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Transient ischemia does not limit subsequent ischemic regional dysfunction in humans: a transesophageal
M J Malkowski1, C M Kramer, S T Parvizi
1Department of Anesthesia, Allegheny General Hospital, Allegheny University of the Health Sciences, MCP-Hahnemann School of Medicine, Pittsburgh, Pennsylvania 15212-4772, USA. Malkowsk@pgh.auhs.edu
Insights
Sequential coronary artery occlusion during minimally invasive coronary artery bypass graft surgery causes temporary ischemic dysfunction. However, a second occlusion does not further impair left ventricular systolic function in humans.
Area of Science:
- Cardiology
- Cardiac Surgery
- Echocardiography
Background:
- Ischemic preconditioning may protect against acute coronary syndromes.
- The impact of repeated myocardial ischemia on human cardiac function remains unclear.
Purpose of the Study:
- To evaluate the effects of sequential coronary artery occlusion during minimally invasive coronary artery bypass graft surgery (CABG).
- To assess hemodynamic variables and left ventricular systolic function using transesophageal echocardiography (TEE).
Main Methods:
- Seventeen patients with significant LAD stenosis undergoing minimally invasive CABG were studied.
- Intraoperative TEE assessed regional left ventricular wall motion and hemodynamics during sequential LAD occlusions and reperfusion.
- Measurements were taken at baseline, during two 5-minute occlusions, and after reperfusion.
Main Results:
- Left ventricular wall motion score significantly worsened during both occlusions compared to baseline.
- Pulmonary artery systolic and diastolic pressures increased significantly during both occlusions.
- No significant differences in left ventricular wall motion or pulmonary artery pressures were observed between the first and second occlusions.
Conclusions:
- A 5-minute LAD occlusion precipitates ischemic dysfunction, evidenced by increased LVWMS and pulmonary artery pressure.
- Repeated 5-minute coronary occlusion does not further compromise regional left ventricular systolic function in humans.
Objectives:
This study sought to assess the effects of sequential coronary artery occlusion during minimally invasive coronary artery bypass graft surgery (CABG) on hemodynamic variables and left ventricular systolic function by means of transesophageal echocardiography (TEE).
Background:
Clinical and experimental studies suggest a protective effect of ischemic preconditioning in patients with acute coronary syndromes. However, the effect of repetitive myocardial ischemia on myocardial mechanical function in humans is not completely understood.
Methods:
Seventeen patients with left anterior descending coronary artery (LAD) stenosis > or =70% and normal rest left ventricular systolic function referred for minimally invasive CABG underwent intraoperative TEE for assessment of regional left ventricular wall motion and measurement of hemodynamic variables at baseline (baseline 1), during a 5-min coronary occlusion (occlusion 1), after a 5-min reperfusion period (baseline 2) and a during a second coronary occlusion during bypass anastomosis (occlusion 2).
Results:
Left ventricular wall motion score (LVWMS) increased significantly from baseline (16.0) to occlusion 1 (21.4+/-3.1 [mean +/- SD], p < 0.05) and occlusion 2 (21.8+/-3.1, p < 0.05). No difference in LVWMS was noted between occlusions 1 and 2. Pulmonary artery systolic pressure increased significantly from baseline (25+/-6 mm Hg) to occlusion 1 (32+/-7 mm Hg, p < 0.05) and occlusion 2 (33+/-6 mm Hg, p < 0.05). Pulmonary artery diastolic pressure also increased significantly from baseline (12+/-4 mm Hg) to occlusion 1 (16+/-4 mm Hg, p < 0.05) and occlusion 2 (16+/-4 mm Hg, p < 0.05). No significant differences in pulmonary artery pressures were noted between occlusions 1 and 2.
Conclusions:
Ischemic dysfunction was precipitated by the 5-min LAD occlusion, as shown by the increase in LVWMS and pulmonary artery pressure. However, a 5-min coronary occlusion and the resulting ischemia do not alter regional left ventricular systolic function during subsequent ischemia in humans.