Premature Acute Myocardial Infarction Research Articles

Prothrombotic genetic risk factors in patients with very early ST-segment elevation myocardial infarction

The contribution of prothrombotic genetic risk factors in the pathogenesis of premature acute myocardial infarction (MI) is controversial. We examined the prevalence of prothrombotic polymorphisms (G1691A of factor V gene [FV Leiden] and G20210A of prothrombin [FII] gene), deficiencies of natural anticoagulants (protein C, protein S and antithrombin III) and antiphospholipid syndrome (APS) in patients with early ST-segment elevation MI (STEMI). We recruited 255 consecutive patients who had survived a STEMI ≤ 35 years of age (224 men). The control group consisted of 400 healthy individuals matched with cases for age and sex. G20210A polymorphism of FII gene was more frequent in young patients than in controls (7.4 vs. 3.5%, p = 0.023). The odds ratio (OR) for STEMI for carriers versus non-carriers was 2.239 (95% CI 1.102-4.250). The adjusted OR for major cardiovascular risk factors was 2.569 (95% CI 1.086-6.074). The risk was increased by 22-fold (95% CI 9.192-66.517) when G20210A polymorphism was present in combination with smoking. There was no difference in the prevalence of FV Leiden between patients and controls (7.8 vs. 6.5%, p = 0.512). There was only one patient (0.4%) with protein C deficiency and one with APS (0.4%). G20210A polymorphism of FII gene may be associated with increased risk of premature STEMI and the risk increases substantially when smoking is present. The contribution of other prothrombotic disorders such as deficiencies of protein C, protein S and antithrombin III and APS was minimal in this cohort.

Long-term outcome and risk assessment in premature acute myocardial infarction: A 10-year follow-up study

BackgroundPremature acute myocardial infarction (AMI) is a rare disease carrying significant morbidity and mortality. Existing data on outcome in these patients is based on retrospective analysis of angiographic reports or refer to time periods with incomparable treatment regimes, making them unusable for risk assessment in times of widespread use of reperfusion therapy. Aim of this study was to assess the outcome of premature AMI in a prospectively recruited study population enrolled in the times of modern reperfusion therapy. MethodsWe included 102 consecutive AMI survivors (≤40years) in this prospective multicentre study. Outcome was assessed via retrieval query of the Austrian Death Registry and the centralized patient management system of Vienna. ResultsDuring a median follow up time of 10.3years (IQR:8.9–11.1), 23% of all patients experienced MACE, of those 6% died, 17% experienced re-AMI and 5% patients an ischemic stroke. Furthermore, forty patients underwent cardiac re-catheterization and twenty-five needed recurrent revascularization. MACE were associated among the classic cardiovascular risk factors with elevated levels of HbA1c (adj. HR 1.32; 95%CI 1.06–1.64; P=0.012), total cholesterol (adj. HR 2.16; 95%CI 1.27–3.48; P=0.004), and c-reactive protein (adj. HR 1.67; 95%CI 1.29–2.17; P=0–003) for an increase of 1-standard deviation. ConclusionAlthough myocardial re-infarction was the driving force of morbidity in premature myocardial infarction, we observed an excellent long-term survival opposed to previous reports. We found that persistence risk factors rather than the clinical risk profile at baseline influences the outcome in these patients, emphasizing the importance of secondary prevention in young patients after AMI.

24: ASSOCIATION OF RS3850641 POLYMORPHISM IN OX40 LIGAND GENE AND PREMATURE MYOCARDIAL INFARCTION, SOUTHERN OF IRAN

Background and aims:Tumor necrosis factor (TNF) is one of the inflammatory cytokines which has an important role in inflammation and migration of other inflammatory cells to the atherosclerotic plaques. OX40L...

The fundamental importance of smoking cessation in those with premature ST-segment elevation acute myocardial infarction.

