walls. Accordingly, it is suggested that MAP is the method of choice in determining the infarcted area in clinical cases.

Electrocardiography↗
PubMed2002

The effect of blockade of the CD11/CD18 integrin receptor on infarct size in patients with acute myocardial infarction treated with direct angioplasty: the results of the HALT-MI study.

OBJECTIVE: The purpose of this study was to determine whether Hu23F2G (LeukoArrest), an antibody to the CD11/CD18 integrin receptors, would reduce infarct size in patients undergoing primary angioplasty for an acute myocardial infarction. BACKGROUND: Reperfusion injury in acute myocardial infarction has been shown experimentally to be related to neutrophil accumulation. Inhibitors of the CD11/CD18 or CD18 integrin receptors have been shown to reduce infarct size in experimental models. METHODS: Patients within 6 h of onset of chest pain with ST-segment elevation were randomized to receive either 0.3 mg/kg or 1.0 mg/kg of Hu23F2G or placebo just before angioplasty of occluded arteries (Thrombolysis in Myocardial Infarction TIMI flow grade 0 or 1). The primary end point was infarct size as measured by sestamibi single-photon emission computed tomography (SPECT) scan five to nine days later. RESULTS: Four-hundred and twenty patients were enrolled and received a placebo or the study drug. The groups did not differ in baseline or angiographic characteristics or angioplasty results. Infarct size was 16%, 17.2% and 16.6%, for placebo, 0.3 mg/kg and 1.0 mg/kg, respectively, of the left ventricle (p = NS). No differences were evident in those patients with anterior myocardial infarction or those presenting within 2 h of onset of chest pain. Corrected TIMI frame count was also not different between groups. Clinical events at 30 days were very low, with a mortality of 0.8%, 1.4% and 3.3%, respectively. The drug was well tolerated, with a slight increase in minor infections in the high dose group. CONCLUSIONS: The results of this multicenter, double-blind, placebo-controlled, randomized clinical trial demonstrated that an antibody to CD11/CD18 leukocyte integrin receptor did not reduce infarct size in patients who underwent primary angioplasty.

Angioplasty, Balloon, Coronary↗
PubMed1983

Comparison of radionuclide and enzymatic estimate of infarct size in patients with acute myocardial infarction.

A comparison was made of the estimated size of the myocardial infarction occurring in 26 patients with a first infarction using creatine kinase (CK) enzyme release between radionuclide gated blood pool measurement of total and regional ventricular function and thallium-201 scintigraphic measurement of myocardial perfusion defects. Creatine kinase estimates of infarct size (enzymatic infarct size) correlated closely with the percent of abnormal contracting regions, left ventricular ejection fraction and thallium-201 estimates of percent of abnormal perfusion area (r = 0.78, 0.69 and 0.74, respectively, p less than 0.01). A close correlation also existed between percent abnormal perfusion area and percent of abnormal contracting regions (r = 0.81, p less than 0.01) and left ventricular ejection fraction (r = 0.69, p less than 0.01). Enzymatic infarct size was larger in anterior (116 +/- 37 CK-g-Eq) than inferior (52 +/- 29 CK-g-Eq) myocardial infarction (p less than 0.01) and was associated with significantly more left ventricular functional impairment as determined by left ventricular ejection fraction (33 +/- 7 versus 60 +/- 10%) (p less than 0.01) and percent abnormal perfusion area (58 +/- 14 versus 13 +/- 12) (p less than 0.01). No significant correlation was observed between enzymatic infarct size and right ventricular ejection fraction. These different methods of estimating infarct size correlated closely with each other in these patients with a first uncomplicated myocardial infarction.

Adult↗
PubMed1985

Coronary angiographic morphology in myocardial infarction: a link between the pathogenesis of unstable angina and myocardial infarction.

It has previously been shown that analysis of coronary morphology can separate unstable from stable angina. An eccentric stenosis with a narrow neck or irregular borders, or both, is very common in patients who present with acute unstable angina, whereas it is rare in patients with stable angina. To extend these observations to myocardial infarction, the coronary morphology of 41 patients with acute or recent infarction and nontotally occluded infarct vessels was studied. For all patients, 27 (66%) of 41 infarct vessels contained this eccentric narrowing, whereas only 2 (11%) of 18 noninfarct vessels with narrowing of 50 to less than 100% had this lesion (p less than 0.001). In addition, a separate group of patients with acute myocardial infarction who underwent intracoronary streptokinase infusion were also analyzed in similar fashion. Fourteen (61%) of 23 infarct vessels contained this lesion after streptokinase infusion compared with 1 (9%) of 11 noninfarct vessels with narrowing of 50 to less than 100% (p less than 0.01). Therefore, an eccentric coronary stenosis with a narrow neck or irregular borders, or both, is the most common morphologic feature on angiography in both acute and recent infarction as well as unstable angina. This lesion probably represents either a disrupted atherosclerotic plaque or a partially occlusive or lysed thrombus, or both. The predominance of this morphology in both unstable angina and acute infarction suggests a possible link between these two conditions. Unstable angina and myocardial infarction may form a continuous spectrum with the clinical outcome dependent on the subsequent change in coronary supply relative to myocardial demand.

Angina Pectoris↗
PubMed1985

Prevalence and significance of residual flow to the infarct zone during the acute phase of myocardial infarction.

