Abstract 16334: An Artificial Intelligence Derived Method for Instantaneous Detection of Elevated Left Ventricular End Diastolic Pressure

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Niema M Pahlevan ◽  
Rashid Alavi ◽  
Melissa Ramos ◽  
Antreas Hindoyan ◽  
Ray V Matthews
Keyword(s):  
Systems Approach ◽  
Diastolic Pressure ◽  
Medical Center ◽  
Aortic Pressure ◽  
Outcome Data ◽  
Left Ventricular ◽  
Heart Catheterization ◽  
Pressure Waveform ◽  
Arterial Waveform ◽  
Artificial Neural Network Ann

Introduction: Instantaneous, non-invasive detection of an elevated left ventricular end-diastolic pressure (LVEDP) offers a significant benefit in diagnosis and treatment of heart failure. We recently proposed a systems approach, called cardiac triangle mapping (CTM), that uses intrinsic frequencies (IFs) of the arterial waveform and pre-ejection period (PEP) to map the global ventricular function (Pahlevan et al. Fluids 4.1 (2019): 16). Here, we tested the hypothesis that an elevated LVEDP can be detected using ECG and arterial pressure waveform by applying an artificial neural network (ANN) combined with CTM approach. Methods: This study included 46 patients (12 females, age 39-90 (66.4±9.9), BMI 20.2-36.8 (27.6±4.1)) who were scheduled for a clinical left heart catheterization or coronary angiogram at the Keck Medical Center of USC. Exclusion criteria were valvular heart disease, atrial fibrillation, or left bundle branch block. Invasive LVEDP and aortic pressure waveforms were measured using a 3F Millar transducer tipped catheter with simultaneous 3 channel ECG. The IFs were computed from pressure waveforms. PEPs were calculated as the time difference between the beginning of QRS and the uprising of the pressure waveform. A 3-layer network consisted of 6 input, 6 hidden and one output nodes was developed. LVEDP=18 mmHg was used as the cut-off for a binary outcome. Data from 34 patients were used to design the ANN (27 for training, 7 for validation). The model was tested on 12 additional patients. Results: Our results showed a specificity of 87% and a sensitivity of 96% in detecting an elevated LVEDP (Fig.1). Conclusions: Here, we demonstrated the proof-of-concept that an AI model based on reduced-order parameters (extracted from arterial waveform and ECG) can instantaneously detect an elevated LVEDP. Although our hemodynamic measurements were done invasively, all variables that are required for this AI-LVEDP calculation can be collected noninvasively.

INFLUENCE OF ACIDEMIA ON LEFT VENTRICULAR FUNCTION IN THE NEWBORN LAMB

PEDIATRICS ◽  
1966 ◽  
Vol 38 (3) ◽  
pp. 457-464
Author(s):  
Norman S. Talner ◽  
Thomas H. Gardner ◽  
S. Evans Downing
Keyword(s):  
Left Ventricle ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Newborn Lamb ◽  
Precise Control ◽  
Significant Impairment ◽  
Ph Range

The performance of the left ventricle in 20 newborn lambs was examined in a preparation which allowed precise control of aortic pressure, cardiac output, heart rate, and temperature. Reduction of arterial pH from a normal range (7.35 to 7.5) to severe acidemia (6.8 to 7.0) by hydrochloric or lactic acid infusion resulted in no significant impairment of left ventricular function. Prolonged acidemia (over 2 hours) failed to produce a reduction in left ventricular stroke volume or mean ejection rate for a given left ventricular end-diastolic pressure. Responsiveness of the left ventricle of the lamb to catecholamine stimulation was not diminished over the pH range 7.5 to 6.8. Under conditions of these investigations the apparent resistance of the myocardium of the newborn lamb, as well as the adult cat, to wide variations in pH may reflect a buffering capacity of cardiac muscle which would allow minimal change in intracellular pH, even though extracellular pH may indicate the presence of severe metabolic acidosis.

