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PubMedDate not supplied

Afterload mismatch and preload reserve: a conceptual framework for the analysis of ventricular function.

A two-dimensional framework can be used for considering the characteristics of left ventricular ejection in terms of the appropriateness of the matching between afterload and the level of inotropic state, as modulated by the preload reserve. An afterload mismatch (reduced velocity and extent of shortening) can be induced acutely in the normal heart under controlled conditions if the preload is not allowed to compensate for an increased afterload, or if the limit of preload (Frank-Starling) reserve has been reached. In the intact circulation the normal heart is sensitive to some degree to acute changes in afterload, perhaps due to impaired venous return; but under basal resting conditions the ejection phase measures (such as the ejection fraction and the mean velocity of circumferential fiber shortening or VCF, corrected for heart size) encompass a relatively narrow range. This finding, and the lack of change in ejection phase measures after the normal heart has adapted to a chronic pressure or volume overload, provides justification for the use of ejection phase indices for detecting depressed inotropic state under basal conditions. When there is mild depression of myocardial inotropic state, with or without accompanying mechanical overload, enhanced preload may allow full compensation, but acute pressure loading may allow early detection of a less than normal preload reserve. When the inotropic state is substantially reduced, however, a mismatch between afterload and contractility (a reduction in mean VCF) will become evident even in the basal state (venous return being presumed to be adequate under these conditions). The concept of afterload mismatch with limited preload reserve provides an explanation for the value of ejection phase indices compared to isovolunic phase measures in assessing the basal level of inotropic state: the former may be more reliable because they are sensitive to afterload. The effects and implications of therapeutic afterload reduction as modulated by the preload also are understood within this framework.

Animals↗
PubMed1976

Rate of change of ventricular power: an indicator of ventricular performance during ejection.

An expression representative of the rate of change of ventricular power during ejection was derived. The primary advantages of the expression are its theoretical value and its ability to characterize ventricular performance. The rate of change of ventricular power, measured during ejection, is virtually free of assumptions. It has a fluid dynamic as well as a physiological meaning. It serves in an integrative fashion by combining terms previously shown to be of functional significance. Studies in dogs show that it reflects alterations of the inotropic state yet is relatively independent of alterations of preload or afterload. In nine dogs isoproterenol caused the peak rate of change of power to increase from (10 +/- 2) X 10(8) to (15 +/- 3) X 10(8) dynes-cm. sec.-2 (mean +/- S.E.) (P less than 0.01). Propranolol produced a reduction from (10 +/- 2) X 108 to (6 +/- 1) X 10(8) dynes-cm. sec.-2 (P less than 0.001). An increased afterload induced by angiotensin caused no change of the peak rate of change of power. Augmentation of the preload with dextran, which caused a 40 per cent increase of the end-diastolic volume, produced a statistically insignificant increase of the peak rate of change of power from (12 +/- 3) X 10(8) TO (16 +/- 4) X 10(8) dynes-cm. sec.-2 The rate of change of ventricular power, measured during ejection, therefore appears to be a useful and meaningful indicator of ventricular performance that has many desirable characteristics.

Animals↗
PubMed2000

The measurement of impedance to assess myocardial contractility and rhythm stability.

By introducing an alternating current through the ventricular cavity via a multipolar catheter the potential difference measured between adjacent electrodes can be used to assess ventricular volume. This is possible by the measurement of intracardiac impedance. The data obtained can be used to construct pressure-volume loops allowing the continuous real-time assessment of myocardial contractility. Clinical applications of this research tool are now becoming apparent. Further derivations of impedance measurement have been incorporated into commercially available permanent pacing systems, allowing effective heart rate modulation.

Electric Impedance↗
PubMed1991

[Chronic active hepatitis and possible relationship with immunosuppressive therapy].

A 54-year-old man with Chagas cardiomyopathy that was submitted to a heart transplantation and five months later presented a progressive increase in liver enzymes. Diagnosis of chronic active hepatitis was confirmed by histopathologic studies. A transitory interruption of treatment with azathioprine and the posterior re-introduction of small doses, as well as the use of lesser amounts of cyclosporin-A improved the clinical and laboratory pictures. Despite several investigations the pathogenesis of hepatitis remained undetermined, although some type of drug injury was presumed to be involved. The eventual role of viruses as the primary inciting event could not be completely ruled out.

Chagas Cardiomyopathy↗
PubMedDate not supplied

Myocardial contractility in healthy rabbits.

In 75 healthy rabbits the systolic times intervals (STI) and their indexes of the left-ventricle were determined for establishing the normal range of these values. In the analysis the effects of the heart rate on the values of these parameters were taken into account. A correlation was found between the heart rate and the QT interval (r = -0.8673), total electromechanical systole - QS2 (r = -0.5557), heart sounds interval - S1S2 (r = -5696), left ventricular ejection time - LVET (r = -0.4745), pre-ejection period - PEP (r = -2288), isovolumic contraction time - ICT (r = -0.2570). No correlation was found between the heart rate and the electromechanical delay - Q-1 (r = -0.0226).

Animals↗