Affect Heart Rate Research Articles

The effects of acute operational stress and passive heat stress on physiological and subjective stress responses in military personnel.

Military personnel often encounter situations that can trigger acute stress, which may affect operational performance. Therefore, it is important to examine stress responses in controlled environments to obtain more insights in performance-influencing effects of acute stress. This study investigated the impact of passive heat exposure combined with virtual combat scenarios on cardiovascular and psychophysiological parameters in a controlled setting. Sixty-eight healthy servicemembers were randomized into a low-stress or high-stress condition. Both groups engaged in two virtual combat scenarios. The low-stress group, however, underwent testing under thermoneutral conditions (MTemp = 22.4 °C, MRelativeHumidity = 41.4 %) whereas the high-stress group was exposed to passive heat exposure (MTemp = 35.9 °C, MRelativeHumidity = 66.4 %) using a portable environmental facility. While virtual combat scenarios alone led to a decrease in heart rate variability (HRV) without affecting heart rate (HR), the addition of passive heat exposure elicited a more pronounced physiological stress response, characterized by significantly higher HR and lower HRV in the high-stress condition. However, no significant changes were observed in respiratory rate, salivary cortisol, or alpha-amylase levels across the conditions, suggesting that there was no activation of either the hypothalamic-pituitary-adrenal or the sympathetic-adrenal-medullary axis. Furthermore, subjective stress and anxiety scores did not differ between conditions, underscoring the physiological nature of the observed changes. Resultantly, the physiological response was likely a thermal reaction rather than an acute stress response. These findings highlight the importance of incorporating environmental stressors into military training protocols to enhance realism and prepare personnel for operational stressors. However, the mild response observed suggests that higher ambient temperatures and longer exposure times may be necessary to evoke a more robust stress response for effective stress inoculation training.

Acute metformin intake on exercise performance in healthy participants during functional fitness training.

The study aimed to assess whether prior intake of metformin enhances performance in the FRAN workout, a popular Functional Fitness Training protocol. Fourteen men (mean±SD: 24.2±3.5 years; height: 173.3±7.8 cm; weight: 78.3±14.1 kg; body mass index: 25.9±3.0 kg/m2) participated. During the first visit, anthropometric measurements were taken, and participants performed the FRAN workout. After 72-96 hours, a retest was conducted to establish test-retest reliability. In the third and fourth visits, participants completed the FRAN workout under two conditions: metformin and placebo, using a crossover, counterbalanced, and double-blind design. The FRAN workout consisted of barbell thrusters (43.2 kg) and bodyweight butterfly pull-ups, performed in 21, 15, and 9 repetitions across three rounds. Significant differences were observed in partial times between rounds (F=28.91; P<0.01), but no significant differences were found between metformin and placebo conditions (F=0.08; P=0.77) or interaction effects (F=0.87; P=0.42). Similarly, total time differed significantly between rounds (F=158.04; P<0.01), with no significant differences between conditions (F=0.02; P=0.88) or interaction effects (F=0.30; P=0.73). Acute metformin intake did not enhance FRAN workout performance, nor did it affect heart rate or perceived exertion. Coaches and athletes should consider that metformin's impact on exercise performance appears nonexistent, and its use in this context might not provide the desired ergogenic effect.

Visceral Fat Affects Heart Rate Recovery but Not the Heart Rate Response Post-Single Bout of Vigorous Exercise: A Cross-Sectional Study in Non-Obese and Healthy Participants.

Body composition could influence exercise physiology. However, no one has ever studied the effect of visceral fat (VF) on heart rate (HR) trends during and after exercise by using bioimpedance analysis (BIA). This study aims to investigate BIA variables as predictors of HR trends during vigorous exercise. Ninety-six participants (age 22.5 ± 4.8 years) were included in the data analysis. After performing BIA, the HR was recorded at three time points: baseline HR (BHR), peak HR (PHR) at the end of vigorous exercise, and resting HR (RHR) 1 min after the end of the exercise. After BHR, a 30 s squat jump test was performed. Linear regression analysis showed the body fat percentage and VF as a predictor of HR recovery post-exercise (p < 0.01). However, body weight has no association with HR recovery (p > 0.05). On the other hand, BIA variables were not associated with the variation of HR from the baseline to the end of the exercise. The results show that higher VF is associated with a slower HR recovery. To schedule a training program, it would be safer to monitor visceral fat before prescribing recovery time.

