Investigating autonomic nervous system dysfunction among patients with post-COVID condition and prolonged cardiovascular symptoms.

Heart Rate Variability (HRV) and arterial pressure (AP) variability and their responses to head-up tilt test (HUTT) were investigated in Post-COVID-19 syndrome (PCS) patients reporting tachycardia and/or postural hypotension. Besides tachycardia, PCS patients also showed attenuation of the following HRV parameters: RMSSD [square root of the mean of the sum of the squares of differences between adjacent normal-to-normal (NN) intervals] from statistical measures; the power of RR (beat-to-beat interval) spectra at HF (high frequency) from the linear method spectral analysis; occurrence of 2UV (two unlike variation) pattern of RR from the nonlinear method symbolic analysis; and the new family of statistics named sample entropy, when compared to control subjects. Basal AP and LF (low frequency) power of systolic AP were similar between PCS patients and control subjects, while 0 V (zero variation) patterns of AP from the nonlinear method symbolic analysis were exacerbated in PCS patients. Despite tachycardia and a decrease in RMSSD, no parameter of HRV changed during HUTT in PCS patients compared to control subjects. PCS patients reassessed after 6 months showed higher HF power of RR spectra and a higher percentage of 2UV pattern of RR. Moreover, the reassessed PCS patients showed a lower occurrence of 0 V patterns of AP, while the HUTT elicited HR (heart rate) and AP responses identical to control subjects. The HRV and AP variability suggest an autonomic dysfunction with sympathetic predominance in PCS patients. In contrast, the lack of responses of HRV and AP variability indices during HUTT indicates a marked impairment of autonomic control. Of note, the reassessment of PCS patients showed that the noxious effect of COVID-19 on autonomic control tended to fade over time.

Autonomic modulation of arterial pressure and heart rate variability in hypertensive diabetic rats.

OBJECTIVE: The aim of the present study was to evaluate the autonomic modulation of the cardiovascular system in streptozotocin (STZ)-induced diabetic spontaneously hypertensive rats (SHR), evaluating baroreflex sensitivity and arterial pressure and heart rate variability. METHODS: Male SHR were divided in control (SHR) and diabetic (SHR+DM, 5 days after STZ) groups. Arterial pressure (AP) and baroreflex sensitivity (evaluated by tachycardic and bradycardic responses to changes in AP) were monitored. Autoregressive spectral estimation was performed for systolic AP (SAP) and pulse interval (PI) with oscillatory components quantified as low (LF:0.2-0.6Hz) and high (HF:0.6-3.0Hz) frequency ranges. RESULTS: Mean AP and heart rate in SHR+DM (131+/-3 mmHg and 276+/-6 bpm) were lower than in SHR (160+/-7 mmHg and 330+/-8 bpm). Baroreflex bradycardia was lower in SHR+DM as compared to SHR (0.55+/-0.1 vs. 0.97+/-0.1 bpm/mmHg). Overall SAP variability in the time domain (standard deviation of beat-by-beat time series of SAP) was lower in SHR+DM (3.1+/-0.2 mmHg) than in SHR (5.7+/-0.6 mmHg). The standard deviation of the PI was similar between groups. Diabetes reduced the LF of SAP (3.3+/-0.8 vs. 28.7+/-7.6 mmHg2 in SHR), while HF of SAP were unchanged. The power of oscillatory components of PI did not differ between groups. CONCLUSIONS: These results show that the association of hypertension and diabetes causes an impairment of the peripheral cardiovascular sympathetic modulation that could be, at least in part, responsible for the reduction in AP levels. Moreover, this study demonstrates that diabetes might actually impair the reduced buffer function of the baroreceptors while reducing blood pressure.

Autonomic modulation of arterial pressure and heart rate variability in hypertensive diabetic rats

OBJECTIVE: The aim of the present study was to evaluate the autonomic modulation of the cardiovascular system in streptozotocin (STZ)-induced diabetic spontaneously hypertensive rats (SHR), evaluating baroreflex sensitivity and arterial pressure and heart rate variability. METHODS: Male SHR were divided in control (SHR) and diabetic (SHR+DM, 5 days after STZ) groups. Arterial pressure (AP) and baroreflex sensitivity (evaluated by tachycardic and bradycardic responses to changes in AP) were monitored. Autoregressive spectral estimation was performed for systolic AP (SAP) and pulse interval (PI) with oscillatory components quantified as low (LF:0.2-0.6Hz) and high (HF:0.6-3.0Hz) frequency ranges. RESULTS: Mean AP and heart rate in SHR+DM (131±3 mmHg and 276±6 bpm) were lower than in SHR (160±7 mmHg and 330±8 bpm). Baroreflex bradycardia was lower in SHR+DM as compared to SHR (0.55±0.1 vs. 0.97±0.1 bpm/mmHg). Overall SAP variability in the time domain (standard deviation of beat-by-beat time series of SAP) was lower in SHR+DM (3.1±0.2 mmHg) than in SHR (5.7±0.6 mmHg). The standard deviation of the PI was similar between groups. Diabetes reduced the LF of SAP (3.3±0.8 vs. 28.7±7.6 mmHg2 in SHR), while HF of SAP were unchanged. The power of oscillatory components of PI did not differ between groups. CONCLUSIONS: These results show that the association of hypertension and diabetes causes an impairment of the peripheral cardiovascular sympathetic modulation that could be, at least in part, responsible for the reduction in AP levels. Moreover, this study demonstrates that diabetes might actually impair the reduced buffer function of the baroreceptors while reducing blood pressure.

