Echocardiographie Detection of Elevated Left Ventricular End-Diastolic Pressure by Left Atrial Contractile Function

1993 ◽  
Vol 7 (3) ◽  
pp. 152-159 ◽  
Author(s):  
Shuji Yonekura ◽  
Kazufumi Tsuchihashi ◽  
Tomoaki Nakata ◽  
Nobuichi Hikita ◽  
Kazuhiko Nagao ◽  
...  
Keyword(s):  
Left Atrial ◽  
Diastolic Pressure ◽  
Contractile Function ◽  
Left Ventricular

Left ventricular end-diastolic pressure is associated with left atrial functional measures by echocardiography

2021 ◽  
Author(s):  
Flemming Javier Olsen ◽  
Rasmus Møgelvang ◽  
Martina Chantal de Knegt ◽  
Søren Galatius ◽  
Sune Pedersen ◽  
...  
Keyword(s):  
Left Atrial ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Functional Measures

Role of endogenous testosterone in myocardial proinflammatory and proapoptotic signaling after acute ischemia-reperfusion

2005 ◽  
Vol 288 (1) ◽  
pp. H221-H226 ◽  
Author(s):  
Meijing Wang ◽  
Ben M. Tsai ◽  
Ajay Kher ◽  
Lauren B. Baker ◽  
G. Mathenge Wairiuko ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Functional Recovery ◽  
Caspase 3 ◽  
Diastolic Pressure ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Acute Ischemia ◽  
Caspase 1 ◽  
Tnf Α

Myocardial ischemia is the leading cause of death in both men and women; however, very little information exists regarding the effect of testosterone on the response of myocardium to acute ischemic injury. We hypothesized that testosterone may exert deleterious effects on myocardial inflammatory cytokine production, p38 MAPK activation, apoptotic signaling, and myocardial functional recovery after acute ischemia-reperfusion (I/R). To study this, isolated, perfused rat hearts (Langendorff) from adult males, castrated males, and males treated with a testosterone receptor blocker (flutamide) were subjected to 25 min of ischemia followed by 40 min of reperfusion. Myocardial contractile function (left ventricular developed pressure, left ventricular end-diastolic pressure, positive and negative first derivative of pressure) was continuously recorded. After reperfusion, hearts were analyzed for expression of tissue TNF-α, IL-1β, and IL-6 (ELISA) and activation of p38 MAPK, caspase-1, caspase-3, caspase-11, and Bcl-2 (Western blot). All indices of postischemic myocardial functional recovery were significantly higher in castrated males or flutamide-treated males compared with untreated males. After I/R, castrated male and flutamide-treated male hearts had decreased TNF-α, IL-1β, and IL-6; decreased activated p38 MAPK; decreased caspase-1, caspase-3, and caspase-11; and increased Bcl-2 expression compared with untreated males. These results show that blocking the testosterone receptor (flutamide) or depleting testosterone (castration) in normal males improves myocardial function after I/R. These effects may be attributed to the proinflammatory and/or the proapoptotic properties of endogenous testosterone. Further understanding may allow therapeutic manipulation of sex hormone signaling mechanisms in the treatment of acute I/R.

Reduction of Carnitine Content by Inhibition of Its Biosynthesis Results in Protection of Isolated Guinea Pig Hearts against Hypoxic Damage

1996 ◽  
Vol 1 (3) ◽  
pp. 235-242 ◽  
Author(s):  
Pradip K. Dhar ◽  
Ingrid L. Grupp ◽  
Arnold Schwartz ◽  
Gunter Grupp ◽  
Mohammed A. Matlib
Keyword(s):  
Guinea Pigs ◽  
Initial Rate ◽  
Diastolic Pressure ◽  
Contractile Function ◽  
Dry Weight ◽  
Treated Group ◽  
Left Ventricular ◽  
Untreated Group ◽  
Free Carnitine ◽  
Isolated Hearts

Background 3-(2,2,2-trimethylhydrazinium) propionate (THP or mildronate) is an inhibitor of carnitine biosynthesis. This study was carried out to determine whether feeding of guinea pigs with THP results in decreased myocardial-free carnitine content and, as a result, attenuates hypoxic damage in isolated and paced work-performing hearts. Methods and Results Guinea pigs were administered either distilled water or 100 mg THP/kg/day orally for 10 days. The treatment resulted in about a 50% decline in myocardial-free carnitine content, from 11.1 ± 0.2 (n = 5) to 5.6 ± 0.2 (n = 5) μM/g dry weight of the heart. The left ventricular contractile function of the hearts was measured during normoxic perfusion (PO2 = 590 mmHg), hypoxic perfusion (PO2 = 149 mmHg), and reperfusion (PO2 = 590 mmHg). In both untreated and THP-treated groups, the rate of development of intraventricular pressure (+dP/dt) under normoxic perfusion was similar; however, +dP/dt declined to about 10% of the initial rate within 20 minutes of hypoxic perfusion. In the THP-treated group of hearts, the initial decline was slower than that of the untreated animal hearts. After 20 minutes of normoxic reperfusion following 60 minutes of hypoxic perfusion, the recovery of +dP/dt and -dP/dt was greater in the THP-treated group than in the untreated group. The elevation of end-diastolic pressure during hypoxia was completely reversed by normoxic reperfusion of the THP-treated group but not in the untreated group. Mitochondria isolated from hearts from the THP-treated group after normoxic reperfusion following hypoxic perfusion exhibited better respiratory function than those from untreated hearts. Conclusion The data suggest that feeding guinea pigs with THP results in reduced myocardial-free carnitine content and attenuation of hypoxic and reperfusion injury in isolated hearts.