Smoking is the most prevalent risk factor among young patients suffering acute myocardial infarction (AMI). In this review, we will present data on the detrimental consequences of continued smoking with regard to the recurrence of coronary events after an AMI at an early age. A prospective study with long-term follow-up of young survivors of AMI showed that continuation of smoking after a first episode of AMI was the strongest independent predictor of further cardiac events. In particular, persistent smokers had ∼2.5 times higher risk of a new coronary event when compared with nonsmokers. This emphasizes the fundamental importance of initiating smoking cessation treatment in all smokers with AMI during hospitalization. Extrapolating the results of previous studies showing the benefits of smoking cessation in middle-aged or elderly coronary patients, an even greater benefit should be expected in young patients because of their specific characteristics, which are presented in the current review. Young persistent smokers after a premature AMI constitute a high-risk subgroup for a recurrence of cardiac events. Therefore, smoking cessation is a key issue for improving their prognosis and all smokers should be offered effective antismoking treatment at the time of initial hospitalization.

Soluble galectin-3 is associated with premature myocardial infarction.

Inflammatory responses are pivotal in the initiation and development of premature atherosclerotic lesions. Galectin-3 represents a valuable biomarker for both progression and destabilization of atherosclerotic lesions. This study aims to assess the involvement of galectin-3 in premature myocardial infarction. In this multicentre case-control study, we assessed circulating galectin-3 levels in 144 patients comprising 72 consecutive survivors of acute myocardial infarction (≤ 40 years) and 72 hospital controls frequency matched for age, gender and centre. Patients with acute myocardial infarction showed significantly higher galectin-3 levels as compared to controls in the acute phase of acute myocardial infarction (2552 ± 1992 vs. 1666 ± 829 pg/mL; P < 0·001) as well as in the stable phase 1 year after the index event (3692 ± 1774 vs. 1666 ± 829 pg/mL; P < 0·001). Circulating galectin-3 was significantly and independently associated with premature myocardial infarction in the logistic regression analysis (acute phase: adj. OR per 1-SD change 2·03, 95% CI 1·30-3·19; P = 0·002; stable phase: adj. OR of 6·54 (95% CI 2·56-16·68; P < 0·001). Moreover, we observed a significant correlation between circulating galectin-3 and leucocyte count (r = 0·35, P < 0·001), non-HDL cholesterol (r = 0·23, P = 0·014) and HDL cholesterol (r = -0·29, P = 0·002). We demonstrated that elevated levels of circulating galectin-3 are strongly associated with premature myocardial infarction. Galectin-3 might serve as link between dyslipidaemia as driving force of plaque formation with inflammation as initiator of plaque rupture in patients with premature acute myocardial infarction.

Lack of Association Between rs17568 Polymorphism in OX40 Gene and Myocardial Infarction, Southern of Iran.

Tumor necrosis factor (TNF) is one of the inflammatory cytokines which has an important role in inflammation and migration of other inflammatory cells to the atherosclerotic plaques. OX40 is a member of the TNF super family receptor protein. OX40 and OX40 ligand are co-stimulators for T-cells and can increase inflammatory response in atherosclerotic plaques. The aim of this study was to determine the association of rs17568 polymorphism in OX40 gene with premature myocardial infarction. This case control study was done on 100 patients with premature acute myocardial infarction (AMI) and a similar number of sex, age and some other cardiovascular risk factor matched healthy people. The OX40 rs17568 polymorphism was genotyped, using PCR-RFLP method. A-allele frequency of rs17568 SNP was lower non-significantly in Premature AMI, compared to healthy subjects (49% vs. 51%). The analysis of rs17568 (A/G) polymorphism showed an odds ratio of 1.127 (95% CI: 0.635-1.999; P= 0.686) for the GG genotype and 5.761 (95% CI: 1.200-27.655; P= 0.029) for the AG genotype, compared to the AA genotype. The results of this study indicate that the rs17568 SNP of OX40 gene is not associated with premature AMI in the evaluated population.

Genetic Variants of Cytochrome b-245, Alpha Polypeptide Gene and Premature Acute Myocardial Infarction Risk in an Iranian Population.

