Electrical Cardiometry and Cardiac Biomarkers in 24-h and 48-h Ultramarathoners

Author(s):  
Che-Hung Liu ◽  
Li-Hua Li ◽  
Ming-Long Chang ◽  
Wei-Fong Kao ◽  
Chorng-Kuang How ◽  
...  

AbstractOur study aimed to (i) utilize novel electrical cardiometry and observe acute changes in cardiac biomarkers among 24-h and 48-h ultra-marathoners, and (ii) examine whether alterations in cardiac responses were associated with the average running speed of these participants. Twenty-four 24-h and sixteen 48-h ultra-marathoners were recruited. Electrical cardiometry in the 2 groups showed significant post-race drops in systolic pressure (24-h: p=0.001; 48-h: p=0.016) and rapid increases in heart rate (24-h, p=0.004; 48-h, p=0.001). Cardiac output increased in 48-h runners (p=0.012) and stroke volume decreased in 24-h runners (p=0.009) at post-test. Six of 20 (30%) 24-h and 4 of 16 (25%) 48-h runners had high-sensitivity troponin T values above the reference interval after the races. N-terminal proB-type natriuretic peptide levels showed a 15-fold increase in 24-h runners and a 10-fold increase in 48-h runners at post-race. There was a positive correlation between delta N-terminal proB-type natriuretic peptide and running mileage (rs=0.629, p=0.003) in 24-h ultra-marathoners. In conclusion, stroke volume and cardiac output showed inconsistent changes between the 2 groups. Average running speed has a significant effect on post-exercise elevation in cardiac biomarkers.

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Sasha Z Prisco ◽  
Megan Eklund ◽  
Kurt W Prins

Introduction: Pulmonary arterial hypertension (PAH) is caused by obstructive remodeling of the pulmonary arteries which ultimately causes right ventricle (RV) failure and death. Increased expression of the glucose membrane transporters Glut1 and Glut4 occurs in the failing RV, but the upstream regulators of these proteins are unknown. The With-no-Lysine (WNK) kinase-1, a kinase activated in low chloride conditions, promotes expression of Glut1/4 in skeletal muscle, but its regulation in the RV in PAH is unexplored. Furthermore, the relationship between WNK1 and protein O-GlcNAcylation, a glucose based post-translational modification, has not been examined. Methods: Immunoblots quantified the abundance of WNK1, Glut1, Glut4, and total protein O-GlcNAcylation in the RV of control, monocrotaline (MCT) rats, and MCT rats treated with a WNK inhibitor two weeks after MCT injection. Echocardiography and pressure-volume loop analysis assessed RV function and pulmonary vascular disease severity. Results: Treatment with WNK inhibitor improved TAPSE (2.4±0.1 vs 1.8±0.1 mm, p =0.0007), cardiac output (86.0±9.1 vs 52.5±5.6 ml/min, p =0.02), and cardiac output normalized body weight (0.26±0.03 vs 0.15±0.02 ml/min/g, p =0.0032). Importantly, the WNK inhibitor did not alter pulmonary vascular disease severity as there were no differences in pulmonary artery acceleration time (18.2±1.5 vs 14.2±0.9 sec, p =0.22), Ea (0.58±0.07 vs 0.58±0.08 mmHg/μL, p=1.00), or right ventricular systolic pressure (71.8±7.6 vs 72.0±4.0 mmHg, p =1.00) compared to MCT. At the molecular level, WNK1 inhibition decreased expression of WNK1 (MCT: 1.3±0.2 fold increase, MCT-WNK: 3.4±2.2 fold decrease), Glut1 (MCT: 2.7±0.9 fold increase, MCT-WNK: 1.2±0.2 fold increase), Glut4 (MCT: 1.7±0.4 fold increase, MCT-WNK: 1.0±0.2 fold increase), and protein O-GlcNAcylation (MCT: 2.4±0.7 fold increase, MCT-WNK: 1.1±0.1 fold increase). Conclusions: WNK inhibition normalized Glut1/4 expression and protein O-GlcNAcylation in the RV. These molecular changes resulted in improved RV function without a change in pulmonary vascular disease burden.


