Ultrastructural and functional features of the developing mammalian heart: a brief overview

1995 ◽  
Vol 7 (3) ◽  
pp. 451 ◽  
Author(s):  
JJ Smolich
Keyword(s):  
Blood Flow ◽  
Sarcoplasmic Reticulum ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Postnatal Development ◽  
Vascular Resistance ◽  
Ventricular Myocytes ◽  
Left Ventricular ◽  
The Right

The heart undergoes marked ultrastructural alterations during fetal and postnatal development. Early in fetal development, cardiac myocytes contain abundant pools of glycogen, scattered mitochondria and sparse, peripheral myofibrils. Transverse tubules are absent, and sarcoplasmic reticulum and intercalated discs are poorly developed. During late fetal and early postnatal development, myofibrils extend into the myocyte interior and attain a mature appearance, and the glycogen pools are reduced in size. In addition, transverse tubules develop and the morphological appearance of the sarcoplasmic reticulum and intercalated disc becomes increasingly complex. Experimental studies in sheep, corroborated by clinical studies in humans, also point to marked functional changes during development. In the fetus, the right ventricle is the dominant pumping chamber because right ventricular output exceeds left ventricular output, while pulmonary arterial and aortic pressures are similar. This functional difference is reflected in myocardial blood flow patterns, with blood flow to the right ventricle exceeding that to the left ventricle. The ventricular outputs equalize after birth, but a functional left ventricular dominance rapidly emerges following a postnatal increase in systemic vascular resistance and a decrease in pulmonary vascular resistance. This postnatal switchover in functional dominance is accompanied by a corresponding alteration in the relative level of ventricular myocardial blood flows. Consistent with right ventricular dominance in utero, myocytes in the right ventricle of the fetal sheep are larger and contain more myofibrillar material than those in the left ventricle. Left ventricular myocytes become larger than right ventricular myocytes after birth, but this adaptation to altered postnatal haemodynamics requires some weeks to become fully established.

Right Ventricular Perfusion

2018 ◽  
Vol 128 (1) ◽  
pp. 202-218 ◽  
Author(s):  
George J. Crystal ◽  
Paul S. Pagel
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Coronary Circulation ◽  
Contractile Function ◽  
Left Ventricular ◽  
Oxygen Extraction ◽  
Pulmonary Arterial ◽  
The Right

Abstract Regulation of blood flow to the right ventricle differs significantly from that to the left ventricle. The right ventricle develops a lower systolic pressure than the left ventricle, resulting in reduced extravascular compressive forces and myocardial oxygen demand. Right ventricular perfusion has eight major characteristics that distinguish it from left ventricular perfusion: (1) appreciable perfusion throughout the entire cardiac cycle; (2) reduced myocardial oxygen uptake, blood flow, and oxygen extraction; (3) an oxygen extraction reserve that can be recruited to at least partially offset a reduction in coronary blood flow; (4) less effective pressure–flow autoregulation; (5) the ability to downregulate its metabolic demand during coronary hypoperfusion and thereby maintain contractile function and energy stores; (6) a transmurally uniform reduction in myocardial perfusion in the presence of a hemodynamically significant epicardial coronary stenosis; (7) extensive collateral connections from the left coronary circulation; and (8) possible retrograde perfusion from the right ventricular cavity through the Thebesian veins. These differences promote the maintenance of right ventricular oxygen supply–demand balance and provide relative resistance to ischemia-induced contractile dysfunction and infarction, but they may be compromised during acute or chronic increases in right ventricle afterload resulting from pulmonary arterial hypertension. Contractile function of the thin-walled right ventricle is exquisitely sensitive to afterload. Acute increases in pulmonary arterial pressure reduce right ventricular stroke volume and, if sufficiently large and prolonged, result in right ventricular failure. Right ventricular ischemia plays a prominent role in these effects. The risk of right ventricular ischemia is also heightened during chronic elevations in right ventricular afterload because microvascular growth fails to match myocyte hypertrophy and because microvascular dysfunction is present. The right coronary circulation is more sensitive than the left to α-adrenergic–mediated constriction, which may contribute to its greater propensity for coronary vasospasm. This characteristic of the right coronary circulation may increase its vulnerability to coronary vasoconstriction and impaired right ventricular perfusion during administration of α-adrenergic receptor agonists.