RHRVEasy: Heart rate variability made easy.

Heart Rate Variability (HRV) analysis aims to characterize the physiological state affecting heart rate, and identify potential markers of underlying pathologies. This typically involves calculating various HRV indices for each recording of two or more populations. Then, statistical tests are used to find differences. The normality of the indices, the number of groups being compared, and the correction of the significance level should be considered in this step. Especially for large studies, this process is tedious and error-prone. This paper presents RHRVEasy, an R open-source package that automates all the steps of HRV analysis. RHRVEasy takes as input a list of folders, each containing all the recordings of the same population. The package loads and preprocesses heart rate data, and computes up to 31 HRV time, frequency, and non-linear indices. Notably, it automates the computation of non-linear indices, which typically demands manual intervention. It then conducts hypothesis tests to find differences between the populations, adjusting significance levels if necessary. It also performs a post-hoc analysis to identify the differing groups if there are more than two populations. RHRVEasy was validated using a database of healthy subjects, and another of congestive heart failure patients. Significant differences in many HRV indices are expected between these groups. Two additional groups were constructed by random sampling of the original databases. Each of these groups should present no statistically significant differences with the group from which it was sampled, and it should present differences with the other two groups. All tests produced the expected results, demonstrating the software's capability in simplifying HRV analysis. Code is available on https://github.com/constantino-garcia/RHRVEasy.

Orthostatic intolerance with tachycardia (postural tachycardia syndrome) and without (hypocapnic cerebral hypoperfusion) represent a spectrum of the same disorder.

Spectrum of chronic orthostatic intolerance without orthostatic hypotension includes postural tachycardia syndrome (POTS), with orthostatic tachycardia and hypocapnic cerebral hypoperfusion (HYCH), without orthostatic tachycardia. This study compared autonomic, cerebrovascular, and neuropathic features of POTS and HYCH. This retrospective study evaluated patients with orthostatic intolerance referred for autonomic testing. Analyzed data included surveys (Survey of Autonomic Symptoms, Compass-31, Neuropathy Total Symptom Score-6, Central Sensitization Inventory) and autonomic tests (Valsalva maneuver, deep breathing, sudomotor and tilt tests), cerebrovascular (cerebral blood flow velocity (CBFv) monitoring in the middle cerebral artery), respiratory (capnography), neuropathic (skin biopsies for assessment of small fiber neuropathy) and invasive cardiopulmonary exercise testing (iCPET). A total of 127 HYCH, 125 POTS, and 42 healthy controls were analyzed. Compared HYCH to POTS patients, there was no difference in the duration of symptoms, the prevalence of younger women, comorbidities, sensory and autonomic complaints, central sensitization syndrome, supine/standing norepinephrine levels, inflammatory markers and medical therapy except for gastrointestinal medication. Autonomic testing showed widespread but similar abnormalities in POTS and HYCH that included: reduced orthostatic CBFv and end-tidal CO2, preload failure (assessed in 16/19 POTS/HYCH), mild autonomic failure, and frequent small fiber neuropathy. HYCH and POTS are syndromes of orthostatic intolerance with cerebral hypoperfusion associated with reduced orthostatic cerebral blood flow, hypocapnia, mild autonomic failure and small fiber neuropathy of a similar degree and distribution; except for tachycardia in POTS. Similarities in peripheral domain abnormalities that affect heart rate suggest that orthostatic tachycardia in POTS is driven by the central nervous system overcompensation of orthostatic challenge. These findings provide additional evidence that HYCH and POTS represent a spectrum of the same disorder. Reduced orthostatic cerebral blood flow is a key unifying feature of HYCH and POTS.

