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PubMed1983

Correlation between divalent cation concentration and electrocardiogram in canine myocardial infarction.

Myocardial infarction is accompanied by changes in serum divalent cation concentrations. The effects of these changes on the electrical activity of the heart have not been fully determined. In six mongrel dogs, major coronary arteries were catheterized and occluded with metal beads; in five dogs the arteries were catheterized, but left patent. Serum magnesium concentrations ([Mg++]), zinc concentrations ([ZN++1]), copper concentrations ([Cu++]), calcium concentrations ([Ca++]), and ECGs were monitored in each dog at one, 24, 48, and 72 hours after surgery. Only dogs with coronary artery occlusion had ST segment changes (1.9 +/- 0.4 mm) in chest lead V4. Serum [Mg++] and [Zn++] decreased (approximately 20%) only after coronary artery occlusion and only at 24 hours after the procedure. Runs of ventricular tachycardia and premature beats were prevalent at this time. Serum [Cu++] was different in that it increased (approximately 30%) at 48 and 72 hours in the dogs with and without coronary artery occlusion. No changes were observed in serum [Ca++]. Decreases in serum [Mg++] and Zn++] coincided with the periods of dysrhythmia in the ischemic hearts. Elevation of serum [Cu++] was not specifically associated with myocardial ischemia and, within these physiologic limits, it appeared to be without effect on cardiac electrical activity.

Animals↗

PubMed1999

Envisioning a network of care for at-risk patients after myocardial infarction.

Myocardial infarction (MI) continues to be a significant health care issue because of its prevalence. As treatment options improve the survival rate, an increasing number of individuals have to learn how to adjust to this major life event and prevent recurrence. Recovery can be difficult. Many patients experience emotional distress, fear of dying, and family turmoil, fail to return to work when physiologically capable of doing so, are unable to return to their previous levels of sexual activity, and are not capable of making the necessary diet and exercise changes. Acute management strategies continue to be aimed at limiting the infarct size, whereas holistic approaches to the patient and family adjustment must target seeking prompt treatment when symptoms present, psychologic adjustment, stress reduction, and patient and family education for self-care and risk reduction. As hospital length of stay for acute MI decreases, health care professionals must provide an interdisciplinary, collaborative approach to ensure that the at-risk MI patient is provided all of the information and support needed to lead a satisfying, productive, healthy life. An excellent way for nurses to not only address this challenge, but to lead the effort, would be to develop a network of care for the at-risk MI patient.

Community Networks↗

PubMed2006

Genome-wide association study to identify single-nucleotide polymorphisms conferring risk of myocardial infarction.

Myocardial infarction (MI) is characterized by abrupt occlusion of coronary artery resulting in irreversible damage to cardiac muscle. This disease might result from the interactions of multiple genetic and environmental factors, none of which can cause disease solely by themselves. To reveal the genetic bases of MI, we performed a large-scale, case-control association study using 92,788 gene-based single-nucleotide polymorphism (SNP) markers. We have identified functional SNPs within the lymphotoxin-alpha gene located on chromosome 6p21 conferred susceptibility to MI. This chapter describes a detailed protocol for performing a genome-wide association study as used in our MI study.

Case-Control Studies↗

PubMed1999

Diabetes and myocardial infarction.

Myocardial infarction (MI) is a common cause of mortality in people with diabetes. The case fatality from MI is high and may be reduced by thrombolysis and treatment with aspirin, beta-blockers and angiotensin-converting enzyme inhibitors. Poor metabolic control is common among diabetic patients with MI, but the importance of controlling blood glucose during and following an MI is debatable. Treatment with statins reduces cardiovascular end-points in diabetic patients with previous MI (secondary prevention). Large studies in diabetic patients without existing heart disease have shown statistically insignificant reductions in heart disease and MI with improved glycaemic control of the diabetes (primary prevention). The treatment of hypertension in people with diabetes prevents cardiovascular end-points, and studies on whether the treatment of hyperlipidaemia reduces heart disease and MI are proceeding.

