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PubMed2001

Attenuation of infarct size in rats and dogs after myocardial infarction by low-energy laser irradiation.

BACKGROUND AND OBJECTIVE: The aim of the present study was to investigate the possibility that low-energy laser irradiation attenuates infarct size formation after induction of chronic myocardial infarction (MI) in small and large experimental animals. STUDY DESIGN/MATERIALS AND METHODS: Laser irradiation was applied to the infarcted area of rats and dogs at various power densities (2.5 to 20 mW/cm(2)) after occlusion of the coronary artery. RESULTS: In infarcted laser-irradiated rats that received laser irradiation immediately and 3 days after MI at energy densities of 2.5, 6, and 20 mW/cm(2), there was a 14%, 62% (significant; P < 0.05), and 2.8% reduction of infarct size (14 days after MI) relative to non--laser-irradiated rats, respectively. In dogs, a 49% (significant; P < 0.01) reduction of infarct size was achieved. CONCLUSION: The results of the present study indicate that delivery of low-energy laser irradiation to infarcted myocardium in rats and dogs has a profound effect on the infarct size after MI.

Animals↗

PubMed1998

Increase in the expression of biglycan mRNA expression Co-localized closely with that of type I collagen mRNA in the infarct zone after experimentally-induced myocardial infarction in rats.

Biglycan, a small dermatan sulphate proteoglycan, has been postulated to interact with other components of the extracellular matrix (ECM), specifically collagens. We hypothesized that biglycan messenger ribonucleic acid (mRNA) is increased in the myocardial infarct zone. Biglycan mRNA expression after acute myocardial infarction (AMI) in rats was determined with the use of Northern blotting and in situ hybridization, and its expression pattern was compared to that of type I collagen mRNA [alpha1(I) collagen]. The left coronary artery was ligated in male Sprague-Dawley rats, and the hearts were excised on days 2 and 7. The Northern blot analysis demonstrated that expression of biglycan mRNA in the infarct on days 2 and 7 were 4.0- and 6.8-fold higher, respectively, compared to the sham-operated hearts. The in situ hybridization revealed intense signals for both biglycan and alpha1(I) collagen mRNA on day 2 in the spindle-shaped mesenchymal cells located between the surviving myocytes in the infarct peripheral zone. On day 7, biglycan mRNA signals were observed in the interior of the infarct around the infarct granulation tissue, a distribution that was essentially the same as that of alpha1(I) collagen. These results demonstrated that the increases in the infarct biglycan mRNA expression produced by mesenchymal cells (presumably myofibroblasts and fibroblasts) was closely co-localized with that of type I collagen mRNA, indicating that biglycan contributes to the infarct healing processes.

Animals↗

PubMed1982

Evaluation of a QRS scoring system for estimating myocardial infarct size. II. Correlation with quantitative anatomic findings for anterior infarcts.

The ability of an independently developed QRS point score to estimate the size of infarcts predominantly within the anterior third of the left ventricular was evaluated by quantitative pathologic-electrocardiographic correlation. The study was limited to 21 patients with a single infarct documented by postmortem examination, for whom an appropriately timed standard 12 lead electrocardiogram was available that did not exhibit signs of left or right ventricular hypertrophy, left or right bundle branch block or anterior or posterior fascicular block. At necropsy the heart was cut into five to seven slices. The location and size of the infarct was quantitated by computer-assisted planimetry of the slices. The electrocardiogram of 19 (90 percent) of the patients exhibited either a Q wave or an R wave of no more than 20 ms in lead V2. The infarct in the two patients without this electrocardiographic finding was small, occupying 2 and 3 percent of the left ventricle, respectively. The percent infarction of the left ventricle correlated with the QRS point score (r=0.80). Thus in patients without complicating factors in the electrocardiogram and with a single infarct, the electrocardiogram provides a marker for infarction in the anterior third of the left ventricle and permits estimation of infarct size.

Adult↗

PubMed1982

Quantitative comparison of extent of coronary narrowing and size of healed myocardial infarct in 33 necropsy patients with clinically recognized and in 28 with clinically unrecognized ("silent") previous acute myocardial infarction.