Interaction of interval-force relationship with aortic pressure and stroke volume

1976 ◽  
Vol 230 (4) ◽  
pp. 893-900 ◽  
Author(s):  
ER Powers ◽  
Foster ◽  
Powell WJ
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Right Heart ◽  
Anesthetized Dogs ◽  
Right Heart Bypass ◽  
Force Relationship

The modification by aortic pressure and stroke volume of the response in cardiac performance to increases in heart rate (interval-force relationship) has not been previously studied. To investigate this interaction, 30 adrenergically blocked anesthetized dogs on right heart bypass were studied. At constant low aortic pressure and stroke volume, increasing heart rate (over the entire range 60-180) is associated with a continuously increasing stroke power, decreasing systolic ejection period, and an unchanging left ventricular end-diastolic pressure and circumference. At increased aortic pressure or stroke volume at low rates (60-120), increases in heart rate were associated with an increased performance. However, at increased aortic pressure or stroke volume at high rates (120-180), increases in heart rate were associated with a leveling or decrease in performance. Thus, an increase in aortic pressure or stroke volume results in an accentuation of the improvement in cardiac performance observed with increases in heart rate, but this response is limited to a low heart rate range. Therefore, the hemodynamic response to given increases in heart rate is critically dependent on aortic pressure and stroke volume.

scholarly journals Acute stimulation of the soluble guanylate cyclase does not impact on left ventricular capacitance in normal and hypertrophied porcine hearts in vivo

2018 ◽  
Vol 315 (3) ◽  
pp. H669-H680 ◽  
Author(s):  
Alessio Alogna ◽  
Michael Schwarzl ◽  
Martin Manninger ◽  
Nazha Hamdani ◽  
Birgit Zirngast ◽  
...  
Keyword(s):  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Concentric Hypertrophy ◽  
Ventricular Compliance ◽  
Left Ventricular Compliance ◽  
Stimulation Of

Experimental data indicate that stimulation of the nitric oxide-soluble guanylate cyclase(sGC)-cGMP-PKG pathway can increase left ventricular (LV) capacitance via phosphorylation of the myofilamental protein titin. We aimed to test whether acute pharmacological sGC stimulation with BAY 41-8543 would increase LV capacitance via titin phosphorylation in healthy and deoxycorticosteroneacetate (DOCA)-induced hypertensive pigs. Nine healthy Landrace pigs and 7 pigs with DOCA-induced hypertension and LV concentric hypertrophy were acutely instrumented to measure LV end-diastolic pressure-volume relationships (EDPVRs) at baseline and during intravenous infusion of BAY 41-8543 (1 and 3 μg·kg−1·min−1 for 30 min, respectively). Separately, in seven healthy and six DOCA pigs, transmural LV biopsies were harvested from the beating heart to measure titin phosphorylation during BAY 41-8543 infusion. LV EDPVRs before and during BAY 41-8543 infusion were superimposable in both healthy and DOCA-treated pigs, whereas mean aortic pressure decreased by 20–30 mmHg in both groups. Myocardial titin phosphorylation was unchanged in healthy pigs, but total and site-specific (Pro-Glu-Val-Lys and N2-Bus domains) titin phosphorylation was increased in DOCA-treated pigs. Bicoronary nitroglycerin infusion in healthy pigs ( n = 5) induced a rightward shift of the LV EDPVR, demonstrating the responsiveness of the pathway in this model. Acute systemic sGC stimulation with the sGC stimulator BAY 41-8543 did not recruit an LV preload reserve in both healthy and hypertrophied LV porcine myocardium, although it increased titin phosphorylation in the latter group. Thus, increased titin phosphorylation is not indicative of increased in vivo LV capacitance. NEW & NOTEWORTHY We demonstrate that acute pharmacological stimulation of soluble guanylate cyclase does not increase left ventricular compliance in normal and hypertrophied porcine hearts. Effects of long-term soluble guanylate cyclase stimulation with oral compounds in disease conditions associated with lowered myocardial cGMP levels, i.e., heart failure with preserved ejection fraction, remain to be investigated.

