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PubMed2005

Myeloperoxidase-generated oxidants modulate left ventricular remodeling but not infarct size after myocardial infarction.

BACKGROUND: Inflammation after myocardial infarction (MI) heralds worse left ventricular (LV) function and clinical outcomes. However, whether inflammation affects LV function by extending myonecrosis and/or altering LV remodeling remains unknown. We hypothesized that cytotoxic aldehydes generated during oxidative stress may adversely affect remodeling and infarct size. One theoretical source of reactive aldehydes is oxidation of common alpha-amino acids by myeloperoxidase (MPO) released by leukocytes. However, a role for MPO in formation of aldehydes in vivo and the functional consequences of MPO-generated oxidants in ischemia/reperfusion models of MI have not been established. METHODS AND RESULTS: In studies with cell types found in vascular tissue, MPO-oxidation products of glycine (formaldehyde) and threonine (acrolein) were the most cytotoxic. Mass spectrometry studies of myocardial tissue from murine models of acute MI (both chronic left anterior descending coronary artery ligation and ischemia/reperfusion injury) confirmed that MPO serves as a major enzymatic source in the generation of these cytotoxic aldehydes. Interestingly, although MPO-null mice experienced 35.1% (P<0.001) less LV dilation and a 52.2% (P<0.0001) improvement in LV function compared with wild-type mice 24 days after ischemia/reperfusion injury, no difference in infarct size between wild-type and MPO-null mice was noted. CONCLUSIONS: The present data separate inflammatory effects on infarct size and LV remodeling and demonstrate that MPO-generated oxidants do not significantly affect tissue necrosis after MI but rather have a profound adverse effect on LV remodeling and function.

Acrolein↗
PubMed2005

Mortality and morbidity remain high despite captopril and/or Valsartan therapy in elderly patients with left ventricular systolic dysfunction, heart failure, or both after acute myocardial infarction: results from the Valsartan in Acute Myocardial Infarction Trial (VALIANT).

BACKGROUND: The elderly constitute an increasing proportion of acute myocardial infarction patients and have disproportionately high mortality and morbidity. Those with heart failure or impaired left ventricular left ventricular function after acute myocardial infarction have high complication and mortality rates. Little is known about outcomes with contemporary therapies in these patients. METHODS AND RESULTS: The Valsartan in Acute Myocardial Infarction Trial (VALIANT) randomized 14,703 patients with heart failure and/or left ventricular ejection fraction <40% to receive captopril, valsartan, or both. Mortality and a composite end point, including cardiovascular mortality, readmission for heart failure, reinfarction, stroke, and resuscitated cardiac arrest, were compared for the age groups of <65 (n=6988), 65 to 74 (n=4555), 75 to 84 (n=2777), and > or =85 (n=383) years. With increasing age, 3-year mortality almost quadrupled (13.4%, 26.3%, 36.0%, and 52.1%, respectively), composite end-point events more than doubled (25.2%, 41.0%, 52.3%, and 66.8%), and hospital admissions for heart failure almost tripled (12.0%, 23.1%, 31.3%, and 35.4%). Outcomes did not differ between the 3 study treatments in any age group. Adverse events associated with captopril and valsartan were more common in the elderly and in patients receiving combination therapy. With increasing age, use of aspirin, beta-blockers, and statins declined, and use of digoxin, calcium-channel blockers, and non-potassium-sparing diuretics increased. On 3-year multivariable analysis, each 10-year age increase was associated with a hazard ratio of 1.49 (95% CI, 1.426 to 1.557; P<0.0001) for mortality and an odds ratio of 1.38 (95% CI, 1.31 to 1.46; P<0.0001) for readmission with heart failure. CONCLUSIONS: Outcomes remained poor in elderly patients with heart failure and/or impaired left ventricular systolic function after acute myocardial infarction, although most received beta-blockers and all received an ACE inhibitor and/or an angiotensin receptor blocker. Better therapies and increased use of aspirin, beta-blockers, and statins are needed in this important and increasing patient group.

