Left ventricular strain rate is reduced during voluntary apnea in healthy humans

2017 ◽  
Vol 123 (6) ◽  
pp. 1730-1737 ◽  
Author(s):  
Joshua R. Smith ◽  
Shelbi L. Sutterfield ◽  
Dryden R. Baumfalk ◽  
Kaylin D. Didier ◽  
Shane M. Hammer ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Strain Rate ◽  
Blood Pressure Response ◽  
Left Ventricular ◽  
Rate Pressure Product ◽  
Healthy Humans ◽  
Arterial Blood ◽  
Strain And Strain Rate ◽  
Cardiac Afterload

During an apneic event, sympathetic nerve activity increases resulting in subsequent increases in left ventricular (LV) afterload and myocardial work. It is unknown how cardiac mechanics are acutely impacted by the increased myocardial work during an apneic event. Ten healthy individuals (23 ± 3 yr) performed multiple voluntary end-expiratory apnea (VEEA) maneuvers exposed to room air, while a subset ( n = 7) completed multiple VEEA exposed to hyperoxic air (100% [Formula: see text]). Beat-by-beat blood pressure, heart rate, and stroke volume were measured continuously. Effective arterial elastance (EA) was calculated as an index of cardiac afterload, and myocardial work was calculated as the rate pressure product (RPP). Tissue Doppler echocardiography was used to measure LV tissue velocities, deformation via strain, and strain rate (SR). Systolic blood pressure (Δ18 ± 13 mmHg, P < 0.01), EA (Δ0.13 ± 0.10 mmHg/ml, P < 0.01), and RPP (Δ9 ± 10 beats/min × mmHg 10−2, P < 0.01) significantly increased with room air VEEA. This occurred in parallel with decreases in peak longitudinal systolic (Δ−0.62 ± 0.41 cm/s, P < 0.01) and early LV filling (Δ−2.81 ± 1.99 cm/s, P < 0.01) myocardial velocities. Longitudinal SR (Δ−0.30 ± 0.32 1/s, P = 0.01) was significantly decreased during room air VEEA. VEEA with hyperoxia did not alter ( P > 0.18) EA or RPP and attenuated the systolic blood pressure response compared with room air. Myocardial velocities and LV strain rate response to VEEA were unchanged ( P = 0.30) with hyperoxia. Consistent with our hypotheses, VEEA-induced increases in EA and myocardial work impact LV mechanics, which may depend, in part, on stimulation of peripheral chemoreceptors. NEW & NOTEWORTHY Transient increases in arterial blood pressure and systemic vascular resistance occur during sleep apnea events and may contribute to the associated daytime hypertension and risk of overt cardiovascular disease. To date, the link between this apnea pressor response and acute changes in left ventricular function remains poorly understood. We demonstrate that in parallel to increases in cardiac afterload a depressed left ventricular systolic function occurs at end apnea.

P4372Left atrial strain: a potential marker of early diastolic dysfunction in patients with Marfan syndrome

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
E Garcia-Izquierdo Jaen ◽  
S Mingo Santos ◽  
M Torres Sanabria ◽  
V Monivas Palomero ◽  
S Moreno Casado ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Ejection Fraction ◽  
Strain Rate ◽  
Diastolic Dysfunction ◽  
Left Atrial ◽  
Left Ventricular ◽  
Healthy Controls ◽  
Left Atrial Strain ◽  
Strain And Strain Rate ◽  
Atrial Strain

