scholarly journals Noninvasive estimation of aortic hemodynamics and cardiac contractility using machine learning

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Vasiliki Bikia ◽  
Theodore G. Papaioannou ◽  
Stamatia Pagoulatou ◽  
Georgios Rovas ◽  
Evangelos Oikonomou ◽  
...  

Abstract Cardiac and aortic characteristics are crucial for cardiovascular disease detection. However, noninvasive estimation of aortic hemodynamics and cardiac contractility is still challenging. This paper investigated the potential of estimating aortic systolic pressure (aSBP), cardiac output (CO), and end-systolic elastance (Ees) from cuff-pressure and pulse wave velocity (PWV) using regression analysis. The importance of incorporating ejection fraction (EF) as additional input for estimating Ees was also assessed. The models, including Random Forest, Support Vector Regressor, Ridge, Gradient Boosting, were trained/validated using synthetic data (n = 4,018) from an in-silico model. When cuff-pressure and PWV were used as inputs, the normalized-RMSEs/correlations for aSBP, CO, and Ees (best-performing models) were 3.36 ± 0.74%/0.99, 7.60 ± 0.68%/0.96, and 16.96 ± 0.64%/0.37, respectively. Using EF as additional input for estimating Ees significantly improved the predictions (7.00 ± 0.78%/0.92). Results showed that the use of noninvasive pressure measurements allows estimating aSBP and CO with acceptable accuracy. In contrast, Ees cannot be predicted from pressure signals alone. Addition of the EF information greatly improves the estimated Ees. Accuracy of the model-derived aSBP compared to in-vivo aSBP (n = 783) was very satisfactory (5.26 ± 2.30%/0.97). Future in-vivo evaluation of CO and Ees estimations remains to be conducted. This novel methodology has potential to improve the noninvasive monitoring of aortic hemodynamics and cardiac contractility.

2003 ◽  
Vol 81 (2) ◽  
pp. 125-128 ◽  
Author(s):  
Ghada S Hassan ◽  
Fazila Chouiali ◽  
Takayuki Saito ◽  
Fu Hu ◽  
Stephen A Douglas ◽  
...  

Recent studies have shown that the vasoactive peptide urotensin-II (U-II) exerts a wide range of action on the cardiovascular system of various species. In the present study, we determined the in vivo effects of U-II on basal hemodynamics and cardiac function in the anesthetized intact rat. Intravenous bolus injection of human U-II resulted in a dose-dependent decrease in mean arterial pressure and left ventricular systolic pressure. Cardiac contractility represented by ±dP/dt was decreased after injection of U-II. However, there was no significant change in heart rate or diastolic pressure. The present study suggests that upregulation of myocardial U-II may contribute to impaired myocardial function in disease conditions such as congestive heart failure.Key words: urotensin-II, rat, infusion, heart.


1997 ◽  
Vol 273 (6) ◽  
pp. H2826-H2831 ◽  
Author(s):  
John N. Lorenz ◽  
Evangelia G. Kranias

Phospholamban (PLB) regulates Ca2+- adenosinetriphosphatase activity in cardiac sarcoplasmic reticulum and participates in the regulation of myocardial performance. Animal models with altered levels of PLB permit in vivo evaluation of the physiological role of PLB. This study examined left ventricular (LV) performance in intact PLB heterozygous and homozygous mice under basal and stimulated conditions. A Millar Mikro-Tip transducer was inserted into the right carotid artery and advanced into the LV for direct measurement of ventricular pressure and the first derivative of intraventricular pressure (dP/d t). Baseline blood pressures were increased in PLB heterozygotes and even more so in PLB homozygotes compared with wild types (WT), and there were no differences in heart rate or LV end-diastolic pressure. The increase in pressure was primarily caused by an increase in systolic pressure. Baseline values for positive and negative dP/d t were linearly correlated with PLB levels. In PLB heterozygotes, contractile response to isoproterenol (Iso) was blunted compared with WT, but maximum rates of contraction were similar between the two groups. Contractile performance in PLB homozygous mice, which under baseline conditions was similar to maximum levels seen in WT, showed a blunted response to Iso, and maximum rates of contraction were significantly greater than in either of the other groups, indicating an essential but perhaps not exclusive role for PLB in mediating the inotropic effects of β-adrenergic agonists. The effects of Iso on negative dP/d t were also blunted in both PLB heterozygous and PLB homozygous animals. Our results demonstrate that myocardial function is highly dependent on PLB level and suggest that the cardiovascular effects of PLB perturbations are largely uncompensated for in the intact mouse.


