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PubMed1996

Acute and long-term effects of thrombolysis after anterior wall acute myocardial infarction with serial assessment of infarct expansion and late ventricular remodeling.

This study investigates the impact of thrombolysis on infarct expansion and subsequent left ventricular (LV) remodeling in patients with anterior wall acute myocardial infarction (AMI). We evaluated 51 consecutive patients (24 treated with thrombolysis) with anterior wall AMI by 2-dimensional echocardiography in the following sequence: days 1, 2, 3, and 7, after 3 and 6 weeks, and after 3, 6, and 12 months. LV end-diastolic and end-systolic volume indexes were determined from apical 2- and 4-chamber views using Simpson's biplane formula. Infarct and total LV perimeters were determined in the same views and their ratio expressed as infarct percentage. Infarct expansion was defined as: (1) an increase in infarct percentage and total perimeter >5% on days 2 to 3 in either of the views, or (2) initial infarct percentage >50% with an increase in total perimeter >5% on days 2 to 3. Coronary angiography was performed in 43 patients before discharge, and patency of the infarct-related artery was assessed using Thrombolysis in Myocardial Infarction trial criteria. Infarct expansion was detected in 23 patients. Infarct perimeter steadily decreased in patients with versus without thrombolysis and in patients with patent versus occluded infarct-related arteries. Furthermore, by logistic regression, thrombolysis (p = 0.007) and potency of the infarct-related artery (p = 0.02) were strong negative predictors of expansion, whereas initial infarct perimeter (p = 0.009) was directly associated with subsequent expansion. End-systolic volume index was higher in patients with expansion from day 1 (p = 0.003) through the end of the study (p = 0.021), and end-diastolic volume index was higher in these patients from day 2 (p = 0.012) through 12 months (p = 0.015). Thus thrombolysis, initial infarct size, and infarct-related artery patency are major predictors of infarct expansion after anterior wall AMI.

Confounding Factors, Epidemiologic↗
PubMed2000

[Influence of pre-infarction angina on mid-term mortality after acute myocardial infarction].

INTRODUCTION AND OBJECTIVES: Pre-infarction angina may reduce the extent of myocardial cell necrosis and improves the prognosis after myocardial infarction. The aim of this study was to analyze the total mortality six-month after acute myocardial infarction according to the presence or absence of pre-infarction angina. METHODS: One hundred seventy-five consecutive patients with acute myocardial infarction were prospectively included, 72 (41.4%) with pre-infarction angina. They were followed for 6 months. There were 16 deaths (15.5%) in the group of patients without pre-infarction angina and 7 (9.7%) in the group with pre-infarction angina (log-rank = 1.03; p = 0.311). The hazard-risk function curves showed a higher risk of death during the entire follow-up in the group without pre-infarction angina. In the multivariate logistic regression model, the presence of pre-infarction angina does not significantly reduce the risk of death (OR = 0.43; CI 95% = 0.09-2. 22; p = 0.303). We detected a significant interaction between treatment with sulfonylureas before the infarction and the presence of pre-infarction angina (p = 0.017). CONCLUSIONS: In this study no significant differences were observed in total mortality six months after acute myocardial infarction according to the presence of pre-infarction angina. However, the risk of death seemed to be higher in the group of patients without pre-infarction angina during the entire follow-up. A significant interaction was found between the treatment with sulfonylurea drugs before infarction and the presence of pre-infarction angina.

Aged↗
PubMed1984

Is anterior ST depression with acute transmural inferior infarction due to posterior infarction? A vectorcardiographic and scintigraphic study.

The hypothesis that anterior ST segment depression represents concomitant posterior infarction was tested in 49 patients admitted with a first transmural inferior myocardial infarction. Anterior ST depression was defined as 0.1 mV or more ST depression in leads V1, V2 or V3 on an electrocardiogram recorded within 18 hours of infarction. Serial vectorcardiograms and technetium pyrophosphate scans were obtained. Eighty percent of the patients (39 of 49) had anterior ST depression. Of these 39 patients, 34% fulfilled vectorcardiographic criteria for posterior infarction, and 60% had pyrophosphate scanning evidence of posterior infarction. Early anterior ST depression was neither highly sensitive (84%) nor specific (20%) for the detection of posterior infarction as defined by pyrophosphate imaging. Of patients with persistent anterior ST depression (greater than 72 hours), 87% had posterior infarction detected by pyrophosphate scan. In patients with inferior myocardial infarction, vectorcardiographic evidence of posterior infarction correlated poorly with pyrophosphate imaging data. Right ventricular infarction was present on pyrophosphate imaging in 40% of patients with pyrophosphate changes of posterior infarction but without vectorcardiographic evidence of posterior infarction. It is concluded that: 1) the majority of patients with acute inferior myocardial infarction have anterior ST segment depression; 2) early anterior ST segment depression in such patients is not a specific marker for posterior infarction; and 3) standard vectorcardiographic criteria for transmural posterior infarction may be inaccurate in patients with concomitant transmural inferior myocardial infarction or right ventricular infarction, or both.