The role of beta blockers in the treatment of cardiovascular diseases

Beta-blockers are used to treat various cardiovascular diseases, including hypertension and chronic heart failure. They act by suppressing the effects of catecholamines through various pathways and affect heart rate, strength, and renin release, providing antihypertensive and anti-ischemic effects. The individual effects of various drugs on clinical outcomes in this group were determined according to characteristics of the patient, underlying disease, and type of beta-blocker used. In recent years, beta-blockers have faced a serious obstacle when new guidelines on hypertension suggest their use as second-line therapy after angiotensin converting enzyme inhibitors, angiotensin receptor blockers and slow calcium channel blockers in the absence of clear indications. In fact, these recommendations were based on meta-analyses that showed that beta-blockers have fewer beneficial effects on overall mortality, cardiovascular events, and brain stroke. In addition, according to currently available data, the appointment of beta-blockers for diseases such as heart failure with preserved ejection fraction and stable coronary heart disease can cause more harm than good outcomes. Bisoprolol is a beta-blocker with the highest selectivity for beta1-adrenergic receptors, which determines the rare frequency of side effects that develop because of its use. This review presents current data on the use of beta-blockers for treating cardiovascular diseases, with an emphasis on the use of bisoprolol.

Empagliflozin's role in reducing ventricular repolarization heterogeneity: insights into cardiovascular mortality decline from the EMPATHY-HEART trial

Abstract Introduction The incidence of myocardial infarction (MI) and sudden cardiac death (SCD) is significantly higher in individuals with Type 2 Diabetes Mellitus (T2DM). Predictive measures for fatal arrhythmias are often inadequate, highlighting the need for novel non-invasive diagnostic tools. The T-wave heterogeneity (TWH) index, which measures variations in ventricular repolarization, has emerged as a promising predictor for severe ventricular arrhythmias. Although the EMPA-REG trial reported reduced cardiovascular mortality with empagliflozin, the underlying mechanisms remain unclear. This study investigates the potential of empagliflozin in mitigating electrical instability in patients with T2DM and coronary heart disease (CHD) by examining changes in TWH. Methods Participants were adult outpatients with T2DM and CHD, exhibiting a baseline TWH of at least 80 µV. They received a 25mg daily dose of empagliflozin and were evaluated clinically, including ECG measurements at baseline and after 4 weeks. TWH was computed from leads V4, V5, and V6 using a validated technique. The primary study outcome was the alteration in TWH following empagliflozin administration, assessed via the Wilcoxon test, with a significance threshold of p&amp;lt;0.05. Results An initial review of 6,000 medical records pinpointed 800 patients for TWH evaluation. Of these, 412 exhibited TWH above 80 µV, with 144 completing clinical assessments and 90 meeting the criteria for high cardiovascular risk enrollment. Empagliflozin adherence exceeded 80%, resulting in notable reductions in blood pressure without affecting heart rate. Side effects were generally mild, with 13.3% experiencing mostly Level 1 hypoglycemia, alongside infrequent urinary and genital infections. The treatment consistently reduced median TWH from 116 to 103 µV (p=0.01), as detailed in Figure 1. Conclusion The EMPATHY-HEART trial preliminarily suggests that empagliflozin decreases heterogeneity in ventricular repolarization among patients with T2DM and CHD. This reduction in TWH may provide insight into the mechanism behind the decreased cardiovascular mortality observed in previous trials, potentially offering a therapeutic pathway to mitigate the risk of severe arrhythmias in this population.Table 1 Figure 1

Developmental Toxicity and Teratogenic Effects of Dicarboximide Fungicide Iprodione on Zebrafish (Danio rerio) Embryos

Iprodione (IDN) is a broad-spectrum fungicide used to treat various fungal infections in plants. Despite its extensive use, assessment of its toxicity in aquatic organisms remains incomplete. This study investigated the deleterious effects of IDN using zebrafish (ZF) as a model organism. ZF embryos, beginning at 2 h post-fertilization (hpf), were exposed to IDN (3.75–40 mg/L), and both mortality and deformities were assessed. The impact of IDN on mortality was concentration-dependent and significant from 14 mg/L. Importantly, IDN induced several deformities at sublethal concentrations, including abnormal somites, reduced retinal pigment accumulation, yolk sac edema, hatching failure, abnormal swim bladders, and spinal curvature. The EC50 values for IDN-induced deformities were 3.44 ± 0.74 to 21.42 ± 6.00 mg/L. The calculated teratogenic index values for all deformities were above 1, indicating that IDN is teratogenic to ZF. IDN-exposed ZF also displayed abnormalities in touch-evoked escape responses. IDN significantly affected heart rate and blood flow, and induced pericardial edema and hyperemia in a concentration-dependent manner, suggesting its influence on cardiac development and the function of ZF. In conclusion, these results suggest that IDN exerts toxic effects on ZF embryos, affecting mortality, development, and behavior.

