Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Infarction”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
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↗
PubMed2005

Hypoxia-inducible factor 1-alpha reduces infarction and attenuates progression of cardiac dysfunction after myocardial infarction in the mouse.

OBJECTIVES: The aim of this research was to test whether constitutive expression of hypoxia-inducible factor 1-alpha (HIF-1alpha) influences infarction size and cardiac performance after myocardial infarction. BACKGROUND: A major question in clinical medicine is whether infarction size and border zone remodeling of the heart can be influenced by the overexpression of specific genes in the peri-infarction region. METHODS: We investigated the role of constitutive HIF-1alpha expression in acute myocardial infarction using a transgenic model. Transgenic mice containing the HIF-1alpha gene under the control of the alpha-myosin heavy chain promoter were constructed. Myocardial infarction was produced by coronary ligation in HIF-1alpha transgenic mice and control animals. Extent of infarction was then quantitated by two-dimensional and M-mode echocardiography as well as by molecular and pathologic analysis of heart samples in infarct, peri-infarct, and remote heart regions at serial time points. RESULTS: Constitutive overexpression of HIF-1alpha in the murine heart resulted in attenuated infarct size and improved cardiac function 4 weeks after myocardial infarction. Significantly, we found an increase in both capillary density as well as vascular endothelial growth factor and inducible nitric oxide synthase expression in peri-infarct and infarct regions in the hearts of constitutive HIF-1alpha-expressing animals compared to control animals. CONCLUSIONS: These observations suggest the involvement of HIF-1alpha in myocardial remodeling and peri-infarct vascularization. Our results show that supranormal amounts of this peptide protect against extension of infarction and improve border zone survival in myocardial infarction.

Animals↗
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↗
PubMed1998

[Evolution of the filling pattern of the left ventricle during the first year after an acute myocardial infarct. The influence of the infarct size].

OBJECTIVES: Acute myocardial infarction induces diastolic dysfunction as a result of the alteration of left ventricular relaxation and stiffness caused by ischemia and fibrosis. This study analyzes the association of infarct size with the diastolic filling pattern and the evolution of the latter during the first postinfarction year. PATIENTS AND METHODS: The study group consisted of 68 patients with a first acute myocardial infarction treated with thrombolytic agents. A Doppler echocardiography was performed at 8 +/- 2, 32 +/- 7 and 370 +/- 23 days after infarction. Five measurements of the ratio between E and A waves peak velocities (E/A ratio) and of the E deceleration time (EDT, ms) were averaged in each echocardiographic study. The patients were divided according to infarct size into a large infarct group (creatine kinase > 1,000 U/ml; 1,913 +/- 883; n = 26) and a small infarct group (creatine kinase < 1,000 U/ml; 556 +/- 227; n = 42). RESULTS: The large infarct group exhibited a greater E/A ratio and shorter EDT than the small infarct group in the first week (E/A ratio: 1.4 +/- 0.7 vs 0.8 +/- 0.3; p = 0.0001; EDT: 159 +/- 49 vs 192 +/- 56; p = 0.02) and at one month (E/A ratio: 1.2 +/- 0.7 vs 0.9 +/- 0.3; p = 0.01; EDT: 170 +/- 55 vs 207 +/- 40; p = 0.004); however no differences were observed between either group at one year in either E/A ratio (0.8 +/- 0.2 vs 0.9 +/- 0.4; NS) or EDT (207 +/- 44 vs 219 +/- 54; NS). In the large infarct group, E/A ratio decreased and EDT increased at one year compared to the first week (E/A ratio: p = 0.0004; EDT: p = 0.0001) and the first month (E/A: p = 0.02; EDT: p = 0.003); in contrast, in the small infarct group there were no significant differences in E/A ratio nor EDT during the first year postinfarction. CONCLUSIONS: In the first month postinfarction, large infarcts exhibit a greater E/A ratio and shorter EDT than small infarcts. The evolution of large infarcts is characterized by an attenuation of this pattern, with a progressive reduction of E/A ratio and prolongation of EDT during the first year post-infarction.

