Abstract Data support that hypertension (HTN) is prevalent among human immunodeficiency virus (HIV) patients contributing to increased risk of cardiovascular disease. Immunodeficiency and prolonged antiretroviral treatment along with common risk factors including older age, male gender, and high body mass index might conduce to greater incidence of HTN. The purpose of this review was to summarize recent evidence of the increased cardiovascular risk in these patents linking HIV infection to HTN. blood pressure, cardiovascular disease, HIV, hypertension Human immunodeficiency virus (HIV) patients are facing several non-HIV comorbidities including cardiovascular disease (CVD) that usually occurs earlier compared with non-HIV individuals.1,2 The risk of CVD is attributed to immunodeficiency, antiretroviral drugs, family history of coronary artery disease, and traditional cardiovascular risk factors such as age, smoking, hypertension (HTN), and dyslipidemia.1 In Europe and the United States, patients with HIV infection have a 1.5-fold increased risk of myocardial infarction (MI) compared with uninfected counterparts.3 In terms of HTN, it is still debatable whether there is a higher prevalence in HIV subjects or not. In addition, the exact relationship of antiretroviral treatment (ART) to blood pressure (BP) remains unclear. The aim of this review was to summarize recent evidence linking HIV infection and both CVD and HTN. RISK FACTORS IN HIV PATIENTS Both modifiable and nonmodifiable risk factors are present among HIV individuals contributing to CVD. In a total of 394 HIV subjects in England, 62% were 40 years of age or older, 37% had family history of coronary artery disease, 14% had HTN, 3% had diabetes mellitus, 20% had body mass index (BMI) higher than 26 kg/m3, and 18% had high cholesterol levels.4 According to a cross-sectional analysis of Data Collection on Adverse Effects of Anti-HIV Drugs (D:A:D) study, 25% of HIV patients were in an older age group (over 45 years for males; over 55 years for females), 11.4% had family history of coronary artery disease, more than 8% had HTN, and 2.5% had diabetes mellitus.5 The prevalence of CVD risk factors by age and gender was also investigated in Swiss HIV Cohort Study (SHCS). The most common risk factors were smoking (57%), low high-density lipoprotein cholesterol (37%), hypertriglyceridemia (36%), and HTN (26%). Among hypertensive HIV patients, the minority was younger than 40 years old.6 Given the fact that the prevalence of HTN in general population is approximately 30%, the aforementioned data do not clearly demonstrate higher prevalence of HTN among HIV patients.7 PATHOPHYSIOLOGY HIV infection and following inflammation might contribute to the development of atherosclerosis and thus to increased risk of CVD. The activation of endothelial cells promotes the expression of adhesion molecules and proinflammatory cytokines. In turn, monocytes/macrophages and T-cells are attracted and the former phagocytize oxidized low-density lipoprotein leading to foam cell formation and development of atherogenic plaque.8,9 During HIV infection, proinflammatory cytokines are elevated promoting the migration of monocytes/macrophages and thereby the HIV-related atherosclerosis. Furthermore, viral proteins such as Tat and Nef proteins are produced in T-cells and monocytes modifying their function. Tat protein can cause endothelial dysfunction and secretion of chemokine monocyte chemoattractant protein 1 accumulating the monocytes into the vascular intima. Nef protein influences the normal function of ATP-binding cassette transporter A1 damaging cholesterol efflux from infected macrophages and subsequently accelerating foam cells formation.8,9 Proportions of activated T-cells might be higher among HIV patients promoting the progressive CD4+ T-cell loss even without measurable viremia. Chronic immune activation might also contribute to the endothelial activation. In the plaques, T-cells produce proatherogenic mediators inducing the development of lesions and worsening atherosclerosis. During ART, the virus remains in a latent state in immune cells and incorporates into the host genome triggering molecular mechanisms such as oxidative stress, endoplasmic reticulum stress, inflammasome activation, and autophagy inhibition conducive to atherosclerosis.8 Higher levels of inflammatory markers including C-reactive protein, interleukin-6, and tumor necrosis factor have been reported among HIV individuals. Numerous immune activation markers such as soluble CD163, CXCL10, CD14+, and CD16+ monocytes are also elevated promoting the development of noncalcified coronary artery plaques. In addition, higher levels of interleukin-6, D-dimer, soluble tumor necrosis factor receptor I, and soluble tumor necrosis factor II have been correlated with the occurrence of MI and stroke after 1 year of ART exposure.10 The noncalcified coronary artery plaques represent an early stage of atherosclerosis and are considered as more vulnerable plaques. Studies have revealed the higher prevalence of subclinical coronary atherosclerosis and noncalcified plaques in HIV individuals.11,12 Imaging study using coronary computed tomography angiography showed that 59% of infected men had coronary atherosclerosis compared with uninfected subjects (34%).11 Abnormalities in platelet function might also contribute to the