Acute right-sided transcutaneous vagus nerve stimulation improves cardio-vagal baroreflex gain in patients with chronic heart failure.

The aim of this paper is to investigate the acute effects of short-term transcutaneous vagus nerve stimulation (tVNS) on cardio-vagal baroreflex gain and heart rate variability in patients with chronic heart failure (CHF). A total of 16 adults with CHF and left ventricular ejection fraction (LVEF) < 50% in sinus rhythm were enrolled (65 ± 8years, 63% men, LVEF 40 ± 5%, 88% on beta-blockers, 50% on quadruple CHF therapy). Over a single experimental session, after a 10-min baseline recording, each patient underwent two trials of 10-min tVNS (Parasym Device, 200µs, 30Hz, 1mA below discomfort threshold) at either the right or left tragus in a randomized order, separated by a 10-min recovery. Compared with baseline, tVNS did not affect heart rate, blood pressure, and respiratory rate (p > 0.05), and no patients complained of discomfort or any adverse effect. Right-sided tVNS was associated with a significant increase in cardio-vagal baroreflex gain (from 5.6 ± 3.1 to 7.5 ± 3.8ms/mmHg, ∆ 1.9 ± 1.6ms/mmHg, p < 0.001), while no change was observed with left-sided tVNS (∆ 0.5 ± 2.0ms/mmHg, p = 0.914). These findings were independent of stimulation-side order (excluding any carry-over effect) and consistent across sex, LVEF category, and HF etiology subgroups (p-value for interaction > 0.05). Acute right-sided tVNS increases cardio-vagal baroreflex gain in patients with CHF and LVEF < 50%, with no tolerability concerns.

The role of NAADP in maintaining spontaneous heart contractions: comparative physiological studies

The goal of the work was to study the role of the second messenger NAADP (Nicotinic Acid Adenine Dinucleotide Phosphate), which causes the release of Ca2+ ions from lysosomes and endosomes, in the regulation of heart contractions. Isolated hearts of the grape snail Helix pomatia and a chicken embryo were used as models. Using the membrane-permeable acetooxymethyl ester NAADP-AM, we showed that NAADP at nanomolar concentrations increases the frequency and amplitude of spontaneous cardiac contractions in H. pomatia. The NAADP antagonist NED19, without affecting the amplitude of contractions, dose-dependently reduces their frequency, completely blocking spontaneous contractions of the mollusk heart at a concentration of 5 μM. The V-type H+-ATPase inhibitor bafilomycin A1 suppresses the accumulation of calcium ions in lysosomes and acidic endosomes. We have shown that bafilomycin A1 causes attenuation of spontaneous contractions and cardiac arrest in H. pomatia. Serotonin increases the amplitude of contractions of the H. pomatia heart without affecting heart rate. NED19 at saturating concentrations (10 μM) reduces the frequency of contractions when the snail heart is activated by serotonin, but only partially reduces their amplitude. In experiments with the isolated chick embryo heart, we showed that NED19 reduces the frequency of spontaneous contractions without affecting the amplitude of contractions. Based on the data obtained, a hypothesis was put forward that the release of calcium ions from lysosomes and endosomes under the influence of endogenous NAADP ensures the maintenance of spontaneous contractions of the heart.

Feet-heating and calf-heating have opposing effects on glucose tolerance and heart rate variability: a randomized, controlled, crossover trial.

