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PubMed1998

[Regeneration of the heart muscle after myocardial infarct].

Myocardial infarction is characterized by the loss of contractile cardiomyocytes. This results in an increased load on the spared myocardium. The aim of this article is to describe the response of the non-affected myocardium after infarction. Human hearts were investigated by microscopical, biochemical and cytophotometrical methods. The number of nuclei was calculated from the numerical ratio of connective tissue nuclei/myocyte nuclei, the values of the total DNA amount and the percentage proportion of the various ploidy classes in the myocyte nuclei. After myocardial infarction the DNA concentration as well as the DNA content was increased. Different DNA distribution pattern could be found in infarcted hearts. Percentage proportion of higher ploid nuclei and aneuploid nuclei was increased. Number of connective tissue nuclei was increased in infarcted hearts. And, in spite fibrosis of the necrotic area, number of myocyte nuclei did not change significantly. Beside scarring of the necrotic tissue, hypertrophy and hyperplasia of cardiomyocytes occur after myocardial infarction and may compensate the loss of contractile fibres to guarantee myocardial function.

Cardiomegaly↗
PubMed2006

Autoimmunity in myocardial infarction.

Myocardial infarction is associated with an immune response. Physiological inflammation response causes self-repair and protection, while pathological autoimmune response leads to ventricular remodeling and heart failure. Laying emphasis on regulating the immune function may become a new target for the prevention of heart failure after myocardial infarction. This review focuses on the mechanism of immune-mediated ventricular remodeling and the immune therapy after myocardial infarction.

Animals↗
PubMed1995

Good exercise capacity at hospital discharge predicts recovery of baroreflex sensitivity after myocardial infarction.

Myocardial infarction results in depressed baroreflex sensitivity, which has been shown to be associated with increased risk of ventricular arrhythmias and sudden death. We measured baroreflex sensitivity in 37 patients with acute myocardial infarction before hospital discharge and 3 months after the infarction to find out whether the baroreflex sensitivity recovers during that period. In addition, baroreflex sensitivity was assessed in 15 healthy controls. Baroreflex sensitivity was assessed from the regression line relating the change in R-R interval to the change in systolic blood pressure following an intravenous bolus injection of phenylephrine. There was a wide inter-individual variation in the change of baroreflex sensitivity (delta baroreflex sensitivity) in infarction patients, but the average baroreflex sensitivity showed no significant change during the 3-month follow-up (10.2 + 5.6 to 11.8 +/- 7.5 ms.mmHg-1, ns) and remained lower than the baroreflex sensitivity of the controls (16.4 +/- 9.7 ms.mmHg-1, P < 0.05). delta Baroreflex sensitivity correlated significantly with exercise capacity measured before hospital discharge. When the patients were divided into tertiles according to the delta baroreflex sensitivity (-3.3 +/- 1.5 ms.mmHg-1 in the lowest tertile, 1.0 +/- 1.0 ms.mmHg-1 in the middle tertile and 7.5 +/- 4.0 ms.mmHg-1 in the highest tertile) the exercise capacity was found to increase from the lowest to the highest tertile (exercise time 357 +/- 115 s, 418 +/- 126 s and 461 +/- 141 s, respectively; P < 0.05 lowest vs highest tertile). Patients with a low exercise tolerance (exercise time < 360 s) showed a significantly smaller delta baroreflex sensitivity than patients with a good exercise tolerance (exercise time > or = 480 s) (-0.5 +/- 4.4 vs 5.3 +/- 5.4 ms.mmHg-1, P < 0.05), respectively. delta Baroreflex sensitivity was not related to the location or type of infarction, thrombolytic therapy, presence of angina pectoris or left ventricular function at the time of discharge. In conclusion, exercise capacity assessed before hospital discharge seems to be a predictor of baroreflex sensitivity recovery in patients with a recent myocardial infarction.

Aged↗
PubMed1995

Intravascular ultrasound imaging in patients with acute myocardial infarction.

