scholarly journals Acute and Long-Term Effects of Aortic Compliance Decrease on Central Hemodynamics: A Modeling Analysis

2021 ◽  
Vol 12 ◽  
Author(s):  
Stamatia Pagoulatou ◽  
Dionysios Adamopoulos ◽  
Georgios Rovas ◽  
Vasiliki Bikia ◽  
Nikolaos Stergiopulos
Keyword(s):  
Augmentation Index ◽  
Left Ventricular ◽  
Central Hemodynamics ◽  
Aortic Compliance ◽  
Long Term Effects ◽  
Wave Separation ◽  
Modeling Analysis ◽  
Lv Remodeling ◽  
Type C

Aortic compliance is an important determinant of cardiac afterload and a contributor to cardiovascular morbidity. In the present study, we sought to provide in silico insights into the acute as well as long-term effects of aortic compliance decrease on central hemodynamics. To that aim, we used a mathematical model of the cardiovascular system to simulate the hemodynamics (a) of a healthy young adult (baseline), (b) acutely after banding of the proximal aorta, (c) after the heart remodeled itself to match the increased afterload. The simulated pressure and flow waves were used for subsequent wave separation analysis. Aortic banding induced hypertension (SBP 106 mmHg at baseline versus 152 mmHg after banding), which was sustained after left ventricular (LV) remodeling. The main mechanism that drove hypertension was the enhancement of the forward wave, which became even more significant after LV remodeling (forward amplitude 30 mmHg at baseline versus 60 mmHg acutely after banding versus 64 mmHg after remodeling). Accordingly, the forward wave’s contribution to the total pulse pressure increased throughout this process, while the reflection coefficient acutely decreased and then remained roughly constant. Finally, LV remodeling was accompanied by a decrease in augmentation index (AIx 13% acutely after banding versus −3% after remodeling) and a change of the central pressure wave phenotype from the characteristic Type A (“old”) to Type C (“young”) phenotype. These findings provide valuable insights into the mechanisms of hypertension and provoke us to reconsider our understanding of AIx as a solely arterial parameter.

scholarly journals Benefits of long-term β-blockade in experimental chronic aortic regurgitation

2008 ◽  
Vol 294 (4) ◽  
pp. H1888-H1895 ◽  
Author(s):  
Eric Plante ◽  
Dominic Lachance ◽  
Serge Champetier ◽  
Marie-Claude Drolet ◽  
Élise Roussel ◽  
...  
Keyword(s):  
Adrenergic Receptor ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Prolonged Treatment ◽  
Adrenergic System ◽  
Lv Function ◽  
Adrenergic Blockade ◽  
Long Term Effects ◽  
Lv Remodeling

The objective of this study was to assess the long-term effects of β-blockade on survival and left ventricular (LV) remodeling in rats with aortic valve regurgitation (AR). The pharmacological management of chronic AR remains controversial. No drug has been definitively proven to delay the need for valve replacement or to affect morbidity and/or mortality. Our group has reported that the adrenergic system is activated in an animal model of AR and that adrenergic blockade may help maintain normal LV function. The effects of prolonged treatment with a β-blocker are unknown. Forty Wistar rats with severe AR were divided into 2 groups of 20 animals each and treated with metoprolol (Met, 25 mg·kg−1·day−1) or left untreated for 1 yr. LV remodeling was evaluated by echocardiography. Survival was assessed by Kaplan-Meir curves. Hearts were harvested for tissue analysis. All Met-treated animals were alive after 6 mo vs. 70% of untreated animals. After 1 yr, 60% of Met-treated animals were alive vs. 35% of untreated animals ( P = 0.028). All deaths, except one, were sudden. There were no differences in LV ejection fraction (all >50%) or LV dimensions. LV mass tended to be lower in the Met-treated group. There was less subendocardial fibrosis in this group, as well as lower LV filling pressures (LV end-diastolic pressure). β-Adrenergic receptor ratio (β1/β2) was improved. One year of treatment with Met was well tolerated. Met improved 1-yr survival, minimized LV hypertrophy, improved LV filling pressures, decreased LV subendocardial fibrosis, and helped restore the β-adrenergic receptor ratio.

