Reducing residual vascular risk in patients with atherogenic dyslipidemia: where do we go from here?

Hermans, Michel P.; Fruchart, Jean‐Charles

doi:10.2217/clp.10.65

Cited by 25 publications

(46 citation statements)

References 134 publications

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“…Given the continuous progression of the obesity pandemic and worldwide rising rates of metabolic syndrome, identifying and impacting upon RCVR in patients benefiting from current, evidence-based standards of care is increasingly becoming an unmet need in CV risk reduction [1,10,11]. Current guidelines for standards of care emphasize the importance of multifactorial intervention to achieve recommended levels of LDL-C, blood pressure and, in diabetic patients, glycemic control [12][13][14].…”

Section: Residual Cardiovascular Risk In Lipid Lowering Trialsmentioning

confidence: 99%

“…• A substantial fraction of RCVR remains modifiable, • A major component of RCVR is lipid-or hypertensionrelated, • RCVR is amenable to reduction through various lifestyle or pharmacologic interventions [1].…”

Section: Residual Cardiovascular Risk In Lipid Lowering Trialsmentioning

confidence: 99%

“…Relative cardiovascular risk reduction after statin therapy is approximately 25-35%, depending on the baseline level of risk. Additional lowering of LDL-C with high-dose statins or the administration of ezetimibe, while allowing for further CV risk reduction and target attainment, leaves out a considerable lipid-related RCVR due to abnormal non-LDL lipid constituents, unaddressed or little improved by statins [1]. A considerable part of poststatin lipid abnormalities associated with RCVR appear to result from abnormal levels of triglyceride (TG)-rich lipoproteins, of their remnants and from a decreased number and/or functionality of HDLs.…”

Section: Residual Cardiovascular Risk In Lipid Lowering Trialsmentioning

confidence: 99%

“…A considerable part of poststatin lipid abnormalities associated with RCVR appear to result from abnormal levels of triglyceride (TG)-rich lipoproteins, of their remnants and from a decreased number and/or functionality of HDLs. [1] These non-LDL lipoproteins are the main effectors of TG transport from liver or gut to TG-consuming organs and of reverse cholesterol transport (RCT). The most prevalent form of non-LDL dyslipidemia is known as atherogenic dyslipidemia or atherogenic dyslipoproteinemia.…”

Section: Residual Cardiovascular Risk In Lipid Lowering Trialsmentioning

confidence: 99%

“…recommendations and state-of-the-art consensuses defining standards of care [1]. The concept clearly derives from interventional trials, mainly the statin trials, and there is a lot of debate about the residual risk conferred by other lipid components, in particular low levels of HDL cholesterol and high levels of triglycerides.…”

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confidence: 99%

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The epidemiological concept of residual risk

Vanuzzo¹

2011

Intern Emerg Med

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Residual cardiovascular risk can be defined as the residual risk of incident vascular events or progression of established vascular damage persisting in patients treated with current evidence-based recommended care including the risk that established from risk factors, such as dyslipidemia, high blood pressure, and the risk related to emerging or newer risk factors. The concept clearly derives from intervention trials, mainly the statin trials, and there is a lot of debate about the residual risk conferred by other lipid components, in particular low levels of HDL cholesterol and high levels of triglycerides. A meta-analysis of 53 fibrates (16,802 subjects) and 30 niacin trials (4,749 subjects) revealed an average HDL-C increase of 10% with fibrates and 16% with niacin, a triglyceride decrease of 36% with fibrates and 20% with niacin, and a LDL-C decrease of 8% with fibrates and 14% with niacin. These lipid changes resulted in similar overall reductions in major coronary events evidenced by a 25% decrease with fibrates and 27% with niacin. However, recent analyses of the primary and secondary prevention trials like JUPITER, Treating to New Targets (TNT) and PROVE-IT TIMI 22 force to reconsider the issue. In these three trials, HDL-C was useful in the initial risk assessment but when LDL-C was aggressively lowered the residual risk predictive value of HDL-C was markedly attenuated. Also epidemiological studies evaluate the residual risk in treated hypertensives and dyslipidemic subjects within a general population. The PRIME study in Northern Ireland and France and the Progetto CUORE study in Italy, both with a 10-year follow-up were able to test the hypothesis of the residual cardiovascular risk in treated hypertensives, because the proportion of treated dyslipidemic subjects was too low at baseline. In both studies treatment with antihypertensive agents was associated with a sizeable residual cardiovascular risk with the hazard ratio of 1.5-1.7, suggesting that more efficient risk reduction strategies in hypertension should be developed as a priority. In conclusion residual cardiovascular risk should be better studied in cardiovascular epidemiology, refining the methods to evaluate it, to consider measures of exposure to the modifiable risk factors and indicators of treatment (both at pharmacological and lifestyle level) over the time. Repeated measures and cohortal follow-up are needed and also new statistical methods are necessary to evaluate the residual risk to understand how to reduce it.

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Section: Residual Cardiovascular Risk In Lipid Lowering Trialsmentioning

confidence: 99%

Section: Residual Cardiovascular Risk In Lipid Lowering Trialsmentioning

confidence: 99%

Section: Residual Cardiovascular Risk In Lipid Lowering Trialsmentioning

confidence: 99%

Section: Residual Cardiovascular Risk In Lipid Lowering Trialsmentioning

confidence: 99%

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confidence: 99%

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The epidemiological concept of residual risk

Vanuzzo¹

2011

Intern Emerg Med

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Colchicine for the primary prevention of cardiovascular events

Martí‐Carvajal

Sanctis

Hidalgo

et al. 2022

Cochrane Database of Systematic Reviews

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ObjectivesThis is a protocol for a Cochrane Review (intervention). The objectives are as follows:To assess the clinical benefit and harms of colchicine as primary prevention of cardiovascular outcomes in the general population. Background Description of the conditionCardiovascular diseases (CVDs) include coronary heart disease (CHD), sudden cardiac death/sudden cardiac arrest, cerebrovascular disease, stroke/transient ischemic attack, rheumatic heart disease, congenital heart disease, deep venous thrombosis, pulmonary embolism, and peripheral arterial disease. From 1990 to 2019, the prevalence of cases of total CVDs has been nearly doubled from 271 million (95% uncertainty interval: 257 to 285 million) to 523 million (95% UI: 497 to 550 million), respectively (Roth 2020). In addition, it has been estimated that CVDs caused 18.6 million (95% uncertainty interval: 17.1 to 19.7 million) deaths in 2019 (Roth 2020). Doubtlessly, CVDs yield a high socioeconomic burden in the general population (Flora 2019).The main cause of CVDs is atherosclerosis which is the result of cellular-molecular interactions in the artery wall (Gotlieb 1991); therefore, it is a chronic inflammatory disease with autoimmune foundations (

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