Cardiac adaptation of sarcomere dynamics to arterial load: a model of hypertrophy

1992 ◽  
Vol 263 (4) ◽  
pp. H1054-H1063 ◽  
Author(s):  
G. M. Drzewiecki ◽  
E. Karam ◽  
J. K. Li ◽  
A. Noordergraaf
Keyword(s):  
Left Ventricle ◽  
Element Model ◽  
Left Ventricular ◽  
Arterial System ◽  
Optimal Point ◽  
The Past ◽  
Cardiac Adaptation ◽  
Arterial Load ◽  
Myocardial O2 Consumption ◽  
Physiological Hypertrophy

In the past, the dynamics of the left ventricle were studied by its response to altered venous and arterial load for a given heart. This led researchers to propose the concept of an arterioventricular match or optimal point of function. The model of this paper reverses that idea by fixing preload and afterload while computing cardiac function due to altered left ventricular size or shape, resulting from modification of the number of parallel and series sarcounits. A mathematical model of physiological hypertrophy is introduced. Series and parallel arrangements of sarcounits constitute a cylindrical model of the left ventricle. Filling occurs from a venous reservoir with constant pressure through a valve, while ejection takes place into a three-element model of the systemic arterial system through another valve. It is found that the dynamics of the myofibrils can be matched to those of the left ventricle by choosing a ventricular shape that results in a minimum in myocardial O2 consumption (MVO2) for any constant ventricular load. A unique solution for the size of the ventricle results if the rate of MVO2 is specified. The model is able to predict correctly hypertrophy due to hypoxia and due to pressure (concentric) and volume (eccentric) overloads.

scholarly journals A ventricular-vascular coupling model in presence of aortic stenosis

2005 ◽  
Vol 288 (4) ◽  
pp. H1874-H1884 ◽  
Author(s):  
Damien Garcia ◽  
Paul J. C. Barenbrug ◽  
Philippe Pibarot ◽  
André L. A. J. Dekker ◽  
Frederik H. van der Veen ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Left Ventricle ◽  
Aortic Stenosis ◽  
Vascular System ◽  
Severe Aortic Stenosis ◽  
Left Ventricular ◽  
Arterial System ◽  
Coefficient Of Determination ◽  
Ventricular Afterload ◽  
Good Agreement

In patients with aortic stenosis, the left ventricular afterload is determined by the degree of valvular obstruction and the systemic arterial system. We developed an explicit mathematical model formulated with a limited number of independent parameters that describes the interaction among the left ventricle, an aortic stenosis, and the arterial system. This ventricular-valvular-vascular (V3) model consists of the combination of the time-varying elastance model for the left ventricle, the instantaneous transvalvular pressure-flow relationship for the aortic valve, and the three-element windkessel representation of the vascular system. The objective of this study was to validate the V3 model by using pressure-volume loop data obtained in six patients with severe aortic stenosis before and after aortic valve replacement. There was very good agreement between the estimated and the measured left ventricular and aortic pressure waveforms. The total relative error between estimated and measured pressures was on average (standard deviation) 7.5% (SD 2.3) and the equation of the corresponding regression line was y = 0.99 x − 2.36 with a coefficient of determination r2 = 0.98. There was also very good agreement between estimated and measured stroke volumes ( y = 1.03 x + 2.2, r2 = 0.96, SEE = 2.8 ml). Hence, this mathematical V3 model can be used to describe the hemodynamic interaction among the left ventricle, the aortic valve, and the systemic arterial system.

Staphylococcus aureusSepticemia with a Fatal Transmural Myocardial Infarction in a 27-Week-Gestation Twin Infant: A Case Study

2010 ◽  
Vol 29 (2) ◽  
pp. 75-85 ◽  
Author(s):  
Amanda Hines ◽  
Patricia Rawlins
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Neonatal Period ◽  
Left Ventricular ◽  
Central Venous Catheters ◽  
Arterial System ◽  
Central Venous ◽  
Low Birth Weight Infants ◽  
Percutaneous Central Venous Catheters

Septicemia, one of the major causes of morbidity and mortality in the neonatal period, often has a rapid and fulminant course. Low-birth-weight infants with persistentStaphylococcus aureussepticemia, possibly associated with percutaneous central venous catheters, may develop metastatic infections including endocarditis with large vegetations. This article describes a neonate withS. aureusbacteremia that resolved with treatment who died secondary to decreased left ventricular function. At autopsy, organizing microthrombi were seen within both atria, the left ventricle, and the left coronary arterial system. Extensive infarcts were noted throughout the entire myocardium of the left ventricle. It was suspected, but not proven, that the thrombotic sequelae from septicemia caused this neonate’s death.

