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PubMed1987

Effectiveness of intravenous streptokinase on infarct size and left ventricular function in acute myocardial infarction. Prospective and randomized study.

Within 3 h after the onset of symptoms of myocardial infarction, 64 patients were randomly assigned to receive either a 1-h intravenous infusion of 1,500,000 IU of streptokinase (SK) or a conventional therapy. Infarct size was estimated in CK gram equivalent (CKg) by measurement of CK-MB every 3 hours during a 48-h period. Enzymatic study revealed that myocardial infarction of the SK group was significantly smaller (61.4 +/- 45 vs. 89.4 +/- 56 CKg, p less than .05). Angiograms were performed at early stage and five weeks after myocardial infarction. At first coronary angiogram, the infarct-related vessel was open in 82% in the SK group versus 12% in controls. The SK group had higher global ejection fraction at second angiogram (57 +/- 11% vs. 49 +/- 11%, p less than .02), but differences in regional wall motion were not significant. By analysis according to patency or occlusion of infarct-related vessel, global and regional ejection fractions were significantly better at first and at second angiograms in all patients and in anterior infarctions with a patent infarct-related coronary artery. There was no significant difference for inferior infarction. We conclude that intravenous streptokinase infusion early after the onset of myocardial infarction reduces infarct size and improves left ventricular function, chiefly in anterior infarction. This benefit appears to be closely correlated to patency of infarct-related vessels.

Acute Disease↗
PubMed1997

Adenosine technetium-99m sestamibi single-photon emission tomography for the assessment of jeopardized myocardium early after acute myocardial infarction. Paradoxical scintigraphic underestimation of jeopardized myocardium in patients with a severe infarct-related stenosis.

This study investigated the value of technetium-99m sestamibi scintigraphy in identifying patients at risk for post-infarct ischaemia (=jeopardized myocardium), especially within the reperfused infarct region. In 51 patients with a recent (<1 month) myocardial infarction, adenosine 99mTc-sestamibi single-photon emission tomography (SPET) and dobutamine stress echocardiography (DSE) were performed and correlated with the presence of significant coronary artery stenosis [% diameter stenosis (DS) >50%] on quantitative coronary angiography. Regional perfusion activity was analysed semi-quantitatively (score 0-4) on a 13-segment left ventricular model. DSE was used for the estimation of the infarct size (low-dose DSE) and for concomitant evaluation of ischaemia (high-dose DSE). A reversible perfusion defect within the infarct region was observed in 20 of the 37 patients with a significant infarct-related lesion (sensitivity of 54%) and only in one patient without a significant infarct-related lesion (specificity of 93%). Further analysis revealed that the scintigraphic assessment of jeopardized myocardium was fairly good in patients with a moderate (DS 51%-64%) infarct-related stenosis but was inadequate in patients with a severe (DS>/=65%) infarct-related stenosis (sensitivity of 80% vs 36%, P<0.01), while the echocardiographic detection of ischaemia was not influenced by stenosis severity (sensitivity of 73% in both subgroups). This scintigraphic underestimation of jeopardized myocardium was mainly related to a severely impaired myocardial perfusion under baseline conditions, as was evidenced by a significantly more severe rest perfusion score in the infarct region in patients with a severe stenosis as compared to those with a moderate stenosis (average score: 1.5+/-0.7 vs 2.1+/-0.6, P<0.01), while infarct size on echocardiography was similar for both subgroups. It may be concluded that early after an acute myocardial infarction, adenosine 99mTc-sestamibi SPET may underestimate reperfused but still jeopardized myocardium, particularly in patients with a severe infarct-related stenosis. In these patients the evaluation of the ischaemic burden on rest-stress scintigraphy is hampered by the presence of a severely impaired myocardial perfusion in resting conditions.

Adenosine↗
PubMedDate not supplied

Comparison of reinjection thallium 201 and resting technetium 99m sestamibi tomographic images for the quantification of infarct size after acute myocardial infarction.