Diphosphates↗
PubMed1984

Myocardial infarct size determined by computed transmission tomography in canine infarcts of various ages and in the presence of coronary reperfusion.

Thirty-one dogs underwent in vivo scanning with computed transmission tomography; 15 dogs were studied within 7 days (mean 4) after coronary occlusion, 10 dogs 21 to 25 days (mean 28) after occlusion and 6 dogs 4 days after coronary reperfusion of a 2 to 3 hour coronary ligation. Ungated scans (1 cm in depth) of the left ventricle were obtained from apex to base to determine infarct size. In all animals with documented (postmortem) infarction (n = 26), contrast medium caused delayed enhancement of the entire infarct or the periphery of the infarct. Infarct size was calculated from scans showing contrast enhancement of the infarct. Infarct size was also determined from the postmortem heart using histochemical morphometry (nitroblue tetrazolium) and then compared with infarct size derived from tomography using the outer margin of the contrast-enhanced periphery of the infarct as the border of the infarct. Infarct size calculated by the tomographic technique (excluding the animals without an infarct) correlated well with infarct size determined at autopsy (r = 0.90, p less than 0.001). The tomographic estimate (18.2 +/- 11.3 g) of infarct size was similar to autopsy values (18.6 +/- 11.8 g, p = NS). Thus, ungated computed transmission tomographic imaging of the heart can reliably estimate infarct size in a variety of potential clinical circumstances, particularly when the area of rim enhancement of the infarct is included within the presumed infarct region.

Animals↗
PubMed1994

Limitation of infarct size and preservation of left ventricular function after primary coronary angioplasty compared with intravenous streptokinase in acute myocardial infarction.

BACKGROUND: Early and effective flow through the infarct-related vessel is probably of paramount importance for limitation of infarct size and preservation of left ventricular function in patients with acute myocardial infarction. Primary coronary angioplasty may offer advantages in these respects compared with thrombolytic therapy. The purpose of the present study was to assess the effects on estimated enzymatic infarct size and left ventricular function in patients with acute myocardial infarction randomly assigned to undergo primary angioplasty or to receive intravenous streptokinase. METHODS AND RESULTS: We evaluated 301 patients with signs of acute myocardial infarction and without contraindications for thrombolysis who presented within 6 hours after onset of symptoms or between 6 and 24 hours if there was evidence of ongoing ischemia. One hundred fifty-two patients were randomly assigned to undergo primary angioplasty, and 149 patients were assigned to receive treatment with streptokinase (1.5 million U i.v.). Infarct size was estimated from enzyme release. Global left ventricular ejection fraction and regional wall motion, if possible in combination with exercise testing, were evaluated by radionuclide ventriculography before discharge. Thrombolysis in Myocardial Infarction (TIMI) flow grade 3 through the infarct-related vessel within 120 minutes after admission was achieved in 92% of all patients assigned to receive primary angioplasty therapy. Myocardial infarct size was 23% smaller in the angioplasty group compared with patients assigned to receive streptokinase (1003 +/- 784 versus 1310 +/- 1198 U/L, P = .012). Global left ventricular ejection fraction (50 +/- 9% versus 45 +/- 11%, P < .001) and regional wall motion in the infarct-related zones (42 +/- 14% versus 34 +/- 13%, P < .001) were better in the angioplasty group, which could mainly be contributed to myocardial salvage in the infarct-related areas. The observed differences were more pronounced in patients with an anterior wall myocardial infarction, although patients with a nonanterior infarct location also showed a beneficial effect of primary coronary angioplasty on left ventricular function compared with streptokinase therapy. Furthermore, the observed differences appeared to be more pronounced in patients presenting relatively early (within 2 hours) after onset of symptoms. CONCLUSIONS: In patients with acute myocardial infarction, primary angioplasty results in a smaller infarct size and a better preserved myocardial function compared with patients randomized to receive treatment with intravenous streptokinase. This is probably due to early and optimal blood flow through the infarct-related vessel, as can be accomplished in a very high percentage of patients undergoing primary coronary angioplasty.

