CE: Swati; COH/120603; Total nos of Pages: 5;

COH 120603

REVIEW

CURRENT
OPINION HIV and myocarditis
Ntobeko A.B. Ntusi a,b,c

Purpose of review
The purpose of this article is to review the literature on HIV and myocarditis and HIV-associated heart
failure.
Recent findings
Currently, 17 million people are receiving antiretroviral therapy (ART) globally. There is a decrease in
mortality from HIV in the last decade with increased survival in those receiving ART. HIV-associated cardiac
failure is on the increase, with more cases of diastolic dysfunction reported in the ART era. The
pathophysiology of HIV-associated myocarditis is multifactorial. Cardiovascular magnetic resonance (CMR),
through tissue characterization, demonstrates increased native T1 values which reflect both increased
myocardial inflammation and fibrosis in HIV infection.
Summary
HIV-associated myocarditis is common and may be an important cause of HIV-associated cardiac failure.
CMR is an important imaging modality for the study of myocardial inflammation.
Keywords
AIDS, cardiovascular magnetic resonance, heart failure, HIV, myocarditis

INTRODUCTION With many people surviving with HIV for many

The latest Joint United Nations Programme on HIV/ years, chronic noncommunicable disorders have
AIDS data, covering 160 countries, demonstrate become an important cause of morbidity and mor-
&&

that just in the last 2 years, the number of people
living with HIV on antiretroviral therapy (ART) has
increased by about a third, reaching 17.0 million
people – 2 million more than the 15 million by
2015 target set by the United Nations General Assem-
tality [4 ]. HIV-associated cardiovascular disease
(CVD) involves every segment of the cardiovascular
tree and commonly affects all layers of the heart,
including the myocardium, valves, pericardium and
coronary, pulmonary, cerebrovascular and peri-
&&

bly in 2011 – refer to Table 1 for abbreviations [1]. pheral vasculature [4 ].

Since the first global treatment target was set in 2003,
annual AIDS-related deaths have decreased by 43%.
In the world’s most affected region, eastern and
southern Africa, the number of people on treatment
has more than doubled since 2010, reaching nearly
10.3 million people. AIDS-related deaths in the region
have decreased by 36% since 2010 [1]. However, huge
challenges lie ahead: In 2015, there were 2.1 million
new HIV infections worldwide, adding up to a total of
36.7 million people living with HIV globally [1].
The survival of people living with HIV/AIDS has
dramatically increased since the widespread use of
ART [2,3]. Global coverage of ART reached 46% at
the end of 2015 [1]. Gains were greatest in the
world’s most affected region. South Africa alone
had nearly 3.4 million people on treatment, more
than any other country in the world. After South
Africa, Kenya has the largest treatment programme
in Africa, with nearly 900 000 people on treatment
at the end of 2015 [1].
Myocardial inflammation and myocarditis are
likely the most studied causes of HIV-associated
heart disease and heart failure in HIV-infected per-
sons not on ART. The incidence of HIV-associated
myocarditis appears to be on the decline in the ART
era. In contrast, the incidence of HIV/AIDS-related
heart failure is on the increase, and current evidence
suggests that diastolic, rather than systolic,
a
Division of Cardiology, Department of Medicine, University of Cape
Town and Groote Schuur Hospital, bThe Cape Universities Body Imaging
Centre and cThe Hatter Institute for Cardiovascular Research in Africa,
Department of Medicine, University of Cape Town, Cape Town, South
Africa
Correspondence to Ntobeko A.B. Ntusi, Head and Chair, Department of
Medicine, University of Cape Town and Groote Schuur Hospital, Main
Road, Observatory, 7925 Cape Town, South Africa.
Tel: +27 214066200; fax: +27 214486815; e-mail: ntobeko.ntusi@uct.ac.za
Curr Opin HIV AIDS 2017, 12:000–000
DOI:10.1097/COH.0000000000000416

