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PubMed1976

Myocardial necrosis, fibrosis, and DNA synthesis in experimental cardiac hypertrophy induced by sudden pressure overload.

The development of myocardial fibrosis as a result of cardiac hypertrophy was studied in 11 cats in which the pulmonary artery was banded, six rabbits in which the ascending aorta was banded, and eight cats with various congenital cardiac anomalies. Histological examination of the myocardium revealed multifocal areas of degeneration and necrosis with healing by fibrosis in the right ventricle of cats in which the pulmonary artery was banded and in the left ventricle of rabbits in which the aorta was banded. In five of eight cats with congenital anomalies, myocardial necrosis and fibrosis were not present in spite of heart weight to body weight ratios 2-4 times greater than in the experimental models. In the other three cats, fibrosis was subendocardial or diffuse rather than multifocal as in the banded animals. This suggests that the increased connective tissue found in animals with cardiac hypertrophy induced by banding the aorta or pulmonary artery is an artifact of the preparation. Autoradiographic studies of the myocardium of pulmonary artery-banded cats indicated that all newly synthesized DNA in this model is restricted to interstitial cell and endothelial cell proliferation.

Animals↗
PubMed1977

Quantitation of left ventricular myocardial fiber hypertrophy and interstitial tissue in human hearts with chronically increased volume and pressure overload.

Using new techniques, we quantitated left ventricular myocardial fiber hypertrophy and interstitial tissue in four groups of autopsied hearts free of coronary disease: 1) 22 normal hearts, 2) 20 hearts from patients with mitral incompetence (NYHA Class II-III) who died early after mitral valve replacement from causes other than cardiac failure, 3) 22 hearts from patients with mitral incompetence (NYHA Class III-IV) who died early after mitral valve replacement from cardiac failure with low cardiac output syndrome, and 4) 22 hearts from patients with hypertensive heart disease (NYHA Class II-III). Myocardial fiber hypertrophy was quantitated by measuring cross-sectional myocardial fiber diameter; the proportion of interstitial tissue was quantitated by using a computerized, high-resolution video image-digitizing system. Myocardial fiber average diameter in groups 2, 3 and 4 was significantly higher than group 1. The proportion of interstitial tissue was significantly increased in group 3. In chronic mitral incompetence an increase in left ventricular interstitial tissue may play a role in the development of severe cardiac failure.

Cardiomegaly↗
PubMed1978

Canine cardiac myosin with special referrence to pressure overload cardiac hypertrophy. I. Subunit composition.

In studies of myosin from left and right ventricles of normal hearts and hypertrophic hearts at 5 weeks and 13 weeks after aortic banding, polyacrylamide gel electrophoresis shows intermediate molecular weight components which derive from heavy chains fragmented in the presence of dodecyl sulfate. The proportion of degraded heavy chains is greater in myosin from hypertrophic hearts than normal hearts, with comparable degradation in left and right ventricle myosin. The observed fragmentation of myosin results from proteolysis due to contaminant proteases or a thermally activated, heat-stable nonenzymatic process, or both. The susceptibility of heavy chains to crude myofibrillar proteases differs in normal and hypertrophic cardiac myosin; however, the kinetics of tryptic digestion are identical for both myosins. With precautions to minimize proteolytic artifacts on dodecyl sulfate-polyacrylamide gel electrophoresis, preparations of myosin from left and right ventricles of normal and hypertrophic hearts exhibit comparable subunit composition, with approximately molar ratios of heavy chains, light chain L1, and light chain L2. Comparable stoichiometry for the light chain fraction is determined by high speed sedimentation equilibrium at pH 11 and direct fractionation of the different cardiac myosins. We do not confirm reports (e.g. Wikman-Coffelt, J., Fenner, C., Smith, A., and Mason, D. T. (1975) J. Biol. Chem. 250, 1257-1262) of different proportions of light chains in left and right ventricle myosin of normal and hypertrophic canine hearts. The light chains display microheterogeneity, with L1 generating two isoelectric variants and L2 generating two major and two minor variants, but identical mobilities and isoelectric values are obtained in the different myosin preparations.

