The effect of left ventricular contractility on arterial hemodynamics: A model-based investigation

Ventricular-arterial coupling is a major determinant of cardiovascular performance, however, there are still inherent difficulties in distinguishing ventricular from vascular effects on arterial pulse phenotypes. In the present study, we employed an extensive mathematical model of the cardiovascular system to investigate how sole changes in cardiac contractility might affect hemodynamics. We simulated two physiologically relevant cases of high and low contractility by altering the end-systolic elastance, Ees, (3 versus 1 mmHg/mL) under constant cardiac output and afterload, and subsequently performed pulse wave analysis and wave separation. The aortic forward pressure wave component was steeper for high Ees, which led to the change of the total pressure waveform from the characteristic Type A phenotype to Type C, and the decrease in augmentation index, AIx (-2.4% versus +18.1%). Additionally, the increase in Ees caused the pulse pressure amplification from the aorta to the radial artery to rise drastically (1.86 versus 1.39). Our results show that an increase in cardiac contractility alone, with no concomitant change in arterial properties, alters the shape of the forward pressure wave, which, consequently, changes central and peripheral pulse phenotypes. Indices based on the pressure waveform, like AIx, cannot be assumed to reflect only arterial properties.

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

Frontiers in Physiology ◽

10.3389/fphys.2021.701154 ◽

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.

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Effects of CCM (Cardiac Contractility Modulation) signal delivery on left ventricular contractility

Heart Rhythm ◽

10.1016/j.hrthm.2005.02.902 ◽

2005 ◽

Vol 2 (5) ◽

pp. S286-S287

Author(s):

Thomas Lawo ◽

Thomas Deneke ◽

Andreas Mügge ◽

Matthias Vogt

Keyword(s):

Cardiac Contractility ◽

Left Ventricular ◽

Ventricular Contractility ◽

Left Ventricular Contractility ◽

Cardiac Contractility Modulation ◽

Modulation Signal

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Augmentation Index, Left Ventricular Contractility, and Wave Reflection

Hypertension ◽

10.1161/hypertensionaha.109.133066 ◽

2009 ◽

Vol 54 (5) ◽

pp. 1099-1105 ◽

Cited By ~ 63

Author(s):

James E. Sharman ◽

Justin E. Davies ◽

Carly Jenkins ◽

Thomas H. Marwick

Keyword(s):

Wave Reflection ◽

Augmentation Index ◽

Left Ventricular ◽

Ventricular Contractility ◽

Left Ventricular Contractility

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P1573Chemotherapy-induced vasotoxicity in patients undergoing therapy for breast cancer

European Heart Journal ◽

10.1093/eurheartj/ehz748.0333 ◽

2019 ◽

Vol 40 (Supplement_1) ◽

Author(s):

M Anastasiou ◽

A S Antonopoulos ◽

E Oikonomou ◽

F Zagouri ◽

G Siasos ◽

...

Keyword(s):

Breast Cancer ◽

Arterial Stiffness ◽

Vascular Function ◽

Augmentation Index ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Flow Mediated Dilation ◽

Vascular Effects ◽

Ventricular Ejection Fraction ◽

Her 2

Abstract Background Cardiotoxicity is a well-known adverse effect of anthracycline and HER-2 monoclonal antibodies, however the vascular effects of these agents remain less-well studied. Purpose To explore the effects of breast chemotherapy on vascular function. Methods A total of 57 female patients undergoing breast diagnosed with breast cancer and scheduled for anthracycline-based and HER-2 chemotherapy were included in this study. At baseline, at 3, 6 and 12 months, patients underwent assessment of cardiac function by transthoracic echocardiography, endothelial function assessment by brachial flow mediated dilation (FMD) and assessment of arterial stiffness by carotid-radial pulse wave velocity (PWV) and augmentation index (Aix). Results There was a significant decrease in left ventricular ejection fraction (LVEF) overtime compared to baseline (A). This was paralleled by a significant decrease in brachial FMD at 6 months (B) and a significant increase in PWV compared to baseline (C). There was no significant change in Aix compared to baseline levels (D). Chemotherapy-induced cardiotoxicity (expressed by the change in LVEF) was not associated with either the change in FMD or PWV at 6 months. Conclusions Breast chemotherapy-induced cardiotoxicity is paralleled by vasotoxicity, which is manifested as endothelial dysfunction and increased arterial stiffness. Systemic vasotoxicity is not directly related to cardiotoxicity, suggesting that monitoring of both cardiac and vascular function could be useful in identifying early signs of cardiovascular toxicity.