Effect of exercise on left ventricular-arterial coupling assessed in the pressure-volume plane

1993 ◽  
Vol 264 (5) ◽  
pp. H1629-H1633 ◽  
Author(s):  
W. C. Little ◽  
C. P. Cheng
Keyword(s):  
Left Ventricle ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Arterial System ◽  
Adrenergic Blockade ◽  
Stroke Work ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Lv Volume ◽  
Left Ventricular Arterial Coupling

The left ventricle (LV) and arterial system are nearly optimally coupled to produce stroke work (SW) at rest. However, the effect of exercise on the coupling between the LV and arterial system has not been directly determined. We evaluated 11 dogs who were instrumented to determine LV volume from three diameters. The LV end-systolic pressure (Pes)-volume (Ves) relation was determined by transient caval occlusion at rest and while the animals ran at 5-7 mph on a treadmill. During exercise, the Pes-Ves relation was shifted toward the left and the slope [end-systolic elastance (Ees)] increased from 7.7 +/- 2.8 to 12.7 +/- 4.2 (SD) mmHg/ml (P < 0.05). The arterial end-systolic elastance (Ea), calculated as Pes divided by stroke volume, increased during exercise (8.8 +/- 3.0 to 10.9 +/- 4.7 mmHg/ml, P < 0.05). The ratio of Ees to Ea increased during exercise from 0.89 +/- 0.31 to 1.27 +/- 0.12 (P < 0.05). The portion of the pressure-volume area expressed as SW increased during exercise from 0.63 +/- 0.07 to 0.69 +/- 0.10 (P < 0.05). After adrenergic blockade, the Ees-to-Ea ratio was not significantly altered during exercise (0.90 +/- 0.24 vs. 0.83 +/- 0.15, P = NS). At rest and during exercise, both with intact reflexes and after beta-adrenergic blockade, the ratio of Ees to Ea remained within the range in which SW is > 95% of maximum. We conclude that during exercise, beta-adrenergic stimulation shifts the LV Pes-Ves relation to the left with an increased slope. This more than offsets the increase in Ea.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic vasoconstriction limits coronary blood flow during exercise in hypertrophied left ventricle

1991 ◽  
Vol 260 (5) ◽  
pp. H1489-H1494 ◽  
Author(s):  
R. J. Bache ◽  
D. C. Homans ◽  
X. Z. Dai
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Ventricular Hypertrophy ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Additional Contribution ◽  
Adrenergic Blockade ◽  
Myocardial O2 Consumption

This study was carried out to test the hypothesis that alpha-adrenergic vasoconstriction limits coronary blood flow (CBF) during exercise in the chronically pressure overloaded, hypertrophied left ventricle. Studies were performed in dogs in which left ventricular hypertrophy had been produced by banding the ascending aorta at 9 wk of age. Left circumflex coronary artery blood flow and myocardial O2 consumption (MVO2) were examined at rest and during treadmill exercise during control conditions, after selective alpha 1-adrenergic blockade with prazosin, and after nonselective alpha-adrenergic blockade with phentolamine. All studies were performed after beta-adrenergic blockade with propranolol. During control conditions CBF and MVO2 increased progressively during exercise, while coronary sinus O2 tension decreased. Neither prazosin nor phentolamine altered CBF at rest but, in comparison with control measurements, both agents significantly increased CBF during exercise and abolished the decrease in coronary sinus O2 tension that normally occurred during exercise. Both prazosin and phentolamine caused similar significant increases of MVO2 relative to the heart rate times systolic left ventricular pressure during exercise, indicating that the increased CBF produced by these agents enhanced MVO2. Similar findings after prazosin and phentolamine indicate that adrenergic restraint of CBF during exercise resulted principally from alpha 1-adrenergic vasoconstrictions with little additional contribution from postjunctional alpha 2-adrenergic mechanisms.

Pressure-Circumference Relations of Left Ventricle

1956 ◽  
Vol 186 (1) ◽  
pp. 115-121 ◽  
Author(s):  
Robert F. Rushmer
Keyword(s):  
Left Ventricle ◽  
Myocardial Contractility ◽  
Left Ventricular Pressure ◽  
Cardiovascular Responses ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Work Output ◽  
External Work ◽  
Cardiac Adaptation

Changes in left ventricular pressure and left ventricular circumference of intact animals have been recorded simultaneously during spontaneous and induced cardiovascular responses. Mechanisms by which the left ventricular myocardium alters its ‘work output’ are indicated by pressure-circumference loops displayed on a cathode ray oscilloscope. Evidence is presented that the external work of the heart is not necessarily related to the diastolic dimensions in accordance with Starling's law of the heart. Instead, changes in both myocardial contractility and distensibility may play important roles in cardiac adaptation to various conditions.