Angioplasty, Balloon, Coronary↗
PubMedDate not supplied

Contribution of contractile state of the non-infarcted area to global ventricular performance after acute myocardial infarction: assessment by quantitative radionuclide angiography.

To evaluate the regional contractile state of the non-infarcted zone and to determine the contribution of this area to left ventricular (LV) performance, 112 patients (42 anterior and 70 inferior infarction) with their first acute myocardial infarction were investigated by radionuclide ventriculography at admission and 10 days after admission. Wall motion at the non-infarcted area was defined as hyperkinetic, normal, or hypokinetic, if radial chord shortening had above normal, normal, or below normal values, respectively, by quantitative wall motion analysis. Hyperkinetic, normal, and hypokinetic wall motion of the non-infarcted area were observed in three (7%), 12 (29%), and 27 (64%) patients in anterior infarction and 14 (20%), 28 (40%), and 28 (40%) in inferior infarction, respectively. In the patients with hypokinetic wall motion at the non-infarcted area, the infarct involved more than 30% of the left ventricle manifesting akinetic contractile segment (ACS), radial chord shortening in the infarcted area was severely depressed, and the incidence of multi-vessel involvement was higher compared with those with hyperkinetic or normal wall motion. In serial measurements, radial chord shortening in the infarcted and non-infarcted area, percent ACS, left ventricular ejection fraction, and left ventricular end-diastolic volume index did not change significantly from acute to follow-up study in any group. In conclusion, our data indicated that the non-infarcted area following acute infarction had various contractile states and these conditions were determined primarily by the severity and extent of infarct and underlying coronary artery disease. Furthermore, the contractile state of the non-infarcted area has a supplemental role in determination of LV function following acute infarction.

Adult↗
PubMed2000

Differences in time course of myocardial mRNA expression in non-infarcted myocardium after myocardial infarction.

In non-infarcted myocardium after myocardial infarction, the change of cardiac phenotypic modulation of contractile protein, extracellular matrix and intracellular Ca2+ transport protein, such as sarcoplasmic reticulum Ca2+(SR-Ca2+)-ATPase, Na+-Ca2+ exchanger, have a important role during cardiac remodeling. However, the time course in this gene expression in the adjacent and remote left ventricular, or right ventricular myocardium after myocardial infarction has not been well examined. The purpose of this study was to examine the left ventricular function and regional cardiac gene expression after myocardial infarction. Myocardial infarction was produced in Wistar rats by the ligation of the left anterior descending coronary artery. After 3 weeks, 2 months and 4 months from myocardial infarction, we performed Doppler echocardiography and measured the systolic and diastolic function. Then, we analyzed the contractile protein, extracellular matrix and intracellular Ca2+ transport protein mRNAs of cardiac tissues in the adjacent and the remote noninfarcted myocardium, and right ventricular myocardium by Northern blot hybridization. Fractional shortening of infarcted heart progressively decreased. Peak early diastolic filling wave (E wave) velocity increased, and the deceleration rate of the E wave velocity was more rapid in myocardial infarction areas. Atrial filling wave (A wave) velocity decreased, resulting in a marked increase in the ratio of E wave to A wave velocity. Expression of myocardial alpha-skeletal actin, beta-MHC and ANP mRNA, or collagen I and III mRNA were higher at 3 weeks after myocardial infarction. SR Ca2+-ATPase mRNA in the adjacent non-infarcted myocardium was decreased at 2 months, and that in remote myocardium was decreased at 4 months after infarction. Na+-Ca2+ exchanger mRNA levels were increased at 3 weeks, but was decreased at 2 months in the adjacent non-infarcted myocardium and at 4 months in the remote myocardium. These findings suggest that the compensation for myocardial infarction by myocardial gene expression in non-infarcted myocardium may occur at an early phase after myocardial infarction, and myocardial dysfunction may begin from adjacent to remote non-infarcted myocardium during progressive cardiac remodeling.