Myocardial infarction is the result of acute thrombotic occlusion of a coronary artery secondary to rupture of an atherosclerotic plaque. Intracoronary ultrasonic examinations (ICUS) were performed in patients with acute myocardial infarction in order to describe intraluminal ultrasonic findings at the site of an acute coronary occlusion. Coronary angiography and ICUS studies were performed consecutively within 6 h after the onset of chest pain in 50 patients with acute myocardial infarction (AMI) prior to percutaneous coronary angioplasty (PTCA). Following angiographic documentation of a proximal occlusion, a 3.5 mechanical ultrasound catheter (30 MHz) was advanced successfully through the lesion in 42 of 50 patients (84%). In 37 of the 42 patients (88.1%), ICUS differentiated between pulsatile, low echogenic, intraluminal material suggesting thrombus, and mural more highly echogenic atherosclerotic plaque. A negative imprint of the ICUS catheter was documented within the low echogenic material in 25 of 42 (60%) patients with AMI. Low echogenic intraluminal material was found in 31 of 42 (73.4%) segments proximal to the highly echogenic plaque and in 28 of 42 (66.7%) segments distal to it, indicating pre- and post-stenotic thrombus in AMI. The plaque appeared eccentric in 32 of 42 patients (76.2%) with AMI. Cross-sectional area stenosis due to highly echogenic plaque averaged 48 +/- 14%. Calcification of plaque was evident in 35 of 42 patients (83.3%) and the surface of the plaque was rough in 30 of 42 (42.4%). Fissures were found in 10 (23.8%) and a dissection was detected in four (9.5%) cases.

Adult↗
PubMedDate not supplied

[Secondary prevention in acute myocardial infarction].

Myocardial infarction is still one of the main causes of mortality and morbidity in Western countries. The advances made in the last 30 years have made it possible to reduce mortality significantly (which is currently below two digits) as well as morbidity. The subject of secondary prevention of myocardial infarction gains particular significance in this context since 10 to 15% of the patients who survive the hospital phase of myocardial infarction die during the first year following discharge and, of these deaths, half occur in the first three months. Therefore, it is necessary to make an early definition of the risk of another coronary event, that is, to make a risk stratification. This should occur throughout hospitalization and should be complete at the time of discharge, never beyond the first weeks of evolution. Bearing in mind the age, sex, coronary risk factors, ischemia persistence, the degree of left ventricular dysfunction and the presence of malignant disrhythmias, there are three risk levels: high; intermediate; and low. An overall approach to secondary prevention of infarction should take into account that, apart from the factors of such high prognostic value (Chapter II) assessed in the definition of risk groups, the measures to reduce reinfarction and sudden death (Chapter III) and the control of the risk factors for heart disease (Chapter IV) should also be considered. The principal late complications of infarction with significant prognostic influence are described in Chapter III: left ventricular dysfunction; rhythm disturbances and residual ischemia. The diagnostic criteria and therapeutic objectives are considered in each of the groups with relevance to consolidated advances according to the modern concept of evidence based medicine, according to international regulations. The grading of scientific evidence into three distinct categories (A, B and C), based on five levels of evidence classified from I to V, is presented accordingly in relation to the therapeutic proposals. Chapter III deals with a set of therapeutic interventions used in secondary prevention because they reduce reinfarction and sudden death: platelet antiaggregants; anticoagulants; Beta blockers; calcium channel blockers; antioxidants and nitrates. A concept of particular clinical significance is presented for each of these groups of drugs. The last part contains an eminently clinical overall review of the principal advances in coronary risk factor control, new therapeutic acquisitions in atherosclerotic disease with natural relevance to hypolipidemic agents and statins, which apart from controlling the plasmatic levels of cholesterol, also stabilize the atherosclerotic plaque and reduce acute coronary events significantly. Apart from dyslipidemia, the classic risk factors are: smoking; hypertension; obesity; diabetes and sedentary life. In each case, reference is made to the general measures and specific approaches, as well as the pharmacological therapy according to evidence based medicine. The recommended attitudes are pointed out. The role of cardiac rehabilitation and postmenopausal hormone replacement therapy are also discussed in the last part of these recommendations, in which the on-going controversy regarding hormone replacement therapy is pointed out in view of the results of more recent clinical trials.

Clinical Protocols↗
PubMed2000

Beneficial effects of MET-88, a gamma-butyrobetaine hydroxylase inhibitor in rats with heart failure following myocardial infarction.