Age Factors↗
PubMed1993

The clinical outcome of acute myocardial infarction is related to the circadian rhythm of myocardial infarction onset.

In order to study whether the circadian rhythm of acute myocardial infarction (AMI) onset has any impact on the clinical outcome, in terms of enzymatically estimated infarct size, circulatory arrest from ventricular tachyarrhythmias, and in-hospital mortality, the authors studied a representative population of 10,791 AMIs treated in the same center between 1973 and 1987. In 6,763 cases (63%) the time of symptom onset was known. In these cases a major peak in AMI incidence was observed between 7:01 AM and 10:00 AM, and minor peaks at 12:01 noon, 3:01 PM-4:00 PM, and 8:01 PM-9:00 PM. In a set of multivariate analyses including several clinical characteristics, symptom onset between 6:00 AM and 12:00 noon significantly predicted a greater infarct size, and symptom onset between 12:00 AM and 6:00 AM was associated with a significantly lower risk of circulatory arrests from ventricular tachyarrhythmias. The time of symptom onset was not significantly associated with in-hospital mortality after adjustment for other clinical characteristics, including infarct size. The authors suggest that the time of day has an impact, not only on the incidence, but also on the severity of AMI and that the ability of beta blockers to blunt the morning increase in AMI incidence may possibly contribute to the beneficial secondary preventive effects of such drugs after AMI.

Aged↗
PubMed2005

Quantitative assessment of harmonic power doppler myocardial perfusion imaging with intravenous Levovist in patients with myocardial infarction: comparison with myocardial viability evaluated by coronary flow reserve and coronary flow pattern of infarct-related artery.

BACKGROUND: Myocardial contrast echocardiography and coronary flow velocity pattern with a rapid diastolic deceleration time after percutaneous coronary intervention has been reported to be useful in assessing microvascular damage in patients with acute myocardial infarction. AIM: To evaluate myocardial contrast echocardiography with harmonic power Doppler imaging, coronary flow velocity reserve and coronary artery flow pattern in predicting functional recovery by using transthoracic echocardiography. METHODS: Thirty patients with anterior acute myocardial infarction underwent myocardial contrast echocardiography at rest and during hyperemia and were quantitatively analyzed by the peak color pixel intensity ratio of the risk area to the control area (PIR). Coronary flow pattern was measured using transthoracic echocardiography in the distal portion of left anterior descending artery within 24 hours after recanalization and we assessed deceleration time of diastolic flow velocity. Coronary flow velocity reserve was calculated two weeks after acute myocardial infarction. Left ventricular end-diastolic volumes and ejection fraction by angiography were computed. RESULTS: Pts were divided into 2 groups according to the deceleration time of coronary artery flow pattern (Group A; 20 pts with deceleration time > or = 600 msec, Group B; 10 pts with deceleration time < 600 msec). In acute phase, there were no significant differences in left ventricular end-diastolic volume and ejection fraction (Left ventricular end-diastolic volume 112 +/- 33 vs. 146 +/- 38 ml, ejection fraction 50 +/- 7 vs. 45 +/- 9 %; group A vs. B). However, left ventricular end-diastolic volume in Group B was significantly larger than that in Group A (192 +/- 39 vs. 114 +/- 30 ml, p < 0.01), and ejection fraction in Group B was significantly lower than that in Group A (39 +/- 9 vs. 52 +/- 7%, p < 0.01) at 6 months. PIR and coronary flow velocity reserve of Group A were higher than Group B (PIR, at rest: 0.668 +/- 0.178 vs. 0.248 +/- 0.015, p < 0.0001: during hyperemia 0.725 +/- 0.194 vs. 0.295 +/- 0.107, p < 0.0001; coronary flow velocity reserve, 2.60 +/- 0.80 vs. 1.31 +/- 0.29, p = 0.0002, respectively). CONCLUSION: The preserved microvasculature detecting by myocardial contrast echocardiography and coronary flow velocity reserve is related to functional recovery after acute myocardial infarction.

