Genetic Susceptibility of Myocardial Infarction

2007 ◽  
Vol 10 (6) ◽  
pp. 848-852 ◽  
Author(s):  
Slobodan Zdravkovic ◽  
Andreas Wienke ◽  
Nancy L. Pedersen ◽  
Ulf de Faire
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Genetic Factors ◽  
First Episode ◽  
Phenotypic Variance ◽  
Genetic Analyses ◽  
Quantitative Genetic ◽  
Equal Variance ◽  
First Occurrence ◽  
Mz Twins

AbstractThe aim of this study was to determine the influence of genetic factors on the first episode of acute myocardial infarction. Probandwise concordances, tetrachoric correlations and quantitative genetic analyses of liability were applied to data drawn from the Swedish Twin Registry and the Swedish Acute Myocardial Infarction Register. All same-sexed twin pairs born between 1886 and 1958 who were alive in 1987 were included in the analyses. Our results show that concordance rates for acute myocardial infarction in monozygotic (MZ) twins were similar across sexes (among males .26 and females .27). For dizygotic (DZ) twins the concordances were .20 for males and .16 for females, yielding a greater MZ–DZ concordance differential for females than males. Tetrachoric correlations were greater for MZ than DZ twins for both sexes (.49 for male MZ and .34 for male DZ-twins and .56 and .35 for female MZ and DZ twins respectively). Quantitative genetic analyses of liability resulted in equal variance components for males and females (.36) but significantly different thresholds (prevalences). In conclusion, liability to first occurrence of acute myocardial infarction is moderately influenced by genetic variants in both sexes. The familial influence on phenotypic variance is exclusively explained by additive genetic factors.

scholarly journals Unexpected Coexisting Myocardial Infarction Detected by Delayed Enhancement MRI

2009 ◽  
Vol 2009 ◽  
pp. 1-4
Author(s):  
Edouard Gerbaud ◽  
Henri De Clermont-Galleran ◽  
Matthew Erickson ◽  
Pierre Coste ◽  
Michel Montaudon
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Chest Pain ◽  
Imaging Technique ◽  
Delayed Enhancement ◽  
First Episode ◽  
Ecg Changes ◽  
Anterior Myocardial Infarction ◽  
Prognostic Implications ◽  
Inferior Acute Myocardial Infarction

We report a case of an unexpected coexisting anterior myocardial infarction detected by delayed enhancement MRI in a 41-year-old man following a presentation with a first episode of chest pain during inferior acute myocardial infarction. This second necrotic area was not initially suspected because there were no ECG changes in the anterior leads and the left descending coronary artery did not present any significant stenoses on emergency coronary angiography. Unrecognised myocardial infarction may carry important prognostic implications. CMR is currently the best imaging technique to detect unexpected infarcts.

Successful Direct PTCA on LAD after First Episode of Acute Myocardial Infarction: Does It Improve Cardiac Function?

Angiology ◽  
1990 ◽  
Vol 41 (9) ◽  
pp. 724-730
Author(s):  
Hirohiko Asonuma ◽  
Yasuhiro Tanji ◽  
Hiroshi Nakatoh ◽  
Takanobu Nakajima ◽  
Hirotoshi Akita ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Function ◽  
First Episode

scholarly journals Dietary iron intake and risk of non-fatal acute myocardial infarction

2006 ◽  
Vol 9 (4) ◽  
pp. 480-484 ◽  
Author(s):  
Alessandra Tavani ◽  
Silvano Gallus ◽  
Cristina Bosetti ◽  
Maria Parpinel ◽  
Eva Negri ◽  
...  
Keyword(s):  
Risk Factors ◽  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Total Iron ◽  
Alcoholic Beverages ◽  
First Episode ◽  
Italian Population ◽  
Inverse Association ◽  
Dietary Iron ◽  
Iron Intake

AbstractObjectiveThe relation between several measures of body iron and atherosclerotic disease, particularly acute myocardial infarction (AMI), is debated. This is of specific interest since iron is frequently included in supplementation and fortification of foods. We assessed the relation between dietary iron intake and the risk of non-fatal AMI.DesignCase–control study. The information was collected by interviewers using a food-frequency questionnaire tested for validity and reproducibility. Adjusted odds ratios (OR) and 95% confidence intervals (CI) were obtained by multiple unconditional logistic regression models, including terms for energy and alcohol intakea, as well as for sociodemographic factors, tobacco and other major recognised risk factors for AMI.SettingMilan, Italy, between 1995 and 1999.SubjectsCases were 507 patients, below age 79 years, with a first episode of non-fatal AMI, and controls were 478 patients admitted to hospital for a wide spectrum of acute conditions unrelated to known or potential AMI risk factors.ResultsCompared with patients in the lowest tertile of total iron intake, the OR was 0.48 (95% CI 0.29–0.82) for those in the highest tertile. The corresponding value for haem iron was 0.71 (95% CI 0.48–1.06), for non-haem, non-alcohol iron was 0.80 (95% CI 0.51–1.24) and for iron derived from alcoholic beverages was 0.60 (95% CI 0.40–0.90). Sex-specific OR for total iron intake were not heterogeneous.ConclusionsIn this Italian population dietary iron intake was inversely related to AMI risk. This inverse association may depend on other nutrients present in the major sources of iron in the Italian diet.

