Larger Myocardial Infarction Size Research Articles

Coronary artery disease in patients aged 35 or less - A different beast?

Aim:To assess the extent and severity of coronary artery disease (CAD) in 200 consecutive patients aged 35 years or less undergoing diagnostic coronary angiography.Patients and Methods:Findings in these 200 patients (≤ 35 years of age) were analyzed to find the extent and severity of CAD. The mean age was 31.69 (±3.76) years. Majority were males (94%) and from the Arab ethnicity (70.5%).Result:Smoking (71%) and history of premature CAD (27%) were the most frequent risk factors (RF). History of previous ST elevation myocardial infarction (MI) was present in 68%. Anterior wall MI was the most frequent location (63.3%). The majority (54.3%) had moderate or large size MI. Ejection fraction (EF) less than 50% was noted in 30.3%. Left main or triple vessel CAD was seen in 15%. One- and two-vessel CAD was seen in 32.5% and 19% patients, respectively. Coronary angiogram was completely normal in 23.5%. The majority (54.5%) were treated conservatively and the rest (45.5%) needed percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG). The mean number of stents used was 1.3 ± 0.67 and the mean length of stents used was 20.3 ± 12.6 mm.Conclusion:The extent and severity of CAD was very significant in this subgroup of very young (≤35 years) Asian patients. Smoking was the main risk factor and half of the patients needed either PCI or CABG.

Effect of insulin and glucose infusion on myocardial infarction size in uraemic rats

The post myocardial infarction (MI) mortality rate is high in renal patients. One possible explanation is the reduced ischemia tolerance caused by uraemia. Previous investigations showed larger MI size in uraemic rats when compared with sham-operated controls. To explore a possible link between uraemic insulin resistance syndrome and MI size in uraemia, we studied an intervention model with administration of insulin and glucose during acute MI in subtotally nephrectomized (SNX) rats and sham-operated controls. In 16 SNX rats and 16 sham-operated controls, the left coronary artery was ligated for 60 min, followed by reperfusion for 90 min. To visualize the perfused myocardium, lissamine-green ink was injected. The nonperfused area (lissamine exclusion) and the area of total infarction (TTC stain) were assessed in sections of the left ventricle (LV) using image analysis. While eight SNX rats and eight sham-operated controls were treated with a placebo during the procedure, the other animals received an insulin bolus of 85 mU/kg and then a continuous insulin infusion of 8 mU/kg per minute. Blood glucose levels were clamped to baseline levels with an infusion of 25% glucose. Insulin receptor substrates (IRS-1 and IRS-2) and glucose transporter (GLUT 4) were studied by western blot in another seven SNX and seven sham-operated controls without further intervention. The infarcted area, given as a proportion of the nonperfused risk area, was not different in sham-operated controls treated with a hyperinsulinaemic clamp versus untreated (0.55 +/- 0.07 vs. 0.51 +/- 0.13, p = 0.477). The eight SNX animals treated with the hyperinsulinaemic clamp utilized significantly less glucose to stabilize baseline glucose levels when compared with the sham-operated controls (5,637 vs. 3,207 microl Glc 25%, p = 0.007). The infarcted area was significantly lower in SNX rats treated with the hyperinsulinaemic clamp compared to non-treated SNX animals (0.56 +/- 0.06 vs. 0.79 +/- 0.09, p < 0.001). SNX rats with the insulin clamp had the same infarcted area size as sham-operated controls (0.56 +/- 0.06 vs. 0.51 +/- 0.13, p = 0.357). Western blotting did not show any change in the expression of GLUT 4 and IRS-1/IRS-2 in SNX animals when compared with sham-operated controls. The size of MI in uraemic rats is significantly reduced by a glucose/insulin infusion. The results suggest an insulin resistance in uraemic rats with similar benefits of glucose/insulin application during acute MI, as found in diabetic individuals. Further analysis did not reveal a down regulation in GLUT 4 and IRS-1/IRS-2.

Acute hyperglycemia enhances oxidative stress and exacerbates myocardial infarction by activating nicotinamide adenine dinucleotide phosphate oxidase during reperfusion