Clinical and necropsy observations are described in 61 patients with a healed transmural myocardial infarction, 33 with and 28 without a clinical history of acute myocardial infarction. There were no significant differences between the 2 groups of patients in mean age, sex, or frequency of angina pectoris, chronic congestive heart failure, systemic hypertension, sudden coronary death, or fatal acute myocardial infarction. Compared with the patients with clinically recognized acute myocardial infarction, the patients with clinically unrecognized (silent) infarction had a significantly (p less than 0.05) higher incidence of diabetes mellitus (43 versus 15%), death from noncardiac causes (39 versus 9%), posterior (inferior) wall infarcts (82 versus 55%), and smaller infarcts (mean size 7 versus 17% of left ventricular wall). The patients with and without clinically recognized infarction had similar numbers of the 4 major coronary arteries severely (76 to 100% in cross-sectional area) narrowed (mean 2.8 versus 2.9/4.0 per patient), insignificant differences in incidence of severe narrowing of the left main coronary artery (18 versus 29%), similar overall percents of 5 mm segments of the 4 major coronary arteries severely narrowed (43 versus 42%), and similar percents of severely narrowed 5 mm segments of the right (46 versus 55%), left anterior descending (39 versus 33%), and left circumflex (41 versus 41%) coronary arteries.

Adult↗

PubMed1985

Relation between the transmural extent of acute myocardial infarction and associated myocardial contractility two weeks after infarction.

To characterize the relation between the transmural extent of acute myocardial infarction (AMI) and associated regional contractility after recovery from ischemia, 11 mongrel dogs underwent occlusion of the proximal left anterior descending coronary artery and were evaluated 2 weeks after infarction. Occlusion was permanent in 5 dogs, and reperfusion was allowed after 2 hours of occlusion in 6 dogs. All dogs had computer-assisted quantitative wall-thickening analysis by 2-dimensional echocardiography and infarct localization by the triphenyl-tetrazolium chloride technique. Percent systolic wall thickening was correlated with the transmural extent of AMI in 40 regions of interest, each measuring approximately 60 arc degrees in circumference. In 11 non-infarct-containing regions, the mean wall thickening was 59 +/- 16% (+/- standard deviation). In 29 infarct-containing segments (with transmural extent of infarction 11 to 100%) systolic wall thickening ranged from -4% to 47%. Wall thickening and transmural extent of AMI were inversely related. Least-squares regression analysis found the relation to be best described by the logarithmic function, percent wall thickening = 61 - 26 log (percent transmural extent of infarction +1), r = -0.87. The nature of this relation between structure and function suggests that salvage of small amounts of myocardium (transmural extent less than 30 to 40%) by coronary reperfusion or other means may have little effect on systolic myocardial function when compared with the function of transmural infarcts. Alternatively, salvage of more than 40% of the jeopardized myocardium should be expected to appreciably augment myocardial function.

Animals↗

PubMed1986

Relation of size of transmural acute myocardial infarct to mode of death, interval between infarction and death and frequency of coronary arterial thrombus.

Seventy-eight necropsy patients with transmural acute myocardial infarction (AMI) were studied to correlate the mode of death, the interval between onset of AMI and death and the presence or absence of coronary thrombus with the extent of the infarct. Infarct size was assessed quantitatively as a percentage of total left ventricular (LV) mass. Death was caused by cardiogenic shock in 16 patients (21%), arrhythmia in 31 patients (40%) and cardiac rupture in 24 patients (31%). The mean interval between the onset of AMI and death was 12 +/- 13 days. Infarct size averaged 23 +/- 14% of LV mass. Patients who died in cardiogenic shock had the largest infarcts (37 +/- 11%) and those who died of cardiac rupture had the smallest infarcts (15 +/- 9%) and the shortest interval between onset of AMI and death (7 +/- 8 days). Coronary thrombi were present in 58 patients (74%). When present, thrombus was observed in the coronary artery that had supplied the infarct area and was superimposed on advanced atherosclerotic plaque, but no relation was found between extent of luminal obstruction by thrombus and AMI size. The absence of coronary thrombus at necropsy was associated with either small infarcts or prolonged survival after AMI.

Aged↗

PubMed1993

Effect of cigarette smoking on coronary patency after thrombolytic therapy for myocardial infarction. TEAM-2 Investigators. Second Multicenter Thrombolytic Trials of Eminase in Acute Myocardial Infarction.

