Role of Diastole in Left Ventricular Function, I: Biochemical and Biomechanical Events

2004 ◽  
Vol 13 (5) ◽  
pp. 394-403 ◽  
Author(s):  
Penelope S. Villars ◽  
Shannan K. Hamlin ◽  
Andrew D. Shaw ◽  
Joseph T. Kanusky
Keyword(s):  
Left Ventricle ◽  
Calcium Release ◽  
Troponin I ◽  
Regulatory Protein ◽  
Systolic Pressure ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Release Mechanism ◽  
Adrenergic Stimulation ◽  
Inotropic State

Left ventricular diastolic function plays an important role in cardiac physiology. Lusitropy, the ability of the cardiac myocytes to relax, is affected by both biochemical events within the myocyte and biomechanical events in the left ventricle. β-Adrenergic stimulation alters diastole by enhancing the phosphorylation of phospholamban, a substrate within the myocyte that increases the uptake of calcium ions into the sarcoplasmic reticulum, increasing the rate of relaxation. Troponin I, a regulatory protein involved in the coupling of excitation to contraction, is vital to maintaining the diastolic state; depletion of troponin I can produce diastolic dysfunction. Other biochemical events, such as defects in the voltage-sensitive release mechanism or in inositol triphosphate calcium release channels, have also been implicated in altering diastolic tone. Extracellular collagen determines myocardial stiffness; impaired glucose tolerance can induce an increase in collagen cross-linking and lead to higher end-diastolic pressures. The passive properties of the left ventricle are most accurately measured during the diastasis and atrial contraction phases of diastole. These phases of the cardiac cycle are the least affected by volume status, afterload, inherent viscoelasticity, and the inotropic state of the myocardium. Diastolic abnormalities can be conceptualized by using pressure-volume loops that illustrate myocardial work and both diastolic and systolic pressure-volume relationships. The pressure-volume model is an educational tool that can be used to demonstrate isolated changes in preload, afterload, inotropy, and lusitropy and their interaction.

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)

scholarly journals Computational modeling of Takotsubo cardiomyopathy: effect of spatially varying β-adrenergic stimulation in the rat left ventricle

2014 ◽  
Vol 307 (10) ◽  
pp. H1487-H1496 ◽  
Author(s):  
Sander Land ◽  
Steven A. Niederer ◽  
William E. Louch ◽  
Åsmund T. Røe ◽  
Jan Magnus Aronsen ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Takotsubo Cardiomyopathy ◽  
Troponin I ◽  
Contractile Function ◽  
Single Cells ◽  
Apical Ballooning ◽  
Calcium Sensitivity ◽  
Takotsubo Syndrome ◽  
Adrenergic Stimulation ◽  
Inotropic Effects

In Takotsubo cardiomyopathy, the left ventricle shows apical ballooning combined with basal hypercontractility. Both clinical observations in humans and recent experimental work on isolated rat ventricular myocytes suggest the dominant mechanisms of this syndrome are related to acute catecholamine overload. However, relating observed differences in single cells to the capacity of such alterations to result in the extreme changes in ventricular shape seen in Takotsubo syndrome is difficult. By using a computational model of the rat left ventricle, we investigate which mechanisms can give rise to the typical shape of the ventricle observed in this syndrome. Three potential dominant mechanisms related to effects of β-adrenergic stimulation were considered: apical-basal variation of calcium transients due to differences in L-type and sarco(endo)plasmic reticulum Ca2+-ATPase activation, apical-basal variation of calcium sensitivity due to differences in troponin I phosphorylation, and apical-basal variation in maximal active tension due to, e.g., the negative inotropic effects of p38 MAPK. Furthermore, we investigated the interaction of these spatial variations in the presence of a failing Frank-Starling mechanism. We conclude that a large portion of the apex needs to be affected by severe changes in calcium regulation or contractile function to result in apical ballooning, and smooth linear variation from apex to base is unlikely to result in the typical ventricular shape observed in this syndrome. A failing Frank-Starling mechanism significantly increases apical ballooning at end systole and may be an important additional factor underpinning Takotsubo syndrome.

