Diastolic dysfunction was associated with multiple alterations in cardiac structure and function in a contemporary HIV-positive population receiving antiretroviral therapy, according to results published in the Journal of Cardiac Failure.

A multicenter, cross-sectional, case-control study of people with HIV who were receiving treatment and demonstrated viral suppression was conducted. There were 94 patients with diastolic dysfunction and 101 patients without diastolic dysfunction. All patients had ejection fraction >50%, no significant valvular disease, and no history of coronary revascularization or persistent atrial fibrillation.

The groups were similar in CD4 cell count, HIV RNA copies, sex, and race. Individuals with diastolic dysfunction were older, had higher body mass index, and were more likely to have higher blood pressure, renal dysfunction, dyslipidemia, and longer QRS interval (all P <.04). Levels of N-terminal-pro-B-type natriuretic peptide (median 36 vs 26 pg/mL; P <.01) and high-sensitivity troponin I (3.6 vs 2.5 pg/mL; P <.01) were also higher in patients with diastolic dysfunction than in those without diastolic dysfunction. The patients with diastolic dysfunction also had similar left atrial size but increased wall stiffness (conduit strain, 23.5 vs 30.0; P <.01) and impaired relaxation (reservoir strain, 39.7 vs 45.9; P =.04).

Furthermore, on cardiac magnetic resonance imaging, the prevalence of focal fibrosis was higher among patients with diastolic dysfunction (19.0% vs 5.3%, P <.01) and results further demonstrated higher levels of carboxyl-terminal telopeptide of collagen type I (P =.04), and trends toward higher interlukin-6 and oxidized low-density lipoprotein levels (P ≤.08). Finally, both Kansas City Cardiomyopathy Questionnaire physical limitation (87.1 ± 21.4 vs 93.1 ± 18.1; P =.01) and symptom frequency scores were lower among patients with diastolic dysfunction (86.0 ± 21.5 vs 92.5 ± 16.8; P =.01).

It is important to note that this study used a cross-sectional design that could not prove causality or directionality of the reported relationships. Further, patients were assessed on a single visit; statistical models were univariate and designed as non-parametric rank-based models. No tested multivariable models were able to meet minimum assumptions for validity. The hypothesis-generating nature of this work also meant correction for multiple comparisons was not performed and that samples sixes were small which may have limited the power for detecting significant relationships. Also of note, while cardiac magnetic resonance was performed in nearly all patients, data for the myocardial T1 value pre-contrast and extracellular volume fraction was only available for a subset of participants.

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According to investigators, “collectively, these findings support the clinical relevance of even mild diastolic dysfunction among adequately-treated patients with HIV and suggest a pathophysiologic role for myocardial fibrosis and potentially systemic inflammation.” They recommended further work that assesses changes in fibrosis and inflammatory parameters over time and their abilities to predict onset of symptomatic heart failure. The potential of these conditions as therapeutic targets to attenuate or halt progressive cardiac remodeling and dysfunction could then also be investigated.

Reference

Butler J, Greene SJ, Shah SH, et al. Diastolic dysfunction in patients with human immunodeficiency virus receiving antiretroviral therapy: Results from the CHART study [published online November 1 2019]. J Card Fail. doi: 10.1016/j.cardfail.2019.10.011