SummaryBackgroundOxidative stress induced by superoxide anion plays critical roles in the pathogenesis of coronary artery disease (CAD) and hence acute myocardial infarction (AMI). The major source of superoxide production in vascular smooth muscle and endothelial cells is the NADPH oxidase complex. An essential component of this complex is p22phox, that is encoded by the cytochrome b-245, alpha polypeptide (CYBA) gene. The aim of this study was to investigate the association of CYBA variants (rs1049255 and rs4673) and premature acute myocardial infarction risk in an Iranian population.MethodsThe study population consisted of 158 patients under the age of 50 years, with a diagnosis of premature AMI, and 168 age-matched controls with normal coronary angiograms. Genotyping of the polymorphisms was performed by the polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP).ResultsThere was no association between the genotypes and allele frequencies of rs4673 polymorphism and premature acute myocardial infarction (P>0.05). A significant statistical association was observed between the genotypes distribution of rs1049255 polymorphism and AMI risk (P=0.037). Furthermore, the distribution of AA+AG/GG genotypes was found to be statistically significant between the two groups (P=0.011).ConclusionsOur findings indicated that rs1049255 but not rs4673 polymorphism is associated with premature AMI.

Premature myocardial infarction is strongly associated with increased levels of remnant cholesterol

Remnant cholesterol has been defined as the cholesterol present in triglyceride-rich remnant lipoproteins. Elevated levels of remnant cholesterol have been associated with increased cardiovascular risk. Acute myocardial infarction (AMI) in very young individuals (≤40 years) represents a rare disease with a typical risk factor profile and a lipid phenotype that is characterized by a predominance of elevated triglyceride-rich lipoproteins. The aim of this study was to investigate the role of remnant cholesterol in premature AMI. We prospectively enrolled 302 patients into our multicenter case-control study comprising 102 consecutive myocardial infarction survivors (≤40 years) and 200 hospital controls. Myocardial infarction patients were frequency matched for age, gender, and center. Remnant cholesterol was calculated from standard lipid parameters. Remnant cholesterol was 1.7-fold higher in premature AMI patients compared with controls (61.1 ± 36.8 vs 35.8 ± 16.8 mg/dL; P < .001). Remnant cholesterol was the lipid fraction most strongly associated with premature myocardial infarction (odds ratio 3.87; 95% confidence interval 2.26-6.64; P < .001) for an increase of 1-standard deviation. This observation was independent from clinical risk factors and plasma lipid levels. Remnant cholesterol is strongly associated with premature myocardial infarction, can be easily calculated, and might serve as a new potent risk marker in this young patient population.

Impaired antioxidant HDL function is associated with premature myocardial infarction.

There is growing evidence that the predictive value of HDL cholesterol levels for cardiovascular risk stratification is limited in patients with coronary artery disease (CAD). HDL function seems to be a more sensitive surrogate of cardiovascular risk estimation than simple serum levels. Therefore, we aimed to assess whether impaired antioxidant HDL function is involved in the development of premature acute myocardial infarction (AMI). In this multicentre case-control study, we compared the antioxidant function of HDL, measured by the HDL inflammatory index (HII), and HDL particle size in 184 patients comprising 92 patients with AMI at a very young age (≤40years of age) and 92 age- and gender-matched controls. Antioxidant capacities of HDL were significantly impaired in the acute phase of AMI (HII of 1·50 [IQR 1·10-1·74] vs. 0·56 [IQR 0·41-0·86] in controls, P<0·001 as well as in the chronic stable phase 1year after the event (HII of 0·85 [IQR 0·72-1·03] vs. 0·56 [IQR 0·41-0·86], P<0·001) compared to controls. Moreover, HDL function in the stable phase remained significantly associated with premature MI in adjusted logistic regression analysis with an OR of 2·24 per SD increase of HII (95% CI 1·28-3·91; P=0·005). Analyses of HDL size revealed a significant correlation between all HDL subfractions and HDL function in controls, whereas this correlation was lost for large and intermediate HDL in AMI patients. Impaired antioxidant function of HDL is independently associated with the development of premature AMI. The maintenance of HDL function might evolve into a significant therapeutic target, especially in patients with premature CAD.

