Systole wall thickening

Figure 4. Posterior systolic wall thickening (PWT) at baseline, with immediate coronary microembolization (ME) and 5-10 min, 1, 4, and 8 h later. In the placebo-group (PLA), posterior systolic wall thickening after an initial recovery from microembolization was progressively decreased, whereas it remained unchanged in the groups receiving methylprednisolone before (MPpre) or after microembolization (MPpost) (by permission from Skyschally41).

LeGrice, I.J., Takayama, Y, and Coveil, J.W., Transverse shear along myocardial cleavage planes provides a mechanism for normal systolic wall thickening, Circ. Res., 77,182-193,1995. 

Figure 1.2 Echocardiography see example of volumes, wall thickening and myocardium mass in a normal case and in a patient with post-MI. Above (A) End-diastolic and (B) end-systolic apical long-axis views of a normal left ventricle. The endocardial and epicardial contours are traced and the built-in computer software of the ultrasound system allows calculation of volumes, wall thickening and myocardial mass. Below Segmental wall...

Figure 12. Contoured wall thickening map (T/r - Tps) derived from circumferential wall measurement in the images of Figure 13. The difference in wall thickness between end diastole and end systole is related to the contractile state of a region of heart muscle. The horizontal axis is distance along the left ventricular long axis from apex to base. The ordinate is circumferential dimension of the left ventricle. Intensity is the scaled rate of wall thickening (maximum = 40 mm/s minimum = 4 mm/s) (Schwartz et ai, 1983a).

Myocardial hypertrophy The heart increases in size, and the chambers dilate. Initially, stretching of the heart muscle leads to a stronger contraction of the heart. However, excessive elongation of the fibers results in weaker contractions. This type of failure is termed systolic failure and is a result of a ventricle unable to pump effectively. Less commonly, patients with CHF may have diastolic dysfunction—a term applied when the ventricles ability to relax and accept blood is impaired by structural changes, such as hypertrophy. The thickening of the ventricular wall and subsequent decrease in ventricular volume decreases the ability of heart muscle to relax. In this case, the ventricle does not fill adequately, and the inadequacy of cardiac output is termed diastolic heart failure. 

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