© 1992 by European Society of Cardiology
Copyright © 1992, European Society of Cardiology
Effects of progressive myocardial ischaemia on systolic function, diastolic dysfunction, and load dependent relaxation
Nuffield Department of Anaesthetics, Radcliffe Infirmary, Oxford, United Kingdom: B J Leone, R M Norris, A Safwat, P Foex, W A Ryder. Correspondence to Dr Leone, at Department of Anesthesiology, Duke University Medical Center, PO Box 3094, Durham, NC 27710, USA. Dr Norris's present address: Coronary Care Unit, Green Lane Hospital, Auckland, New Zealand. Dr Safwat's present address: Cardiothoracic Anesthesia, University of California, Davis, CA, USA.
Objective: The aims were to determine (1) the relationship between changes in contractile function (systolic shortening) and the appearance of diastolic dysfunction (postsystolic shortening) during progressive regional left ventricular ischaemia; (2) the effects of increased afterload (acute constriction of the descending thoracic aorta) on ischaemic contractile dysfunction; and (3) the effects of loading during ischaemia on load dependent relaxation. Methods: Regional myocardial function, using sonomicrometry, was measured in the short and long axes of the apex of the left ventricle of eight open chest anaesthetised dogs (16-20 kg). Progressive apical ischaemia was induced by graded reductions in left anterior descending coronary artery flow (critical constriction, ischaemia 1, ischaemia 2, total coronary occlusion, and postocclusive maximum reactive hyperaemia). Acute afterloading was induced by a snare placed around the descending aorta. Results: Consistent decreases in systolic shortening and increases in postsystolic shortening relative to the total segmental shortening in the short axis of the apical region were seen with worsening ischaemia. Aortic constriction increased the magnitude of apical postsystolic shortening and decreased apical systolic shortening in the short axis during critical constriction, ischaemia 1, and ischaemia 2. Long axis function changed in a qualitatively similar but quantitatively different manner. There was a significant decrease in the load dependency of relaxation with total coronary occlusion. Conclusions: (1) Changes in systolic and diastolic function occurred concomitantly as mild regional myocardial ischaemia developed and intensified; (2) afterloading significantly worsened regional systolic and diastolic dysfunction during mild ischaemia; and (3) progression of regional ischaemia resulted in loss of load dependent relaxation.
KEYWORDS regional myocardial ischaemia; sonomicrometry; isovolumetric relaxation
The authors wish to express their appreciation to Mrs A L Nunn for her preparation of the manuscript and to Dr D M Philbin for his thoughtful review of the manuscript. This study was sponsored by grants nos G8002204SA and G830685SA from the Medical Research Council of Great Britain. Dr Noms was supported by the Medical Research Council of New Zealand and the Wellcome Trust.
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