Smokers have been reported to have an improved short-term prognosis after myocardial infarction when compared with nonsmokers. This study examines the effect of smoking status on infarct-related artery patency, a determinant of outcome, following thrombolytic therapy for acute myocardial infarction (AMI). To evaluate patency outcome by smoking status, the database of the Second Thrombolytic Trial of Eminase in Acute Myocardial Infarction was reviewed, and baseline characteristics were compared with infarct-related artery patency early (90 to 240 minutes) after thrombolysis in smokers versus nonsmokers. Smokers were younger (mean age 53 vs 59 years, p = 0.0001), more likely to be men (86 vs 73%, p = 0.008), normotensive (74 vs 58%, p = 0.004), to have an inferior infarction (66 vs 51%, p = 0.007), and tended to have higher hematocrits and fibrinogen levels than nonsmokers. Smokers had a significantly greater chance of achieving complete perfusion (Thrombolysis in Myocardial Infarction trial grade 3) (66 vs 51% p = 0.007) than nonsmokers, although the combination of grades 2 and 3 did not differ. After correcting for imbalances in baseline and angiographic variables, multivariate logistic regression identified smoking (odds ratio 1.8, p = 0.01) and infarct location (odds ratio 1.7, p = 0.03) as independent predictors of achieving grade 3 flow. The independent predictive component of smoking for achieving grade 3 patency after thrombolysis suggests the hypothesis that more active thrombogenic mechanisms may be operative in smokers, leading to a larger thrombus component that is more susceptible to lytic therapy.

Anistreplase↗

PubMed1990

Prevalence and extent of right ventricular dysfunction after myocardial infarction--relation to location and extent of infarction and left ventricular function.

In view of today's efforts to preserve myocardial function in acute myocardial infarction, the prevalence and extent of persistent right ventricular dysfunction was analysed in a prospective study of 127 patients admitted with a first myocardial infarction without thrombolysis. Right ventricular ejection fraction measured at hospital discharge by radionuclide angiocardiography was related to the location of infarction as judged electrocardiographically, its size as estimated enzymatically, and by the simultaneously measured left ventricular ejection fraction. Two opposite patterns of right and left ventricular function were observed in relation to the location of infarction: the right ventricular ejection fraction was significantly depressed in inferior, but not in anterior, infarction and the reverse was true for left ventricular ejection fraction (P less than 0.001 between infarct locations for both right ventricular ejection fraction and left ventricular ejection fraction). There were significant correlations between peak levels of creatine kinase and left ventricular ejection fraction for anterior (r = 0.76, P less than 0.001) and inferior (r = 0.57, P less than 0.001) infarction, while peak levels of creatine kinase and right ventricular ejection fraction correlated only in inferior infarction (r = 0.45, P less than 0.01). There was no overall correlation for left ventricular ejection fraction and right ventricular ejection fraction (r = 0.28, P NS), despite the fact that right ventricular ejection fraction was lower in patients with severely reduced left ventricular ejection fraction than in those with normal left ventricular function (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1996

Electrocardiographic identification of the infarct-related artery in acute inferior myocardial infarction.

Differentiation between left circumflex occlusion and right coronary occlusion in inferior acute myocardial infarction is a common clinical problem. This study investigated new electrocardiographic markers for differentiation, including T wave inversion, and individual inferior and precordial lead ST level, versus the traditional criterion of lateral ST elevation. In 95 angiographically characterised patients, ST elevation in lateral chest lead V5 or V6 had a sensitivity of 56% and specificity of 92% to predict left circumflex related acute myocardial infarction while the absence of lateral T inversion in I and AVL was even more sensitive (89%) though less specific (74%). A criterion of ST depression in V1 > 0.1 mV has a sensitivity of 61% and specificity of 84% whereas a criterion of ST level in III minus II < or = 0.1 mV has a sensitivity of 94% and specificity of 37% in predicting left circumflex related acute myocardial infarction. These criteria were then tested in another 49 patients subsequently recruited with inferior acute myocardial infarction. Useful parameters that discriminated left circumflex related acute myocardial infarction from right coronary related acute myocardial infarction include lateral ST elevation (38% vs. 7%, P < 0.05), absence of lateral T inversion (50% vs. 15%, P < 0.05), and ST depression in V1 of more than 0.1 mV (50% vs. 7%, P < 0.05). The present study revealed new electrocardiographic clues to suggest a left circumflex related inferior acute myocardial infarction other than lateral ST elevation. However, it should be noted that no single electrocardiographic variable or their combinations could identify the infarct-related artery with complete certainty.

Coronary Vessels↗

PubMed1992

Effects of diltiazem on recurrent myocardial infarction in patients with non-Q wave myocardial infarction.