Acute hyperglycemia is independently associated with larger myocardial infarct size in both diabetic and nondiabetic patients. We hypothesized that the oxidative stress imposed by acute hyperglycemia contributes to the exacerbation of infarct size during reperfusion. C57BL/6 mice underwent 30 minutes of occlusion of the left anterior descending coronary artery followed by 60 minutes of reperfusion. Acute hyperglycemia was induced with an intraperitoneal injection of dextrose (2g/kg body weight) 30 minutes before left anterior descending occlusion. An antioxidant, N-2-mercaptopropionyl glycine, was injected intravenously 2 minutes before the onset of reperfusion at a dose of 20 mg/kg. A nicotinamide adenine dinucleotide phosphate oxidase inhibitor, apocynin (50 mg/kg), was applied either before or after the induction of hyperglycemia. Blood glucose level before left anterior descending occlusion was 153 +/- 19 mg/dL in control mice and 444 +/- 26 mg/dL in hyperglycemic mice (P < .05). Plasma lipid peroxidation product (malondialdehyde) was significantly increased in both control and hyperglycemic mice at 1 hour after reperfusion, and levels of malondialdehyde in hyperglycemic mice were higher than that in control mice (3.38 +/- 0.21 vs 2.33 +/- 0.12 micromol/L; P < .05). N-2-mercaptopropionyl glycine administered just before reperfusion significantly reduced malondialdehyde levels in both control and hyperglycemic mice (1.21 +/- 0.06 and 1.03 +/- 0.24 micromol/L). Acute hyperglycemia increased infarct size (percent of risk region) from 34.0 +/- 2.7 to 49.4 +/- 1.6 (P < .05). N-2-mercaptopropionyl glycine reduced infarct size to 19.5 +/- 2.3 in control mice and to 26.2 +/- 2.9 in hyperglycemic mice. Apocynin also reduced malondialdehyde levels and infarct size in hyperglycemic mice if administered 5 minutes before injection of dextrose, but not before reperfusion. Acute hyperglycemia enhances oxidative stress and exacerbates myocardial infarction in mice through activation of nicotinamide adenine dinucleotide phosphate oxidase.

Performance of two-dimensional Doppler echocardiography for the assessment of infarct size and left ventricular function in rats

Although echocardiography has been used in rats, few studies have determined its efficacy for estimating myocardial infarct size. Our objective was to estimate the myocardial infarct size, and to evaluate anatomic and functional variables of the left ventricle. Myocardial infarction was produced in 43 female Wistar rats by ligature of the left coronary artery. Echocardiography was performed 5 weeks later to measure left ventricular diameter and transverse area (mean of 3 transverse planes), infarct size (percentage of the arc with infarct on 3 transverse planes), systolic function by the change in fractional area, and diastolic function by mitral inflow parameters. The histologic measurement of myocardial infarction size was similar to the echocardiographic method. Myocardial infarct size ranged from 4.8 to 66.6% when determined by histology and from 5 to 69.8% when determined by echocardiography, with good correlation (r = 0.88; P < 0.05; Pearson correlation coefficient). Left ventricular diameter and mean diastolic transverse area correlated with myocardial infarct size by histology (r = 0.57 and r = 0.78; P < 0.0005). The fractional area change ranged from 28.5 +/- 5.6 (large-size myocardial infarction) to 53.1 +/- 1.5% (control) and correlated with myocardial infarct size by echocardiography (r = -0.87; P < 0.00001) and histology (r = -0.78; P < 00001). The E/A wave ratio of mitral inflow velocity for animals with large-size myocardial infarction (5.6 +/- 2.7) was significantly higher than for all others (control: 1.9 +/- 0.1; small-size myocardial infarction: 1.9 +/- 0.4; moderate-size myocardial infarction: 2.8 +/- 2.3). There was good agreement between echocardiographic and histologic estimates of myocardial infarct size in rats.

Myocardial Performance Index in Female Rats with Myocardial Infarction: Relationship with Ventricular Function Parameters by Doppler Echocardiography

The aim of the study was to analyze the myocardial performance index (MPI), its relationship with the standard variables of systolic and diastolic functions, and the influence of time intervals in an experimental model of female rats with myocardial infarction (MI). Forty-one Wistar female rats were submitted to surgery to induce MI. Six weeks later, Doppler echocardiography was performed to assess infarct size (IS,%), fractional area change (FAC,%), ejection fraction biplane Simpson (EF), E/A ratio of mitral inflow, MPI and its time intervals: isovolumetric contraction (IVCT, ms) and relaxation (IVRT, ms) times, and ejection time (ET, ms); MPI = IVCT + IVRT/ET. EF and FAC were progressively lower in rats with small, medium and large-size MI ( P < .001). E/A ratio was higher only in rats with large-size MI (6.25 +/- 2.69; P < .001). MPI was not different between control rats and small-size MI (0.37 +/- 0.03 vs 0.34 +/- 0.06, P = .87), but different between large and medium-size MI (0.69 +/- 0.08 vs 0.47 +/- 0.07; P < .001) and between these two compared to small-size MI. MPI correlated with IS (r = 0.85; P < .001), EF (r = -0.86; P < .001), FAC (r = -0.77; P < .001) and E/A ratio (r = 0.77; P < .001, non-linear). IVCT was longer in large size MI compared to medium-size MI (31.87 +/- 7.99 vs 15.92 +/- 5.88; P < .001) and correlated with IS (r = 0.85; P < .001) and MPI (r = 0.92; P < .001). ET was shorter only in large-size MI (81.07 +/- 7.23; P < .001), and correlated with IS (r = -0.70; P < .001) and MPI (r = -0.85; P < .001). IVRT was shorter only in large-size compared to medium-size MI (24.40 +/- 5.38 vs 29.69 +/- 5.92; P < .037), had borderline correlation with MPI (r = 0.34; P = .0534) and no correlation with IS (r = 0.26; p = 0.144). The MPI increased with IS, correlated inversely with systolic function parameters and had a non-linear relationship with diastolic function. These changes were due to the increase of IVCT and a decrease of ET, without significant influence of IVRT.

