End-systolic pressure/volume ratio: A new index of ventricular contractility

Sagawa, Kiichi; Suga, Hiroyuki; Shoukas, Artin A.; Bakalar, Kenneth M.

doi:10.1016/0002-9149(77)90192-8

Cited by 572 publications

(216 citation statements)

References 8 publications

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“…Ea, that is the value of ventricular pressure developed for each milliliter of blood transferred to the arterial system, expresses the input impedance of the arterial bed 15 and is considered a good noninvasive method to estimate ventricular elastance, the index of myocardial contractility in vivo. 16,17 This parameter was calculated according to Kelly et al 18 (Ea ϭ 0.9 ϫ systolic pressure/SVI). Mitral flow was recorded at the end of normal expiration with color flowguided pulsed-wave Doppler from the apical 4-chamber view, by placing the sample volume (2-mm width) at the tips of the mitral valve leaflets, without angle correction.…”

Section: Methodsmentioning

confidence: 99%

Cardiovascular effects of canrenone in patients with preascitic cirrhosis

et al. 2002

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In patients with cirrhosis and portal hypertension, standing induces a reduction in cardiac index (CI) and an increase in systemic vascular resistance index. Our previous studies indicate that this abnormal hemodynamic response to standing is due to an altered myocardial function, because cirrhotic patients are unable to compensate for the reduced preload with an increase in left ventricular (LV) ejection fraction (EF) and stroke volume. To evaluate whether the cardiac dysfunction in cirrhosis is influenced by canrenone, an aldosterone antagonist, 8 patients with preascitic, nonalcoholic cirrhosis, and portal hypertension underwent echocardiographic assessment of LV function and systemic hemodynamics and determinations of plasma volume, urinary sodium excretion, and plasma renin activity T he hemodynamic pattern of cirrhosis with portal hypertension, with high blood volume and cardiac output and low systemic vascular resistance (SVR), is thought to play a major role in the development of sodium retention and ascites. 1 Bernardi et al. [2][3][4] showed that this hemodynamic pattern occurs only in the supine position; standing is associated with a reduction in cardiac output and an increase in SVR, that is, a "normalization" of systemic hemodynamics. This response to standing is quite different from that of healthy subjects, who do not show any appreciable changes in either cardiac output or SVR. 2-4 However, "normalization" of systemic hemodynamics during standing is associated with activation of vasoconstricting and sodium retaining systems. 3,4 In patients with preascitic cirrhosis, sodium retention occurs only during standing, 3 whereas, in those with ascites, it occurs in either position but worsens during standing. 4 We recently evaluated cardiovascular function in healthy subjects and cirrhotic patients with ascites and hyperdynamic circulation. 5 When supine, patients had increased left ventricular ejection fraction (LVEF) and cardiac index (CI) and reduced LV end-systolic volume index (LVESVI) and SVR. On standing, LV end-diastolic volume index (LVEDVI) decreased in all subjects. Healthy subjects maintained CI and stroke volume index (SVI) by decreasing LVESVI. In contrast, cirrhotic patients experienced a fall in SVI and CI and a disproportionate increase in arterial elastance (Ea), despite marked

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Section: Methodsmentioning

confidence: 99%

Cardiovascular effects of canrenone in patients with preascitic cirrhosis

et al. 2002

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“…Laffi et al [5] assessed the isotropic and chronotropic response in a group of nonalcoholic cirrhotic patients and reported a significantly decreased stroke volume in response to active tilting, leading to a reduced cardiac index despite a significant increase in heart rate. Wong et al [9] demonstrated in both alcoholic and nonalcoholic cirrhotic patients, with or without ascites, an abnormal and inverse systolic pressure to end-systolic volume relationship, an index of myocardial contractility [22]. With graded exercise test by using upright bicycle ergometry, both the absolute and the percentage increases in cardiac output in the cirrhotic patients were significantly decreased compared with the controls [6].…”

Section: Systolic Dysfunctionmentioning

confidence: 99%

Cirrhotic cardiomyopathy

2008

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Cirrhotic cardiomyopathy is a recently recognized condition in cirrhosis consisting of systolic incompetence under condition of stress, diastolic dysfunction related to altered diastolic relaxation, and electrophysiological abnormalities in the absence of any known cardiac disease. It can be diagnosed by using a combination of electrocardiograph, 2-dimensional echocardiography, and various serum markers such as brain natriuretic factor. The underlying pathogenetic mechanisms include abnormalities in the b-adrenergic signaling pathway, altered cardiomyocyte membrane fluidity, increased myocardial fibrosis, cardiomyocyte hypertrophy, and ion channel defects. Various compounds for which levels are elevated in cirrhosis such as nitric oxide and carbon monoxide can also exert a negative inotropic effect on the myocardium, whereas excess sodium and volume retention can lead to myocardial hypertrophy. Various toxins can also aggravate the ion channel defects, thereby widening the QRS complex causing prolonged QT intervals. Clinically, systolic incompetence is most evident when cirrhotic patients are placed under stress, whether physical or pharmacological, or when the extent of peripheral arterial vasodilatation demands an increased cardiac output as in the case of bacterial infections. Acute volume overload such as immediately after insertion of a transjugular intrahepatic portosystemic shunt or after liver transplantation can also tip these cirrhotic patients into cardiac failure. Treatment of cirrhotic cardiomyopathy is unsatisfactory. There is some evidence that b-blockade may help some cirrhotic patients with baseline prolonged QT interval. Long-term aldosterone antagonism may help reduce myocardial hypertrophy. Future studies should include further elucidation of pathogenetic mechanisms so as to develop effective treatment strategies.

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“…The model was further supported by the demonstration of the straight regression line of isochronal pressure-volume ratios for differently loaded beats at steady inotropic state [11]. End systolic pressure-volume relationship was widely accepted as an index of cardiac contractility and has been named ESPVR (end systolic pressure volume relationship).…”

Section: Lumped Parameters Modelsmentioning

confidence: 95%

Open-Source Programming of Cardiovascular Pressure-Flow Dynamics Using SimPower Toolbox in Matlab and Simulink

Barnea¹

2013

TOPETJ

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Abstract:A toolbox for simulation of the cardiovascular system has been constructed for use in Matlab Simulink (The MathWorks Inc.). The toolbox contains basic elements such as vessel segments, cardiac chambers, valves and shunts that can be graphically arranged and connected to directly simulate the circulation with the desired level of detail. The toolbox is based on the SimPower toolbox to allow simple connections between the different elements. One difficulty that remains is the need to know the values of the various parameters. The toolbox is an open-source script that is available for download. It is expected that researchers that will use the toolbox will refine it, enhance its capabilities and share their code with others.

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End-systolic pressure/volume ratio: A new index of ventricular contractility

Cited by 572 publications

References 8 publications

Cardiovascular effects of canrenone in patients with preascitic cirrhosis

Cardiovascular effects of canrenone in patients with preascitic cirrhosis

Cirrhotic cardiomyopathy

Open-Source Programming of Cardiovascular Pressure-Flow Dynamics Using SimPower Toolbox in Matlab and Simulink

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