Blood Flow Velocity↗
PubMed2006

Close association of regional interleukin-6 levels in the infarct-related culprit coronary artery with restenosis in acute myocardial infarction.

BACKGROUND: The involvement of interleukin (IL)-6 in restenosis of the recanalized coronary artery after the percutaneous coronary intervention (PCI) was examined. METHODS AND RESULTS: There were 40 patients enrolled in the study who had acute myocardial infarction and whose infarct-related coronary arteries were treated by new thrombectomy devices and stenting. Blood samples were collected from the culprit coronary artery before and immediately after the maneuver of the PCI. Restenosis was defined as residual stenosis because it accounted for more than 50% at the follow-up coronary angiography. Plasma IL-6 levels in the infarct-related coronary artery were 12.8 and 13.2 pg/ml before and after the initial maneuver of the PCI, respectively, values that were significantly greater than that of 7.2 pg/ml in the peripheral vein (p<0.0001). The levels of IL-6 in the pre- and the post-stage of PCI were significantly greater in the patients with restenosis than those without restenosis. The plasma IL-6 levels in the post-stage of PCI had significant correlations with late loss and loss index. CONCLUSIONS: The present study findings indicate that plasma IL-6 levels in the culprit coronary artery at the post-stage of PCI are closely associated with the future restenosis of the revasculized coronary artery in acute myocardial infarction.

Acute Disease↗
PubMed1985

Macroscopic hemorrhagic infarction following selective coronary thrombolysis in acute myocardial infarction.

Macroscopic hemorrhagic infarction was studied in 14 autopsied hearts with selective coronary thrombolysis (SCT) after acute myocardial infarction (AMI). In all patients urokinase, 240,000 - 720,000 units, had been selectively injected into ischemia-related coronary artery at 2 - 7 hours after the onset of AMI. The degree of stenosis after SCT was 90 - 99% in 13 patients and 100% in one patient. According to the duration of illness at death, the 14 patients were classified into 3 stages; stage I: 4 - 9 hours; stage II: 15 hours to 11 days; stage III: 19 days to 12 months. Three hearts in stage I had no macroscopic hemorrhage. In stage II, marked and diffuse hemorrhage in the infarct area was macroscopically evident in 6 of 7 hearts. In a stage II patient, extravasation of contrast medium into the myocardium was found at 3 hours after the onset of AMI. In stage III, 4 hearts had massive fibrosis or granulation in the left ventricular wall without macroscopic hemorrhage. Cardiac rupture was seen in 4 of 10 patients from stages I and II. It is concluded that macroscopic bleeding appears in most patients with AMI treated with coronary thrombolysis. In the majority of cases, the hemorrhage increases gradually after SCT and becomes macroscopically definite approximately 15 hours after the onset of AMI. Rarely, massive bleeding appears earlier. Hemorrhagic infarction is replaced by massive fibrosis after approximately 2 weeks.

Aged↗
PubMed1993

Estimation of infarct size using serum troponin T concentration in patients with acute myocardial infarction.

To estimate the size of myocardial infarction, serum troponin T concentration was measured in 34 patients with acute myocardial infarction. Left ventriculography, 2-dimensional echocardiography and resting 201thallium myocardial single photon emission computed tomography (SPECT) were performed about 4 weeks after the onset of myocardial infarction and used for correlation with the late serum troponin T peak concentration which occurred on the 3rd to 5th day after onset. Both left ventricular ejection fraction (LVEF) obtained from left ventriculography and wall motion index (WMI) obtained from 2-dimensional echocardiography were inversely related to late troponin T peak value (LVEF: r = 0.68, p < 0.001, WMI: r = 0.70, p < 0.001). Extent score (ES) and severity score (SS), which were estimated from the initial resting 201thallium SPECT image, showed excellent linear correlations with late troponin T peak concentrations (ES: r = 0.77, p < 0.001, SS: r = 0.66, p < 0.001). This correlation was present both in patients with an early troponin T peak on day 1 (group A-16 patients) and in those without an early peak (group B-10 patients). Thus, late troponin T peak concentration can be used to predict infarct size regardless of the kinetics of its appearance in serum.

