Key result
Combined CPET and CMR in HIV patients with unexplained dyspnea revealed reduced exercise capacity and impaired ventilation without evidence of exercise-induced pulmonary hypertension.
Why the study?
HIV patients commonly experience dyspnea without an apparent immediate cause, prompting evaluation using CPET coupled with exercise CMR to elucidate underlying etiologies.
Does combined CPET and exercise CMR identify the etiology of unexplained dyspnea in well-treated HIV patients?
Cohort (n=34)
No
Does combined CPET and exercise CMR identify the etiology of unexplained dyspnea in well-treated HIV patients?
Combined CPET and exercise CMR demonstrated that unexplained dyspnea in well-treated HIV patients is likely due to non-cardiopulmonary peripheral limitations rather than occult heart failure or exercise-induced pulmonary hypertension.
Answers are grounded in this paper and cite their sources.
Suggests peripheral mechanisms underlie dyspnea in treated HIV; hypothesis-generating for combined CPET-CMR, needing prospective validation.
Human Immunodeficiency Virus (HIV) patients commonly experience dyspnea for which an immediate cause may not be always apparent. In this prospective cohort study of HIV patients with exercise limitation, we use cardiopulmonary exercise testing (CPET) coupled with exercise cardiovascular magnetic resonance (CMR) to elucidate etiologies of dyspnea. Thirty-four HIV patients on antiretroviral therapy with dyspnea and exercise limitation (49.7 years, 65% male, mean absolute CD4 count 700) underwent comprehensive evaluation with combined rest and maximal exercise treadmill CMR and CPET. The overall mean oxygen consumption (VO2) peak was reduced at 23.2 ± 6.9 ml/kg/min with 20 patients (58.8% of overall cohort) achieving a respiratory exchange ratio > 1. The ventilatory efficiency (VE)/VCO2 slope was elevated at 36 ± 7.92, while ventilatory reserve (VE: maximal voluntary ventilation (MVV)) was within normal limits. The mean absolute right ventricular (RV) and left ventricular (LV) contractile reserves were preserved at 9.0% ± 11.2 and 9.4% ± 9.4, respectively. The average resting and post-exercise mean average pulmonary artery velocities were 12.2 ± 3.9 cm/s and 18.9 ± 8.3 respectively, which suggested lack of exercise induced pulmonary artery hypertension (PAH). LV but not RV delayed enhancement were identified in five patients. Correlation analysis found no relationship between peak VO2 measures of contractile RV or LV reserve, but LV and RV stroke volume correlated with PET CO2 (p = 0.02, p = 0.03). Well treated patients with HIV appear to have conserved RV and LV function, contractile reserve and no evidence of exercise induced PAH. However, we found evidence of impaired ventilation suggesting a non-cardiopulmonary etiology for dyspnea.
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Patterson et al. (2020) conducted a cohort in HIV with unexplained dyspnea (n=34). Combined cardiopulmonary exercise testing (CPET) and cardiovascular magnetic resonance (CMR) was evaluated on Peak oxygen consumption (VO2). Combined CPET and CMR in HIV patients with unexplained dyspnea revealed reduced exercise capacity and impaired ventilation without evidence of exercise-induced pulmonary hypertension.
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