Animals↗
PubMed2026

Non-telomeric function deficiency of TERT enhances pressure overload-induced mouse cardiac remodeling by activation of CNBP-mediated THBS3/ITGB1 pathway.

Recent studies show that telomerase reverse transcriptase (TERT) possesses important new biological functions in gene transcription regulation, signal transduction, tumorigenesis, vascular development and mitochondrial DNA protection independent of the maintenance of telomere length. In this study we investigated the role and mechanisms of TERT in regulating the gene expression and signal transduction during pressure overload-induced cardiac remodeling. The first-generation TERT knockout (Tert-/-) and wild-type littermate control (Tert+/+) male mice were subjected to transverse aortic constriction (TAC) surgery to establish a pressure overload-induced cardiac remodeling model. We showed that pressure overload significantly increased TERT expression in the hearts at 8 weeks after TAC, whereas TERT deficiency remarkably exacerbated pressure overload-induced cardiac dysfunction, cardiac hypertrophy and fibrosis, and reduced the survival rate of the mice. In contrast, TERT overexpression reversed phenylephrine (PE)-stimulated cardiomyocyte hypertrophy and fibrosis in neonatal rat ventricular myocytes (NRVMs). Ttranscriptomic and proteomic analyses revealed that extracellular matrix (ECM)-receptor interaction was a key Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway regulated by TERT in hemodynamic overload-induced cardiac remodeling. TERT knockdown greatly enhanced, while TERT overexpression inhibited the activation of the THBS3/ITGB1 signaling pathway, in which transcription factor cellular nucleic acid-binding protein (CNBP) played a pivotal mediating role by interacting with TERT. In conclusion, the non-telomeric function of TERT in gene transcription regulation and signaling transduction plays an important role during pressure overload-induced myocardial remodeling via modulating CNBP-mediated THBS3/ITGB1 signaling pathway, which provides new targets and strategies for the prevention and treatment of pressure overload-induced cardiac remodeling.

Animals↗
PubMed1975

Wall stress and patterns of hypertrophy in the human left ventricle.

It is generally recognized that chronic left ventricular (LV) pressure overload results primarily in wall thickening and concentric hypertrophy, while chronic LV volume overload is characterized by chamber enlargement and an eccentric pattern of hypertrophy. To assess the potential role of the hemodynamic factors which might account for these different patterns of hypertrophy, we measured LV wall stresses throughout the cardiac cycle in 30 patients studied at the time of cardiac catheterization. The study group consisted of 6 subjects with LV pressure overload, 18 with LV volume overload, and 6 with no evidence of heart disease (control). LV pressure, meridional wall stress (sigman), wall thickness (h), and radius (R) were measured in each patient throughout the cardiac cycle. For patients with pressure overload, LV peak systolic and end diastolic pressures were significantly increased (220 plus or minus 6/23 plus or minus 3 mm Hg) compared to control (117 plus or minus 7/10 plus or minus 1 mm Hg, P less than 0.01 for each). However, peak systolic and end diastolic (sigman) were normal (161 plus or minus 24/23 plus or minus 3 times 10-3 dyn/cm-2) compared to control (151 plus or minus 14/17 plus or minus 2 times 10-3 dyn/cm-2, NS), reflecting the fact that the pressure overload was exactly counterbalanced by increased wall thickness (1.5 plus or minus 0.1 cm for pressure overload vs. 0.8 plus or minus 0.1 cm for control, P less than 0.01). For patients with volume overload, peak systolic (sigman) was not significantly different from control, but end diastolic (sigmam) was consistently higher than normal (41 plus or minus 3 times 10-3 dyn/cm-2 for volume overload, 17 plus or minus 2 times 10-3 dyn/cm-2 for control, P less than 0.01). LV pressure overload was associated with concentric hypertrophy, and an increased value for the ratio of wall thickness to radius (h/R ratio). In contrast, LV volume overload was associated with eccentric hypertrophy, and a normal h/R ratio. These data suggest the hypothesis that hypertrophy develops to normalize systolic but not diastolic wall stress. We propose that increased systolic tension development by myocardial fibers results in fiber thickening just sufficient to return the systolic stress (force per unit cross-sectional area) to normal. In contrast, increased resting or diastolic tension appears to result in gradual fiber elongation or lengthening which improves efficiency of the ventricular chamber but cannot normalize the diastolic wall stress.