scholarly journals Epigenetics, inflammation and metabolism in right heart failure associated with pulmonary hypertension

2017 ◽  
Vol 7 (3) ◽  
pp. 572-587 ◽  
Author(s):  
Nolwenn Samson ◽  
Roxane Paulin
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Pressure Overload ◽  
Right Heart Failure ◽  
Left Ventricular ◽  
Ventricular Failure ◽  
Pulmonary Arterial ◽  
Ventricle Hypertrophy ◽  
The Right

Right ventricular failure (RVF) is the most important prognostic factor for both morbidity and mortality in pulmonary arterial hypertension (PAH), but also occurs in numerous other common diseases and conditions, including left ventricle dysfunction. RVF remains understudied compared with left ventricular failure (LVF). However, right and left ventricles have many differences at the morphological level or the embryologic origin, and respond differently to pressure overload. Therefore, knowledge from the left ventricle cannot be extrapolated to the right ventricle. Few studies have focused on the right ventricle and have permitted to increase our knowledge on the right ventricular-specific mechanisms driving decompensation. Here we review basic principles such as mechanisms accounting for right ventricle hypertrophy, dysfunction, and transition toward failure, with a focus on epigenetics, inflammatory, and metabolic processes.

Measurement of left and right ventricular volume from implanted radiopaque markers

1981 ◽  
Vol 240 (6) ◽  
pp. H896-H900
Author(s):  
W. P. Santamore ◽  
R. Carey ◽  
D. Goodrich ◽  
A. A. Bove
Keyword(s):  
Standard Deviation ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Ventricular Volumes ◽  
Radiopaque Markers ◽  
Left And Right ◽  
The Right

To better understand biventricular mechanics, an algorithm was developed to simultaneously calculate right and left ventricular volumes from randomly placed subendocardial radiopaque markers. Mathematically, the ventricle is represented as a stack of circular discs. The radius R of each disc is calculated as the distance from the subendocardial radiopaque marker to a computer generated base-to-apex line, and the height H of each disc is determined by the projected distance between radiopaque markers along the base-to-apex line. Accordingly, the volume (V) is calculated as V = pi . sigma Hi . Ri2. The validity of this algorithm was tested on 10 canine left ventricular casts, on 10 human right ventricular casts, and in five experiments. For the left ventricle, the regression line between the casts (VT) and calculated (VC) volumes was VC = 0.55 VT + 6.6, with r = 0.95, standard error of estimate (Sy) = 1.9 ml, and the standard deviation of percent error = 12.6%. For the right ventricle, VC = 1.75 VT = 42.5, with r = 0.86, Sy = 16.2 ml, and the standard deviation of percent error = 24.8%. In five animal experiments, radiopaque markers were implanted into the endocardium of the left and right ventricles and comparisons were made between angiographic- and marker-determined ventricular volumes. For the five experiments, the mean correlation coefficient, relating the marker volumes to the angiographic volumes, were 0.92 +/- 0.01 for the left ventricle and 0.89 +/- 0.02 for the right ventricle. The results, which are similar to other volume-determination methods, indicate that this method can be applied to determine right and left ventricular volume. Once implanted, fluoroscopy of these markers provides a noninvasive means of calculating ventricular volume.

A 24-segment fractional shortening of the fetal heart using FetalHQ

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Toshiyuki Hata ◽  
Aya Koyanagi ◽  
Tomomi Yamanishi ◽  
Saori Bouno ◽  
Riko Takayoshi ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Speckle Tracking ◽  
Fetal Heart ◽  
Correlation Coefficients ◽  
Left Ventricular ◽  
Basal Segment ◽  
The Right ◽  
Fractional Shortening