Adult↗
PubMed1994

Clinico-pathological study of the role of infarct expansion in patients with cardiac rupture following acute myocardial infarction.

The purpose of this study was to clarify whether the infarct expansion with cardiac rupture following acute myocardial infarction pathomorphologically differed from expansion without rupture. Eighteen autopsied patients with rupture were classified into acute phase (time between the onset of myocardial infarction and death < or = 36 h) and subacute phase (> 36 h). These patients were compared with 25 patients with no rupture using new parameters of expansion: radius index, cavity index, expansion area index and thinning-dilatation index of the left ventricle. In the acute phase, each parameter was significantly higher in the ruptured group than in the non-ruptured group (radius index: 0.49 +/- 0.28 vs 0.14 +/- 0.16, p < 0.005, cavity index: 0.21 +/- 0.09 vs 0.08 +/- 0.06, p < 0.005, expansion area index: 0.75 +/- 0.25 vs 0.34 +/- 0.23, p < 0.001, thinning-dilatation index: 2.89 +/- 1.31 vs 1.53 +/- 0.52, p < 0.001). However, in the subacute phase there were no differences in these parameters between the two groups. These data suggest that in the acute phase, but not the subacute phase, the degree of expansion and the proportion of expansion to infarcted area are associated with rupture.

Aged↗
PubMed1995

Gender difference in long-term prognosis after myocardial infarction--clinical characteristics in 1000 patients. The Kyoto and Shiga Myocardial Infarction (KYSMI) Study Group.

To examine gender differences in the long-term prognosis of patients with myocardial infarction, 1000 patients with myocardial infarction were studied after coronary arteriography. Over a follow-up period of 3.3 +/- 2.0 years, 65 patients died from cardiac causes and 301 experienced cardiac events (death, reinfarction and revascularization). Overall, the 5-year cardiac mortality was 8%: that in females (12.4%) was significantly higher than that in males (6.6%) (p = 0.0073). The overall 5-year cardiac event-rate was 35%, with no significant difference between females and males (41.1% vs 33.3%). Univariate analysis revealed that differences in age (57.8 +/- 9.8 years in males vs 64.8 +/- 8.9 years in females, p < 0.0001), presence of smoking habit, obesity, hypercholesterolemia, hypertension, heart failure, right coronary artery disease, nicorandil administration, hypolipidemic, diuretic and anti-hypertensive treatment, and warfarin administration were present between men and women. The mortality rate in elderly females tended to be higher than that in their male counterparts. Multivariate analysis demonstrated that number of diseased vessels, post-infarction angina and left main trunk disease were significant predictors for cardiac death in both sexes, while gender was not. Therefore, gender did not appear to affect the long-term prognosis after age-adjustment among patients with myocardial infarction in the Western part of Japan.

Adult↗
PubMed1995

Cocaine-associated myocardial infarction. Clinical safety of thrombolytic therapy. Cocaine Associated Myocardial Infarction (CAMI) Study Group.

