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PubMed1991

Carvedilol (Kredex) reduces infarct size in a canine model of acute myocardial infarction.

Carvedilol (Kredex) is a multiple action, antihypertensive agent that may also prove to be useful in the treatment of angina and congestive heart failure. Carvedilol combines in one molecule both beta-adrenoceptor blocking and vasodilating activities. Inasmuch as beta-adrenoceptor blocking agents are known to be cardioprotective and thereby reduce infarct size, it is logical to assume that carvedilol, likewise, would possess this desirable activity. Furthermore, the additional vasodilating activity of carvedilol could contribute to further reductions in infarct size by reducing myocardial work (and therefore myocardial oxygen demand) through reductions in both afterload and myocardial wall tension. As such, we have investigated the ability of carvedilol to reduce infarct size in a canine model of acute myocardial infarction. Carvedilol (1 mg/kg i.v.) or its vehicle, dimethylformamide, were administered 15 min before left circumflex coronary artery (LCX) occlusion. Following 1 h of LCX occlusion, dogs were reperfused through a critical stenosis and then allowed to recover for 24 h. Carvedilol-treated animals exhibited a 78% reduction in infarct size compared to vehicle controls, such that the percentage of the left ventricle infarcted was reduced significantly from 16.2 +/- 4.1% in control animals to 3.6 +/- 1.3% in animals treated with carvedilol (p = 0.017, n = 6). Stained tissue sections of the left ventricle were photographed, digitized and color-enhanced using an Image Analysis Computer System, and three-dimensional reconstruction of the left ventricle, including the infarcted areas, was performed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed2003

Immediate administration of mineralocorticoid receptor antagonist spironolactone prevents post-infarct left ventricular remodeling associated with suppression of a marker of myocardial collagen synthesis in patients with first anterior acute myocardial infarction.

BACKGROUND: Aldosterone (ALD) has been shown to stimulate cardiac collagen synthesis and fibroblast proliferation via activation of local mineralocorticoid receptors. In patients with acute myocardial infarction, we demonstrated that ALD was extracted through the infarct heart and extracting ALD-stimulated post-infarct left ventricular (LV) remodeling. METHODS AND RESULTS: To evaluate the effect of mineralocorticoid receptor antagonist (MRA) spironolactone on post-infarct LV remodeling, 134 patients with first anterior acute myocardial infarction were randomly divided into the MRA (n=65) or non-MRA (n=69) groups after revascularization. All patients were administered angiotensin-converting enzyme (ACE) inhibitor and study drug just after revascularization. Left ventriculography with contrast medium was performed at the acute stage and after 1 month to evaluate LV remodeling. ALD was measured at aortic root and coronary sinus. There was no difference in the baseline characteristics including infarct size and LV performance between the two groups. However, LV ejection fraction was significantly improved in the MRA group compared with that in the non-MRA group (46.0+/-0.6% to 53.2+/-0.8% versus 46.5+/-0.8% to 51.0+/-0.8%, Pinteraction=0.012). LV end-diastolic volume index was significantly suppressed in the MRA group compared with that in non-MRA group (86.5+/-1.0 to 90.6+/-2.4 versus 87.5+/-1.3 to 106.8+/-3.5 mL/m2, Pinteraction=0.002). Transcardiac extraction of ALD through the heart was significantly suppressed in the MRA group (Pinteraction=0.001), and plasma procollagen type III aminoterminal peptide level, a biochemical marker of fibrosis, was significant lower in the MRA group compared with the non-MRA group (Pinteraction=0.002). CONCLUSIONS: These findings indicate that MRA combined with ACE inhibitor can prevent post-infarct LV remodeling better than ACE inhibitor alone in association with the suppression of a marker of collagen synthesis.

Adrenergic beta-Antagonists↗
PubMed2003

Effect of pexelizumab, an anti-C5 complement antibody, as adjunctive therapy to fibrinolysis in acute myocardial infarction: the COMPlement inhibition in myocardial infarction treated with thromboLYtics (COMPLY) trial.