Adrenergic beta-Antagonists↗

PubMed1998

Genetic risk factors for myocardial infarction.

Myocardial infarction (MI) is a complex phenotype caused by interaction of a number of genetic and environmental factors. A genetic susceptibility to MI was observed in a familial aggregation and studies in twins. Advances in molecular genetics have led to identification of a number of potential genetic risk factors for MI, such as variants of genes involved in vascular homeostasis, thrombosis, and lipid metabolism. Functional variants of angiotensin-1-converting enzyme (ACE), beta-fibrinogen, plasminogen activator inhibitor-1, methylenetetrahydrofolate reductase, glycoprotein Illa, and many apolipoprotein genes are considered excellent candidate risk factors for MI. Interaction of the susceptibility genes with modifier genes, environmental factors, and conventional risk factors results in the final phenotype of MI. Understanding the complex interaction between these factors is expected to provide significant insights into the pathogenesis of MI and lead to development of genetic-based risk stratification, prevention, and treatment.

Genetic Markers↗

PubMed2004

Warfarin and herbal products interaction causing prosthetic aortic valve thrombosis presenting as acute myocardial infarction.

Myocardial infarction (MI) due to coronary artery embolization is a rare and potentially lethal complication of prosthetic heart valve thrombosis. A 58-year-old man in whom the aortic valve was replaced with a bileaflet mechanical valve presented with an acute anterior MI. Valvular dysfunction was detected by physical examination, and confirmed by two-dimensional echocardiography and cinefluoroscopy. Coronary angiography disclosed embolization of the left anterior descending artery. Thrombotic encroachment of one of the prosthetic valve leaflets was found at reoperation. Failure to achieve adequate anticoagulation was likely due to an interaction between warfarin and herbal products. These findings have significant implications regarding the diagnosis and treatment of acute MI in patients with left-sided prosthetic heart valves, and emphasizes the importance of appropriate anticoagulation in this setting.

Anticoagulants↗

PubMed1996

Effect on prolonged inhibition of neutral endopeptidase on cardiac hypertrophy in rats with myocardial infarction.

Myocardial infarction was induced by rats by ligation of the left coronary artery. Treatment with TM1, a prodrug of SQ 28,603, an inhibitor of neutral endopeptidase (NEP, EC 3.4.24.11), was started 18-20 hours after ligation and was continued for 4 weeks (100 mg/kg, orally, twice daily). Morphological and biochemical parameters were assessed at the endo of therapy. The treatment resulted in a significant reduction of heart hypertrophy, which was restricted to the parts of myocardium hemodynamically upstream of the infarcted left ventricle. The weights of the right ventricle and atria were reduced by 15-20%, whereas the treatment had no effect on the left ventricle and septum weights. Treatment led to an almost complete inhibition of plasma NEP activity and to a slight decrease (-14%, p < 0.05) in plasma ACE activity. Plasma ANF level increased 3.8-fold after ligation, and treatment resulted in a slight ( + 29%) and nonsignificant additional increase in the ANF level. The amount of hydroxyproline in the right ventricle was enhanced by + 207% in control ligated rats and by +140% (NS) in treated rats. These data indicated that prolonged NEP inhibition exerts a favorable effect in heart failure by reducing the development of right ventricular and atrial hypertrophy. These effects may result from an improvement in hemodynamic conditions, leading to a reduction in cardiac preload.

Alanine↗

PubMed2007

A functional SNP in ITIH3 is associated with susceptibility to myocardial infarction.

