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Published on: October 7, 2010
Ventricular Ectopy and Arrhythmia Characteristics for Persons Living with HIV and Uninfected Controls
Alexander Meyer1, Sanjay Dandamudi2, Chad Achenbach1
11 Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Insights
People with HIV (human immunodeficiency virus) do not have a higher risk of ventricular ectopy and tachycardia (VE/VT) compared to uninfected individuals. However, poorer HIV control in HIV+ persons was linked to increased VE/VT odds.
Area of Science:
- Cardiology
- Infectious Diseases
- Electrophysiology
Background:
- Individuals with HIV face increased cardiovascular disease risk.
- Limited data exists on ventricular ectopy and tachycardia (VE/VT) in HIV-infected (HIV+) populations.
Purpose of the Study:
- To assess the prevalence and likely anatomic origin of VE/VT in HIV+ individuals compared to controls.
- To investigate the relationship between HIV control and VE/VT occurrence.
Main Methods:
- Cohort screening using International Classification of Diseases codes.
- Chart review adjudication for positive screens.
- Electrocardiogram analysis to determine VE/VT origin.
Main Results:
- No significant difference in VE/VT prevalence between HIV+ and uninfected persons.
- Worse HIV control correlated with significantly higher odds of VE/VT among HIV+ individuals.
- Exploratory findings suggest a potential higher likelihood of left ventricular origin for VE/VT in HIV+ persons.
Conclusions:
- While poorer HIV control increases VE/VT odds in HIV+ individuals, overall VE/VT prevalence is not higher than in uninfected populations.
- Further research into the specific origins and mechanisms of VE/VT in HIV+ individuals is warranted.
Background:
Persons with HIV have elevated risk for cardiovascular disease, but little is known about the risk of ventricular ectopy and ventricular tachycardia (VE/VT) for HIV-infected (HIV+) persons.
Methods:
We evaluated the presence and anatomic origin of VE/VT for HIV+ persons and controls by screening a cohort using International Classification of Diseases codes and adjudicating positive screens by chart review. We sought to evaluate (1) presence of VE/VT and (2) likely anatomic origin of the VE/VT based on electrocardiogram.
Results:
There was no significant difference in the prevalence of VE/VT for HIV+ or uninfected persons. Among HIV+ persons, worse HIV control was associated with significantly greater odds of VE/VT. Exploratory analyses suggested that HIV+ persons may have a greater likelihood of VE/VT originating from the left ventricle.
Conclusion:
Although worse HIV control was associated with higher odds of VE/VT among persons with HIV, odds of VE/VT were not higher for persons with HIV than uninfected persons.
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