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COH 120603
Cardiovascular disease in HIV-infected persons
KEY POINTS
 Currently, 17 million people are receiving
ART worldwide.
 There is a decrease in mortality from HIV in the last
decade with increased survival in those receiving ART.
 HIV-associated cardiac failure is on the increase, with
more cases of diastolic dysfunction reported in the
ART era.
 The pathophysiology of HIV-associated myocarditis
is multifactorial.
 CMR is an ideal technique for the study of HIV-
associated myocarditis, through its tissue
characterization and ability to demonstrate both
myocardial inflammation and fibrosis.
dysfunction is the predominant form of heart failure
in the era of ART [5–7]. The pathophysiology of
heart failure in HIV-infected persons is multifacto-
rial and includes presence of traditional risk factors,
myocardial inflammation, opportunistic infections,
myocardial fibrosis, coronary artery disease, pericar-
dial disease, impaired vascular compliance, myocar-
dial steatosis, pulmonary vascular and renal disease
&& &
[4 ,8,9 ,10]. It is timely to place into perspective
the evolving concepts and comprehension of HIV-
associated myocarditis and heart failure through sys-
tematic review and critical appraisal of the literature.
EPIDEMIOLOGY OF HIV-ASSOCIATED
HEART FAILURE
A meta-analysis of 11 studies conducted during the
ART era assessed 2242 well controlled, asymptom-
atic HIV-infected persons who had a prevalence of
systolic dysfunction of 8.3% and diastolic dysfunc-
tion of 43.4% [5]. Risk factors for systolic dysfunc-
tion included elevated high-sensitivity C-reactive
protein more than five, tobacco use and prior myo-
cardial infarction (MI); for diastolic dysfunction,
Table 1. Abbreviations
AIDS ¼ acquired immunodeficiency syndrome
ART ¼ antiretroviral therapy
CMR ¼ cardiovascular magnetic resonance
CVD ¼ cardiovascular disease
DCM ¼ dilated cardiomyopathy
EMB ¼ endomyocardial biopsy
HIV ¼ human immunodeficiency virus
UNAIDS ¼ the Joint United Nations Programme on HIV/AIDS
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risk factors were hypertension and older age [5].
In the Heart of Soweto Study, designed to investigate
the impact of the HIV/AIDS on de-novo manifesta-
tions of heart disease, 518 of 5328 cases (9.7%) of
newly diagnosed heart disease were HIV infected
[11]. Of those, almost 29% had systolic dysfunction,
and 38% had HIV-associated cardiomyopathy; the
incidence of coronary artery disease was 2.7% [11].
The DAD study recently published a follow-up
of trends in all-cause mortality and specific causes of
death in people with HIV from 1999 to 2011 and
found that the crude incidence mortality rate was
12.7 per 1000 person-years, with leading causes of
death being AIDS-related (29%), non-AIDS-defining
cancers (15%), liver disease (13%) and CVD (11%)
[12]. A study of 81 000 people, a third of whom were
HIV-infected in the Veterans Aging Cohort Study
Virtual Cohort, reported that acute MI was com-
monly associated with HIV, especially in those
with prehypertension and hypertension during
&&
the 6-year follow-up period [13 ]. Another recent
report on risk of non-AIDS-defining events among
HIV-infected persons not yet on ART found that
CVD and other non-AIDS complications were higher
in those with a CD4 count less than 200 cells/ml and
was related to degree of immunodeficiency rather
&&
than HIV RNA levels [14 ]. Two recently published
meta-analyses, including observational and random-
ized controlled trial data, have reported that HIV-
associated coronary artery and cerebrovascular dis-
ease is common [15,16]. Moreover, compared with
HIV-uninfected populations, the relative risk (RR) of
events was higher both for untreated and ART-treated
HIV-infected persons [RR ¼ 1.61 (1.43–1.81) and
RR ¼ 2.00 (1.70–2.37), respectively]. Moreover, the
RR was higher for protease inhibitor-based therapies
versus nonprotease inhibitor treatments.
HIV-ASSOCIATED MYOCARDITIS
A myocarditis directly due to HIV has been
described, but the virus appears to infect the myo-
cardial cells in a patchy distribution [17], without a
clear association between HIV viral load and cardi-
omyocyte dysfunction. However, myocarditis in
HIV may be related to other microorganisms. For
instance, Mycobacterium tuberculosis [18], Mycobacte-
rium avium [18], Toxoplasma gondii [19], Cryptococcus
neoformans [20], Histoplasma capsulatum [21], Herpes
simplex [22], Parvovirus [22], cocksackievirus B3 [23]
and Cytomegalovirus [17] have been described as
causes of myocarditis and pericarditis in HIV infec-
tion. In an autopsy series performed in the pre-ART
era, myocarditis was documented in 40–52% of
patients who died of AIDS [17,24]. In more than
80% of these patients, no specific aetiologic factor
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was found, whereas the remaining cases were attrib-
utable to above-mentioned infectious agents. In
another historic study of HIV-associated cardiomy-
opathy, endomyocardial biopsy (EMB) revealed
myocarditis with cardiotropic viral infection in
almost all cases [25].
In a seminal study, Shaboodien et al. [26] have
compared the prevalence of myocarditis and cardio-
tropic viral genomes in HIV-associated cardiomyop-
athy cases with HIV-negative idiopathic dilated
cardiomyopathy (DCM) patients and heart trans-
plant recipients using EMB and the immunohisto-
logical criteria of the World Heart Federation in 33
patients. In this study, myocarditis was present in
44% of HIV-associated cardiomyopathy cases, 36% of
heart transplant recipients and 25% of participants
with idiopathic DCM. Although myocarditis was
acute in 50% of HIV-associated and heart- trans-
plant-associated myocarditis, it was chronic in all
