Juvenile Myocardial Infarction Research Articles

Sudden cardiac death after early-onset myocardial infarction: a multicentre longitudinal cohort study with a 20-year follow-up.

Sudden cardiac death (SCD) is a serious consequence of a myocardial infarction (MI), but identifying patients at risk of developing SCD remains a major clinical challenge, especially in the case of juvenile MI. The aim of this study is to identify predictors of SCD after early-onset MI using long-term follow-up data relating to a large nationwide patient cohort. The Italian Genetic Study on Early-onset MI enrolled 2000 patients experiencing a first MI before the age of 45 years, who were followed up for a median of 19.9 years. Fine-Gray proportional hazard models were used to assess the associations between their clinical, demographic, and index event data and the occurrence of SCD. Sudden cardiac death occurred in 195 patients, who were more frequently males, were hypertensive and/or diabetic, had a history of previous thrombo-embolic events with a greater atherosclerotic burden, and had a lower left ventricular ejection fraction (LVEF) after the index event. A multivariable analysis showed that the independent predictors of SCD were diabetes, hypertension, previous thrombo-embolic events, a higher SYNTAX score, and a lower LVEF. There was no clear evidence of the clustering of SCD events during the follow-up. Sudden cardiac death was the first post-MI clinical event in 101 patients; the remaining 94 experienced SCD after a non-fatal MI or hospitalization for coronary revascularization. Sudden cardiac death frequently occurs during the 20 years after early-onset MI. The nature of the identified predictors and the absence of clustering suggest that the pathophysiological basis of SCD may be related to progressive coronary atherosclerosis.

Bayesian Mendelian randomization with an interval causal null hypothesis: ternary decision rules and loss function calibration

We enhance the Bayesian Mendelian Randomization (MR) framework of Berzuini et al. (Biostatistics 21(1):86–101, 2018) by allowing for interval null causal hypotheses, where values of the causal effect parameter that fall within a user-specified interval of “practical equivalence” (ROPE) (Kruschke, Adv Methods Pract Psychol Sci 1(2):270–80, 2018) are regarded as equivalent to “no effect”. We motivate this move in the context of MR analysis. In this approach, the decision over the hypothesis test is taken on the basis of the Bayesian posterior odds for the causal effect parameter falling within the ROPE. We allow the causal effect parameter to have a mixture prior, with components corresponding to the null and the alternative hypothesis. Inference is performed via Markov chain Monte Carlo (MCMC) methods. We speed up the calculations by fitting to the data a simpler model than the intended, "true", one. We recover a set of samples from the “true” posterior distribution by weighted importance resampling of the MCMC-generated samples. From the final samples we obtain a simulation consistent estimate of the desired posterior odds, and ultimately of the Bayes factor for the interval-valued null hypothesis, H0\\documentclass[12pt]{minimal} \\usepackage{amsmath} \\usepackage{wasysym} \\usepackage{amsfonts} \\usepackage{amssymb} \\usepackage{amsbsy} \\usepackage{mathrsfs} \\usepackage{upgreek} \\setlength{\\oddsidemargin}{-69pt} \\begin{document}$$H_0$$\\end{document}, vs H1\\documentclass[12pt]{minimal} \\usepackage{amsmath} \\usepackage{wasysym} \\usepackage{amsfonts} \\usepackage{amssymb} \\usepackage{amsbsy} \\usepackage{mathrsfs} \\usepackage{upgreek} \\setlength{\\oddsidemargin}{-69pt} \\begin{document}$$H_1$$\\end{document}. In those situations where the posterior odds is neither large nor small enough, we allow for an uncertain outcome of the test decision, thereby moving to a ternary decision logic. Finally, we present an approach to calibration of the proposed method via loss function. We illustrate the method with the aid of a study of the causal effect of obesity on risk of juvenile myocardial infarction based on a unique prospective dataset.

A Case of Father–Son Juvenile Acute Myocardial Infarction

Coronary artery ectasia (CAE) is a cause of juvenile myocardial infarction. The causes of CAE include arteriosclerosis, vasculitis such as Kawasaki disease, and genetic contribution. There are few reports about familial aggregation of CAE-related juvenile myocardial infarction. We report an unusual case of father-son juvenile myocardial infarction owing to CAE. (Level of Difficulty: Beginner.)

