Right ventricular distension and left ventricular compliance

1981 ◽  
Vol 240 (1) ◽  
pp. H87-H98 ◽  
Author(s):  
B. H. Lorell ◽  
I. Palacios ◽  
W. M. Daggett ◽  
M. L. Jacobs ◽  
B. N. Fowler ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Time Course ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Leftward Shift ◽  
Ventricular Compliance ◽  
Left Ventricular Compliance ◽  
The Right ◽  
Relationship Of ◽  
Isovolumic Relaxation

The constraint of the right ventricle (RV) on the end-diastolic pressure-volume (PV) relationship of the nonischemic and ischemic left ventricle (LV) was studied. The model used was the isovolumic beating LV, with separately perfused ejecting RV with controlled RV distension. The effect of augmented RV distension on the nonischemic LV PV relationship was examined. A change from mild [right ventricular end-diastolic pressure (RVEDP) = 1.5 mm Hg] to severe (RVEDP = 16 mmHg) RV distension resulted in a significant leftward shift of the LV PV relationship. Ischemia was produced for 90 min by reducing flow in the cannulated left main coronary artery and the effect of two levels of stable RV distension on the PV relationship of the ischemic LV was examined. Mild RV distension and moderate (RVEDP = 6 mmHg) RV distension were used. In both groups, there was a progressive leftward shift in the LV PV relationship that was significant by 60 min of ischemia. No change was seen in nonischemic controls. Ventricular relaxation, as described by the time constant of isovolumic relaxation, T, was impaired throughout ischemia but was not sufficiently prolonged to explain the above changes. Thus, the time course of change in the LV PV relationship during ischemia differs from that previously reported after pacing-induced ischemia in humans. Neither the external constraint of the RV nor incomplete relaxation explains this difference.

scholarly journals Acute stimulation of the soluble guanylate cyclase does not impact on left ventricular capacitance in normal and hypertrophied porcine hearts in vivo

2018 ◽  
Vol 315 (3) ◽  
pp. H669-H680 ◽  
Author(s):  
Alessio Alogna ◽  
Michael Schwarzl ◽  
Martin Manninger ◽  
Nazha Hamdani ◽  
Birgit Zirngast ◽  
...  
Keyword(s):  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Concentric Hypertrophy ◽  
Ventricular Compliance ◽  
Left Ventricular Compliance ◽  
Stimulation Of

Experimental data indicate that stimulation of the nitric oxide-soluble guanylate cyclase(sGC)-cGMP-PKG pathway can increase left ventricular (LV) capacitance via phosphorylation of the myofilamental protein titin. We aimed to test whether acute pharmacological sGC stimulation with BAY 41-8543 would increase LV capacitance via titin phosphorylation in healthy and deoxycorticosteroneacetate (DOCA)-induced hypertensive pigs. Nine healthy Landrace pigs and 7 pigs with DOCA-induced hypertension and LV concentric hypertrophy were acutely instrumented to measure LV end-diastolic pressure-volume relationships (EDPVRs) at baseline and during intravenous infusion of BAY 41-8543 (1 and 3 μg·kg−1·min−1 for 30 min, respectively). Separately, in seven healthy and six DOCA pigs, transmural LV biopsies were harvested from the beating heart to measure titin phosphorylation during BAY 41-8543 infusion. LV EDPVRs before and during BAY 41-8543 infusion were superimposable in both healthy and DOCA-treated pigs, whereas mean aortic pressure decreased by 20–30 mmHg in both groups. Myocardial titin phosphorylation was unchanged in healthy pigs, but total and site-specific (Pro-Glu-Val-Lys and N2-Bus domains) titin phosphorylation was increased in DOCA-treated pigs. Bicoronary nitroglycerin infusion in healthy pigs ( n = 5) induced a rightward shift of the LV EDPVR, demonstrating the responsiveness of the pathway in this model. Acute systemic sGC stimulation with the sGC stimulator BAY 41-8543 did not recruit an LV preload reserve in both healthy and hypertrophied LV porcine myocardium, although it increased titin phosphorylation in the latter group. Thus, increased titin phosphorylation is not indicative of increased in vivo LV capacitance. NEW & NOTEWORTHY We demonstrate that acute pharmacological stimulation of soluble guanylate cyclase does not increase left ventricular compliance in normal and hypertrophied porcine hearts. Effects of long-term soluble guanylate cyclase stimulation with oral compounds in disease conditions associated with lowered myocardial cGMP levels, i.e., heart failure with preserved ejection fraction, remain to be investigated.