AbstractObjectivesTo evaluate 24-segment fractional shortening (FS) of the fetal heart using FetalHQ by speckle-tracking regarding reproducibility and the change with advancing gestation.MethodsEighty-one pregnant women at 18–21 + 6 and 28–31 + 6 weeks of gestation were studied using FetalHQ with the speckle-tracking technique to calculate 24-segment FS of left and right ventricles. Intra- and inter-class correlation coefficients and intra- and inter-observer agreements of measurements for FS were assessed in each segment.ResultsWith respect to intra-observer reproducibility, all FS values showed correlations between 0.575 and 0.862 for the left ventricle, with good intra-observer agreements except for left ventricular segments 14–24. Right ventricular FS values showed correlations between 0.334 and 0.685, with good intra-observer agreements. With respect to inter-observer reproducibility, all FS values showed correlations between 0.491 and 0.801 for the left ventricle, with good intra-observer agreements except for left ventricular segments 16–22. Right ventricular FS values showed correlations between 0.375 and 0.575, with good inter-observer agreements. There were significant differences in the mean FS values in the basal segment (segments 1–5) of the left ventricle between 18 and 21 + 6 and 28–31 + 6 weeks of gestation (p<0.05), whereas there were significant differences in all mean FS values in the right ventricle between both gestational ages (p<0.05).ConclusionsThese results suggest that the reproducibility of the 24-segment FS of the fetal heart using FetalHQ is fair. However, there may be significant differences in FS values with advancing gestational age, especially for the right ventricle.

Mechanisms of Oxygen Demand/Supply Balance in the Right Ventricle

2005 ◽  
Vol 230 (8) ◽  
pp. 507-519 ◽  
Author(s):  
Pu Zong ◽  
Johnathan D. Tune ◽  
H. Fred Downey
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Coronary Blood Flow ◽  
Oxygen Demand ◽  
Coronary Vasodilation ◽  
External Work ◽  
Coronary Conductance ◽  
The Right

Few studies have investigated factors responsible for the O2 demand/supply balance in the right ventricle. Resting right coronary blood flow is lower than left coronary blood flow, which Is consistent with the lesser work of the right ventricle. Because right and left coronary artery perfusion pressures are Identical, right coronary conductance is less than left coronary conductance, but the signal relating this conductance to the lower right ventricular O2 demand has not been defined. At rest, the left ventricle extracts ~75% of the O2 delivered by coronary blood flow, whereas right ventricular O2 extraction Is only ~50%. As a result, resting right coronary venous PO2 is ~30 mm Hg, whereas left coronary venous PO2 is ~20 mm Hg. Right coronary conductance does not sufficiently restrict flow to force the right ventricle to extract the same percentage of O2 as the left ventricle. Endogenous nitric oxide impacts the right ventricular O2 demand/supply balance by increasing the right coronary blood flow at rest and during acute pulmonary hypertension, systemic hypoxia, norepinephrine infusion, and coronary hypoperfusion. The substantial right ventricular O2 extraction reserve is used preferentially during exercise-induced increases in right ventricular myocardial O2 consumption. An augmented, sympathetic-mediated vasoconstrictor tone blunts metabolically mediated dilator mechanisms during exercise and forces the right ventricle to mobilize its O2 extraction reserve, but this tone does not limit resting right coronary flow. During exercise, right coronary vasodilation does not occur until right coronary venous PO2 decreases to ~20 mm Hg. The mechanism responsible for right coronary vasodilation at low PO2 has not been delineated. In the poorly autoregulating right coronary circulation, reduced coronary pressure unloads the coronary hydraulic skeleton and reduces right ventricular systolic stiffness. Thus, normal right ventricular external work and O2 demand/supply balance can be maintained during moderate coronary hypoperfusion.

Pulmonary Vascular Versus Right Ventricular Function Changes During Targeted Therapies of Pulmonary Hypertension – An Argument for Upfront Combination Therapy?

2012 ◽  
Vol 8 (3) ◽  
pp. 209
Author(s):  
Wouter Jacobs ◽  
Anton Vonk-Noordegraaf ◽  
◽  
Keyword(s):  
Combination Therapy ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Meta Analysis ◽  
Right Heart Failure ◽  
Functional Class ◽  
Pulmonary Vasculature ◽  
The Right

Pulmonary arterial hypertension is a progressive disease of the pulmonary vasculature, ultimately leading to right heart failure and death. Current treatment is aimed at targeting three different pathways: the prostacyclin, endothelin and nitric oxide pathways. These therapies improve functional class, increase exercise capacity and improve haemodynamics. In addition, data from a meta-analysis provide compelling evidence of improved survival. Despite these treatments, the outcome is still grim and the cause of death is inevitable – right ventricular failure. One explanation for this paradox of haemodynamic benefit and still worse outcome is that the right ventricle does not benefit from a modest reduction in pulmonary vascular resistance. This article describes the physiological concepts that might underlie this paradox. Based on these concepts, we argue that not only a significant reduction in pulmonary vascular resistance, but also a significant reduction in pulmonary artery pressure is required to save the right ventricle. Haemodynamic data from clinical trials hold the promise that these haemodynamic requirements might be met if upfront combination therapy is used.