Red Cell Distribution Width and Elongation Index in a Cohort of Patients With Juvenile Acute Myocardial Infarction.

In a cohort of patients with juvenile myocardial infarction, we considered the red cell distribution width (RDW), hematocrit, hemoglobin, and elongation index values at the initial phase and at 3 and 12 months from the acute event. In the initial phase, only the elongation index values turn out reduced if compared with those of the control group, and that only turn out to discriminate the infarcted ST-segment elevation myocardial infarction (STEMI) from non-STEMI. Dividing the patients according to the traditional risk factors and the extent of coronary heart disease, there are no significant variations in the analyzed parameters. No major changes are observed after 12 months from the acute event. Both to 3 and to 12 months from the infarct episode, the negative statistical correlation between RDW and the value of elongation index remains. These data make us reflect on the role of the degree of anisocytosis of red blood cell expressed by the RDW on the determinism of erythrocyte deformability, which plays its role in the microcirculation district and that is essential in the transfer of tissue oxygen.

Incidence trends and long-term outcomes of myocardial infarction in young adults: Does gender matter?

AimsData about long-term clinical outcomes of young patients experiencing an acute myocardial infarction (MI) and about the potential impact of gender on juvenile MI incidence and prognosis are scant. Methods and resultsHospital Discharge Register records of Piedmont region (Italy) from 2007 to 2018 were interrogated to identify incident juvenile MI cases and MI recurrences. Patients were considered young if the first MI occurred before or at 47 years of age (5th percentile). Incidence of first juvenile MI event and overall survival were the primary outcomes. Gender differences and survival rate after an MI recurrence were secondary outcomes. Out of 114.816 hospitalizations due to MI, 4482 (3.9%) occurred in people aged ≤47. Average incidence rate of juvenile MI over the study period was 24.5 (23.8-25.2) per 100.000 person-years, with a decline among men and a stable trend among women through the years. The risk of in hospital death was higher for women (1.9% vs. 0.9%, p = 0.02), while the survival rate at 10 years after the first MI was 94.8%, without gender differences (HR 1.05: 0.69-1.60). MI recurrence occurred in 348 (7.8%) and was less common in women (HR 0.72: 0.52-0.99). After multivariate adjustment, MI recurrence was associated with a significantly higher risk of death at follow-up as compared with a single MI episode (HR 3.05: 1.9-4.80, all CI 95%). ConclusionAmong young patients with MI, women had a higher in-hospital mortality compared to men, but long-term prognosis after hospital discharge did not differ. MI recurrences were associated with increased mortality at follow up.

294 Incidence trends and long-term outcomes of juvenile myocardial infarction: does gender matter?

Abstract Aims Data about long-term clinical outcomes of young patients experiencing an acute myocardial infarction (MI), along with the potential impact of gender on incidence and prognosis in such subset are scant and mostly including USA populations. Thus, there is a paucity of data about European patients suffering from a juvenile MI. Purpose. The purpose of the current study was to investigate temporal trends, survival, MI recurrence, and sex differences among subjects who experienced their first MI at young age in the Piedmont region (Italy) between 2007 and 2018. Methods and results Hospital Discharge Register records of Piedmont region (Italy) from 2007 to 2018 were interrogated to identify incident juvenile MI cases and MI recurrences (ICD-9-CM codes: ‘410’, ‘411’, and their subcodes). Patients were considered young if the first MI occurred before or at 47 years of age. Incidence of first Juvenile MI event and subsequent overall survival among patients who survived to hospital discharge were defined as primary outcomes of interest. Subgroup analysis were performed according to sex category, comorbidities and clinical intervention (obtained from the HDRs records). Incidence of MI recurrence among patients who survived to hospital discharge was defined as secondary outcome of interest. Lastly, we evaluated whether experiencing a MI recurrence was associated with a lower overall survival at follow-up. Out of 114 816 hospitalizations due to MI, 4482 occurred in people aged ≤47, with median age 44 years old. At baseline, men had more hypertension (13% vs. 9.4%, P < 0.006) and dyslipidaemia (18.2% vs. 9.9%, P < 0.001), while women more cardiac arrest at presentation (2.9% vs. 1.7%, P = 0.03), cardiogenic shock (2.1% vs. 1.3%, P = 0.06), and less likely to undergone PCI (53.9% vs. 74.3%, P < 0.001). More women (n = 14; 1.9%) than men (n = 33; 0.9%) died while in-hospital, adjusted OR: 2.12; 1.13–3.99. After a median follow-up was 7.2 years (IQR: 4.2–9.9), the survival rate after the first MI was 94.8%, without differences between men and women (HR: 1.05; 0.69–1.60). Age at first MI, year of hospitalization, hospitalization length, chronic kidney disease, cardiogenic shock, third degree atrio-ventricular block, and PCI were found independent predictors of long term survival. 348 (7.8%) experienced at least one MI recurrence and it was more common in men than women (adjusted HR: 0.72; 0.52–0.99). After multivariate adjustment, MI recurrence was associated with a significantly higher risk of death at follow-up as compared with a single MI episode (HR: 3.05; 1.9–4.80, all 95% CI). Conclusions In young patients with a MI, women had more in-hospital mortality compared to men, but among patients who survived to hospital discharge, overall long-term prognosis did not differ. MI recurrences were more common in men and were associated with lower long-term survival rate.