Diltiazem has been reported to reduce the short-term in-hospital reinfarction rate in patients with a non-Q wave myocardial infarction. In the long-term Multicenter Diltiazem Postinfarction Trial, there were 514 patients with non-Q wave myocardial infarction; 279 patients were randomized to the placebo group and 235 to the treatment group. The average follow-up period was 25 months. There was no difference in baseline clinical characteristics between the two groups. Early reinfarction (less than or equal to 6 months) occurred in 17 patients in the placebo group and in 2 patients in the diltiazem group (p less than 0.001). Late reinfarction (greater than 6 months) occurred in 13 patients in the placebo group and in 14 patients in the diltiazem group (p = NS). Initial and reinfarction electrocardiograms (ECGs) were analyzed by using a coding system that permitted identification of standard anatomic areas involved in the infarction process. Thirty-one of the 46 patients had a localized infarction on index and reinfarction ECGs. In the early reinfarction group, 10 (77%) of 13 infarctions occurred in the same ECG region in which the initial infarction had occurred; all 10 were in patients in the placebo group. Among the 18 patients with late reinfarction, the site of the second infarction was the same as that of the first in 9 patients and differed in 9. There was no difference between the placebo and diltiazem groups with respect to location of the infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Cohort Studies↗

PubMed1994

A pilot trial of recombinant desulfatohirudin compared with heparin in conjunction with tissue-type plasminogen activator and aspirin for acute myocardial infarction: results of the Thrombolysis in Myocardial Infarction (TIMI) 5 trial.

OBJECTIVES: The purpose of this study was to assess the value of recombinant desulfatohirudin (hirudin) as adjunctive therapy to thrombolysis in acute myocardial infarction. BACKGROUND: Failure to achieve initial reperfusion and reocclusion of the infarct-related artery remain major limitations of thrombolytic therapy despite aggressive regimens of heparin and aspirin. Hirudin, a direct thrombin inhibitor, has been shown in experimental models to enhance thrombolysis and reduce reocclusion. METHODS: The Thrombolysis in Myocardial Infarction (TIMI) 5 trial was a randomized, dose-ranging, pilot trial of hirudin versus heparin, given with front-loaded tissue-type plasminogen activator and aspirin to 246 patients with acute myocardial infarction. Patients received either intravenous heparin or hirudin at one of four ascending doses for 5 days. Patients underwent coronary angiography at 90 min and at 18 to 36 h, unless rescue angioplasty was performed. RESULTS: The primary end point, TIMI grade 3 flow in the infarct-related artery at 90 min and 18 to 36 h without death or reinfarction before the 18- to 36-h catheterization was achieved in 97 (61.8%) of 157 evaluable hirudin-treated patients compared with 39 (49.4%) of 79 evaluable heparin-treated patients (p = 0.07). All four doses of hirudin led to similar findings in the angiographic and clinical end points. At 90 min, TIMI grade 3 flow was present in 105 (64.8%) of 162 hirudin-treated patients compared with 48 (57.1%) of 84 heparin-treated patients (p = NS). Infarct-related artery patency (TIMI grade 2 or 3 flow) was similar in the two groups (82.1% and 78.6%, respectively). At 18 to 36 h, 129 (97.8%) of 132 hirudin-treated patients had a patent infarct-related artery compared with 58 (89.2%) of 65 heparin-treated patients (p = 0.01). Reocclusion by 18 to 36 h occurred in 2 (1.6%) of 123 hirudin-treated patients versus 4 (6.7%) of 60 heparin-treated patients (p = 0.07). Death or reinfarction occurred during the hospital period in 11 (6.8%) of 162 hirudin-treated patients compared with 14 (16.7%) of 84 heparin-treated patients (p = 0.02). Major spontaneous hemorrhage occurred in 1.2% of hirudin-treated patients versus 4.7% of heparin-treated patients (p = 0.09), and major hemorrhage at an instrumented site occurred in 16.3% and 18.6%, respectively (p = NS). CONCLUSIONS: Hirudin is a promising agent compared with heparin as adjunctive therapy with thrombolysis for acute myocardial infarction, and its evaluation in larger trials is warranted.

Adjuvants, Pharmaceutic↗

PubMed1995

Thrombolysis with recombinant unglycosylated single-chain urokinase-type plasminogen activator (saruplase) in acute myocardial infarction: influence of heparin on early patency rate (LIMITS study). Liquemin in Myocardial Infarction During Thrombolysis With Saruplase.