Lipoprotein lipase gene variants: Association with acute myocardial infarction and lipid profiles

BackgroundStudies showed that lipid metabolism disorders are significant risk factors for myocardial infarction and coronary artery disease (CAD). Therefore, genes involved in lipid and lipoprotein metabolism pathways such as lipoprotein lipase (LPL), are proper candidates for susceptibility to CAD. AimTo investigate the possible association between LPL gene variants (HindIII (rs320) and PvuII (rs285)), acute myocardial infarction (AMI) and serum lipid levels. Subjects and methodsThe study population consisted of 211 patients with a diagnosis of premature AMI, and 203 age-matched individuals with normal coronary angiograms as controls. Genotyping of HindIII and PvuII polymorphisms was done by the PCR-RFLP technique. ResultsAlthough the H+ and P+ alleles were more observed among the patients, there were no significant differences in genotype distributions and allele frequencies of HindIII and PvuII polymorphisms between patient and control subjects (P>0.05). Triglyceride levels were found to be significantly elevated in H+H+ and P+P+ genotypes compared to others (P<0.05). However, there was no association between HindIII and PvuII genotypes and HDL-C, LDL-C and cholesterol levels. ConclusionOur findings indicate that LPL-HindIII and PvuII polymorphisms are not associated with acute myocardial infarction but with triglyceride levels.

Major dietary patterns and risk of acute myocardial infarction in young, urban Pakistani population.

Objective:To investigate the role of dietary intake in the development of premature acute myocardial infarction (AMI) in a hospital-based Pakistani population in Karachi.Methods:In a case control study, 203 consecutive patients (146 males and 57 females) with their first AMI and age below 45 years were enrolled with informed consent. Similarly, 205 gender and age matched (within 3 years) healthy adults were also included as controls. Dietary intake of both cases and controls was assessed by using a simple 14-item food frequency questionnaire. Using factor analysis, 3 major dietary patterns- prudent dietary pattern, combination dietary pattern and western dietary pattern were identified. Fasting plasma/serum of both cases and controls were analyzed for homocysteine, folate, vitamin B12, blood Pb, ferritin, cholesterol, LDL-cholesterol, HDL-cholesterol and triglycerides. ANOVA and conditional logistic regression were used to predict the association of dietary patterns with AMI.Results:Consumption of prudent diet, characterized by high consumption of legumes, vegetables, wheat, chicken and fruits, is protective against the risk of premature AMI. Moderate to high consumption of combination diet, characterized by high intake of eggs, fish, fruits, juices and coffee was associated with decreased risk of AMI. No association was observed between western diet, characterized by high intake of meat, fish and tea with milk and risk of AMI.Conclusions:Consumption of a prudent dietary pattern and a combination dietary pattern is protective against the risk of AMI in a Pakistani population.

The impact of smoking on long-term outcome of patients with premature (≤35 years) ST-segment elevation acute myocardial infarction