1983 ◽  
Vol 104 (1) ◽  
pp. 193-201 ◽  
Author(s):  
B. Grubb ◽  
D. D. Jorgensen ◽  
M. Conner

Cardiovascular variables were studied as a function of oxygen consumption in the emu, a large, flightless ratite bird well suited to treadmill exercise. At the highest level of exercise, the birds' rate of oxygen consumption (VO2) was approximately 11.4 times the resting level (4.2 ml kg-1 min-1). Cardiac output was linearly related to VO2, increasing 9.5 ml for each 1 ml increase in oxygen consumption. The increase in cardiac output is similar to that in other birds, but appears to be larger than in mammals. The venous oxygen content dropped during exercise, thus increasing the arteriovenous oxygen content difference. At the highest levels of exercise, heart rate showed a 3.9-fold increase over the resting rate (45.8 beats min-1). The mean resting specific stroke volume was 1.5 ml per kg body mass, which is larger than shown by most mammals. However, birds have larger hearts relative to body mass than do mammals, and stroke volume expressed per gram of heart (0.18 ml g-1) is similar to that for mammals. Stroke volume showed a 1.8-fold increase as a result of exercise in the emus, but a change in heart rate plays a greater role in increasing cardiac output during exercise.


Children ◽  
2021 ◽  
Vol 8 (10) ◽  
pp. 936
Author(s):  
David B. Healy ◽  
Eugene M. Dempsey ◽  
John M. O’Toole ◽  
Christoph E. Schwarz

Non-invasive cardiac output methods such as Electrical Cardiometry (EC) are relatively novel assessment tools for neonates and they enable continuous monitoring of stroke volume (SV). An in-silico comparison of differences in EC-derived SV in relation to preset length and weight was performed. EC (ICON, Osypka Medical) was simulated using the “demo” mode for various combinations of length and weight representative of term and preterm infants. One-centimetre length error resulted in a SV-change of 1.8–3.6% (preterm) or 1.6–2.0% (term) throughout the tested weight ranges. One-hundred gram error in weight measurement resulted in a SV-change of 5.0–7.1% (preterm) or 1.5–1.8% (term) throughout the tested length ranges. Algorithms to calculate EC-derived SV incorporate anthropomorphic measurements. Therefore, inaccuracy in physical measurement can impact absolute EC measurements. This should be considered in the interpretation of previous findings and the design of future clinical studies of EC-derived cardiac parameters in neonates, particularly in the preterm cohorts where a proportional change was noted to be greatest.


2021 ◽  
pp. 43-46
Author(s):  
Yu.S. Lobanov ◽  
◽  
S.L. Lobanov ◽  
K.G. Shapovalov ◽  
◽  
...  

Aim of the study. To study alterations in macrohaemodynamics in diff erent modes of retropneumoperitoneum during retroperitoneal surgery. Material and methods. A total of 58 patients aged 40-60, both male and female, with previous surgeries on renal cysts through retroperitoneal approach were studied aft er distribution between 2 groups. In the fi rst group, the pressure did not exceed 12 mm Hg. The RPP in the second group was observed to be 12-16 mm Hg. During the surgical intervention, analysis of the cardiovascular system values was carried out using the method of volume compression oscillometry. Results. Evaluation of macrohaemodynamics revealed significant deviation of the indices in patients with high RPP (group 2). Elevated true systolic pressure was revealed, as well as cardiac output decrease by 20 %, decrease of the cardiac index by 24 % and decrease of the stroke volume by 11 %. Th e patients treated with application of the highest gas pressure in the retroperitoneal space were revealed to have decrease in the linear velocity of blood fl ow by 17 % and elevation of total systemic vascular resistance (TSVR) by 12 %. Conclusion. Th erefore, the RPP value of 12-16 mm Hg exerts significant influence on the patient’s macrohaemodynamic status


2002 ◽  
Vol 103 (5) ◽  
pp. 493-499 ◽  
Author(s):  
Alison J. DEARY ◽  
Anne L. SCHUMANN ◽  
Helen MURFET ◽  
Stephen HAYDOCK ◽  
Roger S. FOO ◽  
...  