OBJECTIVES: The Liquemin in Myocardial Infarction During Thrombolysis With Saruplase (LIMITS) study was instituted to evaluate and characterize the effect of a prethrombolytic heparin bolus (5,000 IU) on the efficacy and safety of saruplase in patients with acute myocardial infarction. BACKGROUND: Heparin has been used after thrombolytic therapy for acute myocardial infarction to prevent reocclusion of the infarct-related artery. METHODS: The study was designed as a randomized, parallel-group, double-blind, multicenter trial. Patients were treated within 6 h of onset of symptoms with either a bolus of 5,000 IU of heparin (Liquemin) (n = 56, HSH group) or placebo (n = 62, PSH group) before thrombolytic treatment with saruplase given as a 20-mg bolus followed by an infusion of 60 mg over 60 min. Thirty minutes after completion of thrombolysis, an intravenous heparin infusion was administered for 5 days. Before coronary angiography was performed at 6 to 12 h after start of lysis, an additional bolus of 5,000 IU heparin was given to all patients. End points studied were patency of the infarct-related artery, changes in the hemostatic system and bleeding complications. RESULTS: In the HSH group (heparin-saruplase-heparin), 78.6% of patients had an open infarct-related vessel (Thrombolysis in Myocardial Infarction [TIMI] flow grade 2 or 3) compared with 56.5% in the PSH group (placebo-saruplase-heparin) (intention-to-treat analysis, p = 0.01). No significant difference was observed between the two groups with regard to changes in fibrinogen and fibrin/fibrinogen degradation products. A total of eight bleeding complications (14.3%) were observed in the HSH group and five (8.1%) in the PSH group; no cerebrovascular event occurred, and no allergic reaction was reported. A total of 12 patients died during the hospital stay, 3 in the HSH group (5.4%) and 9 in the PSH group (14.5%). CONCLUSIONS: In acute myocardial infarction, the administration of a heparin bolus before thrombolytic therapy with saruplase is associated with a significantly higher patency at angiography 6 to 12 h after the start of thrombolysis without any appreciable increase in risk of bleeding.

Adult↗

PubMed2004

Comparison of rheolytic thrombectomy before direct infarct artery stenting versus direct stenting alone in patients undergoing percutaneous coronary intervention for acute myocardial infarction.

This randomized trial compared rheolytic thrombectomy before direct infarct artery stenting with direct infarct artery stenting alone in 100 patients with a first acute myocardial infarction (AMI). The primary end point of the study was early ST-segment elevation resolution, and the secondary end points were corrected Thrombolysis In Myocardial Infarction (TIMI) frame count, infarct size, and 1-month clinical outcome. The primary end point rates were 90% in the thrombectomy group and 72% in the placebo group (p = 0.022). Randomization to thrombectomy was independently related to the primary end point (odds ratio 3.56, p = 0.032). The corrected Thrombolysis In Myocaridal Infarctions (TIMI) frame count was lower in the thrombectomy group (18.2 +/- 7.7 vs 22.5 +/- 11.0, p = 0.032), and infarct size was smaller in the thrombectomy group (13.0 +/- 11.6% vs 21.2 +/- 18.0%, p = 0.010). At 1 month, there were no major adverse cardiac events. Rheolytic thrombectomy before routine direct infarct-related artery (IRA) stenting is highly feasible and provides more effective myocardial reperfusion in patients undergoing percutaneous coronary intervention for AMI.

Aged↗

PubMed2006

Myocardial contrast echocardiographic estimates of infarct size predict likelihood of left ventricular remodeling after acute anterior wall myocardial infarction.