There are few data regarding the long-term prognosis of young survivors of acute myocardial infarction (AMI). We explored the long-term outcome in individuals who had sustained a premature ST-segment elevation AMI. We recruited 257 consecutive patients who had survived their first AMI ≤35years of age. Patients were followed up for up to 18years. Clinical end points included all major adverse coronary events (MACE): cardiac death, readmission for acute coronary syndrome, arrhythmias, or coronary revascularization due to clinical deterioration. The most prevalent risk factor at presentation was smoking (93.7%). Follow-up data were obtained from 237 patients (32.2±3.7years old). The median follow-up period was 9.1years. During follow-up, 139 (58.6%) patients reported continuation of smoking. Ninety-one (38.4%) patients had recurrent MACE (13 deaths, 59 acute coronary syndromes, 2 arrhythmias, and 17 revascularizations). Multivariable Cox regression analysis showed that persistence of smoking, left ventricular ejection fraction (LVEF), and reperfusion therapy (fibrinolysis or primary coronary angioplasty) were independent predictors of MACE after adjustment for conventional risk factors. Continuation of smoking remained an independent predictor for MACE after additional adjustments for LVEF (hazard ratio 2.154, 95% CI 1.313-3.535, P=.002) or reperfusion treatment (hazard ratio 2.327, 95% CI 1.423-3.804, P=.001). Harrell c statistic showed that the model with persistent smoking had the best discriminatory power compared with models with LVEF or reperfusion treatment. In the era of statins and reperfusion treatment, continuation of smoking is the strongest independent long-term predictor for recurrent MACE in young survivors of premature AMI.

Comparison of the effect of rosuvastatin and atorvastatin on vascular endothelial and cardiac function of patients with early acute myocardial infarction

Objective To observe the effects of rosuvastatin and atorvastatin on vascular endothelial and car -diac function of patients with early acute myocardial infarction .Methods 162 patients with early acute myocardial infarction were selected and randomly divided into A group and B group by the digital table ,81 cases in each group . The two groups were given conventional treatment of myocardial infarction ,and A group was given rosuvastatin 10mg/d, and B group received atorvastatin 20mg/d,all the patients were treated for 6 months.Results After 6 months of treatment,the total cholesterol（TC）,triglyceride（TG）,low density lipoprotein（LDL-C）,hs-CRP in two groups were significantly reduced,FMD,serum NO were increased,the differences were statistically significant （t=2.573,2.487, 2.422,2.556,3.223,3.175,2.583,2.542,3.528,3.107,3.506,2.982,all P〈0.05）.TC,LDL-C and hs-CRP in A group were significantly lower than those in B group （t=2.327,2.228,2.328,all P〈0.05）.Conclusion Rosuv-astatin and atorvastatin can reduce blood lipids in patients with premature coronary heart disease and acute myocardial infarction,reduce inflammation and improve endothelial function ,they have similar short-term efficacy,but rosuvastatin has stronger lipid-lowering effect and reducing inflammatory function . Key words: Coronary artery disease; Rosuvastatin ; Atorvastatin ; Endothelium, vascular; Heart function tests

Response to Relation Between Time of Symptom Onset of ST‐Segment Elevation Myocardial Infarction and Patient Baseline Characteristics: From the National Cardiovascular Data Registry