Ventricular systolic interdependence: volume elastance model in isolated canine hearts

1987 ◽  
Vol 253 (6) ◽  
pp. H1381-H1390 ◽  
Author(s):  
W. L. Maughan ◽  
K. Sunagawa ◽  
K. Sagawa
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Cross Talk ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Systolic Volume ◽  
The Right

To analyze the interaction between the right and left ventricle, we developed a model that consists of three functional elastic compartments (left ventricular free wall, septal, and right ventricular free wall compartments). Using 10 isolated blood-perfused canine hearts, we determined the end-systolic volume elastance of each of these three compartments. The functional septum was by far stiffer for either direction [47.2 +/- 7.2 (SE) mmHg/ml when pushed from left ventricle and 44.6 +/- 6.8 when pushed from right ventricle] than ventricular free walls [6.8 +/- 0.9 mmHg/ml for left ventricle and 2.9 +/- 0.2 for right ventricle]. The model prediction that right-to-left ventricular interaction (GRL) would be about twice as large as left-to-right interaction (GLR) was tested by direct measurement of changes in isovolumic peak pressure in one ventricle while the systolic pressure of the contralateral ventricle was varied. GRL thus measured was about twice GLR (0.146 +/- 0.003 vs. 0.08 +/- 0.001). In a separate protocol the end-systolic pressure-volume relationship (ESPVR) of each ventricle was measured while the contralateral ventricle was alternatively empty and while systolic pressure was maintained at a fixed value. The cross-talk gain was derived by dividing the amount of upward shift of the ESPVR by the systolic pressure difference in the other ventricle. Again GRL measured about twice GLR (0.126 +/- 0.002 vs. 0.065 +/- 0.008). There was no statistical difference between the gains determined by each of the three methods (predicted from the compartment elastances, measured directly, or calculated from shifts in the ESPVR). We conclude that systolic cross-talk gain was twice as large from right to left as from left to right and that the three-compartment volume elastance model is a powerful concept in interpreting ventricular cross talk.

Abstract 18996: Impact of Infarct Size on Left Ventricular Diastolic Function Following Acute Myocardial Infarction

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Andrew Lin ◽  
Christopher Kwan ◽  
Kristyan Guppy-Coles ◽  
Joanne Sippel ◽  
John Atherton ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Infarct Size ◽  
Diastolic Dysfunction ◽  
Diastolic Function ◽  
Troponin I ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Ventricular Diastolic Function ◽  
St Elevation

Introduction: Severe left ventricular diastolic dysfunction is associated with worse prognosis after acute myocardial infarction (MI). Twenty percent of patients have a restrictive filling pattern (RFP) following MI, and this is associated with a fourfold increase in mortality. The determinants of diastolic function in this setting are not well defined. Aim: We sought to determine the correlation between enzymatic infarct size and RFP in patients with a first ever MI. We hypothesized that a larger infarct size would result in greater impairment of left ventricular diastolic function. Methods: Data analysis was performed on consecutive patients admitted with first ever non-ST elevation MI (NSTEMI) or ST-elevation MI (STEMI) to a single large tertiary referral hospital from January 2013 to December 2014. All patients underwent coronary angiography during the index admission. Infarct size was determined by peak troponin I. Doppler transmitral flow pattern was obtained from the initial transthoracic echocardiogram performed within 48 hours of admission. RFP was defined as: E/A ratio >2.0 and/or E-wave deceleration time <160ms (American Society of Echocardiography Guidelines 2009). Results: Data were available on 645 consecutive patients who underwent coronary angiography for MI. We excluded 160 patients with a previous MI. Of the remaining 485 patients (mean age 62±13 years; mean left ventricular ejection fraction (LVEF) 53±12%), there were 338 NSTEMIs (70%) and 147 STEMIs (30%). PCI was performed in 360 (74%) patients (single vessel (82%), ≥2 vessels (18%)); coronary artery bypass surgery in 58 (13%); and medical management in 67 (13%). Sixty-nine patients (14.4%) had RFP; 52% of these had a LVEF ≥45%. Peak troponin I levels were higher in the RFP group (31.8±30.9μg/L vs 16.8±25.2μg/L, p=<0.001). On multivariate analysis, infarct size by peak troponin I (OR 1.02, 95%CI 1.00-1.03, p=0.026) and low LVEF (OR 0.95, 95%CI 0.91-0.99, p=0.015) were the only independent predictors of RFP. Conclusion: Infarct size was a major determinant of diastolic dysfunction following first ever MI. Whilst LV systolic dysfunction was strongly associated with impaired diastolic function, 52% of patients with severe diastolic dysfunction had relatively preserved LVEF.