BACKGROUND: Complement activation mediates myocardial damage that occurs during ischemia and reperfusion through multiple pathways. We performed 2 separate, parallel, double-blind, placebo-controlled trials to determine the effects of pexelizumab (a novel C5 complement monoclonal antibody fragment) on infarct size in patients receiving reperfusion therapy: COMPlement inhibition in myocardial infarction treated with thromboLYtics (COMPLY) and COMplement inhibition in Myocardial infarction treated with Angioplasty (COMMA). The COMPLY trial is reported here. METHODS AND RESULTS: Overall, 943 patients with acute ST-segment elevation myocardial infarction (MI) (20% with isolated inferior MI) receiving fibrinolysis were randomly assigned <6 hours after symptom onset to placebo, pexelizumab 2.0-mg/kg bolus, or pexelizumab 2.0-mg/kg bolus plus 0.05 mg/kg per h for 20 hours. Infarct size determined by creatine kinase-MB area under the curve was the primary analysis, which included patients who received at least some study drug and fibrinolysis (n=920). The median infarct size did not differ by treatment (placebo, 5230; bolus, 4952; bolus plus infusion, 5557 [ng/mL] x h; bolus versus placebo, P=0.85; bolus plus infusion versus placebo, P=0.81), nor did the 90-day composite incidence of death, new or worsening congestive heart failure, shock, or stroke (placebo, 18.6%; bolus, 18.4%; bolus plus infusion, 19.7%). Pexelizumab inhibited complement for 4 hours with bolus-only dosing and for 20 to 24 hours with bolus-plus-infusion dosing, with no increase in infections. CONCLUSIONS: When used adjunctively with fibrinolysis, pexelizumab blocked complement activity but reduced neither infarct size by creatine kinase-MB assessment nor adverse clinical outcomes.

Aged↗
PubMed2004

Simultaneous evaluation of infarct size and cardiac function in intact mice by contrast-enhanced cardiac magnetic resonance imaging reveals contractile dysfunction in noninfarcted regions early after myocardial infarction.

BACKGROUND: The objective of this study was to noninvasively determine the effects of reperfused myocardial infarction (MI) on regional and global left-ventricular (LV) function 24 hours after MI in intact mice with contrast-enhanced cardiac MRI and a single, gradient-echo pulse sequence. METHODS AND RESULTS: Twenty-three mice received baseline MRI scans followed by either 60 minutes of coronary occlusion (MI group, n=15) or thoracotomy without occlusion (sham group, n=8). Gadolinium-DTPA-enhanced magnetic resonance (MR) images were acquired 24 hours after surgery. Hearts were then excised for conventional infarct size determination via 2,3,5-triphenyl tetrazolium chloride (TTC) staining. In addition to infarct size, analysis of the MR images yielded left ventricular (LV) mass, LV end-systolic volume (LVESV), LV end-diastolic volume (LVEDV), LV ejection fraction (LVEF), cardiac output, and percent LV wall thickening (%WTh). Twenty-four hours after surgery, infarct size was 28.1+/-1.8% of LV mass by MRI and 27.5+/-1.7% by TTC (P=NS). Bland-Altman analysis revealed close agreement between the results obtained by the 2 methods. MI had little effect on LVEDV but caused a 98% increase in LVESV (from 11.3 to 22.4 microL, P<0.05), which resulted in a significant reduction in LVEF (from 70% to 37%, P<0.05). Compared with LV regional function at baseline, %WTh 24 hours after MI was significantly depressed, not only in infarcted myocardium but also in regions remote from the infarct zone. In contrast, sham-operated mice showed a small but significant increase in %WTh 24 hours after surgery (P<0.05). CONCLUSIONS: MRI can accurately assess both infarct size and cardiac function in intact mice early after large, reperfused MI, revealing the existence of contractile dysfunction in noninfarcted regions of the heart.

Animals↗
PubMed1982

Intravenous hyaluronidase therapy for myocardial infarction in man: double-blind trial to assess infarct size limitation.

Patients with their first myocardial infarction not initially complicated by severe atrioventricular block or power failure were given a skin test and then randomized to receive either hyaluronidase or placebo in double-blind fashion. Hyaluronidase, 500 IU/kg i.v., was given every 6 hours for 42 hours. Of the 48 eligible patients, 26 received hyaluronidase and 22 received placebo. The mean CK serum entry was 3140 +/- 2111 mIU/ml (mean +/- SD) in hyaluronidase patients and 3574 +/- 1476 mIU/ml in placebo patients (p less than 0.21). The mean infarct size was 54.6 +/- 35.8 CK gram-equivalents in the hyaluronidase patients and 64.0 +/- 31.1 CK gram-equivalents in the placebo patients (p less than 0.20). Among the 21 patients treated within 6 hours of the onset of infarction, the difference in infarct size was greater (p less than 0.15). There was no significant difference in the incidence of power failure, ventricular arrhythmias, recurrence of ischemic pain, infarct extension or mortality. No benefit of hyaluronidase was demonstrated in this study, which was designed to detect a 50% reduction of infarct size. However, to detect a 20% reduction in infarct size would require a much larger study population.