Measurement of Ejection Fraction After Myocardial Infarction in the Population

To assess the secular trends in left ventricular ejection fraction (LVEF) assessment after myocardial infarction (MI) and to identify the determinants of testing. A population-based MI incidence cohort. The use of tests measuring LVEF (echocardiography, radionuclide, and left ventricular [LV] angiography) was examined among all consecutive residents of Olmsted County, MN, hospitalized for a validated incident MI between 1979 and 1998. Baseline characteristics and outcome were ascertained from community medical records. Among 2,317 patients with incident MI, LVEF assessment increased from 1979 to 1986 (22 to 85%; p value for trend = 0.0001) to stabilize thereafter until 1998. During the most recent decade, LVEF was measured during the hospital stay in 81% of the patients. Characteristics associated with lesser use of tests included older age and measurement of ejection fraction within 1 year prior to the index MI. Larger MI size, prolonged hospital stay, and involvement of a cardiologist as a care provider were positively associated with determination of LVEF. Measurement of LVEF after MI increased in the last 2 decades, but there continues to be a group of patients in whom it is not done. Given the potential benefits of LVEF measurement, including knowledge for risk stratification and therapeutic choices as underscored in recent practice guidelines, there may be additional opportunities for improving outcomes by ensuring its more consistent use. However, as testing for LVEF differs according to patient characteristics, reliance on selected clinically performed LVEF measurements will result in biased estimates of the prevalence of LV dysfunction after MI.

Influence of myocardial infarction size on radionuclide and Doppler echocardiographic measurements of diastolic function

To assess the relation between myocardial infarction size and diastolic function as measured by radionuclide ventriculography and Doppler echocardiography, 83 patients (aged 58 ± 9 years) without significant valvular disease were studied 8 to 12 weeks after an acute myocardial infarction. Myocardial infarction size was measured by resting thallium-201 tomography. Peak early filling rate (in end-diastolic volumes/s) was measured by gated blood pool scintigraphy. Doppler measures of mitral inflow were peak early (E) and atrial (A) filling velocities, slopes of E and A, percent E and A filling, E A ratio and diastolic filling period. In univariate analyses, there was a significant inverse correlation between infarction size and the peak early filling rate (r = −0.59, p < 0.001), and this remained significant (r = −0.63, p < 0.0001) in an analysis that included 2 other determinants of the filling rate, age and diastolic filling period. Infarction size was directly correlated to the peak E velocity (r = 0.37, p < 0.01), deceleration of E (r = 0.41, p < 0.01) and percent E filling (r = 0.31, p < 0.01), and was inversely correlated to peak A (r = −0.27, p < 0.05) and percent A filling (r = −0.26, p < 0.05). The correlation of myocardial infarction size with the E A ratio was r = 0.43 (p < 0.01) and remained significant in a multivariate analysis that included age and diastolic filling period (r = 0.53, p < 0.001). Thus, a larger myocardial infarction size was associated with a reduced peak early filling rate by radionuclide angiography, a higher peak E and a lower peak A velocity, and an increased E A ratio by Doppler. In addition to the other variables known to influence diastolic measurements, these results suggest that myocardial infarction size determines, in part, diastolic function as assessed by either radionuclide or Doppler techniques.

Precordial S-T segment depression in inferior myocardial infarction: Evaluation by quantitative thallium-201 scintigraphy and technetium-99m ventriculography

The relation of initial precordial S-T segment depression to anterior ischemia and eventual prognosis was studied in 70 patients with acute inferior myocardial infarction (MI). Early quantitative thallium-201 scintigraphy and technetium-99m ventriculography were used to evaluate anterior ischemia. In comparison with patients without S-T segment depression, those with depression had lower global ejection fraction (EF), 45 ± 10 versus 52 ± 7 (p <0.01), lower inferoposterior regional EF, 40 ± 14 versus 52 ± 13 (p <0.005), and larger thallium-201 defect index, 21 ± 7 versus 16 ± 6 (p <0.005). In contrast, anteroseptal regional EFs were similar in the 2 groups, 54 ± 13 versus 56 ± 12 (p not significant [NS]), and the frequency of anteroseptal thallium-201 defects or redistribution abnormalities was not significantly different, 17 of 47 versus 5 of 23 and 8 of 31 versus 4 of 11 (p = NS). The predictive value of precordial S-T segment depression for mortality was low (21%) compared with the Killip class (75%), chest radiographs (67%), and EF (60%). Multiple logistic regression confirmed that the presence of S-T segment depression did not significantly improve the prediction of mortality when considered with these other risk factors. Thus, <i>precordial S-T segment depression is a marker of larger MI size and not of anterior ischemia</i>. When examined with other variables reflecting MI size and left ventricular function, precordial S-T segment depression was not a significant independent risk factor.