Abstract: . . .  abnormalities in myocyte shortening are believed to contribute importantly to the development of left ventricular systolic dysfunction in the failing heart. Source: Hypertension Online ( www.hypertensiononline.org ) 2004 Baylor College of Medicine, Houston, . . .
. . .  decrease of speed and extent of shortening of the actin and myosin cross-bridges, as shown in the lower panel of this sequence. These abnormalities in myocyte shortening are believed to contribute importantly to the development of left ventricular systolic dysfunction . . .
. . .  filaments and pull the thin filaments towards the center of the sarcomere in a ratchet like fashion. In this sequence of the normal heart, we have reviewed the process of excitation contraction coupling. As will be discussed subsequently, this process of excitation . . .
. . .  lower panel of this sequence. These abnormalities in myocyte shortening are believed to contribute importantly to the development of left ventricular systolic dysfunction in the failing heart. Source: Hypertension Online ( www.hypertensiononline.org )  . . .
. . .  panel of this sequence. These abnormalities in myocyte shortening are believed to contribute importantly to the development of left ventricular systolic dysfunction in the failing heart. Source: Hypertension Online ( www.hypertensiononline.org ) 2004 . . .
. . .  of these abnormalities are believed to contribute to the depressed systolic performance of the left ventricle. As in cardiac hypertrophy, there are a number of significant abnormalities in excitation contraction coupling that occur in the failing cardiac myocyte. . . .
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