Adult↗
PubMed1983

Right ventricular infarction: role of the moderator band artery in determining infarct size.

We studied 19 patients with proximal right coronary artery occlusions associated with acute myocardial infarcts less than 30 days old. Right ventricular infarct size, determined as a percentage of right ventricular surface area, ranged from 0% to 29%. Correlation of 24 variables measuring infarct size, chamber size and coronary artery disease failed to demonstrate a significant correlation with the extent of right ventricular infarction. However, estimates of the degree of obstruction to potential collateral flow into the right coronary arterial system from the left anterior descending coronary artery, especially through the moderator band artery, showed a significant positive correlation with infarct size (p less than 0.02). Among the five patients with massive (greater than 25%) right ventricular infarction, four had significant (greater than 75%) obstruction of the left anterior descending system, resulting in potentially impaired collateral blood flow; the other patient had normal coronary arteries and embolic occlusion of the proximal right coronary artery with contraction band necrosis. The study suggests that collateral flow to the right ventricular myocardium, especially through the moderator band artery, protects against massive infarction in the presence of proximal right coronary artery occlusion.

Adult↗
PubMed1985

Angiographic findings after myocardial infarction in patients with previous bypass surgery: explanations for smaller infarcts in this group compared with control patients.

The incidence of previous coronary artery bypass surgery (CABS) in patients with acute myocardial infarction admitted to our hospital has risen from 2.3% to 11.2% in 6 years. We compared infarct size and the angiographically determined cause of infarction in 52 control patients and in 52 consecutive patients with acute myocardial infarction at least 2 months after they had undergone CABS. Baseline characteristics were similar in both groups except for a higher incidence of preexisting Q waves in the post-CABS group (22 vs 10; p less than .05). Indexes of myocardial infarct size were smaller in the post-CABS group compared with those in control patients: peak creatine kinease (CK) level (IU/liter) 1113 +/- 1094 (mean +/- SD) vs 1824 +/- 1932 (p less than .01), peak CK-MB level (IU/liter) 173 +/- 230 vs 272 +/- 332 (p less than .02), peak summed ST segment elevation (mm) 3.5 +/- 4.8 vs 8.2 +/- 9.9 (p less than .005), and QRS score on days 7 to 10, 1.9 +/- 3.0 vs 4.3 +/- 3.4 (p less than .001). Postinfarction left ventricular ejection fraction was higher in the post-CABS group (53 +/- 13%) compared with that in control patients (47 +/- 12%; p less than .05). The incidence of total occlusion of the artery to the infarct zone was similar in the post-CABS and control patients (33 vs 27), as was the incidence of one-, two-, and three-vessel disease (artery plus graft). Collateral blood flow to the infarct zone was found in 27 post-CABS patients and in 23 control patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Delayed effects of early infarct-limiting therapies on healing after myocardial infarction.

The effect of early infarct-limiting therapy on the hydroxypyroline (OHP, a marker of collagen) content and topography of 7-day-old infarcts was studied in 76 conscious dogs (69 ligated; seven sham operated). Two hours after their left anterior descending coronary arteries were occluded, 69 dogs were randomly assigned to receive 6 hr intravenous infusions of saline (controls; n = 29), low-dose nitroglycerin (NG; n = 13), prostacyclin (PGI2; n = 14), or ibuprofen (IBU; n = 13). Regional OHP (mg/g dry weight) was measured by spectrophotometry, and size of infarction and topography were determined by computerized planimetry. Infarct size was less in the NG, PGI2, and IBU groups compared with that in the saline group, both when measured as a percent of the arteriographic occluded bed (p less than .001) and as a percent of the left ventricle (p less than .005). For each treatment group (1) the level of OHP was higher (p less than .001) in the region of infarction (saline group, 9.9 +/- 0.7 mg/g; NG group, 14.9 +/- 1.9 mg/g; PGI2 group, 12.9 +/- 0.9 mg/g; IBU group, 10.6 +/- 1.4 mg/g) than in normal zones (4.4 +/- 0.2 mg/g), with more (p less than .05) OHP in border than center regions, and (2) the total OHP in the infarct zone was linearly related to size of infarction as a percent of the left ventricle (r = .89 to .94). However, the slopes of regressions for the NG, PGI2, and IBU groups were greater (p less than .001) than the slope for the saline group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Effects of short-term, diet-induced hypercholesterolemia on systemic hemodynamics, myocardial blood flow, and infarct size in awake dogs with acute myocardial infarction.