Residual flow to the infarct zone was assessed by coronary angiography during the acute phase of myocardial infarction in 130 patients. In 36 patients, the infarct-related coronary artery was not completely obstructed, thereby providing residual anterograde flow to the infarct area (Group I). Complete obstruction of the infarct vessel with residual flow to the infarct zone by means of collateral circulation was observed in 56 patients (Group II). Complete obstruction of the infarct vessel without residual flow was seen in 38 patients (Group III). Ejection fraction during the acute phase of infarction was found to be significantly higher in Group I (55 +/- 13%) than in either Group II (48 +/- 13%) or Group III (50 +/- 10%) (p less than 0.05). Group II patients had a longer history of angina pectoris (14.2 +/- 21.4 months) than did Group III patients (0.7 +/- 3.1 months) (p less than 0.01). Patients in Group I and Group II were more likely to be taking antianginal medication (56 and 54%, respectively) than were the patients in Group III (16%) (p less than 0.01). Thirty-seven patients in whom reperfusion techniques were not employed had repeat angiography in the chronic phase of infarction, enabling assessment of spontaneous changes in left ventricular function and coronary morphology.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Infarct artery perfusion and changes in left ventricular volume in the month after acute myocardial infarction.

The relation between perfusion of the infarct-related artery and changes in left ventricular volume and function during the month after a first myocardial infarction was examined in 40 patients who did not receive thrombolytic therapy. Infarct artery perfusion was documented at predischarge coronary angiography, and left ventricular volume was measured by nongeometric analysis of radionuclide angiograms performed within 48 hours of infarction and at 1 month. Left ventricular dilation (greater than or equal to 20% increase in volume) developed in 16 patients, whereas 5 patients had a decrease in left ventricular volume of greater than or equal to 20% by 1 month. Left ventricular dilation occurred in all 14 patients without perfusion of the infarct-related artery, compared with only 2 of 26 patients with perfusion of this artery due to subtotal occlusion or collateral vessels. All five patients whose left ventricular volume decreased by greater than or equal to 20% had a perfused infarct artery. Multiple linear regression analysis confirmed that the degree of perfusion of the infarct artery (partial r = 0.58, p = 0.001) was a more important predictor of volume change than was infarct size measured by peak creatine kinase (partial r = 0.30, p = 0.009) or QRS score (partial r = 0.20, p = 0.087). Left ventricular ejection fraction decreased from 0.38 +/- 0.10 to 0.30 +/- 0.16 (p = 0.05) in 11 patients with an anterior infarct and ventricular dilation; it increased from 0.45 +/- 0.10 to 0.62 +/- 0.07 (p = 0.02) in the 5 patients with a greater than or equal to 20% decrease in volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

The prehospital electrocardiogram in acute myocardial infarction: is its full potential being realized? National Registry of Myocardial Infarction 2 Investigators.

OBJECTIVES: This study sought to examine the management and subsequent outcomes of patients with a prehospital electrocardiogram (ECG) in a large, voluntary registry of myocardial infarction. BACKGROUND: The prehospital ECG has been proposed as a means of rapidly identifying patients with acute myocardial infarction who might be eligible for reperfusion therapy. METHODS: The characteristics and outcomes of patients with a prehospital ECG were compared with those without a prehospital ECG in the National Registry of Myocardial Infarction 2 data base. Included in the analysis were those patients who presented to the hospital within 12 h of an acute myocardial infarction. Excluded were patients with an in-hospital infarction, transferred-in referrals and self-transported patients. RESULTS: Prehospital ECGs were obtained in 3,768 (5%) of 66,995 National Registry of Myocardial Infarction 2 patients meeting study criteria. Median time from myocardial infarction symptom onset until hospital arrival was longer among those having a prehospital ECG (152 vs. 91 min, p < 0.001). However, once in the hospital, the prehospital ECG group experienced a shorter median time to the initiation of either thrombolysis (30 vs. 40 min, p < 0.001) or primary angioplasty (92 vs. 115 min, p < 0.001). The prehospital ECG group was more likely to receive thrombolytic therapy (43% vs. 37%, p < 0.001) and to undergo primary angioplasty (11% vs. 7%, p < 0.001). Also, the prehospital ECG group was more likely to undergo coronary arteriography (55% vs. 40%, p < 0.001), angioplasty (24% vs. 16%, p < 0.001) or bypass surgery (10% vs. 6%, p < 0.001). The in-hospital mortality rate was 8% in patients with a prehospital ECG and 12% in those without a prehospital ECG (p < 0.001). After adjusting for baseline covariates utilizing multiple logistic regression analysis, this mortality difference remained statistically significant (odds ratio 0.83, 95% confidence interval 0.71 to 0.96, p = 0.01). CONCLUSIONS: The prehospital ECG is infrequently utilized for diagnosing myocardial infarction, and among patients with a prehospital ECG, is associated with a longer time from symptom onset to hospital arrival. Despite these shortcomings, the prehospital ECG is a test that may potentially influence the management of patients with acute myocardial infarction through wider, faster in-hospital utilization of reperfusion strategies and greater usage of invasive procedures, factors that may possibly reduce shortterm mortality. Efforts to implement the prehospital ECG more widely and more rapidly may be indicated.

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