Family History Of Premature Myocardial Infarction Research Articles

How family history of premature myocardial infarction affects patients at cardiovascular risk.

Family history of premature myocardial infarction (FH-MI) increases the risk for coronary heart disease (CHD). Research has shown that this effect cannot be accounted for by increased genetic vulnerability alone. We tested the hypothesis that FH-MI is associated with psychological distress, which is known to increase CHD risk, and that this effect is sustained over years and mediated by personality traits and coping strategies. Levels of distress (i.e., exhaustion, depression, and anxiety) were compared between patients with versus without FH-MI and those with versus without own history of myocardial infarction (MI) from the large observational Diagnostic trial on Prevalence and Clinical Course of Diastolic Dysfunction and Heart Failure (DIAST-CHF) study of patients with cardiovascular risk factors or manifest heart disease (N = 1,470). FH-MI was associated with a range of personality traits and coping strategies and independently predicted psychological distress, whereas own MI did not. In mediation analysis, we found that sociotropy and avoidant coping serially mediated significant portions of the effect of FH-MI on distress. Proportions of explained variance ranged from R2 = .11 for depressive symptoms to R2 = .25 for anxiety. Effects remained stable at 1-year follow-up. Several alternative hypotheses were tested and found to be less well supported by the data. Participants with cardiovascular risk factors and FH-MI report increased distress, even years after the event, which might be one component leading to their increased CHD risk. They should be offered support for dealing with distress and life events recurring on sociotropy and avoidant coping as important diathesis factors. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Family history of premature myocardial infarction modifies the associations between bilateral oophorectomy and cardiovascular disease mortality in a US national cohort of postmenopausal women.

To test the hypothesis that a family history of premature myocardial infarction (FHPMI) will modify the associations between bilateral salpingo-oophorectomy (BSO) and mortality due to heart disease (HD), cardiovascular disease (CVD), or all-cause mortality with stronger associations observed for BSO occurring before 45 years. We analyzed data from 2,763 postmenopausal women aged 40 years or older who participated in the National Health and Nutrition Examination Survey (1988-1994) and were followed through December 31, 2015. Cox regression was used to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for mortality outcomes (HD, CVD, and all-cause). At baseline, the average age was 62 years. There were 610 women with BSO, 338 women with FHPMI, and 95 women with both BSO and FHPMI. During a median follow-up of 22 years, 1,713 deaths occurred of which 395 and 542 were attributed to HD and CVD, respectively. In models adjusting for CVD risk factors and hormone therapy use, HD mortality was greater among women with both BSO and FHPMI compared to those without either of these conditions (HR: 2.88, 95% CI: 1.72-4.82, PInteraction = 0.016). HD mortality was higher among women with FHPMI and BSO at an earlier age (<45 y: HR: 4.32, 95% CI: 1.95-9.50 vs ≥45 y: HR: 1.60, 95% CI: 0.63-4.09). Similar observations were seen for CVD and all-cause mortality. In this study, the risk of HD, CVD, and all-cause mortality in women with BSO was modified by an FHPMI with the risk limited to women undergoing BSO at younger ages.

Determinants of premature familial arterial thrombosis in patients with juvenile ischaemic stroke. The Italian Project on Stroke in Young Adults (IPSYS).

Factors predicting family history (FH) of premature arterial thrombosis in young patients with ischaemic stroke (IS) have not been extensively investigated, and whether they might influence the risk of post-stroke recurrence is still unknown. In the present study we analysed 1,881 consecutive first-ever IS patients aged 18-45 years recruited from January 2000 to January 2012 as part of the Italian Project on Stroke in Young Adults (IPSYS). FH of premature arterial thrombosis was any thrombotic event [IS, myocardial infarction or other arterial events event] < 45 years in proband's first-degree relatives. Compared with patients without FH of premature arterial thrombosis, those with FH (n = 85) were more often smokers (odds ratio [OR], 1.94; 95 % confidence interval [CI], 1.21-3.09) and carriers of procoagulant abnormalities (OR, 3.66; 95 % CI, 2.21-6.06). Smoking (OR, 2.48; 95 % CI, 1.20-5.15), the A1691 mutation in factor V gene (OR, 3.64; 95 % CI, 1.31-10.10), and the A20210 mutation in the prothrombin gene (OR, 8.40; 95 % CI 3.35-21.05) were associated with FH of premature stroke (n = 33), while circulating anti-phospholipids to FH of premature myocardial infarction (n = 45; OR, 3.48; 95 % CI, 1.61-7.51). Mean follow-up time was 46.6 ± 38.6 months. Recurrent events occurred more frequently in the subgroup of patients with FH of premature stroke [19.4 %); p = 0.051] compared to patients without such a FH. In conclusion, young IS patients with FH of premature arterial thrombosis exhibit a distinct risk-factor profile, an underlying procoagulant state and have worse vascular prognosis than those with no FH of juvenile thrombotic events.