Left ventricular-arterial coupling in conscious dogs

1991 ◽  
Vol 261 (1) ◽  
pp. H70-H76 ◽  
Author(s):  
W. C. Little ◽  
C. P. Cheng
Keyword(s):  
Stroke Volume ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Arterial System ◽  
Conscious Dogs ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Inotropic State ◽  
End Diastolic Volume ◽  
Wide Range

We investigated the criteria for the coupling of the left ventricle (LV) and the arterial system to maximize LV stroke work (SW) and the transformation of LV pressure-volume area (PVA) to SW. We studied eight conscious dogs that were instrumented to measure LV pressure and determine LV volume from three ultrasonically determined dimensions. The LV end-systolic pressure (PES)-volume (VES) relation was determined by caval occlusion. Its slope (EES) was compared with the arterial elastance (EA) and determined as PES per stroke volume. At rest, with intact reflexes, EES/EA was 0.96 +/- 0.20 EES/EA was varied over a wide range (0.18-2.59) by the infusion of graded doses of phenylephrine and nitroprusside before and during administration of dobutamine. Maximum LV SW, at constant inotropic state and end-diastolic volume (VED), occurred when EES/EA equaled 0.99 +/- 0.15. At constant VED and contractile state, SW was within 20% of its maximum value when EES/EA was between 0.56 and 2.29. The conversion of LV PVA to SW increased as EES/EA increased. The shape of the observed relations of the SW to EES/EA and SW/PVA to EES/EA was similar to that predicted by the theoretical consideration of LV PES-VES and arterial PES-stroke volume relations. We conclude that the LV and arterial system produce maximum SW at constant VED when EES and EA are equal; however, the relation of SW to EES/EA has a broad plateau. Only when EA greatly exceeds EES does the SW fall substantially. However, the conversion of PVA to SW increases as EES/EA increases. These observations support the utility of analyzing LV-arterial coupling in the pressure-volume plane.

Similar normalized Emax and O2 consumption-pressure-volume area relation in rabbit and dog

1988 ◽  
Vol 255 (2) ◽  
pp. H366-H374 ◽  
Author(s):  
Y. Goto ◽  
B. K. Slinker ◽  
M. M. LeWinter
Keyword(s):  
Left Ventricle ◽  
Systolic Pressure ◽  
Energy Conversion Efficiency ◽  
Left Ventricular ◽  
Energy Transduction ◽  
Base Line ◽  
Contractile State ◽  
Primary Determinant ◽  
Heart Size ◽  
Volume Relation

The end-systolic pressure-volume relation (ESPVR), a measure of ventricular contractile state, and systolic pressure-volume area (PVA), a primary determinant of cardiac oxygen consumption per beat (VO2), have been derived from the pressure-volume diagram of the cross-circulated dog left ventricle. The slope of the PVA-VO2 relation represents the efficiency of chemomechanical energy transduction of the contractile machinery. To see whether these relationships were similar in other animals, we studied the isovolumic ESPVR and the VO2-PVA relation in nine excised, cross-circulated rabbit left ventricles. The base-line ESPVR was linear (r = 0.94-0.99) with the slope (Emax) and volume-axis intercept (V0) equal to 83.4 +/- 18.3 mmHg/ml and 0.43 +/- 0.17 ml, respectively. When normalized for left ventricular weight, Emax (4.1 +/- 1.1 mmHg.ml-1.100 g) and V0 (8.9 +/- 3.7 ml/100 g) were similar to values reported for the dog left ventricle. The correlation between PVA and VO2 was linear (r = 0.93-1.00), and the slope (1.90 X 10(-5) +/- 0.44 X 10(-5) ml O2.mmHg-1.ml-1) and VO2-axis intercept (0.040 +/- 0.009 ml O2.beat-1.100 g-1) were similar to values found in the dog left ventricle. Hence, despite the greatly different heart size, the base-line contractile state and chemomechanical energy conversion efficiency of the excised, cross-circulated rabbit left ventricle are similar to those of the dog left ventricle.

Congestive Heart Failure in Copper-Deficient Mice

2003 ◽  
Vol 228 (7) ◽  
pp. 811-817 ◽  
Author(s):  
Laila Elsherif ◽  
Raymond V. Ortines ◽  
Jack T. Saari ◽  
Y. James Kang
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Left Ventricle ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Experimental Models ◽  
Left Ventricular ◽  
Mouse Heart ◽  
Total Period