Recent studies have suggested a differential influence of mean pressure and pulse pressure on myocardial infarction and stroke, and differences among the major drugs in their efficacy at preventing these individual endpoints. We hypothesized that antihypertensive drugs have differing influences upon the pulse wave even when their effects on blood pressure are the same. We studied 30 untreated hypertensive patients, aged 28—55 years, who were rotated through six 6-week periods of daily treatment with amlodipine 5mg, doxazosin 4mg, lisinopril 10mg, bisoprolol 5mg, bendrofluazide 2.5mg or placebo. The best drug was repeated at the end of the rotation. Blood pressure readings and radial pulse tonometry (by Sphygmocor®) were performed at each visit, and blood was taken for measurement of levels of atrial natriuretic peptide and brain natriuretic peptide (BNP). The Sphygmocor derivation of the central aortic pulse wave was used to measure time for transmission of the reflected wave (TR) and the augmentation index (AI), which is the proportional increase in systolic pressure due to the reflected wave. There was a dissociation between the effects of the drugs on blood pressure and pulse wave analysis. Bisoprolol caused the greatest falls in blood pressure and TR, but was the only drug to increase AI. This paradoxical response to bisoprolol was associated with a 3-fold increase in plasma BNP levels. There was a smaller elevation of BNP in women compared with men, as described previously, and this elevation also was associated with significantly higher values of AI. Other drugs reduced AI, and this was associated with a significant decrease in BNP by amlodipine. In conclusion, antihypertensive drugs differ in their short-term effects on augmentation of the systolic pulse wave and secretion of BNP from the heart, regarded as a sensitive measure of strain on cardiomyocytes. These differences may help to explain cause-specific differences in outcome in recent trials.


1994 ◽  
Vol 266 (4) ◽  
pp. H1572-H1580 ◽  
Author(s):  
M. Toth ◽  
K. H. Vuorinen ◽  
O. Vuolteenaho ◽  
I. E. Hassinen ◽  
P. A. Uusimaa ◽  
...  

We determined the effect of hypoxia on cellular energy state and ventricular atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and endothelin-1 (ET-1) release in an isolated perfused heart preparation after removal of all atrial tissue in 21- to 24-mo-old Wistar-Kyoto rats. After a control period (14 min), the ventricles (n = 6) were exposed to 30 min of hypoxia by changing the gas mixture to N2-CO2 (95:5 vol/vol; hypoxic period) and back to O2-CO2 (95:5 vol/vol) for 30 min (reoxygenation period). Control hearts (n = 6) were perfused throughout the experiment (74 min) with oxygenated Krebs-Henseleit phosphate-free buffer. In parallel experiments, the metabolic state of oxygenated (n = 4) and hypoxic (n = 5) ventricles was assessed using 31P-nuclear magnetic resonance (31P-NMR). Hypoxia caused a rapid decrease in left ventricular peak systolic pressure associated with a 2.1-fold increase (27.6 +/- 2.2 to 58.0 +/- 13.1 fmol/ml; P < 0.05) in the concentration of immunoreactive (ir) ANP and a 1.6-fold increase (2.5 +/- 0.2 to 3.9 +/- 0.5 fmol/ml; P < 0.05) in the [irBNP] (where brackets signify concentration) in the perfusate. In contrast, perfusate [irET-1] (1.2 +/- 0.2 fmol/ml) did not change significantly during hypoxia. 31P-NMR showed that the [ATP]-to-[ADP].[Pi] ratio was reduced during hypoxia with a simultaneous increase in intracellular monophosphates and perfusate [irANP] and [irBNP]. The decrease in the cytosolic pH during hypoxia was small. High-performance liquid chromatography of the perfusates showed that the ANP-like immunoreactive material released corresponded to the processed, low-molecular weight peptide.(ABSTRACT TRUNCATED AT 250 WORDS)


1987 ◽  
Vol 63 (1) ◽  
pp. 270-276 ◽  
Author(s):  
J. M. Hagberg ◽  
S. J. Montain ◽  
W. H. Martin

Recently, systolic and diastolic blood pressure have been reported to be significantly lower for several hours after exercise than when measured at rest before exercise in individuals with essential hypertension. We sought to determine the hemodynamic mechanism underlying this reduction in blood pressure. Twenty-four men and women 60–69 yr of age with persistent essential hypertension completed one of the following protocols: exercise at 50% of maximum O2 consumption (VO2 max) followed by 1 h of recovery, exercise at 70% of VO2 max followed by 3 h of recovery, or a 4-h control study. Systolic pressure was significantly lower during recovery after both intensities of exercise, but diastolic pressure was unchanged. The lower blood pressure was primarily due to a reduction in cardiac output, since total peripheral resistance was increased throughout both recovery periods. Cardiac output was reduced in recovery because of a reduction in stroke volume. Heart rate was above, or no different from, that at rest before exercise. Changes in plasma volume could not entirely account for the reduction in stroke volume. Therefore, other mechanisms altering venous return and/or myocardial contractility appear to be responsible for the reduction in systolic blood pressure evident after a single bout of submaximal exercise in individuals with essential hypertension.


