Regional deficits of myocardial blood flow and function in left ventricular pacing-induced heart failure.
BACKGROUND
Pacing-induced congestive hear, failure has become a preferred model for the study of the pathogenesis of dilated cardiomyopathy. However, little is known regarding regional myocardial blood flow and function during the development of heart failure in this model.


RESULTS
To determine whether regional differences in myocardial blood flow are associated with regional dysfunction in ventricular pacing-induced heart failure, regional myocardial blood flow (radioactive microspheres) and regional wall thickening (transthoracic echocardiography) were measured in pigs studied at weekly intervals during the progression of heart failure induced by rapid pacing from the lateral wall of the left ventricle (220 +/- 9 bpm for 26 +/- 4 days). Echocardiography and hemodynamic measurements with the pacemaker off showed progressive, severe global left ventricular dysfunction. During pacing over the 3- to 4-week period, a progressive decrease in systolic wall thickening in the lateral wall occurred compared with the interventricular septum (IVS; P = .001); at 21 to 28 days, the difference was 50% (lateral wall, 14 +/- 6%; IVS, 28 +/- 6%; P = .0001). A difference in subendocardial blood flow per beat between the left ventricular lateral wall (the site of stimulation) and the IVS was found immediately on the initiation of pacing (IVS, 0.009 +/- 0.002 mL.min-1.g-1.beat-1; lateral wall, 0.005 +/- 0.001 mL.min-1.g-1.beat-1; P = .001), a difference that was sustained during pacing throughout the study. Subendocardial blood flow per beat was normal in both regions with the pacemaker off throughout the study.


CONCLUSIONS
These data indicate that regional myocardial ischemia is associated with the development of contractile dysfunction of the paced wall during prolonged rapid left ventricular pacing and that regional stunning contributes to persistent global left ventricular dysfunction when pacing is discontinued.
Veterans Affairs Medical Center, San Diego, Calif, USA.
G A
GA
Helmer
M D
MD
McKirnan
R
R
Shabetai
G R
GR
Boss
J
J
Ross
H K
HK
Hammond
D000244:Adenosine Diphosphate / Q000032:analysis; D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D003326:Coronary Circulation / Q000502:physiology*; D004195:Disease Models, Animal; D006333:Heart Failure / Q000503:physiopathology*; D017202:Myocardial Ischemia / Q000503:physiopathology; D010138:Pacemaker, Artificial; D013312:Stress, Physiological / Q000503:physiopathology; D013552:Swine; D013599:Systole / Q000502:physiology; D016277:Ventricular Function, Left
D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate