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The myocardial cell nucleus was studied in the rat during its normal growth and under different types of heart overloading. Under overloading of short duration, a disappearance of condensed chromatin and an increase in the nucleolus and nucleolonema were interpreted as representing cell overactivity.With isoproterenol overloading, a first stage of cell necrosis and of its consequences on chromatin and nucleolus was followed by the process of cell repair and overactivity.With overloading of long duration, several different nuclear aspects were encountered: (a) enlarged and distorted nuclei as possible supports of polyploidy; (b) a partial coupling between two adjacent nuclei, interpreted either as nuclear fusion or amitosis; (c) segregation of different proteins, probably due to cell damage.The number of nuclei per myocyte was high (90%) in the adult. It decreased (80%) two days after isoproterenol overloading, as well as in heart hypertrophy of 6–9-months duration.Nuclear size increased under isoproterenol overdosage of 48-h duration.The amount of nuclear DNA also increased two days after isoproterenol overdosage, particularly in mononucleated cells. [ABSTRACT FROM PUBLISHER]

Different aspects of the myocardial cells in cardiac hypertrophy induced by mechanical overload are described. They depend on the severity of the load. The classical three stages of hypertrophy described by Meerson only occur when overload is moderate. Under more severe load, some cells seem to be in a hyperactive state of growth while other ones are damaged. These alterations remain visible throughout the whole duration of the load. In all cases these lesions are predominant in the subendocardial region of the ventricle. [ABSTRACT FROM PUBLISHER]

In a model of heart failure induced in rabbits by a double volume plus pressure overload, sarcoplasmic reticulum (SR) function was measured by Ca uptake and ryanodine receptor analysis. When expressed per mg of proteins, Ca uptake was decreased by 20% in failing hearts (FH) and ryanodine receptor density was similar in control hearts (CH) and in FH. However Ca uptake and ryanodine receptor density were significantly increased when expressed per total left ventricle suggesting SR hypertrophy. On electron microscopic examination, SR morphology not directly examined but large hypertrophied T tubules were observed suggesting a change in the relationship between membranes and contractile apparatus which may lead to alterations in excitation-contraction-relaxation coupling in spite of minimal biochemical alterations of SR.

Endomyocardial biopsies (EMB) of the left ventricle (LV) were performed during cardiac catheterization in 27 patients with apparently primary myocardiopathies (PMC). The results of optical and electron microscopy were compared with ventricular performance indices calculated from hemodynamic and cinematographic data from the left ventricle. The telediastolic pressure of the LV increases with the spread of fibrosis (r = 0.68) suggesting that it disturbs the filling of this cavity. Systolic effort is reduced as this fibrosis increases (r = 0.56), and it contributes to the changes in the pumping function of the LV, but the contractile power of the LV is altered in a less evident and less constant manner. The association of cell and fibro-elastic tissue degeneration is always accompanied by a drop in ventricular performance (p less than 0.0001). Apart from its diagnostic role, which is limited but may be of great value, the EMB can help to clarify the physiopathology of PMC and to formulate a prognosis based on more solid grounds.

Left ventricular myocardial biopsy was carried out at operation in 11 patients with pure, isolated mitral stenosis after preoperative angiocardiographical assessment of left ventricular function. The biopsy specimens were examined by light and electron microscopy. The diameter of the myocytes was normal (20 +/- 1.6 mu). The changes observed were probably of a degenerative type with anarchy and irregularities in the sarcomeres, modification of the Z bands, as seen in Nemaline myopathies, and changes in the intercalatory discs. Moderate interstitial fibrosis with scanty histiocytes was also observed. A quantitative assessment by two dimensional planimetry showed a significant increase in the interstitial space (37 +/- 5.5%) compared to a control group without fibrosis (22 +/- 1.1%). The angiocardiographical indices of left ventricular function were all decreased. The amplitude of circumferential fibre shortening was reduced: 25 +/- 6% the ejection fraction by 52 +/- 9% and the average speed of circumferential fibre shortening by 1.0 +/- 0.3 circ/s. Only four patients had normal left ventricular function (ejection fraction > 55%). However, it was not possible to establish a significant correlation between the degree of fibrosis and the reduction in left ventricular function. Left ventricular fibrosis may be one of the factors responsible for the reduction of myocardial function, but it does not in itself explain all the changes in left ventricular function observed in mitral stenosis.

We assessed coronary reserve, by measuring the increase in coronary sinus blood flow (CSBF) after intravenous administration of dipyridamole (0.14 mg/kg/minute for 4 minutes), in 7 patients with primary scleroderma myocardial disease (PSMD) and in 7 control subjects. Coronary reserve was greatly impaired in PSMD: before administration of dipyridamole, CSBF was similar in patients with PSMD (89 +/- 32 ml/minute/100 gm, mean +/- SD) and in controls (100 +/- 15 ml/minute/100 gm); after dipyridamole infusion, CSBF was significantly lower in patients with PSMD (191 +/- 45 ml/minute/100 gm) than in controls (399 +/- 58 ml/minute/100 gm) (P less than 0.01). Six of the 7 patients with PSMD had angiographically normal epicardial coronary arteries and normal left ventricular function. Decreased coronary reserve may be an important contributor to the pathogenesis of primary scleroderma myocardial disease.

The maximum coronary vasodilator capacity after intravenous dipyridamole (0.14 mg X kg-1 X min-1 X 4 minutes) was studied in seven patients with primary scleroderma myocardial disease and compared to that of seven control subjects. Hemodynamic data and left ventricular angiographic data were not different in the two groups. The coronary flow reserve was evaluated by the dipyridamole/basal coronary sinus blood flow ratio (D/B CSBF) and the coronary resistance reserve by the dipyridamole/basal coronary resistance ratio (D/B CR). Coronary reserve was greatly impaired in the group with primary scleroderma myocardial disease: D/B CSBF was lower than in the control group (2.54 +/- 1.37 vs 4.01 +/- 0.56, respectively; p less than 0.05) and D/B CR was higher than in the control group (0.47 +/- 0.25 vs 0.23 +/- 0.04, respectively; p less than 0.05). Such a decreased coronary flow and resistance reserve in patients with primary scleroderma myocardial disease was not explained by an alteration of left ventricular function. It may be an important contributing factor in the pathogenesis of primary scleroderma myocardial disease.