Influence of pericardium on left atrial compliance and pulmonary venous flow

1993 ◽  
Vol 264 (6) ◽  
pp. H1781-H1787 ◽  
Author(s):  
B. D. Hoit ◽  
Y. Shao ◽  
M. Gabel ◽  
R. A. Walsh

We studied seven open-chest anesthetized dogs to test the hypothesis that left atrial (LA) compliance is increased after pericardiectomy and to determine the effect of pericardiectomy on left atrial reservoir and conduit function. Two orthogonal sonomicrometer crystal pairs were used to estimate LA volume, and LA filling was assessed with a pulmonary vein (PV) flow probe. The left ventricular (LV) systolic (JFTI) and diastolic (KFTI) PV flow integrals were used as indexes of LA reservoir and conduit function, respectively. Diastolic LV transmitral flow was assessed with transesophageal Doppler echocardiography. Data were acquired over a wide range of intracardiac pressures and volumes obtained by intravenous hetastarch infusion both before and after pericardiectomy. The mean dynamic stiffness constant of the LA diastolic pressure-volume relation was significantly greater before pericardiectomy than afterwards (0.15 +/- 0.04 vs. 0.08 +/- 0.03 ml-1, P < 0.05). Data were analyzed before and after pericardiectomy at three matched levels of left atrial pressure (LAP; 7, 13, and 20 mmHg). The J-to-KFTI ratio increased significantly with volume infusion and was significantly less after pericardiectomy than before (1.2 +/- 0.7 vs. 1.2 +/- 0.6, 1.8 +/- 0.6 vs. 2.2 +/- 0.9, and 2.0 +/- 0.8 vs. 2.6 +/- 0.9 at low, mid, and high levels of LAP, respectively; P < 0.05 at mid and high levels of LAP). Peak early transmitral velocity increased with both volume infusion and pericardiectomy. We conclude that pericardiectomy increases LA compliance and early LV filling rate and is accompanied by a relatively greater augmentation in conduit than reservoir function of the left atrium.

1998 ◽  
Vol 275 (1) ◽  
pp. H183-H189 ◽  
Author(s):  
Brian D. Hoit ◽  
Yanfu Shao ◽  
Marjorie Gabel

The objective of this study was to examine the hypothesis that long-term, rapid atrial pacing produces a model of atrial systolic and diastolic dysfunction but does not alter ventricular function. Eight dogs were atrially paced at 400 beats/min (3:1–5:1 ventricular response) for 6 wk and subsequently instrumented with left atrial (LA) and left ventricular (LV) sonomicrometers and micromanometers. Data were compared with those from six sham-operated controls at matched heart rates and mean LA pressures of 10 mmHg. Dogs with rapid pacing had slightly greater LA volume (10.3 ± 4.0 vs. 7.9 ± 4.4 ml) and reduced ejection fraction (2.2 ± 1.4 vs. 13.0 ± 4.0, P < 0.05), systolic ejection rate (0.3 ± 0.1 vs. 2.8 ± 1.2 vol/s, P < 0.05), and reservoir fraction (0.07 ± 0.04 vs. 0.35 ± 0.06, P < 0.05) compared with controls. LA diastolic chamber stiffness was greater after rapid atrial pacing than before (stiffness constant k c, 5.7 ± 2.3 vs. 3.4 ± 0.6, P < 0.05), and the ratio of transesophageal echo-determined pulmonary venous systolic to diastolic integrated flow (a measure of relative reservoir to conduit function of the LA) was less in rapidly paced dogs compared with control dogs (0.41 ± 0.19 vs. 0.68 ± 0.23, P < 0.05). In contrast, rapid atrial pacing did not influence LV systolic performance or lusitropy, because the LV pressure time derivative and the time constant of LV relaxation were similar in both groups. In this model of isolated atrial myopathy, increased atrial stiffness and enhanced conduit function compensate for impaired atrial booster pump and reservoir functions.


1990 ◽  
Vol 259 (2) ◽  
pp. H480-H487 ◽  
Author(s):  
B. D. Hoit ◽  
M. LeWinter ◽  
W. Y. Lew

We examined the influence of left atrial pressure on regional peak lengthening rates in six open-chest dogs. Sonomicrometers were implanted in the midwall of the anterior apex, the midanterior wall, and the posterior wall of the left ventricle. A bolus of blood was injected into the left atrium during ventricular systole by a computer-driven power injector to produce an isolated increase in left atrial pressure without altering the peak rate of left ventricular pressure fall, regional systolic shortening, or end-systolic length. Several left atrial injections of different volumes were performed over a wide range of left ventricular end-diastolic pressure (LVEDP) (from 7 to 22 mmHg). The peak lengthening rate increased in direct proportion to the increase of left atrial pressure. This effect was significantly greater in the apical than midanterior or posterior sites and decreased at all sites at higher LVEDP. Similar size left atrial injections produced greater increases in atrioventricular pressure gradient but smaller increases in left atrial pressure at low compared with high LVEDP. We conclude that left atrial pressure is an independent determinant of regional peak lengthening rates in the intact left ventricle. The influence of left atrial pressure is attenuated at higher LVEDP because of a smaller change in the diastolic pressure gradient, although viscoelastic effects may play a role.


