Key result
Acute Trypanosoma brucei infection reduces LV internal dimensions, EDV, and LV mass in dogs.
Why the study?
Does acute Trypanosoma brucei infection alter left ventricular structural and functional echocardiographic indices in dogs?
Does acute Trypanosoma brucei infection alter left ventricular structural and functional echocardiographic indices in dogs?
p-value: p=<0.05
Acute Trypanosoma brucei infection in dogs causes significant reductions in left ventricular dimensions and mass without altering ejection fraction or fractional shortening, suggesting these functional indices are unsuitable markers for acute myocardial dysfunction in this setting.
This study is aimed at understanding the structural and functional changes that could occur in the left ventricle of dogs acutely infected with Trypanosoma brucei. Twenty clinically healthy adult dogs of both sexes with an average weight of 8.4 kg were used for the study. They were divided into infected and uninfected groups of fifteen and five dogs, respectively. Each dog was intra-peritoneally inoculated with 1 mL of phosphate buffered saline (PBS) diluted blood containing 1x10 6 of Lafenwa strain of T. brucei. M-mode echocardiogram of the left ventricle was obtained from right parasternal short axis view before and at sixteen days after infection. The internal dimension indices were recorded by the in-built caliper of an ultrasound machine and functional indices obtained using appropriate formula. In both systole and diastole, the left ventricular internal dimensional indices of infected dogs were significantly lower than values obtained for uninfected dogs (P<0.05). In comparison to control dogs, the end diastolic volume (EDV) and left venticular mass (LVM) of infected dogs were significantly reduced (P<0.05). The ejection fraction (EF) and fractional shortening (FS) of infected dogs were not statistically different from control dogs (P>0.05). While the reduced end systolic volume index of infected dogs may be due to their smaller systolic ventricular dimension, LVM reduction in infected dogs may be attributable to cardiac muscle necrosis. The stability in both EF and FS of infected dogs may result from left ventricular compensatory efforts against sepsis induced myocardial depression. The preload and after load dependent nature of EF and FS make them unsuitable as candidate markers of myocardial dysfunction in acute canine trypanosomiasis
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Ajibola et al. (2016) studied Trypanosoma brucei infection (n=20). Trypanosoma brucei infection vs. Uninfected dogs was evaluated on M-mode echocardiogram indices of the left ventricle (internal dimensions, EDV, LVM, EF, FS) (p=<0.05). Acute Trypanosoma brucei infection in dogs significantly reduced left ventricular internal dimensions, end-diastolic volume, and left ventricular mass (P<0.05) compared to uninfected controls.
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