Heart rate variability comparison between young males after 4–6 weeks from the end of SARS-CoV-2 infection and controls

Due to the prolonged inflammatory process induced by infection of the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), indices of autonomic nervous system dysfunction may persist long after viral shedding. Previous studies showed significant changes in HRV parameters in severe (including fatal) infection of SARS-CoV-2. However, few studies have comprehensively examined HRV in individuals who previously presented as asymptomatic or mildly symptomatic cases of COVID-19. In this study, we examined HRV in asymptomatic or mildly symptomatic individuals 5–7 weeks following positive confirmation of SARS-CoV-2 infection. Sixty-five ECG Holter recordings from young (mean age 22.6 ± 3.4 years), physically fit male subjects 4–6 weeks after the second negative test (considered to be the start of recovery) and twenty-six control male subjects (mean age 23.2 ± 2.9 years) were considered in the study. Night-time RR time series were extracted from ECG signals. Selected linear as well as nonlinear HRV parameters were calculated. We found significant differences in Porta’s symbolic analysis parameters V0 and V2 (p < 0.001), α2 (p < 0.001), very low-frequency component (VLF;p = 0.022) and respiratory peak (from the PRSA method;p = 0.012). These differences may be caused by the changes of activity of the parasympathetic autonomic nervous system as well as by the coupling of respiratory rhythm with heart rate due to an increase in pulmonary arterial vascular resistance. The results suggest that the differences with the control group in the HRV parameters, that reflect the functional state of the autonomic nervous system, are measurable after a few weeks from the beginning of the recovery even in the post-COVID group—a young and physically active population. We indicate HRV sensitive markers which may be used in long-term monitoring of patients after recovery.

Will a Burst in Federal Infrastructure Spending Accelerate the Recovery from the COVID-19 Recession? (preprint)

Facing a highly uncertain and potentially sluggish recovery in a presidential election year, the president has pressed for increased infrastructure spending to boost the economy. If he continues to promote this idea, members of Congress may go along with this policy as a potential way to speed up the recovery. Because the current transportation funding bill is due to expire in September, there will be a window of opportunity to act.A limited number of research papers have carefully examined the impact of government investment spending on highways and other infrastructure since the Great Recession. Published papers have examined the effectiveness of the spending programs embodied in the American Recovery and Reinvestment Act of 2009 (ARRA). I show in this policy brief that the preponderance of evidence suggests that this type of spending does not significantly boost the economy in the short term. In particular, the most likely impact is a spending multiplier that is less than one. This implies that government investment spending reduces, or crowds out, some private spending.

Hypertension and renin-angiotensin system blockers are not associated with expression of Angiotensin Converting Enzyme 2 (ACE2) in the kidney (preprint)

Angiotensin converting enzyme 2 (ACE2) is the cellular entry point for severe acute respiratory syndrome coronavirus (SARS-CoV-2) - the cause of COVID-19 disease. It has been hypothesized that use of renin-angiotensin system (RAS) inhibiting medications in patients with hypertension, increases the expression of ACE2 and thereby increases the risk of COVID-19 infection and severe outcomes or death. However, the effect of RAS-inhibition on ACE2 expression in human tissues of key relevance to blood pressure regulation and COVID-19 infection has not previously been reported. We examined how hypertension, its major metabolic co-phenotypes and antihypertensive medications relate to ACE2 renal expression using information from up to 436 patients whose kidney transcriptomes were characterised by RNA-sequencing. We further validated some of the key observations in other human tissues and/or a controlled experimental model. Our data reveal increasing expression of ACE2 with age in both human lungs and the kidney. We show no association between renal expression of ACE2 and either hypertension or common types of RAS inhibiting drugs. We demonstrate that renal abundance of ACE2 is positively associated with a biochemical index of kidney function and show a strong enrichment for genes responsible for kidney health and disease in ACE2 co-expression analysis. Collectively, our data indicate that neither hypertension nor antihypertensive treatment are likely to alter individual risk of SARS-CoV-2 infection or influence clinical outcomes in COVID-19 through changes of ACE2 expression. Our data further suggest that in the absence of SARS-CoV-2 infection, kidney ACE2 is most likely nephro-protective but the age-related increase in its expression within lungs and kidneys may be relevant to the risk of SARS-CoV-2 infection.