BACKGROUND: Both thallium 201 and technetium 99m sestamibi have been used to quantitate infarct size at rest. Exercise 201Tl scintigraphy has been shown to have powerful prognostic information after myocardial infarction. A single study using these agents that could provide data on infarct size and prognosis would be of value. The purpose of this study was to compare estimates of infarct size by use of 201Tl and 99mTc sestamibi and to correlate these measurements with left ventricular ejection fraction in patients after acute myocardial infarction. METHODS AND RESULTS: The study group consisted of 20 patients who underwent low-level 201Tl stress studies with reinjection and 99mTc sestamibi resting studies within 4 days. Acute reperfusion was attempted in 18 of 20 patients. For 99mTc sestamibi tomographic imaging, infarct size was quantitated with 60% of maximal counts per slice for five short-axis slices as described in multiple previous studies. The postreinjection delayed 201Tl images acquired 4 hours after stress were quantitated according to the same threshold method. 201Tl patient images were also quantitated with a commercially available polar map program and compared with sex-matched control subjects. Ejection fraction was determined for each patient by radionuclide ventriculography 6 weeks later. Ejection fraction was well preserved for the group: mean 0.53 +/- 0.10. Infarct size with 99mTc sestamibi was 12% +/- 13% of the left ventricle, which was significantly smaller than either method with 201Tl: threshold method, 29% +/- 18% of left ventricle; polar map method, 25% +/- 17% of left ventricle (both 201Tl estimates, p < 0.0001 vs 99mTc sestamibi; 201Tl, 70% threshold vs 201Tl polar map, p = 0.04). There was a significant correlation between infarct size with 99mTc sestamibi and that with 201Tl (r = 0.72 to 0.73; p < 0.001). Infarct size with 99mTc sestamibi, however, provided the closest correlation with ejection fraction (r = 0.81; p < 0.001), with the two 201Tl quantitative methods providing very similar correlations (r = 0.69; p < 0.001). CONCLUSIONS: Infarct size with reinjection 201Tl imaging correlates significantly with resting infarct size with 99mTc sestamibi, although it provides significantly larger estimates. Although both approaches can be combined with a same-day exercise protocol, the closer correlation of infarct size with ejection fraction at 6 weeks suggests that resting infarct size with 99mTc sestamibi may be slightly more accurate.

Aged↗
PubMed1985

Clinical significance of "reciprocal" S-T segment depression in acute myocardial infarction. Relative contributions of infarct size and ischemia at a distance.

The early electrocardiographic results in 100 patients surviving their first myocardial infarction who thereafter underwent serial radionuclide ventriculography were reviewed. Site of infarction was anterior in 46 and inferior in 54, with lateral extension in two patients. Those with "reciprocal" S-T segment depression of more than 1 mm in the acute phase (n = 53) sustained larger infarcts on the basis of enzyme criteria (mean peak serum creatine kinase, +/- SD, 2,203 +/- 1,271 versus 1,544 +/- 1,197 IU/liter, p less than 0.02), with a higher incidence of ventricular akinesis and dyskinesis. Reciprocal change was more common during inferior infarction (n = 33) than anterior infarction (n = 20). Despite equivalent peak enzyme levels following anterior and inferior infarction with reciprocal S-T depression (mean peak creatine kinase 2,330 versus 2,128, NS), there was marked sparing of left ventricular function in the latter group (mean left ventricular ejection fraction 0.31 +/- 0.14 versus 0.42 +/- 0.09, p less than 0.01). Of 17 patients who died within two years of infarction, 14 had reciprocal changes. Patients who died after anterior infarction with reciprocal changes (n = 5) had poor left ventricular function compared with those who died after inferior infarction (n = 9; left ventricular ejection fraction, +/- SD, 0.21 +/- 0.05 versus 0.38 +/- 0.11, p less than 0.01). One third of those recovering from inferior infarction with reciprocal changes subsequently had positive results on exercise testing, and of the nine patients who died, five had good left ventricular function (left ventricular ejection fraction 0.44 to 0.50). Infarct size and ventricular wall motion abnormality proved to be of major importance in the production of inferior reciprocal S-T change during anterior infarction, and subsequent mortality was related to poor left ventricular function. The proximity of the precordial leads to left ventricular myocardium may increase the detection of concomitant anterior ischemia during inferior infarction, and those who exhibit reciprocal change are presumably at risk from left main stem or anterior descending lesions but with reasonably good ventricular function represent a more attractive population for invasive investigation.

Creatine Kinase↗
PubMed1993

Effects of tissue plasminogen activator therapy on the frequency of acute right ventricular myocardial infarction associated with acute left ventricular infarction.

To assess the effects of reperfusion therapy on acute right ventricular myocardial infarction, we studied at necropsy the hearts from 51 patients who died after receiving intravenous recombinant tissue plasminogen activator for acute left ventricular myocardial infarction as part of the Thrombolysis in Myocardial Infarction (TIMI) study. Right ventricular infarction occurred in none of 29 patients with infarction of the anterior wall of the left ventricle and in 8 of 22 patients (36%) with infarction of the posterior (inferior) wall of the left ventricle. Of the 22 patients with posterior wall infarction, the 8 patients with right ventricular infarction were compared to the 14 patients without right ventricular infarction. The patients with right ventricular infarction had a longer mean interval from tissue plasminogen activator infusion to peak creatine phosphokinase level (19 vs. 11 h, P < 0.03), a lower frequency of hemorrhagic necrosis (2 of 8 vs. 10 of 14, P < 0.04) and higher frequency of luminal thrombus in the infarct-related coronary artery (6 of 8 vs. 3 of 14, P = 0.054). Each of these findings is associated with the absence of coronary reperfusion. Thus, successful reperfusion following acute left ventricular myocardial infarction appears to be associated with a decreased frequency of concomitant right ventricular myocardial infarction.

