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Color Key: Yellow: Cohort/Cross Sectional Study Article Number/AMA Citation/Hyperlink 1. Raposeiras-Roubín S, Triant V. Ischemic Heart Disease in HIV: An In-depth Look at Cardiovascular Risk. Revista Espanola De Cardiologia (English Ed.) [serial online]. November 10, 2016;Available from: MEDLINE Complete, Ipswich, MA. Accessed November 17, 2016. Green: Prevalence/Epidemiology Blue: Biomarkers/Inflammation-Related Summary Cardiovascular (CV) risk is increased in HIV-infected patients. “After adjustment for traditional CV risk factors, HIV-infected patients have a 50% higher risk of CV disease than that in uninfected persons.” This risk is due to (See pg. 3 of article for a figure and details): 1. Factors intrinsic to the patient: a. Non-modifiable Factors: age, sex (males have increased risk of CV disease) b. Modifiable Factors: drug use, poor diet, obesity, high blood pressure levels (HIV-patients tend to have higher blood pressure than others), dyslipidemia – elevated total or low-density lipoprotein (LDL) cholesterol levels, or low levels of high-density lipoprotein (HDL) cholesterol (increased incidence among HIV-patients), insulin resistance and diabetes mellitus (increased incidence among patients using HAART), lipodystrophy – abnormal accumulation of body fat (typical in HIV-patients) 2. Contribution of HIV Infection: The HIV Infection alone, despite general CV risk factors, contributes to CV risk. This risk increases as CD4 cells decrease. The role of HIV in CV disease is based on: a. Immune activation, inflammation and oxidative stress, endothelial dysfunction and vasoconstriction, prothrombotic activity 3. Contribution of Antiretroviral Therapy: ART is associated with increased CV risk, although each drug differs in its contribution. (See Table 2, pg. 5) a. Lipid profile alterations, insulin resistance, lipodystrophy The most common CV disease associated with HIV in developed countries with access to ART is ischemic heart disease. It is recommended that HIV-patients with CV risk over 20% should adjust their HAART, adhere to CV therapeutic objectives, and make appropriate lifestyle changes. These changes are detailed on p. 5. However, it is important to note that drug interactions (ART and drugs associated with CV risk reduction) may have a significant clinical impact. The interactions of these drugs are shown on Tables 4, 5, and 6 within the article. 2. De Socio G, Parruti G, Bonfanti P, et al. Identifying HIV patients with an unfavorable cardiovascular risk profile in the clinical practice: results from the SIMONE study. The Journal Of Infection [serial online]. July 2008;57(1):33-40. Available from: MEDLINE Complete, Ipswich, MA. Accessed November 17, 2016. This study analyzed 1230 HIV+ subjects (71% male) from Italy across 4 different algorithmic estimates of CVD risks. The diagnosis of Metabolic Syndrome (MS) was also analyzed in connection to risk to assess any factors associated with high CV risk. Overall, the Framingham Scale Scores (FRS) provided the highest risk estimates in this sle. Even so, higher FSR was associated with a diagnosis of MS. Lipodystrophy and higher CD4 count were both individually associated with both having a high FRS and having both high FRS and MS. Although higher BMIs were Color Key: Yellow: Cohort/Cross Sectional Study **Cross Sectional 3. Secemsky E, Scherzer R, Hsue P, et al. Novel Biomarkers of Cardiac Stress, Cardiovascular Dysfunction, and Outcomes in HIV-Infected Individuals. JACC. Heart Failure [serial online]. August 2015;3(8):591-599. Available from: MEDLINE Complete, Ipswich, MA. Accessed November 17, 2016. Green: Prevalence/Epidemiology Blue: Biomarkers/Inflammation-Related associated with high FRS or MS, this association was not present among those with both high FRS and MS – possibly due to the small sle size. Smoking was the greatest predictor of high CV risk independent other factors. This study analyzed 4 cardiac biomarkers [ST2, growth differentiation factor (GDF)-15, N terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitivity troponin I (hsTnI)] and 4 non-specific biomarkers [highsensitivity C-reactive protein (hCRP) and Interleukin-6 (IL-6); cystatin C; and D-dimer] in HIV+ patients to assess not only if these biomarkers are elevated in these patients, but also if these biomarkers are associated with cardiovascular dysfunction and all-cause mortality. These biomarkers were assessed because among HIVpatients, these biomarkers have previously been predictive of cardiovascular events and mortality. Results from these study indicated that HIV+ participants had higher levels of all biomarkers except ST2, IL-6, and the prevalence of detectable hsTnI. However, all HIV+ participants exceeded pre-define CVD risk thresholds for ST2, GDF-15, and NT-proBNP. ST2 was significantly associated with DD even after adjusting for demographics and remained significant when adjusting for CVD and HIV-related risk factors, with each doubling of ST2 conferring a 43% risk increase. NT-proBNP and GDF-15 were significantly associated with pulmonary hypertension after adjusting for demographics, with the doubling of each biomarker conferring a 15% and 19% increased risk, respectively. This association remained significant after adjusting for other variable as well. In the fully adjusted analysis, the biomarkers significantly associated with all-cause mortality were ST2, GDF15, hsCRP, and D-dimer. The strong association with all-cause mortality was ST2, with each doubling of ST2 conferring a 104% increased risk. The cause of death for 12 out of the 38 HIV+ patients who died, were cardiovascular-related. Of these 12, 9 patients exceeded pre-defined CVD risk thresholds for either ST2 and/or GDF-15. Considering this, it is possible that non-specific biomarkers are useful markers of global risk for all-cause mortality, but less useful for identifying cardiovascular dysfunction. The authors suggest that cardiovascular health become apart of the regular health maintenance of HIV+ patients and that biomarkers should be further assessed not only in connection to cardiovascular health and Color Key: Yellow: Cohort/Cross Sectional Study Green: Prevalence/Epidemiology Blue: Biomarkers/Inflammation-Related risk, but also to all-cause mortality as some biomarkers may vary in their usefulness for predicting various outcomes. 