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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 sample. 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
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**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 sample 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
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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 < 0.001). Risk of heart failure was highest among younger age groups, specifically ages
20-29 years old, and decreased with age. HIV-associated risk was also higher amongst females regardless of
age. Furthermore, the prevalence of heart failure was highest amongst HIV-positive patients with CD4 counts
below 200; this prevalence decreased as CD4 count increased. Similarly, prevalence of heart failure was
Color Key:
Yellow: Cohort/Cross Sectional Study
Green: Prevalence/Epidemiology
Blue: Biomarkers/Inflammation-Related
highest amongst HIV-positive patients with higher viral loads and prevalence decreased as viral load
decreased. Risk was marginally lower for HIV-positive patients prescribed ART within the last year compared
to those who were not on any HIV-medication regimen. HIV-positive patients with heart failure that had
sought care from a cardiologist had higher rates of heart failure treatment, but HIV-positive patients overall
were less likely to receive treatment.
Overall, risk of heart failure is nearly 2 times higher in HIV-positive patients compared to HIV-negative
patients. Among HIV-positive patients, younger age groups and females have the highest risk. Those receiving
specialty care from a cardiologist were more likely to receive treatment for heart failure, but HIV-positive
patients were less likely to receive specialty care in general compared to their HIV-negative counterparts.
Heart failure is a significant cause of mortality among HIV-positive patients. The authors of the article suggest
exploring if interventions aimed to reduce chronic inflammation lead to risk reduction.
7. Kuller L, Tracy R, Neaton J, et al.
Inflammatory and coagulation biomarkers
and mortality in patients with HIV infection.
Plos Medicine [serial online]. October 21,
2008;5(10):e203. Available from: MEDLINE
Complete, Ipswich, MA. Accessed December
1, 2016.
This study analyzed six biomarkers (hsCRP, IL-6, amyloid A, amyloid P, D-dimer, and prothrombin fragment
1+2 in connection with all-cause mortality and the effects of continuous versus intermittent ART. The data
analyzed in this study was collected from the SMART trial.
8. Capili B, Anastasi J, Ogedegbe O. HIV and
general cardiovascular risk. The Journal Of
The Association Of Nurses In AIDS Care:
JANAC [serial online]. September
2011;22(5):362- 375. Available from:
This cross-sectional study analyzed the CVD risk of 123 HIV+ adults with no previous cardiovascular
complications or surgeries (MI, angina pectoris, coronary artery bypass graft surgery, coronary angioplasty or
stent placement, symptoms of congestive heart failure, insert of pacemaker or known atrial fibrillation,
stroke, peripheral arterial disease (intermittent claudication), or history of surgery for peripheral arterial
disease.) Results indicated that the only significant gender difference among cardiovascular risk factors was
In previous studies, IL-6 has been evidenced to be associated with HIV-RNA levels among patients with
advanced HIV and CRP has been evidenced to increase over time among HIV+ patients and individuals with
AIDS have greater increases. Results indicated that elevated levels of IL-6 or D-dimer were significantly
associated with all-cause mortality. Both IL-6 and D-dimer were increased in the intermittent ART group
compared to the continuous ART group. Overall, this evidence suggests that inflammation and coagulation
can have a negative effect in all-cause mortality, even among patients with preserved CD4 count. Interrupting
ART can increase IL-C and D-dimer; however, the relationships between IL-6 and D-dimer levels and all-cause
mortality were strong in both ART groups. Out of the 85 deaths that occurred, 21 were classified as CVD or
were unwitnessed. Overall, IL-6 and D-dimer predicted all-cause mortality among HIV+ patients.
Color Key:
Yellow: Cohort/Cross Sectional Study
MEDLINE Complete, Ipswich, MA. Accessed
December 1, 2016.
**Cross Sectional
9. Gupta M, Miller C, Neaton J, et al.
Biomarkers and electrocardiographic
evidence of myocardial ischemia in patients
with human immunodeficiency virus
infection. The American Journal Of
Cardiology [serial online]. March 1,
2013;111(5):760-764. Available from:
MEDLINE Complete, Ipswich, MA. Accessed
December 1, 2016.
**Cross Sectional
10. Currier J, Lundgren J, Smieja M, et al.
Epidemiological evidence for cardiovascular
disease in HIV-infected patients and
relationship to highly active antiretroviral
therapy. Circulation [serial online]. July 8,
2008;118(2):e29-e35. Available from:
MEDLINE Complete, Ipswich, MA. Accessed
December 1, 2016.
Green: Prevalence/Epidemiology
Blue: Biomarkers/Inflammation-Related
abdominal obesity – with women having a greater proportion of abdominal obesity compared to men for
individuals living with HIV from 1 to 10 year and 11 to 20 years, but no differences were found for individuals
loving with HIV for more than 21 years. Longer duration of smoking was also a predictor of increased risk.