Creatine Kinase↗
PubMed1988

A comprehensive analysis of myocardial infarction due to left circumflex artery occlusion: comparison with infarction due to right coronary artery and left anterior descending artery occlusion.

Forty consecutive patients with creatine kinase-MB confirmed myocardial infarction due to circumflex artery occlusion (Group 1) were prospectively evaluated and compared with 107 patients with infarction due to right coronary artery occlusion (Group 2) and 94 with left anterior descending artery occlusion (Group 3). All 241 patients underwent exercise thallium-201 scintigraphy, radionuclide ventriculography, 24 h Holter electrocardiographic (ECG) monitoring and coronary arteriography before hospital discharge and were followed up for 39 +/- 18 months. There were no significant differences among the three infarct groups in age, gender, number of risk factors, prevalence and type of prior infarction, Norris index, Killip class and frequency of in-hospital complications. Acute ST segment elevation was present in only 48% of patients in Group 1 versus 71 and 72% in Groups 2 and 3, respectively (p = 0.012), and 38% of patients with a circumflex artery-related infarct had no significant ST changes (that is, elevation or depression) on admission (versus 21 and 20% for patients in Groups 2 and 3, respectively) (p = 0.001). Abnormal R waves in lead V1 were more common in Group 1 than in Group 2 (p less than 0.003) as was ST elevation in leads I, aVL and V4 to V6 (p less than or equal to 0.048). These differences in ECG findings between Group 1 and 2 patients correlated with a significantly higher prevalence of posterior and lateral wall asynergy in the group with a circumflex artery-related infarct. Infarct size based on peak creatine kinase levels and multiple radionuclide variables was intermediate in Group 1 compared with that in Group 2 (smallest) and Group 3 (largest). During long-term follow-up, the probability of recurrent cardiac events was similar in the three infarct groups. When patients with a circumflex artery-related infarct were stratified according to the presence or absence of abnormal R waves in lead V1 or V2, the abnormal R wave group had more admission ST elevation (p = 0.025), a larger infarct (p less than 0.05) and more extensive coronary artery disease (p = 0.027). In fact, all patients with a circumflex artery-related infarct and an abnormal R wave in lead V1 had multivessel disease. An abnormal R wave in lead V1 had a 96% specificity for circumflex versus right coronary artery-related infarction but a sensitivity of only 21%. Discriminate function analysis of all admission historical and ECG variables identified inferior and lateral ST elevation as independent predictors of circumflex artery-related infarction...

Angiography↗
PubMed1989

Multicenter trial of intravenous anisoylated plasminogen streptokinase activator complex (APSAC) in acute myocardial infarction: effects on infarct size and left ventricular function.

Two hundred thirty-one patients with a first acute myocardial infarction were randomly allocated within 5 h after the onset of symptoms either to treatment with anisoylated plasminogen streptokinase activator complex (APSAC), 30 U over 5 min, or to conventional heparin therapy, 5,000 IU in a bolus injection. Heparin was reintroduced in both groups 4 h after initial therapy at a dosage of 500 IU/kg per day. One hundred twelve patients received APSAC and 119 received heparin within a mean period of 188 +/- 62 min after the onset of symptoms. Both groups were similar in age, location of the acute myocardial infarction, Killip functional class and time of randomization. Elective coronary arteriography was performed on an average of 4 +/- 1.2 days after initial therapy. Follow-up radionuclide angiography and thallium-201 single photon emission computed tomography were performed before hospital discharge. Infarct size was estimated from single photon emission computed tomography and expressed as a percent of total myocardial volume. The patency rate of the infarct-related artery was 77% in the APSAC group and 36% in the heparin group (p less than 0.001). Left ventricular ejection fraction determined from contrast angiography was significantly higher in the APSAC group than in the heparin group. This was true for the entire study group (0.53 +/- 0.13 versus 0.47 +/- 0.12; p = 0.002) as well as for the subgroups of patients with anterior and inferior wall infarction (0.47 +/- 0.13 versus 0.40 +/- 0.11; p = 0.04 and 0.56 +/- 0.10 versus 0.51 +/- 0.11; p = 0.02, respectively). At 3 weeks, the difference remained significant for the anterior myocardial infarction subgroup. A significant 31% reduction in infarct size was found in the APSAC group (33% for the anterior infarction subgroup [p less than 0.05] and 16% for the inferior infarction subgroup [p = NS]). A close inverse relation was found between the values of left ventricular ejection fraction and infarct size (r = -0.73, p less than 0.01). By the end of a 3 week follow-up period, seven APSAC-treated patients and six heparin-treated patients had died. In conclusion, the early infusion of APSAC in acute myocardial infarction produced a high early patency rate, significant limitation of infarct size and significant preservation of left ventricular systolic function, mainly in anterior wall infarction.