Matching between feline left ventricle and arterial load: optimal external power or efficiency

1988 ◽  
Vol 254 (2) ◽  
pp. H279-H285 ◽  
Author(s):  
G. P. Toorop ◽  
G. J. Van den Horn ◽  
G. Elzinga ◽  
N. Westerhof
Keyword(s):  
Left Ventricle ◽  
Left Ventricular ◽  
Or Efficiency ◽  
Isolated Hearts ◽  
Arterial Load ◽  
External Power ◽  
Left Ventricular Output ◽  
Optimal Efficiency ◽  
Working Point

We tested the hypothesis that the feline left ventricle normally works at optimal external power as opposed to optimal efficiency by (re)analyzing data from five isolated, blood-perfused cat hearts and 39 open-thorax cats. In the isolated hearts, we measured pump function, external steady power, myocardial oxygen consumption, and efficiency. Optimal external power and optimal efficiency were found at different left ventricular outputs (6.94 +/- 0.33 and 8.35 +/- 0.37 ml/s, respectively; P less than 0.001). In the in situ cat hearts the working point was found at an output of 4.72 +/- 0.32 ml/s, whereas optimal external power was found at 4.84 +/- 0.26 ml/s. These values were not significantly different. Assuming that the point of optimal efficiency was located at the same fraction of the maximal unloaded left ventricular output (Fmax) as in the isolated hearts, i.e., 0.7, we found the point of optimal efficiency for the in situ heart at a flow of 5.83 +/- 0.32 ml/s, which was significantly different (P less than 0.001) from the flow in the working point. Our data therefore indicate that the left ventricle in the open-thorax cat is matched to the arterial load such that its external power output rather than efficiency is optimized.

Left ventricular interaction with arterial load studied in isolated canine ventricle

1983 ◽  
Vol 245 (5) ◽  
pp. H773-H780 ◽  
Author(s):  
K. Sunagawa ◽  
W. L. Maughan ◽  
D. Burkhoff ◽  
K. Sagawa
Keyword(s):  
Analytical Formula ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Arterial System ◽  
Ejection Time ◽  
Arterial Impedance ◽  
Final Output ◽  
Arterial Load ◽  
Highly Correlated ◽  
Impedance Conditions

We developed a framework of analysis to predict the stroke volume (SV) resulting from the complex mechanical interaction between the ventricle and its arterial system. In this analysis, we characterized both the left ventricle and the arterial system by their end systolic pressure (Ps)-SV relationships and predicted SV from the intersection of the two relationship lines. The final output of the analysis was a formula that gives the SV for a given preload as a function of the ventricular properties (Ees, V0, and ejection time) and the arterial impedance properties (modeled in terms of a 3-element Windkessel). To test the validity of this framework for analyzing the ventriculoarterial interaction, we first determined the ventricular properties under a specific set of control arterial impedance conditions. With the ventricular properties thus obtained, we used the analytical formula to predict SVs under various combinations of noncontrol arterial impedance conditions and four preloads. The predicted SVs were compared with those measured while actually imposing the identical set of arterial impedance conditions and preload in eight isolated canine ventricles. The predicted SV was highly correlated (P less than 0.0001) with the measured one in all ventricles. The average correlation coefficient was 0.985 +/- 0.004 (SE), the slope 1.00 +/- 0.04, and the gamma-axis intercept 1.0 +/- 0.2 ml, indicating the accuracy of the prediction. We conclude that the representations of ventricle and arterial system by their Ps-SV relationships are useful in understanding how these two systems determine SV when they are coupled and interact.

scholarly journals Arterial-ventricular coupling: mechanistic insights into cardiovascular performance at rest and during exercise

2008 ◽  
Vol 105 (4) ◽  
pp. 1342-1351 ◽  
Author(s):  
Paul D. Chantler ◽  
Edward G. Lakatta ◽  
Samer S. Najjar
Keyword(s):  
Left Ventricle ◽  
Left Ventricular ◽  
The Body ◽  
Arterial System ◽  
Energetic Efficiency ◽  
Arterial Elastance ◽  
Ventricular Performance ◽  
Men And Women ◽  
Left Ventricular Chamber ◽  
Cardiovascular Performance

