scholarly journals Simulation of Exercise-Induced Syncope in a Heart Model with Severe Aortic Valve Stenosis

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Matjaž Sever ◽  
Samo Ribarič ◽  
Marjan Kordaš
Keyword(s):  
Heart Rate ◽  
Aortic Valve ◽  
Vascular Resistance ◽  
Aortic Valve Stenosis ◽  
Case Reports ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Lumped Parameter ◽  
Pulmonary Arterial ◽  
Exercise Induced

Severe aortic valve stenosis (AVS) can cause an exercise-induced reflex syncope (RS). The precise mechanism of this syncope is not known. The changes in hemodynamics are variable, including arrhythmias and myocardial ischemia, and one of the few consistent changes is a sudden fall in systemic and pulmonary arterial pressures (suggesting a reduced vascular resistance) followed by a decline in heart rate. The contribution of the cardioinhibitory and vasodepressor components of the RS to hemodynamics was evaluated by a computer model. This lumped-parameter computer simulation was based on equivalent electronic circuits (EECs) that reflect the hemodynamic conditions of a heart with severe AVS and a concomitantly decreased contractility as a long-term detrimental consequence of compensatory left ventricular hypertrophy. In addition, the EECs model simulated the resetting of the sympathetic nervous tone in the heart and systemic circuit during exercise and exercise-induced syncope, the fluctuating intra-thoracic pressure during respiration, and the passive relaxation of ventricle during diastole. The results of this simulation were consistent with the published case reports of exertional syncope in patients with AVS. The value of the EEC model is its ability to quantify the effect of a selective and gradable change in heart rate, ventricular contractility, or systemic vascular resistance on the hemodynamics during an exertional syncope in patients with severe AVS.

scholarly journals A Novel Control Method for Rotary Blood Pumps as Left Ventricular Assist Device Utilizing Aortic Valve State Detection

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Dmitry Petukhov ◽  
Leonie Korn ◽  
Marian Walter ◽  
Dmitry Telyshev
Keyword(s):  
Heart Rate ◽  
Aortic Valve ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Control Method ◽  
Left Ventricular ◽  
Pump Speed ◽  
Pump Flow ◽  
Blood Pumps ◽  
Rotary Blood Pumps

A novel control method for rotary blood pumps is proposed relying on two different objectives: regulation of pump flow in accordance with desired value and the maintenance of partial support with an open aortic valve by the variation of pump speed. The estimation of pump flow and detection of aortic valve state was performed with mathematical models describing the first- and second generation of Sputnik rotary blood pumps. The control method was validated using a cardiovascular system model. The state of the aortic valve was detected with a mean accuracy of 91% for Sputnik 1 and 96.2% for Sputnik 2 when contractility, heart rate, and systemic vascular resistance was changed. In silico results for both pumps showed that the proposed control method can achieve the desired pump flow level and maintain the open state of the aortic valve by periodically switching between two objectives under contractility, heart rate, and systemic vascular resistance changes. The proposed method showed its potential for safe operation without adverse events and for the improvement of chances for myocardial recovery.

Cardiovascular responses to metabolic acidosis

1965 ◽  
Vol 208 (2) ◽  
pp. 237-242 ◽  
Author(s):  
S. Evans Downing ◽  
Norman S. Talner ◽  
Thomas H. Gardner
Keyword(s):  
Heart Rate ◽  
Metabolic Acidosis ◽  
Vascular Resistance ◽  
Diastolic Pressure ◽  
Cardiovascular Responses ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Precise Control ◽  
Arterial Ph

The performance of the left ventricle was examined in a feline preparation which allowed precise control of aortic pressure, cardiac output, heart rate, and temperature. The arterial pH, Po2, and Pco2 were continuously measured with a Jewett flow-through electrode assembly. Reduction of arterial pH from 7.45 to 6.80 by HCl or lactic acid infusion was associated with a minimal reduction or no change of left ventricular contractility as measured by the stroke volume or mean ejection rate for a given left ventricular end-diastolic pressure at a constant aortic pressure and heart rate. No evidence for a diminished positive inotropic response to norepinephrine was found. Simultaneous systemic and pulmonary pressure-flow curves demonstrated that metabolic acidosis caused a reduction of systemic vascular resistance and a concurrent increase of pulmonary vascular resistance.