We read the article by Mogabgab et al with great interest.1 The authors aimed to investigate the relationship between patient characteristics and outcomes in ST-segment elevation myocardial infarction (STEMI). This study revealed that the circadian rhythm of STEMI with a morning peak continues to exist and represents a potential target for preventative strategies. Additionally, the authors observed that some patient characteristics were consistently varied with time of symptom onset and might reflect underlying physiologic differences that alter the timing of events. The study was successfully planned and the results were presented well; thanks to the authors for their contribution. It has long been known that circadian rhythm plays a pivotal role in many biologic phenomena, including secretion of hormones and activities of the nervous system, and it has also been noted to occur in the incidences of certain cardiovascular events. Circadian variation for the onset of STEMI has been well investigated in many studies, and an early morning peak has been reported frequently. This early morning peak is often described with the changes in autonomic nervous system activity, blood fibrinolytic activity, platelet aggregability, activity of hemostasis, endothelial function, and coronary tone during the daily cycle, especially in the early morning hours.2-5 However, it is a well-known fact that different regions of the world have different circadian variations with regard to cardiovascular diseases. Studies showing the early morning peak of the onset of STEMI are very common and often come from Western populations. Furthermore, other studies that examined the circadian variation of STEMI in different population cohorts found that onset of STEMI happened between midnight and noon in British Caucasians and Indo-Asians,6 between noon and midnight in a Mediterranean Caucasian6 and Bulgarian cohort,7 between midnight and morning in a Chinese cohort,8 and with afternoon predominance in a Turkish population.9 Environmental and genetic background, customs, education, socioeconomic status, sociocultural habits, physical activity level, working hours (night people or morning people), and eating and sleeping habits might be possible underlying causes of ethnic disparities in cardiovascular risk factor profiles in different populations and should be evaluated. With respect to the effect of circadian variation in outcomes of cardiovascular disease, Khan et al10 examined the risk of cardiovascular disease outcomes among South Asian, Chinese, and white patients, and they assumed that South Asian and Chinese patients had a lower risk of death and of developing cardiovascular outcomes compared to whites. In their study, Hulten et al11 aimed to predict all-cause mortality and nonfatal myocardial infarction among Caucasian, African, and East Asian ethnicities, and found that compared to other ethnicities, East Asians had fewer events than expected. Wong et al12 showed that among the 3 ethnic groups (Malay, Chinese, and Indian), Indians had the highest risk of developing premature acute myocardial infarction. Additionally, circadian variation at the time of onset of chest pain in patients with STEMI may be different regarding infarction site in different population cohorts.13, 14 Circadian variation of STEMI might not be equally effective throughout the world. Ethnic disparities may be partly responsible for cardiovascular risk prevalence and outcomes of STEMI. Thus, instead of the term circadian rhythm, it might be more accurate to use the term population rhythm. Further large-scale clinical studies are needed to analyze the underlying pathophysiological mechanisms causing those ethnic disparities in the chronobiology of STEMI. Murat Celik, MD Baris Bugan, MD Emre Yalcinkaya, MD Uygar Cagdas Yuksel, MD Turgay Celik, MD Department of Cardiology, School of Medicine Gulhane Military Medical Academy Ankara, Turkey

Association of Body Iron Status with the Risk of Premature Acute Myocardial Infarction in a Pakistani Population

BackgroundCoronary artery disease is very common in Pakistani population. Some of the studies carried out on Western populations have shown a relationship between body iron status as determined by the ratio of concentrations of serum soluble transferrin receptor (sTfR) to ferritin and the risk of acute myocardial infarction (AMI). In order to investigate whether increased body iron status has any relationship with the risk of premature AMI in Pakistani population, a case-control study was carried out.Methodology/Principal findingsIn this case-control study, 203 consecutive AMI patients [146 males and 57 females; age range 18–45 years] admitted to the National Institute for Cardiovascular Diseases, Karachi, were enrolled with informed consent. In addition, 205 healthy controls whose gender and age (within 3 years) matched the patients, and who had a similar socio-economic background were recruited. Fasting venous blood was obtained and assessed for plasma/serum folate, vitamin B12, homocysteine, total cholesterol, triglycerides, LDL-cholesterol, HDL-cholesterol, sTfR and ferritin and blood lead. It was found that serum concentration of ferritin and blood lead levels were significantly higher in AMI patients compared to their age and gender-matched healthy controls (p value <0.05), while the concentrations of vitamin B12 and HDL-cholesterol were significantly lower in AMI patients compared to controls (p value <0.01). The ratio of sTfR to ferritin was significantly lower in AMI patients compared to controls [mean±SD/median (IQR) values 84.7±295/28.9 (38.4) vs 255±836/49.4 (83.8), respectively; p value <0.001]. Compared with the highest quartile of sTfR/ferritin (low body iron status), the OR for the risk of AMI was 3.29(95% CI, 1.54–7.03) for the lowest quartile (quartile 1) when the model was adjusted for vitamin B12 and HDL-cholesterol (p value for trend <0.01).Conclusions/SignificanceThis study shows a positive association between total body iron status and risk of premature AMI in a Pakistani population.