Myocardial infarction (MI) results from complex interactions of multiple genetic and environmental factors. To disclose genetic backgrounds of MI, we performed a large-scale, case-control association study using 52,608 gene-based single-nucleotide polymorphism (SNP) markers, and identified a candidate SNP located on chromosome 3p21.2-p21.1. Subsequent linkage-disequilibrium mapping indicated very significant association between MI and a SNP in exon 2 of the inter-alpha (globulin) inhibitor 3 gene (ITIH3; chi(2) = 24.88, P = 6.1 x 10(-7), 3,353 affected individuals versus 3,807 controls). In vitro functional analyses showed that this SNP enhanced the transcriptional level of the ITIH3 gene. Furthermore, we found expression of the ITIH3 protein in the vascular smooth muscle cells and macrophages in the human atherosclerotic lesions, suggesting ITIH3 SNP to be a novel genetic risk factor of MI.

Alpha-Globulins↗

PubMed1988

Relation of left ventricular perfusion and wall motion with metabolic activity in persistent defects on thallium-201 tomography in healed myocardial infarction.

Myocardial viability in persistent thallium (TI)-201 defect is a controversial subject. To assess metabolic activity in segments with persistent defect, stress TI-201 tomography and positron emission tomography using nitrogen-13 ammonia and fluorine-18 2-fluoro-deoxyglucose (FDG) were performed in 28 patients with healed myocardial infarction. The segments with TI-201 perfusion defect in electrocardiogram-determined infarcted areas were selected for assessment. Stress perfusion defect was detected in 61 segments by TI-201 tomography. Twenty-two patients (36%) showed transient defects with redistribution (group 1) and 39 showed persistent defects (group 2). Increase in FDG uptake was observed in 95% in group 1. Among group 2 patients, 15 segments (38%) showed an increase in FDG uptake (group 2A) while the remaining 24 (62%) did not have an increased uptake (group 2B). The decrease in nitrogen-13 ammonia perfusion was more severe in group 2B (-23 +/- 7%) than in group 2A (-13 +/- 9%) (p less than 0.005) and group 1 (-10 +/- 4%) (p less than 0.001). In addition, wall motion scores tended to be lower in group 2B (0.21 +/- 0.71), compared with group 2A (0.67 +/- 0.70) (p = 0.05) and group 1 (0.77 +/- 0.60) (p less than 0.01). These data indicate that metabolic viability was observed in approximately 40% of the segments with persistent TI-201 defect. Preservation of regional perfusion and wall motion in these areas was similar to that in areas with transient TI-201 defect.

Aged↗

PubMed2004

Differences in tail vascular bed reactivity in rats with and without heart failure following myocardial infarction.

Myocardial infarction (MI) was induced in rats by coronary ligation to compare changes in vascular reactivity from animals that developed heart failure (InfHF) with those that did not (Inf). Infarct size was similar in both groups. In vitro preparations of tail vascular bed were used to investigate the vascular responses to acetylcholine, sodium nitroprusside, and phenylephrine. Acetylcholine-induced relaxation was impaired in the Inf group (53 +/- 2%, n = 6) when compared with Sham (80 +/- 2%, n = 6, P < 0.05). The maximal response (E(max)) to phenylephrine increased in the Inf group (423 +/- 10 mm Hg, n = 9, P < 0.01) and decreased in InfHF (279 +/- 10 mm Hg, n = 7, P < 0.05) when compared with Sham (319 +/- 11 mm Hg, n = 8). Regardless of endothelial integrity, E(max) to phenylephrine increased in the Inf, nitro-l-arginine methyl ester, and indomethacin groups. An increased release of a prostanoid vasodilator was detected in the Inf group. Differently, the InfHF group presented a reduction of the E(max) to phenylephrine and an increment of nitric oxide release. This study demonstrates that MI without heart failure impairs endothelium-dependent relaxation and increases the reactivity to phenylephrine. This increase seems to involve a muscular component. The endothelium participates with an increased release of a vasodilator prostanoid, possibly to compensate the increased smooth muscle response. When heart failure follows MI, the reactivity to phenylephrine decreases, possibly due to an increased nitric oxide release.

Animals↗

PubMed1988

Changes in platelet membrane fatty acids after myocardial infarction.