Participants who were male, older, had clinical histories of MS (Metabolic Syndrome), DM (Diabetes Mellitus),
or HTN (Hypertension), were more likely to belong to the high-risk group. Overall, 25% of these participants
had a greater than 20% 10-year risk for developing general CVD.
The data analyzed in this study was collected from the SMART trial. Data from this trial had previously been
analyzed in connection to CVD and all-cause mortality, yielding results indicating that baseline biomarkers
levels of hsCRP, IL-6, and D-dimer predicted both CVD and all-cause mortality. This study analyzed these 3
biomarkers in connection to prevalence and incidence of ischemic ECG abnormalities, hypothesizing that
greater levels of these biomarkers would be associated with greater prevalence and incidence.
Results indicated that 19% of the participants had at least one major or minor abnormality and biomarker
levels among these participants were greater than biomarker levels among patients with no abnormalities.
Although this associating was significant before adjusting for covariates, none of the biomarkers remained
significant once adjusting for covariates. Furthermore, although those who later developed incident ECG
abnormalities at follow-up had greater baseline biomarker levels, the associations were not significant on
either unadjusted or adjusted analysis. Overall, this study’s results in connection with previous studies
indicated that biomarkers predict clinical CVD, but not subclinical CVD as measured by ischemic ECG
abnormalities. The authors advise that it is possible that the ECG abnormalities reported reflect cardiac
conditions other than ischemic heart disease. Also, considering that biomarker levels were only captured at a
single point and used for baseline and follow up analyses, it is possible that associations have been
underestimated and did not capture temporary biomarker elevations.
“HIV and ART can contribute to an altered risk of CVD in 3 principal ways: (1) HIV may serve as a marker to
identify a subgroup of the general population with an altered prevalence of traditional cardiovascular risk
factors, unrelated to HIV or ART (eg, HIV-infected patients may have higher smoking rates); (2) HIV or ART
may affect the risk of developing a traditional cardiovascular risk factor (eg, HIV or ART may worsen
dyslipidemia); and (3) HIV or ART may affect the pathogenetic process that leads to CVD in ways other than
via an effect on traditional risk factors (eg, through inflammation or endothelial function).” In other words,
HIV-infected patients may engage in factors connected to traditional CVD risk, thus increasing risk (eg,
smoking); development of factors associated with the HIV virus and/or ART that are also traditional CVD risk
factors may increase risk (eg, HIV/ART may worsen dyslipidemia, which is a CVD risk); and underlying
Color Key:
Yellow: Cohort/Cross Sectional Study
Green: Prevalence/Epidemiology
Blue: Biomarkers/Inflammation-Related
biological mechanisms associated with HIV and/or ART may affect effect traditional risk factors thereby
increasing CVD risk (eg, through effects on inflammation or endothelial function). (p. 1) Although many
studies have demonstrated increased risk among HIV-positive patients, it is not possible to determine the
cause of this increased risk, whether it is specifically the HIV infection or exposure to ART, other HIV-specific
factors or a difference in prevalence of traditional risk factors among HIV-positive patients such as smoking.
Even so, age, smoking, hypertension, and diabetes mellitus are prevalent among HIV-positive patients and
have been evidenced to strong predictors of CVD risk among these patients. Smoking and dyslipidemia in
particular has been evidenced to be consistently prevalent among HIV-positive patients compared to HIVnegative patients.
In 2008, the largest study that had been conducted (DAD) analyzing ART and increased MI risk showed results
pointing to increased risk with increased duration of ART; however absolute risk of CVD would likely remain
low for most patients. Even so, it would be beneficial to analyze the causal relationship of this finding via
randomized, controlled trials. Furthermore, it would be beneficial to determine the relative risk of individual
ART drugs. At that time in 2008, there were a few studies that found evidence suggesting that protease
inhibitor-based ART was significantly associated with MI risk. There has definitely been research conducted
since 2008 following up on this finding.
As of 2008, two questions Professor Gurung hopes to review that were not yet addressed by the studies
reviewed in this article, as indicated by the authors are:
•
11. Serhal M, Longenecker C. Preventing Heart
Failure in Inflammatory and Immune
Disorders. Current Cardiovascular Risk
Reports [serial online]. June
2014;8(8)Available from: MEDLINE
“What is the impact of unmeasured confounding factors, such as intensity of smoking, cocaine use,
concomitant infections, low socioeconomic status, and depression, on the association between HIV
infection and CHD risk?”
• “Is HIV viral replication itself a risk factor? Can this be measured through use of established and
novel markers of inflammation and immune activation?”
Inflammation has been evidenced to be associated with CV afflictions since 1956; some of the inflammatory
biomarkers that have known associations previously evidenced in prior research include: CRP, IL-1, IL-6, IL-18,
and TNF-α. Furthermore, the incidence of CVD is increase among patients with comorbid inflammatory
disorders such as HIV. HIV-infection has been evidenced to be independently associated with about 1.5-fold
higher risk of myocardial infarction and heart failure. Current hypotheses regarding the underlying
Color Key:
Yellow: Cohort/Cross Sectional Study
Complete, Ipswich, MA. Accessed December
1, 2016.