Heat exposure's effect on glucose tolerance depends on the amount of body exposed, likely relating to autonomic nervous system balance. We assessed how partial-body heat exposure at two different levels of the lower extremities affects glucose tolerance and autonomic nervous system balance, measured via heart rate variability. We hypothesized feet-heating would improve glucose tolerance without affecting heart rate variability, while calf-heating would worsen glucose tolerance and decrease heart rate variability compared to a thermoneutral control condition. In a randomized, controlled, crossover trial, healthy participants' (N=31, 23(3) years, 45% male) glucose tolerance was measured in (A) thermoneutral; (B) feet-heating; and (C) calf-heating conditions. Every 30 min for 2 h, blood glucose, heart rate, heart rate variability, tympanic temperature, thermal comfort scores, and blood pressure were measured. There were significant interactions between condition and time for blood glucose (F (4.6,72.6)=2.6, p=0.036), heart rate (F (3.4, 54.5)=3.5, p=0.017), heart rate variability (F (4.3,63.2)=7.5, p<.0001), tympanic temperature (F (8, 268)=2.4, p=0.014), and thermal comfort scores (F (8, 248)=22.1, p<0.0001). Calf-heating increased 90 min glucose (+12 (95% confidence interval, CI: 3-21) mg/dL, p=0.013) and decreased heart rate variability throughout (mean decrease: 13%-22%, p<0.007), while feet-heating lowered 90 min glucose (-7 (95% CI: -16 to+1) mg/dL, p=0.090) without affecting heart rate variability (p=0.14-0.99). Blood pressure and body temperature were similar between conditions, but heart rate and thermal comfort scores increased with heating. Calf-heating worsens, while feet-heating may improve, glucose tolerance. Changes in heart rate variability coincided with changes in glucose tolerance despite unchanged body temperature. Whether heart rate variability can be used to monitor autonomic nervous system balance during heating to optimize its acute effect on glycemic indices should be further explored.

Effect of Caffeine and Nitrates Combination on Exercise Performance, Heart Rate and Oxygen Uptake: A Systematic Review and Meta-Analysis.

The evidence about the synergy of combining caffeine (CAF) and nitrates on exercise performance has not been summarized, although there is a possibility of additive/synergistic effects of the co-ingestion of these substances given their different mechanisms of action in central (CAF) and peripheral tissues (nitrates). The aim was to analyze the effects of co-supplementation of CAF and nitrates on sports performance in comparison to the isolated ingestion of these substances. The databases of PubMed, Web of Science, Medline, CiNAHL and SPORTDiscus were used until June 2024 following PRISMA guidelines. Randomized controlled trials, at least one single-blind trial, conducted in adults were considered. A meta-analysis was performed using the random effects model to calculate the standardized mean difference estimated by Hedges' g and 95% confidence intervals (CIs) for studies with four arms. Six studies were included (N = 95). The meta-analysis revealed that caffeine and nitrates supplementation (CAF+nitrates) did not enhance performance in time trials (TTs) over the CAF alone (g = -0.06; 95% CI = -0.46 to 0.35; p = 0.78) or nitrates alone (g = 0.29; 95% CI = -0.12 to 0.70; p = 0.17). CAF+nitrates did not affect heart rate during submaximal exercise trials over CAF alone (g = 0.04; 95% CI = -0.31 to 0.40; p = 0.80) or nitrates alone (g = -0.15; 95% CI = -0.50 to 0.20; p = 0.40). Likewise, CAF+nitrates did not affect oxygen uptake during submaximal exercise trials over CAF alone (g = -0.04; 95% CI = -0.45 to 0.37; p = 0.84) or nitrates alone (g = -0.29; 95% CI = -0.70 to 0.12; p = 0.16). CAF+nitrates did not offer further benefits on exercise performance or physiological variables from the isolated intake of CAF and nitrates.