2020 ◽  
Author(s):  
Reidun Aarsetøy ◽  
Torbjørn Omland ◽  
Helge Røsjø ◽  
Heidi Strand ◽  
Thomas Werner Lindner ◽  
...  

Abstract Background: Early risk stratification applying cardiac biomarkers may prove useful in sudden cardiac arrest patients. We investigated the prognostic utility of early-on levels of high sensitivity cardiac troponin-T (hs-cTnT), copeptin and N-terminal pro-B-type natriuretic peptide (NT-proBNP) in patients with out-of-hospital cardiac arrest (OHCA).Methods: We conducted a prospective observational unicenter study, including patients with OHCA of assumed cardiac origin from the Southwestern part of Norway from 2007 until 2010. Blood samples for later measurements were drawn during cardiopulmonary resuscitation or at hospital admission. Results: A total of 114 patients were included, 37 patients with asystole and 77 patients with VF as first recorded heart rhythm. Forty-four patients (38.6%) survived 30-day follow-up. Neither hs-cTnT (p = 0.49), nor copeptin (p = 0.39) differed between non-survivors and survivors, whereas NT-proBNP was higher in non-survivors and significantly associated with time to death, with a hazard ratio (HR) for patients in the highest compared to the lowest quartile of 4.6 (95% CI 2.1 – 10.1), p < 0.001. This association was attenuated in the multivariable analysis [HR 2.18 (95% CI 0.83 – 5.72)], p = 0.11. NT-proBNP was significantly higher in asystole- as compared to VF-patients, p < 0.001.Conclusions: In OHCA, NT-proBNP was significantly associated with 30-day survival in univariate analysis, but associations were attenuated after multivariable adjustment. Hs-cTnT and copeptin did not provide prognostic information following OHCA.Clinical Trial Registration: ClinicalTrials. gov, NCT02886273.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Efstratios Koutroumpakis ◽  
Tariq Thannoun ◽  
Jason Pang ◽  
Ritesh Patel ◽  
Cullen Grable ◽  
...  

Introduction: In a time span of 6 months, COVID-19 has infected more than 7 million and cost the lives of more than 400,000 people worldwide. Cardiovascular involvement is associated with adverse clinical outcomes. Hypothesis: Increased plasma troponin and brain natriuretic peptide (BNP) or NT-proB-type natriuretic peptide (NT-proBNP) levels are associated with the presence of underlying cardiovascular disease and predict increased in-hospital mortality. Methods: Here we present a multicenter observational study of patients diagnosed with COVID-19, who were hospitalized in 5 hospitals (4 in Texas and 1 in New York) between March 16 th and May 22 nd , 2020. Demographic and clinical characteristics were abstracted after patient’s discharge or death. To address the non-standard troponin and BNP/NT-proBNP assays across institutions we used the upper 99th percentile as the cut-off for abnormal on each test. Results: We identified 297 consecutive patients hospitalized with COVID-19. Troponin levels were available in 84% and BNP/NT-proBNP levels in 47% of patients. Troponin levels were increased in 14% and BNP/NT-proBNP in 46% of patients. In multivariate Cox analysis, history of coronary artery disease was independently associated with elevated troponin levels (Hazard Ratio [HR]: 5.24; 95% confidence interval [CI]: 1.37-19.97; p=0.015), while history of congestive heart failure was independently associated with elevated BNP/NT-proBNP levels (HR: 2.58; 95% CI: 1.05 6.31; p=0.038). Older age, history of hypertension, dyslipidemia, or stroke, were associated with elevated troponin or BNP/NT-proBNP levels only in the univariate analysis. Other demographic and clinical characteristics were not significantly associated with cardiac biomarker elevation. Collectively, elevated troponin or BNP/NT-proBNP were significantly associated with in-hospital mortality (HR: 3.47 95% CI: 1.90-6.35 and HR: 3.56; 95% CI: 1.44-8.77, respectively; both p<0.01). Conclusions: Increased levels of cardiac biomarkers were associated with a 3-fold increase of in-hospital mortality among patients with COVID-19. Troponin or BNP/pro-BNP testing has a prognostic value and may guide treatment.


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