Regulation of K+ and Ca2+ channels in experimental cardiac failure

1991 ◽  
Vol 261 (6) ◽  
pp. H1979-H1987 ◽  
Author(s):  
M. Gopalakrishnan ◽  
D. J. Triggle ◽  
A. Rutledge ◽  
Y. W. Kwon ◽  
J. A. Bauer ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Cardiac Failure ◽  
Radioligand Binding ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
The Right

To examine the status of ATP-sensitive K+ (K+ATP) channels and 1,4-dihydropyridine-sensitive Ca2+ (Ca2+DHP) channels during experimental cardiac failure, we have measured the radioligand binding properties of [3H]glyburide and [3H]PN 200 110, respectively, in tissue homogenates from the rat cardiac left ventricle, right ventricle, and brain 4 wk after myocardial infarction induced by left coronary artery ligation. The maximal values (Bmax) for [3H]glyburide and [3H]PN 200 110 binding were reduced by 39 and 40%, respectively, in the left ventricle, and these reductions showed a good correlation with the right ventricle-to-body weight ratio in heart-failure rats. The ligand binding affinities were not altered. In the hypertrophied right ventricle, Bmax values for both the ligands were not significantly different when data were normalized to DNA content or right ventricle weights but showed an apparent reduction when normalized to unit protein or tissue weight. Moderate reductions in channel densities were observed also in whole brain homogenates from heart failure rats. Assessment of muscarinic receptors, beta-adrenoceptors and alpha 1-adrenoceptors by [3H]quinuclidinyl benzilate, [3H]dihydroalprenolol, and [3H]prazosin showed reductions in left ventricular muscarinic and beta-adrenoceptor densities but not in alpha 1-adrenoceptor densities, consistent with earlier observations. It is suggested that these changes may in part contribute to the pathology of cardiac failure.

Ventricular systolic interdependence: volume elastance model in isolated canine hearts

1987 ◽  
Vol 253 (6) ◽  
pp. H1381-H1390 ◽  
Author(s):  
W. L. Maughan ◽  
K. Sunagawa ◽  
K. Sagawa
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Cross Talk ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Systolic Volume ◽  
The Right

To analyze the interaction between the right and left ventricle, we developed a model that consists of three functional elastic compartments (left ventricular free wall, septal, and right ventricular free wall compartments). Using 10 isolated blood-perfused canine hearts, we determined the end-systolic volume elastance of each of these three compartments. The functional septum was by far stiffer for either direction [47.2 +/- 7.2 (SE) mmHg/ml when pushed from left ventricle and 44.6 +/- 6.8 when pushed from right ventricle] than ventricular free walls [6.8 +/- 0.9 mmHg/ml for left ventricle and 2.9 +/- 0.2 for right ventricle]. The model prediction that right-to-left ventricular interaction (GRL) would be about twice as large as left-to-right interaction (GLR) was tested by direct measurement of changes in isovolumic peak pressure in one ventricle while the systolic pressure of the contralateral ventricle was varied. GRL thus measured was about twice GLR (0.146 +/- 0.003 vs. 0.08 +/- 0.001). In a separate protocol the end-systolic pressure-volume relationship (ESPVR) of each ventricle was measured while the contralateral ventricle was alternatively empty and while systolic pressure was maintained at a fixed value. The cross-talk gain was derived by dividing the amount of upward shift of the ESPVR by the systolic pressure difference in the other ventricle. Again GRL measured about twice GLR (0.126 +/- 0.002 vs. 0.065 +/- 0.008). There was no statistical difference between the gains determined by each of the three methods (predicted from the compartment elastances, measured directly, or calculated from shifts in the ESPVR). We conclude that systolic cross-talk gain was twice as large from right to left as from left to right and that the three-compartment volume elastance model is a powerful concept in interpreting ventricular cross talk.

