Circulation, Vol 85, 717-729, Copyright © 1992 by American Heart Association
FG Spinale, R Tanaka, FA Crawford and MR Zile
BACKGROUND. Chronic supraventricular tachycardia (SVT) causes a dilated
cardiomyopathy and myocyte injury. Termination of SVT improves left
ventricular (LV) function but is associated with LV hypertrophy. Changes in
myocardial blood flow (MBF) that may accompany the development of and
recovery from SVT cardiomyopathy might have a significant effect on LV
function and myocyte structure. The goal of this study was to relate
changes in LV function, myocyte composition, and coronary vascular
structure to changes in MBF with the development and recovery of SVT
cardiomyopathy. METHODS AND RESULTS. LV function and MBF were measured in
three groups of conscious pigs: sham control (control; n = 8), after 3
weeks of atrial pacing (SVT, 240 beats per minute; n = 8), and after a
4-week recovery from SVT (post-SVT; n = 8) by echocardiography
catheterization and microspheres. Measurements were made under three
states: 1) at rest with a basal heart rate, 2) rapid atrial pacing (240
beats per minute), and 3) during adenosine infusion (1.5
mumol/l.kg-1.min-1) without pacing. LV myocyte, capillary, and arteriole
morphometric studies were performed in five additional pigs from each group
using histochemistry and electron microscopy. LV fractional shortening was
lower and left atrial pressure was significantly higher in the SVT group
compared with control at rest, during pacing, and with adenosine (p less
than 0.05). In the post-SVT group, fractional shortening returned to
control values at rest and with adenosine, but fell from control values
with pacing (p less than 0.05). Left atrial pressure fell in the post-SVT
but remained significantly higher than control (p less than 0.05). LV/body
weight ratio was significantly increased in the post-SVT group (p less than
0.05). In all states, SVT LVMBF was significantly reduced from control
values (rest, 0.8 +/- 0.3 versus 1.6 +/- 0.3 ml-min-1.g-1; pacing, 1.2 +/-
0.2 versus 3.1 +/- 0.3 ml.min-1.g-1; adenosine, 1.4 +/- 0.3 versus 4.4 +/-
0.4 ml.min-1.g-1, respectively, p less than 0.05). In the post- SVT group,
LVMBF was similar to control at rest (1.3 +/- 0.2 ml.min-1.g- 1) but was
significantly lower than control with pacing and adenosine (2.0 +/- 0.4 and
2.5 +/- 0.5 ml.min-1.g-1, respectively, p less than 0.05). Myofibrillar
content fell significantly with SVT compared with control (42 +/- 5 versus
61 +/- 3%, p less than 0.05) and returned to control values in the post-SVT
group (64 +/- 3%). Capillary density remained unchanged in the SVT and
post-SVT groups, but capillary luminal diameter decreased and arteriole
diameter increased in the SVT group (p less than 0.05). CONCLUSIONS. The LV
dysfunction and myocyte injury with SVT cardiomyopathy were associated with
reduced MBF. Early recovery from SVT cardiomyopathy resulted in hypertrophy
with normal MBF at rest, but significantly reduced coronary reserve.
ARTICLES
Changes in myocardial blood flow during development of and recovery from tachycardia-induced cardiomyopathy
Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston 29425.
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