Abstract Background/Introduction Previous studies using conventional echocardiographic measurements have reported subclinical left diastolic dysfunction in patients with Marfan syndrome (MFS). Left atrial strain (LAS) has been shown to be an accurate predictor of left ventricular diastolic dysfunction. However, there is no evidence regarding the use of LAS in MFS. Purpose To assess feasibility of LAS and compare LAS derived measurements along with traditional diastolic parameters in MFS patients vs healthy controls. Methods 46 MFS patients (normal LV ejection fraction, no previous cardiovascular surgery, no significant valvular regurgitation) vs. 20 healthy controls (age and sex-matched). We performed LAS analysis using 2D speckle-tracking (QLAB 10, Philips). LA strain was determined as the average value of the longitudinal deformation (7 segments) in the apical 4-chamber view (RR gating). Results LAS analysis was feasible in 40 MFS patients (87%). All participants had normal diastolic function according to current guidelines (ASE/EACVI 2016). MFS patients showed lower TDI e' velocities and higher average E/e' ratio, but still within normal range. Similarly, LVEF was normal but slightly reduced in MFS patients. LA strain and strain rate parameters during reservoir and conduit phase were significantly impaired in MFS patients compared to controls. MFS vs controls MFS patients (n=40) Controls (n=20) p MFS patients (n=40) Controls (n=20) p Age 33.8±12.4 34.4±8.3 0.846 Septal e' (cm/s) 9.7±2.5 11.7±2.3 0.006 Male (%) 24 (60%) 12 (60%) 1.000 Average E/e' ratio 6.8±1.5 5.5±1.1 0.002 SBP (mmHg) 120.3±12.4 120.1±9.4 0.969 TR velocity (cm/s) 208.6±21.4 201.6±22.9 0.390 DBP (mmHg) 72.0±10.1 67.1±6.2 0.069 LAVi (ml/m2) 23.5±7.1 25.5±4.8 0.260 Aortic root (mm) 40.3±4.6 31.7±3.7 <0.001 LASr (%) 32.6±8.8 43.0±8.3 <0.001 LVEF (%) 60.9±5.6 64.2±4.2 0.022 LAScd (%) −20.1±8.0 −29.4±5.5 <0.001 E-wave (cm/s) 74.6±16.5 76.7±16.5 0.651 LASct (%) −12.8±6.1 −13.6±5.2 0.622 A-wave (cm/s) 55.2±10.9 52.0±12.8 0.327 LASRr 2.02±0.49 2.31±0.43 0.030 E/A ratio 1.4±0.4 1.5±0.4 0.287 LASRcd −2.22±0.61 −3.07±0.68 <0.001 Lateral e' (cm/s) 13.0±3.6 16.3±3.3 0.002 LASRct −2.24±0.90 −2.35±0.75 0.600 SBP: Systolic blood pressure. DBP: Diastolic blood pressure. LVEF: Left ventricular ejection fraction. LAVi: Left atrial volume index. LAS: Left atrial strain. LASR: Left atrial strain rate. (r): Reservoir. (cd): Conduit. (ct): Contraction. Example of LA strain and strain rate Conclusion MFS patients showed a subtle impairment in diastolic function compared to controls. Although further evidence is needed, LAS derived parameters could be early markers of diastolic dysfunction in this group of patients. Acknowledgement/Funding Programa de Actividades de I+D de la Comunidad de Madrid

scholarly journals A METHOD TO DETERMINE THE PERIPHERAL ARTERIAL BLOOD PRESSURE IN THE MOUSE

1941 ◽  
Vol 74 (1) ◽  
pp. 29-40 ◽  
Author(s):  
Philip D. McMaster
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Arterial Blood Pressure ◽  
Close Agreement ◽  
Carotid Arteries ◽  
Systolic Pressure ◽  
Arterial Blood ◽  
Relative Transparency ◽  
Direct Measurements ◽  
Peripheral Arterial

Advantage has been taken of the relative transparency of the claw of the mouse to devise a method, here described, to measure the blood pressure in the animal's leg. Direct measurements of the systolic blood pressure from the carotid arteries of anesthetized mice have also been made. Simultaneous blood pressure readings by both these methods applied to the same animal showed close agreement. The systolic pressure ranged from 60 to 126 mm. Hg, according to the conditions.

scholarly journals Association arterial stiffness reduction with improved left ventricular longitudinal and torsional deformation after 3 years of antihypertensive treatment

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Tzortzis ◽  
I Ikonomidis ◽  
H Triantafyllidi ◽  
J Thymis ◽  
A Frogoudaki ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Stiffness ◽  
Ace Inhibitors ◽  
Antihypertensive Treatment ◽  
Left Ventricular ◽  
Torsional Deformation ◽  
Flow Reserve ◽  
Stiffness Reduction ◽  
Arterial Blood ◽  
Lv Mass