Myocardial ischemia can cause myocardial infarction and as a consequence, heart failure. 3-(2,2,2-trimethylhydrazinium) propionate (MET-88) inhibits gamma-butyrobetaine hydroxylase and has cardioprotective effects on the ischemic heart. We now examined the effects of MET-88 in rats with congestive heart failure following myocardial infarction. Congestive heart failure was produced by left coronary artery ligation in rats. MET-88 at 100 mg/kg/day was orally administered from the 2nd day after surgery. We performed a survival study for 181 days, and measured ventricular remodeling, cardiac function, and myocardial high-energy phosphate levels after treatment for 20 days. MET-88 prolonged survival with a median 50% survival of 103 days compared to 79 days for the heart-failure control rats. The expansion of the left ventricular cavity (ventricular remodeling) in heart-failure rats was prevented by treatment with MET-88, and the effect of MET-88 was similar to that of captopril at 20 mg/kg. MET-88 attenuated the rise in right atrial pressure in heart-failure rats and augmented cardiac functional adaptability against an increased load. Also, MET-88 improved the myocardial energy state in heart-failure rats. The present results indicate that MET-88 improves the pathosis in rats with heart failure induced by myocardial infarction.

Adenosine Diphosphate↗
PubMed1981

[Effect of nitroglycerin on the extent of myocardial infarction].

Myocardial infarction in rabbits was caused by ligation of the anterior descending artery. Nitroglycerin was given intravenously (100 micrograms/min) 120--180 min after the operation. In both control and experimental groups, precordial ECG maps were recorded 30, 120, 180 and 360 min after the operation. 7 days after the operation the size of myocardial infarction was measured by planimetry. Rapid and statistically significant dynamics of ECG was observed in the control group under the effect of nitroglycerin. Bradycardia under the effect of nitroglycerin was recorded in the experimental group but was not seen in the control group or in the complementary one where nitroglycerin was given to anesthetized but non-operated animals. Therefore bradycardia under the effect of nitroglycerin was observed only in animals with acute myocardial infarction. Planimetry demonstrated a statistically significant reduction of the area of necrosis in the experimental group (by 41.2%) as compared with the control one.

Animals↗
PubMed1998

[Platelet activation in the early phases of acute myocardial infarction].

Myocardial infarction and thrombolysis are proven to be associated with platelet activation. However, the time relationship of platelet activation with the onset of symptoms and with thrombolysis, and the response to aspirin are not well defined. In this study we measured platelet activity in the early phase of myocardial infarction treated with either streptokinase or recombinant tissue-type plasminogen activator (rt-PA) and evaluated whether and to what extent it may be counteracted by aspirin. Fourty-one patients (mean age 57 +/- 6 years) received thrombolytic therapy after coronary occlusion: 1.5 million units of streptokinase (Group 1; 21 patients) or 100 mg of rt-PA (Group 2; 20 patients). Ten randomly selected patients in either group were given 500 mg aspirin i.v. prior to infusion of the thrombolytic compound and, then, 325 mg/die of aspirin orally. Beta-thromboglobulin (BTG), a marker of platelet activity, was determined at admission, after thrombolysis and in the subsequent 48 hours. At admission, BTG plasma levels averaged 125 +/- 31 IU/ml in Group 1 and 134 +/- 35 IU/ml in Group 2 (NS). Thrombolysis produced a similar increase in platelet activity in both groups, and maximal values were reached at the third hour (196 +/- 43 IU/ml in Group 1 and 192 +/- 39 in Group 2, p < 0.001 vs baseline and NS between groups). Levels of BTG were higher in streptokinase-treated group starting from 24 hours (p < 0.05). Differences in BTG levels between aspirin-treated and aspirin-untreated patients became significant at 48 hours after thrombolysis in both groups. An inverse correlation was found between time elapsed from onset of symptoms and BTG value on admission (r = -0.86, p < 0.001); in patients admitted within 2 hours after the beginning of symptoms, and having the higher BTG levels, thrombolysis did not induce a significant increase in platelet activity; this, on the contrary, was observed in patients admitted later. Platelet activation is greater early after myocardial infarction and is differently influenced by thrombolytic treatment, depending on the delay of the patient's admission. Streptokinase and rt-PA induce a similar increase in platelet activity which is more persistent after streptokinase; cycloxygenase inhibition with aspirin seems to influence platelet activity only starting from the second day.

Adult↗
PubMed1999

Fibrinolytic and antithrombotic regimens in recently completed, ongoing and planned clinical trials in myocardial infarction.

Myocardial infarction carries significant short-term and long-term risks of morbidity and mortality. Traditional treatment for acute myocardial infarction has significantly improved the outcomes of patients suffering from this condition. Recent clinical trials have focused on the use of novel fibrinolytics, glycoprotein IIb/IIIa receptor antagonists, low-molecular-weight heparin, direct thrombin inhibitors and myocardial protection, in an attempt to improve the prognosis of these patients. This clinical trials report reviews the rationale and design of recently completed, ongoing and planned major Phase II and III clinical trials on fibrinolytic and antithrombotic regimens for the treatment of myocardial infarction.

