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Sudden Cardiac Death in Patients With HIV and Heart Failure
Study Questions:
What is the incidence of sudden cardiac death (SCD) among persons living with human immunodeficiency virus infection (PHIV) with heart failure (HF), who were hospitalized for HF, and the risk factors associated with it?
Methods:
This was a retrospective study of 2,578 patients hospitalized with HF from a single academic center, of whom 344 were PHIV. The primary outcome was SCD. SCD was defined using the standardized definition as death within 1 hour of onset of symptoms if witnessed or within 24 hours of being observed alive and asymptomatic if unwitnessed, or unexpected out-of-hospital death. Subgroup analyses were performed by strata of viral load (VL), and left ventricular ejection fraction (LVEF) <35%, 35-49%, and ≥50%. Categorical data were compared using the chi-square or the Fisher exact test. Survival curves were plotted using Kaplan-Meier curves. Univariate and multivariate analyses (Cox proportional hazard regression adjusting for confounding factors such as age, beta-blocker use, CD4 count, cocaine use, and history of coronary artery disease [CAD]), electrocardiographic parameters, and LVEF were performed to determine the association between covariates and the occurrence of SCD.
Results:
There were 2,149 of 2,578 (86%) patients with HF who did not have an implantable cardioverter-defibrillator (ICD); of these, there were 344 PHIV and 1,805 uninfected controls. Among PHIV with HF, the presence of CAD and pulmonary artery systolic pressure was higher (47 ± 9.2 vs. 40 ± 9.0 mm Hg, p < 0.001), as was cocaine use (34 vs. 19%, p < 0.001), and co-infection with hepatitis C virus (13% vs. 7%, p < 0.001) compared to the non-HIV group with HF. Among PHIV with HF, 91% (n = 313) were prescribed anti-retroviral therapy and 64% were virally suppressed. There were 191 SCDs over a median follow-up period of 19 months. Compared to controls, PHIV had a threefold increase in SCD (21 vs. 6.4%; p < 0.001; adjusted odds ratio, 3.0; 95% confidence interval, 1.78-4.24). The SCD rate was higher among African Americans living with HIV compared to non-African Americans living with HIV (27 vs. 18%, p = 0.02). In a multivariable model, after adjusting for confounding factors, CAD was the strongest predictor of SCD followed by lower CD4 count (or nonsuppressed VL), cocaine use, nonprescription of beta-blockers, a low LVEF, wider QRS, and an increased corrected QT interval duration. The SCD rate among PHIV with an undetectable VL was similar to the rate among HIV-uninfected individuals. Similar findings were observed when stratified by LVEF. Also, the SCD rate was higher among PHIV with a preserved LVEF as compared to HIV-uninfected individuals with a preserved LVEF (18 vs. 5.4%, p < 0.001). Among PHIV with HF without a conventional indication for an ICD, the rate of SCD was 10% per year.
Conclusions:
PHIV hospitalized with HF are at a markedly increased risk for SCD. SCD risk was increased in patients with a lower LVEF, lower CD4 count, and a higher VL.
Perspective:
This is an important study because it confirms that there is a significantly higher risk of SCD in PHIV. Further studies are needed to confirm these findings and develop a risk score to determine which patients will benefit with prophylactic strategies such as beta-blockers, LifeVest, and subcutaneous ICDs. Also, it would also be interesting to determine whether statins would reduce the burden of CAD and SCD death since anti-retroviral therapy is known to be associated with dyslipidemia.
Keywords: Arrhythmias, Cardiac, Blood Pressure, CD4 Lymphocyte Count, Cocaine, Coronary Artery Disease, Death, Sudden, Cardiac, Defibrillators, Implantable, Dyslipidemias, Electrocardiography, Geriatrics, Heart Failure, HIV, HIV Infections, Metabolic Syndrome, Risk Factors, Secondary Prevention, Stroke Volume, Viral Load
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