137 DIAGNOSIS AND MANAGEMENT OF FAMILIAL HYPERCHOLESTEROLAEMIA IN A TERTIARY CARDIAC CENTRE

<h3>Introduction</h3> Familial hypercholesterolaemia (FH) is a treatable risk factor for premature myocardial infarction (MI), yet it remains poorly diagnosed in the UK. Current NICE guidance (2008) recommends use of Simon Broome (S-B) criteria for diagnosis of ‘definite’ or ‘possible’ FH with referral to a specialist for confirmation of diagnosis and initiation of cascade testing. Cardiac centres have valuable opportunities to identify such patients and implement these recommendations. We examined diagnosis and referral patterns for FH in light of NICE guidance at our tertiary centre. <h3>Methods</h3> Using hospital electronic records we identified all patients with a total cholesterol (TC) ≥7.5 mmol/l, who presented to our cardiac services from January to December 2011. For the visit relating to the high TC measurement, we examined patient records to determine if they were assessed by a physician and if there was sufficient documentation to apply S-B criteria, namely (1) family history of premature MI or FH, (2) physical examination for FH stigmata or (3) consideration of a diagnosis of FH with referral to a lipid clinic. <h3>Results</h3> We examined records for 126 patients and excluded 45 who had not directly seen a physician relating to the index TC measurement. Among the 81 patients included in this study (mean age 57.8, 56% male), approximately half were seen as in-patients. A total of 4% (n=3) were classified as ‘definite’ FH (2 had a prior diagnosis and 1 was not referred), 16% (n=13) as ‘possible’ (none referred), and 7% (n=6) as ‘other known lipid disorders’. Over 2/3 (n=59) could not be classified due to insufficient information available to apply the S-B criteria, although 4 of these patients were referred for a specialist opinion and 3 were known to the lipid clinic. Documentation of examination for FH stigmata was absent in almost all cases (98%, n=79). Family history of coronary heart disease (CHD) was documented in 67% (n=54) of cases, of whom 54% (n=29) had a positive history. Of the latter, the type of CHD and age of onset were adequately documented in only 69% and 66% respectively. Documentation of family history of high cholesterol was absent in 89% of cases. In 43% (n=35) of all cases there was no documentation that the cholesterol result had been noted. Finally we estimated that approximately 4–6% of acute coronary syndrome patients had TC levels &gt;7.5, thus representing a potentially enriched population for FH. <h3>Conclusions</h3> While a significant opportunity exists in tertiary cardiac units to identify and refer potential FH cases, S-B criteria are not being routinely documented to consider such patients for onward referral. Universal focus on high dose statin therapy after ACS may in part have contributed to diminished consideration of the wider implications of FH and familial risk. Raising awareness of FH in cardiac units across the country could have significant population health benefits through cascade screening.

Relation of the Leu40Arg variant of glycoprotein IIIA to personal and family history of myocardial infarction

Relation of the Leu40Arg variant of glycoprotein IIIA to personal and family history of myocardial infarction GPIIb/IIIa fibrinogen receptor is a key element of the thrombotic pathway. In this study, we investigated the possible relation of PlA1/A2 polymorphism (1565T&gt;C; Leu33Pro) and a rare 1586T&gt;G (Leu40Arg) variation of GPIIIa gene to personal and family history of myocardial infarction (MI) among 601 patients with angiographically confirmed coronary heart disease. Four hundred and fifteen patients had MI and 94 of individuals reported family history of premature MI. The Arg40 (1586G) variant (n = 4) was present exclusively in MI-patients and significantly correlated with a family history of premature MI (P = 0.013), whereas the Pro33 (1565C; PlA2) allele (n = 204) was similarly prevalent among different groups of patients. These data indicate the importance of the Arg40 variant but do not support a significant role of Pro33 allele in susceptibility to MI.