BACKGROUND: Short-term cholesterol feeding has been shown to affect vasomotor tone and increase infarct size in anesthetized rabbits. The purpose of the study was to determine whether acute hypercholesterolemia reduced collateral flow to ischemic myocardium and increased infarct size in the awake dog. METHODS AND RESULTS: Acute myocardial infarction was produced in awake dogs by a 4-hour left anterior descending coronary artery occlusion followed by 6-hour reperfusion after either a cholesterol-supplemented diet (n = 14) or a control diet of dog chow (n = 15) for 10 days. Infarct size was determined using nitroblue tetrazolium staining. In two subgroups, a 15-minute transient occlusion of the left anterior descending coronary artery was produced before the diet treatments and was compared with occlusion after diet treatments, so that the effects of hypercholesterolemia of collateral flow could be determined by paired comparisons. Cholesterol feeding increased plasma cholesterol to 288 +/- 52 mg/dl, which was twofold to threefold that in the control group (127 +/- 35 mg/dl), but had no effects on baseline systemic hemodynamics and myocardial blood flow. Coronary artery occlusion produced similar increases in heart rate, mean aortic pressure, left atrial pressure, and plasma norepinephrine in both groups of animals. However, cholesterol feeding reduced collateral flow to ischemic myocardium and increased infarct size, compared with the control group. The infarct size correlated with ischemic myocardial blood flow in both groups, but the slopes of regression lines relating the two variables did not differ between the two groups. CONCLUSIONS: Short-term, diet-induced hypercholesterolemia increased infarct size in awake dogs. This change results, at least in part, from a decrease in collateral blood flow to ischemic myocardium during coronary artery occlusion.

Animals↗
PubMed1994

Serum antioxidants and myocardial infarction. Are low levels of carotenoids and alpha-tocopherol risk factors for myocardial infarction?

BACKGROUND: In vitro, animal and epidemiological studies suggest that lipoprotein oxidation may play an important role in atherosclerosis. Antioxidants may protect against lipoprotein oxidation and in that way inhibit atherosclerosis and its clinical sequelae. To investigate this possibility, we examined the association between levels of several antioxidants and myocardial infarction using serum specimens collected 7 to 14 years before the onset of myocardial infarction. METHODS AND RESULTS: A nested case-control design was used. Cases and control subjects were selected from the 25,802 persons who had donated 15 mL of blood in 1974 for a serum bank. Cases comprised 123 persons with a subsequent first diagnosis of myocardial infarction who ranged from 23 through 58 years of age in 1974 and who had had their first diagnosis of myocardial infarction during 1981 to 1988. Two groups of control subjects matched to the cases for sex and age were selected from donors to the serum bank, one from those with hospital admissions during the same period and the other from the total group of donors. Sera were assayed for four carotenoids (beta-carotene, lycopene, lutein, and zeaxanthin), alpha-tocopherol, and cholesterol. Because associations with these serum nutrients showed similar trends whether based on hospital or community controls, the two control groups were combined. There was a significantly increasing risk for subsequent myocardial infarction with decreasing levels of beta-carotene in 1974 (P value for trend, .02) and a suggestive trend with decreasing levels of lutein (P = .09). When the results were stratified by smoking status, the excess risk of myocardial infarction associated with low serum levels of carotenoids was limited to smokers. A protective association with higher levels of alpha-tocopherol was suggested only among persons with high levels of serum cholesterol. CONCLUSIONS: Low serum levels of carotenoids were associated with an increased risk of subsequent myocardial infarction among smokers.

Adult↗
PubMed1997

Influence of infarct-zone viability on left ventricular remodeling after acute myocardial infarction.