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Impaired Cardiac Contractility Response to Hemodynamic Stress in S100A1-Deficient Mice

Molecular and Cellular Biology ◽

10.1128/mcb.22.8.2821-2829.2002 ◽

2002 ◽

Vol 22 (8) ◽

pp. 2821-2829 ◽

Cited By ~ 89

Author(s):

Xiao-Jun Du ◽

Timothy J. Cole ◽

Nora Tenis ◽

Xiao-Ming Gao ◽

Frank Köntgen ◽

...

Keyword(s):

Cardiac Contractility ◽

Pressure Overload ◽

Left Ventricular ◽

Ventricular Contractility ◽

Adrenergic Stimulation ◽

Protein Levels ◽

Hemodynamic Stress ◽

Gene Coding ◽

Ef Hand

ABSTRACT Ca2+ signaling plays a central role in cardiac contractility and adaptation to increased hemodynamic demand. We have generated mice with a targeted deletion of the S100A1 gene coding for the major cardiac isoform of the large multigenic S100 family of EF hand Ca2+-binding proteins. S100A1−/− mice have normal cardiac function under baseline conditions but have significantly reduced contraction rate and relaxation rate responses to β-adrenergic stimulation that are associated with a reduced Ca2+ sensitivity. In S100A1−/− mice, basal left-ventricular contractility deteriorated following 3-week pressure overload by thoracic aorta constriction despite a normal adaptive hypertrophy. Surprisingly, heterozygotes also had an impaired response to acute β-adrenergic stimulation but maintained normal contractility in response to chronic pressure overload that coincided with S100A1 upregulation to wild-type levels. In contrast to other genetic models with impaired cardiac contractility, loss of S100A1 did not lead to cardiac hypertrophy or dilation in aged mice. The data demonstrate that high S100A1 protein levels are essential for the cardiac reserve and adaptation to acute and chronic hemodynamic stress in vivo.

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Reflex cardiac effects of local cutaneous cold exposure in dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1980.239.1.h114 ◽

1980 ◽

Vol 239 (1) ◽

pp. H114-H120

Author(s):

J. F. Borgia ◽

S. M. Horvath

Keyword(s):

Heart Rate ◽

Cardiac Contractility ◽

Oxygen Demand ◽

Cardiovascular Responses ◽

Left Ventricular ◽

Myocardial Oxygen Demand ◽

Adrenergic Blockade ◽

Stroke Index ◽

Ventricular Contractility ◽

Cold Stimulation

Cardiovascular responses initiated by local cutaneous cooling were evaluated in 16 anesthetized dogs of which 8 were pretreated with propranolol. Heart rate, cardiac index (CI), and indices of ventricular contractility were significantly elevated in untreated animals during cold stimulation. Myocardial oxygen uptake (MVo2) and left ventricular work (LVW) were also increased, and cardiac mechanical efficiency was significantly reduced. Total peripheral vascular resistance remained unchanged. In the propranolol group, heart rate decreased by 12 beats/min, but CI was maintained constant during cold by a rise in stroke index. Left ventricular dP/dtmax was reduced and ventricular preload elevated, but LVW, MVo2, and cardiac efficiency were unchanged. These data indicate that local cutaneous cooling increases myocardial oxygen demand by reflexly elevating heart rate and cardiac contractility rather than by increasing cardiac afterload. The response is completely eliminated by beta-adrenergic blockade. The significance of these observations in regard to the cold-intolerant individual with coronary disease is discussed.

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Penatalaksanaan Anestesi untuk Seksio Sesarea pada Multigravida dengan Kardiomiopati Peripartum

Jurnal Anestesi Obstetri Indonesia ◽

10.47507/obstetri.v1i1.21 ◽

2020 ◽

Vol 1 (1) ◽

pp. 18-22

Author(s):

Purwoko Purwoko ◽

Andi Rizki Caprianu

Keyword(s):