Alterations in left ventricular compliance due to changes in right ventricular volume, pressure and compliance

1988 ◽  
Vol 22 (11) ◽  
pp. 768-776 ◽  
Author(s):  
W. P SANTAMORE ◽  
M. CONSTANTINESCU ◽  
J. VINTEN-JOHANSEN ◽  
W. E JOHNSTON ◽  
W. C LITTLE
Keyword(s):  
Right Ventricular ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Right Ventricular Volume ◽  
Ventricular Compliance ◽  
Left Ventricular Compliance

Cascade model of ventricular-arterial coupling and arterial-cardiac baroreflex function for cardiovascular variability in humans

2006 ◽  
Vol 291 (5) ◽  
pp. H2142-H2151 ◽  
Author(s):  
Shigeki Shibata ◽  
Rong Zhang ◽  
Jeff Hastings ◽  
Qi Fu ◽  
Kazunobu Okazaki ◽  
...  
Keyword(s):  
Diastolic Pressure ◽  
Function Analysis ◽  
Left Ventricular ◽  
Cascade Model ◽  
Respiratory Frequency ◽  
Cardiovascular Variability ◽  
Baroreflex Function ◽  
Ventricular Compliance ◽  
Transfer Function Analysis ◽  
Left Ventricular Compliance

Cardiovascular variability reflects autonomic regulation of blood pressure (BP) and heart rate (HR). However, systolic BP (SBP) variability also may be induced by fluctuations in stroke volume through left ventricular end-diastolic pressure (LVEDP) variability via dynamic ventricular-arterial coupling during respiration. We hypothesized that dynamic ventricular-arterial coupling is modulated by changes in left ventricular compliance associated with altered preload and that a cascade control mechanism of ventricular-arterial coupling with arterial-cardiac baroreflex function contributes to the genesis of cardiovascular variability at the respiratory frequency. Seven healthy young subjects underwent 6-min recordings of beat-by-beat LVEDP, SBP, and HR in the supine position with controlled respiration at 0.2 Hz during hyper- and hypovolemia. Spectral and transfer function analysis of these variables was conducted between 0.18 and 0.22 Hz. Dynamic ventricular-arterial coupling gain (Gain LVEDP-SBP) was smaller by 25% ( P = 0.009) during hypervolemia than during hypovolemia, whereas arterial-cardiac baroreflex function gain (Gain SBP-HR) was similar. As predicted from a cascade model, a linear relationship between Gain LVEDP-HR and LVEDP-SBP times Gain SBP-HR was identified ( R2 = 0.93, P < 0.001). Gain LVEDP-HR was smaller by 40% ( P = 0.04) during hypervolemia than during hypovolemia, leading to a reduction in spectral power of HR variability by 45% ( P = 0.08). We conclude that dynamic ventricular-arterial coupling gain is reduced during hypervolemia because of a decrease in left ventricular compliance. A cascade model of ventricular-arterial coupling with the arterial-cardiac baroreflex contributes to the genesis of cardiovascular variability at the respiratory frequency.

Effect of acute ventricular dilatation on fibrillation thresholds in the isolated rabbit heart

1992 ◽  
Vol 263 (4) ◽  
pp. H1306-H1310 ◽  
Author(s):  
S. Jalal ◽  
G. R. Williams ◽  
D. E. Mann ◽  
M. J. Reiter
Keyword(s):  
Right Ventricular ◽  
Diastolic Pressure ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Ventricular Dilatation ◽  
Excitation Wavelength ◽  
Ventricular Fibrillation Threshold ◽  
Fibrillation Thresholds ◽  
The Right ◽  
Right Ventricular Dilatation