OBJECTIVE: To determine the safety of thrombolytic use in patients with cocaine-associated myocardial infarction. DESIGN: Retrospective cross-sectional survey. SETTING: Twenty-nine acute care institutions. PATIENTS: Patients who sustained cocaine-associated myocardial infarction from 1987 to 1993 were identified through medical record review. Those who received thrombolytic therapy (n = 25) were compared with those who met electrocardiographic TIMI criteria but did not receive thrombolytic therapy (n = 41). INTERVENTIONS: None. RESULTS: Both groups of patients were similar with respect to age, gender, race, cardiac risk factors, time from last cocaine use until presentation, and duration of chest pain at the time of presentation (p > 0.20). There were no major complications or deaths in patients who received thrombolytic therapy (95% confidence interval, 0 to 12%). Minor complications occurred in only two patients. The presence or absence of clinical criteria for reperfusion was noted in the charts of 21 patients who received thrombolytic therapy: 67% were believed to reperfuse. The patients who did and did not receive thrombolytic therapy had similar median peak creatine kinase-MB (CK-MB) levels (180 vs 154 mg/dL, p = NS) and time until peak CK-MB (11.3 vs 13.6 h; p = NS). CONCLUSION: Thrombolytic therapy for cocaine-associated myocardial infarction appears to be safe. It remains unclear whether thrombolytic therapy is an important therapeutic intervention for patients with cocaine-associated myocardial infarction. Further study on efficacy is recommended prior to routine use.

Adult↗
PubMed2002

Use of biochemical markers of infarction for diagnosing perioperative myocardial infarction and early graft occlusion after coronary artery bypass surgery.

STUDY OBJECTIVES: Perioperative myocardial infarction (PMI) during coronary artery bypass grafting (CABG) is an important clinical problem because it is closely associated with increased morbidity and mortality. The diagnosis of PMI is, however, associated with several problems. Due to the surgical trauma, the usual indicators of myocardial infarction (pain, ECG changes, and elevated biochemical markers of infarction) have uncertain diagnostic value. The primary aim of this study was to illustrate the levels of the biochemical markers after uncomplicated bypass surgery defined as no clinical or ECG evidence of PMI, and no graft occlusion at 7 days by repeat angiography; and secondarily, to establish biochemical diagnostic discrimination limits for detection of in-hospital graft occlusion. METHODS AND RESULTS: One hundred three patients undergoing elective CABG were closely monitored by serial measurements of creatine kinase (CK)-MB mass, myoglobin, troponin T, and troponin I, and underwent a repeat angiography before discharge. Seven patients had ECG evidence of PMI. Peak troponin T and CK-MB values were significantly higher in these seven patients, although the diagnostic performances of the optimally chosen cutoff levels for diagnosing AMI were fair. Twelve patients had at least one occluded graft shown by repeat angiography. Peak values of CK-MB and troponin T were significantly higher in patients with graft occlusion (52.2 microg/L vs 24.7 microg/L, p = 0.01; and 3.7 microg/L vs 1.0 microg/L, p = 0.05, respectively). By multivariate analysis, a diagnostic discrimination level of 30 microg/L for CK-MB did not reach statistical significance; however, the independent diagnostic value of a cutoff level for troponin T at 3 microg/L reached a level of significance (p = 0.06). DISCUSSION: We have suggested normal values of four different biochemical markers of infarction after uncomplicated coronary bypass surgery. Patients with in-hospital graft occlusion had higher peak CK-MB and troponin T values. However, the overlap with patients without graft occlusion is substantial, and the patency status in the individual cannot be reliably predicted from these noninvasive tests.

Adult↗
PubMed1986

Right ventricular infarction mimicking extensive anterior infarction.

Two patients with inferior infarction complicated by right ventricular infarction are presented. Both manifested electrocardiographic changes involving the anterior chest leads with initial S-T segment elevation followed by loss of R waves and the development of QS complexes mimicking anterior infarction. Cardiac catheterization showed right coronary artery occlusion with normal left coronary system and anterior wall motion in each case. Radionuclide angiocardiography showed dilated poorly contracting right ventricles. The ECG changes of "anterior infarction" in these patients were therefore due solely to right ventricular injury.

Adult↗
PubMed1975

The incidence of myocardial infarction in hospitalized patients and the risk factors of myocardial infarction.