those with idiopathic DCM. Cardiotropic viral infec-
tion was present in all HIV-associated cardiomyopa-
thy and idiopathic DCM cases and in 90% of heart
transplant recipients. Multiple viruses were identified
in the majority of cases, with HIV-associated cardio-
myopathy, heart transplant recipients and idiopathic
DCM patients having an average of 2.5, 2.2 and 1.1
viruses per individual, respectively [26].
A recent cardiovascular magnetic resonance
(CMR) publication has revealed that HIV-infected
person had lower left ventricular (LV) ejection frac-
tion, higher LV mass, lower peak diastolic strain and
strain rates and higher native T1 values, a measure of
&&
myocardial inflammation and fibrosis [27 ]. Pericar-
dial effusions and focal fibrosis on late gadolinium
enhancement (LGE) CMR were more common in
&&
HIV-infected persons [27 ]. Similarly, another publi-
cation revealed that lower LV ejection fraction, lower
global circumferential and longitudinal strain, native
FIGURE 1. Cardiovascular magnetic resonance image of myocarditis in HIV. Phase-sensitive inversion recovery late
gadolinium enhancement cardiovascular magnetic resonance image showing linear midwall fibrosis in the inferolateral and
anterior walls in short-axis (a), vertical long-axis (b) and horizontal long-axis views (c).
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HIV and myocarditis Ntusi
T1 values and positive LGE CMR were much more
&&
common in HIV-infected patients [28 ].
HIV-ASSOCIATED CARDIOMYOPATHY
HIV has long been recognized as a significant
cause of acquired cardiomyopathy [29]. The current
prevalence of HIV-associated cardiomyopathy is
substantially lower in industrial countries compared
with the pre-ART era, mainly due to the ease of
access to ART and reduction in opportunistic infec-
&&
tions [4 ,30]. In the era of ART, the epidemiology of
HIV-associated cardiomyopathy has changed sub-
stantially; however, very few studies have measured
the incidence at a population level in recent times.
In The Heart of Soweto Study, cardiomyopathy was
reported in 38% of HIV-infected patients studied,
comprising systolic and diastolic dysfunction in both
symptomatic and asymptomatic patients [11]. Path-
ologic features of HIV-associated cardiomyopathy are
similar to those observed in HIV-uninfected patients
with DCM [31]. The macroscopic pathological
features include dilated cardiac chambers with endo-
cardial fibrosis and mural thrombus. Histologically,
there is evidence of myocyte hypertrophy and degen-
eration, with increased interstitial and endocardial
fibrillar collagen and evidence of prior myocarditis
[31]. Echocardiography is the first-line imaging
modality for diagnosis of HIV-associated cardiomy-
opathy and is useful for assessment of LV systolic
function and for looking for wall motion abnormali-
ties, as well as assessment of diastolic function and
differential diagnosis. CMR, where available, should
always be considered and provides an accurate
assessment of ventricular morphology and function,
myocardial fibrosis, myocardial oedema, LGE and
prognosis as well as comprehensive assessment of
differential diagnosis (Fig. 1). EMB, although not
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Cardiovascular disease in HIV-infected persons
FIGURE 2. Pathophysiology of HIV-associated myocarditis and heart failure.
routinely performed, remains the gold standard
tool for diagnosis of the aetiologic agent of the
HIV-associated cardiomyopathy.
PATHOPHYSIOLOGY OF HIV-ASSOCIATED
CARDIAC FAILURE AND MYOCARDITIS
The pathophysiology of HIV-associated heart failure
is multifactorial. Postulated mechanisms include
consequences of direct HIV infection and toxicity
of HIV components, opportunistic infections and
autoimmunity [32,33]. Increased myocardial inflam-
mation, endothelial dysfunction, capillary leak syn-
drome and abnormal coagulation have also been
implicated in the pathophysiology (Fig. 2) [34,35].
HIV-associated wasting disease, malignancies and
nutritional deficiencies have also been associated
with cardiovascular abnormalities in HIV-infected
persons [36,37]. There is increasing evidence of the
importance of myocardial fibrosis and steatosis in
&
driving cardiovascular dysfunction in HIV [8,9 ]. In
the DAD study of 4000 HIV-infected persons and over
1 million HIV-uninfected controls, hypertension,
diabetes, dyslipidaemia and smoking were all found
more commonly in the HIV-infected cohort [38].
PROGNOSIS OF HIV-ASSOCIATED
MYOCARDITIS
The prognosis of HIV-associated myocarditis in the
pre-ART era was poor with high rates of progression
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to heart failure, DCM and premature mortality
[17,24,25]. However, reduction in incidence of
opportunistic infections in HIV-infected persons
receiving ART may be responsible for the impressive
drop in myocarditis rates and declining prevalence of
mortality and DCM, seen in high-income countries.
CONCLUSION
The HIV pandemic appears to be under control.
Although the recorded cases of HIV-associated car-
diomyopathy appear to be on the decrease, the
incidence of HIV-associated cardiac failure is on
the increase. CMR, through tissue characterization,
is able to detect both increased myocardial inflam-
mation and fibrosis in HIV and may be a useful
tool to track disease activity in HIV-associated
myocarditis.
Acknowledgements
N.A.B.N. gratefully acknowledges support from the
National Research Foundation, the Medical Research
Council of South Africa and the Harry Crossley Founda-
tion.
Financial support and sponsorship
None.
Conflicts of interest
There are no conflicts of interest.
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COH 120603
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