OBJECTIVES: We sought to determine the utility of myocardial contrast echocardiography (MCE) in predicting left ventricular (LV) remodeling (LVR) in patients with a recent anterior wall myocardial infarction and residual regional LV akinesis. BACKGROUND: Although recent studies have shown that MCE predicts recovery of regional and global LV systolic function after myocardial infarction, the relationship between myocardial perfusion patterns and likelihood of subsequent LVR has not been extensively studied. METHODS: In all, 50 patients (mean age 62 years) underwent contrast-enhanced echocardiography for determination of LV volumes and ejection fraction, and MCE, 2 days after admission, with follow-up contrast-enhanced echocardiography 6 months later. LVR was defined as greater than 15% increase in LV end-diastolic volume index at follow-up. RESULTS: LVR occurred in 19 patients (38%) (group 1), with stable LV volumes in 31 patients (62%) (group 2). Routine clinical and angiographic variables did not differ between groups 1 and 2. Both transmural extent of infarction and number of abnormally perfused myocardial segments (assessed by MCE) predicted LVR. LVR occurred in 55% of patients with transmural perfusion defects, and was less common in those with subendocardial perfusion defects or normal perfusion (31% and 21%, respectively). The mean percent increase in LV size was significantly greater for transmural infarcts (15 +/- 7%) versus subendocardial infarcts or normal perfusion (-1 +/- 8 and 8 +/- 8, respectively). When more than 5 myocardial segments were abnormally perfused, remodeling always occurred and was extensive. CONCLUSIONS: MCE markers of infarct size are useful in predicting subsequent risk of LVR after myocardial infarction. Routine performance of MCE studies in select patients early after infarction may be helpful in further refining risk stratification.

Echocardiography↗

PubMed1998

Differential uptake of myocardial perfusion radiotracers in normal, infarcted, and acutely ischemic peri-infarction myocardium.

OBJECTIVES: We measured the uptake of technetium-99m tetrofosmin (99m Tc) and thallium-201 (201 TI) in areas of healed transmural myocardial infarction and in the regions of acute peri-infarction ischemia. METHODS: Anesthetised pigs with a 1-month old transmural infarction elicited by permanent ligature of the left anterior descending (LAD) coronary artery below the first branch underwent one hour of proximal LAD occlusion followed by injection of 99m Tc-tetrofosmin and 201TI either in the left atrium (GI, n= 19) or in the jugular vein (GII, n = 6). Twelve other pigs (GIII) with similar acute peri-infarction ischemia received 99m Tc-tetrofosmin and 201Tl into the left ventricle during cardiocirculatory arrest to rule out the effect of coronary collaterals. Radiotracer counting was determined in samples from normal, acute ischemic and necrotic regions. RESULTS: Uptake of 99m Tc-tetrofosmin and 201 Tl was greater in the infarct scar (median % of normal tissue: 20 for 99m Tc and 8.6 for 201 Tl in GI; 22 and 15 in GII) than in acute ischemic myocardium (3.2 and 2.5 in GI; 6.4 and 3.3 in GII). Radiotracer injection in arrested hearts (GIII) depicted a similar pattern (median % of injected dose: 6.2 for 99m Tc and 10 for 201Tl in the scar; 2.3 and 4.0 in acute ischemia; 2.9 and 3.5 in normal tissue). The infarcted region showed connective tissue and lack of viable myocardium. CONCLUSION: A 1-month old infarct scar with no viable myocardial tissue can take up significant fractions of 99mTc-tetrofosmin and 201Tl even in the absence of coronary collateral perfusion. Data suggest that the infarct scar can extract these radiotracers from the intraventricular blood.

Animals↗

PubMed2000

Large-scale test of hypothesised associations between the angiotensin-converting-enzyme insertion/deletion polymorphism and myocardial infarction in about 5000 cases and 6000 controls. International Studies of Infarct Survival (ISIS) Collaborators.

BACKGROUND: The original report of a possible association between myocardial infarction and the insertion/deletion (I/D) polymorphism of the gene for the angiotensin-1-converting enzyme (ACE) indicated a risk ratio for myocardial infarction with the DD genotype of 1.34 (95% CI 1.05-1.70), and the association was claimed to be particularly strong in a retrospectively defined low-risk subgroup (3.2 [95% CI 1.7-5.9). Subsequent investigations reached varying conclusions, but all were small, and much larger studies were needed. METHODS: 4629 myocardial infarction cases and 5934 controls were compared. Cases were UK men aged 30-54 years and women aged 30-64 years recruited on presentation to hospital with confirmed myocardial infarction. Controls were aged 30-64 years with no history of cardiovascular disease, but were siblings or children of myocardial infarction survivors, or spouses of such relatives. All risk-ratio calculations allow for this relatedness of some of the controls. An updated meta-analysis of previous studies was also conducted. FINDINGS: The ACE DD genotype was found in 1359 (29.4%) of the myocardial infarction cases and in 1637 (27.6%) of the controls (risk ratio 1.10 [95% CI 1.00-1.21]). The association between myocardial infarction and the DD genotype did not seem to be stronger in the subgroup defined as low risk by previously used criteria (234 [28%] of 836 cases and 911 [28%] of 3253 controls: risk ratio 1.04 [95% CI 0.87-1.24]), or in any other subgroup. Nor was the ACE I/D genotype predictive of subsequent survival. INTERPRETATION: This study involved many more cases than any previously reported study of this question, but did not confirm the existence of any substantial association. In an updated meta-analysis of these results with those of previously published studies, the risk ratio for myocardial infarction with the DD genotype seems to lie in the range 1.0 to about 1.1. Although an increase in risk of up to about 10-15% cannot be ruled out, substantially more extreme risks can be. Moreover, there are not especially strong associations in the subgroups previously selected for emphasis. These findings illustrate the need for some studies of candidate genes to involve much larger populations than is customary, without undue emphasis on retrospectively defined subgroups.