Understanding the performance of the left ventricle (LV) requires not only examining the properties of the LV itself, but also investigating the modulating effects of the arterial system on left ventricular performance. The interaction of the LV with the arterial system, termed arterial-ventricular coupling (EA/ELV), is a central determinant of cardiovascular performance and cardiac energetics. EA/ELV can be indexed by the ratio of effective arterial elastance (EA; a measure of the net arterial load exerted on the left ventricle) to left ventricular end-systolic elastance (ELV; a load-independent measure of left ventricular chamber performance). At rest, in healthy individuals, EA/ELV is maintained within a narrow range, which allows the cardiovascular system to optimize energetic efficiency at the expense of mechanical efficacy. During exercise, an acute mismatch between the arterial and ventricular systems occurs, due to a disproportionate increase in ELV (from an average of 4.3 to 13.2, and 4.7 to 15.5 mmHg·ml−1·m−2 in men and women, respectively) vs. EA (from an average of 2.3 to 3.2, and 2.3 to 2.9 mmHg·ml−1·m−2 in men and women, respectively), to ensure that sufficient cardiac performance is achieved to meet the increased energetic requirements of the body. As a result EA/ELV decreases from an average of 0.58 to 0.34, and 0.52 to 0.27 in men and women, respectively. In this review, we provide an overview of the concept of EA/ELV, and examine the effects of age, hypertension, and heart failure on EA/ELV and its components (EA and ELV) in men and women. We discuss these effects both at rest and during exercise and highlight the mechanistic insights that can be derived from studying EA/ELV.

LV-arterial coupling: interactive model to predict effect of wave reflections on LV energetics

1991 ◽  
Vol 261 (4) ◽  
pp. H1026-H1033 ◽  
Author(s):  
D. H. Fitchett
Keyword(s):  
Arterial Compliance ◽  
Element Model ◽  
Energy Utilization ◽  
Arterial System ◽  
Time Varying ◽  
Wave Reflections ◽  
Efficient Energy ◽  
Arterial Resistance ◽  
Arterial Load ◽  
Optimal Coupling

The interaction between the left ventricle (LV) and the arterial system was simulated using sequential convolution of the flow output generated by a time-varying elastance model of the LV with an impulse response calculated from a 128-element model of the arterial system. The model illustrates the effect of independent changes of components of the arterial load on LV performance and energetics. This report studies the response of the model LV to an increase in arterial resistance, a decrease in arterial compliance, and an increase in discrete vascular reflections. Although arterial resistance exerts the greatest effect on ventricular stroke output, a reduction of arterial compliance or an increase in early reflections resulted in less optimal coupling of the heart to the arteries and less efficient energy utilization by the LV. In addition, the earlier the reflections return, the greater the disturbance of ventricular arterial coupling.

Acute effects of methoxamine on left ventricular-arterial coupling in streptozotocin-diabetic rats: a pressure-volume analysis

2000 ◽  
Vol 78 (5) ◽  
pp. 415-422 ◽  
Author(s):  
Ying-I Peng ◽  
Kuo-Chu Chang
Keyword(s):  
Left Ventricle ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Arterial System ◽  
Acute Effects ◽  
Energy Transmission ◽  
Arterial Elastance ◽  
Streptozotocin Diabetic Rats ◽  
Effective Arterial Elastance ◽  
Left Ventricular Arterial Coupling

We determined the acute effects of methoxamine, a specific alpha1-selective adrenoceptor agonist, on the left ventricular-arterial coupling in streptozotocin (STZ)-diabetic rats, using the end-systolic pressure-stroke volume relationships. Rats given STZ 65 mg·kg-1 iv (n = 8) were compared with untreated age-matched controls (n = 8). A high-fidelity pressure sensor and an electromagnetic flow probe measured left ventricular (LV) pressure and ascending aortic flow, respectively. Both LV end-systolic elastance ELV,ES and effective arterial elastance Ea were estimated from the pressure-ejected volume loop. The optimal afterload Qload determined by the ratio of Ea to ELV,ES was used to measure the optimality of energy transmission from the left ventricle to the arterial system. In comparison with controls, diabetic rats had decreased LV end-systolic elastance ELV,ES, at 513 ± 30 vs. 613 ± 29 mmHg·mL-1, decreased effective arterial elastance Ea, at 296 ± 20 vs. 572 ± 48 mmHg·mL-1, and decreased optimal afterload Qload, at 0.938 ± 0.007 vs. 0.985 ± 0.009. Methoxamine administration to STZ-diabetic rats significantly increased LV end-systolic elastance ELV,ES, from 513 ± 30 to 602 ± 38 mmHg·mL-1, and effective arterial elastance Ea, from 296 ± 20 to 371 ± 28 mmHg·mL-1, but did not change optimal afterload Qload. We conclude that diabetes worsens not only the contractile function of the left ventricle, but also the matching condition for the left ventricular-arterial coupling. In STZ-diabetic rats, administration of methoxamine improves the contractile status of the ventricle and arteries, but not the optimality of energy transmission from the left ventricle to the arterial system. Key words: streptozotocin-diabetic rats, left ventricular-arterial coupling, left ventricular end-systolic elastance, effective arterial elastance, optimal afterload.

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