Abstract P138: Long-term Effects Of Severe Caloric Restriction To The Heart Function

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Aline M De Souza ◽  
Jonathas Almeida ◽  
Nataliia Shults ◽  
Hong Ji ◽  
Kathryn Sandberg
Keyword(s):  
Cardiovascular Disease ◽  
Caloric Restriction ◽  
Heart Function ◽  
Left Ventricular ◽  
Structure And Function ◽  
Long Term Effects ◽  
Isolated Hearts ◽  
Ad Libitum ◽  
And Function

Severe caloric restriction (sCR) increases the risk for acute cardiovascular disease. Less understood are the long-term effects on cardiovascular disease risk after the sCR period has ended. We investigated the effects of sCR on heart structure and function months after refeeding (sCR-Refed). Female Fischer rats (3-months-old) were maintained on (CT) ad libitum or a 60% caloric restricted diet for 2 weeks. Thereafter, all rats received ad libitum chow for 3 months and they were analyzed by precision ultrasound to assess their heart function. After imaging, the animals were sacrificed and the hearts were subjected to ischemia-reperfusion (I/R) using a Langendorff preparation. After 2 weeks of sCR, rats lost 15% of their initial body weight (BW) [% (100*(Final-Initial/Initial)): CT, 1.5±0.8 vs sCR, -15.4±1.1; p<0.001;n=8]. After 3 months of refeeding, there was no detectable difference in BW between CT and sFR-Refed groups. Isolated hearts from the sCR-Refed rats exhibited worse myocardial pathology after I/R compared to CT rats. The parallel orientation of myofibers and striations normally present in cardiomyocytes was lost in sCR-Refed rats. Further analysis revealed uneven blood-filling of the microcirculatory vessels and prominent interstitial edema of the myocardium. Hearts from sCR-Refed rats had more atrophied cardiomyocytes than CT [Atrophied/Total (%): CT, 0.2±0.1 vs sCR-Refed, 50.6±1.1; p<0.001; n=5]. The number of arrhythmic events during a 30 min ischemic interval in isolated hearts doubled after 2 weeks on the sCR diet ( data not shown ) and remained doubled 3 months later [Arrhythmias (% of time): CT, 34±8 vs sCR-Refed, 68±9; p=0.02; n=8]. Ultrasound imaging showed no difference in stroke volume, coronary perfusion pressure and left ventricular mass. However, the thickness of the left ventricular posterior wall was significantly reduced in sCR-Refed rats [(mm): CT, 2.55 ±0.03 vs sCR-Refed, 2.10±0.04; p=0.002; n=4]. These findings indicate heart structure and function remained damaged months after the sCR period ended and BW was restored. These studies have adverse cardiovascular risk implications for who are subjected either voluntarily (crash diets) or involuntarily (very low food security) to periods of inadequate caloric intake.

Abstract 13947: The Acute and Long-term Effects of Transcatheter Aortic Valve Implantation on Aortic Stiffness and Hemodynamics

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Vasiliki Gardikioti ◽  
Dimitrios Terentes-printzios ◽  
Konstantinos Aznaouridis ◽  
George Latsios ◽  
Gerasimos Siasos ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Arterial Stiffness ◽  
Transcatheter Aortic Valve Implantation ◽  
Augmentation Index ◽  
Long Term Effects ◽  
Transcatheter Aortic Valve ◽  
Aortic Valve Implantation ◽  
One Year ◽  
Valve Implantation

