Noninvasive estimation of the end systolic pressure-volume relationship using impedance cardiography.
Traditional measures of cardiac contractility such as dp/dt and ejection fraction has been noted to be sensitive to preload and afterload conditions. The end systolic pressure-volume relationship of the left ventricle (ESPVR, Suga Index or Emax) has been found to be the best load independent measure of the cardiac contractile state. However, determination of the ESPVR requires very highly invasive procedures. Impedance cardiography (IC) is a reliable noninvasive method for calculating stroke volume and may also be useful for estimating the end systolic volume.
An equation was derived using the systolic time intervals (PEP = pre-ejection period, LVET = left ventricular ejection time) and determined stroke volume (SV) as calculated from the impedance cardiograph to estimate the end systolic volume of the left ventricle. Likewise, and systolic pressure (ESP) was estimated from brachial cuff pressures using a previously published method. The resulting ESPVR was then calculated from tracings recorded in healthy normal subjects and compared to those obtained from patients in decompensated congestive heart failure (ejection fraction < 30% by echocardiogram) using the standard t test (p < 0.05).
Using the derived equation (ESPVR = ESP/(SV/(1.125-1.25(PEP/LVET)) - SV), the ESPVR for the normal group of 6 averaged 2.72 +/- 0.71 and was significantly different from the 1.04 +/- 0.45 found in 6 patients with known systolic dysfunction. In a further test of the method, 15 patients who received concurrent echocardiographic and IC evaluations were found to have calculated ESPVR values that significantly correlated with determined ejection fractions (r = 0.83, p < 0.01).
A noninvasive method for estimating the ESPVR that differentiates the myocardial contractile state in the clinically setting was derived using parameters obtained from IC. While further studies are needed to correlate this new equation with invasive measurements, this method has the potential for easily estimating load independent contractility in patients with cardiac dysfunction.
Available from: George Kunos
- "This intervention was performed by placing a saline-soaked cotton tip applicator on the inferior vena cava through an abdominal incision. Changes in the slope of the ESPVR are well-accepted as a relatively preload-and afterload-independent measure of contractility in a single experiment . Again because of the involvement of volume measurement in this index, it was not possible to compare the results among different animals. "
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ABSTRACT: Background & aims:
Cirrhosis is associated with blunted cardiovascular response to stimuli such as hemorrhage, but the mechanism remains unclear. We aimed to clarify the role of endocannabinoids in blunted hemorrhage response in cirrhotic rats.
Cirrhosis was induced by bile duct ligation (BDL). Hemodynamics were measured. Cannabinoid receptor-1 (CB1) antagonist, AM251, and macrophage inhibitor gadolinium chloride (GdCl3) were administered. Myocardial levels of anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) were measured and resident monocytes and macrophages quantified by immunohistochemistry. Isolated cardiomyocyte contractility was measured before and after incubation with monocytes from BDL and sham controls.
Hemorrhage significantly decreased arterial pressure and left ventricular dP/dT. After hemorrhage, these changes quickly reversed in controls, but were severely prolonged in BDL rats. Chronic AM251 treatment restored this impaired response. AEA and 2-AG levels were increased in BDL hearts and further increased after hemorrhage. Sham hearts showed virtually no monocytes or macrophages before or after hemorrhage, whereas BDL hearts had significantly more white blood cells which further increased after hemorrhage. GdCl3 treatment significantly reduced cardiac endocannabinoid levels both at baseline and after hemorrhage. This treatment also restored cardiovascular response to hemorrhage in BDL rats but did not affect sham controls. Monocytes isolated from BDL rats more potently inhibited cardiomyocyte contractility than sham control monocytes.
The cirrhotic heart showed increased monocyte recruitment and endocannabinoid levels. CB1 blockade or GdCl3 treatment restored blunted cardiovascular response to hemorrhage. Endocannabinoids released by monocytes blunt cardiac response to hemorrhage. Preventing monocyte recruitment or blocking endocannabinoid signaling may improve cardiovascular homeostasis in cirrhosis.
Journal of Hepatology 01/2015; 62(6). DOI:10.1016/j.jhep.2015.01.021 · 11.34 Impact Factor
Available from: Ilan Hay
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ABSTRACT: Whereas end-systolic and end-diastolic pressure-volume relations (ESPVR, EDPVR) characterize left ventricular (LV) pump properties, clinical utility of these relations has been hampered by the need for invasive measurements over a range of pressure and volumes. We propose a single-beat approach to estimate the whole EDPVR from one measured volume-pressure (Vm and Pm) point. Ex vivo EDPVRs were measured from 80 human hearts of different etiologies (normal, congestive heart failure, left ventricular assist device support). Independent of etiology, when EDPVRs were normalized (EDPVRn) by appropriate scaling of LV volumes, EDPVRns were nearly identical and were optimally described by the relation EDP = An.EDV (Bn), with An = 28.2 mmHg and Bn = 2.79. V0 (the volume at the pressure of approximately 0 mmHg) was predicted by using the relation V0 = Vm.(0.6 - 0.006.Pm) and V30 by V30 = V0 + (Vm,n - V0)/(Pm/An) (1/Bn). The entire EDPVR of an individual heart was then predicted by forcing the curve through Vm, Pm, and the predicted V0 and V30. This technique was applied prospectively to the ex vivo human EDPVRs not used in determining optimal An and Bn values and to 36 in vivo human, 12 acute and 14 chronic canine, and 80 in vivo and ex vivo rat studies. The root-mean-square error (RMSE) in pressure between measured and predicted EDPVRs over the range of 0-40 mmHg was < 3 mmHg of measured EDPVR in all settings, indicating a good predictive value of this approach. Volume-normalized EDPVRs have a common shape, despite different etiology and species. This allows the entire curve to be predicted by a new method with a potential for noninvasive application. The results are most accurate when applied to groups of hearts rather than to individual hearts.
AJP Heart and Circulatory Physiology 08/2006; 291(1):H403-12. DOI:10.1152/ajpheart.01240.2005 · 3.84 Impact Factor
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