Guidelines on cardiovascular risk reduction in HIV-infected patients have been published and generally follow those for the general population ((96),(97),98). It is important to highlight the treatment of atherogenic dyslipidemia frequently found in HIV-infected patients taking cART. Serum concentrations of lipids, particularly triglycerides, should be evaluated in the fasting patient before cART is started, at 3 to 6 months after initiation, and then yearly in the absence of abnormalities. National Cholesterol Education Program III guidelines should be applied to HIV-infected patients, as suggested by other guidelines for the management of dyslipidemia in HIV-infected patients ((96),(97),(98),99). Lipid-lowering therapy should be prescribed with caution in HIV-infected patients because of the potentially severe interaction between statins and fibrates, as well as PIs (Table 6). Several statins are metabolized via the cytochrome P450 (CYP) 3A4 pathway. PIs and ritonavir mainly inhibit CYP and could increase the toxicity of some statins (Table 6). NNRTIs (e.g., efavirenz) are inducers of CYP and could reduce statin efficacy. In the HIV-infected patient taking a PI, if a statin is prescribed (e.g., for primary or secondary prevention in the high-risk patient), the preferable choice is pravastatin, fluvastatin, low-dose atorvastatin, or low-dose rosuvastatin, as these statins have a low risk for interaction with PIs ((99),(100),101). Pitavastatin—a new statin not metabolized by the CYP 3A4 isozyme and primarily excreted unchanged in the bile with little renal elimination—has not been evaluated in this context but could present a therapeutic option; this statin has not, however, shown any clinical benefit in randomized trials (102). Whether a PI should be switched to an NNRTI or to a new drug such as integrase or chemokine (C-C motif) receptor 5 (CCR5) inhibitors when dyslipidemia is present, to avoid adjunctive therapy with a statin, is debatable. In fact, physicians treating HIV-infected patients have several therapeutic options in this context: to continue PI therapy and add a statin or to switch the PI to an NNRTI or a novel drug such as an integrase inhibitor. No trials comparing the 2 strategies in terms of cardiovascular prevention have been performed. The impact on lipids of switching from first-generation NRTIs to second-generation NRTIs is low (as they are less proatherogenic), and the associated beneficial impact on CHD is unknown. Fibrates should be prescribed when the triglyceride concentration is above 500 mg/dL ((96),(97),98). In this case, the measurements of non–high-density lipoprotein cholesterol, apolipoprotein B, or both may be useful because low-density lipoprotein cholesterol measurement may underestimate the true CHD risk, especially in lipodystrophic patients. Ezetimibe may be useful and well tolerated in achieving the low-density lipoprotein goal in association with a statin (103), as HIV-infected patients are susceptible to muscular pain before statin prescription. However, no clinical benefit of ezetimibe has been shown in the general population except for patients with chronic kidney disease in primary prevention (104). The risk–benefits ratio of treating HIV-infected patients with dyslipidemia is unknown. Male patients age >45 years and female patients >55 years with hypertension and/or diabetes and/or familial premature CHD are candidates for lipid-lowering therapy. In secondary prevention, whether PI therapy should be discontinued after an ACS and cART switched, if virologically possible, to a drug class with a better “atherogenic profile,” needs further investigation. Finally, statins as potent lipid-lowering drugs and major agents in primary and secondary cardiovascular prevention, along with their properties to reverse PI-related senescence of cells and accumulation of prelamin A in vitro (74) and inflammation in vivo (105), need to be tested in a large study of primary prevention in HIV-infected patients.