Incidence trends and long-term outcomes of juvenile myocardial infarction: does gender matter?

Abstract Background Data about long-term clinical outcomes of young patients experiencing an acute myocardial infarction (MI), along with the potential impact of gender on incidence and prognosis in such subset are scant and mostly including USA populations. Thus, there is a paucity of data about European patients suffering from a juvenile MI. Purpose The purpose of the current study was to investigate temporal trends, survival, MI recurrence and sex differences among subjects who experienced their first MI at young age in the Piedmont region (Italy) between 2007 and 2018. Methods Hospital Discharge Register records of Piedmont region (Italy) from 2007 to 2018 were interrogated to identify incident juvenile MI cases and MI recurrences (ICD-9-CM codes: “410”, “411” and their subcodes). Patients were considered young if the first MI occurred before or at 47 years of age. Incidence of first Juvenile MI event and subsequent overall survival among patients who survived to hospital discharge were defined as primary outcomes of interest. Subgroup analysis were performed according to sex category, comorbidities and clinical intervention (obtained from the HDRs records). Incidence of MI recurrence among patients who survived to hospital discharge was defined as secondary outcome of interest. Lastly, we evaluated whether experiencing a MI recurrence was associated with a lower overall survival at follow-up. Results Out of 114.816 hospitalizations due to MI, 4482 occurred in people aged ≤47, with median age 44 years old. At baseline, men had more hypertension (13% vs 9.4%, p<0.006) and dyslipidemia (18.2% vs 9.9%, p<0.001), while women more cardiac arrest at presentation (2.9% vs 1.7%, p=0.03), cardiogenic shock (2.1% vs 1.3%, p=0.06) and less likely to undergone PCI (53.9% vs 74.3%, p<0.001). More women (n=14; 1.9%) than men (n=33; 0.9%) died while in-hospital, adjusted OR 2.12: 1.13–3.99. After a median follow up was 7,2 years (IQR: 4.2–9.9), the survival rate after the first MI was 94.8%, without differences between men and women (HR 1.05: 0.69–1.60). Age at first MI, year of hospitalization, hospitalization length, chronic kidney disease, cardiogenic shock, third degree atrio-ventricular block and PCI were found independent predictors of long term survival. 348 (7.8%) experienced at least one MI recurrence and it was more common in men than women (adjusted HR 0.72: 0.52–0.99). After multivariate adjustment, MI recurrence was associated with a significantly higher risk of death at follow-up as compared with a single MI episode (HR 3.05: 1.9–4.80, all CI 95%). Conclusions In young patients with a MI, women had more in-hospital mortality compared to men, but among patients who survived to hospital discharge, overall long-term prognosis did not differ. MI recurrences were more common in men and were associated with lower long-term survival rate. Funding Acknowledgement Type of funding sources: None.

Behaviour of carbonyl groups in several clinical conditions: Analysis of our survey.