Author(s):  
António Fontes ◽  
Nuno Dias-Ferreira ◽  
Anabela Tavares ◽  
Fátima Neves

Abstract Background Myocarditis is an uncommon, potentially life-threatening disease that presents with a wide range of symptoms. In acute myocarditis, chest pain (CP) may mimic typical angina and also be associated with electrocardiographic changes, including an elevation of the ST-segment. A large percentage (20–56%) of myxomas are found incidentally. Case summary A 62-year-old female presenting with sudden onset CP and infero-lateral ST-elevation in the electrocardiogram. The diagnosis of ST-elevation myocardial infarction was presumed and administered tenecteplase. The patient was immediately transported to a percutaneous coronary intervention centre. She complained of intermittent diplopia during transport and referred constitutional symptoms for the past 2 weeks. Coronary angiography showed normal arteries. The echocardiogram revealed moderate to severe left ventricular systolic dysfunction due to large areas of akinesia sparing most of the basal segments, and a mobile mass inside the left atrium attached to the septum. The cardiac magnetic resonance (CMR) suggested the diagnosis of myocarditis with concomitant left atrial myxoma. The patient underwent resection of the myxoma. Neurological evaluation was performed due to mild vertigo while walking and diplopia in extreme eye movements. The head magnetic resonance imaging identified multiple infracentimetric lesions throughout the cerebral parenchyma compatible with an embolization process caused by fragments of the tumour. Discussion Myocarditis can have various presentations may mimic acute myocardial infarction and CMR is critical to establish the diagnosis. Myxoma with embolic complications requires emergent surgery. To the best of our knowledge, this is the first case reported in the applicable literature of a myxoma diagnosed during a myocarditis episode.


Author(s):  
Flemming Javier Olsen ◽  
Rasmus Møgelvang ◽  
Martina Chantal de Knegt ◽  
Søren Galatius ◽  
Sune Pedersen ◽  
...  

2003 ◽  
Vol 81 (2) ◽  
pp. 125-128 ◽  
Author(s):  
Ghada S Hassan ◽  
Fazila Chouiali ◽  
Takayuki Saito ◽  
Fu Hu ◽  
Stephen A Douglas ◽  
...  

Recent studies have shown that the vasoactive peptide urotensin-II (U-II) exerts a wide range of action on the cardiovascular system of various species. In the present study, we determined the in vivo effects of U-II on basal hemodynamics and cardiac function in the anesthetized intact rat. Intravenous bolus injection of human U-II resulted in a dose-dependent decrease in mean arterial pressure and left ventricular systolic pressure. Cardiac contractility represented by ±dP/dt was decreased after injection of U-II. However, there was no significant change in heart rate or diastolic pressure. The present study suggests that upregulation of myocardial U-II may contribute to impaired myocardial function in disease conditions such as congestive heart failure.Key words: urotensin-II, rat, infusion, heart.


1998 ◽  
Vol 274 (3) ◽  
pp. H945-H954 ◽  
Author(s):  
Steven B. Solomon ◽  
Srdjan D. Nikolic ◽  
Stanton A. Glantz ◽  
Edward L. Yellin

In patients with heart failure, decreased contractility resulting in high end-diastolic pressures and a restrictive pattern of left ventricular filling produces a decrease in early diastolic filling, suggesting a stiff ventricle. This study investigated the elastic properties of the myocardium and left ventricular chamber and the ability of the heart to utilize elastic recoil to facilitate filling during pacing-induced heart failure in the anesthetized dog. Elastic properties of the myocardium were determined by analyzing the myocardial stress-strain relation. Left ventricular chamber properties were determined by analyzing the pressure-volume relation using a logarithmic approach. Elastic recoil was characterized using a computer-controlled mitral valve occluder to prevent transmitral flow during diastole. We conclude that, during heart failure, the high end-diastolic pressures suggestive of a stiff ventricle are due not to stiffer myocardium but to a ventricle whose chamber compliance characteristics are changed due to geometric remodeling of the myocardium. The restrictive filling pattern is a result of the ventricle being forced to operate on the stiff portion of the diastolic pressure-volume relation to maintain cardiac output. Slowed relaxation and decreased contractility result in an inability of the heart to contract to an end-systolic volume below its diastolic equilibrium volume. Thus the left ventricle cannot utilize elastic recoil to facilitate filling during heart failure.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Shahryar M Chowdhury ◽  
Ryan J Butts ◽  
Anthony M Hlavacek ◽  
Carolyn L Taylor ◽  
Varsha M Bandisode ◽  
...  