Acute Disease↗
PubMed2005

Analysis of the extension of Q-waves after infarction with body surface map: relationship with infarct size.

AIMS: We aimed to characterize the extension of Q-waves after a first ST-segment elevation myocardial infarction using body surface map (BSM) and its relationship with infarct size quantified with cardiovascular magnetic resonance imaging (CMR). METHODS AND RESULTS: Thirty-five patients were studied 6 months after a first ST-segment elevation myocardial infarction (23 anterior, 12 inferior). All cases had single-vessel disease and an open artery. The extension of Q-waves was analyzed by means of a 64-lead BSM. Infarct size was quantified with CMR. Absence of Q-waves in BSM was observed in 5 patients (14%), 2 of whom (40%) had >1 segment with transmural necrosis. Absence of Q-waves in 12-lead ECG was observed in 8 patients (23%), 7 of whom (87%) had >1 segment with transmural necrosis. Patients with inferior infarctions (n=12, 34%) showed a larger number of Q-waves in BSM (18+/-7.1 leads) than patients with anterior infarctions (n=23, 66%; 3.7+/-3.6 leads; p<0.0001). When the study group was analysed as a whole, the total number of Q-waves detected in BSM did not correlate with the number of necrotic segments (r=0.15; p=0.4). In anterior infarctions, a number of Q-waves >median (2 leads) was related to a higher number of necrotic segments (5.1+/-2.4 vs. 2+/-2.2 segments; p=0.004). The same was observed in inferior infarctions (median 20 leads: 3.5+/-1.9 vs. 1.2+/-1.2 segments; p=0.03). CONCLUSION: In a stable phase after a first ST-segment elevation myocardial infarction, absence of Q-waves does not mean non-transmural necrosis. Using BSM, extension of Q-waves is much higher in inferior infarctions; a separate analysis depending on infarct location is necessary. A major BSM-derived extension of Q-waves is related to larger infarct size both in anterior and in inferior infarctions.

Aged↗
PubMed1994

Reduced coronary vasodilator function in infarcted and normal myocardium after myocardial infarction.

BACKGROUND: The ability of the coronary vascular bed to dilate and thus increase blood flow to the myocardium may be impaired in coronary artery disease, even in regions of myocardium supplied by an angiographically normal coronary artery. If this kind of vasomotor dysfunction was present or accentuated after acute myocardial infarction, it might influence the extent of ischemia and necrosis in areas not directly injured by the infarction. METHODS: We studied 13 patients (mean [+/- SD] age, 62 +/- 11 years) with single-vessel coronary artery disease after they had received thrombolytic therapy for myocardial infarction. Using positron-emission tomography (PET) with oxygen-15-labeled water, we measured regional myocardial blood flow under basal conditions and after the intravenous administration of dipyridamole (0.5 mg per kg of body weight over a period of four minutes) 8 +/- 3 days after infarction in all 13 patients (1-week study) and 6 +/- 2 months after infarction in 9 of the 13 (6-month study). On both occasions we measured blood flow both in the infarcted region and in a region of myocardium that was remote from the infarcted region and supplied by a normal artery. RESULTS: At the one-week PET study, the coronary vasodilator response (the ratio of the myocardial blood flow after the administration of dipyridamole to basal blood flow) was 1.12 +/- 0.50 in the infarct-related artery and 1.53 +/- 0.36 in the remote region (P = 0.015). At the six-month study, the coronary vasodilator response was 1.42 +/- 0.37 in the infarcted region and 2.19 +/- 0.69 in the remote region (P = 0.004 for the comparison with the infarcted region; P = 0.011 for the comparison with the remote region at the one-week study). The value in remote myocardium remained lower than that in similar regions in 10 control patients, who had single-vessel coronary artery disease but no evidence of myocardial infarction (3.17 +/- 0.72; P = 0.009). CONCLUSIONS: After acute myocardial infarction, there is a severe vasodilator abnormality involving not only resistance vessels in infarcted myocardium, but also those in myocardium perfused by normal coronary vessels. This dysfunction may affect the extent of myocardial ischemia and necrosis after coronary occlusion.

Adult↗
PubMed2000

Radio frequency heating of chronic ovine infarct leads to sustained infarct area and ventricular volume reduction.

OBJECTIVE: Myocardial infarct expansion and subsequent left ventricular remodeling are associated with increased incidence of congestive failure and mortality. Collagen is known to denature and contract when heated above 65 degrees C. We therefore tested the hypothesis that radio frequency heating of myocardial infarct tissue with application of a restraining patch causes a sustained reduction in myocardial infarct area and left ventricular volume. METHODS: Thirteen male Dorset sheep underwent surgical coronary artery ligation. At least 14 weeks later, animals were randomized to either radio frequency infarct heating (95 degrees C) with application of a restraining patch or a sham operation. Before treatment, after treatment, and 10 weeks later, left ventricular volume was measured with transdiaphragmatic echocardiography and myocardial infarct area was measured with an array of sonomicrometry crystals. RESULTS: Radio frequency infarct heating causes an acute decrease of 34% (-215 +/- 82 mm(2); P =.0002) in infarct area at end-diastole that is maintained at 10 weeks (-144 +/- 79 mm(2); P =.0002). Radio frequency infarct heating causes a downward trend in end-diastolic left ventricular volume measured by echocardiography of 20% (-15.7 +/- 6.3 mL; P = no significant difference) and end-systolic left ventricular volume of 32% (-17.1 +/- 9.8 mL; P =.09), which are significantly decreased at 10 weeks (-13.6 +/- 22.3 mL; P =.007 and -15.3 +/- 21.9 mL; P =.008, respectively). Radio frequency infarct heating causes an acute improvement in systolic function (P <.001), a sustained increase in left ventricular ejection fraction (+0.11%; P =.06), and preserved stroke volume. CONCLUSION: Radio frequency heating of chronic left ventricular myocardial infarct causes a sustained reduction in infarct area and left ventricular volume. This technique may beneficially reverse infarct expansion and left ventricular remodeling after myocardial infarction.

Animals↗
PubMed1997

Influence of late reopening of the infarct-related artery on left ventricular remodelling after myocardial infarction. IRIS Study Group.

AIMS: This trial was undertaken to assess the impact of late reopening of the infarct-related artery on left ventricular remodelling in post-myocardial infarction patients. METHODS: One hundred and fifty seven patients with recent myocardial infarction were routinely submitted to delayed (second week) catheterization. They also underwent systematic angioplasty of a significantly narrowed infarct-related artery with a suitable anatomy, or reopening of a totally occluded infarct-related artery, and repeat follow-up catheterization after 4 months. Changes in left ventricular ejection fraction, left ventricular volumes, and percent of regional hypokinesia were assessed over the study period. RESULTS: One hundred and thirty-two patients had two interpretable left ventriculograms and two interpretable coronary angiograms. At initial angiography, 56 out of 96 patients with a patent infarct-related artery were successfully submitted to percutaneous coronary angioplasty, of whom 25 had restenosis and eight had total reocclusion at follow-up angiography. Percutaneous transluminal coronary angioplasty was not attempted in the remaining 40 patients due to unsuitable anatomy in 18 or a nonsignificant lesion in 22. The infarct-related artery was totally occluded in 36 patients at initial angiography, and successfully reopened by means of angioplasty in 19, of whom seven showed a reocclusion at follow-up angiography. The independent predictors of left ventricular enlargement, identified by means of multivariate regression analysis, were initial stroke volume index < 40 ml.m-2 (odds ratio = 6.3, 95% confidence interval = [2.5; 16.6]), initial end-systolic volume index > 50 ml.m-2 (odds ratio = 7.1, 95% confidence interval = [1.5; 25.8]), anterior infarct location (odds ratio = 4.1, 95% confidence interval = [1.4; 11.5]) and reocclusion of the infarct-related artery (odds ratio = 7.3, 95% confidence interval = [1.3; 27.3]). Angioplasty of a patent but significantly narrowed infarct-related artery was not found predictive. CONCLUSIONS: This study demonstrates that reocclusion of a previously open infarct-related artery, as well as the initial low stroke volume index, enlarged end-systolic volume index and anterior infarct location are independent predictors of long-term left ventricular enlargement. These results emphasize the impact of long-term sustained patency of the infarct-related artery on the prevention of left ventricular dysfunction. The need for a larger randomized trial is recognised.

Adrenergic beta-Antagonists↗
PubMed1995

Use of changes in ST segment elevation for prediction of infarct artery recanalization in acute myocardial infarction.

BACKGROUND: The role of the ECG in evaluating reperfusion status after thrombolytic treatment in acute myocardial infarction is not clear. Dramatic ST segment changes have been observed during recanalization of an infarct-related artery, but ST criteria have not been definitively established for prediction of coronary artery patency. Differences in ST segment changes in relation to infarct localization have not been evaluated, and further investigation is required into reciprocal ST depression, which provides information independent from ST elevation. Therefore, the aim of this study was to evaluate how early changes in ST segment elevations and depressions predict vessel patency after fibrinolysis for patients with anterior and inferior/lateral infarcts. METHODS AND RESULTS: Two hundred patients with a Pardee wave in the ECG and chest pain of less than 6 h duration were given thrombolytic treatment. The result of the therapy was assessed simultaneously with coronary angiography. Patients were divided into two groups: I (50 patients) without recanalization (TIMI grade 0, 1 or 2), and II (150 patients) with successful recanalization (TIMI grade 3). Before and after therapy, analysis of the 12 lead ECG included maximum ST elevation measurement (H1, H2 respectively), the sum of ST elevations (sigma H1, sigma H2), the sum of ST segment depressions (sigma h1, sigma h2), and the ratios of ST segment changes (R1 = H2:H1, R2 = sigma H2:sigma H1, R3 = sigma h2:sigma h1). The mean interval from the first to the second ECG was 3.5 +/- 1 h. Successive values of R1 and R2 were examined to find that which best distinguished between the two groups. The best values for prediction of reperfusion were: (1) For anterior wall infarct [table: see text] (2) For inferior and lateral infarct [table: see text] In 13 patients with a complete right or left bundle branch block in the first or second ECG, the result of treatment was predicted in 11 patients using criteria for factor R1 and in 12 patients using criteria for R2. Analysis of ST segment depressions revealed a significant correlation between normalization of ST segment depressions and elevations (R3 vs R1: r = 0.60, P < 0.05; R3 vs R2 r = 0.59, P < 0.05). Multivariate discriminant analysis showed an independent value of R3 for discrimination between the two groups, but only in patients with inferior/lateral infarcts. The overall accuracy of the common algorithm in predicting reperfusion was significantly better in patients with inferior/lateral infarcts (Chi2 test, P = 0.0078). When separate algorithms were used, there was no significant difference between patients with anterior or inferior/lateral infarcts because of the significant improvement in prediction of reperfusion in patients with anterior infarcts (McNemar's test: P = 0.041). CONCLUSIONS: We conclude that analysis of ST segments on the standard 12-lead ECG offers valuable help in the early identification of successful recanalization of infarct-related arteries after thrombolytic therapy in patients with acute myocardial infarction. Use of the ratio of ST segment normalization according to the separate criteria for anterior and inferior/lateral infarcts gives the test a high sensitivity and specificity, even in the presence of interventricular conduction disturbances.

Adult↗
PubMed1984

CT-detected hemorrhagic infarction; relation with the size of the infarct, and the presence of midline shift.

The incidence of mass effect indicated by midline shift, and the incidence of hemorrhagic infarction were studied in 952 consecutive CT scans with supratentorial infarcts. Hemorrhagic infarction was found in 5.1% indicating that the incidence of hemorrhagic infarction during life is far less than was suggested from pathological studies. Midline shift was found in 3.6% and, accordingly, the chance of finding a hemorrhagic infarct with mass effect indicated by a shift of the midline would be 0.2% if these 2 phenomena were not related. However, this incidence appeared to be 12 times higher, indicating they are closely related. In addition, the incidence of hemorrhagic infarcts and midline shift were both related to large infarcts with bad outcome. Cardiac emboli were not more prevalent in patients with hemorrhagic infarcts than in a control series, indicating that cardiac emboli do not produce hemorrhagic infarction more often than other causes of cerebral infarction, and that cardiac embolic cause cannot be inferred from hemorrhagic infarction on CT. This probably also applies to carotid emboli. When anticoagulation is considered in patients with cerebral infarction, CT-confirmed hemorrhagic infarction and shift of midline structures as well as decreased consciousness are contraindications to such treatment. In their absence, and in the absence of general contraindications, anticoagulant treatment can safely be started.

Adult↗
PubMed1996

Significance of perfusion of the infarct related coronary artery for susceptibility to ventricular tachyarrhythmias in patients with previous myocardial infarction.

OBJECTIVE: To study the significance of perfusion of the infarct related coronary artery for susceptibility to ventricular tachyarrhythmias in patients with a remote myocardial infarction. SETTING: Tertiary referral cardiac centre. METHODS: Angiographic filling of the infarct related artery was assessed in a consecutive series of 85 patients with different susceptibilities to ventricular tachyarrhythmias after previous (> 3 months) Q wave myocardial infarction: 30 patients had a history of cardiac arrest (n = 16) or sustained ventricular tachycardia (n = 14), and sustained ventricular tachyarrhythmia was inducible in these by programmed electrical stimulation (arrhythmia group); 47 patients had no clinical arrhythmic events and no inducible ventricular tachyarrhythmias during programmed ventricular stimulation (control group). Eight patients without a history of any arrhythmic events were inducible into ventricular tachycardia. RESULTS: The patients in the arrhythmia group were older (63 (SD 8) years) than the control patients (59 (6) years, P < 0.05), and had larger left ventricular volumes in cineangiography (P < 0.01), but ejection fraction, severity of left ventricular wall motion abnormalities, previous thrombolytic therapy, and time from previous infarction did not differ between the groups. Patients with susceptibility to ventricular tachyarrhythmias more often had a totally occluded infarct related artery on angiography (77%) than patients without arrhythmia susceptibility (21%) (P < 0.001), and complete collateral filling of the infarct artery in cases without complete anterograde filling was less common in the arrhythmia group than in the control group (P < 0.001). Patients without a history of malignant arrhythmia but with inducible ventricular tachyarrhythmia also had no or poor perfusion of the infarct artery more often than the patients without inducible arrhythmia (P < 0.001). Logistic multiple regression showed that no or poor anterograde or collateral filling of the infarct related artery was the most powerful predictor of susceptibility to ventricular tachyarrhythmias (P < 0.001). Left ventricular size and function were not independently related to arrhythmic susceptibility. CONCLUSIONS: No or poor angiographic filling of the infarct related artery is closely associated with susceptibility to ventricular tachyarrhythmias late after acute myocardial infarction, suggesting that perfusion of the infarct artery will modify favourably the electrophysiological substrate of the infarct scar independently of the myocardial salvage achieved by early reperfusion.

Coronary Angiography↗
PubMed1978

Myocardial infarction size from serial CPK: variability of CPK serum entry ratio with size and model of infarction.

To study the variability of the fraction of CPK released from the infarcted heart which enters the serum (serum entry ratio, or SER) with size and model of infarction, nine dogs underwent homogeneous infarctions (LAD ligation) of varying sizes, and 10 dogs underwent scattered infarctions (left coronary embolization). In homogeneous infarcts there was an inverse linear relationship of SER to infarct size (IS) (SER = -0.8514% LV + 0.345, r = 0.98). No such relationship was found for scattered infarcts. CPK Kd (exponential disappearance constant for CPK) was not significantly different in homogeneous (-0.00178 min-1) vs scattered infarcts (-0.00195 min-1). Although similar IS was produced in each (homogeneous 19.9% LV, scattered 18.4% LV) cumulative CPK serum entry (CPKr) was much lower in homogeneous (4175 mlU/ml) vs scattered infarcts (7,296 mlU/ml). SER was also much lower in homogeneous (17.7%) vs scattered infarcts (29.0%) (P less than 0.025). Cumulative CPK plateau occurred significantly later in homogeneous (15.8 hours) vs scattered infarcts (11.7 hours) (P less than 0.01). Further corrections to the serial CPK equations for IS determination are indicated. The method may not be applicable in some infarct situations, e.g., scattered infarction.

Animals↗
PubMed1985

Prognosis after extension of myocardial infarct: the role of Q wave or non-Q wave infarction.

We examined whether or not subsets of patients with extension of myocardial infarct were at high risk for early and late mortality. Some data suggest increased risk in patients with non-Q wave infarcts and we hypothesized that infarct extension in this group might be associated with a poorer prognosis than that for patients with extension of Q wave infarcts. A total of 1253 patients with acute myocardial infarction who were included in our data base were followed prospectively. The patients were classified according to electrocardiographic results into the following groups: those with non-Q wave (n = 277) infarcts and those with Q-anterior (n = 462) and Q-inferior (n = 497) infarcts. Extension was diagnosed by two of the following criteria: (1) recurrent chest pain 24 hr or more after admission to the hospital, (2) new persistent electrocardiographic changes, and (3) elevation or reappearance of creatine kinase. By these criteria 85 (6%) patients had extension (8% of non-Q wave infarcts, 6% of Q-anterior infarcts, and 6% of Q-inferior infarcts). Hospital mortality in patients with extension was 15% in those with Q wave infarcts vs 43% in those with non-Q wave infarcts (p less than .01). Nine hundred and fifty-two patients were followed for 1 year. In 24% of those who did not survive 1 year there was extension of infarct; only 6% of survivors had extension (p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Measurement of infarct size and percentage myocardium infarcted in a dog preparation with single photon-emission computed tomography, thallium-201, and indium 111-monoclonal antimyosin Fab.