Protein carbonylation is a marker of oxidative protein damage, that is likely involved in the pathogenesis of several diseases. The aim of this study was to evaluate the protein carbonyl (PC) groups in different clinical conditions. It included different groups of subjects: 81 trained subjects; 23 subjects with mild essential hypertension; 31 middle-aged subjects with metabolic syndrome (MS); 106 subjects with MS not selected for age (subdivided into two subgroups, with and without diabetes mellitus); 91 obese adults subdivided in two subgroups (BMI 30-35 Kg/m2 and BMI > 35 kg/m2); 48 subjects with obstructive sleep apnea syndrome (OSAS) subdivided in accordance with the apnea/hypopnea index (AHI); 27 subjects with chronic kidney disease (CKD) on conservative therapy; 31 subjects with CKD on haemodialysis treatment; and 50 subjects with juvenile myocardial infarction. PC groups were reduced in trained subjects in comparison with sedentary controls, while no variation was observed in mild essential hypertension. PC groups were increased in MS subjects and in adult obese subjects. In MS subjects the PC groups were not influenced by the presence of diabetes mellitus and in adult obese subjects were not influenced by the obesity degree. In OSAS subjects only those with AHI > 30 showed an increase of PC groups. PC groups increased in CKD subjects undergoing conservative treatment and haemodialysis therapy. In dialyzed subjects, after a standard dialysis session, there was a marked increase in PC groups. In juvenile myocardial infarction PC groups were higher than in controls; there was no difference between STEMI and NSTEMI and their concentration was unaffected by the number of cardiovascular risk factors or stenosed coronary vessels.

Plasma Viscosity and NLR in Young Subjects with Myocardial Infarction: Evaluation at the Initial Stage and at 3 and 12 Months.

In the “Sicilian study on juvenile myocardial infarction,” we had evaluated plasma viscosity (PV) and neutrophil/lymphocyte ratio (NLR) in patients with acute myocardial infarction (AMI) at the age of ⩽45 years. Now, we examined the relationship between these 2 parameters in 120 subjects (109 men and 11 women) aged ⩽45 years with recent AMI. The patients were classified according to the number of cardiovascular risk factors, the electrocardiographic criteria (ST-segment elevation myocardial infarction [STEMI] or non-ST-segment elevation myocardial infarction [NSTEMI]), and the extent of coronary stenosis, evaluated with coronary angiography. On fasting venous blood, we measured PV at the shear rate of 450 s−1 and NLR. The control group included 50 healthy subjects (mean age = 35.1 ± 7.8 years). At the initial stage, PV and NLR were significantly increased in comparison with controls. Subdividing AMI patients according to the median value of NLR, in the group with high NLR PV was significantly higher, whereas subdividing the patients according to the PV median value, NLR was not different between the 2 groups; 3 and 12 months after AMI, we observed only a significant decrease in NLR. Only PV was discriminant regarding the cardiovascular complications registered during an 18-month follow-up. The evaluation of PV may be of prognostic value in juvenile AMI.

Analysis of the Blood Viscosity Behavior in the Sicilian Study on Juvenile Myocardial Infarction.

Considering the role of hemorheology in coronary circulation, we studied blood viscosity in patients with juvenile myocardial infarction. We examined whole blood viscosity at high shear rate using the cone-on-plate viscosimeter Wells-Brookfield ½ LVT and at low shear rate employing a viscometer Contraves LS30 in 120 patients (aged <46 years) with myocardial infarction, at the initial stage and subsequently 3 and 12 months after. At the initial stage, patients had an increased whole blood viscosity in comparison to normal controls. This hemorheological profile was not influenced by the cardiovascular risk factors, nor by the extent of coronary lesions, even if some differences were evident between patients with ST-segment elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI). The blood viscosity pattern at the initial stage did not influence recurring ischemic events or the onset of heart failure during an 18 months’ follow-up. The neutrophil to lymphocyte ratio did not affect the blood viscosity pattern. We reevaluated 83 patients 3 months after and 70 patients 12 months after the acute coronary syndrome, and we found that the hemorheological parameters were still altered in comparison to normal controls at both times. We observed an impairment of the hemorheological pattern in young patients with myocardial infarction, partially influenced by the infarction type (STEMI and NSTEMI) and persisting in the long term.

Behaviour of the neutrophil to lymphocyte ratio in young subjects with acute myocardial infarction.

