Key result
Pacing-induced congestive heart failure significantly reduced global brain blood flow at rest (0.81 vs 1.06 mL/min/g; p<.05) and during treadmill exercise (2.01 vs 4.58 mL/min/g; p<.05).
Why the study?
Does pacing-induced congestive heart failure alter brain blood flow patterns at rest and during treadmill exercise in adult pigs?
Does pacing-induced congestive heart failure alter brain blood flow patterns at rest and during treadmill exercise in adult pigs?
Absolute Event Rate: 0.81% vs 1.06%
p-value: p=<.05
Pacing-induced congestive heart failure in pigs is associated with significantly diminished global and regional brain perfusion both at rest and during exercise, which may contribute to central cardiovascular dysregulation.
May indicate cerebral hypoperfusion in experimental CHF; hypothesis-generating in pigs and should not yet inform clinical practice.
OBJECTIVE: Congestive heart failure (CHF) is associated with left ventricular (LV) failure, neurohormonal system activation, and diminished exercise capacity. Although alterations in systemic vascular resistive properties have been recognized to occur with CHF, whether and to what degree perfusion abnormalities occur within the brain after the development of CHF remain poorly understood. Accordingly, the present study measured brain blood flow patterns in pigs after the development of pacing-induced CHF at rest and after treadmill-induced exercise. MEASUREMENTS AND MAIN RESULTS: Adult pigs (n = 6) were studied before and after the development of pacing-induced CHF (240 beats/min, 3 wks) at rest and with treadmill exercise (3 mph, 15 degrees incline, 10 mins). At rest, LV stroke volume was reduced nearly 45% with CHF compared with normal (20+/-2 vs. 36+/-3 mL; p<.05) and was associated with a more than four-fold increase in plasma catecholamines, renin activity, and endothelin concentration. At rest, global brain blood flow was reduced with CHF compared with the normal state (1.06+/-0.13 vs. 0.81+/-0.06 mL/min/g; p<.05). At rest, blood flow to the frontal lobe, cerebellum, and medullary regions was reduced by approximately 30% in the CHF group (p<.05). With treadmill exercise, LV stroke volume remained lower and neurohormonal concentrations remained higher in the pacing CHF state. Global brain blood flow increased significantly with treadmill exercise in both the normal and CHF states (4.58+/-1.36 and 2.01+/-0.29 mL/min/g; p<.05) but remained reduced in the CHF state compared with normal values (p<.05). In the CHF group, the relative increase in blood flow with exercise was significantly blunted in the parietal and occipital regions of the cerebrum and the suprapyramidal region of the medulla. CONCLUSIONS: The development of pacing-induced CHF was associated with diminished brain perfusion under resting conditions and with treadmill exercise. These perfusion abnormalities with pacing CHF were pronounced in specific regions of the brain. The defects in brain perfusion with the development of CHF may contribute to abnormalities in centrally mediated processes of cardiovascular regulation.
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Caparas et al. (2000) studied Congestive heart failure (n=6). Pacing-induced congestive heart failure vs. Normal state (baseline) was evaluated on Global brain blood flow at rest (mL/min/g) (p=<.05). Pacing-induced congestive heart failure significantly reduced global brain blood flow at rest (0.81 vs 1.06 mL/min/g; p<.05) and during treadmill exercise (2.01 vs 4.58 mL/min/g; p<.05).
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