Animals↗
PubMed1992

Effects of amlodipine on myocardial infarction, infarct expansion, and ventricular geometry in the rat.

Infarct expansion remains an important sequela of myocardial infarction. Both angiotensin converting enzyme inhibitors and intravenous nitrates reduce early infarct expansion in humans. This is believed to be caused by the reduction in left ventricular systolic wall stress that results from the arteriolar vasodilatation they produce. Patients are frequently already receiving calcium channel blockers at the time of infarction or these drugs are sometimes administered in the perimyocardial infarction period. The calcium blockers of the dihydropyridine class might be expected to modify infarct expansion. However, their effect on this process has not been studied. We therefore evaluated the effect of early treatment with the calcium blocker amlodipine, a potent arteriolar vasodilator with minimal negative inotropic properties, on chronic myocardial infarction in the rat. Permanent left coronary occlusion was created after pretreatment with amlodipine, 0.25 mg/kg (low dose) or 1.0 mg/kg (high dose), or placebo, intravenously twice a day, and continued for 7 days after infarction. Hearts (n = 50) were perfusion fixed 21 days after infarction and analyzed for infarct extent, scar thickness, left ventricular shape and size, and expansion index. Both doses decreased mean blood pressure (119 +/- 3 to 99 +/- 5 mm Hg low dose, p = 0.004; 110 +/- 5 to 84 +/- 4 mm Hg high dose, p = 0.0003), with reflex tachycardia only after the high dose (heart rate 395 +/- 9 to 434 +/- 11, p = 0.001). Infarct extent was equal in the three groups (39 +/- 2%, 41 +/- 2%, and 41 +/- 3% of left ventricular circumference for control, low, and high doses, respectively). The three groups did not differ significantly with regard to left ventricular cavity cross-sectional area (80 +/- 4, 77 +/- 3, and 87 +/- 3 mm2, control, low, and high doses, respectively; p = 0.07 high dose vs control), mean scar thickness (0.74 +/- 0.06, 0.73 +/- 0.05, and 0.65 +/- 0.06 mm, control, low, and high doses, respectively; p = NS), and expansion index (1.52 +/- 0.10, 1.58 +/- 0.12, and 1.95 +/- 0.19, control, low, and high doses, respectively; p = 0.08 high dose vs control). In the subgroup with larger infarcts (infarct extent greater than 0.39 of left ventricle), the expansion index was higher in the high-dose group (2.37 +/- 0.23 vs 1.64 +/- 0.17 control; p = 0.04). In this model, treatment with amlodipine does not limit infarct extent or reduce early infarct expansion and left ventricular dilatation, even when initiated before infarction.(ABSTRACT TRUNCATED AT 400 WORDS)

Amlodipine↗
PubMed1992

Quantification of antimyosin uptake and infarct size at various stages of myocardial infarction.

We studied with quantitative techniques the clinical efficacy of indium-111 antimyosin at a later stage of myocardial infarction in 18 patients at various stages after infarction. Antimyosin accumulation was detected irrespective of infarct age and size and quantified as an infarct weight with a tomographic technique. Higher intensities in a planar image were observed in anterior Q wave infarct group (36 +/- 5 g) but not in inferior and non-Q wave anterior infarct groups because of the smaller infarct weights (8 +/- 3 g, 13 +/- 6 g, respectively). Infarct area calculated from thallium-201 tomography significantly correlated with left ventricular ejection fraction in both recent (less than 2 weeks) and older (2-week- to 6-month-old) infarct groups (r = -0.969, P less than 0.001; r = -0.860, P less than 0.001, respectively), whereas there was a significant negative correlation between infarct weight and left ventricular ejection fraction in the recent infarct group (r = -0.731, P less than 0.05) but not in the older infarct group. Thus, antimyosin tomography can detect myocardial necrosis with a high sensitivity regardless of infarct age, size, and location. However, the accumulation might be affected by infarct age and correspond to necrotic mass but not necessarily to infarct volume itself at a later stage probably because of the presence of necrosed and scarred tissues in infarcted myocardium.

Aged↗
PubMed1993

Difference in plasminogen activator inhibitor activity between non-Q-wave infarction and Q-wave infarction.