Diastole↗
PubMed1998

Significance of rest technetium-99m sestamibi imaging for the prediction of improvement of left ventricular dysfunction after Q wave myocardial infarction: importance of infarct location adjusted thresholds.

OBJECTIVE: The value of rest technetium-99m (Tc-99m) sestamibi scintigraphy under oral nitrate medication to predict myocardial viability was examined in patients with chronic infarcts. BACKGROUND: The value of rest Tc-99m sestamibi to predict viability in infarct regions has not been fully established because significant underestimation of viability, especially in the inferior myocardial wall, has been reported. METHODS: Forty patients with Q wave myocardial infarction underwent Tc-99m sestamibi single-photon emission computed tomography under nitrate medication before revascularization of the infarct-related artery. Wall motion was quantified from paired angiograms before and 4 months after revascularization. Tracer uptake was quantified in the central infarct region identified on the angiogram. RESULTS: The average Tc-99m sestamibi uptake in the central infarct region of patients with anterior infarcts and improvement of left ventricular function was significantly higher (68+/-12%, mean+/-SD) than in patients without improvement of function (40+/-14%, p < 0.02). The average Tc-99m sestamibi uptake in the central infarct region of patients with improvement of function and inferior infarcts was significantly lower (43+/-7%) than in patients with anterior infarcts (68+/-12%, p < 0.003), but was significantly higher than in patients with inferior infarction and no improvement of function (31+/-7%, p < 0.02). Using an infarct location adjusted optimal threshold (50% for anterior infarcts, 35% for inferior infarcts), Tc-99m sestamibi had a positive predictive value of 90% and a negative predictive value of 91% for improvement of left ventricular function. CONCLUSION: Quantitative rest Tc-99m sestamibi scintigraphy after oral nitrates reliably predicts improvement of left ventricular function after revascularization if infarct location adjusted thresholds are used.

Aged↗
PubMed1998

Early angiotensin converting enzyme inhibitor therapy after experimental myocardial infarction prevents left ventricular dilation by reducing infarct expansion: a possible mechanism of clinical benefits.

OBJECTIVE: To examine the effects of early angiotensin-converting enzyme (ACE) inhibitor therapy after myocardial infarction on infarct expansion in an experimental rat model. BACKGROUND: ACE inhibitor therapy within 24 h of acute myocardial infarction (AMI) reduces mortality by unknown mechanism(s). METHODS: Rats underwent permanent coronary artery occlusion. A treated group received enalapril (1.9+/-0.2 mg/kg) daily in drinking water beginning 2 h after coronary artery occlusion, a time too late to reduce infarct size. Rats were sacrificed 2 days or 2 weeks after myocardial infarction. Hearts were arrested and fixed at a constant pressure, then sectioned and photographed for morphometric analysis. RESULTS: Infarcts in the control group expanded between 2 days and 2 weeks after myocardial infarction (expansion index 0.7+/-0.1 versus 2.5+/-0.4, P< 0.05). However, infarct expansion remained unchanged in the enalapril group between 2 days and 2 weeks after myocardial infarction (expansion index 0.8+/-0.1 versus 1.3+/-0.1, NS). Two weeks after myocardial infarction, the enalapril group had fewer expanded infarcts than the control group (expansion index 1.3+/-0.1 versus 2.5+/-0.4, P< 0.05). While left ventricular volume increased in the control group between 2 days and 2 weeks after myocardial infarction (0.17+/-0.01 ml versus 0.36+/-0.03 ml, P< 0.05), it remained constant in the enalapril group (0.22+/-0.02 ml versus 0.25+/-0.03 ml, NS). Two weeks after myocardial infarction, the left ventricles were larger in the control group than in the enalapril group (0.36+/-0.03 ml versus 0.25+/-0.03 ml, P< 0.05). CONCLUSIONS: Treatment with enalapril initiated 2 h after AMI prevented left ventricular dilation by limiting infarct expansion. This may explain the mechanism by which ACE inhibitor therapy started within 24 h of an AMI improves survival 5-6 weeks after infarction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

Determinants of infarct size in reperfusion therapy for acute myocardial infarction.