Journal Article↗
PubMed1999

[New thrombolytic agents in myocardial infarction].

Myocardial infarction is the result of thrombotic coronary artery occlusion. Although present-day thrombolytics have major value by increasing the frequency of reopening of arteries responsible for myocardial infarction, by preserving myocardial function and, thereby, significantly reduce mortality. Nevertheless, they are subject to the following limitations: 1) excellent arterial partency is only obtained in 50% of cases: 2) reocclusion occurs in 5 to 10% of cases; 3) severe complications such as cerebral haemorrhage are observed in about 0.5% of cases. Therefore, the search to improve thrombolytic agents is intense. This article reports the recent advances in concept and production of new thrombolytic agents. The most recent results concern the production of mutants of T-PA (tissue plasmogen activator). Of these mutants, the reteplase (r-PA) has already received authorization for its commercialisation. Other t-PA mutants under development (phase 3) include TNK-t-PA and lanoteplase. Over the last few years, there has been renewed interest in staphylokinase. The results of the initial clinical trials with this agent have also been reported. Paradoxically, the mode of action of thrombolytic agents has an inherent pro-thrombotic effect. This explains some of the interest for anti-thrombotic agents as an adjuvant treatment of thrombolysis. The initial results of the association of thrombolytics with new glycoprotein IIb/IIIa platelet inhibitors and anti-thrombin agents are reported.

Coronary Disease↗
PubMed2000

Free radicals, cytokines and nitric oxide in cardiac failure and myocardial infarction.

Myocardial infarction is the most common cause of congestive cardiac failure. Free radicals, cytokines, nitric oxide (NO) and antioxidants play a major role both in atherosclerosis and myocardial damage and preservation. In the early stages of atherosclerosis, neutrophils and monocytes infiltrate the intima and generate free radicals which damage the endothelial cells. As a result, production of NO and prostacyclin by the endothelial cells declines, which have cardioprotective actions. This also has relevance to the beneficial action of aspirin since, it can modulate both prostanoid and L-arginine-NO systems and NF-kB translocation. In both acute myocardial infarction and chronic congestive cardiac failure, the plasma levels of various inflammatory mediators such as interleukins and tumour necrosis factor-alpha (TNFalpha) are elevated. TNFalpha, produced by the inflammatory cells and the myocardium, can suppress myocardial contractility and induce the production of free radicals, which in turn can further damage the myocardium. Transforming growth factor beta (TGFbeta), polyunsaturated fatty acids and the glucose-insulin-potassium regimen can antagonize the harmful actions of TNFalpha and protect the myocardium. This explains why efforts made to reduce the levels of pro-inflammatory cytokines have beneficial action and preserve the myocardium.

Animals↗
PubMed1993

Echocardiographic diagnosis of mechanical complications in acute myocardial infarction.

Myocardial infarction occurs with an incidence of approximately 1.5 million cases annually in the United States. Mortality remains at about 12% despite recent advances in medical and interventional therapies. A significant proportion of deaths is due to mechanical complications following infarction. These complications include rupture of the ventricular free wall, septum and papillary muscles. Collectively, they are potentially treatable. However, they require prompt diagnosis and urgent surgical intervention. Traditional measures in the evaluation of these patients include invasive tests such as right heart catheterisation, coronary angiography and contrast left ventriculography, which may be time-consuming and are not without untoward effects. The purpose of this review is to examine the role of echocardiography as an adjunct in the diagnosis of mechanical complications in acute myocardial infarction. Echocardiography is particularly well suited for this purpose as it is safe, performed rapidly and is capable of providing reliable information regarding the presence and location of transmural rupture, interventricular shunts and the evaluation of mitral regurgitation. In addition, echocardiography is capable of assessing overall left ventricular function and regional wall motion abnormalities.

Echocardiography↗
PubMedDate not supplied

[Comparison of initial and delayed myocardial imaging with beta-methyl-p-[123I]-iodophenylpentadecanoic acid in acute myocardial infarction].