Telomere Length Variation in Juvenile Acute Myocardial Infarction

Leukocyte telomere length (LTL) provides a potential marker of biological age, closely related to the endothelial dysfunction and consequently to the atherosclerotic process. To investigate the relationship between the LTL and the risk of premature acute myocardial infarction and to evaluate the predictive value of LTL on the onset of major cardiovascular events, 199 patients from 18 to 48 years old with first diagnosis of acute myocardial infarction were enrolled and were matched with 190 controls for sex and age (±1 year). Clinical data and coronary artery disease were evaluated at enrollment and at follow up. LTL was measured at enrollment using a quantitative PCR-based method. No significant differences were observed in LTL between cases and controls (p = 0.20) and with the presence of coronary artery disease in patients (p = 0.47). Hypercholesterolemic cases presented LTL significantly longer than cases without hypercholesterolemia (t/s: 0.82±0.16 p = 0.79 and t/s norm: 0.79±0.19 p = 0.01), as confirmed in multivariate regression analysis (p = 0.005, β = 0.09). Furthermore, multivariate regression analysis showed LTL significantly shorter in hypertensive cases than in normotensive cases (p = 0.04, β = −0.07). One hundred seventy-one cases (86%) ended the average follow up of 9±5 years, 92 (54%) presented a major cardiovascular event. At multivariate regression analysis the LTL detected at enrollment did not represent a predictive factor of major cardiovascular events nor it significantly impacted with cumulative events. Based on present cohort of young Italian patients, the LTL did not represent a marker of acute myocardial infarction nor had a predictive role at medium term follow up.

Association of platelet collagen receptor polymorphisms with premature acute myocardial infarction

The impact of platelet collagen receptor polymorphisms in the pathogenesis of myocardial infarction at young age remains unknown. To determine whether either of the two platelet collagen receptor polymorphisms (GP VI T13254C and GP Ia C807T) was associated with premature acute myocardial infarction. One hundred patients with premature acute myocardial infarction and 100 age-matched controls with normal coronary angiograms were studied. Genotyping was done using PCR followed by restriction fragment length polymorphism (RFLP). GP Ia C807T polymorphism was more frequent in the patient group (65%) than in the control group (53%). However, there was no association between this polymorphism and premature acute myocardial infarction (P = 0.08). The prevalence of T13254C polymorphism did not differ between patients (38%) and controls (33%), and this polymorphism was not associated with premature acute myocardial infarction (P = 0.46). Logistic regression analysis also indicated no association between these polymorphisms and premature acute myocardial infarction (C807T with P = 0.51 and T13254C with P = 0.20). There is no association between GP VI T13254C or GP Ia C807T polymorphisms and premature acute myocardial infarction.

Acute myocardial infarction: Clinical features and outcomes in young adults in Singapore

To investigate the clinical features and in-hospital outcomes of young adults with acute myocardial infarction (AMI) in Singapore. Between January 2005 to September 2010, 333 consecutive patients aged ≤ 45 years old were diagnosed to have AMI at our institution. As Singapore is a multi-ethnic society, we also analysed whether ethnic differences exist between the three dominant ethnic groups, Malay, Chinese and Indian with regards to the clinical features. Clinical data was collected retrospectively on demographic characteristics, presenting signs and symptoms, blood investigation, angiographic findings and in-hospital clinical outcomes. The mean age at presentation was 40.2 ± 4.0 years with male predominance (94%). The majority of patients were Chinese (51%) followed by Indians (31%) and Malays (18%). The most common risk factor was smoking (74%) followed by hypertension (28.5%) and hyperlipidemia (20.0%). 37% of patients were obese. The majority of patients had single vessel disease (46%) on coronary angiography. The mean total cholesterol, low-density lipoprotein and high-density lipoprotein levels were 5.6 ± 1.2 mmol/L, 3.8 ± 1.1 mmol/L and 0.93 ± 0.25 mmol/L respectively. The mean left ventricular function was 44% ± 10% with the incidence of heart failure 3% and cardiogenic shock 4.5%. Overall in-hospital mortality was low with 4 deaths (1.2%). For ethnic subgroup analysis, Indians have a 3-fold risk of developing premature AMI when compared to other ethnic groups. Young AMI patients in Singapore are characterized by male predominance, high incidence of smoking and obesity. Overall in-hospital clinical outcomes are favourable. Among the 3 ethnic groups, Indians have the highest risk of developing premature AMI.

