scholarly journals Age and blood pressure goal in women with prior coronary events

2020 ◽  
Vol 7 ◽  
pp. 100059
Author(s):  
Luis M. Ruilope ◽  
Gema Ruiz-Hurtado
2015 ◽  
Vol 29 (1) ◽  
pp. 39-45 ◽  
Author(s):  
Sante D. Pierdomenico ◽  
Anna M. Pierdomenico ◽  
Roberta Di Tommaso ◽  
Francesca Coccina ◽  
Silvio Di Carlo ◽  
...  

2018 ◽  
Vol 6 (10) ◽  
pp. 889-890
Author(s):  
Mostafa Ghanim ◽  
Maxwell Eyram Afari ◽  
Lana Tsao

2022 ◽  
Vol 18 ◽  
Author(s):  
McCall Walker ◽  
Paras Patel ◽  
Osung Kwon ◽  
Ryan J Koene ◽  
Daniel A. Duprez ◽  
...  

Abstract: Hypertension is one of the most well-established risk factors for atrial fibrillation. Long-standing untreated hypertension leads to structural remodeling and electrophysiologic alterations causing an atrial myopathy that forms a vulnerable substrate for the development and maintenance of atrial fibrillation. Hypertension-induced hemodynamic, inflammatory, hormonal, and autonomic changes all appear to be important contributing factors. Furthermore, hypertension is also associated with several atrial fibrillation-related comorbidities. As such, hypertension may represent an important target for therapy in atrial fibrillation. Clinicians should be aware of pitfalls of the blood pressure measurement in atrial fibrillation. While the auscultatory method is preferred, the use of automated devices appears to be an acceptable method in the ambulatory setting. There are pathophysiologic bases and emerging clinical evidence suggesting the benefit of renin-angiotensin system inhibition in risk reduction of atrial fibrillation development particularly in patients with left ventricular hypertrophy or left ventricular dysfunction. A better understanding of hypertension’s pathophysiologic link to atrial fibrillation may lead to the development of novel therapies for the primary prevention of atrial fibrillation. Finally, future studies are needed to address optimal blood pressure goal to minimize the risk of atrial fibrillation-related complications.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Panafidina ◽  
T V Popkova ◽  
D S Novikova

Abstract Background Nephritis in systemic lupus erythematosus (SLE) is a factor contributing to early development of atherosclerosis (AS). Objectives The aim of the study is to determine differences in cardiovascular risk factors and AS in SLE pts with and without lupus nephritis (LN). Methods The study included 162 females, age 35 [26–43] years (median [interquartile range 25–75%])) with SLE (ACR,1997). We divided SLE pts on two groups, comparable in age: the 1st group is the pts with LN (n=84, 52%), the 2nd - without LN (n=78, 48%). We considered traditional factors of cardiovascular disease (CVD): (smoking, family history of CVD, blood pressure, cholesterol (total, HDL, LDL) and triglyceride (TG) levels, body mass index, diabetes mellitus) and SLE-related factors (age at onset, duration, clinical features, SLE Disease Activity Index (SLEDAI-2K) and the Systemic Lupus International Collaborating Clinics damage index (SLICC/DI), treatment with steroids); intima-media thickness (IMT) and the 10-year risk for coronary events. Carotid intima-media wall thickness of common carotid arteries was measured by high resolution B-mode ultrasound. The 10-year risk for coronary events was estimated by the Framingham risk equation. Results Median SLE duration was 8,0 [2,3–17,0] years, SLEDAI 2K – 8 [3–16], SLICC/DI score – 2 [0–3], duration of prednisone treatment – 72 [26–141] months. SLE pts from the 1st group had higher prevalence of hypertension (61% vs 36%, p<0,01), systolic blood pressure (130 [110–150] vs 120 [110–130]mm Hg, p<0,01), diastolic blood pressure (80 [70–95] vs 70 [70–80] mm Hg, p<0,05), TG concentration (136 [98–184] vs 100 [61–162] mg/dl, p<0,01), Framingham Risk Score (5 [1–30] vs 1 [1–27]%, p<0,05), SLEDAI-2K (12 [5–19] vs 4 [2–10], p<0,ehz745.08501), SLICC/DI score (2 [0–4] vs 0 [0–2], p<0,01), prednisone therapy duration (95 [26–192] vs 44 [14–98] months, p<0,05), prednisone cumulative dose (34,4 [13,6–82,5] vs 15,7 [6,2–35,2] g, p<0,001), mean IMT (0,73 [0,65–0,83] vs 0,67 [0,61–0,75] mm, p<0,01), than the pts from the 2nd group. There is no difference in CVD frequency in these groups (17% vs 8%, p=0,084). Conclusions SLE patients with and without LN had no difference in frequency of clinical manifestations of AS (CVD), but had a greater value of mean IMT, Framingham Risk Score and a higher incidence of both traditional (hypertension, TG concentration) and SLE-related (disease activity, prednisone therapy) risk factors for AS.


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