1) Patients with myocardial infarction constituted 2.36% of all the hospitalized patients during 1961-1968. The mortality of the hospitalized patients with myocardial infarction during the same term was 19.1%. The ratio of the male to female patients with myocardial infarction was 5.2. 2) As the risk factors of myocardial infarction, the following items were considered to be of importance: 1. gout in past history, 2. angina pectoris in family history, 3. diabetes mellitus in family history, 4. cigaret smoking over 40 pieces per day, 5. diabetes mellitus in past history, 6. administrative occupation, 7. serum cholesterol level over 250 mg/100 ml, 8. obesity of 20% excess over standard body weight, 9. hypertension in family history. 3) According to the statistical analysis, several groups of risk factors and interrelationship of risk factors are recognized.

Adult↗
PubMed1992

Doppler assessment of left ventricular diastolic filling pattern during the convalescent stage of acute myocardial infarction. Effects of infarct size and coronary thrombolysis.

Pulsed Doppler echocardiography was used to study left ventricular diastolic filling pattern (LVDFP) over the convalescent stage of acute myocardial infarction (AMI) in 25 patients. Twelve normal subjects served as a control group. The patients were divided on the basis of enzymatically estimated infarct size into 2 groups: 7 as the large AMI group, and the other 18 as the small AMI group. Peak early diastolic filling velocity (E) and the ratio of E to peak filling velocity at atrial contraction (E/A ratio) were determined from the Doppler transmitral flow velocity recordings at 1 and 4 weeks after the onset of AMI. At 1 week E and E/A ratio were significantly lower in the small AMI group compared to the control and the large AMI groups, however, there was no significant difference in E and E/A ratio between the control and the large AMI groups. E/A increased with cumulative CK release among the patients (r = 0.54, p < 0.01). In the following 3 weeks E and E/A ratio decreased only in the large AMI group, and E and E/A ratio at 4 weeks weakly correlated with pulmonary capillary wedge pressure (r = 0.63, p < 0.01 and r = 0.65, p < 0.01) and ejection fraction (r = 0.50, p < 0.05 and r = 0.62, p < 0.01) among the patients. There was no significant difference in E or E/A ratio between patients with and without coronary thrombolysis. Thus, LVDFP in the early convalescent stage of AMI was characterized by low E and E/A ratio in patients with small AMI, however, a "pseudonormalized" pattern was observed in patients with large AMI. The effect of the infarct size on LVDFP diminished in the late convalescent stage of AMI. LVDFP in patients with AMI appears to be influenced by the infarct size and by the time of study. The effect of coronary thrombolysis on LVDFP was not evident throughout the convalescent stage of AMI in this study.

Convalescence↗
PubMed2004

Progression of coronary atherosclerosis relates to the onset of myocardial infarction in an animal model of spontaneous myocardial infarction (WHHLMI rabbits).

Recently, we developed myocardial infarction-prone WHHLMI rabbits from coronary atherosclerosis-prone WHHL rabbits (WHHLCA rabbits) by selective breeding. In this study, we examined the relation of atherosclerotic plaques to the onset of myocardial infarction. We examined myocardial lesions of 378 WHHL rabbits born between 1992 and 2000, and atherosclerosis lesions of 93 WHHLCA and 82 WHHLMI rabbits. The aortic lesions were evaluated as percent surface lesion area. The coronary lesions were evaluated as cross sectional narrowing using sections prepared at 500 or 1,000 microm intervals. Serum lipid levels were assayed with enzymatic methods. The cumulative incidence of fatal myocardial infarction between 11 and 35 months old was 90% in WHHLMI rabbits and 21% in WHHLCA rabbits, respectively. Selective breeding increased the serum cholesterol levels by about 200 mg/dl despite there being no changes in triglyceride levels. Aortic and coronary atherosclerosis progressed markedly in WHHLMI rabbits compared to WHHLCA rabbits. Especially, WHHLMI rabbits over 15 months old showed more than 90% cross sectional narrowing of the left circumflex arteries, main stem of the left coronary artery, and the origin portion of the right coronary artery. In addition, there were no gender differences in atherosclerotic lesions of both aortas and coronary arteries. In conclusion, the present study showed that marked progression of coronary atherosclerosis was probably associated with spontaneous development of myocardial infarction in WHHLMI rabbits.

