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Regional deficits of myocardial blood flow and function in left ventricular pacing-induced heart failure
G A Helmer1, M D McKirnan, R Shabetai
1Veterans Affairs Medical Center, San Diego, Calif, USA.
Insights
Rapid ventricular pacing causes reduced blood flow and dysfunction in the left ventricle, contributing to heart failure. This study shows regional ischemia is linked to contractile dysfunction during pacing.
Area of Science:
- Cardiology
- Physiology
Background:
- Pacing-induced heart failure is a model for dilated cardiomyopathy.
- Regional myocardial blood flow and function during heart failure development are poorly understood.
Purpose of the Study:
- To investigate regional differences in myocardial blood flow and their association with regional dysfunction in pacing-induced heart failure.
Main Methods:
- Pigs underwent rapid left ventricular pacing for 26 days.
- Regional myocardial blood flow was measured using radioactive microspheres.
- Regional wall thickening was assessed via transthoracic echocardiography.
Main Results:
- Pacing induced progressive global left ventricular dysfunction.
- The paced lateral wall showed decreased systolic wall thickening compared to the interventricular septum.
- Reduced subendocardial blood flow per beat was observed in the lateral wall immediately upon pacing initiation and was sustained.
Conclusions:
- Regional myocardial ischemia is associated with contractile dysfunction in the paced wall.
- Regional stunning contributes to persistent global left ventricular dysfunction after pacing cessation.
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.
Methods And 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.