We examined the plasma levels of tissue plasminogen activator antigen and plasminogen activator inhibitor activity in 14 patients with non-Q-wave infarction and in 27 patients with Q-wave infarction before the start of thrombolytic therapy and in 34 control subjects. The mean level of plasma tissue plasminogen activator antigen (ng/ml) was higher (P < 0.01) both in the patients with non-Q-wave infarction and in those with Q-wave infarction than in the control subjects (10.3 +/- 1.9, 9.5 +/- 0.8 vs. 5.8 +/- 0.3), and there was no difference in the level between the patients with non-Q-wave infarction and those with Q-wave infarction. The mean level of plasma plasminogen activator inhibitor activity (IU/ml) was lower (P < 0.01) in the patients with non-Q-wave infarction than in those with Q-wave infarction (7.3 +/- 2.0 vs. 17.1 +/- 2.2), and there was no difference in the level between the patients with non-Q-wave infarction and the control subjects (7.3 +/- 2.0 vs. 4.1 +/- 2.6). The patency rate of infarct-related coronary artery before thrombolytic therapy was higher (P < 0.01) in the patients with non-Q-wave infarction than in those with Q-wave infarction (54% vs. 15%). We conclude that plasminogen activator inhibitor activity was lower in non-Q-wave infarction than in Q-wave infarction and this may be related to the higher patency rate of infarct-related coronary artery in non-Q-wave infarction.

Aged↗
PubMedDate not supplied

Right ventricular infarction associated with anteroseptal myocardial infarction: a clinicopathologic study of nine cases.

The association of right ventricular (RV) infarction with inferoseptal myocardial infarction is well established. However, a question remains about the occurrence of RV infarction in association with anteroseptal myocardial infarction. To determine the frequency and clinical correlates of this entity, we studied autopsied hearts from patients with isolated anteroseptal left ventricular (LV) infarcts. Among 3,249 autopsy specimens, 88 cases were identified. From each, sections were taken from the RV anterior, lateral, and inferior regions at basal, middle, and apical levels. All 1,584 slides were reviewed by blinded assessment. RV and LV infarcts were compared to confirm similarity in age. Patient records and cardiac investigations were reviewed for evidence of RV involvement. Of the 88 hearts with anteroseptal LV infarcts, 9 (10%) had coexistent RV infarction (6, old; 3, new). For these 9, the RV infarction involved 11% to 33% of the RV area, and the left anterior descending coronary artery was the infarct-related artery in each. All 3 patients who had an echocardiographic examination within 4 weeks of anteroseptal LV infarction had RV dysfunction. One patient, studied 15 years after infarction, had a normal right ventricle by echocardiography. In 3 patients with acute myocardial infarction, right heart catheterization during the acute phase revealed increased right-sided diastolic pressures out of proportion to left-sided diastolic pressures (right atrial pressure to pulmonary capillary wedge pressure, 60% to 95%). In conclusion, 10% of patients with an isolated anteroseptal LV infarct had evidence of RV free wall infarction. The RV infarction was associated with identifiable hemodynamic and echocardiographic features.

Adult↗
PubMed1986

Prognostic significance of electrocardiographic site of infarction after correction for enzymatic size of infarction.

To assess whether the site of myocardial infarction is an independent prognostic indicator, the outcome of patients with anterior myocardial infarction was compared with that of patients with inferior infarction. A consecutive series of patients who had suffered their first myocardial infarction was analyzed (398 with anterior and 391 with inferior infarction). Patients with anterior myocardial infarction had a higher 1 year mortality than those with inferior infarction (18.3% vs 10.5%, p = .002). When patients were matched for infarct size determined by peak creatine kinase (CK) level expressed as a multiple of the upper limit of normal, those with anterior myocardial infarction tended to have a higher 1 year mortality than those with inferior infarction for all subgroups of peak CK. Early mortality (day 1 to 28 after myocardial infarction) was greater in the anterior than in the inferior myocardial infarction group (10% vs 6.4%, p = .03); this was most significant when peak CK was greater than four times normal (12.4% vs 7.0%, p = .04). Late mortality was also higher in the anterior (8.4% vs 4.1%, p = .04) than the inferior infarction group and this was most significant when peak CK was less than two times normal (15.2% vs 0%, p = .02) or greater than eight times normal (10.6% vs 4.1%, p = .04). Multivariate analysis with proportional-hazards regression confirmed the prognostic significance of location of infarction independent of peak CK level. Thus, infarct location was found to be a predictor of prognosis that is independent of infarct size based on peak CK levels.

Actuarial Analysis↗
PubMed1988

Inducible sustained ventricular tachycardia 4 years after experimental canine myocardial infarction: electrophysiologic and anatomic comparisons with early healed infarcts.

We studied a group of 17 dogs 4 to 6 years after infarction produced by 2 hr occlusion of the anterior descending coronary artery followed by reperfusion. Dogs in this "late" infarct group were compared with a group of 24 dogs with "early" healed infarcts (2 to 24 weeks old). With signal-averaging techniques body surface potentials were recorded during sinus rhythm. After thoracotomy epicardial electrograms were recorded from 45 standardized sites within the infarcted region and characteristics of selected electrograms were compared with anatomic features of underlying myocardium. Epicardial recordings from the late infarct group demonstrated earlier local activation (p less than .001) and shorter electrogram duration (p less than .001) when compared with recordings from the early infarct group. There was less temporal dispersion of activation and electrogram duration among the 45 sites in dogs with late infarcts as measured by respective coefficients of variance (p = .007 and less than .001). With programmed stimulation six dogs in the late and eight in the early infarct group exhibited inducible sustained ventricular tachycardia. Mean cycle length of the tachycardia in dogs with late infarcts was significantly shorter (p = .035). Late potentials were notably less prominent in dogs in the late infarct group with ventricular tachycardia than in dogs in the early infarct group. Fewer abnormal electrophysiologic characteristics of late infarcts coincided with relatively less scar in the underlying myocardium. Moreover, the strength of electrophysiologic-anatomic correlations differed in late as opposed to early infarcts. The latter findings suggest long-term evolution of infarct anatomy. We conclude that a substrate for reentrant tachycardia is present in dogs 4 to 6 years after reperfused infarction. Conduction characteristics are less abnormal in these late healed infarcts and are associated with a shorter ventricular tachycardia cycle length and less pronounced late potentials on the body surface.

Animals↗
PubMed2002

Plasminogen activator inhibitor in patients with acute myocardial infarction and re-infarction in syndrome X.

Plasminogen activator inhibitor was determined in myocardial infarction and re-infarction patients along with other parameters relevant for the Syndrome X, such as triglycerides, HDL-cholesterol and body mass index. Plasminogen activator inhibitor was determined in 58 patients with myocardial infarction and 18 patients with re-infarction as well as in 57 healthy individuals. Significantly higher plasminogen activator inhibitor values were found in re-infarction patients (6.53 +/- 0.39 U/mL) than in myocardial infarction patients (4.32 +/- 0.19 U/mL), whereas the values were significantly higher in both groups in comparison to healthy individuals (2.81 +/- 0.74 U/mL). Triglyceride values were also significantly higher in myocardial infarction (2.05 +/- 0.1 mmmi/L) and re-infarction patients (2.02 +/- 0.99 mmol/L) than in healthy individuals (1.35 +/- 0.58 mmol/L), although the difference between the triglyceride values obtained for myocardial infarction and re-infarction patients was not statistically significant. HDL-cholesterol values for myocardial infarction (1.18 +/- 0.04 mmol/L) and re-infarction (1.14 +/- 0.18 mmol/L) patients were significantly lower than in healthy individuals (1.46 +/- 0.5 mmol/L). However, the difference was not statistically significant between the myocardial infarction and the re-infarction group. The difference in body mass index between myocardial infarction (26.65 +/- 0.39 kg/m2) and re-infarction (25.49 +/- 0.39 kg/m2) patients and healthy individuals (24.45 +/- 3.41 kg/m2) was evidenced.

Acute Disease↗
PubMed1978

Relationship of myocardial infarction to presence of angina pectoris in patients with coronary heart disease: lack of abolition of angina by infarction.