Animals↗
PubMed2002

Analysis of the prevalence of ventricular late potentials in the late phase of myocardial infarction based on the site of infarction.

OBJECTIVE: The initial site of myocardial infarction (MI) may influence the prevalence of ventricular late potentials (VLP), high-frequency signals, due to the time course of ventricular activation. The prevalence of VLP in a period of more than 2 years after acute MI was assessed focusing on the initially injured wall. METHODS: The prevalence of VLP in a late phase after MI (median of 924 days) in anterior/antero-septal and inferior/infero-dorsal wall lesion was analyzed using signal-averaged electrocardiogram in time domain. The diagnostic performance of the filters employed for analysis on was tested at high-pass cut-off frequencies of 25 Hz, 40 Hz and 80 Hz. RESULTS: The duration of the ventricular activation and its terminal portion were larger in inferior than anterior infarction, at high-pass cut-off frequencies of 40 Hz and 80 Hz. In patients with ventricular tachycardia, these differences were more remarked. The prevalence of ventricular late potentials was three times greater in inferior than anterior infarction. CONCLUSION: Late after myocardial infarction, the prevalence and the duration of ventricular late potentials are greater in lesions of inferior/infero-dorsal than anterior/antero-septal wall confirming their temporal process, reflecting their high-frequency content.

Action Potentials↗
PubMed2000

Basic fibroblast growth factor caused no change in collateral flow or infarct size of acutely-infarcted myocardium in rats.

The extent to which local administration of basic fibroblast growth factor (bFGF) increased regional myocardial blood flow (Qm) to acutely-infarcted areas of the heart, thereby mediating myocardial salvage, was examined in this study. Myocardial infarction was induced in two groups of rats by ligation of the left coronary artery. The bFGF group (n = 16) received 100 microg bFGF in physiological saline by intramyocardial injection into the infarcted area, while the control group (n = 7) received only saline. The rats were then maintained for four weeks. Among the controls, Qm decreased in the infarcted areas to 6.5+/-6.7% of that in the noninfarcted areas immediately after coronary ligation, then increased to 11.5+/-8.6% during the four-week maintenance period. In the bFGF group, Qm immediately decreased to 17.5+/-14.7% following ligation and remained stable thereafter (18.3+/-9.1%). There were no significant differences between the bFGF and control groups with respect to Qm, the number of viable myocardial cells or the extent of myocardial fibrosis. In this study we failed to show any significant effect of bFGF on coronary angiogenesis in acutely-ischemic myocardium in rats. Application of bFGF using different dosage, different routes of administration, measuring new capillaries morphologically will be needed to confirm the present negative results.

Acute Disease↗
PubMed2004

Early association of electrocardiogram alteration with infarct size and cardiac function after myocardial infarction.

OBJECTIVE: Myocardial infarction (MI) is the main cause of heart failure, but the relationship between the extent of MI and cardiac function has not been clearly determined. The present study was undertaken to investigate early changes in the electrocardiogram associated with infarct size and cardiac function after MI. METHODS: MI was induced by ligating the left anterior descending coronary artery in rats. Electrocardiograms, echocardiographs and hemodynamic parameters were assessed and myocardial infarct size was measured from mid-transverse sections stained with Masson's trichrome. RESULTS: The sum of pathological Q wave amplitudes was strongly correlated with myocardial infarct size (r = 0.920, P < 0.0001), left ventricular ejection fraction (r = -0.868, P < 0.0001) and left ventricular end diastolic pressure (r = 0.835, P < 0.0004). Furthermore, there was close relationship between MI size and cardiac function as assessed by left ventricular ejection fraction (r = -0.913, P < 0.0001) and left ventricular end diastolic pressure (r = 0.893, P < 0.0001). CONCLUSION: The sum of pathological Q wave amplitudes after MI can be used to estimate the extent of MI as well as cardiac function.

Animals↗