Adolescent↗
PubMed1978

[Dynamics of left ventricular hypertrophy and function in spontaneous hypertension of rats (author's transl)].

Left ventricular dynamics and papillary muscle mechanics were examined in 44 spontaneously hypertensive rats (SHR) (Okamoto, 9-21 weeks old), in 38 normotensive Wistar Kyoto inbred rats and in 31 control rats. In spite of marked pressure overload, SHR had normal peak systolic wall stress and reduced (21%) diastolic wall stress due to an increased proportion between left ventricular wall thickness and radius. Left ventricular function was normal (isovolumic contractility indices before and after aortic clamping) or augmented (pressure development per gramm of left ventricular weight before and after clamping). Papillary muscle mechanics showed decreases of contraction velocities (isometric and isotonic), whereas shortening and maximum tension development were nearly unaffected. Left ventricular hypertrophy in proportion to pressure overload, the increase in wall thickness/radius ratio and hence the normalisation or decrease of wall stress, provides normal left ventricular function even at extreme pressure overload.

Animals↗
PubMed1977

Left ventricular contractile function in aortic stenosis evaluated by isovolumic and ejection phase indexes.

This study is to reappraise the usefulness of isovolumic as compared to ejection phase indexes for detecting abnormal left ventricular contractile function patients with a common hemodynamic abnormality, namely, chronic left ventricular pressure overload. In 41 subjects with pure or predominant aortic stenosis left ventricular pressure measurements were performed by micromanometry. Single-plane left ventricular cineangiograms were carried out in the right anterior oblique (RAO) and the A-P position. The isovolumic contractile indexes we used in this study were peak measured velocity of shortening of the contractile elements (Vpm) and Vmax obtained from linear extrapolation of total pressure-velocity curves. The end-diastolic and end-systolic RAO cineventriculograms served for the calculation of the ejection phase parameters mean velocity of circumferential fiber shortening (VCF) and mean normalized systolic ejection rate (MNSER). Of the 41 patients, Vpm was depressed in 16 (39 per cent), Vmax in 17 (42 per cent), VCF in 12 (29 per cent), and MNSER in 14 (34 per cent). When the isovolumic and the ejection phase parameters were combined, 24 patients (59 per cent) were found to have at least one of the four contractile indexes below normal. In 26 of the 41 patients the isovolumic and the ejection phase indexes provided the same conclusions as to normality of left ventricular function. In contrast, 15 patients showed discordant isovolumic and ejection phase indexes. An increased left ventricular end-diastolic pressure was only inconsistently related to an abnormal left ventricular function because in 7 of 28 patients with an end-diastolic pressure above 14 mm. Hg all contractile indexes were normal. Furthermore, a normal end-diastolic pressure was present in three of 24 patients with depressed myocardial function. It is concluded that in chronic left ventricular pressure overload from aortic stenosis neither the isovolumic nor the ejection phase indexes are superior in sensitivity for assessing contractile function. In this clinical setting the combination of both types of indexes appears to be the most reliable way for identifying patients with depressed contractile function of theleft ventricle in the basal state.

Adolescent↗
PubMed1979

Effects of exerimental right ventricular hypertrophy on myocardial blood flow in conscious dogs.