2002 ◽  
Vol 282 (5) ◽  
pp. H1642-H1647 ◽  
Author(s):  
Satoshi Mohri ◽  
Kun-Lun He ◽  
Marc Dickstein ◽  
Yuval Mika ◽  
Juichiro Shimizu ◽  
...  

Inotropic effects of electric currents applied during the refractory period have been reported in cardiac muscle in vitro using voltage-clamp techniques. We investigated how electric currents modulate cardiac contractility in normal canine hearts in vivo. Six dogs were instrumented to measure regional segment length, ventricular volume (sonomicrometry), and ventricular pressure. Cardiac contractility modulating (CCM) electric currents (biphasic square pulses, amplitude ±20 mA, total duration 30 ms) were delivered during the refractory period between pairs of electrodes placed on anterior and posterior walls. CCM significantly increased index of global contractility ( E es) from 5.9 ± 2.9 to 8.3 ± 4.6 mmHg/ml with anterior CCM, from 5.3 ± 1.8 to 8.9 ± 4.0 mmHg/ml with posterior CCM, and from 6.1 ± 2.6 to 11.0 ± 7.0 mmHg/ml with combined CCM ( P < 0.01, no significant change in volume axis intercept). End-systolic pressure-segment length relations showed contractility enhancement near CCM delivery sites, but not remotely. Relaxation was not influenced. CCM increased mean aortic pressure, but did not change peripheral resistance. Locally applied electrical currents enhanced global cardiac contractility via regional changes in myocardial contractility without impairing relaxation in situ.


2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Rafael Jaimes ◽  
Meredith Sherman ◽  
Adam Swiercz ◽  
Narine Muselimyan ◽  
Paul Marvar ◽  
...  

Di-2-ethylhexyl phthalate (DEHP) is a plasticizer that is used to impart flexibility to polyvinyl chloride products. Patients have an increased exposure to phthalates through contact with DEHP-containing medical devices, including: storage bags containing blood, plasma, intravenous fluids, total parenteral nutrition, tubing associated with their administration, nasogastric tubes, enteral feeding tubes, catheters, extracorporeal membrane oxygenation (ECMO) circuits, hemodialysis tubing, respiratory masks and endotracheal tubes. Human health concerns pertaining to DEHP exposure are linked to its endocrine-disrupting properties. Accordingly, increased exposure has been associated with cancer, metabolic disturbances, reproductive and neurological disorders, and cardiovascular disease. As an example, epidemiological studies have shown a link between DEHP exposure and elevated systolic blood pressure in adolescents. Despite bans and restrictions on the use of DEHP-containing medical devices in other countries, there is currently no mandate from the Food & Drug Administration for the use of DEHP-free devices and storage containers. The objective of this study was to quantify the impact of in vivo DEHP exposure on cardiovascular function; thereby, providing additional information for regulatory decisions by the scientific, medical and regulatory community. Healthy C57BL/6 male mice were implanted with radiotelemetry transmitters; briefly, the transmitter catheter was placed in the carotid artery and biopotential leads were routed subcutaneously to collect electrocardiogram (ECG) signals. After surgical recovery, pre-exposure data was collected, and thereafter, animals were exposed to 0.2 mg/g DEHP or control diet. We observed a significant increase in systolic pressure in DEHP-treated (145 + 3 mmHg) vs control animals (136 + 1 mmHg). We also detected an increase in diastolic and mean arterial pressure in DEHP-treated (119 + 5 and 132 + 3 mmHg, respectively) vs control animals (107 + 2 and 121 + 2 mmHg). Our previous reports have shown that DEHP diminishes cardiac contractility, which suggests that these effects on blood pressure are likely attributed to alterations in sympathetic tone and/or an increase in vascular resistance.


2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S598-S598 ◽  
Author(s):  
Laurent Martarello ◽  
Vincent J Cunningham ◽  
Julian C Matthews ◽  
Eugenii Rabiner ◽  
Steen Jakobsen ◽  
...  

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S595-S595 ◽  
Author(s):  
Wynne K Schiffer ◽  
Deborah Pareto-Onghena ◽  
HaiTao Wu ◽  
Kuo-Shyan Lin ◽  
Andrew R Gibbs ◽  
...  

Planta Medica ◽  
2010 ◽  
Vol 76 (12) ◽  
Author(s):  
J Bauer ◽  
F Dehm ◽  
A Koeberle ◽  
F Pollastro ◽  
G Appendino ◽  
...  

2008 ◽  
Vol 56 (S 1) ◽  
Author(s):  
D Ruzicka ◽  
W Eichinger ◽  
I Hettich ◽  
S Bleiziffer ◽  
R Guenzinger ◽  
...  
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