In the last years the neutrophil to lymphocyte ratio (NLR) has been examined in cardiovascular disorders and in particular in coronary artery disease and acute myocardial infarction (AMI). Now we examined this parameter in subjects with juvenile myocardial infarction at the initial stage and after 3 and 12 months. We enrolled 123 young subjects (112 men and 11 women, mean age 39.4 ± 5.8 yrs) with AMI. The time interval between the AMI onset and the investigation was 13 ± 7 days. The mean value of NLR observed in young AMI subjects was significantly increased compared to normal controls (N = 1.817 ± 0.711; young AMI subjects = 2.376 ± 0.873, p < 0.0001). NLR does not discriminate STEMI (2.427 ± 0.878) and non STEMI (2.392 ± 0.868) or diabetics (2.604 ± 1.000) and non diabetics (2.324 ± 0.853), but it differentiates smokers (2.276 ± 0.853) and non smokers (2.837 ± 1.072). NLR at the initial stage is not correlated with the number of cardiovascular risk factors or with the extent of the coronary disease. In this study we found a significant decrease of neutrophil count at 3 and 12 months later AMI without any significant variation of lymphocyte and consequently we observed a decrease in NLR at these two intervals of time in comparison with the initial stage. Despite some limitations present in this study, it is interesting to underline that also in juvenile myocardial infarction this low-cost haematological marker may be considered together with other inflammatory indicators.

A novel polymorphism in the PAI-1 gene promoter enhances gene expression. A novel pro-thrombotic risk factor?

IntroductionPlasminogen activator inhibitor-1 (PAI-1) is the major physiological inhibitor of tissue-type plasminogen activator in plasma and the most important regulator of the fibrinolytic pathway. The 4G/5G polymorphism (rs1799889) in the PAI-1 promoter is associated with altered PAI-1 transcription. We have identified a new 4G/5G allele, in which a T is inserted near the 4G tract or replaces a G in the 5G tract, forming a T plus 4G (T4G) region. Materials and MethodsThis new variant was first identified in two women, one had experienced juvenile myocardial infarction, the other repeated miscarriage; both had increased PAI-1 plasma activity. In view of the important influence of this promoter region on PAI-1 protein plasma level, we performed in vitro evaluation of the effects of the T4G variant on the transcription activity of the PAI-1 gene promoter. Results and ConclusionsIn silico prediction analysis showed that presence of the T4G allele disrupts the E-Box region upstream of the T4G variant, altering the affinity of the target sequence for E-Box binding factors like upstream stimulatory factor-1 (USF-1). Basal T4G promoter activity was 50% higher compared to 4G and 5G variants, but it was less stimulated by USF-1 overexpression. We also analyzed the effects of IL-1β and IL-6 on the PAI-1 promoter activity of our three constructs and showed that the T4G variant was less affected by IL-1β than the other variants. These findings indicate that the T4G variant may be a novel risk factor for thrombotic events.

Behaviour of protein carbonyl groups in juvenile myocardial infarction

Acute myocardial infarction (AMI) is accompanied by oxidative stress, and protein oxidation is among the consequences of oxidative stress. We examined the plasma concentration of protein carbonyl groups (PC), a marker of protein oxidation, in a group of young subjects with AMI (45 men and 5 women; mean age 40.4 ± 4.8 yrs). We found a significant increase of PC (p < 0.001) in comparison with normal controls. No difference was observed between patients with AMI characterized by elevated ST segment and those without elevation of ST segment. There was no correlation between the ejection fraction and PC in the whole group nor in the subgroups of STEMI and non-STEMI patients. Subdividing the whole group of AMI patients according to the number of risk factors and the number of stenosed coronary vessels, the difference in PC level was not statistically significant among the subgroups. This study showed an increased protein oxidation in young subjects with recent AMI. Further investigation is needed to ascertain whether this can be a target of therapeutic intervention.

