Chronic obstructive pulmonary disease (COPD) increases the
risk of heart attack in people with HIV, US researchers reported at the Conference on Retroviruses and Opportunistic Infections (CROI 2019) in Seattle this week.
COPD refers to chronic lung disease that causes breathing
difficulties (including emphysema and bronchitis). COPD tends to be progressive
and is mainly caused by smoking.
COPD is one of the most common chronic diseases in people
with HIV, with recent studies estimating that around one in ten people with HIV
may suffer from COPD. Even after adjusting for smoking, a recent meta-analysis
found that people with HIV had a 15% higher risk of suffering from COPD. HIV
may cause direct damage to the lungs or may raise the risk of other infections
that lead to lung damage.
As COPD is a progressive condition, it is likely that the
prevalence will increase where the average age of the population living with
HIV is rising, as in North America, Europe and Australasia.
Severe COPD is associated with an increased risk of myocardial
infarction (heart attack) in the general population. However, previous studies have
not shown an increased rate of heart attack in people with HIV, even through
subclinical markers of cardiovascular risk in people with HIV are elevated in
people with COPD.
Researchers from the University of Washington, Seattle, investigated
whether COPD raised the risk of heart attack, especially type 2 heart attacks
in which the vessels in the heart contract rather than becoming blocked by a
ruptured plaque. Type 2 heart attacks are more common in younger people,
cocaine users and people not judged to be at high risk of cardiovascular disease,
and in people suffering from sepsis.
They looked at the risk in 22,596 people with HIV included
in the CNICS cohort, which covers eight large HIV clinics in the United States.
They identified COPD cases according to clinical definition and receipt of at
least 90 days of COPD controller medication, and two reviewers evaluated
potential myocardial infarctions, categorising them as probable type 1 or type
2 events.
The prospective review identified 895 people with COPD at
baseline and 415 people diagnosed with COPD during a median follow-up period
of 3.44 years. People with COPD at baseline were older than those without
COPD (47 vs 40) and had a lower nadir CD4 count (211 vs 271). They were more likely
to smoke (48% vs 25%), to have hypertension (21% vs 12% and to be taking statins
(14% vs 7%).
People who developed COPD during follow-up had a median age
of 45 at baseline and had a similar frequency of cardiovascular risk factors to
those who did not have COPD, but were almost as likely to smoke as those who already
had COPD (45%). They had accumulated 5.25 pack-years of smoking history when follow-up
began compared to 10 pack-years in those who already had COPD. Nevertheless, it
is worth noting that just over half the people in this study who had COPD had
never smoked.
A total of 704 heart attacks occurred during the
follow-up period (55% type 1). Around two-thirds of the type 2 heart attacks
were not the result of sepsis (201/314).
After adjustment for smoking and duration of smoking, people
with COPD were twice as likely to suffer a heart attack during the follow-up period
(aHR 2.02, 95% CI 1.61-2.70). The risk of type 2 heart attack was higher than
the risk of type 1 heart attack, after adjusting for smoking duration (aHR
2.65, 95% CI 1.82-3.86, vs aHR 1.73, 95% CI 1.21-2.48).
The researchers also explored possible reasons for the
association, especially the possibility that heart attacks are linked to exacerbation
of COPD due to sub-optimal disease control.
People who had a heart attack appeared more likely to be
using a short-acting inhaler at their last visit before heart attack (45% vs
15% on long-acting), but over a third were not receiving any medication to
control COPD at the time of heart attack. But investigators said it was still
unclear if inadequate COPD control was raising the risk of heart attack, or if
other factors such as inflammation and pneumonia also play a role.
More research is needed into the mechanisms leading to a
raised risk of heart attack, and into preventative and therapeutic strategies.