Abstract 10878: Validation of Non-invasive Measures of Diastolic Function in Children: A Simultaneous Echocardiography and Conductance Catheterization Study

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Shahryar M Chowdhury ◽  
Ryan J Butts ◽  
Anthony M Hlavacek ◽  
Carolyn L Taylor ◽  
Varsha M Bandisode ◽  
...  
Keyword(s):  
Diastolic Function ◽  
Diastolic Pressure ◽  
Ductus Arteriosus ◽  
Left Ventricular ◽  
Balloon Occlusion ◽  
Heart Catheterization ◽  
Active Relaxation ◽  
Non Invasive ◽  
Stiffness Constant ◽  
Lv Diastolic Function

Introduction: The accuracy of echocardiography in evaluating left ventricular (LV) diastolic function has not been validated in children. The objective of this study was to compare echocardiographic and gold-standard measures of LV diastolic function in children. Methods: Patients undergoing routine left heart catheterization were prospectively enrolled. Pressure-volume loops (PVL) were obtained via conductance catheters. The end-diastolic pressure-volume relationship was obtained via balloon occlusion of the vena cavae. PVL measures of diastolic function were divided into early active relaxation (the isovolumic relaxation time constant, tau), and ventricular stiffness (the chamber stiffness constant, β). End-diastolic pressure (EDP) was also recorded. Echocardiographic measures of diastolic function were derived from spectral Doppler, tissue Doppler, and 2D speckle-tracking. The relationships between PVL and echocardiographic measures were determined using Spearman’s correlation. Results: Of 24 patients, 18 patients were s/p heart transplant, 5 patients had a small patent ductus arteriosus or coronary fistula. Mean age was 9.1 ± 5.6 years. The median τ was 24.9 ms (IQR 22.8 - 28.4 ms), median β was 0.094 (IQR 0.035 - 0.154), and median EDP was 9 mmHg (IQR 8 - 13 mmHg). Statistically significant correlations between invasive and echocardiographic measures of diastolic function are reported in the Table. No echocardiographic measures correlated with β. Conclusion: Early diastolic echocardiographic measures correlate with tau and may accurately represent early active relaxation in children. Modest associations exist between echocardiographic measures and EDP. The use of these non-invasive measures in accurately assessing LV diastolic function appears promising in children. However, no echocardiographic measures correlate with chamber stiffness. The development of such measures merits further study.

Abstract 2432: Effect of Left Ventricular Systolic Dysfunction on Wasted Left Ventricular Energy and Tension-Time Index

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Scott J Denardo ◽  
Wilmer W Nichols
Keyword(s):  
Heart Failure ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Systemic Hypertension ◽  
Pressure Waveform ◽  
Ventricular Systolic Dysfunction ◽  
Time Index ◽  
Tension Time

Information obtained from the aortic pressure waveform is affected by age, physical condition, systemic hypertension, diabetes mellitus and coronary artery disease. However, alterations in the aortic pressure waveform in patients (pts) with heart failure and left ventricular systolic dysfunction (LVSD) have not been fully described, including a description of the effect on wasted LV pressure energy and tension-time index. Non-invasive high-fidelity radial artery tonometry was used for data acquisition, and a mathematical transfer function used to generate aortic pressure waveforms (see figure ). Pulse wave analysis (PWA) of the aortic pressure waveform was used to obtain information associated with LV/vascular coupling in 23 pts age 55±9.5 yrs with LVSD (mean LV ejection fraction, 22±6%) and compared to data collected from 23 normal subjects matched for age, gender, height, weight and heart rate. Measurements obtained using PWA in heart failure pts with LVSD demonstrate decreased wasted LV energy and tension time index, consistent with poor LV mechanical performance, in addition to decreased unaugmented pressure, pulse pressure, ejection duration and augmentation index. Further standardization of these aortic pressure waveform findings in heart failure pts may allow for the clinical use of arterial PWA to non-invasively estimate LVSD.

Abstract 15865: Analysis of Left Ventricular Assist Device Hemodynamics During Right Heart Catheterization Ramp Studies

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Alexander G Hajduczok ◽  
Katharine Julian ◽  
Carly Maucione ◽  
John P Boehmer
Keyword(s):  
Left Ventricular Assist Device ◽  
Ventricular Assist Device ◽  
Heart Function ◽  
Medical Center ◽  
Left Ventricular ◽  
Heart Catheterization ◽  
Right Heart ◽  
Assist Device ◽  
Ventricular Assist ◽  
Left Ventricular Assist