Abstract 4992: Cardiovascular Disease Risk Prediction with and without Knowledge of Genetic Variation at Chromosome 9p21.3: The Women’s Genome Health Study

Background : While genetic variation at chromosome 9p21.3 is associated with incident cardiovascular disease (CVD), it is unclear whether screening for this polymorphism improves risk prediction. We sought to determine whether knowledge of variation at chromosome 9p21.3 adds to the information provided by traditional risk factors using data from a prospective cohort study of female Caucasian health professionals in the United States. Methods : 22,129 initially healthy participants in the Women’s Genome Health Study were prospectively followed over a median of 10.2 years for incident CVD. We determined genotype for rs10757274 in chromosome 9p21.3 as well as blood pressure, smoking status, diabetes, blood levels of cholesterol, high sensitivity C-reactive protein (hsCRP), and family history of premature myocardial infarction (MI). Models were compared overall using the C-index and for reclassification across commonly used categories of 10-year CVD risk (&lt;5%, 5% to &lt;10%, 10% to &lt;20%, 20+%). Results : Genotype for rs10757274 was associated with an adjusted hazard ratio (HR) for incident CVD of 1.25 (95% CI 1.04 – 1.51) for the AG genotype (present in 49% of the women) and 1.32 (95% CI 1.07 – 1.63) for the GG genotype (present in 24% of the women) compared to the AA genotype. However, the addition of the genotype to traditional CVD risk factors had no effect on the C-index (0.805 to 0.807) with correct reclassification of 526 women (2.4%). When the genotype was added to previously validated prediction models that additionally included hsCRP and family history of premature MI, there was again no effect on the C-index (0.809 to 0.807), and only 214 women (1.0%) were reclassified correctly. Conclusion : In this large prospective cohort of Caucasian women, genetic variation in chromosome 9p21.3 was associated with incident CVD but did not improve discrimination or classification of predicted risk.

Implications of family history of myocardial infarction in young women

Family history of premature myocardial infarction (FHMI) may be a useful marker of cardiovascular disease (CVD) risk in young subjects, but comparisons of its implications for CVD risk factor burden, prevalent atherosclerosis, and risk awareness between young men and women have not been reported. We analyzed data from 2404 young subjects with ages 30 to 50 in the Dallas Heart Study, which is a population-based study. Family history of premature MI was defined as a first-degree relative with myocardial infarction (MI) before age 50 (men) or 55 (women). Coronary artery calcification was measured by computed tomography scan, and perceived lifetime risk of MI was assessed by questionnaire. Analyses were sex-stratified. Women with versus without FHMI had an increased composite risk factor burden (> or = 2 CVD risk factors, 49.1% vs 39.1%; P < .001), an association not seen in men (P = .6). Family history of premature MI was independently associated with coronary artery calcification among women (adjusted odds ratio, 2.0; 95% confidence interval, 1.0-4.1) but not among men (adjusted odds ratio, 1.7; 95% confidence interval, 0.9-3.2). A higher proportion of subjects with FHMI versus no FHMI perceived their lifetime risk of MI to be at > or = average in women (59.7% vs 47.4%; P < .001) and men (75.0% vs 48.3%; P = .004), with the increment greatest among men (P interaction = .02). Despite a stronger association with CVD risk factors and atherosclerosis prevalence with FHMI among young women compared with men, young women with FHMI demonstrated less CVD risk awareness and worse lifestyle choices. Family history of premature MI may be an especially useful risk assessment tool in young women, and greater efforts are needed to promote CVD risk awareness among young women with FHMI.

C-Reactive Protein Levels and Arterial Abnormalities in the Offspring of Patients with Premature Myocardial Infarction

Aims: To determine whether high C-reactive protein (CRP) levels and increased intima-media thickness of the common carotid arteries are coexistent in adolescents and young adults with a family history (FH) of premature myocardial infarction (MI). Methods: 50 healthy young subjects whose parents had had premature MI and 50 control matched subjects were enrolled in the study. CRP levels and the intima-media thickness of the distal common carotid arteries were evaluated in all subjects. Results: As compared with the control subjects, the offspring of patients with premature MI had a higher CRP concentration (mean ± SD 8.8 ± 2.6 versus 3.9 ± 0.6 mg/l, p < 0.02) and greater intima-media thickness of the common carotid arteries (values for combined sides, mean ± SD 0.48 ± 0.02 versus 0.43 ± 0.02 mm, p < 0.03). Conclusion: High serum levels of CRP and arterial structural changes are coexistent at an early age in subjects with an FH of premature MI.