Heritability of platelet-leukocyte conjugates and cell activation markers in families with and without juvenile myocardial infarction

Heritability of platelet-leukocyte conjugates and cell activation markers in families with and without juvenile myocardial infarction

Genetic regulation of inflammation-mediated activation of haemostasis: Family-based approaches in population studies

Blood coagulation and inflammation play a key role in atherosclerosis and thrombosis. Candidate gene and genome wide association studies have identified potential specific genes that might have a causal role in these pathogenic processes. The analysis of quantitative traits is more powerful as they are closer to direct gene action than disease phenotypes. Thus linkage-based studies on extended families might be useful both to estimate the heritability and to map the genetic loci responsible for the regulation of the trait.Family-based studies may estimate high heritability for thrombosis and quantitative traits regarding both platelet aggregation and blood coagulation. Some specific loci relevant to thrombosis have been identified, with some of them showing a direct pleiotropic effect on the risk of thrombosis.Haemostasis factors can be activated by inflammatory stimuli. Fibrinogen level is genetically correlated with C-reactive protein levels with a link for both traits on chromosomes 12 and 21. Genes related to prostanoid biosynthesis, involved both in inflammation and thrombosis, show high heritability levels in both enzyme expression and prostanoid production.Considering that few large family-based linkage studies have as yet been performed on haemostasis and inflammation-related traits, additional studies are highly needed. We are performing a family-based linkage study on large pedigrees (750 subjects from 23 families with juvenile myocardial infarction and 31 control families), to identify genes responsible for quantitative traits involved in the pathway progressively going from inflammation to haemostasis, cell activation, thrombus formation and cardiovascular events.

Tissue factor gene polymorphisms and haplotypes and the risk of ischemic vascular events: four studies and a meta-analysis.

The exposure of tissue factor (TF) to blood flow is the initial step in the coagulation process and plays an important role in thrombogenesis. We investigated the role of genetic polymorphisms and haplotypes of the TF gene in the risk of ischemic vascular disease. Four hundred and twenty-two Italian patients with juvenile myocardial infarction (MI) and 434 controls, 808 US cases with MI and 1005 controls, 267 Italian cases with juvenile ischemic stroke and 209 controls and 148 German cases with juvenile ischemic stroke and 191 controls were studied. rs1361600, rs3917629 (rs3354 in the US population), rs1324214 and rs3917639 Tag single nucleotide polymorphisms were genotyped. Additionally, a meta-analysis of all previous studies on TF loci and the risk of ischemic coronary disease (ICD) was performed. After multivariable analysis none of the SNPs, major SNP haplotypes or haplotype-pairs showed any consistent association with MI. Pooled meta-analysis of six studies also suggested that TF polymorphisms are not associated with CHD. A significant, independent association between SNP rs1324214 (C/T) and juvenile stroke was found in Italian and German populations (OR for TT homozygotes = 0.47, 95% CI 0.24-0.92, in combined analysis). Pooled analysis also showed a significant association for haplotype H3 (OR = 0.76, 95% CI 0.57-1.00) and haplotype-pair H3-H3 (OR = 0.43, 95% CI 0.20-0.92). TF genetic variations were associated with the risk of ischemic stroke at young age, but did not affect ischemic coronary disease.

Influence of risk factors on nitric oxide metabolites at the initial stage of juvenile acute myocardial infarction

Few data are accessible about the nitric oxide (NO) stable end-products (nitrite/NO2 − and nitrate/NO3 − :N O x) in acute coronary syndromes. An increase in inducible NO synthase (iNOS) was found during experimental myocardial infarction [13] and this increase persisted for 2 weeks. In experimental models of acute myocardial infarction (AMI) other authors [2] observed a NOx increase, a correlation between NOx level and iNOS activity and an inhibitory action carried out by S-methylisothiourea, that is an iNOS inhibitor [5]. The NOx level was also measured in a small group of patients with myocardial infarction in whom the peak of NOx elevation occurred 2 and 3 days after the onset of symptoms, suggesting that the NOx increase was dependent on the macrophagical iNOS activation induced by cytokines [1]. Similar results were recently observed in large groups of patients with AMI [6,11]. Now we report the evaluation of the plasma NOx in a group of young patients with recent AMI, subdivided according to the number of main cardiovascular risk factors (RF). We enrolled 105 subjects (97 men and 8 women) aged <46 years; the mean age was 39.6 ± 5.5 years (range 19–45 years). The time interval between AMI onset and the NOx determination was 13 ± 7 days. Regarding the main risk factors, 83% were cigarette smokers or ex-smokers and 49% had family history of coronary artery disease; hypercholesterolemia was present in 51%, essential hypertension in 24% and diabetes mellitus in 12%. According to the number of cardiovascular RF we subdivided AMI subjects into three groups: 33 subjects had 0–1 RF, 35 had 2 RF and 37 had 3–5 RF. On fasting venous blood the NOx level was evaluated by a micromethod which measures the concentration of both NO metabolites (nitrite plus nitrate). At first nitrate was converted into nitrite by a nitrate reductase, then nitrite was measured by spectrophotometry after addition of the Griess reagent. The data were expressed as means ± SD. The statistical difference between normal controls and the subgroups of AMI subjects was examined using the one-way ANOVA model while the Bonferroni posttest was used to compare each pair of subgroups. The obtained results showed that in each subgroup of AMI subjects the mean value of NOx was increased in comparison with normal controls, in whom the NOx level was 24.38 ± 15.67 µM. The mean values of NOx were in fact respectively 57.11±24.75 µM in the subgroup with 0–1 RF, 63.76±31.93 µM