BACKGROUND: Experimental animal studies have demonstrated that myocardium at risk, residual collateral flow, and duration of coronary artery occlusion are important determinants of final infarct size. The present study examined these variables in patients with acute myocardial infarction in relation to final infarct size. METHODS AND RESULTS: Myocardium at risk was assessed with hexakis(2-methoxyisobutyl isonitrile) technetium (I) (99mTc sestamibi) in 89 patients with first-time myocardial infarction (anterior, 48 patients; inferior, 41 patients). All patients had successful reperfusion therapy with either intravenous thrombolysis (32 patients) or primary coronary angioplasty (57 patients) within 24 hours of the onset of chest pain (4.7 +/- 3.9 hours; range, 0.5-21.5 hours) documented by coronary angiography. 99mTc sestamibi was injected intravenously before reperfusion therapy, and tomographic imaging was performed 1-6 hours later. Myocardium at risk was quantitated for each patient and expressed as a percentage of the left ventricle: 35 +/- 19%; range, 2-73%. Collateral flow was estimated by both invasive and noninvasive methods. Fifty-three patients with TIMI grade 0 or I flow who underwent primary coronary angioplasty had collateral flow graded angiographically (0-3) before the first balloon inflation. All patients had collateral flow estimated noninvasively from the acute sestamibi short-axis profile curve by three methods that assess the severity of the perfusion defect. Each of these three methods was significantly associated with angiographic collateral grade. Final infarct size was determined at hospital discharge by a second sestamibi study (17 +/- 17%; range, 0-59%). Myocardium at risk (r = 0.61, p less than 0.0001), angiographic collateral grade (p = 0.0003), and radionuclide estimates of collateral flow (r = 0.69-0.70, all p less than 0.0001) were all significantly associated with final infarct size. The time to reperfusion therapy was not significantly associated with final infarct size by univariate analysis (r = 0.18, p = 0.10). Two multivariate models were constructed to determine which variables were independently associated with final infarct size. In the invasive model, myocardium at risk, angiographic collateral grade with an interaction term for infarct location, and time to reperfusion were all independently significant and accounted for 70% of the variability in final infarct size. The noninvasive model, which substituted a radionuclide estimate of collateral flow for angiographic collateral grade, showed nearly identical results, accounting for 68% of the variability in infarct size in patients where the infarct artery was known to be occluded. When all patients were included (patients with and without acute angiography), the noninvasive model accounted for 59% of the variability in infarct size. CONCLUSIONS: Myocardium at risk, collateral flow, and duration of coronary occlusion are each independently associated with final infarct size and account for most of its variability. Ideally, all three parameters should be examined in evaluation of the efficacy of new treatment strategies for acute myocardial infarction.

Adult↗
PubMed1993

Cerebellar infarction. Clinical and neuroimaging analysis in 293 patients. The Tohoku Cerebellar Infarction Study Group.

BACKGROUND AND PURPOSE: We performed this multicenter study to explore the full spectrum of the clinical characteristics and neuroimaging findings of cerebellar infarction, including patients with mild to severe illnesses. METHODS: We studied 293 consecutive patients with cerebellar infarction diagnosed by computed tomography and/or magnetic resonance imaging who were admitted to 36 hospitals during 5 years. RESULTS: Cerebellar infarcts constituted 2.3% of the total patients with acute brain infarction. The backgrounds and risk factors were similar to those in patients with infarctions of the cerebral hemispheres. At least 24% were embolic, and the diagnosis of embolism could not be ruled out in 27%. Infarcts involving the superior cerebellar artery (SCA) region (52%) and the posterior inferior cerebellar artery (PICA) region (49%) were far more frequent than those involving the anterior inferior cerebellar artery (AICA) region (20%). Patients with SCA infarcts exhibited obtunded consciousness and ataxia more frequently than those with PICA infarcts (P < .05). Infarcts in the PICA regions were associated with abnormalities of the PICA (64%) or the vertebral arteries (57%), whereas infarcts in the SCA and AICA regions were associated with abnormalities in the SCA or AICA, respectively, in approximately 30% of patients, in the basilar artery in approximately 16%, and in the vertebral artery in more than 60% of patients. Outcomes were poorer with SCA infarcts than with AICA and PICA infarcts. CONCLUSIONS: These data indicate similar frequencies of SCA and PICA infarcts and illustrate the difference in clinical presentation and outcomes between SCA and PICA infarcts. They also indicate that not only in situ thrombosis but also cardiogenic or artery-to-artery embolism and the insufficiency of collateral circulation play important roles in the pathogenesis of cerebellar infarction.