Myocardial infarction (MI) is a common cause of morbidity and mortality, and platelets may contribute to its development. Platelet membrane composition can influence platelet function. In this study changes in platelet membrane fatty acids with time following MI were explored. Platelet membrane fatty acid profiles were studied in 40 patients after MI, at a mean of 8 days, and compared with a control group of 17 subjects awaiting minor surgery. They were restudied at 1 month and 3 months. Significant changes were found within the patient group in 18:1, which fell with time (19.99% +/- 1.24 to 18.73% +/- 1.16 at 3 months, P less than 0.001), 22:3 + 24:1, which also fell (1.97% +/- 0.48 to 1.46% +/- 0.49, P less than 0.001), and in 18:2, which increased (3.92% +/- 0.77 to 5.04% +/- 1.15 P less than 0.001). Comparison with controls showed no significant differences at baseline, a small increase in 22:4 at 1 month and 3 months in MI group and a decrease in 22:3 + 24:1 in MI group at 3 months. No changes were noted in 20:4, 20:5 or in the polyunsaturated/saturated fatty acid ratio. The explanation for these findings is not known. The possible influence of diet and other factors is discussed.

Adult↗

PubMed2004

Studies on serum triglyceride level in patients with myocardial infarction.

Myocardial Infarction (MI) is the most common form of heart disease and the single most important cause of premature death in the developed and developing world. Unfortunately the incidence of the condition is increasing rapidly in many developing countries like Bangladesh. Effort should therefore be taken to minimize the risk factors of MI. Large scale randomized clinical trials have shown that lowering high triglyceride concentration mainly by drugs reduces the risk of cardiac events like MI. So the present work has been designed to see the serum triglyceride levels in normal healthy subjects, to compare serum triglyceride levels in patients with MI and those of healthy subjects and to evaluate the association of serum triglyceride in Bangladeshi MI patients. The present study was carried out in the Department of Biochemistry, BSMMU in collaboration with Department of Cardiology, BSMMU and NICVD, Dhaka during the period of July 2001 to December 2002. A total of 50 subjects were selected, Group A (30 subjects of control ) and Group B (20 subjects of test ). The mean level of serum triglyceride in control subjects were 117.07 +/- 32.41 mg/d1 and in test subjects were 176.87 +/- 37.15 mg/d1. So the present study showed that serum triglyceride level is significantly higher in patients with MI. From the present study, it is difficult to draw any definite conclusion but suggested that high serum triglyceride concentration is a cause of the incidence of MI.

Adult↗

PubMed2004

["Heart attack in humans"--the health belief model in comparison with the health reality of patients with myocardial infarction].

Myocardial infarction (MI) is the direct cause of 40% of all deaths, independently of the high standard of medical treatment. The main aim of the study was to define the relationship between the declarative health model (declarations) and the real health activity of the sufferers (realization). The research was performed on 107 patients after acute MI, hospitalized in the Cardiology Department Medical University of Silesia. They were questioned in direct interviews. In addition, the modified form of Shalit's circle was applied. The results indicated the coexistence of two health models of patients. In declarations, there is a model of person with interior attribution of MI (90.65%) that has a feeling of ability to influence his/her health (e.g. through the lifestyle: 63.55%; an individual's character: 41.12%). In realization, there is a model of sick patient with exterior attribution of heart attack (e.g. political and economic crisis, innate predisposition). A similar tendency in the perception of health factors and planning of changes after MI was observed. For instance, 50.47% patients talked about "the increase caution" or "slowing down" as a new planned form of activity. Moreover, of 92% patients who have the social support only 33.64% consider that as an important factor for health. The results suggest a divergence between declarations and real health activity. The launched health model of beliefs seems to be too costly and not attractive enough. Taking into consideration the complete risk factors in MI and making the proposed health belief system more accessible seem to be essential for creating an adequate prevention program.