Cognitive control processes and emotion regulation in adolescence: Examining the impact of affective inhibition and heart-rate-variability on emotion regulation dynamics in daily life

Cognitive control processes likely influence the extent to which adolescents can successfully regulate their emotions. This study examined whether individual differences in affective inhibition and heart rate variability (HRV), as a peripheral index of cognitive control, moderated the association between momentary emotion regulation and negative affect (NA). Ecological Momentary Assessments (EMA) over 14 days were obtained in 235 adolescents (Mage = 13.48 years; 106 females). At each assessment, participants reported their current NA and the extent to which they used cognitive reappraisal and rumination. Moreover, at three time points (approximately 1 year, 6 months, and just before the EMA), affective inhibition was assessed using an affective go/no-go task and HRV was recorded at rest. Results indicate that adolescents with lower affective inhibition reported lower average levels of daily rumination. However, affective inhibition did not moderate the association between either daily cognitive reappraisal or rumination and momentary NA. Consistent with hypotheses, the association between momentary rumination and NA was weaker in adolescents showing higher levels of resting HRV. Overall, findings may underscore the importance of interventions targeting HRV as a malleable factor for enhancing adolescents’ affective well-being.

Beta-Blocker in Heart Rate Control and Cardio Protection: The Role of ADRB1 Variants and HCN4 Regulation – A Systematic Review

Elevated heart rate is linked to adverse cardiovascular outcomes. Sinoatrial (SA) nodes, hyperpolarization-activated cyclic nucleotide-gated-4 (HCN4) channels, and beta1-adrenergic receptor (ADRB1) are responsible for generating the heart rate. Beta-blockers have a cardioprotective effect on heart failure, including controlling heart rate. However, the responses to beta-blockers can vary among individuals. ADRB1 genetic variability may be contributed to the differential beta-blocker effect in heart failure. HCN4 also performs a crucial function in the pacemaker cells of the heart. Exploring the effect of beta-blockers in pacemaker cells is expanding the view of their role and their therapeutic response in heart failure. The objectives of this study were to identify ADRB1 genetic variants affecting heart rate response in heart failure subjects with beta-blocker treatment and to explore the effect of beta-blockers on HCN4 channels and SA nodes. A systematic review was performed using three databases. Eight of 668 manuscripts were selected. The systematic review found that ADRB1 genetic variants (A145G (Ser49Gly) and C1165G (Arg389Gly)) can affect heart rate response in beta-blocker-treated heart failure. The study also found that the percentage of patients with the Ser49Ser-Gly389X haplotype achieved a heart rate target was higher than other haplotypes. Individuals with the Arg389Arg genotype necessitated a markedly increased amount of beta-blocker dose to reach the identical heart rate target compared to those with the Gly389X gene variation. In addition, the review found that carvedilol, a beta-blocker derivative, demonstrated beneficial effects in inhibiting HCN-gated channels. Bisoprolol and carvedilol improved channel regulation in the SA Node by reversing the downregulation of HCN4 and sodium channels. In general, this systematic review provides important insights into beta-blockers in treating heart failure, specifically concerning the genetic variability of ADRB1 and the beta-blockers effect on the SA node and HCN4 channels.

Low-intensity focused ultrasound to the insula differentially modulates the heartbeat-evoked potential: A proof-of-concept study

ObjectiveThe heartbeat evoked potential (HEP) is a brain response time-locked to the heartbeat and a potential marker of interoceptive processing that may be generated in the insula and dorsal anterior cingulate cortex (dACC). Low-intensity focused ultrasound (LIFU) can selectively modulate sub-regions of the insula and dACC to better understand their contributions to the HEP. MethodsHealthy participants (n = 16) received stereotaxically targeted LIFU to the anterior insula (AI), posterior insula (PI), dACC, or Sham at rest during continuous electroencephalography (EEG) and electrocardiography (ECG) recording on separate days. Primary outcome was HEP amplitudes. Relationships between LIFU pressure and HEP changes and effects of LIFU on heart rate and heart rate variability (HRV) were also explored. ResultsRelative to sham, LIFU to the PI, but not AI or dACC, decreased HEP amplitudes; PI effects were partially explained by increased LIFU pressure. LIFU did not affect heart rate or HRV. ConclusionsThese results demonstrate the ability to modulate HEP amplitudes via non-invasive targeting of key interoceptive brain regions. SignificanceOur findings have implications for the causal role of these areas in bottom-up heart-brain communication that could guide future work investigating the HEP as a marker of interoceptive processing in healthy and clinical populations.

