| 1. |
- Back, M, et al.
(författare)
-
Biomarkers in Mitral Regurgitation
- 2017
-
Ingår i: Progress in cardiovascular diseases. - : Elsevier BV. - 1873-1740 .- 0033-0620. ; 60:3, s. 334-341
-
Tidskriftsartikel (refereegranskat)
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
- Björck, Martin, et al.
(författare)
-
Pathophysiology of AAA : Heredity vs Environment
- 2013
-
Ingår i: Progress in cardiovascular diseases. - : Elsevier BV. - 0033-0620 .- 1873-1740. ; 56:1, s. 2-6
-
Forskningsöversikt (refereegranskat)abstract
- Abdominal aortic aneurysm (AAA) has a complex pathophysiology, in which both environmental and genetic factors play important roles, the most important being smoking. The recently reported falling prevalence rates of AAA in northern Europe and Australia/New Zeeland are largely explained by healthier smoking habits. Dietary factors and obesity, in particular abdominal obesity, are also of importance. A family history of AAA among first-degree relatives is present in approximately 13% of incident cases. The probability that a monozygotic twin of a person with an AAA has the disease is 24%, 71 times higher than that for a monozygotic twin of a person without AAA. Approximately 1000 SNPs in 100 candidate genes have been studied, and three genome-wide association studies were published, identifying different diverse weak associations. An example of interaction between environmental and genetic factors is the effect of cholesterol, where genetic and dietary factors affect levels of both HDL and LDL. True epigenetic studies have not yet been published.
|
|
| 6. |
- Bouchard, Claude, et al.
(författare)
-
Personalized Preventive Medicine : Genetics and the Response to Regular Exercise in Preventive Interventions
- 2015
-
Ingår i: Progress in cardiovascular diseases. - : Elsevier BV. - 0033-0620 .- 1873-1740. ; 57:4, s. 337-346
-
Tidskriftsartikel (refereegranskat)abstract
- Regular exercise and a physically active lifestyle have favorable effects on health. Several issues related to this theme are addressed in this report. A comment on the requirements of personalized exercise medicine and in-depth biological profiling along with the opportunities that they offer is presented. This is followed by a brief overview of the evidence for the contributions of genetic differences to the ability to benefit from regular exercise. Subsequently, studies showing that mutations in TP53 influence exercise capacity in mice and humans are succinctly described. The evidence for effects of exercise on endothelial function in health and disease also is covered. Finally, changes in cardiac and skeletal muscle in response to exercise and their implications for patients with cardiac disease are summarized. Innovative research strategies are needed to define the molecular mechanisms involved in adaptation to exercise and to translate them into useful clinical and public health applications.
|
|
| 7. |
|
|
| 8. |
- Khawaja, Tasveer, et al.
(författare)
-
Coronary artery calcium, hepatic steatosis, and atherosclerotic cardiovascular disease risk in patients with type 2 diabetes mellitus: Results from the Dallas heart study
- 2023
-
Ingår i: Progress in cardiovascular diseases. - : W B SAUNDERS CO-ELSEVIER INC. - 0033-0620 .- 1873-1740. ; 78, s. 67-73
-
Forskningsöversikt (refereegranskat)abstract
- Introduction: Cardiovascular disease (CVD) risk amongst those with type 2 diabetes (T2D) is heterogenous. The role of imaging-based cardiometabolic biomarkers (e.g., coronary artery calcium [CAC] score, and hepatic triglyceride content [HTC]) in CVD risk stratification in T2D is unclear. To better understand this, we sought to evaluate the individual and joint associations between CAC and hepatic steatosis (HS) with clinical atherosclerotic CVD (ASCVD) in Dallas Heart Study (DHS) participants with and without T2D. Methods: We examined participants in the DHS, a multi-ethnic cohort study, without self-reported ASCVD. CAC scoring was performed via computed tomography with the mean of two consecutive scores used. HTC was measured using magnetic resonance spectroscopy, and HS was defined as HTC >5.5% The primary outcome was incident ASCVD, defined as coronary heart disease (CHD; myocardial infarction, percutaneous coronary intervention, or coronary artery bypass graft surgery), ischemic stroke, transient ischemic attack, or CVD death. Cox regression analyses, and interaction testing was performed to evaluate the individual and joint associations between CAC and HS with ASCVD. The association between HS and coronary heart disease was validated in the UK Biobank (UKB).Results: A total of 1252 DHS participants were included with mean age 44.8 & PLUSMN; 9.3 years, mean body mass index 28.7 & PLUSMN; 5.9 kg/m2, 55% female, and 59% black with an overall prevalence of T2D of 9.7%. CAC scores were significantly higher (p < 0.01) and HS was significantly more prevalent in those with T2D (p < 0.01). Over a median of 12.3 years, 8.3% of participants experienced ASCVD events. The ASCVD event rate was significantly higher in participants with T2D (20.5% vs 7.0%, p < 0.01). Continuous CAC was associated with ASCVD events in the overall cohort regardless of T2D status with a significant interaction present between CAC and T2D status on ASCVD, Pinteraction = 0.02. HTC was not associated with ASCVD risk in participants without T2D but was inversely associated with risk in participants with T2D (HR 0.91, 95% CI 0.83-0.99 per 1% increase in HTC, p = 0.02), Pinteraction = 0.02. Amongst 37,266 UKB participants, 4.5% had T2D. CHD events occurred in 2.2% of participants, with 10.2% of events occurring amongst those with T2D. An inverse relationship between HTC and CHD was also found amongst those with T2D in UKB with a significant interaction between T2D status and HTC on CHD (HR per 1% increase in HTC 0.95, 95% CI 0.91-0.99, p = 0.01, Pinteraction = 0.02).Conclusions: In the DHS, we found that CAC was associated with ASCVD risk independent of T2D status. We did not observe an association between HTC and ASCVD in participants without T2D, but there was an inverse association between HTC and ASCVD in those with T2D that was replicated in the UKB cohort. Further investigation is warranted to understand the possible protective association of HS in participants with T2D.& COPY; 2023 Elsevier Inc. All rights reserved.
|
|
| 9. |
|
|
| 10. |
|
|
