Myocardial edema and compromised left ventricular function attributable to dirofilariasis and cardiopulmonary bypass in dogs

Douglas A. Rohn From the Department of Physiology and Pharmacology, College of Veterinary Medicine, Texas A&M University, College Station, TX 77843 (Rohn, Laine), and the Center for Microvascular and Lymphatic Studies, Department of Anesthesiology, The University of Texas Medical School, Houston, TX 77030 (Davis, Mehlhorn, Allen).

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Karen L. Davis From the Department of Physiology and Pharmacology, College of Veterinary Medicine, Texas A&M University, College Station, TX 77843 (Rohn, Laine), and the Center for Microvascular and Lymphatic Studies, Department of Anesthesiology, The University of Texas Medical School, Houston, TX 77030 (Davis, Mehlhorn, Allen).

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Uwe Mehlhom From the Department of Physiology and Pharmacology, College of Veterinary Medicine, Texas A&M University, College Station, TX 77843 (Rohn, Laine), and the Center for Microvascular and Lymphatic Studies, Department of Anesthesiology, The University of Texas Medical School, Houston, TX 77030 (Davis, Mehlhorn, Allen).

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Steven J. Allen From the Department of Physiology and Pharmacology, College of Veterinary Medicine, Texas A&M University, College Station, TX 77843 (Rohn, Laine), and the Center for Microvascular and Lymphatic Studies, Department of Anesthesiology, The University of Texas Medical School, Houston, TX 77030 (Davis, Mehlhorn, Allen).

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Glen A. Laine From the Department of Physiology and Pharmacology, College of Veterinary Medicine, Texas A&M University, College Station, TX 77843 (Rohn, Laine), and the Center for Microvascular and Lymphatic Studies, Department of Anesthesiology, The University of Texas Medical School, Houston, TX 77030 (Davis, Mehlhorn, Allen).

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SUMMARY

We investigated the relation between left ventricular dysfunction and myocardial edema in dogs with heartworm (Dirofilaria immitis) infection that were undergoing cardiopulmonary bypass. Dogs with and without D immitis were anesthetized by continuous thiopental infusion and were mechanically ventilated. Sonomicrometry crystals were placed on the long and short axes of the left ventricle, and a Millar pressure transducer was placed in the left ventricular chamber. Pressure-volume loops were digitized and continuously recorded. Dogs with and without D immitis were placed on standard hypothermic cardiopulmonary bypass, with 1 hour of aortic cross-clamp. Wet-to-dry weight ratio corrected for residual blood volume was used to quantitate the volume of myocardial edema. Preload recruitable stroke work was used as a preload-independent index of systolic function. Tau, the isovolumic relaxation time constant, was determined to assess diastolic relaxation. Dogs with D immitis had increased baseline myocardial wet-to-dry weight ratio. After cardiopulmonary bypass, myocardial edema increased in all dogs. Acute edema attributable to cardiopulmonary bypass decreased preload recruitable stroke work in all dogs of both groups, and dogs with D immitis could not be weaned from cardiopulmonary bypass. Myocardial edema increased diastolic relaxation times (τ) in dogs with and without D immitis. We conclude that cardiopulmonary bypass and heartworm infection induce myocardial edema. This edema compromises left ventricular systolic and diastolic function making D immitis an important confounding factor in weaning dogs from cardiopulmonary bypass.

SUMMARY

We investigated the relation between left ventricular dysfunction and myocardial edema in dogs with heartworm (Dirofilaria immitis) infection that were undergoing cardiopulmonary bypass. Dogs with and without D immitis were anesthetized by continuous thiopental infusion and were mechanically ventilated. Sonomicrometry crystals were placed on the long and short axes of the left ventricle, and a Millar pressure transducer was placed in the left ventricular chamber. Pressure-volume loops were digitized and continuously recorded. Dogs with and without D immitis were placed on standard hypothermic cardiopulmonary bypass, with 1 hour of aortic cross-clamp. Wet-to-dry weight ratio corrected for residual blood volume was used to quantitate the volume of myocardial edema. Preload recruitable stroke work was used as a preload-independent index of systolic function. Tau, the isovolumic relaxation time constant, was determined to assess diastolic relaxation. Dogs with D immitis had increased baseline myocardial wet-to-dry weight ratio. After cardiopulmonary bypass, myocardial edema increased in all dogs. Acute edema attributable to cardiopulmonary bypass decreased preload recruitable stroke work in all dogs of both groups, and dogs with D immitis could not be weaned from cardiopulmonary bypass. Myocardial edema increased diastolic relaxation times (τ) in dogs with and without D immitis. We conclude that cardiopulmonary bypass and heartworm infection induce myocardial edema. This edema compromises left ventricular systolic and diastolic function making D immitis an important confounding factor in weaning dogs from cardiopulmonary bypass.

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