Green: Prevalence/Epidemiology
Blue: Biomarkers/Inflammation-Related
mechanisms in connection to this association focus on the role of residual inflammation and immune
activation. This article focuses on CVD, HIV, and Rheumatoid arthritis. Details below will focus on HIV and
CVD.
Intervention and prevention strategies to reduce the risk of progression to heart failure include life-style
modifications (e.g. weight loss, exercise, and smoking cessation) and pharmacologic therapy for risk factors
(e.g. hypertension, diabetes, and dyslipidemia). A recent trial that that demonstrated effectiveness at
reducing incident of heart failure, left ventricular systolic and diastolic dysfunction is the Screening To Prevent
Heart Failure (STOP-HF) trial, which can also be employed as a strategy.
Exercise: In a small pilot trial of HIV+ patients, a supervised exercise and resistance training program did not
improve MI sensitivity or LV diastolic function; although whether or not continued training would reduce risk
over time is unknown.
Statins: In trials that have been conducted analyzing statin use among HIV+ patients, use of statins have been
associated with significant reductions in total mortality. At the time of this study, several trials were being
conducted to further explore station use among HIV+ patients.
Hypertension: Hypertension is a prevalent issue among HIV+ patients. Several trials have provided evidence
suggesting that Telmisartan effectively reduced blood pressure, improved lipid metabolism and improved
renal function without interfering with ART or being negatively tolerated. However, as of the time of this
study, there had been no clinical trials assessing the effect of RAAS blockade on hard CVD events among HIV+
patients.
Immune Modulating Agents: Immune therapies to reduce inflammation and immune activation have not been
extensively studied among HIV+ populations at the time of this study. Two trials were, however, underway at
the time of publication: one a study assessing Methotrexate and the other assessing IL-6 receptors
antagonists among HIV+ populations.
Although the authors admit that more research is needed before a comprehensive prevention strategy can be
developed, it is important for HIV-providers to refer their patients to CV specialists in order to begin riskprevention.
12. Guaraldi G, Orlando G, Palella F, et al.
Premature age-related comorbidities among
Although HIV-associated morbidity and mortality have decreased considerably with the introduction and
widespread use of effective ART, mortality rates among HIV-infected people remain 3 to 15 times higher than
Color Key:
Yellow: Cohort/Cross Sectional Study
HIV-infected persons compared with the
general population. Clinical Infectious
Diseases: An Official Publication Of The
Infectious Diseases Society Of America
[serial online]. December 2011;53(11):11201126. Available from: MEDLINE Complete,
Ipswich, MA. Accessed December 13, 2016.
Green: Prevalence/Epidemiology
Blue: Biomarkers/Inflammation-Related
that of the general population (p. 1). Despite some of these mortalities being due to the HIV-infection, more
than 50% of these deaths are due to noninfectious comorbidities (NICMs) including cardiovascular disease
(CVD), hypertension (Htn), bone fractures, renal failure, and diabetes mellitus (DM). (p. 1-2) In fact, people
living with HIV tend to have a greater risk of NICMs compared to the general population and these NICMs are
associated with advancing age. Many researchers hypothesize that these NICMs are prevalent among HIV+
patients due to premature aging. (p. 2). This study compared the aforementioned NICMs within a group of
HIV+ patients to a group of age-, sex-, and race-matched HIV- control patients from 2002 through 2009 in
Italy. CVD included the diagnoses of myocardial infarction, stroke, angina pectoris, coronary artery bypass
grafting, and/or angioplasty.
Among the mostly male (63%) sample with an average age of 46 (±8 years), renal failure, bone fractures, and
DM had a significantly higher prevalence among HIV+ patients in all age strata. NICM risk among HIV+ patients
was significantly greater than controls and occurred at younger ages (p < .001 for all NICMs). DM, CVD, bone
fracture, and renal failure remained significantly higher among HIV+ patients after adjustment for sex, age,
and presence of Htn.
Among HIV+ patients across all strata the prevalence of polypathology (Pp), defined as the concurrent
presence of 2 or more NICMs, was significantly higher than controls (all p < .001). The only exception was Pp
prevalence among HIV+ patients 41-50 years old, which did not significantly differ from Pp prevalence among
the controls within same age group (p = .282). The age difference in connection to the risk of Pp “varied from
15 to 12 years for patients aged 40 or 60 years, respectively.” For example, a 40 year old HIV+ patient had a
Pp risk similar to that of a 55 year old control subject and a 60 year old HIV+ patient had a Pp risk similar to
that of a 72 year old control subject. Factors significantly associated with Pp (p
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