3-methoxycatechol causes vasodilation likely via KV channels: ex vivo, in silico docking and in vivo study

Substituted catechols include both natural and synthetic compounds found in the environment and foods. Some of them are flavonoid metabolites formed by the gut microbiota which are absorbed afterwards. Our previous findings showed that one of these metabolites, 4-methylcatechol, exerts potent vasorelaxant effects in rats. In the current study, we aimed at testing of its 22 structural congeners in order to find the most potent structure and to investigate the mechanism of action. 3-methoxycatechol (3-MOC), 4-ethylcatechol, 3,5-dichlorocatechol, 4-tert-butylcatechol, 4,5-dichlorocatechol, 3-fluorocatechol, 3-isopropylcatechol, 3-methylcatechol and the parent 4-methylcatechol exhibited high vasodilatory activities on isolated rat aortic rings with EC50s ranging from ∼10 to 24 μM. Some significant sex-differences were found. The most potent compound, 3-MOC, relaxed also resistant mesenteric artery but not porcine coronary artery, and decreased arterial blood pressure in both male and female spontaneously hypertensive rats in vivo without affecting heart rate. It potentiated the vasodilation mediated by cAMP and cGMP, but did not impact L-type Ca2+-channels. By using two inhibitors, activation of voltage-gated potassium channels (KV) was found to be involved in the mechanism of action. This was corroborated by docking analysis of 3-MOC with the KV7.4 channel. None of the most active catechols decreased the viability of the A-10 rat embryonic thoracic aorta smooth muscle cell line. Our findings showed that various catechols can relax vascular smooth muscles and hence could provide templates for developing new antihypertensive vasodilator agents without affecting coronary circulation.

Thyroid Hormone Receptors in Control of Heart Rate.

Thyroid hormone has profound effects on cardiovascular functions, including heart rate. These effects can be mediated directly, for example, by changing the expression of target genes in the heart through nuclear thyroid hormone receptors, or indirectly by altering the autonomic nervous systems output of the brain. The underlying molecular mechanisms as well as the cellular substrates, however, are far from being understood. In this review, we summarize the recent key findings on the individual contributions of the two thyroid hormone receptor isoforms on the regulation of heart rate, challenging the role of the pacemaker channel genes Hcn2 and Hcn4 as sole mediators of the hormone's effect. Furthermore, we discuss the possible actions of thyroid hormone on the autonomic nervous system affecting heart rate distribution, and highlight the possibility of permanent alterations in heart and brain by impaired thyroid hormone action during development as important factors to consider when analyzing or designing experiments.

Predicting Sleep Quality through Biofeedback: A Machine Learning Approach Using Heart Rate Variability and Skin Temperature.

Sleep quality (SQ) is a crucial aspect of overall health. Poor sleep quality may cause cognitive impairment, mood disturbances, and an increased risk of chronic diseases. Therefore, assessing sleep quality helps identify individuals at risk and develop effective interventions. SQ has been demonstrated to affect heart rate variability (HRV) and skin temperature even during wakefulness. In this perspective, using wearables and contactless technologies to continuously monitor HR and skin temperature is highly suited for assessing objective SQ. However, studies modeling the relationship linking HRV and skin temperature metrics evaluated during wakefulness to predict SQ are lacking. This study aims to develop machine learning models based on HRV and skin temperature that estimate SQ as assessed by the Pittsburgh Sleep Quality Index (PSQI). HRV was measured with a wearable sensor, and facial skin temperature was measured by infrared thermal imaging. Classification models based on unimodal and multimodal HRV and skin temperature were developed. A Support Vector Machine applied to multimodal HRV and skin temperature delivered the best classification accuracy, 83.4%. This study can pave the way for the employment of wearable and contactless technologies to monitor SQ for ergonomic applications. The proposed method significantly advances the field by achieving a higher classification accuracy than existing state-of-the-art methods. Our multimodal approach leverages the synergistic effects of HRV and skin temperature metrics, thus providing a more comprehensive assessment of SQ. Quantitative performance indicators, such as the 83.4% classification accuracy, underscore the robustness and potential of our method in accurately predicting sleep quality using non-intrusive measurements taken during wakefulness.