Aged↗
PubMed1989

[Clinical methods for evaluating infarct size and its anatomic correlations. Study carried out in 193 cases. III. Comparison of data on the evaluation of the infarct size using the QRS score and a method of maximal creatine kinase determination in the serum].

AIMS: To compare two methods concerning the clinical evaluation of infarct size--one using a QRS score, the other based on peak Ck values--applied to the same population. CONCEPT AND PLACE OF THE STUDY: to determine--based on previously established correlations between a QRS score and the anatomic total infarct size on one hand, and between the peak CK values and the anatomic recent infarct size on the other hand--which myocardial infarction subgroup constitutes the best indication for each method. The study took place in a Coronary Care Unit of a Central Hospital. MATERIAL AND METHODS: 193 patients who died successively of acute myocardial infarction through out 4 years were studied. After establishing the exclusion critéria, the QRS score was calculated according to the method of Selvester modified by Wagner, and peak CK values were evaluated. Infarct size, either recent or old, was determined by means of an anatomical method developed by the authors and based on Hackel's and Alonso's previous works. Correlations were established between data from each clinical method and those from the anatomical method. Several myocardial infarction subgroups were considered for comparison of the correlations found in each subset. RESULTS AND CONCLUSIONS: As long as QRS score was regarded, significant correlations were found between the evaluation by QRS score and anatomical infarct size in the subgroups of patients with severe pump failure, prior myocardial infarction, or total loss of ventricular muscle mass of at least 20 percent; however, a significant correlation was missing when the whole myocardial infarction group was taken into consideration. When peak CK value were considered, a weak significant correlation was found between the evaluation by enzyme determination and anatomical infarct size in the whole group of patients, but a stronger correlation was present in the subgroups of patients with survival longer than 24 hours, anterior wall myocardial infarction, free wall cardiac rupture, or first acute myocardial infarction. In conclusion the choice of the method to be used in the clinical evaluation of infarct size should take into account the type of population beeing studied, and follow the results obtained in different myocardial infarction subgroups as mentioned above.

Creatine Kinase↗
PubMed1983

[Diagnosis of myocardial infarction by CT: the study of an initial filling defect and late enhancement of the infarcted myocardium after injection of contrast material].

Several animal experimental studies have shown that the enhanced CT gives the direct evidence of acute myocardial infarction characterized by an initial filling defect and late enhancement in the site of the damaged myocardium. Therefore, we studied experimentally and clinically the diagnostic value of these CT findings in detecting and quantitating recent and remote myocardial infarctions. Sixteen mongrel dogs with anterior myocardial infarction were subjected to the present study. The cardiac infarction within one month after coronary arterial ligation was visualized as a filling defect by early CT scan after intravenous injection of contrast material. The delayed scan after the injection showed late enhancement of the infarcted area in both acute and chronic phases. Post mortem histologic studies confirmed that the area of filling defect coincided with the necrotic myocardium and late enhancement coincided with the totally infarcted myocardium including healed scar. The total infarct size measured from CT images was closely correlated with histo-pathological infarct volume (r = 0.96). In the clinical study, the enhanced CT was performed on 112 patients with myocardial infarction and 12 patients with angina pectoris. The filling defect and late enhancement of the infarcted myocardium in the antero-septal or apical wall were detected as clearly as in the animal experiment; the former was found in 85% of the patients with recent infarction, and the latter was detected in about a half of the patients with both recent and remote infarctions. However, these CT findings were not clearly recognized in the patients with infero-posterior infarction, subendocardial infarction or angina pectoris. These results indicate the usefulness of CT in the noninvasive diagnosis and a follow-up study of myocardial infarction.

Animals↗