Different outcome of six homozygotes for prothrombin A20210A gene variant

Prothrombin G20210A gene variant (FII G20210A) is a risk factor for venous thrombotic disease while conflicting results have been reported for the risk of arterial thrombotic events. However, vascular episodes were absent in up to 40% of the 67 homozygotes for the G20210A described so far, which indicates that the clinical expression depends on additional risk/trigger factors. We describe six homozygotes for the G20210A variant, among which the first pair of siblings (cases n. 3 and 4) reported so far that displayed a strongly heterogeneous clinical outcome. Case 1, a female of 27 years, developed a full thrombosis of common femoral, superficial and popliteal veins. She assumed oral contraceptives in the last two years. Case n. 2, 34 years old, suffered of recurrent pregnancy loss in absence of any causative alteration. Cases n. 3 and n. 5 experienced arterial thrombotic disease, i.e., juvenile myocardial infarction (40 years old) and stroke (48 years old), respectively, in absence of other risk factors. Finally, cases n. 4 and 6 identified as homozygotes for the FII G20210A variant being consanguineous of symptomatic subjects bearing the variant, did not experience any episode of venous nor arterial disease. Both of them have chronic liver disease with an impairement of the prothrombin time INR. Thus, homozygotes for the G20210A are at risk for arterial (in addition to venous) thromobotic events; chronic liver disease might modulate this risk.

Knowledge of cardiovascular risk factors and awareness of non-pharmacological approach for risk prevention in young survivors of acute myocardial infarction. The cardiovascular risk prevention project “Help Your Heart Stay Young”

Background and aims Knowledge of cardiovascular disease (CVD) risk factors in young patients who experienced myocardial infarction (MI) is poorly described. Methods and results Knowledge of traditional CVD risk factors, non-fatal cardiovascular events and of non-pharmacological factors able to reduce CVD risk and education level were evaluated by questionnaires in subjects who visited their family doctors. Sixty-one participants with history of MI in age <50 years (MI+) were compared with 3749 subjects with age <50 years, from the same population source, but without history of MI (MI−). MI+ were more frequently men ( p < 0.01), did not have significantly higher prevalences of family history of CVD, diabetes and hypertension. MI+ individuals reported previous non-fatal stroke (13% vs. 0.5%, p < 0.001), overweight, diabetes, and hypercholesterolemia (all p < 0.001) more frequently than controls, whereas prevalence of arterial hypertension, smoking habit and physical inactivity did not differ between the two groups; MI+ and MI− individuals did not differ in terms of the proportion of those who were unaware of being hypertensive, diabetic or hypercholesterolemic. MI+ participants reported more frequently lower education level than controls ( p < 0.05). Knowledge of non-pharmacological approach for CVD risk reduction was similar in MI+ and MI−. In a logistic multivariate analysis, male gender (adjusted odds ratio = 5.8) and high cholesterol level (adjusted odds ratio 2.8, both p < 0.01) were independent correlates of MI+. CVD risk factors distribution was similar between participants with juvenile MI+ and MI in age ≥50 years ( n = 167) extracted from the same population source; however, stroke was reported more frequently in juvenile MI+ than in those who had MI at age ≥50 years/old (13% vs. 4%, p < 0.01). Conclusions Juvenile non-fatal MI was associated with metabolic CVD risk factors, with higher cerebrovascular co-morbidity and lower education level.

We-W35:2 Inherited and acquired risk factors for juvenile myocardial infarction in an European cohort

We-W35:2 Inherited and acquired risk factors for juvenile myocardial infarction in an European cohort