BACKGROUND: The relation between residual myocardial viability after acute myocardial infarction (AMI) and ventricular remodeling has yet to be fully elucidated. We hypothesized that the presence of residual viability would favorably influence left ventricular remodeling after AMI and that serial changes in left ventricular dimensions might be related to the extent of myocardial viability in the infarct zone. METHODS AND RESULTS: Ninety-three patients with a first AMI successfully treated with primary coronary angioplasty underwent two-dimensional echocardiography within 24 hours of admission and low-dose dobutamine echocardiography at a mean of 3 days after AMI. Two-dimensional echocardiography and coronary angiography were obtained in all patients 1 and 6 months after coronary angioplasty. On the basis of dobutamine echocardiography responses, patients were divided in two subsets: those with (n=48; group I) and those without (n=45; group II) infarct-zone viability. There was no difference in minimal lesion diameter and infarct-related artery patency at 1 and 6 months between the two groups. Group II patients had significantly greater end-diastolic (76+/-18 versus 53+/-14 mL/m2; P<.0003) and end-systolic (42+/-17 versus 22+/-11 mL/m2; P<.0003) volumes at 6 months than did patients in group 1. The extent of infarct-zone viability was significantly inversely correlated with percent changes in end-diastolic volumes at 6 months (r=-.66; P<.000001) and was the most powerful independent predictor of late left ventricular dilation. CONCLUSIONS: After reperfused AMI, the degree of left ventricular dilation, when it occurs, is inversely related to the extent of residual myocardial viability in the infarct zone. Thus, the absence of residual infarct-zone viability discriminates patients who develop progressive left ventricular dilation after reperfused AMI from those who maintain normal left ventricular geometry.

Aged↗
PubMedDate not supplied

Restraining infarct expansion preserves left ventricular geometry and function after acute anteroapical infarction.

BACKGROUND: Expansion of an acute myocardial infarction predicts progressive left ventricular (LV) dilatation, functional deterioration, and early death. This study tests the hypothesis that restraining expansion of an acute infarction preserves LV geometry and resting function. METHODS AND RESULTS: In 23 sheep, snares were placed around the distal left anterior descending and second diagonal coronary arteries. In 12 sheep, infarct deformation was prevented by Marlex mesh placed over the anticipated myocardial infarct. Snared arteries were occluded 10 to 14 days later. Serial hemodynamic measurements and transdiaphragmatic quantitative echocardiograms were obtained up to 8 weeks after anteroapical infarction of 0.23 of LV mass. In sheep with mesh, circulatory hemodynamics, stroke work, and end-systolic elastance return to preinfarction values 1 week after infarction and do not change subsequently. Ventricular volumes and ejection fraction do not change after the first week postinfarction. Control animals develop large anteroapical ventricular aneurysms, increasing LV dilatation, and progressive deterioration in circulatory hemodynamics and ventricular function. At week 8, differences in LV end-diastolic pressure, cardiac output, end-diastolic and end-systolic volumes, ejection fraction, stroke work, and end-systolic elastance are significant (P<0.01) between groups. CONCLUSIONS: Preventing expansion of acute myocardial infarctions preserves LV geometry and function.

Analysis of Variance↗
PubMedDate not supplied

Cause of cerebral infarction in the carotid territory. Its relation to the size and the location of the infarct and to the underlying vascular lesion.

Seventy-three patients with acute nonhemorrhagic stroke in the carotid territory were investigated for the cause of the stroke: middle cerebral artery (MCA) occlusion/stenosis or internal carotid artery (ICA) occlusion/stenosis; embolus from the heart and extra-cranial arteries or thrombosis. The study is prospective and consecutive comprising stroke patients below the age of 75 years, admitted in the acute state i.e. within 3 days after stroke onset. Excluded were patients with intracerebral hematoma, subarachnoid hemorrhage, vertebrobasilar stroke and patients in whom another severe disease was present. Cerebral angiography and CT-scan were performed in all patients within one and two days after admission. CT-scan was repeated 2 weeks and 6 months later. Forty percent had MCA occlusion, none had MCA stenosis, 12% had ICA occlusion, 14% had severe ICA stenosis (half of these were associated with MCA occlusion) and 41% were without significant MCA/ICA lesions. Twenty-seven percent had large infarcts with a diameter greater than 3 cm; 34% had medium-sized infarcts with a diameter between 3 and 1.5 cm; 21% had small infarcts with a diameter less than 1.5 cm; 18% had no identifiable infarct on CT-scan. MCA occlusion was responsible for 62% of the large or medium-sized infarcts. ICA occlusion or severe ICA stenosis were responsible for only 27% of the large or medium-sized infarcts. Only 11% of the patients with small or no infarct on CT-scan had significant MCA/ICA lesion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Prediction of infarct-related coronary artery of patients with acute inferior myocardial infarction by a predischarge exercise test index.

