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[Hemodilution tolerance in coronary heart disease: single vessel versus multiple vessel disease]
Insights
Isovolemic hemodilution is tolerated in single-vessel coronary artery disease. However, multivessel disease impairs tolerance, as healthy myocardium is crucial for compensatory function during hemodilution.
Area of Science:
- Cardiovascular Physiology
- Hemodynamics
- Myocardial Function
Context:
- Isovolemic hemodilution (IVH) is a technique used to reduce blood viscosity.
- Tolerance to IVH in single-vessel coronary artery disease (CAD) is established.
- Limited data exists on IVH tolerance in multivessel CAD.
Purpose:
- To investigate the tolerance of dogs with multivessel coronary artery disease to isovolemic hemodilution.
- To compare myocardial function in territories with and without critical stenoses during hemodilution.
Summary:
- Forty-two dogs with surgically induced single (LC) or multivessel (LC and LAD) coronary stenoses underwent progressive isovolemic hemodilution.
- Myocardial contractile function in the stenotic LC territory declined similarly in both groups.
- In contrast, the non-stenotic LAD territory showed preserved or increased function in single-vessel stenosis but decreased function in multivessel stenosis.
Impact:
- The presence of healthy, non-compromised myocardium is critical for maintaining compensatory function during hemodilution in CAD.
- Findings suggest that hemodilution strategies may need careful consideration in patients with multivessel coronary artery disease.
Abstract:
Isovolemic hemodilution is well tolerated in experimental models of single vessel coronary artery disease. Little information, however, is available on the hemodilution tolerance in presence of multivessel coronary artery disease. 42 dogs were anesthetized and instrumented to determine global cardiovascular and regional myocardial functions (systolic shortening, SS) in the anterior apical LV territory supplied by the left anterior descending coronary artery (LAD) as well as in the posterior apical LV wall supplied by the circumflex coronary artery (LC) using sonomicrometry. Critical coronary stenoses were imposed on the proximal LAD and LC according to the experimental group assignment and group 1V-HD (LC stenosis only) and group 2V-HD (LC and LAD stenoses) were then progressively hemodiluted using Dextran 70,000. 1000 ml blood per hour was thereby continuously exchanged with 900 ml Dextran until the animal expired or 120 minutes were reached. 12 dogs (LAD and LC stenoses) served as controls (2V-C). All groups started with similar hemoglobin values and these decreased similarly in both hemodiluted groups. Myocardial contractile function in the LC territory failed similarly in the 1V-HD and 2V-HD groups during progressive hemodilution. The LAD myocardium, however, responded markedly different in the 2V-HD as compared to the 1V-HD group: In the 2V-HD group, SSLAD started to decrease shortly into hemodilution, whereas SSLAD progressively increased during the first 60 min of continuous hemodilution in the 1V-HD group. The presence of non-compromised LV myocardium with the ability of a compensatory increase in contractile function thus seems to crucial for the hemodilution tolerance in the setting of coronary artery disease.