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Genetic predisposition of elevated nighttime blood pressure (BP) in patients with coronary heart disease is unknown. We evaluated genetic predisposition and the relationship between elevated nighttime BP and cardiovascular complications over a median of 8.6 years of observation of hypertensive subjects with coronary atherosclerosis confirmed by coronary angiography. Genetic Risk Score (GRS19) was constructed to evaluate the additive effect of single-nucleotide polymorphisms for daytime and nighttime BP. The Receiver Operating Characteristic was used for determination of cutoff points for daytime BP (systolic BP (SBP) 133 mm Hg and diastolic BP (DBP) 77 mm Hg) and nighttime BP (SBP 122 mm Hg and DBP 73 mm Hg). The curves of cumulative incidence revealed an increased risk of major advanced cardiovascular events in subjects with elevated nighttime BP compared with those without elevated nighttime BP during the follow-up period. Subjects with normal daytime and elevated nighttime BP exhibited increased GRS19 compared with those with normal daytime and nighttime BPs (8.6±3.0 vs. 7.9±3.0, P<0.01). After adjustment for cardiovascular risk factors, GRS19 determined nighttime SBP (β 0.4, 95% confidence interval (CI) 0.3-0.5, P<0.01). Our study confirmed that elevated nighttime SBP was genetically determined and related to an increased risk of major adverse coronary events in patients with confirmed coronary atherosclerosis.

Aim: The aim of this study was to compare coronary calcium scores and aortic calcium scores between patients with severe hypercholesterolemia having a DNA-based diagnosis of FH (FH group) versus patients with severe hypercholesterolemia without the FH gene mutation (NFH group)., Method: A total of 89 FH and 50 NFH patients underwent CT with coronary and thoracic aorta calcium scoring. Their CCS and TCS in ascending aorta (TCSasc) and descending aorta (TCSdesc) were determined and compared between the two patient groups., Results: TCSasc was significantly higher in the FH group when compared to the NFH group (30.6± 59 vs 4.7±13.4, p＜0.001. After adjusting for age, sex, smoking, blood pressure, history of diabetes mellitus and LDL cholesterol levels, FH gene mutation was an independent risk factor of having non-zero TCSasc 3.6 (95% CI, 1.4-9.5, p＜0.01), high TCSasc 9.6 (95% CI, 2.4-38.2, p＜0.01) and high CCS of 4.1 (95% CI, 1.2-13.2. p＜0.05)., Conclusion: We found that when computed tomography calcium scores were used as an assessment, patients with familial hypercholesterolemia displayed an increased burden of ascending aorta atherosclerosis when compared to patients with nonfamilial severe hypercholesterolemia. This phenomenon appears to be more dependent on the presence of FH genotype than hypercholesterolemia itself.

The aim of this study was to assess the relationship between 24 h blood pressure (BP) profile, extent of significant coronary artery stenosis, confirmed by coronary angiography, and cardiovascular events in patients with coronary artery disease. Coronary angiographies were performed for all included subjects and significant coronary artery stenosis was considered as ≥ 50% stenosis by atherosclerotic plaque. Twenty-four-hour ambulatory BP monitoring was performed. Major advanced cardiovascular events (MACE) included revascularization, cardiovascular mortality, total mortality, acute coronary syndromes and stroke. BP analysis revealed higher night-time systolic blood pressure (SBP) values in patients with three or more significant coronary artery stenoses than in those without significant stenosis (120.7 ± 16.4 vs 116.7 ± 14.3 mmHg,p < 0.001), lower night-time SBP dip in patients with three or more significant coronary artery stenoses than in those without significant stenosis (5.7 ± 3.2 vs 7.4 ± 6.8 mmHg,p < 0.001) and lower night-time diastolic blood pressure dip in patients with three or more significant stenoses than in patients without significant stenosis (9.4 ± 7.4 vs 11.9 ± 7.4 mmHg,p < 0.001). Night-time SBP values, night-time/daytime SBP dip and extent of significant coronary artery stenosis were risk factors for MACE, revascularization and cardiovascular mortality. In conclusion, the study shows that advanced coronary artery disease is related to blunted night-time BP dipping and cardiovascular complications. [ABSTRACT FROM AUTHOR]

The objective of the present study was to analyse the potential synergistic influence of the insertion/deletion polymorphism of the angiotensin-converting enzyme gene (I/D ACE) and the A1166C polymorphism of the angiotensin-II type 1 receptor gene polymorphisms (A1166C AT1R) on the left ventricular size and performance. Three hundred sixty and one consecutive, Caucasian patients with angiographically confirmed coronary artery disease (CAD) were enrolled into the study. Left ventricular diameter, mass and function were evaluated by echocardiography. Screening for the I/D ACE and A1166C AT1R genotypes was performed by polymerase chain reaction of genomic DNA, followed by restriction enzyme digestion and agarose gel electrophoresis. The I/D ACE and A1166C AT1R genotypes separately were not significantly associated with the left ventricular size and function parameters in CAD patients. However, trends towards decreased left ventricular ejection fraction (LVEF) as well as increased left ventricular end-diastolic diameter (LVEDD) and left ventricular mass index (LVMI) were observed when patients with genotype DD+CC/AC and DD+CC were compared to patients homozygous only in one locus (DD or CC). Significant increase in LVEDD and LVMI was observed only in patients with a history of anterior myocardial infarction with combined genotype DD+CC/AC or DD+CC. This study does not support the role of the ACE I/D and AT1R A1166C polymorphisms in the determination of the left ventricular size and performance in patients with significant coronary atherosclerosis. However, it indicates that the influence of polymorphisms may be present in specific patient populations. [ABSTRACT FROM AUTHOR]