Pitavastatin versus pravastatin in adults with HIV-1 infection and dyslipidaemia (INTREPID): 12 week and 52 week results of a phase 4, multicentre, randomised, double-blind, superiority trial

Aberg, Judith A.; Sponseller, Craig A.; Ward, Douglas J.; Kryzhanovski, Vladimir A.; Campbell, Stuart; Thompson, Melanie

doi:10.1016/s2352-3018(17)30075-9

Cited by 77 publications

(56 citation statements)

References 28 publications

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“…Statins have been shown to effectively reduce LDL in HIV, with specific effects shown for rosuvastatin 99 and pitavastatin, which was superior to pravastatin in the HIV-infected Patients and Treatment with Pitavastatin vs Pravastatin for Dyslipidemia (INTREPID) study. 100 In this study, pitavastatin also significantly decreased key indices of inflammation and immune activation, sCD14, oxidized LDL (oxLDL), and lipoprotein-associated phospholipase 2 (Lp-PLA2) to a greater extent that pravastatin. 101 In a multisite, randomized trial of lipid reduction strategies, rosuvastatin more effectively reduced total and LDL cholesterol when compared with switching off a PI.…”

Section: Management and Prevention Of Ischemic Heart Disease In Hivmentioning

confidence: 57%

Epidemiology of ischemic heart disease in HIV

Triant

Grinspoon

2017

Current Opinion in HIV and AIDS

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Purpose of review The purpose of this review is to summarize and synthesize recent data on the risk of ischemic heart disease (IHD) in HIV-infected individuals. Recent findings Recent studies in the field demonstrate an increasing impact of cardiovascular disease (CVD) on morbidity and mortality in HIV relative to AIDS-related diagnoses. Studies continue to support an approximately 1.5 to 2-fold increased risk of IHD conferred by HIV, with specific risk varying by gender and virologic/immunologic status. Risk factors include both traditional CVD risk factors and novel, HIV-specific factors including inflammation and immune activation. Specific antiretroviral therapy (ART) drugs may increase CVD risk, yet the net effect of ART with viral suppression is beneficial with regards to CVD risk. Management of cardiovascular risk and prevention of CVD is complex, because current general population strategies target traditional CVD risk factors only. Extensive investigation is being directed at developing tailored CVD risk prediction algorithms and interventions to reduce CVD risk to HIV. Summary Increased IHD risk is a significant clinical and public health challenge in HIV. The development and application of HIV-specific interventions to manage CVD risk factors and reduce CVD risk will improve the long-term health of this aging population.

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Section: Management and Prevention Of Ischemic Heart Disease In Hivmentioning

confidence: 57%

Epidemiology of ischemic heart disease in HIV

Triant

Grinspoon

2017

Current Opinion in HIV and AIDS

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“…59 In a randomized, double-blind comparison study in 252 subjects with HIV, pitavastatin 4 mg/d reduced LDL-C by 31% and pravastatin 40 mg/d reduced LDL-C by 21%, with similar low rates of adverse events in the 2 treatment groups. 60 Levels of soluble CD14, oxidized LDL-C, and lipoproteinassociated phospholipase 2 were significantly lower in the pitavastatin group compared with the pravastatin group. 61 As with other patients, statins should be the mainstay of lipid-lowering drug therapy for persons living with HIV.…”

Section: Treating Lipids In Hiv Patientsmentioning

confidence: 87%

Lipid Abnormalities in Persons Living With HIV Infection

Waters

Hsue

2019

Canadian Journal of Cardiology

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Lipid abnormalities are prevalent among persons living with HIV infection and contribute to increasing the risk of cardiovascular events. Antiretroviral therapy (ART) is associated with lipid abnormalities, most commonly hypertriglyceridemia, but also increases in low-density lipoprotein cholesterol and total cholesterol. Different classes of ART, and different drugs within classes, have differing effects on lipid levels, but in general newer drugs have more favourable effects compared with older ones. Low-level inflammation and chronic immune activation act on lipids through a variety of mechanisms to make them more atherogenic. As a consequence, risk is higher than would be expected for any given cholesterol level. Clinical outcome trials of cholesterollowering therapies have not yet been completed in people living with HIV, so that treatment decisions depend on extrapolation from studies in uninfected populations. Traditional risk assessment tools underestimate cardiovascular risk in individuals with HIV. Statins are the mainstay of lipid-lowering drug treatment; however, drugedrug interactions with ART must be considered.

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“…Statins, which are both lipid-lowering and anti-inflammatory, were used in the INTREPID (HIV+ Patients and Treatment with Pitavastatin vs Pravastatin for Dyslipidemia) and the current REPRIEVE (Randomized Trial to Prevent Vascular Events in HIV) trial. Data from INTREPID have shown that pitavastatin was superior to pravastatin in LDL reduction after 12 weeks of therapy in HIV + individuals with dyslipidemia (124). The REPRIEVE trial is ongoing, and recruiting HIV + patients between 40 and 75 years of age who are taking an antiretroviral regimen, who have no known CVD or substantial kidney or liver disease, and have a CD4 + cell count higher than 100/µl (125).…”

Section: Clinical Trials Of Hiv-associated Atherosclerosismentioning

confidence: 99%

HIV-1–Associated Atherosclerosis

Kearns

Gordon

Burdo

et al. 2017

Journal of the American College of Cardiology

135

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Cardiovascular disease, including atherosclerosis and atherosclerosis-associated complications, is an increasing cause of morbidity and mortality in HIV patients in the post-antiretroviral therapy era. HIV alone accelerates atherosclerosis. Antiretroviral therapy, HIV-associated comorbidities, such as dyslipidemia, drug abuse, opportunistic infections, and lifestyle, are risk factors for HIV-associated atherosclerosis. However, our current understanding of HIV-associated atherogenesis is very limited and largely obtained from clinical observation. There is a pressing need to experimentally unravel the missing link between HIV and atherosclerosis. Understanding these mechanisms will help to better develop and design novel therapeutic interventions for the treatment of HIV-associated cardiovascular disease. HIV mainly infects T cells and macrophages resulting in the induction of oxidative and endoplasmic reticulem stress, the formation of the inflammasome, and the dysregulation of autophagy. These mechanisms may contribute to HIV-associated atherogenesis. In this review, we will summarize our current understanding and propose potential mechanisms of HIV-associated atherosclerosis.

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Pitavastatin versus pravastatin in adults with HIV-1 infection and dyslipidaemia (INTREPID): 12 week and 52 week results of a phase 4, multicentre, randomised, double-blind, superiority trial

Cited by 77 publications

References 28 publications

Epidemiology of ischemic heart disease in HIV

Epidemiology of ischemic heart disease in HIV

Lipid Abnormalities in Persons Living With HIV Infection

HIV-1–Associated Atherosclerosis

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