Adult↗

PubMed2006

Inflammation as a risk factor for myocardial infarction.

Myocardial infarction (MI) is one of the common diseases whose pathogenesis includes genetic factors. To reveal genetic backgrounds of this clinically heterogeneous disorder, we started our case-control association study by examining large-scale gene-based single nucleotide polymorphism (SNP) sets for approximately 1,000 patients and controls. As a core genotyping method, a combination of multiplex PCR and Invader method was used, and after genotyping approximately 65,000 SNPs, we found two SNPs located within lymphotoxin-alpha (LTA) gene showing significant association with MI. LTA is one of the cytokines produced in the early stages of vascular inflammatory processes. These SNPs seem to be involved in inflammation by both qualitatively and quantitatively modifying the function of LTA protein, thereby conferring a risk of MI. The genetic association was further confirmed by other researchers using white European trios. To further understand the roles of LTA protein in the pathogenesis of MI, we searched for proteins that interact directly with LTA protein and identified galectin-2 protein as a binding partner of LTA protein. It is a member of galactose-binding lectin family whose function has not been well characterized. Genetic association study again revealed that an SNP in LGALS2 encoding galectin-2 was also associated with susceptibility to MI. This genetic substitution seemed to affect the transcriptional level of galectin-2, which led to altered secretion of LTA, thereby affecting the degree of inflammation. Thus, our findings indicate the importance of inflammation, especially the LTA cascade, in the pathogenesis of MI. Also, combined strategy of genetic and molecular-cellular biological approaches may be useful for clarification of the pathogenesis of common diseases in general.

Case-Control Studies↗

PubMed2005

Haplotype effect of the matrix metalloproteinase-1 gene on risk of myocardial infarction.

Myocardial infarction (MI) is commonly caused by atherosclerotic plaque rupture following excessive degradation of collagen fibers in the atherosclerotic lesion. We investigated whether interindividual variability in risk of MI was related to polymorphisms in the gene encoding matrix metalloproteinase (MMP)-1, a key fibrillar collagen-degrading enzyme. Several single nucleotide polymorphisms in the MMP1 gene promoter were identified following sequencing DNA samples from 30 individuals. An analysis of the polymorphisms in a cohort of British whites with coronary atherosclerosis, including 639 patients with MI and 538 non-MI subjects, revealed a haplotype effect of the -519A>G and -340T>C polymorphisms on risk of MI, with the A(-519)-C(-340) and G(-519)-T(-340) haplotypes being protective (odds ratio=0.70 [0.57 to 0.86]; P=0.0007), whereas the G(-519)-C(-340) haplotype increased MI risk (odds ratio=1.94 [1.15 to 3.28]; P=0.013). This finding was replicated in a subsequent analysis of 387 Swedish MI patients and 387 healthy controls (odds ratio=0.70 [0.55 to 0.89], P=0.003, for A(-519)-C(-340) and G(-519)-T(-340); odds ratio=1.54 [0.97 to 2.46], P=0.07, for G(-519)-C(-340)). In vitro assays showed that compared with the A(-519)-T(-340) haplotype, the A(-519)-C(-340) and G(-519)-T(-340) haplotypes had lower promoter activity, whereas the G(-519)-C(-340) haplotype had greater promoter strength, in driving gene expression in human macrophages. Haplotype-specific differences in MMP1 mRNA level in atherosclerotic tissues were also detected. The data indicate that MMP1 gene variation is a genetic factor contributing to interindividual differences in MI risk.

Adult↗

PubMed2004

Alterations in myofilament function contribute to left ventricular dysfunction in pigs early after myocardial infarction.