Single photon-emission tomography (SPECT) and indium 111-labeled monoclonal antimyosin Fab fragments were used to measure myocardial infarct size in 12 dogs, six subjected to balloon catheter-induced coronary artery occlusion for 6 hr (late reperfusion) and six subjected to occlusion with reperfusion at 2 hr (early reperfusion). Tomographic imaging was performed 24 hr after the intravenous injection of labeled Fab fragments with the use of a dual-head SPECT camera with medium-energy collimators. Immediately after the first tomographic scan, thallium-201 was injected into nine of 12 dogs and imaging was repeated. Estimated infarct size in grams was calculated from transaxially reconstructed, normalized, and background-corrected indium SPECT images with the use of a threshold technique for edge detection. Estimated noninfarcted myocardium in grams was calculated from obliquely reconstructed thallium SPECT images by a similar method. The animals were killed and infarct size in grams and true infarct size as a percentage of total left ventricular myocardial volume were measured by triphenyl tetrazolium chloride staining. Estimated infarct size from indium SPECT images showed an excellent correlation with true infarct size (r = .95, SEE = 4.1 g). Estimated percentage myocardium infarcted was calculated by dividing estimated infarct size from indium images by the sum of estimated infarct size plus estimated noninfarcted myocardium obtained from thallium images. Correlation between the estimated percentage of myocardium infarcted and true percentage of myocardium infarcted was excellent (r = .93, SEE = 4.4%). We conclude that dual-isotope SPECT with indium 111-monoclonal antimyosin antibodies and thallium-201 can accurately estimate infarct size and percentage myocardium infarcted.

Animals↗
PubMed1995

ST segment elevation at the surface of a healed transmural myocardial infarction in pigs. Conditions for passive transmission from the ischemic peri-infarction zone.

BACKGROUND: Ischemia of the myocardium surviving an infarction induces ST segment elevation in infarct-related ECG leads. In cases with no viable tissues, ischemia adjacent to the infarction could induce a similar ECG pattern if there is ST segment potential transmission through the necrotic scar. We analyzed whether acute ischemia adjacent to a healed infarction with no viable tissue may induce ST segment elevation on the surface of the necrotic scar. METHODS AND RESULTS: Epicardial ST segment changes elicited during 30 minutes of acute reocclusion of the left anterior descending (LAD) coronary artery 2 cm above the first diagonal branch were analyzed by 32-channel mapping in 18 chloralose-anesthetized open-chest pigs with 1-month-old anterior infarctions induced by permanent ligature below the first diagonal branch (group 1). The effect of a previous infarction on the magnitude of ischemic ST segment changes was assessed by similar mapping in 21 control pigs submitted to a LAD ligature 2 cm above the first diagonal branch (group 2, n = 11) or just below this branch (group 3, n = 10). Myocardial perfusion after coronary ligature was estimated in 7 pigs with chronic infarction and in 3 control pigs by mapping of myocardial technetium-99m-methoxyisobutyl isonitrile (99mTc-MIBI) activity in transmural samples underlying each epicardial electrode. The width of cell layers surviving the infarction was measured and their viability after 60 minutes of coronary reocclusion was assessed by intracellular glycogen staining. Reocclusion of the LAD induced parallel ST segment elevation at the periinfarction zone and at the necrotic scar, although in the latter region the changes were less marked (maximal ST segment, 8.4 +/- 3.0 mV versus 2.7 +/- 1.8 mV, ANOVA, P < .001). ST segment elevation inside the scar was greater at the margins (3.9 +/- 1.8 mV) than at sites 20 mm toward the center (2.8 +/- 1.7 mV, P = .003). The necrotic area was virtually devoid of surviving cells except for a 0.22 +/- 0.04-mm-wide subendocardial band that continued to show a positive intracellular glycogen reaction after the second LAD ligature. Acute ischemia adjacent to the infarction (group 1) induced lower ST segment elevation than acute ischemia at a comparable cardiac region in noninfarcted pigs (group 2) (ANOVA, P = .02), despite the fact that these areas developed similar underperfusion after coronary occlusion (percent MIBI activity of that in normal myocardium, 7 +/- 8 versus 7 +/- 6, P = NS). ST segment changes in group 2 pigs were comparable to those induced in group 3 pigs with a 2-cm-lower coronary occlusion. CONCLUSIONS: Acute ischemia adjacent to a chronic infarction induces ST segment elevation at the surface of the scar despite the virtual absence of viable tissue within the infarction. Data suggest a passive ST segment potential transmission through the infarction. Moreover, ischemia adjacent to a chronic infarction induces lower ST segment elevation than ischemia not adjacent to a necrosis. The mechanisms accounting for these regional differences are probably independent of collateral myocardial perfusion and ischemia extension.

Animals↗