Childhood appendectomy, tonsillectomy, and risk for premature acute myocardial infarction--a nationwide population-based cohort study

Although inflammation contributes to cardiovascular disease, the associations of appendectomy and tonsillectomy, which remove mucosa-associated lymphoid tissue, with risk of acute myocardial infarction (AMI) are unknown. Our aim was to assess the association between these operations performed in childhood and AMI risk later in life. We conducted a prospective matched cohort study among all Swedish residents born between 1955 and 1970. A national register identified all appendectomies and tonsillectomies. For each patient undergoing appendectomy or tonsillectomy, we randomly selected five controls without the history of the respective operation, matched on sex, age, and county of residence. Participants were followed for fatal and non-fatal AMI for an average of 23.5 years. Because appendiceal and tonsillar tissues have reduced function after adolescence, our primary analyses were restricted to individuals below age 20 at the time of surgery (54 449 appendectomies and 27 284 tonsillectomies). We derived hazard ratios (HRs) from proportional hazard models adjusted for parental occupation and parental history of AMI. Operations before 20 years of age were associated with an increased risk for AMI (417 and 216 events in the appendectomy and tonsillectomy datasets, respectively), with adjusted HRs of 1.33 [95% confidence interval (CI), 1.05-1.70] for appendectomy and 1.44 (95% CI, 1.04-2.01) for tonsillectomy. This association was graded, with the highest risk among those undergoing both procedures, and generally similar among both males and females. Appendectomy and tonsillectomy performed at or above 20 years of age were not associated with the risk of AMI. We found a higher risk of AMI related to surgical removal of the tonsils and appendix before age 20. These results are consistent with the hypothesis that subtle alterations in immune function following these operations may alter the subsequent cardiovascular risk, but further studies are needed to confirm these findings and to explore possible mechanisms.

Markers of bone metabolism in premature myocardial infarction (≤ 40 years of age)

Introduction Acute myocardial infarction (AMI) at young age is a rare disease with a poor prognosis. Bone metabolism parameters such as 1,25 (OH) 2 vitamin D 3, 25 (OH) vitamin D 3 and osteocalcin have been recently implicated in the development of coronary heart disease (CHD). We evaluated the role of these serum markers in a study population of very young AMI survivors (≤ 40 years). Methods and results We prospectively enrolled 302 subjects into our multi-center case control study, including 102 young myocardial infarction patients (≤ 40 years) and 200 control subjects who were frequency-matched on gender and age in an approximate 2:1 ratio per case patient. In the adjusted logistic regression analysis, we used baseline laboratory measurements for the first analysis (acute phase analysis) and measurements from one-year follow-up visits (stable phase analysis). In both, elevated levels of 25 (OH) vitamin D 3 (acute phase: OR per IQR 2.02, 95% CI 1.13–3.58, p = 0.017; stable phase: OR 4.07, 95% CI 1.8–9.21, p = 0.001) and 1,25 (OH) 2 vitamin D 3 (acute phase: OR 2.82, 95% CI 1.7–4.7, p < 0.001; stable phase: OR 4.57, 95% CI 2.31–9.05, p < 0.001) were associated with premature AMI. Conversely, osteocalcin was inversely associated with premature myocardial infarction (acute phase: OR 0.53, 95% CI 0.28–1.03, p = 0.059; stable phase: OR 0.26, 95% CI 0.12–0.6, p < 0.001). The observed associations were independent of the acute phase of myocardial infarction. Conclusion In our study, elevated levels of 25 (OH) vitamin D 3 and 1,25 (OH) 2 vitamin D 3, as well as decreased levels of osteocalcin were associated with myocardial infarction in very young patients. The precise mechanism and implications of these findings will have to be elucidated in future studies.