Faculty mentor/PI email address

Brandon.Velazquez@hudsonregionalhealth.com

Is your research Teaching and Learning based?

1

Keywords

QTc prolongation, Moxifloxacin, Drug-resistant tuberculosis (MDR/RR-TB), Population pharmacokinetic modeling, Cardiac arrhythmia risk (Torsades de Pointes), Multifactorial risk stratification

Date of Presentation

5-6-2026 12:00 AM

Poster Abstract

Tuberculosis treatment is undergoing its most significant transformation in decades. In recent years, updated ATS/CDC/ERS/IDSA guidelines introduced a new 4-month drug-susceptible TB regimen that incorporates moxifloxacin as a core component. These landmark guideline shifts mean that moxifloxacin exposure among TB patients globally is set to expand dramatically. This drug replaces the ethambutol component of standard TB regiment commonly associated with optic neuritis as a side effect. Yet there is a critical blind spot: while individual studies have documented moxifloxacin’s QT interval-prolonging effects, no research has modeled what happens when this drug is rolled out to millions of patients who simultaneously carry multiple cardiac risk factors. TB patients typically present with multiple comorbidities. Globally, 40–57% are malnourished at diagnosis, a condition that independently prolongs QTc. ~8% of patients have a genetic burden of reduced-function SLCO1B1 variant, leading to ~46% higher moxifloxacin exposure, which may significantly amplify QT-related cardiotoxic risk at a population level. HIV coinfection is common, introducing further drug interactions and cardiac vulnerability. Each risk factor is well characterized in isolation but has not been evaluated collectively at the mass-population level. This study reviews the existing evidence on moxifloxacin-associated cardiac risk, identifies this gap, and demonstrates the need for population-level modeling. We propose a Monte Carlo simulation to integrate these risk factors, which would require individual patient-level pharmacokinetic data and collaboration with clinical pharmacometrics in order to appreciate the probability of different outcomes in unpredictable settings.

Disciplines

Bacterial Infections and Mycoses | Cardiovascular Diseases

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May 6th, 12:00 AM

Quantifying QTc Prolongation Risk at Scale: Cardiac Safety Implications of Moxifloxacin-Based TB Regimens

Tuberculosis treatment is undergoing its most significant transformation in decades. In recent years, updated ATS/CDC/ERS/IDSA guidelines introduced a new 4-month drug-susceptible TB regimen that incorporates moxifloxacin as a core component. These landmark guideline shifts mean that moxifloxacin exposure among TB patients globally is set to expand dramatically. This drug replaces the ethambutol component of standard TB regiment commonly associated with optic neuritis as a side effect. Yet there is a critical blind spot: while individual studies have documented moxifloxacin’s QT interval-prolonging effects, no research has modeled what happens when this drug is rolled out to millions of patients who simultaneously carry multiple cardiac risk factors. TB patients typically present with multiple comorbidities. Globally, 40–57% are malnourished at diagnosis, a condition that independently prolongs QTc. ~8% of patients have a genetic burden of reduced-function SLCO1B1 variant, leading to ~46% higher moxifloxacin exposure, which may significantly amplify QT-related cardiotoxic risk at a population level. HIV coinfection is common, introducing further drug interactions and cardiac vulnerability. Each risk factor is well characterized in isolation but has not been evaluated collectively at the mass-population level. This study reviews the existing evidence on moxifloxacin-associated cardiac risk, identifies this gap, and demonstrates the need for population-level modeling. We propose a Monte Carlo simulation to integrate these risk factors, which would require individual patient-level pharmacokinetic data and collaboration with clinical pharmacometrics in order to appreciate the probability of different outcomes in unpredictable settings.

 

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