Open AccessSystolic and Diastolic Myocardial Dysfunction in Cats with Hypertrophic Cardiomyopathy or Systemic Hypertension
Author(s) -
Sampedrano Carolina Carlos,
Chetboul Valerie,
Gouni Vassiliki,
Nicolle Audrey P.,
Pouchelon JeanLouis,
Tissier Renaud
Publication year - 2006
Publication title -
journal of veterinary internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.356
H-Index - 103
eISSN - 1939-1676
pISSN - 0891-6640
DOI - 10.1111/j.1939-1676.2006.tb00708.x
Subject(s) - medicine , cardiology , hypertrophic cardiomyopathy , diastole , left ventricular hypertrophy , cats , muscle hypertrophy , cardiomyopathy , interventricular septum , concentric hypertrophy , heart failure , blood pressure , ventricle
Background:Hypertrophic Cardiomyopathy (HCM) and chronic systemic hypertension (SHT) can both lead to left‐ventricular hypertrophy (LVH) in cats. Assessment of LVH‐associated myocardial dysfunction could provide new insights in the understanding of the pathophysiology of these diseases. Hypothesis:Quantification of left‐ventricular free‐wall (LVFW) motion using tissue Doppler imaging (TDI) could permit differentiation of feline HCM from SHT‐related LVH (LVH‐SHT). Animals:A total of 108 cats of different breeds were enrolled in this study: 35 cats with HCM, 17 with concentric LVH and SHT, and 56 healthy cats as a control group. Methods:All cats were examined by conventional echocardiography and 2‐dimensional color TDI. Results:Radial and longitudinal diastolic LVFW velocities were similarly altered in cats with HCM and LVH‐SHT, compared to controls. Systolic velocities were also lower in the groups with hypertrophy than in the controls, for longitudinal but not radial motion. To determine whether these diastolic and systolic alterations could also be observed in cats without LVFW hypertrophy, we performed a subgroup analysis in cats with a normal M‐mode examination, that is, with only a localized subaortic interventricular septum hypertrophy. A significant radial and longitudinal diastolic dysfunction was still observed in both the HCM and LVH‐SHT groups compared to controls, and systolic dysfunction was detected in the longitudinal motion. Conclusions: LVFW motion is similarly altered in cats with HCM and LVH‐SHT. This dysfunction occurs independently of the presence of myocardial hypertrophy, demonstrating that TDI is capable of detecting systolic and diastolic segmental functional changes in nonhypertrophied wall segments in cats with HCM and SHT.