Empagliflozin’s role in reducing ventricular repolarization heterogeneity: insights into cardiovascular mortality decline from the EMPATHY-HEART trial

BackgroundThe incidence of myocardial infarction (MI) and sudden cardiac death (SCD) is significantly higher in individuals with Type 2 Diabetes Mellitus (T2DM) than in the general population. Strategies for the prevention of fatal arrhythmias are often insufficient, highlighting the need for additional non-invasive diagnostic tools. The T-wave heterogeneity (TWH) index measures variations in ventricular repolarization and has emerged as a promising predictor for severe ventricular arrhythmias. Although the EMPA-REG trial reported reduced cardiovascular mortality with empagliflozin, the underlying mechanisms remain unclear. This study investigates the potential of empagliflozin in mitigating cardiac electrical instability in patients with T2DM and coronary heart disease (CHD) by examining changes in TWH.MethodsParticipants were adult outpatients with T2DM and CHD who exhibited TWH > 80 µV at baseline. They received a 25 mg daily dose of empagliflozin and were evaluated clinically including electrocardiogram (ECG) measurements at baseline and after 4 weeks. TWH was computed from leads V4, V5, and V6 using a validated technique. The primary study outcome was a significant (p < 0.05) change in TWH following empagliflozin administration.ResultsAn initial review of 6,000 medical records pinpointed 800 patients for TWH evaluation. Of these, 412 exhibited TWH above 80 µV, with 97 completing clinical assessments and 90 meeting the criteria for high cardiovascular risk enrollment. Empagliflozin adherence exceeded 80%, resulting in notable reductions in blood pressure without affecting heart rate. Side effects were generally mild, with 13.3% experiencing Level 1 hypoglycemia, alongside infrequent urinary and genital infections. The treatment consistently reduced mean TWH from 116 to 103 µV (p = 0.01).ConclusionsThe EMPATHY-HEART trial preliminarily suggests that empagliflozin decreases heterogeneity in ventricular repolarization among patients with T2DM and CHD. This reduction in TWH may provide insight into the mechanism behind the decreased cardiovascular mortality observed in previous trials, potentially offering a therapeutic pathway to mitigate the risk of severe arrhythmias in this population.Trial registrationNCT: 04117763.

Cardiovascular Dysautonomy as a Sequel of SARS COV 2. Case Series

The impact of COVID-19, caused by the SARS-CoV-2 virus, a pandemic that originated in Wuhan, China, can lead to serious complications, in addition to mild symptoms, with special interest in the autonomic nervous system (ANS). Damage to the ANS by SARS-CoV-2 can cause dysautonomia, an imbalance between the sympathetic and parasympathetic system, with unclear mechanisms such as cytokine storm, excessive inflammation, and virus neurotropism. A significant sequelae of COVID-19 is cardiac dysautonomia, which affects heart rate, blood pressure and other autonomic reflexes, causing postural tachycardia, orthostatic hypotension, arrhythmias and fatigue. There is decreased heart rate variability (HRV) in patients, suggesting dysautonomia. Long COVID syndrome can also include cardiac dysautonomia. To diagnose cardiac autonomic neuropathy, at least two of six criteria must be met, such as an SDNN less than 50 ms and an RMSSD less than 15 ms. The cases of cardiac dysautonomia below present several of these criteria met. Methods to evaluate cardiac dysautonomia include the COMPASS 31 scale and the orthostatic hypotension questionnaire (OHQ), but more research is still needed, especially in Mexico. The case study shows that those who followed non-pharmacological recommendations such as cardiovascular exercise, increased water intake and BMI control had improvement, while cases that did not follow these recommendations did not show significant improvements. Cardiac dysautonomia is a post-COVID-19 sequelae with high prevalence, highlighting the importance of non-invasive methods for its diagnosis. Even without symptoms, people can have this sequelae, so it is important to suspect cardiovascular disorders. The need for early intervention and monitoring of hygienic-dietary measures is emphasized to avoid the worsening and chronicity of cardiac dysautonomia, with the hope of preventing the development of chronic diseases and fatal outcomes.