Abstract Background We investigated the effects of antihypertensive treatment on vascular function, longitudinal and torsional deformation in hypertensives. Methods In 200 untreated patients with arterial hypertension (age 52.5±11.6 years, 56% females), we measured at baseline and after a 3-year of antihypertensive treatment (160 received ACEi± diuretics and 40 CCBs± diuretics): a) 24h ambulatory blood pressure b) Carotid-femoral pulse wave velocity (PWV) b) Coronary flow reserve (CFR), LV mass index (LVMI), the global longitudinal strain (GLS) and diastolic (LongSRSE) strain rate, peak twisting (Tw-deg) and untwisting at mitral valve opening (UtwMVO), at peak E (UtwE) and at the end of the E wave (UtwendE) of the mitral inflow as well as twisting (TwVel-deg/sec) velocity using speckle tracking imaging. We calculated the % change of LV untwisting as difference between peakTw and UtwMVO, UtwpeakE and UtwendE. Results Compared to baseline, there was an improvement of GLS (−19.9±3.4 vs. −18.7±3.1%), LongSRS (−1.08±0.22 vs. −0.98±0.26 1/s), LongSRE (1.09±0.36 vs. 0.99±0.31 1/s), peak Tw (16.2±5.1 vs. 18.7±5.9 deg), Tw velocity, and the %LV untwisting (31.04±19.28 vs 26.02±15.69% at MVO, 60.04±19.78 vs 53.96±19.76% at peakE and 79.98±14.24 vs 75.90±17.01% at endE) post-treatment. In parallel, CFR (2.72±0.61 vs. 2.55±0.64), PWV (10.34±1.93 vs. 11.2±2.08 m/s) and LVMI were improved (p&lt;0.01 for all comparisons). By ANOVA, the interaction term between changes of all the above parameters and antihypertensive treatment (ACE inhibitors vs calcium channel blockers) was not significant (p&gt;0.05). By multivariate analysis, the reduction of 24h meanBP and PWV independently determined the respective improvement of GLS (b=0.478 and b=0.248 respectively), LongS (b=0.428 and b=0.201 respectively) as well as Twisting (b=0.449 and b=0.294 respectively) after adjusting for changes in LV mass, CFR and atherosclerotic risk factors (p&lt;0.05). Conclusions Long-term optimal blood pressure control with ACE inhibitors and CCBs improves LV longitudinal and torsional mechanics in hypertensives in parallel with arterial stiffness and blood pressure. This improvement in LV deformation and twisting was independently related to changes in arterial blood pressure and arterial stiffness. Funding Acknowledgement Type of funding source: None

Effect of chronic left ventricular failure on beta-endorphin

1992 ◽  
Vol 73 (6) ◽  
pp. 2675-2680 ◽  
Author(s):  
E. Mellow ◽  
E. Redei ◽  
K. Marzo ◽  
J. R. Wilson
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Chronic Heart Failure ◽  
Left Ventricular ◽  
Plasma Norepinephrine ◽  
Endogenous Opiates ◽  
Beta Endorphin ◽  
Arterial Blood ◽  
Norepinephrine Concentration ◽  
C 30

Stimulation of endogenous opiate secretion worsens circulatory dysfunction in several forms of shock, in part by inhibiting sympathetic activity. To investigate whether endogenous opiates have a similar effect in chronic heart failure (HF), we measured beta-endorphin concentrations and hemodynamic responses to naloxone infusion (2 mg/kg bolus + 2 mg.kg-1 x h-1) in six control (C) dogs and eight dogs with low-output HF produced by 3 wk of rapid ventricular pacing. The dogs with HF exhibited reduced arterial blood pressure (C, 123 +/- 4 vs. HF, 85 +/- 7 mmHg; P < 0.01) and cardiac outputs (C, 179 +/- 14 vs. HF, 76 +/- 2 ml.min-1 x kg-1; P < 0.01) and elevated plasma norepinephrine concentrations (C, 99 +/- 12 vs. HF, 996 +/- 178 pg/ml; P < 0.01) but normal beta-endorphin concentrations (C, 30 +/- 11 vs. HF, 34 +/- 12 pg/ml; P = NS). Naloxone produced similar transitory increases in blood pressure (C, 14 +/- 5 vs. HF, 26 +/- 25%) and cardiac output (C, 37 +/- 13 vs. HF, 22 +/- 15%) in both groups (both P = NS). No significant changes in norepinephrine concentration or systemic vascular resistance were observed in either group. These findings suggest that beta-endorphin secretion does not exacerbate circulatory dysfunction in chronic heart failure.

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