OBJETIVO: O objetivo do presente estudo foi investigar a modulação autonômica do sistema cardiovascular em ratos espontâneamente hipertensos (SHR) e diabéticos por estreptozotocina (STZ), avaliando a sensibilidade do reflexo barorreceptor e a variabilidade da pressão arterial e da freqüência cardíaca. MÉTODOS: Ratos SHR machos foram divididos em grupos controle (SHR) e diabéticos (SHR+DM, 5 dias após STZ). A pressão arterial (PA) e a sensibilidade dos barorreceptores (avaliada pelas respostas taquicárdicas e bradicárdicas a alterações da PA) foram monitoradas. Os sinais de pressão arterial sistólica (PAS) e o intervalo de pulso (IP) foram analisados no domínio do tempo e da freqüência pelo método autoregressivo sendo quantificados os componentes oscilatórios de baixa (BF: 0,2-0,6Hz) e alta (AF:0,6-3,0Hz) freqüência. RESULTADOS: A PA média e a freqüência cardíaca estavam reduzidas no grupo SHR+DM (131±3 mmHg e 276±6 bpm) em relação ao grupo SHR (160±7 mmHg e 330±8 bpm). A bradicardia reflexa a aumentos de PA estava atenuada no grupo SHR+DM quando comparada ao grupo SHR (0,55±0,1 vs 0,97±0,1 bpm/mmHg). A variabilidade da PAS no domínio do tempo (desvio padrão batimento-a-batimento da série temporal da PAS) foi menor no grupo SHR+DM (3,1±0,2 mmHg) quando comparada ao grupo SHR (5,7±0,6 mmHg). O desvio padrão do IP foi semelhante entre os grupos. O diabetes reduziu o componente BF da PAS (3,3±0,8 vs 28,7±7,6 mmHg² no SHR), mas não alterou o componente AF da PAS. Em relação aos componentes oscilatórios do IP não houve diferença entre os grupos. CONCLUSÕES: Estes resultados sugerem que a associação de hipertensão e diabetes causa uma importante diminuição da modulação simpática cardiovascular periférica que poderia, pelo menos em parte, ser responsável pela redução da PA. Além disso, este estudo demonstra que o diabetes pode, de fato, piorar a já reduzida função de tamponamento dos barorreceptores ao mesmo tempo em que reduz a pressão arterial.

Frequency-dependent baroreflex modulation of blood pressure and heart rate variability in conscious mice.

The goal of this study was to determine the baroreflex influence on systolic arterial pressure (SAP) and pulse interval (PI) variability in conscious mice. SAP and PI were measured in C57Bl/6J mice subjected to sinoaortic deafferentation (SAD, n = 21) or sham surgery (n = 20). Average SAP and PI did not differ in SAD or control mice. In contrast, SAP variance was enhanced (21 +/- 4 vs. 9.5 +/- 1 mmHg2) and PI variance reduced (8.8 +/- 2 vs. 26 +/- 6 ms2) in SAD vs. control mice. High-frequency (HF: 1-5 Hz) SAP variability quantified by spectral analysis was greater in SAD (8.5 +/- 2.0 mmHg2) compared with control (2.5 +/- 0.2 mmHg2) mice, whereas low-frequency (LF: 0.1-1 Hz) SAP variability did not differ between the groups. Conversely, LF PI variability was markedly reduced in SAD mice (0.5 +/- 0.1 vs. 10.8 +/- 3.4 ms2). LF oscillations in SAP and PI were coherent in control mice (coherence = 0.68 +/- 0.05), with changes in SAP leading changes in PI (phase = -1.41 +/- 0.06 radians), but were not coherent in SAD mice (coherence = 0.08 +/- 0.03). Blockade of parasympathetic drive with atropine decreased average PI, PI variance, and LF and HF PI variability in control (n = 10) but had no effect in SAD (n = 6) mice. In control mice, blockade of sympathetic cardiac receptors with propranolol increased average PI and decreased PI variance and LF PI variability (n = 6). In SAD mice, propranolol increased average PI (n = 6). In conclusion, baroreflex modulation of PI contributes to LF, but not HF PI variability, and is mediated by both sympathetic and parasympathetic drives in conscious mice.

Variabilidade da pressão arterial e freqüência cardíaca, e sensibilidade do barorreflexo, em animais geneticamente manipulados / Arterial pressure and heart rate variability, and baroreflex sensitivity, in genetically manipulated animals

As doenças cardiovasculares estão entre as mais prevalentes e incidentes nos países industrializados. Entre elas, hipertensão arterial sistêmica, coronariopatias, insuficiência cardíaca congestiva e acidente vascular cerebral são as afecções mais comuns, apresentando causas multifatoriais, incluindo uma base genética peculiar. Sabe-se que tais afecções cursam com diversos acometimentos cardiovasculares, sendo que o comprometimento do controle barorreflexo da freqüência cardíaca (FC), e também da variabilidade da FC e da pressão arterial (PA), é comumente observado. Recentemente, diversos modelos experimentais, envolvendo camundongos geneticamente modificados, foram gerados com a expectativa de oferecer melhor compreensão dos mecanismos genéticos envolvidos na fisiopatogenia de doenças cardiovasculares. Alguns dos modelos mais estudados envolvem o sistema reninaangiotensina, o simpático, e outros mecanismos neurohumorais que participam da regulação cardiocirculatória. Em todos estes casos, priorizou-se o estudo fenotípico dos animais, observando-se o desenvolvimento e o acometimento de órgãos e sistemas conforme a manipulação genética realizada, a qual poderia ser tanto a superexpressão como a exclusão de um ou mais genes. A proposta do presente artigo é revisar aspectos importantes da fisiologia cardiovascular, observados em alguns dos modelos mais utilizados de manipulação genética, com enfoque nos estudos da variabilidade da FC e da PA, e no controle barorreflexo da FC.