The predictive accuracy of electrocardiographic markers in identifying the infarct-related artery of myocardial infarctions has been a subject of extensive investigation. The present study was designed to test whether the index L II/L III ratio adapted to exercise electrocardiograms could be utilized as a marker to distinguish right coronary and left circumflex arteries as culprit coronaries in acute inferior myocardial infarctions. For this purpose, 82 patients with a positive-symptom-limited and/or submaximal treadmill exercise test with modified Bruce protocol after an acute inferior myocardial infarction were studied. Those patients with ST segment elevation during the stress test were included in the study. ST segment index was defined as the ratio of exercise-induced ST elevation amplitude in L II/L III. Patients were classified as having an index > 1 (n=24) and < 1 (n=58), and the findings were compared with the findings on coronary angiography. The groups were comparable with respect to age, gender, peak exercise level, and double products achieved. Circumflex artery was the infarct-related one in the majority (21/24; 88%) of patients with an index > 1, whereas most (51/58; 88%) patients with an index < 1 had the culprit lesion in their right coronary artery (p<0.001). The ratio of exercise-induced ST elevations in leads L II and L III has a significantly high ability to discriminate the infarct-related coronary artery in patients with uncomplicated inferior myocardial infarction. Considering the prognostic importance of the type of coronary involvement, this index could be a part of predischarge evaluation in this patient group.

Coronary Angiography↗
PubMed1996

The effect of low molecular weight heparin (fragmin) on myocardial neutrophil accumulation and infarct size in a rat model of myocardial infarction.

BACKGROUND: Heparin molecules possess immunomodulating properties, which are thought to complement their established antithrombotic activity. The purpose of this study was to evaluate whether the antiinflammatory properties of low molecular weight heparin (LMWH) can attenuate polymorphonuclear neutrophil accumulation and infarct size in a rat model of myocardial infarction. METHODS: Myocardial infarction was induced by ligating the left main coronary artery. LMWH (fragmin 500 anti-FXa u/kg) or vehicle (saline) were administered subcutaneously thirty minutes prior to coronary artery occlusion. Significant anticoagulant activity was attained with LMWH for more than eight hours. Twenty-four hours later, neutrophil accumulation and infarct size were determined by measuring left ventricular free wall myeloperoxidase and residual creatine kinase activity, respectively. RESULTS: As compared with rats administered vehicle, myeloperoxidase activity was insignificantly decreased in rats treated with LMWH (1.24 +/- 0.28 u/g vs 1.66 +/- 0.15 u/g, P = 0.16. Infarct size was also not significantly different between the groups (62.48 +/- 3.5% and 50.67 +/- 7.2% of left ventricular free wall with vehicle and LMWH, respectively, P = 0.1). CONCLUSION: The authors conclude that LMWH does not significantly reduce myocardial neutrophil accumulation and infarct size twenty-four hours after myocardial infarction in the rat.

Animals↗
PubMed2000

Atrial (ANP) and brain natriuretic peptide (BNP) expression after myocardial infarction in sheep: ANP is synthesized by fibroblasts infiltrating the infarct.