Myocardial imaging using beta-methyl-p-[123I]-iodophenylpentadecanoic acid (BMIPP) of 15 patients with acute myocardial infarction was performed to assess "fill-in" and "washout" defects in the delayed myocardial image. The initial and delayed images were evaluated by a visual and quantitative washout rate method. Visual judgement found 8/180 (4%) segments showed "fill-in" defects, and 24/180 segments (13%) showed "washout" defects. There was no relationship between days from onset to the study and the frequency of fill-in and washout defects. The mean washout rate in the segments with "fill-in" defects was 9.0 +/- 16.6%, and that of "washout" defects was 24.9 +/- 18.1% which was significantly higher than in controls (8.7 +/- 15.4%, p < 0.05). There was no correlation between mean washout rate and total blood lipids, total cholesterol, triglyceride and HDL-cholesterol. Therefore, neither time from onset nor blood lipids level was related to changes from the initial image to the delayed image. These changes may be due to relative (false) findings due to changes in circumference, and may be based on myocardial characteristics after myocardial infarction and/or reperfusion.

Adult↗
PubMed2000

Tackling myocardial infarction.

Myocardial infarction is dangerous. Among people in the UK who develop an acute coronary event, in particular myocardial infarction, around 35-40% die within 24 hours of the condition's onset and 40-50% within a month. Here, we discuss management up to and following admission to hospital, concentrating on the use of aspirin, thrombolytic therapy, coronary angioplasty, angiotensin-converting-enzyme (ACE) inhibitors and beta-blockers.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

[Stem cell perspectives in myocardial infarctions].

Myocardial infarction is the leading cause of congestive heart failure and death in industrializated countries. The cellular cardiomyoplasty has emerged as an alternative treatment in the regeneration of infarted myocardial tissue. In animals' models, different cellular lines such as cardiomyocites, skeletal myoblasts, embryonic stem cells and adult mesenchymal stem cells have been used, resulting in an improvement in ventricular function and decrease in amount of infarcted tissue. The first three cells lines have disvantages as they are allogenics and are difficult to obtain. The adult mesenchymal stem cells are autologous and can be obtained throught the aspiration of bone marrow or from peripherical circulation, after stimulating with cytokines (G-CSF). The implantation in humans with recent and old myocardial infarction have shown improvements similar to those shown in animal models. These findings encourage the continued investigation in the mechanism of cellular differentiation and implantation methods in infarcted myocardial tissue.

Animals↗
PubMed1992

Drug-induced myocardial ischemia and acute myocardial infarction.

Myocardial infarction generally occurs in the presence of known risk factors and identifiable coronary artery disease. Atypical presentations due to therapeutic and illicit drug use are documented, however, and lead to the consideration of alternative pathophysiologic rationales for myocardial infarction. This article discusses central nervous system stimulants and other drugs that have the potential for myocardial damage and their nursing implications.

Amphetamines↗
PubMed2003

Inflammatory mechanisms in myocardial infarction.

Myocardial infarction is associated with an inflammatory response, ultimately leading to healing and scar formation. Reperfused myocardial infarcts exhibit an enhanced inflammatory reaction, and are associated with improved cardiac repair and patient survival. This review summarizes our current knowledge of the inflammatory mechanisms mediating injury and repair following myocardial ischemia and reperfusion. Myocardial necrosis is associated with complement activation and free radical generation, triggering a cytokine cascade and chemokine upregulation. Interleukin (IL)-8 and C5a are released in the ischemic myocardium, and may have a crucial role in neutrophil recruitment. Extravasated neutrophils may induce potent cytotoxic effects through the release of proteolytic enzymes and the adhesion with Intercellular Adhesion Molecule (ICAM)-1 expressing cardiomyocytes. However, despite these potentially injurious effects, the post-reperfusion inflammatory response may significantly enhance healing. Monocyte Chemoattractant Protein (MCP)-1 is induced in the infarcted area and may regulate mononuclear cell recruitment. Accumulation of monocyte-derived macrophages, and mast cells may increase expression of growth factors inducing angiogenesis and fibroblast accumulation in the infarct. In addition, expression of cytokines inhibiting the inflammatory response, such as Interleukin (IL)-10 may suppress injury. Matrix Metalloproteinases (MMPs) and their inhibitors regulate extracellular matrix deposition and play an important role in mediating ventricular remodeling. Inflammatory mediators may induce recruitment of blood-derived primitive stem cells in the healing infarct, which may differentiate into endothelial cells and even lead to limited myocardial regeneration. Understanding the cellular and molecular steps involved in regulating infarct healing may lead to specific interventions aimed at optimizing cardiac repair.

Animals↗