HIV causes structural heart
disease according to research presented at EuroEcho-Imaging 2013 by Dr Nieves
Montoro from Madrid, Spain. The findings support the idea of introducing
cardiovascular screening in all HIV patients, particularly those with a
positive blood viral load. Dr Montoro said: “It is well known that patients
with HIV have a high incidence of structural heart disease (mainly diastolic
dysfunction and pulmonary hypertension) as measured by echocardiography but the
reason is not clear. We decided to conduct a study to evaluate whether the
stage of HIV or the detectable blood viral load were related to the degree of
heart disease”. The prospective cohort study included 65 HIV patients (63%
male, average age 48 years) who had dyspnea graded as >II on the NYHA scale.
The stage of HIV was determined by the CD4 count and the presence of opportunistic
diseases.
The viral blood load was also determined. Patients underwent a
transthoracic echocardiogram to assess whether they had structural heart
disease (ventricular hypertrophy, systolic or diastolic dysfunction, or
pulmonary hypertension). Several cardiovascular risk factors were assessed:
hypertension, diabetes, smoking status, dyslipidemia and renal failure. Nearly
half of patients (47%) had some form of structural heart disease, mainly left
ventricular hypertrophy, left ventricular dysfunction, pulmonary hypertension
and signs of right ventricle failure.
Patients with a positive blood viral load
had a significantly higher incidence of structural heart disease than those
with an undetectable load (75% vs 43%, p <0.04), independent of their cardiovascular
risk profile or type of antiretroviral therapy. Dr Montoro said: “We found that
half of HIV patients with dyspnea had echocardiographic evidence of structural
heart disease. Our most interesting finding was that patients with a positive
blood viral load had a significantly higher incidence of structural heart
disease. In fact, having a detectable blood viral load nearly doubled the
prevalence of heart disease, suggesting that HIV itself might be an independent
causal agent.”
The amount of structural
heart disease was not affected by whether or not the patient had AIDS, their
gender, age, or presence of cardiovascular risk factors, although these are
still preliminary results and will have to be confirmed in further analysis.
The findings open the door to the hypothesis that HIV is involved in the
etiology of cardiac damage. It is known that HIV can produce a pro-inflammatory
response and this could involve the heart too. We are conducting further
studies to test this idea.” She added: “One of the main objectives in HIV
treatment is that blood virus levels are undetectable. When this is not
achieved, the treatment is usually changed. Our findings show that having any
detectable level of virus in the blood nearly doubles the risk of heart
disease.”
Dr Montoro continued: “Because of the high incidence of cardiac
problems in our study (almost 50%) we think that all HIV patients with dyspnea
should undergo a transthoracic echocardiogram to check for structural heart
disease. She concluded: “Detecting cardiac problems in HIV patients sooner
using a simple diagnostic tool like echocardiography will enable us to treat
them in the very early stage of the heart damage and improve their prognosis.
Patients found to have a detectable blood viral load and/or structural heart
disease should have closer follow up by a cardiologist and their HIV specialist
doctor.”