Left Ventricular Remodeling in Degenerative Aortic Valve Stenosis

2021 ◽  
Vol 46 (5) ◽  
pp. 100801
Author(s):  
João Abecasis ◽  
Daniel Gomes Pinto ◽  
Sância Ramos ◽  
Pier Giorgio Masci ◽  
Nuno Cardim ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Aortic Valve Stenosis ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular

Regional blood volume distribution during positive and negative airway pressure breathing in supine humans

1993 ◽  
Vol 75 (4) ◽  
pp. 1740-1747 ◽  
Author(s):  
J. Peters ◽  
B. Hecker ◽  
D. Neuser ◽  
W. Schaden
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Airway Pressure ◽  
Left Ventricular ◽  
Whole Body ◽  
Blood Content ◽  
Calf Blood Flow ◽  
Negative Airway Pressure

To assess the effects of continuous positive (CPAP) or negative airway pressure (CNAP) breathing (+/- 10#x2013;12 cmH2O, duration 25 min) on blood content in the body's capacitance vasculature, regional distribution of labeled red blood cells was evaluated in seven spontaneously breathing supine volunteers. Counts were acquired by whole body scans and detectors overlying the liver, intestine, left ventricle, and lower arm, and arterial pressure, heart rate, calf blood flow and vascular resistance, hematocrit, vasopressin, and atrial natriuretic peptide plasma concentrations were also obtained. With CPAP, thoracic, cardiac, and left ventricular counts diminished significantly by 7#x2013;10%, were accompanied by significant increases in counts over both the gut and liver, and remained decreased during CPAP but reversed to baseline with zero airway pressure. Calf blood flow and vascular resistance significantly decreased and increased, respectively, whereas limb counts, arterial pressure, heart rate, and hormone concentrations remained unchanged. With CNAP, in contrast, regional counts and other variables did not change. Thus, moderate levels of CPAP deplete the intrathoracic vascular bed and heart, shifting blood toward the gut and liver but not toward the limbs. No short-term compensation increasing cardiac filling during CPAP was seen. In contrast, CNAP did not alter intrathoracic or organ blood content and, therefore, does not simply mirror the effects evoked by CPAP.

scholarly journals Upregulated Autophagy in Calcific Aortic Valve Stenosis Confers Protection of Valvular Interstitial Cells

2019 ◽  
Vol 20 (6) ◽  
pp. 1486 ◽  
Author(s):  
Miguel Carracedo ◽  
Oscar Persson ◽  
Peter Saliba-Gustafsson ◽  
Gonzalo Artiach ◽  
Ewa Ehrenborg ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Aortic Valve Stenosis ◽  
Interstitial Cells ◽  
Left Ventricular ◽  
Autophagic Flux ◽  
Valvular Interstitial Cells ◽  
Survival Mechanism ◽  
Calcified Tissue ◽  
Left Ventricular Outflow

Autophagy serves as a cell survival mechanism which becomes dysregulated under pathological conditions and aging. Aortic valve thickening and calcification causing left ventricular outflow obstruction is known as calcific aortic valve stenosis (CAVS). CAVS is a chronic and progressive disease which increases in incidence and severity with age. Currently, no medical treatment exists for CAVS, and the role of autophagy in the disease remains largely unexplored. To further understand the role of autophagy in the progression of CAVS, we analyzed expression of key autophagy genes in healthy, thickened, and calcified valve tissue from 55 patients, and compared them with nine patients without significant CAVS, undergoing surgery for aortic regurgitation (AR). This revealed a upregulation in autophagy exclusively in the calcified tissue of CAVS patients. This difference in autophagy between CAVS and AR was explored by LC3 lipidation in valvular interstitial cells (VICs), revealing an upregulation in autophagic flux in CAVS patients. Inhibition of autophagy by bafilomycin-A1 led to a decrease in VIC survival. Finally, treatment of VICs with high phosphate led to an increase in autophagic activity. In conclusion, our data suggests that autophagy is upregulated in the calcified tissue of CAVS, serving as a compensatory and pro-survival mechanism.

Sign in / Sign up

Export Citation Format

Share Document