Background: Although hemodynamic-driven Left Ventricular Assist Device (LVAD) speed changes have been shown to improve patient outcomes, there is no standardized algorithm for how to best adjust LVAD speed for optimization of cardiac output (CO) and decompression of left sided filling pressures as measured by pulmonary capillary wedge (PCW). Methods: We performed a retrospective study of LVAD patients at Penn State Hershey Medical Center from 2015 to present, to identify those that ramp studies during right heart catheterizations. 470 patients were identified, of which 60 had ramp studies. Only studies with at least 4 of 5 standard ramp speeds were included. Any study that did not exhibit at least a 20% decrease in PCW, suggesting improper LVAD function or recovered heart function, was also excluded. 32 studies were included in final analysis: 11 HVAD, 12 HMIII, and 9 HMII. CO measured by thermodilution was reported. Standard ramp speeds, in rpm, were as follows: HVAD (2100, 2400, 2700, 3000, 3300), HMIII (4500, 5000, 5500, 6000, 6500), and HMII (8000, 9000, 10,000, 11,000, 12,000). Results: Combined data showed an average CO improvement of 22.3% and average PCW decrease of 89.7%. HMII and HMIII had similar improvements in CO, 44.4% and 43.8%, respectively; much greater than HVAD (17.2%). HMIII had the largest magnitude of decompression 141.5% versus 106.4% for HMII and 56.1% for HVAD. Suction events occurred at an overall rate of 9.4%, and were greatest in HVADs. Conclusion: We report the ramp study hemodynamics for three separate LVADs. Overall, our results suggest the HMIII is most responsive to changes in speed in terms of improvement of CO and decreased PCW. Addition of samples to this analysis may allow for algorithm development to provide clinical guidance regarding LVAD speed settings.

Nitric oxide modulates epicardial coronary basal vasomotor tone in awake dogs

1990 ◽  
Vol 258 (4) ◽  
pp. H1250-H1254 ◽  
Author(s):  
A. Chu ◽  
D. E. Chambers ◽  
C. C. Lin ◽  
W. D. Kuehl ◽  
F. R. Cobb
Keyword(s):  
Nitric Oxide ◽  
Coronary Flow ◽  
Diastolic Pressure ◽  
Coronary Vessels ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Vasomotor Tone ◽  
Coronary Vasomotor Tone ◽  
Endogenous Nitric Oxide

This study evaluates the role of endogenous nitric oxide in the modulation of basal coronary vasomotor tone by studying the effects of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide formation from L-arginine, on resting epicardial coronary diameter and coronary flow. L-NMMA (5 mg/kg) was infused in seven awake dogs chronically instrumented with coronary dimension crystals for measurement of epicardial coronary diameter, and Doppler flow probes for quantitation of phasic coronary flow (vasomotion of distal regulatory resistance coronary vessels). Epicardial coronary diameter decreased 5.5% from 3.47 +/- 0.17 to 3.28 +/- 0.15 mm (mean +/- SE). The diameter change was gradual, reaching a maximum at 13 +/- 2 min after infusion, and persistent, lasting greater than 90 min. Phasic coronary flow did not change. Mean aortic pressure significantly increased from 99 +/- 3 to 111 +/- 3 mmHg and heart rate decreased from 56 +/- 4 to 46 +/- 3 beats/min. Left ventricular end-diastolic pressure and contractility were not significantly altered. L-Arginine (66 mg/kg) but not D-arginine reversed all hemodynamic parameters. These data support an important role of nitric oxide in modulating basal epicardial coronary vasomotor tone and systemic vascular resistance.

Aortic pressure reduction redistributes transmural blood flow in dog left ventricle

1988 ◽  
Vol 254 (2) ◽  
pp. H361-H368 ◽  
Author(s):  
J. J. Smolich ◽  
P. L. Weissberg ◽  
A. Broughton ◽  
P. I. Korner
Keyword(s):  
Blood Flow ◽  
Diastolic Pressure ◽  
Blood Pressure Reduction ◽  
Wall Stress ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Pressure Reduction ◽  
Flow Ratio ◽  
Flow Reserve ◽  
Aortic Blood Pressure