Differential Influence of Family History of Hypertension and Premature Myocardial Infarction on Systolic Blood Pressure and Left Ventricular Mass Trajectories in Youth

To examine the influence of genetic susceptibility to essential hypertension (EH) and the genetic susceptibility to premature myocardial infarction (MI) on longitudinal development of systolic blood pressure (SBP) and left ventricular mass (LVM) in youth. Individual SBP and LVM growth curves across age were created for a sample of 745 subjects (age range: 4.9-27.5 years) and a sample of 687 subjects (age range: 8.2-27.5 years), respectively. Each sample had an approximately equal proportion of African American and European American males and females, with annual assessments over a 10-year period. Family history (FH) of EH and FH of premature MI were used as measures of genetic susceptibility to EH and to premature MI, respectively. Positive FH (FH(+)) of EH and of premature MI were defined, respectively, as verified EH in 1 or both biological parents, and verified MI in any biological parent or grandparent before 55 years of age. Subjects with an FH(+) of EH had higher SBP levels and stronger increases in SBP over time than subjects with a negative FH (FH(-)) of EH. Subjects with an FH(+) of EH also showed higher LVM levels than subjects with an FH(-) of EH. In addition, the effect of an FH(+) of EH on LVM was stronger in females than males. The effects of FH of EH on SBP and LVM could not be explained by differences in socioeconomic status, but the effect on LVM was no longer significant after adjustment for BMI. FH of MI had no significant effects on SBP or LVM. Effects of genetic susceptibility to EH on SBP and LVM trajectories were observed in childhood, whereas no such effects were found for FH of MI. Genetic markers of EH may improve the understanding of individual differences in susceptibility to develop hypertension and LV hypertrophy.

Time urgency and risk of non-fatal myocardial infarction

Inconsistencies in the literature linking Type A behaviour pattern (TAB) to coronary heart disease (CHD) may be due to differences in the effects of various components of TAB, namely aggressiveness, hostility, ambitiousness, competitive drive, and a chronic sense of time urgency. We investigated the association between sense of time urgency/impatience and non-fatal myocardial infarction (MI) in a study of 340 cases and an equal number of age-, sex-, and community-matched controls. A dose-response relation was apparent among subjects who rated themselves higher on the four-item time urgency/impatience scale (P-value for trend <0.001), with a matched odds ratio (OR) for non-fatal MI of 4.45 (95% CI : 2.20-8.99) comparing those with the highest rating to those with the lowest. After further adjustment for family history of premature MI, physical activity, body mass index, occupation, cigarette smoking, total caloric intake, per cent calories from saturated fat, alcohol intake, lipid levels, treated hypertension and diabetes, the dose-response relation remained (P-value for trend = 0.015) and the adjusted OR for MI was 3.99 (95% CI : 1.32-12.0) comparing those with the highest rating to those with the lowest. In these data, a sense of time urgency/impatience was associated with a dose-response increase in risk of non-fatal MI, independent of other risk factors. Prospective cohort studies of time urgency/impatience and incident CHD events are needed to confirm or refute these observations from a case-control study.

Psychosocial Risk Factors and Nonfatal Myocardial Infarction

Numerous psychosocial factors have been hypothesized to play a role in coronary heart disease. However, existing studies have yielded inconsistent results. The relations between type A personality as well as suppressed versus expressed anger and risk of nonfatal myocardial infarction (MI) were studied in 340 patients and 340 age-, sex-, and community-matched control subjects. Subjects were interviewed at home to assess behavioral and medical cardiovascular risk factors, and fasting blood samples were obtained. Type A personality was associated with nonfatal MI in crude matched-pair analysis (OR, 1.57; 95% CI, 1.12 to 2.20; P = .008). Adjusting for known cardiovascular risk factors (including treated hypertension, body mass index, treated diabetes, family history of premature MI, physical activity, smoking, alcohol, total calories per day, and saturated fat) did not substantially change the magnitude of the point estimate, although the finding was no longer statistically significant (OR, 1.43; 95% CI, 0.97 to 2.09; P = .069). Further adjustment for lipids, including total cholesterol, total HDL, its subfractions (HDL2, HDL3), LDL, VLDL, and triglycerides, markedly attenuated the association (OR, 1.12; 95% CI, 0.66 to 1.90; P = .687), an effect due almost entirely to HDL cholesterol. Suppressed anger was positively but not statistically significantly associated with increased risk of MI in crude matched-pair analysis (OR, 1.33; 95% CI, 0.98 to 1.81; P = .065), in analysis adjusted for behavioral and medical cardiovascular risk factors (OR, 1.26; 95% CI, 0.89 to 1.78; P = .193), or after adjustment for lipids (OR, 1.11; 95% CI, 0.67 to 1.82; P = .695). These findings suggest a possible association of type A but not suppressed anger with risk of nonfatal MI that may be mediated by alterations in HDL cholesterol level. If decreases in HDL are not in the same causal pathway, then the apparent association between type A personality and risk of MI is due to confounding, principally by HDL.