Copper Deficiency (CuD) leads to hypertrophic cardiomyopathy in various experimental models. The morphological, electrophysiological, and molecular aspects of this hypertrophy have been under investigation for a long time. However the transition from compensated hypertrophy to decompensated heart failure has not been investigated in the study of CuD. We set out to investigate the contractile and hemodynamic parameters of the CuD mouse heart and to determine whether heart failure follows hypertrophy in the CuD heart. Dams of FVB mice were fed CuD or copper-adequate (CuA) diet starting from the third day post delivery and the weanling pups were fed the same diet for a total period of 5 weeks (pre- and postweanling). At week 4, the functional parameters of the heart were analyzed using a surgical technique for catheterizing the left ventricle. A significant decrease in left ventricle systolic pressure was observed with no significant change in heart rate, and more importantly contractility as measured by the maximal rate of left ventricular pressure rise (+dP/dt) and decline (−dP/dt) were significantly depressed in the CuD mice. However, left ventricle end diastolic pressure was elevated, and relaxation was impaired in the CuD animals; the duration of relaxation was prolonged. In addition to significant changes in the basal level of cardiac function, CuD hearts had a blunted response to the stimulation of the β-adrenergic agonist isoproterenol. Furthermore, morphological analysis revealed increased collagen accumulation in the CuD hearts along with lipid deposition. This study shows that CuD leads to systolic and diastolic dysfunction in association with histopathological changes, which are indices commonly used to diagnose congestive heart failure.

ESPVR of in situ rat left ventricle shows contractility-dependent curvilinearity

1998 ◽  
Vol 274 (5) ◽  
pp. H1429-H1434 ◽  
Author(s):  
Takayuki Sato ◽  
Toshiaki Shishido ◽  
Toru Kawada ◽  
Hiroshi Miyano ◽  
Hiroshi Miyashita ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Linear Regression Analysis ◽  
Systolic Pressure ◽  
Quadratic Equation ◽  
Left Ventricular ◽  
Conductance Catheter ◽  
Electromagnetic Flowmetry ◽  
Significant Difference ◽  
Pressure Volume Relationship

We developed a miniaturized conductance catheter for in situ rat left ventricular (LV) volumetry. After the validation study of the conductance volumetry in 11 rats, we characterized the end-systolic pressure-volume relationship (ESPVR) in 24 sinoaortic-denervated, vagotomized and urethan-anesthetized rats. Stroke volume (SV) measured with the conductance catheter correlated closely with that measured by electromagnetic flowmetry ( r > 0.95). No significant difference was found between the in situ LV end-diastolic volumes measured by conductance volumetry and postmortem morphometry; a linear regression analysis indicated that the correlation coefficient was 0.934, that the slope was not significantly different from 1, and that the intercept was not significantly different from 0. During cardiac sympathotonic conditions, the ESPVR was curvilinear. The estimated slope of ESPVR (end-systolic elastance, E es) by quadratic curve fitting at end-systolic pressure of 100 mmHg was 2,647 ± 846 mmHg/ml. Bilateral cervical and stellate ganglionectomy depressed contractility and made the ESPVR linear; a quadratic equation did not improve the fit. E es was 946 ± 55 mmHg/ml with the volume-axis ( V 0) intercept of 0.076 ± 0.007 ml. Administration of propranolol (1 mg/kg) further reduced E es (573 ± 61 mmHg/ml, P < 0.001) and increased V 0 slightly (0.091 ± 0.011 ml). We conclude that the conductance catheter method is useful for the assessment of the ESPVR of the in situ rat left ventricle and that the ESPVR displays contractility-dependent curvilinearity.

Effect of regional myocardial ischemia on cardiac pump performance during exercise

1978 ◽  
Vol 234 (2) ◽  
pp. H157-H162
Author(s):  
L. D. Horwitz ◽  
D. F. Peterson ◽  
V. S. Bishop
Keyword(s):  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Adrenergic Stimulation ◽  
Circumflex Coronary Artery ◽  
Pump Performance ◽  
Regional Myocardial Ischemia ◽  
Exercise Hemodynamics ◽  
Stimulation Of

The effect of brief periods of regional ischemia upon left ventricular pump performance was studied in nine dogs standing quietly at rest and during running exercise on a treadmill. Transient occlusions of the left circumflex coronary artery resulted in increase in heart rate at rest (+30 beats/min) but not during exercise. Other changes due to occlusion were similar at rest and during exercise and included decreases in stroke volume (-25% standing, -23% running); in dP/dt max, the maximum first derivative of the left ventricular pressure (-20% standing or running); and in left ventricular peak systolic pressure (-13% standing, -21% running); and rises in left ventricular end-diastolic pressure (+4.5 mmHg standing, +6.3 mmHg running). Cardiac output was unchanged by occlusions at rest but fell (-18%) during occlusions while the dogs were running. Propranolol reduced absolute levels of cardiac performance during exercise occlusions but had no effect at rest. Inotropic agents with ischemia had some effects at rest but did not alter exercise hemodynamics. It is concluded that integrated left ventricular function during ischemia is not impaired by exercise, probably because of beta-adrenergic stimulation of nonischemic myocardium.

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