Introduction: Transcatheter aortic valve implantation (TAVI) is a procedure that alters dramatically the hemodynamics in patients with severe aortic valve stenosis who undergo this procedure. Hypothesis: We investigated the hypothesis that arterial properties and hemodynamics are affected immediately after TAVI as well as in the long-term. Methods: We enrolled 90 patients (mean age 80.2 ± 8.1 years, 50% males) with severe symptomatic aortic stenosis undergoing TAVI. Carotid-femoral and brachial-ankle pulse wave velocity (cfPWV and baPWV) were used for the assessment of arterial stiffness. Augmentation index corrected for heart rate (AIx@75) and subendocardial viability ratio (SEVR) were measured non-invasively. Measurements were conducted at baseline, after the procedure (during hospitalization) and at 1 year. Results: Acutely after TAVI we observed a statistically significant increase in arterial stiffness (7.5 ± 1.5 m/s vs 8.4 ± 1.9 m/s, p=0.001 for cfPWV and 1,773 ± 459 cm/s vs 2,383 ± 645 cm/s, p<0.001 for baPWV) without a concomitant change in systolic blood pressure (Figure). One year later, arterial stiffness was still increased compared to pre-TAVI measurements (7.5 ± 1.5 m/s vs 8.7 ± 1.7 m/s, p<0.001 for cfPWV and 1,773 ± 459 cm/s vs 2,286 ± 575 cm/s, p<0.001 for baPWV). We also found a decrease in AIx@75 (32.2 ± 12.9 % vs 27.9± 8.4 %, p=0.016) after TAVI that was attenuated at 1-year follow-up (32.2 ± 12.9 % vs 29.8± 9.1 %, p=0.38). SEVR displayed an increase acutely after TAVI (131.2 ± 30.0 % vs 148.4± 36.1 %, p=0.002) and remained improved 1 year after the procedure (131.2 ± 30.0 % vs 146± 32.2 %, p=0.01). Conclusions: In conclusion, shortly after TAVI the aorta exhibits a "stiffer" behavior in response to the acute change in hemodynamics, which settles in the long term. Our findings further elucidate the hemodynamic consequences of TAVI and may entail a prognostic role in this growing population.

Abstract 15170: Persistent Microvascular Obstruction Leads to Localized Iron Deposition and Active Inflammation Within Chronic Myocardial Infarctions

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Avinash Kali ◽  
Ivan Cokic ◽  
Hsin-Jung Yang ◽  
Richard Tang ◽  
Rohan Dharmakumar
Keyword(s):  
Microvascular Obstruction ◽  
Iron Deposition ◽  
Myocardial Infarctions ◽  
Long Term Effects ◽  
Gadolinium Enhancement ◽  
Tnf Α ◽  
Sphericity Index ◽  
Lv Remodeling ◽  
Active Inflammation

Introduction: The mechanism by which persistent microvascular obstruction (PMO) post myocardial infarction (MI) exerts adverse long-term effects is not well understood. Hypothesis: We hypothesized that PMO, with or without reperfusion hemorrhage, can resolve into iron deposition within chronic MI (CMI) territories, and is associated with prolonged inflammation and adverse LV remodeling. Methods: Canines subjected to reperfused (n=17) and non-reperfused (n=16) MI underwent Cardiovascular Magnetic Resonance (CMR) at 7 (acute) and 56 days (chronic) post-MI. Cine, T2*-weighted and Late Gadolinium Enhancement images were used to characterize LV remodeling (End-Diastolic Sphericity Index (EDSI)), iron and PMO respectively. Histological analysis was used to examine chronic inflammation. Results: In the reperfused group, 9 canines had PMO and hemorrhage with subsequent chronic iron deposition (PMO+/T2*+), while 4 canines had no PMO, hemorrhage, or chronic iron deposition (PMO-/T2*-). The remaining 4 canines had PMO without hemorrhage (PMO+/T2*-), but all subsequently had chronic iron deposition. In the non-reperfused group, 15 canines had PMO, and acute and subsequent chronic iron deposition (NR-PMO+/T2*+); 1 canine had no PMO, acute or chronic iron deposition (NR-PMO-/T2*-). In both groups, PMO volume was significantly associated with both acute and chronic iron volumes (p<0.001 all cases). In both groups, infarct and iron volumes measured in both acute and chronic phases were significant predictors of change in EDSI between acute and chronic phases (p<0.01 all cases). Histological sections of the harvested hearts post day 56 CMR showed extensive newly recruited macrophage, IL-1β, TNF-α and MMP-9 activities highly localized with iron in CMI regions (p<0.001 all cases). Conclusions: PMO, with or without reperfusion hemorrhage, can lead to iron deposition within CMIs, and is associated with active inflammation and adverse LV remodeling in canines.

Long-Term Effects of Growth Hormone on Infarct Size and Left Ventricular Function in Sheep With Coronary Artery Occlusion

2010 ◽  
Vol 55 (3) ◽  
pp. 255-261
Author(s):  
Fernanda D Olea ◽  
Andrea De Lorenzi ◽  
Claudia Cortés ◽  
Patricia Cabeza Meckert ◽  
Oscar Cendoya ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Coronary Artery ◽  
Left Ventricular Function ◽  
Infarct Size ◽  
Ventricular Function ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Long Term Effects
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