Why the study?
Does the injection of glass beads into the circumflex coronary artery induce progressive myocardial dysfunction and increased vascular resistance in a dog model?
Does the injection of glass beads into the circumflex coronary artery induce progressive myocardial dysfunction and increased vascular resistance in a dog model?
In a dog model, myocardial lesions cause early left ventricular dysfunction followed by high systemic vascular resistance and low cardiac output, suggesting peripheral circulation plays a key role in heart failure progression.
Peripheral vascular changes may contribute to HF progression in this canine model; leaves open translation to human disease.
To study heart failure from a myocardial lesion, we injected glass beads into the circumflex coronary artery of 11 conscious dogs and followed hemodynamics for 10 mo. Heart rate remained unchanged. Control mean arterial pressure of 112.3 +/- 3.0 (SE) mmHg was unchanged at 1 and 3 mo, but rose to 127.2 +/- 8.5 to 84.0 +/- 7.6 ml . kg-1 . min-1 at 10 mo (P < 0.02), but was unchanged at 1 and 3 mo. Left ventricular end-diastolic pressure (LVEDP) averaged 4.6 +/- 0.8 mmHg at control and rose to 11.8 +/- 1.4 mmHg at 1 mo and 14.9 +/- 2.5 mmHg at 10 mo (both P < 0.01). Systemic vascular resistance rose significantly by 10 mo. The ratio of stroke work to LVEDP fell from 13.1 +/- 0.1 at control to 3.8 +/- 0.5 by 10 mo (P < 0.01). In this dog model, left ventricular dysfunction is manifest early by increased LVEDP and later by high systemic vascular resistance with low cardiac output, thus suggesting a role of the peripheral circulation in the progression of heart failure.
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Franciosa et al. (1980) studied this question.
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