Cardiac gene expression of atrial natriuretic peptide (ANP) and that of brain natriuretic peptide (BNP) are markedly elevated after myocardial infarction. The cellular distribution and temporal responses of ANP and BNP messenger RNA (mRNA) expression were compared by in situ hybridization for 5 weeks after left coronary artery ligation in sheep. Ligation resulted in highly reproducible, transmural, left ventricular infarcts. Within the infarct, ANP mRNA appeared from 7 days after ligation, whereas BNP expression was undetectable in the infarct at any time. The cells synthesizing ANP were shown by in situ hybridization and immunocytochemistry to be fibroblasts invading the infarct. The appearance of ANP expression coincided with the transition of these cells to the myofibroblast phenotype. Treatment of cultured cardiac fibroblasts with transforming growth factor-beta (10 ng/ml) induced the expression of alpha-smooth muscle actin, characteristic of the transformation to myofibroblasts, and raised ANP concentrations in the medium. In the surviving myocardium of the left ventricle, ANP and BNP expression increased in response to ligation, BNP mRNA was particularly strong at the lateral margins of the infarct. In both left and right atria, levels of BNP mRNA increased markedly over the first 18 h, whereas levels of atrial ANP mRNA decreased over 3 days after infarction. This is the first report of ANP expression and synthesis by cardiac fibroblasts invading the fibrotic scar, suggesting that ANP may be involved in regulating fibroblast proliferation during reparative fibrosis.

Animals↗
PubMed2005

Angiotensin blockade inhibits osteopontin expression in non-infarcted myocardium after myocardial infarction.

Osteopontin has been reported to have an important role in cardiac fibrosis. However, little is known about the effects of angiotensin-converting enzyme inhibitor (ACEI) and angiotensin type 1 receptor blockers (ARB) on osteopontin expression in infarcted myocardium. The purpose of this study was to elucidate the effects of an ACEI (perindpril) and an ARB (candesartan cilexitil) on cardiac function as assessed by Doppler echocardiography and cardiac osteopontin expression associated with cardiac remodeling in myocardial infarcted rats. ACEI or ARB was administered after myocardial infarction (MI). At 4 weeks after MI, cardiac function, and mRNAs in non-infarcted myocardium were analyzed. ACEI and ARB equally prevented left ventricular dilatation, reduction of ejection fraction, and the increase in E/A wave velocity ratio and the rate of E wave deceleration by MI. ACEI and ARB significantly suppressed increased mRNA expression of atrial natriuretic peptide, brain natriuretic peptide, osteopontin, and collagen I and III in the non-infarcted ventricle at 4 weeks. Immunohistochemically stained osteopontin was increased in interstitial fibrosis of non-infarcted myocardium. Both ACEI and ARB significantly prevented cardiac fibrosis and osteopontin expression. In conclusion, angiotensin blockade inhibits osteopontin expression in non-infarcted myocardium and prevents cardiac remodeling after MI.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2001

Clinical significance of coronary flow to the infarct zone before successful primary percutaneous transluminal coronary angioplasty in acute myocardial infarction.

STUDY OBJECTIVE: To assess the effect of coronary flow to the infarct zone before primary coronary angioplasty on hospital complications in patients with acute myocardial infarction (MI). DESIGN: Consecutive case series analysis. SETTING: Coronary-care unit in a university hospital. PATIENTS: Two hundred sixty-four consecutive patients with ST-elevation acute MIs who had successful primary percutaneous transluminal coronary angioplasty. INTERVENTIONS: Coronary angiography on hospital admission and serial echocardiography. MEASUREMENTS AND RESULTS: The status of infarct-related artery flow before primary angioplasty was evaluated on hospital admission. Left ventricular wall motion and pericardial effusions were studied by echocardiography. One hundred ninety patients had total occlusions (Thrombolysis in Myocardial Infarction [TIMI] flow grade, 0 to 1) in the infarct-related artery (group 1), and 74 patients had antegrade flow (TIMI flow grade, 2 to 3) [group 2] before undergoing primary angioplasty procedures. When group 1 was subdivided into two groups (for the presence and absence of collateral flow), the patients with total occlusions and no collateral flow had a higher incidence of left ventricular aneurysmal wall motion (11% vs 1%, respectively; p = 0.03) and pericardial friction rub (15% vs 3%, respectively; p = 0.03) than did those in group 2. Moreover, those patients with total occlusions and no collateral flow had higher incidences of pericardial effusion (34% vs 17%, respectively; p = 0.02; and 34% vs 9%, respectively; p < 0.01) and in-hospital mortality (8% vs 1%, respectively; p = 0.04; and 8% vs 1%, respectively; p = 0.06) than did those patients in the other two groups. CONCLUSIONS: Despite successful primary angioplasty, the absence of antegrade flow in the infarct-related artery and collateral flow to the infarct zone before angioplasty resulted in a higher incidence of in-hospital complications.

Aged↗