Direct cardiac effects of vasopressin and their reversal by a vascular antagonist

1986 ◽  
Vol 251 (4) ◽  
pp. H734-H741 ◽  
Author(s):  
W. A. Boyle ◽  
L. D. Segel
Keyword(s):  
Coronary Flow ◽  
Diastolic Pressure ◽  
Contractile Function ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Total Output ◽  
Stroke Work ◽  
Cardiac Effects ◽  
Myocardial O2 Consumption ◽  
Dose Dependent

We studied the direct cardiac effects of arginine vasopressin (AVP) by use of an isolated working rat heart model perfused with Krebs-Henseleit medium. At a concentration of 878 +/- 15 pg/ml, AVP produced significant (P less than 0.05) decreases in coronary flow (-31 +/- 2%); myocardial O2 consumption (-12 +/- 2%); left ventricular peak systolic pressure (-5 +/- 1%); dP/dtmax (-7 +/- 1%); -dP/dtmax (-6 +/- 3%); peak aortic flow rate (-5 +/- 1%); stroke work (-3 +/- 1%); peak power (-8 +/- 1%); and total output (-3 +/- 1%). Aortic output increased significantly (+7 +/- 1%) as did arteriovenous O2 difference (+108 +/- 14 mmHg); left ventricular end-diastolic pressure (+0.4 +/- 0.1 mmHg); efficiency (+1.5 +/- 0.4%); and rate of lactate release (+1.27 +/- 0.21 nmol/ml perfusate/min). Dose-response relationships were studied at 9 +/- 1, 25 +/- 1, 75 +/- 3, 303 +/- 15, and 817 +/- 42 pg AVP/ml. Significant dose-dependent depression of coronary flow occurred at the three highest AVP concentrations; cardiac function was significantly depressed at the highest dose. The AVP analogue d(CH2)5[Tyr(Me)]AVP (20 ng/ml) completely reversed the cardiac effects attributed to AVP. The data indicate that AVP is a potent direct coronary constrictor that produces myocardial ischemia and decreased contractile function at AVP concentrations that are observed in some pathophysiologic states.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular function during lethal and sublethal endotoxemia in swine

1986 ◽  
Vol 251 (2) ◽  
pp. H364-H373 ◽  
Author(s):  
R. D. Goldfarb ◽  
L. M. Nightingale ◽  
P. Kish ◽  
P. B. Weber ◽  
D. J. Loegering
Keyword(s):  
Low Dose ◽  
Diastolic Pressure ◽  
Contractile Function ◽  
Lethal Dose ◽  
Cardiac Contractility ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
High Dose ◽  
Adrenergic Stimulation ◽  
And Function

Our previous studies suggested that after a median lethal dose (LD50) of endotoxin, cardiac contractility was depressed in nonsurviving dogs. The canine cardiovascular system is unlike humans in that dogs have a hepatic vein sphincter that is susceptible to adrenergic stimulation capable of raising hepatic and splanchnic venous pressures. We retested the hypothesis that lethality after endotoxin administration is associated with cardiac contractile depression in pigs, because the hepatic circulation in this species is similar to that of humans. We compared cardiac mechanical function of pigs administered a high dose (250 micrograms/kg) or a low dose (100 micrograms/kg) endotoxin by use of the slope of the end-systolic pressure-diameter relationship (ESPDR) as well as other measurements of cardiac performance. In all the pigs administered a high dose, ESPDR demonstrated a marked, time-dependent depression, whereas we observed no significant ESPDR changes after low endotoxin doses. The other cardiodynamic variables were uninterpretable, due to the significant changes in heart rate, end-diastolic diameter (preload), and aortic diastolic pressure (afterload). Plasma myocardial depressant factor activity accumulated in all endotoxin-administered animals, tending to be greater in the high-dose group. In this group, both subendocardial blood flow and global function were depressed, whereas pigs administered the low dose of endotoxin demonstrated slight, but nonsignificant, increases in flow and function. These observations indicate that myocardial contractile depression is associated with a lethal outcome to high doses of endotoxin. One possible mechanism for this loss of contractile function may be a relative hypoperfusion of the subendocardium.

Effects of hypertrophy on left atrial and ventricular compliance and plasma ANF levels in conscious dogs

1995 ◽  
Vol 268 (2) ◽  
pp. H781-H787 ◽  
Author(s):  
N. Hasebe ◽  
L. Hittinger ◽  
S. Kohin ◽  
Y. T. Shen ◽  
R. M. Graham ◽  
...  
Keyword(s):  
Coronary Sinus ◽  
Left Atrial ◽  
Volume Expansion ◽  
Diastolic Pressure ◽  
Systemic Circulation ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Volume Loading ◽  
Volume Depletion ◽  
Ventricular Compliance

Alterations in left atrial (LA) and left ventricular (LV) compliance and arterial and coronary sinus atrial natriuretic factor (ANF) concentrations at baseline and in response to both volume depletion and expansion were investigated in 15 conscious dogs with aortic banding-induced LV hypertrophy (LVH) (LV/body wt increased by 64%), which also induced LAH (LA/body wt increased by 61%). With volume expansion coronary sinus ANF increased more (P < 0.05) in dogs with LVH (+427 +/- 88 pg/ml) compared with control dogs (+146 +/- 45 pg/ml). Arterial ANF levels also rose more with volume expansion in LVH. In dogs with LVH, the LV end-diastolic pressure-diameter relationship was shifted to the left with a steeper slope with volume expansion, such that at any given diastolic dimension, diastolic pressure was higher. In contrast, the pressure-dimension relationship for the LA appendage was shifted in the opposite direction during both atrial systolic and diastolic phases, with a more shallow slope in hypertrophy compared with control dogs, resulting in an augmented pressure-dimension product during volume loading in LAH. In conclusion, in dogs with LVH and LAH, enhanced ANF was revealed in the coronary sinus and systemic circulation during volume expansion, which could be due, in part, to a more compliant, but hypertrophied, LA, which responded to equivalent volume loading with an augmented pressure-dimension product.

P4351Validation by cardiac catheterization of noninvasive evaluation of left ventricular chamber and myocardial stiffness as a diastolic function using speckle tracking echocardiography

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Yoshizane ◽  
R Tanaka ◽  
M Kawasaki ◽  
M Otsuka ◽  
T Shoji ◽  
...  
Keyword(s):  
Diastolic Function ◽  
Cardiac Catheterization ◽  
Left Atrial ◽  
Speckle Tracking ◽  
Speckle Tracking Echocardiography ◽  
Diastolic Pressure ◽  
Hypertensive Heart Disease ◽  
Left Ventricular ◽  
Minimum Volume ◽  
Myocardial Stiffness

Abstract Background Left ventricular (LV) diastolic function is mainly composed of LV relaxation and LV stiffness. We reported that pulmonary capillary wedge pressure (ePCWP) and LV relaxation assessed by Tau (eTau) are noninvasively evaluated by speckle tracking echocardiography (STE). The minimum LV diastolic pressure (mLVP) was reported to have a strong correlation with Tau. Therefore, LV chamber stiffness (c-stiffness) may be assessed with the use of two LV diastolic pressure-volume coordinates: the mLVP and volume and the end-diastolic pressure (EDP) and volume. Purpose We sought to noninvasively assess LV stiffness using STE and validate the value by cardiac catheterization. Methods Echocardiography and catheterization were performed in 124 patients (age 72±8) (70 angina pectoris, 20 prior myocardial infarction, 19 hypertensive heart disease, 11 congestive heart failure and 4 paroxysmal atrial fibrillation). The ePCWP (mmHg) is noninvasively obtained as 10.8 − 12.4 × Log (left atrial active emptying function/minimum volume) and the eTau (ms) is obtained as isovolumic relaxation time/(ln 0.9 × systolic blood pressure − ln ePCWP) as previously reported. The mLVP (e-mLVP) was estimate using Tau. The estimated EDP (e-EDP) was calculated as 12.3 − 10.1 × Log (left atrial active emptying function / minimum volume). LV c-stiffness (mmHg/ml) was calculated as LV pressure change (from mLVP to EDP) obtained by catheterization divided by LV volume change during diastole which equals to stroke volume by echocardiography. Estimated c-stiffness (e-c-stiffness) was noninvasively obtained using e-mLVP and e-EDP. Furthermore, LV myocardial stiffness (m-stiffness) was calculated by LVED stress / LV longitudinal strain by STE, where LV stress (kdynes/cm2) was calculated as 0.334 × pressure × dimension / [thickness (1 + thickness/dimension)]. The estimated m-stiffness (e-m-stiffness) was calculated using e-EDP. Results The eTau and e-EDP estimated by STE had a good correlation with Tau and EDP invasively obtained by catheterization (r=0.75 and 0.63, respectively, both p<0.001). There was a good correlation between Tau and mLVP (Tau = 2.06 mLVP + 33.7, r=0.70). The estimated LVED stress had good correlation with ED stress obtained by catheterization (r=0.77, p<0.001). The e-c-stiffness and e-m-stiffness had a good correlation with those obtained by catheterization (e-c-stiffness; 0.116±0.07 and c-stiffness; 0.115±0.06, r=0.603, e-m-stiffness; 0.81±0.41 and m-stiffness; 0.85±0.45, r=0.89, respectively). Bland-Altman analysis revealed a good agreement between e-c-stiffness and c-stiffness, and between e-m-stiffness and m-stiffness without fixed and proportional bias. Conclusion This study demonstrated that LV stiffness may be noninvasively assessed by STE with reasonable accuracy and may have utility and value in the routine clinical practice for the diagnosis and treatment in patients with diastolic dysfunction.

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