Myocardial infarction (MI) initiates cardiac remodeling, depresses pump function, and predisposes to heart failure. This study was designed to identify early alterations in Ca2+ handling and myofilament proteins, which may contribute to contractile dysfunction and reduced beta-adrenergic responsiveness in postinfarct remodeled myocardium. Protein composition and contractile function of skinned cardiomyocytes were studied in remote, noninfarcted left ventricular (LV) subendocardium from pigs 3 weeks after MI caused by permanent left circumflex artery (LCx) ligation and in sham-operated pigs. LCx ligation induced a 19% increase in LV weight, a 69% increase in LV end-diastolic area, and a decrease in ejection fraction from 54+/-5% to 35+/-4% (all P<0.05), whereas cardiac responsiveness to exercise-induced increases in circulating noradrenaline levels was blunted. Endogenous protein kinase A (PKA) was significantly reduced in remote myocardium of MI animals, and a negative correlation (R=0.62; P<0.05) was found between cAMP levels and LV weight-to-body weight ratio. Furthermore, SERCA2a expression was 23% lower after MI compared with sham. Maximal isometric force generated by isolated skinned myocytes was significantly lower after MI than in sham (15.4+/-1.5 versus 19.2+/-0.9 kN/m2; P<0.05), which might be attributable to a small degree of troponin I (TnI) degradation observed in remodeled postinfarct myocardium. An increase in Ca2+ sensitivity of force (pCa50) was observed after MI compared with sham (DeltapCa50=0.17), which was abolished by incubating myocytes with exogenous PKA, indicating that the increased Ca2+ sensitivity resulted from reduced TnI phosphorylation. In conclusion, remodeling of noninfarcted pig myocardium is associated with decreased SERCA2a and myofilament function, which may contribute to depressed LV function. The full text of this article is available online at http://circres.ahajournals.org.

Actin Cytoskeleton↗

PubMed1979

[Diagnostic use of myocardial scintiscanning with thallium-201 in myocardial infarct].

Myocardial scintigraphy shows to have diagnostic ability after latest proposal to use Thallium-201. Thus we verified its iconographic effectiveness in 10 normal subjects and 25 patients with myocardial infarction variously localized. In both groups we obtained adequate and expressive results: the former showed omogeneous images and continuous outlines, whereas the latter showed "cold areas" in agreement with the localization provided by electrocardiography. The further utilization of myocardial imaging with Thallium-201 in 2 patients with prior infarction, in whom present ecg is equivocal, provided scintigraphic evidence of prior necrotic lesion. This emphasizes diagnostic sensitivity of myocardial scintigraphy with Thallium-201 encouraging its use in those patients in whom electrocardiography is not able to give its usual diagnostic contribution.

Adult↗

PubMed2002

Morphological characteristics of the microvasculature in healing myocardial infarcts.

Myocardial infarction (MI) is associated with an angiogenic response, critical for healing and cardiac repair. Using a canine model of myocardial ischemia and reperfusion, we examined the structural characteristics of the evolving microvasculature in healing MI. After 7 days of reperfusion, the infarcted territory was rich in capillaries and contained enlarged, pericyte-poor "mother vessels" and endothelial bridges. During scar maturation arteriolar density in the infarct increased, and a higher percentage of microvessels acquired a pericyte coat (60.4 +/- 6.94% after 28 days of reperfusion vs 30.17 +/- 3.65% after 7 days of reperfusion; p<0.05). The microvascular endothelium in the early stages of healing showed intense CD31/PECAM-1 and CD146/Mel-CAM immunoreactivity but weak staining with the Griffonia simplicifolia lectin I (GS-I). In contrast, after 28 days of reperfusion, most infarct microvessels demonstrated significant lectin binding. Our findings suggest that the infarct microvasculature undergoes a transition from an early phase of intense angiogenic activity to a maturation stage associated with pericyte recruitment and formation of a muscular coat. In addition, in the endothelium of infarct microvessels CD31 and CD146 expression appears to precede that of the specific sugar groups that bind the GS-I lectin. Understanding of the mechanisms underlying the formation and remodeling of the microvasculature after MI may be important in designing therapeutic interventions to optimize cardiac repair.

Animals↗