Heart Disease and Stroke Statistics—2009 Update

Lloyd‐Jones, Donald M.; Adams, Robert J.; Carnethon, Mercedes R.; Simone, Giovanni de; Ferguson, T. Bruce; Flegal, Katherine M.; Ford, Earl S.; Furie, Karen L.; Go, Alan S.; Greenlund, Kurt J.; Haase, Nancy; Hailpern, Susan M.; Ho, Michael; Howard, Virginia J.; Kissela, Brett M.; Kittner, Steven J.; Lackland, Daniel T.; Lisabeth, Lynda D.; Marelli, Ariane J.; McDermott, Mary M.; Meigs, James B.; Mozaffarian, Dariush; Nichol, Graham; O’Donnell, Christopher J; Roger, Véronique L.; Rosamond, Wayne D.; Sacco, Ralph L.; Sorlie, Paul D.; Stafford, Randall S.; Steinberger, Julia; Thom, Thomas; Wasserthiel-Smoller, Sylvia; Wong, Nathan D.; Wylie‐Rosett, Judith; Hong, Yuling

doi:10.1161/circulationaha.108.191261

Cited by 1,689 publications

(477 citation statements)

References 537 publications

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“…cholesterol represent a major risk factor that leads to coronary heart disease, the main cause of death and morbidity worldwide (1). LDL particles are cleared mainly from the bloodstream by the hepatic cell surface LDL receptor (LDLR) (2).…”

mentioning

confidence: 99%

Dissection of the Endogenous Cellular Pathways of PCSK9-induced Low Density Lipoprotein Receptor Degradation

Poirier

Mayer

Poupon

et al. 2009

Journal of Biological Chemistry

237

185

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Elevated levels of plasma low density lipoprotein (LDL)-cholesterol, leading to familial hypercholesterolemia, are enhanced by mutations in at least three major genes, the LDL receptor (LDLR), its ligand apolipoprotein B, and the proprotein convertase PCSK9. Single point mutations in PCSK9 are associated with either hyperor hypocholesterolemia. Accordingly, PCSK9 is an attractive target for treatment of dyslipidemia. PCSK9 binds the epidermal growth factor domain A (EGF-A) of the LDLR and directs it to endosomes/ lysosomes for destruction. Although the mechanism by which PCSK9 regulates LDLR degradation is not fully resolved, it seems to involve both intracellular and extracellular pathways. Here, we show that clathrin light chain small interfering RNAs that block intracellular trafficking from the trans-Golgi network to lysosomes rapidly increased LDLR levels within HepG2 cells in a PCSK9-dependent fashion without affecting the ability of exogenous PCSK9 to enhance LDLR degradation. In contrast, blocking the extracellular LDLR endocytosis/degradation pathway by a 4-, 6-, or 24-h incubation of cells with Dynasore or an EGF-AB peptide or by knockdown of endogenous autosomal recessive hypercholesterolemia did not significantly affect LDLR levels. The present data from HepG2 cells and mouse primary hepatocytes favor a model whereby depending on the dose and/or incubation period, endogenous PCSK9 enhances the degradation of the LDLR both extraand intracellularly. Therefore, targeting either pathway, or both, would be an effective method to reduce PCSK9 activity in the treatment of hypercholesterolemia and coronary heart disease.

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mentioning

confidence: 99%

Dissection of the Endogenous Cellular Pathways of PCSK9-induced Low Density Lipoprotein Receptor Degradation

Poirier

Mayer

Poupon

et al. 2009

Journal of Biological Chemistry

237

185

View full text Add to dashboard Cite

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“…Trends in the population burden of cardiovascular disease (CVD) and associated lifestyle factors differ between regions of the world [20–23]. Studies of the temporal association of these patterns suggest that changes in lifestyle factors precede the change in CVD outcomes.…”

Section: Discussionmentioning

confidence: 99%

Treatment of acute myocardial infarction in the sub-arctic region of Norway. Do we offer an equal quality of care?

Norum

Hovland

Balteskard

et al. 2017

International Journal of Circumpolar Health

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Patients, relatives, healthcare workers and administrators are concerned about the quality of care offered. We aimed to explore the treatment of acute myocatrdial infarction (AMI) in Northern Norway, compare it with the national figures, and document whether there is an equal quality of care or not. The retrospective study included data on patients' treatment for AMI. The following sources were employed. The Norwegian Patient Registry, National Quality of Care Database, Norwegian Myocardial Infarction Registry and data from the National Air Ambulance Services of Norway. The period 2012-2014/15 was studied and the variables were: incidence of AMI, gender and age adjusted rates of AMI and revascularization (PCI, CABG) based on patient's place of living (according to hospital catchment area) and 30-day survival rate. The annual incidence of AMI was 9% higher in the northern region. Significant incidence variations (2.7–5.9 AMI/1000 inhabitants) between the hospitals' catchment areas were revealed. The 30-day survival rate varied between 85.1–92.1% between hospitals. The variation in revascularization/AMI rate was 0.72–1.54. Air amublance services' availability varied through the day. In conclusion, significant variations in the AMI rate and an unequal service within the region was revealed.

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“…In Canada, an estimated 8 million deaths are caused by CVD [3]. In the United Kingdom, an estimated 245,000 deaths occur as a result of CVD [4]. The burden of CVD is not only affecting developed countries, instead the burden is worldwide.…”

Section: Introductionmentioning

confidence: 99%

Common Modifiable and Non-Modifiable Risk Factors of Cardiovascular Disease (CVD) among Pacific Countries

Mohammadnezhad¹,

Mangum²,

May³

et al. 2016

WJCS

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Introduction: Modifiable and non-modifiable risk factors contribute to the significant rise of non-communicable diseases (NCDs), most notably cardiovascular disease (CVD), in the Pacific Island nations. The aim of this study is to review previously published articles to understand common modifiable and non-modifiable risk factors of CVD among Pacific countries. Methods: This systematic review is conducted using different databases including; Scopus, Medline, EMBASE, and psycINFO. This systematic review is based on the Cochrane review process. All articles published in the English language from 1 st January 2000 to 1 st September 2016, will be included in the study. After reviewing all of the articles' titles, abstracts, and full text, the final articles were reviewed and the relevant data was included in the data extraction sheet. A descriptive analysis was conducted to measure the common risk factors of CVD in Pacific countries. Results: Overall, 45 articles met the inclusion criteria of the study. The results showed that age was the most common non-modifiable risk factor while diabetes, high blood lipid, and high blood pressure were the most common modifiable risk factors of CVD. There were only three interventional studies which had all of the significant influences in reducing the risk factors of CVD when the results were compared with the control group. Conclusion: While it is not possible to change the non-modifiable risk factors for CVD, we encourage policy makers to use the results of this study to develop health promotion strategies to address the modifiable risk factors for CVD. Interventional strategies are highly recommended in the Pacific countries to tackle the modifiable risk factors for CVD.

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Heart Disease and Stroke Statistics—2009 Update

Cited by 1,689 publications

References 537 publications

Dissection of the Endogenous Cellular Pathways of PCSK9-induced Low Density Lipoprotein Receptor Degradation

Dissection of the Endogenous Cellular Pathways of PCSK9-induced Low Density Lipoprotein Receptor Degradation

Treatment of acute myocardial infarction in the sub-arctic region of Norway. Do we offer an equal quality of care?

Common Modifiable and Non-Modifiable Risk Factors of Cardiovascular Disease (CVD) among Pacific Countries

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