We studied the effect of graded aortic blood pressure reduction on left ventricular (LV) blood flow in anesthetized, autonomically blocked, open-chest dogs at constant heart rate and mean left atrial pressure. Aortic diastolic pressure (ADP) was lowered from rest (average 116 mmHg) to 90, 75, and 60 mmHg with an arteriovenous fistula. Global and regional LV blood flow was measured with radioactive microspheres. Mean LV blood flow fell stepwise from 145 ml.min-1.100 g-1 at rest to 116 ml.min-1.100 g-1 at ADP of 60 mmHg, whereas the endocardial-to-epicardial flow ratio decreased from 1.20 to 0.84. The transmural redistribution of LV blood flow was not accompanied by increases in LV oxygen extraction, depression of LV contractility, LV dilatation or LV electrical dysfunction and also occurred in the presence of considerable coronary vasodilator flow reserve. Electrical evidence of subendocardial ischemia appeared at ADP of 32 mmHg and an endocardial-to-epicardial flow ratio of 0.41 in a subgroup of animals. We conclude that the redistribution of LV flow during moderate aortic pressure reduction was an appropriate physiological adjustment to uneven transmural alterations in regional LV wall stress and that it preceded a more pronounced redistribution evident with myocardial ischemia.

Arterial pressure-flow relations in the awake standing dog

1975 ◽  
Vol 229 (5) ◽  
pp. 1261-1270 ◽  
Author(s):  
W Enrlich ◽  
FV Schrijen ◽  
TA Solomon ◽  
E Rodriguez-Lopez ◽  
RL Riley
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Rate Increase ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Heart Rate Increase ◽  
Underlying Mechanisms ◽  
The Right

The transient circulatory changes following paced heart rate increase are reported from 133 trials with 6 unanesthetized dogs with chronically implanted monitoring devices for heart rate, cardiac output, aortic blood pressure, and mean right atrial pressure. In 62 trials with 2 of the dogs, pulmonary artery, and left ventricular end-diastolic pressure, as well as left ventricular dP/dt were also studied. The sequence of changes in pressures and flows is analyzed in terms of probable underlying mechanisms, particularly with respect to the nature of vascular resistances. The rise in aortic pressure and flow during the first 3 s of paced heart rate increase, before arterial stretch receptor reflexes become active, is more consistent with an effective downstream pressure of about 49 mmHg, presumably at the arteriolar level, than with an effective downstream pressure close to 0 mmHg at the right atrial level. In the pulmonary circulation where vascular reflex effects are less prominent, the pattern of pulmonary arterial pressure and flow for the entire 30 s of observation is consistent with an effective downstream pressure of 9 mmHg, presumably at the alveolar or pulmonary arteriolar level, rather than at the level of the left ventricular end-diastolic pressure.

Effects of L-thyroxine in rats with chronic heart failure after myocardial infarction

1987 ◽  
Vol 253 (2) ◽  
pp. H341-H346 ◽  
Author(s):  
R. Gay ◽  
T. A. Gustafson ◽  
S. Goldman ◽  
E. Morkin
Keyword(s):  
Myocardial Infarction ◽  
Diastolic Pressure ◽  
Treated Group ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Lv Function ◽  
Myosin Isoenzyme ◽  
Pressure Development ◽  
Isoenzyme Composition

The effects of thyroid hormone on left ventricular (LV) function and myosin isoenzyme distribution were evaluated in rats 3 wk after myocardial infarction. When compared with normal rats, animals selected for study had moderately severe LV dysfunction as judged by decreased aortic and LV systolic pressures and a 34% decrease in LV maximum rate of pressure development (dP/dt). Average LV end-diastolic pressure was increased to 26 +/- 1 mmHg from 5 +/- 1 mmHg. The infarcted rats were divided into saline-treated control (n = 10) and treatment (n = 13) groups. The latter group received thyroxine (T4, 1.5 micrograms/100 g body wt) immediately after the first determination of pressures and at 24 and 48 h. At 72 h, aortic and LV pressures and myosin isoenzyme composition were measured. In the thyroxine-treated group LV end-diastolic pressure decreased from 27 +/- 2 to 18 +/- 2 mmHg, and LV dP/dt increased from 5,627 +/- 249 to 6,064 +/- 355 mmHg/s. Heart rate and aortic pressure did not change. After saline injections, LV end-diastolic pressure remained elevated, and the other hemodynamic parameters were unchanged. Determination of ventricular myosin isoenzyme composition in the saline-treated group revealed an increase in the V3 myosin isoform and a decrease in the V1 isoform as compared with the normal values. This pattern was not altered by T4 treatment. A separate group (n = 7) of rats was treated with a 10 times larger dose of thyroxine (15 micrograms/100 g body wt) for the same period of time. In this group, there was neither hemodynamic improvement nor changes in myosin isoenzyme distribution.(ABSTRACT TRUNCATED AT 250 WORDS)

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