To evaluate the relationship between myocardial infarction and angina pectoris, history of symptomatic coronary heart disease was analyzed in 146 patients who had had documented myocardial infarction. There were 126 males and 70 females of mean age 55 years (range 32 to 70 years). Infarction had occurred 6 to 63 months prior to the study (mean: 30 months). Angina pectoris occurred at some time during the clinical course of 75 patients (51%), and 71 patients (49%) had not experienced angina. In the majority of the group with angina (n = 39; 52%) the symptom had not been present before infarction, appearing initially thereafter. Angina was present both before and after infarction in 31 patients (41%). In only 5 patients (7%) was precedent angina lost after infarction. Angina was, therefore, present in 70 of 146 patients (48%) after, compared to 36 patients (25%) before, infarction and in 86% (31/36) of patients with angina before infarction it persisted following the attack. Prior angina following myocardial infarction was not related to increased activity since in the majority of patients activity level was less after than before infarction. Post-infarction cardiac failure, which developed in 9 patients who had prior angina, was not associated with abolition of angina in any of this group. It is concluded that: 1. angina is frequent after myocardial infarction, 2. when present before infarction it usually persists thereafter, 3. angina commonly appears as a new symptom after infarction when not previously present and 4. disappearance of angina after infarction is distinctly uncommon.

Adult↗
PubMed1994

Myocardium at risk and infarct size after thrombolytic therapy for acute myocardial infarction: implications for the design of randomized trials of acute intervention.

OBJECTIVES: The purpose of this study was to estimate the effect of an improved reperfusion therapy for acute myocardial infarction on myocardial salvage and ventricular function for anterior and inferior infarctions and to ascertain the sample size required to detect such an effect. BACKGROUND: There are significant differences in myocardium at risk between anterior and inferior infarctions that affect the benefit of reperfusion therapy. METHODS: We studied 58 patients with acute myocardial infarction (24 anterior, 34 inferior) treated with intravenous recombinant tissue-type plasminogen activator and angioplasty when necessary. Tomographic imaging with technetium-99m sestamibi was performed to measure myocardium at risk, final infarct size and myocardial salvage and to estimate the beneficial effects of an improved therapy. RESULTS: A new therapy that was 30% more effective than existing therapy (with respect to salvage) would increase salvage (and reduce mean infarct size) by 5.2% of the left ventricle and increase late ejection fraction by only 0.012 (95% confidence interval [CI] 0.009 to 0.015) in inferior infarction and by 0.038 (95% CI 0.027 to 0.047) in anterior infarction. If anterior and inferior infarctions occurred with equal frequency, a sample size of 140 patients in each treatment group would be required to detect such a change with 80% power. In a trial of interior infarctions alone, a sample size of 236 patients in each treatment group would be required compared with only 98 patients in a trial of anterior infarctions alone. CONCLUSIONS: The anticipated mean benefit from an improved reperfusion therapy in individual patients with inferior infarction is very small and of questionable clinical significance. The anticipated benefit in anterior infarction is greater and easier to detect. Future randomized trials should be stratified for infarct location and should consider the greater absolute benefit of treatment in anterior infarction.

Adult↗
PubMed2003

Acute myocardial infarction: differing preinfarction and clinical features according to infarct site and gender.

While differences between anterior and inferior acute myocardial infarction have been observed, clinical features of lateral infarction are poorly investigated. However, the impact of gender on clinical course and prognosis after myocardial infarction is not fully understood. Electrocardiographically determined infarct site, demographic and clinical variables were prospectively recorded for 1623 consecutive patients admitted to Clinical Hospital Split between 1990 and 1994 due to a first Q-wave acute myocardial infarction. Anterior infarctions were correlated with a higher prevalence of diabetes (P=4 x 10(-6)) or pulmonary venous congestion (P=2 x 10(-12)); inferior infarctions were correlated with a lower prevalence of hypertension (P=0.001), hypercholesterolemia (P=0.02) or diabetes (P=10(-5)), and a higher prevalence of smoking (P=0.001); lateral infarctions were characterized by a smaller infarction size and lower prevalence of pulmonary congestion (P=0.002). Among men under the age of 50 with inferior infarction there were 90% smokers, which was significantly more than among their gender (P=0.005) or infarct site (P=2 x 10(-5)) counterparts. After adjustment for age and other confounding factors, the prevalence of inferior infarction was higher in men (P=0.002). Increased age (P=0.002), female gender (P=0.0006), anterior site (P=10(-5)), diabetes (P=0.0003), greater creatine kinase-MB fraction level (P=0.001) and pulmonary congestion (P=9 x 10(-6)) were independent predictors of an adverse hospital outcome. Each site of acute myocardial infarction has relatively specific preinfarction and clinical features. Our results suggest a greater importance of vasoconstriction in the pathophysiology of inferior infarction, especially in young male smokers, and greater importance of advanced atherosclerotic process in occurrence of anterior infarction.

Adult↗