Page 114 - Feline Cardiology

Chapter 11: Hypertrophic Cardiomyopathy 113

D D

A A Cardiomyopathies

E E
B B

C C F F

Figure 11.4. Histopathologic examination of the heart and lungs of a Maine coon cat with severe hypertrophic cardiomyopathy. The
heart of a Maine coon with severe hypertrophic cardiomyopathy is shown in cross section (center), where there is severe concentric
hypertrophy of the left ventricle, and end-systolic cavity obliteration. Histopathologic evaluation of the lungs (A) reveals pulmonary
edema caused by left-sided congestive heart failure. (B) and (C) demonstrate severe replacement fibrosis and interstitial fibrosis of the
left ventricular myocardium, respectively. (D), (E), and (F) are different magnifications of the myocardium showing myocyte disarray, a
pathognomonic feature of HCM. Histopathologic images courtesy of Dr. Philip Fox.

plasm by a sodium/calcium exchanger, which causes a once the LV pressure is less than LA pressure, the mitral
release of the myosin heads from actin. Increased cAMP valve opens and the early rapid filling phase begins. LV
and protein kinase A lead to phosphorylation of phos- and LA pressures influence early rapid filling. Increased
pholamban, which causes the sarcoplasmic reticulum LA pressure increases early rapid filling and shortens IVR
(SR) calcium ATPase pump to sequester calcium into the time (IVRT). Elastic recoil also affects passive filling.
SR. During IVR, the LV pressure quickly declines, and Diastasis occurs when the LA and LV diastolic pressures