Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Left ventricular diastolic compliance is determined by the level of operating pressure and the diastolic pressure-volume relation. This relation is curvillinear and the slope of a tangent (operative chamber stiffness) to the pressure-volume curve increases as the chamber progressively fills. Such preload-dependent changes in compliance occur during any acute alteration in ventricular volume. At a given diastolic pressure, operative chamber stiffness (or its reciprocal, operative chamber compliance) is determined by the relative values for ventricular volume and muscle mass and by the stiffness of a unit of myocardium. Thus, there may be a leftward shift of the diastolic pressure-volume curve (increase in the modulus of chamber stiffness) as a consequence of ventricular hypertrophy or an increase in the stiffness of heart muscle itself (increase in modulus of muscle stiffness). To distinguish between hypertrophy and stiff muscle, it is useful to examine the modulus of chamber stiffness, derived from pressure-volume data, together with the volume/mass ratio of the ventricle. In this fashion, changes in the modulus of chamber stiffness that are inappropriate for a given volume/mass ratio may be attributed to changes in the material properties of the heart muscle. Examples of clinical and experimental pressure-volume studies are presented to illustrate the variety of mechanisms by which acute and chronic changes in ventricular chamber compliance evolve during the course of clinical heart disease. The pathophysiology of pulmonary congestion is best understood by considering the factors responsible for producing changes in chamber stiffness of the ventricle, whereas an examination of muscle stiffness is likely to provide more insight into the extent of irreversible functional and structural defects of the myocardium.
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PMID:Left ventricular compliance: mechanisms and clinical implications. 13 86

Titin is the third myofilament of the cardiac muscle sarcomere, with a single molecule spanning the half sarcomere. Titin contains a molecular spring segment that generates passive force in sarcomeres stretched above the slack length and restoring forces in sarcomeres shortened below this length. The roles of titin in heart disease remain to be established. In this work we review recent developments in the understanding of titin's role in cardiac muscle. We focus on both short-term and long-term modulation of titin-based muscle stiffness, as well as on the recently discovered interplay between titin and actomysoin interaction, suggesting a possible role for titin in the Frank-Starling mechanism of the heart. Finally, we present evidence that suggests that titin plays a role in elevating passive stiffness of myocardium of dilated cardiomyopathy (DCM) hearts, via alterations in titin isoform expression.
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PMID:Titin: an endosarcomeric protein that modulates myocardial stiffness in DCM. 1255 33