Prevalence and management of familial hypercholesterolemia in patients with coronary artery disease: The heredity survey

Background and aims Familial hypercholesterolemia (FH) is a genetic disorder characterized by high levels of low density lipoprotein cholesterol (LDL-C) predisposing to premature cardiovascular disease. Its prevalence varies and has been estimated around 1 in 200\u2013500. The Heredity survey evaluated the prevalence of potential FH and the therapeutic approaches among patients with established coronary artery disease (CAD) or peripheral artery disease (PAD) in which it is less well documented. Methods Data were collected in patients admitted to programs of rehabilitation and secondary prevention in Italy. Potential FH was estimated using Dutch Lipid Clinic Network (DLCN) criteria. Potential FH was defined as having a total score 65 6. Results Among the 1438 consecutive patients evaluated, the prevalence of potential FH was 3.7%. The prevalence was inversely related to age, with a putative prevalence of 1:10 in those with 8) had the highest percentages of patients after an ACS (75% vs 52.5% in the whole study population). At discharge, most patients were on high intensity statin therapy, but despite this, potential FH group still had a higher percentage of patients with LDL-C levels not at target and having a distance from the target higher than 50%. Conclusions Among patients with established coronary heart disease, the prevalence of potential FH is higher than in the general population; the results suggest that a correct identification of potential FH, especially in younger patients, may help to better manage their high cardiovascular risk

No evidence of association between prothrombotic gene polymorphisms and the development of acute myocardial infarction at a young age

Background : we investigated the association between 9 polymorphisms of genes encoding hemostasis factors and myocardial infarction in a large sample of young patients chosen because they have less coronary atherosclerosis than older patients, and thus their disease is more likely to be related to a genetic predisposition to a prothrombotic state Methods and Results : this nationwide case-control study involved 1210 patients who had survived a first myocardial infarction at an age of 45 years who underwent coronary arteriography in 125 coronary care units and 1210 healthy subjects matched for age, sex, and geographical origin. None of the 9 polymorphisms of genes encoding proteins involved in coagulation (G-455A -fibrinogen: OR, 1.0; CI, 0.8 to 1.2; G1691A factor V: OR, 1.1; CI, 0.6 to 2.1; G20210A factor II: OR, 1.0; CI, 0.5 to 1.9; and G10976A factor VII: OR, 1.0; CI, 0.8 to 1.3), platelet function (C807T glycoprotein Ia: OR, 1.1; CI, 0.9 to 1.3; and C1565T glycoprotein IIIa: OR, 0.9; CI, 0.8 to 1.2), fibrinolysis (G185T factor XIII: OR, 1.2; CI, 0.9 to 1.6; and 4G/5G plasminogen activator inhibitor type 1: OR, 0.9; CI, 0.7 to 1.2), or homocysteine metabolism (C677T methylenetetrahydrofolate reductase: OR, 0.9; CI, 0.8 to 1.1) were associated with an increased or decreased risk of myocardial infarction Conclusions : this study provides no evidence supporting an association between 9 polymorphisms of genes encoding proteins involved in hemostasis and the occurrence of premature myocardial infarction or protection against it

Self-assembling of Mn12 molecular nanomagnets on FIB-patterned Au dot matrix

AbstractWe have developed a novel strategy to build arrays of magnetic nanodots on the 100 nm scale, which exploits the potentialities of both bottom-up and top-down approaches, by self-assembling sulfur-functionalized Mn12 single molecule magnets (SMMs) on patterned Au dot matrices nanofabricated by FIB (focus ion beam). In this way, we demonstrate the capability to assemble SMMs in ordered arrays, where the magnetic information can be easily addressed, being the single bit represented by a 2D distribution of few hundred Mn12 clusters, grafted on top of each 100 × 100 nm2 Au dot. Moreover, the chosen Mn12 functionalization is expected to favour a preferential orientation of the grafted molecule with the easy magnetization axis normal to the surface

Tuning Anisotropy Barriers in a Family of Tetrairon(III) Single-molecule Magnets with an S=5 Ground State

Tetrairon(III) Single-Mol. Magnets (SMMs) with a propeller-like structure exhibit tuneable magnetic anisotropy barriers in both height and shape. The clusters [Fe4(L1)2(dpm)6] (1), [Fe4(L2)2(dpm)6] (2), [Fe4(L3)2(dpm)6]·Et2O (3·Et2O), and [Fe4(OEt)3(L4)(dpm)6] (4) were prepd. by reaction of [Fe4(OMe)6(dpm)6] (5) with tripodal ligands R-C(CH2OH)3 (H3L1, R = Me; H3L2, R = CH2Br; H3L3, R = Ph; H3L4, R = tBu; Hdpm = dipivaloylmethane). The iron(III) ions exhibit a centered-triangular topol. and are linked by six alkoxo bridges, which propagate antiferromagnetic interactions resulting in an S = 5 ground spin state. Single crystals of 4 reproducibly contain at least two geometric isomers. From high-frequency EPR studies, the axial zero-field splitting parameter (D) is invariably neg., as found in 5 (D = -0.21 cm-1) and amts. to -0.445 cm-1 in 1, -0.432 cm-1 in 2, -0.42 cm-1 in 3·Et2O, and -0.27 cm-1 in 4 (dominant isomer). The anisotropy barrier Ueff detd. by a.c. magnetic susceptibility measurements is Ueff/kB = 17.0 K in 1, 16.6 K in 2, 15.6 K in 3·Et2O, 5.95 K in 4, and 3.5 K in 5. Both |D| and Ueff increase with increasing helical pitch of the Fe(O2Fe)3 core. The 4th-order longitudinal anisotropy parameter B40, which affects the shape of the anisotropy barrier, concomitantly changes from pos. in 1 (compressed parabola) to neg. in 5 (stretched parabola). With the aid of spin Hamiltonian calcns. the obsd. trends were attributed to fine modulation of single-ion anisotropies induced by a change of helical pitch