The effects of right ventricular hypertrophy on the overall and regional distribution of myocardial blood flow in the absence of an elevated coronary arterial driving pressure were evaluated in 18 concscious dogs subjected to a chronic pressure overload of the right ventricle induced by pulmonary artery constriction. The sustained pressure overload for duration of 4--6 wk or 4--5 mo resulted in significant increases in right ventricular mass (45 and 110%, respectively) and right ventricular fiber diameter (22 and 60%, respectively). Moreover, the presence of moderate and severe hypertrophy was associated with marked increases in transmural blood flow per gram to the right ventricle proportional to the observed increases in mass, i.e., of 36 and 109%, respectively, from a normal value of 0.67 +/- 0.04 ml/min per g, whereas left ventricular blood flow remained unaltered from a normal value of 1.00 +/- 0.06 ml/min per g. Despite the large increase in blood flow per gram to moderately and severely hypertrophied right ventricle, no significant changes in the ratio of capillary:muscle fiber number were observe. These data suggest that the development of right ventricular hypertroph is characterized by a sustained compensatory response of the coronary circulation to the augmented work load and mass, and that is not associated with a proliferative response of the vasculature supplying the enlarged ventricle.

Animals↗
PubMed1977

Functional morphology of the pressure- and the volume-hypertrophied rat heart.

We studied hearts in which hypertrophy was caused by both pressure and volume overload. Pressure hypertrophy was induced by an aortic constriction; volume hypertrophy was induced by an iron-copper deficiency (anemia). The ventricular weight was increased by 34% in the pressure-hypertrophied hearts at the end of 6 weeks. The ventricular weight was increased by 54% in the volume-hypertrophied hearts at the end of 3 months. A potassium arrest-formalin fixation technique was used to produce a "diastole-like" ventricle. In the pressure-hypertrophied ventricle, the ventricular wall thickness and external radii were significantly increased, whereas the valve-to-apex distance and internal radii remained unchanged. We also found that in the volume-hypertrophied ventricle there was an increase in the valve-to-apex distance, external radii, internal radii, and wall thickness. Although external and internal dimensions increased, the ventricular shape did not change significantly in the volume-hypertrophied ventricle.

Animals↗
PubMed1975

Echocardiographic left ventricular dimensions in pressure and volume overload. Their use in assessing aortic stenosis.

Left ventricular 'relative wall thickness', determined from the ratio between echocardiographic measurements of end-systolic wall thickness and cavity transverse dimension, was related to peak systolic intraventricular pressure in 15 normal subjects, in 15 patients with left ventricular volume or pressure overload without aortic stenosis, and in 23 patients with aortic stenosis. All these patients had a mean rate of circumferential fibre shortening greater than 1.0 circumference per second and were regarded as having good ventricular function. Relative wall thickness was found to be normal in cases of volume overload and to be increased in pressure overload, being proportional to the systolic intraventricular pressure. Values for the ratio of systolic intraventricular pressure to relative wall thickness in the normal subjects and patients without aortic stenosis were similar (mean 30 +/- 2.5). Based on this relation, estimates of peak systolic intraventricular pressure were made in the cases of aortic stenosis using the formula: systolic intraventricular pressure (kPa) equals 30 x wall thicknes divided by transverse dimension. Peak systolic aortic value gradients derived by subtracting brachial artery systolic pressure, measured by sphygmomanometer, from the echocardiographic estimates of intraventricular pressure compared favourably with the gradients measured at left heart catheterization (r equals 0.87, P less than 0.001). Aortic value orifice areas, derived from echocardiographic estimates of stroke volume, ejection time, and value gradient, ranged from 0.21 to 3.16 cm2 and appeared to correlate with the severity of aortic stenosis. All patients with aortic stenosis, with or without coexistent mild aortic regurgitation, who were recommended for aortic valve surgery, had estimated valve orifice areas of less than 0.8 cm2. A further 10 patients with pressure or volume overload had mean rates of circumferential fibre shortening of less than 1.0 circumference per second and were regarded as having poor ventricular function. In these cases values for relative wall thickness were lower than in those with good ventricular function and were not proportional to systolic intraventricular pressure. In patients with good left ventricular function systolic intraventricular pressure is proportional to, and can be estimated from, echocardiographic measurement of relative wall thickness.

Adolescent↗