Acute prolonged sitting increases blood pressure (BP) and arterial stiffness (AS). Both of these may be mitigated via light physical activity (LPA). Whether long COVID (LC), which partly manifests as Show more
Acute prolonged sitting increases blood pressure (BP) and arterial stiffness (AS). Both of these may be mitigated via light physical activity (LPA). Whether long COVID (LC), which partly manifests as vascular sequelae, predisposes a heightened sensitivity to sitting or diminished benefits from its interruption is unknown. The aims of this study were to identify whether individuals with LC: (i) exhibit a worse BP/AS response to uninterrupted sitting and (ii) a diminished mitigation of BP/AS response to sitting interrupted with LPA, compared to healthy controls. Thirty participants with LC and 15 controls completed 2 h of uninterrupted sitting and sitting interrupted with LPA. Central and peripheral systolic and diastolic BP and carotid-femoral pulse wave velocity (cfPWV) were determined pre and post sitting. Linear mixed-effects models demonstrated no three-way or two-way interactions for any variable. There was a significant main effect of time, with increases in central systolic (MD = 3.37 mmHg, SE = 0.93 mmHg, p < 0.001) and central diastolic (MD = 3.00 mmHg, SE = 0.58 mmHg, p < 0.001) BP. cfPWV was not altered in sitting in either group (MD = 0.13 m/s, SE = 0.09 m/s, p = 0.170). Uninterrupted sitting increases BP similarly, but AS is unchanged. Interrupting sitting with LPA did not mitigate sitting-induced increase in BP regardless of LC diagnosis. Show less
Single-nucleotide polymorphisms in genes involved in lipoprotein and adipocyte metabolism may explain why dyslipidemia and lipoatrophy occur in some but not all antiretroviral therapy (ART)-treated in Show more
Single-nucleotide polymorphisms in genes involved in lipoprotein and adipocyte metabolism may explain why dyslipidemia and lipoatrophy occur in some but not all antiretroviral therapy (ART)-treated individuals. We evaluated the contribution of APOC3 -482C-->T, -455T-->C, and 3238C-->G; epsilon 2 and epsilon 4 alleles of APOE; and TNF -238G-->A to dyslipidemia and lipoatrophy by longitudinally modeling >2600 lipid determinations and 2328 lipoatrophy assessments in 329 ART-treated patients during a median follow-up period of 3.4 years. In human immunodeficiency virus (HIV)-infected individuals, the effects of variant alleles of APOE on plasma cholesterol and triglyceride levels and of APOC3 on plasma triglyceride levels were comparable to those reported in the general population. However, when treated with ritonavir, individuals with unfavorable genotypes of APOC3 and [corrected] APOE were at risk of extreme hypertriglyceridemia. They had median plasma triglyceride levels of 7.33 mmol/L, compared with 3.08 mmol/L in the absence of ART. The net effect of the APOE*APOC3*ritonavir interaction was an increase in plasma triglyceride levels of 2.23 mmol/L. No association between TNF -238G-->A and lipoatrophy was observed. Variant alleles of APOE and APOC3 contribute to an unfavorable lipid profile in patients with HIV. Interactions between genotypes and ART can lead to severe hyperlipidemia. Genetic analysis may identify patients at high risk for severe ritonavir-associated hypertriglyceridemia. Show less