We examined the effects of ventricular dilatation on epicardial refractoriness and ventricular fibrillation threshold (VFT) in the isolated, retrograde-perfused rabbit heart. Ventricular size was modified by acutely changing the volume of a fluid-filled balloon secured within either the left or right ventricle. Left ventricular dilatation (to an end-diastolic pressure of 30-38 mmHg) significantly decreased left ventricular effective refractory period (ERP) and myocardial wavelength (calculated as ERP x conduction velocity). Left VFT (determined by scanning the vulnerable period with a train of pulses) decreased from 6.4 +/- 0.9 to 4.4 +/- 0.5 mA; P < 0.01) with left but not right ventricular dilatation. Right ventricular dilatation was associated with a decrease in the right ventricular ERP and myocardial wavelength, and right VFT decreased from 13.6 +/- 1.8 to 4.1 +/- 0.3 mA (P < 0.01). Changes in VFT correlated with the decrease in local refractoriness and shortening of local excitation wavelength.

Right ventricular performance during ischemia: an anatomic and hemodynamic analysis

1977 ◽  
Vol 233 (4) ◽  
pp. H505-H513 ◽  
Author(s):  
H. Brooks ◽  
R. Holland ◽  
J. Al-Sadir
Keyword(s):  
Right Ventricular ◽  
Diastolic Pressure ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Ventricular Performance ◽  
Time To Peak ◽  
Contractile Parameters ◽  
Significant Depression ◽  
Right Ventricular Performance ◽  
The Right

This study in the pig was designed to characterize right ventricular (RV) contractile responses during infarction involving three areas of the heart--anteroseptal, anterolateral, and inferoseptal. Porcine coronary architecture was studied from multicolor vinyl casts. Distribution of blood supply to ventricular myocardium and papillary muscles was defined by intra-arterial dye injection. High-fidelity pressure and flow data were measured simultaneously in both ventricles following ligation of approximately equal lengths of the anterior descending, left circumflex, or posterior descending arteries. In the three groups, weight of myocardium involved by the occluded artery was comparable and there was significant depression of left ventricular performance, more pronounced in the two anterior infarcts. However, in anterolateral infarction, despite the obligatory drop in RV flow, there was no significant alteration in RV end-diastolic pressure (EDP), peak rate of rise of RV pressure (dP/dt), or time-to-peak developed dP/dt. In contrast, with both anteroseptal and inferoseptal infarctions there were significant alterations in all RV contractile parameters, at increased levels of RVEDP, signifying a primary depression in RV contractile state. With inferoseptal infarction, further occlusion of the right coronary near its origin produced a more exaggerated and selective RV contractile abnormality and, in half of the animals, varying degrees of acute tricuspid insufficiency.

Time course of systolic loading is an important determinant of ventricular relaxation

1987 ◽  
Vol 252 (3) ◽  
pp. H461-H466 ◽  
Author(s):  
F. J. Zatko ◽  
P. Martin ◽  
R. C. Bahler
Keyword(s):  
Time Course ◽  
Isolated Heart ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Time Interval ◽  
Load Step ◽  
Ventricular Relaxation ◽  
Load Effects ◽  
The Right ◽  
Isovolumic Relaxation

We studied the dependency of left ventricular relaxation on the timing of an abrupt increase in systolic load. In 10 canine isolated heart-lung preparations, a load step of 15 mmHg was imposed at specific intervals throughout systole, and the time of loading was defined as the interval from the R wave to the completion of the load step (R-load interval). Preload was held constant. The right atrium was paced at a cycle length of 450 ms. The decay of left ventricular pressure during isovolumic relaxation was described by a single exponential time constant (Texp). Load effects on isovolumic relaxation were expressed as a percent change in Texp as compared with Texp of the beat preceding the load intervention. Loads imposed early in systole consistently prolonged Texp [mean delta Texp = +17.01 +/- 1.64% (SE) for R-load intervals less than or equal to 120 ms]. Load changes late in systole consistently abbreviated Texp [mean delta Texp = -9.49 +/- 0.86% (SE) for R-load intervals greater than or equal to 130 ms]. The transition from augmentation to diminution of Texp always occurred when the R-load interval was 120-130 ms. The mean time interval of electromechanical systole for the test beats was not significantly different (P greater than or equal to 0.05) from that of the control beats [R-load intervals less than or equal to 120: test = 247.0 +/- 27.8 (SD) ms; control = 246.6 +/- 26.8 (SD) ms] [R-load intervals greater than or equal to 130: test = 243.3 +/- 29.1 (SD) ms; control = 243.8 +/- 28.4 (SD) ms].(ABSTRACT TRUNCATED AT 250 WORDS)

