Mechanism of myocardial ischemia with an anomalous left coronary artery from the right sinus of Valsalva

Carlo R. Bartoli, William B. Wead, Guruprasad A. Giridharan, Sumanth D. Prabhu, Steven C. Koenig, Robert Dowling

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Objective: An ectopic coronary artery that courses between the aortic root and the pulmonary trunk may lead to sudden cardiac death, especially in athletes. It has been speculated that during exercise, compression of the coronary artery between the great vessels may impair coronary blood flow and produce myocardial ischemia and fatal arrhythmia. However, this hypothesis cannot be tested in humans, and little experimental data exist to explain this phenomenon. To this end, in a calf with an anomalous left coronary artery that coursed from the right sinus of Valsalva between the great vessels, we assessed for myocardial ischemia during pharmacologically induced tachycardia and hypertension. Methods: We identified a juvenile male calf (103 kg) with an anomalous left coronary artery from the right sinus of Valsalva that coursed between the great vessels. Via thoracotomy, the animal was instrumented for hemodynamic measurements. Intravenous dobutamine increased heart rate and myocardial metabolic demands. Intravenous phenylephrine produced arterial hypertension and increased myocardial metabolic demands. Fluorescent-labeled microspheres were used to map regional myocardial blood flow, and hemodynamics were recorded during each condition. Masson's trichrome staining for fibrosis, wheat-germ agglutinin staining for myocyte size, terminal deoxynucleotidyl transferase dUTP nick end-label staining for apoptosis, and isolectin-B4 staining for capillary density were performed. Results: For the first time, empiric data documented that an ectopic coronary artery produced myocardial ischemia during elevated myocardial metabolic demands. Left coronary artery resistance increased in a cardiac cycle-dependent pattern that was consistent with systolic compression between the great vessels. Increased cardiac fibrosis, myocyte hypertrophy, cardiac apoptosis, and capillary density indicated that regional ischemic, inflammatory-mediated myocardial remodeling was present. Conclusions: These findings confirm the proposed mechanism of sudden death and support early surgical repair of coronary arteries that course between the aortic root and the pulmonary trunk.

Original languageEnglish (US)
Pages (from-to)402-408
Number of pages7
JournalJournal of Thoracic and Cardiovascular Surgery
Volume144
Issue number2
DOIs
StatePublished - Aug 1 2012

Fingerprint

Sinus of Valsalva
Myocardial Ischemia
Coronary Vessels
Staining and Labeling
Fibrosis
Hemodynamics
Apoptosis
Hypertension
Lung
Wheat Germ Agglutinins
Dobutamine
DNA Nucleotidylexotransferase
Sudden Cardiac Death
Regional Blood Flow
Cardiomegaly
Phenylephrine
Thoracotomy
Sudden Death
Microspheres
Lectins

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Surgery
  • Pulmonary and Respiratory Medicine

Cite this

Bartoli, Carlo R. ; Wead, William B. ; Giridharan, Guruprasad A. ; Prabhu, Sumanth D. ; Koenig, Steven C. ; Dowling, Robert. / Mechanism of myocardial ischemia with an anomalous left coronary artery from the right sinus of Valsalva. In: Journal of Thoracic and Cardiovascular Surgery. 2012 ; Vol. 144, No. 2. pp. 402-408.
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Mechanism of myocardial ischemia with an anomalous left coronary artery from the right sinus of Valsalva. / Bartoli, Carlo R.; Wead, William B.; Giridharan, Guruprasad A.; Prabhu, Sumanth D.; Koenig, Steven C.; Dowling, Robert.

In: Journal of Thoracic and Cardiovascular Surgery, Vol. 144, No. 2, 01.08.2012, p. 402-408.

Research output: Contribution to journalArticle

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AU - Wead, William B.

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AU - Koenig, Steven C.

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AB - Objective: An ectopic coronary artery that courses between the aortic root and the pulmonary trunk may lead to sudden cardiac death, especially in athletes. It has been speculated that during exercise, compression of the coronary artery between the great vessels may impair coronary blood flow and produce myocardial ischemia and fatal arrhythmia. However, this hypothesis cannot be tested in humans, and little experimental data exist to explain this phenomenon. To this end, in a calf with an anomalous left coronary artery that coursed from the right sinus of Valsalva between the great vessels, we assessed for myocardial ischemia during pharmacologically induced tachycardia and hypertension. Methods: We identified a juvenile male calf (103 kg) with an anomalous left coronary artery from the right sinus of Valsalva that coursed between the great vessels. Via thoracotomy, the animal was instrumented for hemodynamic measurements. Intravenous dobutamine increased heart rate and myocardial metabolic demands. Intravenous phenylephrine produced arterial hypertension and increased myocardial metabolic demands. Fluorescent-labeled microspheres were used to map regional myocardial blood flow, and hemodynamics were recorded during each condition. Masson's trichrome staining for fibrosis, wheat-germ agglutinin staining for myocyte size, terminal deoxynucleotidyl transferase dUTP nick end-label staining for apoptosis, and isolectin-B4 staining for capillary density were performed. Results: For the first time, empiric data documented that an ectopic coronary artery produced myocardial ischemia during elevated myocardial metabolic demands. Left coronary artery resistance increased in a cardiac cycle-dependent pattern that was consistent with systolic compression between the great vessels. Increased cardiac fibrosis, myocyte hypertrophy, cardiac apoptosis, and capillary density indicated that regional ischemic, inflammatory-mediated myocardial remodeling was present. Conclusions: These findings confirm the proposed mechanism of sudden death and support early surgical repair of coronary arteries that course between the aortic root and the pulmonary trunk.

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