4. Nemeth C, Bekhbat M, Neigh G. Neural effects of inflammation, cardiovascular disease, and HIV: Parallel, perpendicular, or progressive?. Neuroscience [serial online]. August 27, 2015;302:165-173. Available from: MEDLINE Complete, Ipswich, MA. Accessed November 17, 2016. Please keep in mind that this article is a review, thus all information gained from this article has been cited within the article by other sources. Inflammation plays an important role in the development and progression of various diseases, including cardiovascular disease and HIV. In connection to CVD, the contribution of inflammation to the progression of atherosclerosis and cardiovascular events is slow and less obvious, often remaining undetected until a significant event, such as heart attack or stroke, occurs. This contribution tends to be heightened amongst HIV+ patients, with HIV+ patients suffering from CVD and other inflammatory conditions significant more than the general population despite advanced HIV treatment. Dilated cardiomyopathy, atherosclerosis, myocardial infarction, systemic and pulmonary hypertension, thrombosis and cerebrovascular damage are among the most common cardiovascular comorbidities seen in HIV+ patients. Various studies have also provided evidence that some HIV+ patients also experience somatic symptoms, such as shortness of breath, chest pain, and fatigue, as well as behavioral complications, such as comorbid depression and anxiety. Even when patients use ART, the continuous replication of the virus can lead to increases in pro-inflammatory cytokines such as interleukin-6 (IL-6) and inflammatory biomarkers such as sTNF-R75. Chronic inflammation can lead to perpetuated inflammatory responses and the role of inflammation in almost all aspects of CVD leads to atherosclerosis, increased release of inflammatory biomarkers, ischemic events, depression, and dementia. The combination of chronic inflammation and CVD can accelerates damage to brain functioning and behaviors. Overall, the HIV infection and HIV-related inflammation can accelerate or compound processed that eventually lead to CVD and the combination of these afflictions can lead to further detrimental health consequences. Elevated inflammation is also associated with increased risk for diabetes, blood pressure changes and hypertension. Inflammation can also be triggered by cigarette smoking, hyperglycemia, hypertension, and drug abuse alone. Thus, when combined with inflammation stemming from the HIV infection, creates a continuous loop of increasing inflammation and CVD progression as well as CVD-triggered inflammation. The Color Key: Yellow: Cohort/Cross Sectional Study Green: Prevalence/Epidemiology Blue: Biomarkers/Inflammation-Related state of inflammation can also increase the likelihood of processes associated with CVD. Even with the use of continuous ART, low-grade inflammation of the toxic effects of ART can continue to contribute to this loop. The article discusses how the pathogenesis of HIV leading to CVD and how vascular disease affects the brain/neural processes (i.e. cerebrovascular disease and cerebrovascular immune modulators). Less relevant to the paper topic thus not detailed here, but in the article if needed. 5. Bahrami H, Budoff M, Post W, et al. Inflammatory Markers Associated With Subclinical Coronary Artery Disease: The Multicenter AIDS Cohort Study. Journal Of The American Heart Association [serial online]. June 27, 2016;5(6)Available from: MEDLINE Complete, Ipswich, MA. Accessed November 30, 2016. **Cohort Study/Cross Sectional 6. Al-Kindi S, ElAmm C, Longenecker C, et al. Heart failure in patients with human immunodeficiency virus infection: Epidemiology and management disparities. International Journal Of Cardiology [serial online]. September 1, 2016;218:43-46. Available from: MEDLINE Complete, Ipswich, MA. Accessed November 30, 2016. Although the increased risk of CV abnormalities amongst HIV-infected patients is well-documented, the underlying mechanisms involved in this increased risk are not well understood. However, recent studies have provided evidence that inflammation plays a key role in this increased risk. This study hypothesized that inflammatory biomarkers and coagulation would be higher in HIV-positive patients and correlated with subclinical coronary artery disease (CAD) detected on CT scans. Participants in this study were 923 (575 HIVpositive and 348 negative) gay and bisexual men, ages 40-70 years old, weighing less than 300 pounds, with no prior history of cardiac surgery or percutaneous coronary intervention. Overall, results provided evidence that HIV-positive participants had higher level of inflammatory biomarkers, regardless of viral load. Additionally, “results demonstrate that several inflammatory biomarkers representing different domains of inflammation (IL-6, ICAM-1,sTNFαR I, and sTNFαR II) were significantly associated with a greater prevalence of coronary artery stenosis on CTA in HIV+ men, and these associations were independent of traditional risk factors and HIV clinical factors.” Results “also show that IL-6, sTNFαR I, and sTNFαR II were independently related to extent of coronary artery calcification in HIV+ men.” Overall, HIV-mediated inflammation is evidenced in this study to be an important contributor to CAD. This study analyzed a collection of 12,244,830 adult medical records of patients who had active records in the past year. Of this group, 36,400 patients were HIV-positive and the rest (12,208,430) were HIV negative. HIV patients were more likely to use substances such as tobacco, alcohol, cannabinoids, and cocaine. They were also more likely to have co-morbidities such as diabetes, hypertension, myocardial infarction, peripheral vascular disease, coronary artery disease, and hepatitis B and C. Overall, HIV-positive patients had a significantly higher prevalence rate of heart failure compared to their HIV-negative counterparts (7.2% compared to 4.4%, p

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