Adult↗

PubMedDate not supplied

Early and chronic captopril or Losartan therapy reduces infarct size and avoids congestive heart failure after myocardial infarction in rats.

BACKGROUND: Angiotensin converting enzyme (ACE) inhibitors and angiotensin II AT1-receptor antagonists prolong survival in experimental postischemic heart failure (CHF) in rats. The aim of this study was to investigate whether potential beneficial effects of early and long-term therapy with low doses of captopril or losartan occur in hemodynamics and heart morphometry, as well as in infarct size during establishment of CHF after myocardial infarction. METHODS: Male Wistar rats were subjected to myocardial infarction by left coronary ligation. Subsequently, 24 h after surgery captopril (2.5 mg/kg/day/28 days) or losartan (3 mg/kg/day/28 days) was administered by mini-osmotic pump release. Hemodynamics, infarct size, and heart morphometry were measured in sham, untreated, and treated operated rats. RESULTS: Morphometric and hemodynamic parameters were modified after myocardial infarction indicating hypertrophy of the heart and CHF establishment; however, either captopril or losartan partially avoided hypertrophy. Captopril reverted hemodynamics to sham values, while losartan induced further decrease in systolic blood pressure. Both drugs were able to drastically reduce infarct size produced by myocardial infarction. CONCLUSIONS: Data show that early and chronic therapy with low doses of captopril or losartan prevent CHF establishment, probably by limiting extension of infarcted area after coronary occlusion, and suggest AT1 receptor pathway involvement in this pathology.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1999

[Variability in the management and prognosis at short- and medium-term of myocardial infarct in Spain: the PRIAMHO study. Registration Project of Hospital Acute Myocardial Infarct].

BACKGROUND AND PURPOSE: The paucity of data on myocardial infarction management and results in Spain lead to the design of the PRIAMHO study (Proyecto de Registro de Infarto Agudo de Miocardio Hospitalario [Acute Myocardial Infarction Hospital Registration Project]) which developed standard methods to collect information on the management of patients with such a condition and their characteristics. The variability results among hospitals in myocardial infarction management and in one-year mortality are presented. METHODS: A cohort study with a one-year follow-up was designed to register all patients diagnosed with acute myocardial infarction discharged from 24 Spanish hospitals that completed all the requisites to participate. The demographic and clinical characteristics of the patients, their management during the coronary care unit stage, and the outcome and complications were prospectively registered. Standard definitions for diagnosis were used. Confidentiality regarding patient identity and participating centers was guaranteed. RESULTS: 5,242 (77.6%) of the 6,756 patients with myocardial infarction admitted in the 24 participating hospitals were registered in the coronary care units. Half of the centers had an on-site hemodynamic laboratory and in seven coronary surgery. The delay between symptom-onset and emergency room admission was 2 hours. Acute pulmonary edema or cardiogenic shock was developed by 16.6% of patients and 41.8% received thrombolysis. Mean time delay between symptom-onset and thrombolysis was 3 hours. A large variability in the use of beta-blockers, thrombolysis, echocardiography, coronary catheterization angiography and invasive revascularization was observed among hospitals. Mortality in the coronary care unit was 10.9% and increased to 14.0% at 28 days and to 18.5% at one year with considerable variation among hospitals. Four hospitals showed higher mortality among their patients, independently from the proportion of diabetes, hypertension, women, anterior location of myocardial infarction, non-Q-wave infarction, age and severity. CONCLUSIONS: The results of this study show that early and mid-term mortality from myocardial infarction is still high in Spain in the reperfusion era, and that a considerable variability in management and outcome exists among Spanish hospitals, which is not explained by the different case-mix among them.

Cardiovascular Agents↗