Abstract P076: Genetic Factors Modify the Triggering of Acute Myocardial Infarction by Transient Exposure to Coffee Intake

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Ana Baylin ◽  
Sharon Kardia ◽  
Hannia Campos
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Genetic Risk ◽  
Genetic Factors ◽  
P Value ◽  
Coffee Intake ◽  
High Genetic Risk ◽  
Test Of Homogeneity ◽  
Incident Cases ◽  
Slow Metabolizers

Introduction: Caffeinated coffee increases sympathetic nervous activity that may adversely affect a vulnerable atherosclerotic plaque and therefore trigger an acute myocardial infarction (AMI). Additionally, it is possible that genetic variation alter the susceptibility to the acute effects of coffee. Hypothesis: We assessed the hypothesis that genetic factors associated to AMI can modify the triggering of AMI by acute coffee intake. Methods: We collected information on intake of coffee during the 24 hours and days before the myocardial infarction and habitual intake of coffee in 1,234 incident cases of non-fatal AMI from 1994–2004. Data was analyzed as a case-crossover design assuming a hazard period of 1 hour. We used a genetic score with 3 loci from AMI GWAS that has been validated in this population. People with a higher score have a greater risk for AMI. In addition, we also evaluated one polymorphism in the cytochrome P450 1A2 candidate gene that decreases the enzyme inducibility, resulting in impaired caffeine metabolism. Carriers of the variant CYP1A2*1F allele are slow caffeine metabolizers, whereas individuals who are homozygous for the CYP1A2*1A allele are rapid metabolizers. Results: Participants were classified as low AMI genetic risk (1 to 3 alleles) or high genetic risk (4 to 6 alleles) according to the genetic risk score. RR for the association between coffee and AMI were 1.72 (95%CI:1.22, 2.43) and 1.06 (95%CI:0.85, 1.31) for the low and high genetic risk groups respectively (test of homogeneity p-value=0.02). RR were 1.38 (95%CI:1.07, 1.76) and 0.99 (95%CI:0.77, 1.28) for homozygous carriers of the rapid CYP1A2*1A allele and carriers of the slow CYP1A2*1F allele, respectively (test of homogeneity p-value =0.067). Because we have shown previously that coffee intake is not associated with AMI among heavy drinkers (≥ 4 cups/d), we repeated the analysis among light/occasional and moderate drinkers. RR were 1.69 (95%CI:1.28, 2.23) and 1.09 (95%CI:0.80, 1.48) for rapid and slow metabolizers, respectively (test of homogeneity p-value=0.038). Conclusions: In conclusion, people with lower genetic risk seem to be more susceptible to coffee. It is possible that the effect of environmental factors (including triggers like coffee intake) is higher among people who are not at risk because of genetic factors. Light and moderate drinkers who are rapid caffeine metabolizers are also more susceptible to coffee. It is possible that light/moderate drinkers who are slow metabolizers develop more tolerance to caffeine than rapid metabolizers.

scholarly journals The role of cytokines and cortisol in the non-thyroidal illness syndrome following acute myocardial infarction

2000 ◽  
pp. 236-242 ◽  
Author(s):  
H Karga ◽  
P Papaioannou ◽  
K Venetsanou ◽  
F Papandroulaki ◽  
L Karaloizos ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
First Episode ◽  
Necrosis Factor Alpha ◽  
Ventricular Ejection Fraction ◽  
Group I ◽  
Cortisol Levels ◽  
Group Ii

OBJECTIVE: A number of different hormone changes have been described during the acute myocardial infarction (AMI), including those of the non-thyroidal illness syndrome (NTIS). DESIGN AND METHODS: We assessed the alterations of serum thyroid hormones, cytokines and cortisol levels in 30 patients with a first episode of AMI 4, 24, 48h and 10 days (240h) after the onset of the chest pain and we investigated the possible relationship of these alterations with the severity of AMI. RESULTS: Fifteen patients had left ventricular ejection fraction (LVEF) </=50% (group I) and 15 patients had LVEF >50% (group II). A transient decrease of total tri-iodothyronine (T(3)), more prominent in group I (P<0.05, t-test) with a concomitant rise of reverse T(3 )(rT(3)) occurred at 24h. Total thyroxine (T(4)), free T(4) (FT(4)) and free T(4) index did not change significantly, but tended to be higher in group I patients, whereas TSH significantly increased in group II at 48h. Interleukin-6 (IL-6) increased significantly at 24h only in group I and declined thereafter (24 vs 240h, P<0.001) and this temporal change of IL-6 was associated with similar changes of creatine phosphokinase and creatine kinase isoenzyme MB (CK-MB). Tumor necrosis factor-alpha and IL-1beta remained low in both groups. Cortisol was higher at 4h and in 12 patients was above the normal values. Negative correlation was found between LVEF and IL-6 (P<0. 001), whereas T(3), T(4) or cortisol levels were not correlated with the LVEF. CONCLUSIONS: Our data indicate that NTIS, in association with increase of IL-6, occurs in the early post-infarction period. In the NTIS following AMI the high level of IL-6 is the best predictor, among several parameters, of the severity of AMI as assessed by the LVEF and the rise of CK-MB.

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