Introduction: The accuracy of echocardiography in evaluating left ventricular (LV) diastolic function has not been validated in children. The objective of this study was to compare echocardiographic and gold-standard measures of LV diastolic function in children. Methods: Patients undergoing routine left heart catheterization were prospectively enrolled. Pressure-volume loops (PVL) were obtained via conductance catheters. The end-diastolic pressure-volume relationship was obtained via balloon occlusion of the vena cavae. PVL measures of diastolic function were divided into early active relaxation (the isovolumic relaxation time constant, tau), and ventricular stiffness (the chamber stiffness constant, β). End-diastolic pressure (EDP) was also recorded. Echocardiographic measures of diastolic function were derived from spectral Doppler, tissue Doppler, and 2D speckle-tracking. The relationships between PVL and echocardiographic measures were determined using Spearman’s correlation. Results: Of 24 patients, 18 patients were s/p heart transplant, 5 patients had a small patent ductus arteriosus or coronary fistula. Mean age was 9.1 ± 5.6 years. The median τ was 24.9 ms (IQR 22.8 - 28.4 ms), median β was 0.094 (IQR 0.035 - 0.154), and median EDP was 9 mmHg (IQR 8 - 13 mmHg). Statistically significant correlations between invasive and echocardiographic measures of diastolic function are reported in the Table. No echocardiographic measures correlated with β. Conclusion: Early diastolic echocardiographic measures correlate with tau and may accurately represent early active relaxation in children. Modest associations exist between echocardiographic measures and EDP. The use of these non-invasive measures in accurately assessing LV diastolic function appears promising in children. However, no echocardiographic measures correlate with chamber stiffness. The development of such measures merits further study.


1997 ◽  
Vol 273 (2) ◽  
pp. H583-H592 ◽  
Author(s):  
S. Yasuda ◽  
T. Shishido ◽  
Y. Goto

The left ventricular (LV) mechanical performance and the LV myocardial oxygen consumption (VO2)-to-pressure-volume area (PVA; LV total mechanical energy index) relationship were measured in isovolumic contraction of isolated blood-perfused dog hearts before and after direct current (DC) countershocks. At a constant LV volume, DC shocks increased LV end-diastolic pressure progressively and strikingly with the progression of myocardial edema and a marked prolongation of the time constant of LV pressure decay. In contrast, DC shocks changed neither the slope of the LV end-systolic pressure-volume relationship nor the contractile efficiency (the slope of the Vo2-PVA relationship). The oxygen cost of contractility (the slope of the relationship between PVA-independent VO2 and LV contractility) increased 27% after DC shocks. However, the magnitude of this change was considerably smaller than that previously reported in postischemic stunned myocardium (123%), suggesting that the adverse effect of DC shocks on the energy cost of excitation-contraction coupling is relatively minor. Thus, despite the severe diastolic dysfunction, DC shocks do not substantially impair either the efficiency of cross-bridge cycling or calcium cycling. Myocardial interstitial edema is more likely a potential mechanism of diastolic dysfunction after DC shocks.


1980 ◽  
Vol 239 (4) ◽  
pp. H545-H545 ◽  
Author(s):  
Raymond C. Koehler ◽  
Brian W. McDonald ◽  
John A. Krasney

The modulating effect of CO2 on the circulatory response to hypoxia in chronically instrumented conscious dogs was examined over a wide range of arterial partial pressure of O2 [PaO2 (from 80 to 25 Torr)] during a 41-min rebreathing period at three CO2 levels: hypocapnia (from PaCO2 of 32 to 18 Torr), eucapnia (32 Torr), and mild hypercapnia (40 Torr). Eucapnic and hypercapnic hypoxic responses were also measured after sinoaortic denervation (SAD) to assess the arterial chemoreceptor and baroreceptor reflex contributions. Elevating PaCO2 attenuated the tachycardia during hypoxia and produced progressively greater systemic, renal, and splanchnic vasoconstriction before but not after SAD. Vagal block converted the rises in renal and splanchnic flows observed during hypocapnic hypoxia to declines. The increase in left ventricular dP/d tmax was not affected by varying PaCO2 either before or after SAD. Coronary flow increased an additional onefold during hypoxia when PaCO2 was elevated both before and after SAD, but the tension-time indices did not differ significantly. These results indicate that: a) cardiopulmonary vagal afferents effectively counteract chemoreflex-induced vasoconstriction during hypocapnic hypoxia; b) chemoreflex vasoconstriction predominates in the renal and splanchnic beds when PaCO2 is elevated; c) the sinoaortic reflexes restrain the heart rate, but not the contractility response to hypoxia when PaCO2 is increased; and d) the augmented coronary vasodilation produced by CO2 is probably mediated by local CO2-hypoxic interactions.


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