Levels of brain natriuretic peptide in children with right ventricular overload due to congenital cardiac disease

2005 ◽  
Vol 15 (4) ◽  
pp. 396-401 ◽  
Author(s):  
Thomas S. Mir ◽  
Jan Falkenberg ◽  
Bernd Friedrich ◽  
Urda Gottschalk ◽  
Throng Phi Lê ◽  
...  
Keyword(s):  
Right Ventricle ◽  
Brain Natriuretic Peptide ◽  
Right Ventricular ◽  
Natriuretic Peptide ◽  
Cardiac Disease ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Congenital Cardiac Disease ◽  
The Right

Objective:To evaluate the role of the concentration of brain natriuretic peptide in the plasma, and its correlation with haemodynamic right ventricular parameters, in children with overload of the right ventricle due to congenital cardiac disease.Methods:We studied 31 children, with a mean age of 4.8 years, with volume or pressure overload of the right ventricle caused by congenital cardiac disease. Of the patients, 19 had undergone surgical biventricular correction of tetralogy of Fallot, 11 with pulmonary stenosis and 8 with pulmonary atresia, and 12 patients were studied prior to operations, 7 with atrial septal defects and 5 with anomalous pulmonary venous connections. We measured brain natriuretic peptide using Triage®, from Biosite, United States of America. We determined end-diastolic pressures of the right ventricle, and the peak ratio of right to left ventricular pressures, by cardiac catheterization and correlated them with concentrations of brain natriuretic peptide in the plasma.Results:The mean concentrations of brain natriuretic peptide were 87.7, with a range from 5 to 316, picograms per millilitre. Mean end-diastolic pressure in the right ventricle was 5.6, with a range from 2 to 10, millimetres of mercury, and the mean ratio of right to left ventricular pressure was 0.56, with a range from 0.24 to 1.03. There was a positive correlation between the concentrations of brain natriuretic peptide and the ratio of right to left ventricular pressure (r equal to 0.7844, p less than 0.0001) in all patients. These positive correlations remained when the children with tetralogy of Fallot, and those with atrial septal defects or anomalous pulmonary venous connection, were analysed as separate groups. We also found a weak correlation was shown between end-diastolic right ventricular pressure and concentrations of brain natriuretic peptide in the plasma (r equal to 0.5947, p equal to 0.0004).Conclusion:There is a significant correlation between right ventricular haemodynamic parameters and concentrations of brain natriuretic peptide in the plasma of children with right ventricular overload due to different types of congenital cardiac disease. The monitoring of brain natriuretic peptide may provide a non-invasive and safe quantitative follow up of the right ventricular pressure and volume overload in these patients.

CLINICAL CONFERENCE

PEDIATRICS ◽  
1957 ◽  
Vol 19 (6) ◽  
pp. 1139-1147
Author(s):  
Mary Allen Engle
Keyword(s):  
Blood Flow ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Pulmonary Blood Flow ◽  
Ventricular Hypertrophy ◽  
Pulmonary Valve ◽  
Muscular Tissue ◽  
Pulmonic Stenosis ◽  
Infundibular Stenosis ◽  
The Right

Dr. Engle: When pulmonic stenosis occurs as an isolated congenital malformation of the heart, it usually is due to fusion of the valve cusps into a dome with a small hole in the center. In Figure 1 the pulmonary artery has been laid open so that one can see the three leaflets of the pulmonary valve are completely fused, and that there is only a small, central, pinpoint opening which permits blood to leave the right ventricle and enter the pulmonary circulation. Valvular pulmonic stenosis is much more common than subvalvular or infundibular stenosis, where the obstruction to pulmonary blood flow lies within the substance of the right ventricle. There it may be due to a diaphragm of tissue which obstructs the outflow of the right ventricle, or to an elongated narrow tunnel lined with thickened endocardium, or to a ridge of fibrous or muscular tissue just beneath the pulmonary valve. The changes in the cardiovascular system which result from obstructed pulmonary blood flow are so characteristic that they permit the ready recognition of this condition. Proximal to the constriction, these changes manifest the burden placed on the right ventricle, which enlarges and hypertrophies. On physical examination this is demonstrated by the precordial bulge and tapping impulse just to the left of the sternum, where the rib cage overlies the anterior (right) ventricle. Radiographically, both by fluoroscopy and in roentgenograms in the frontal and both oblique views, right ventricular enlargement is seen. In the electrocardiogram, the precordial leads show a pattern of right ventricular hypertrophy.

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