Absence of right ventricular isovolumic relaxation in open-chest anesthetized dogs

1992 ◽  
Vol 263 (5) ◽  
pp. H1587-H1590 ◽  
Author(s):  
E. S. Myhre ◽  
B. K. Slinker ◽  
M. M. LeWinter
Keyword(s):  
Right Ventricular ◽  
Left Ventricular ◽  
Right Atrial ◽  
Relative Timing ◽  
Relaxation Period ◽  
First Derivative ◽  
Open Chest ◽  
Anesthetized Dogs ◽  
The Right ◽  
Isovolumic Relaxation

During the left ventricular (LV) pump cycle, peak negative first derivative of pressure vs. time (dP/dt) occurs very close to the end of LV ejection, and there is a well-defined isovolumic relaxation period. Despite similarities between the right ventricular (RV) and LV pump cycles, recent studies indicate uncertainty as to whether peak negative RV dP/dt occurs simultaneously with RV end ejection and whether there is an isovolumic relaxation period during the RV pump cycle. To study these questions, we recorded relative timing of peak negative RV dP/dt, RV end ejection, and right atrial-RV pressure crossover in the open-chest anesthetized dog. The data demonstrate that peak negative RV dP/dt occurs an average of 60 ms before end ejection and that there is no RV isovolumic relaxation period. These findings have implications for the possible use of peak negative RV dP/dt as a marker of RV end ejection and for how time constants of pressure decay obtained during RV relaxation can be interpreted.

scholarly journals Heart in Acromegaly: The Echocardiographic Characteristics of Patients Diagnosed with Acromegaly in Various Stages of the Disease

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Agata Popielarz-Grygalewicz ◽  
Jakub S. Gąsior ◽  
Aleksandra Konwicka ◽  
Paweł Grygalewicz ◽  
Maria Stelmachowska-Banaś ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Healthy Volunteers ◽  
Global Longitudinal Strain ◽  
Interventricular Septum ◽  
Left Ventricular ◽  
Volume Index ◽  
Control Group ◽  
Glucose Metabolism Disorders ◽  
Acromegalic Cardiomyopathy ◽  
The Right

To determine whether the echocardiographic presentation allows for diagnosis of acromegalic cardiomyopathy. 140 patients with acromegaly underwent echocardiography as part of routine diagnostics. The results were compared with the control group comprising of 52 age- and sex-matched healthy volunteers. Patients with acromegaly presented with higher BMI, prevalence of arterial hypertension, and glucose metabolism disorders (i.e., diabetes and/or prediabetes). In patients with acromegaly, the following findings were detected: increased left atrial volume index, increased interventricular septum thickness, increased posterior wall thickness, and increased left ventricular mass index, accompanied by reduced diastolic function measured by the following parameters: E’med., E/E’, and E/A. Additionally, they presented with abnormal right ventricular systolic pressure. All patients had normal systolic function measured by ejection fraction. However, the values of global longitudinal strain were slightly lower in patients than in the control group; the difference was statistically significant. There were no statistically significant differences in the size of the right and left ventricle, thickness of the right ventricular free wall, and indexed diameter of the ascending aorta between patients with acromegaly and healthy volunteers. None of 140 patients presented systolic dysfunction, which is the last phase of the so-called acromegalic cardiomyopathy. Some abnormal echocardiographic parameters found in acromegalic patients may be caused by concomitant diseases and not elevated levels of GH or IGF-1 alone. The potential role of demographic parameters like age, sex, and/or BMI requires further research.

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