increased incidence of CVD events in infected population. HIV-related thrombocytopenia could be attributed to the peripheral platelet destruction and the reduced production of platelets by the infected megakaryocytes.9,13 HIV AND CVD The risk of CVD in HIV patients is more complex than in general population and is causally associated with traditional risk factors along with CD4+ T-cell count and ART. In this context, several studies investigated the relationship between HIV infection, ART, and CVD since the early 2000s (Figure 1).14–19 Figure 1. View largeDownload slide Risk factors of HTN and CVD. Abbreviations: ART, antiretroviral treatment; BMI, body mass index; CVD, cardiovascular disease; HIV, human immunodeficiency virus; HTN, hypertension. Figure 1. View largeDownload slide Risk factors of HTN and CVD. Abbreviations: ART, antiretroviral treatment; BMI, body mass index; CVD, cardiovascular disease; HIV, human immunodeficiency virus; HTN, hypertension. An observational study showed significantly higher hospitalization rates for CVD among HIV patients compared with uninfected individuals.14 In addition, data from the Veterans Aging Cohort Study (VACS) revealed that HIV infection was associated with a 50% increased risk of MI in HIV veterans while having the same baseline Framingham risk score as uninfected veterans.17 CVD is a major cause of death in infected population. In a large observational study of HIV patients in Europe and North America, CVD deaths were responsible for 6.5% of total deaths. Similarly, 8% of deaths among HIV adults in France and 15% of deaths in a North American HIV outpatient study were correlated with CVD.20–22 The HIV Outpatient Study (HOPS) investigated the relationship between immunodeficiency and incidence of CVD. CD4+ T-cell count below 500 cells/mm3 was considered as an independent risk factor for CVD.15 Likewise, another cohort study demonstrated that even lower CD4+ T-cell count (<200 cells/mm3) increased further the risk of MI. However, infected subjects with CD4+ T-cell below 500 cells/mm3 did not have excess risk compared with uninfected counterparts. The incidence of MI was independent of the exposure to protease inhibitors (PIs) or nonnucleoside reverse-transcriptase inhibitors (NNRTIs).16 Nevertheless, no association between risk of MI and low CD4+ T-cell count was found in a substudy of D:A:D. On the other hand, long-term exposure to ART was correlated with increased incidence of CVD. The relative rate per year of exposure to PIs was 1.16, whereas for NNRTIs it was 1.05.18 Another substudy of D:A:D demonstrated that among antiretroviral drugs, cumulative exposure to indinavir or lopinavir-ritonavir and recent exposure to abacavir or didanosine were associated with higher risk of MI.19 Conversely, 2 studies revealed that exposure to abacavir was not associated with excess ACS or cerebrovascular events among HIV patients.23,24 The interruption of ART might also contribute to elevated CVD event rates. The Strategies for Management of Anti-Retroviral Therapy (SMART) trial showed that consistent use of ART is superior to its episodic use as guided by the CD4+ T-cell count. More CVD events occurred in the group of patients with episodic therapy.25 HIV AND HTN Several studies have demonstrated that HTN in HIV population is correlated with older age, male gender, hypertriglyceridemia, diabetes mellitus, high BMI, low CD4+ T-cell count, and long-term exposure to ART (Table 1).26–32 However, these data remain conflicting. Table 1. Studies that investigated the risk factors of HTN in HIV population Study Year Patients Findings Seaberg et al. 2005 5,578 Prolonged ART Palacios et al. 2006 95 Prolonged ART Arruda Junior et al. 2010 958 Older age, male gender, high BMI, hypertriglyceridemia, prolonged ART, low CD4+ T-cell count Medina-Torne et al. 2011 707 Older age, high BMI, diabetes mellitus, long duration of HIV Diouf et al. 2012 242 Older age, male gender, high BMI, hypertriglyceridemia Okeke et al. 2016 3,141 High BMI, low eGFR, diabetes mellitus, prolonged ART, low CD4+ T-cell count Rodriguez-Arboli et al. 2017 834 Older age, high BMI, low eGFR Study Year Patients Findings Seaberg et al. 2005 5,578 Prolonged ART Palacios et al. 2006 95 Prolonged ART Arruda Junior et al. 2010 958 Older age, male gender, high BMI, hypertriglyceridemia, prolonged ART, low CD4+ T-cell count Medina-Torne et al. 2011 707 Older age, high BMI, diabetes mellitus, long duration of HIV Diouf et al. 2012 242 Older age, male gender, high BMI, hypertriglyceridemia Okeke et al. 2016 3,141 High BMI, low eGFR, diabetes mellitus, prolonged ART, low CD4+ T-cell count Rodriguez-Arboli et al. 2017 834 Older age, high BMI, low eGFR Abbreviations: ART, antiretroviral treatment; BMI, body mass index; eGFR, estimated glomerular filtration rate; HIV, human immunodeficiency virus View Large According to a study that compared HIV and control groups, HIV individuals had significantly higher proportions of HTN (21% vs. 16%), dyslipidemia (23% vs. 18%), and diabetes mellitus (12% vs. 7%).26 Nonetheless, another study found no significant difference of HTN between HIV patients (13.1%) and controls (13.5%). By gender, 16% of men and 7% of women with HIV had HTN, similar to the 15% of men and 9% of women in the control group, respectively.27 In both studies, mean age was similar between the 2 groups. In a solely HIV cohort