Ejection Fraction ◽

General Anesthesia ◽

Anesthetic Management ◽

Cardiac Contractility ◽

Caesarian Section ◽

Left Ventricular ◽

Peripartum Cardiomyopathy ◽

Reproductive Age ◽

Ventricular Contractility ◽

Sudden Decrease

Peripartum Cardiomyopathy (PPCM) merupakan salah satu jenis kardiomiopati dilatasi tanpa diketahui penyebabnya yang terjadi pada wanita hamil usia reproduktif yang jarang terjadi. Patofisiologi PPCM masih kontroversial, penyebab PPCM tidak bisa dijelaskan dengan etiologi tunggal, karena memiliki penyebab multifaktor. Pasien wanita, 43 tahun, ASA III dengan preeklamsi berat pada multigravida hamil preterm belum dalam persalinan dengan PPCM NYHA II riwayat seksio sesarea 10 tahun rencana dilakukan re-seksio sesarea elektif. Pada pasien ini didapatkan pada pemeriksaan kardiovaskuler dengan murmur pansistolik. Ekokardiografi ventrikel kiri dilatasi, kontraktilitas ventrikel kiri menurun ejection fraction 31%, fungsi diastolik restriktif, mitral regurgitasi ringan. Rencana dilakukan anestesi dengan teknik epidural namun dalam pelaksanaannya gagal epidural kemudian dikonversi menjadi anestesi umum intubasi oral. Secara umum, target hemodinamik pada berbagai teknik anestesi adalah sama, yaitu mengurangi kardiak preload dan afterload serta mencegah penurunan kontraktilitas kardiak yang sudah buruk sebelumnya. Teknik anestesi yang menghasilkan penurunan mendadak pada tahanan pembuluh darah sistemik sebaiknya dihindari. Manajemen anestesi pada pasien dengan PPCM, teknik regional anestesi maupun anestesi umum dapat diterapkan. Namun tetap mempertimbangkan beberapa faktor seperti kondisi pasien dan kemampuan dari dokter anestesi itu sendiri. Anesthetic Management for Caesarean Section in Multygravida with Peripartum Cardiomyopathy Abstract Peripartum Cardiomyopathy (PPCM) is one type of dilated cardiomyopathy without known cause in pregnant women in reproductive age are rare. Pathophysiology of PPCM is still controversial, the cause of PPCM can not be explained by a single etiology because it has multifactor. Female patient, 43 years, ASA III with severe preeclamsia pregnancy, preterm, multigravida and not yet in labor with PPCM NYHA II and history of caesarian section 10 years ago planned for elective re-caesarian section. In this patient was obatained pansistolic murmur on cardiovascular examination. Echocardiography was obtained dilated left ventricle, left ventricular contractility decrease with ejection fraction 31%, restrictive diastolic function, mild mitral regurgitation. Planned for anesthesia with epidural technique but in implementation the epidural was fail then converted into general anesthesia oral intubation. In general, hemodynamic targets in anesthesia techniques are the same, ie reducing cardiac preload and afterload and preventing a decline in bad cardiac contractility. Anesthesia techniques that produce a sudden decrease in systemic vascular resistance should be avoided. Anesthesia management in patient with PPCM both regional and general anesthesia technique can be applied. But still considering several factors such as patient’s condition and the ability of the anesthesiologist itself.

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Applanation Tonometry for Assessment of Left Ventricular Systolic Load

Journal of Biomedical and Clinical Research ◽

10.2478/jbcr-2019-0014 ◽

2019 ◽

Vol 12 (2) ◽

pp. 94-99

Author(s):

Rene D. Mileva-Popova ◽

Nina Y. Belova

Keyword(s):

Arterial Stiffness ◽

Augmentation Index ◽

Age Groups ◽

Systolic Pressure ◽

Left Ventricular ◽

Applanation Tonometry ◽

Non Invasive ◽

Pressure Area ◽

Older Subjects ◽

And Gender

Summary Vascular-ventricular coupling is a major determinant of left ventricular load. The aim of our study was to assess non- invasively left ventricular load and its dependency on central hemodynamics. Sixty-five healthy and gender-matched individuals were divided in two groups according to their age: 20y/o and 50y/o. Applanation tonometry was performed using the Sphygmocor device. Central pressures and pulse wave analysis indices were computed. Central systolic (120±3 vs. 98±2 mm Hg) and pulse pressures (43±3 vs. 29±1 mm Hg) as well as the augmentation index (AIx75) (23±3 vs. 6±2%) were significantly higher in the 50y/o group (p<0.01). These parameters are relevant markers of arterial stiffness and evidenced the development of central arterial morphological and functional alterations in the older subjects. The time-tension index (TTI) computed from the systolic pressure area was significantly higher in the 50y/o subjects as compared to the 20y/o group (2378±66 vs. 1954±73 mmHg×s, p<0.01). Moreover, we have shown the presence of significant correlation between TTI and AIx75 (p<0.01) in both age groups. This finding confirmed the contribution of arterial stiffness for the impaired vascular-ventricular coupling. In conclusion, applanation tonometry might be utilized for non-invasive evaluation of the left ventricular load, which is an important parameter of cardiovascular risk.

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