of 958 patients, 26% were hypertensive. Of those, the majority was older than 40 years old. Traditional risk factors, such as age over 40 years, male gender, BMI greater than 25 kg/m3, high triglyceride levels, CD4+ T-cell count below 200 cells/mm3, and exposure to ART for more than 1 year were associated with the presence of HTN. Nonetheless, no correlation between HTN and antiretroviral drugs was found.28 In a prospective study of 834 normotensive HIV patients, 10% developed HTN during a medium follow-up period of 144 days. Traditional risk factors including age over 50 years and BMI higher than 25 kg/m2 along with estimated glomerular filtration rate below 60 ml/min contributed significantly to the elevated risk of HTN. Then again, no association between HTN and immunological status or ART was reported.29 Existing evidence suggests that prolonged therapy contributes to the development of HTN. Although only 7% of HIV patients were hypertensive before initiating ART, the prevalence of HTN was 26% after 48 weeks of treatment. High systolic BP was observed in 26% and high diastolic BP in 18%. The mean raise in systolic BP was 8 mm Hg and that in diastolic BP was 5 mm Hg.30 Likewise, another large cohort study of 5,622 HIV men showed that exposure to ART for more than 2 years was significantly correlated with HTN, particularly among African American and former smokers.31 In another study, 24% of normotensive HIV patients developed HTN during a median follow-up time of 5.5 years. The incidence rate of HTN increased each year, especially among individuals that were on ART for 5 years or more. Diabetes mellitus, renal insufficiency, high BMI, and CD4+ T-cell count below 500 cells/mm3 conduced to increased risk of HTN.32 Based on a cross-sectional study, only 6% of HIV patients were hypertensive before the initiation of ART, whereas 28% of them had HTN 9 years later. Patients over 45 years of age were more likely to have HTN. Male gender, BMI higher than 25 kg/m2 at treatment initiation, and hypertriglyceridemia were also associated with higher risk of HTN, but differences were not statistically significant. Longer duration of indinavir exposure increased the risk of HTN, whereas longer exposure to lopinavir-ritonavir reduced it.33 Conversely, another cross-sectional study showed that HTN was not significantly correlated with ART. The prevalence of HTN was similar among those receiving and not receiving ART (32% vs. 29%). Factors related to HTN were older age, long duration of HIV infection, high BMI, and diabetes mellitus.34 HTN TREATMENT IN HIV PATIENTS In the absence of specific guidelines for the management of HTN among HIV patients, evidence supports the use of current recommendations available for the general population. The American College of Cardiology (ACC) and the American Heart Association (AHA) have recently issued revised guidelines on the management of HTN.35 The appropriate management of HTN should include lifestyle changes such as weight loss if needed, aerobic exercise, diet low in total and saturated fat, salt restriction, and limitation in alcohol consumption. Pharmacological therapy must be initiated if either BP is not controlled with lifestyle modifications after several months or CVD risk and/or BP levels are significantly elevated at diagnosis. The recommended BP target is less than 130/80 mm Hg.35 Interactions between antiretroviral and antihypertensive drugs might occur and depend on their pharmacokinetic characteristics. In this context, the choice of antihypertensive drugs should be individualized. Antiretroviral agents are metabolized by cytochrome P450 isoenzymes and thereby, drugs interactions are less reported with diuretics, b-blockers excreted by the kidney, angiotensin-converting enzyme inhibitors (ACEIs), and angiotensin II receptor blockers (ARBs) other than losartan and irbesartan.36 Coadministration of propranolol or metoprolol with PIs might raise the plasma concentrations of b-blockers prolonging their therapeutic effect. On the other hand, no significant interactions between NNRTIs that are CYP3A4 inducers and b-blockers have been mentioned, since b-blockers are mainly metabolized by CYP2D6.36 CCBs might interact with both NNRTIs and PIs. However, if they must be prescribed, decrease of initial dose and titrate up while monitoring is required. Side effects including hypotension, conduction block, bradycardia, and peripheral edema have been mentioned.36,37 Diuretics and ACEIs are not involved in significant CYP450-mediated interactions with antiretroviral drugs. Of ARBs, only losartan and ibresartan are metabolized by CYP2C9. Drugs that inhibit CYP2C9, such as efavirenz or etravirine, might decrease their efficacy. Moreover, losartan is thereafter metabolized by CYP3A4; thus, PIs that are CYP3A4 inhibitors should be used with caution.36 CONCLUSIONS Available data are still inconclusive whether the prevalence of HTN is higher among HIV patients or not. However, HTN in HIV population seems to be associated with older age, male gender, high BMI, low CD4+ T-cell count, and prolonged ART. As a major CVD risk factor, HTN should be treated following the same guidelines as in general population. 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American Journal of Hypertension – Oxford University Press
Published: Apr 1, 2018
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