Anomalous Left Coronary Artery From the Pulmonary Artery Medication

  • Author: Mary C Mancini, MD, PhD; Chief Editor: Steven R Neish, MD, SM   more...
 
Updated: Dec 1, 2011
 

Medication Summary

Medications used at the time of presentation in patients with anomalous left coronary artery from the pulmonary artery (ALCAPA), including the judicious use of diuretics, focus on afterload reduction and inotropic support for the treatment of congestive heart failure (CHF) symptoms. Except for diuretics, medications may have immediate deleterious effects that could lead to worsening myocardial ischemia, further reductions in cardiac output, and the potential for ventricular arrhythmias. Following surgical revascularization, these same medications may be used more aggressively for the continued treatment of CHF, left ventricular dysfunction, and mitral valve insufficiency.

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Diuretics

Class Summary

These agents promote excretion of water and electrolytes by the kidneys. They are used to treat heart failure or hepatic, renal, or pulmonary disease when sodium and water retention has resulted in edema or ascites. These medications ease the work of breathing by decreasing the degree of pulmonary venous congestion (pulmonary edema) secondary to mitral valve insufficiency or elevated left atrial pressures resulting from diminished left ventricular compliance. Diuretics also may decrease systemic venous congestion (preload reduction) if right heart failure also has occurred.

Furosemide (Lasix)

 

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. Diuretic effect occurs within 10-20 min following an IV dose and peaks 1-1.5 hours later.

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Afterload-reducing agents

Class Summary

These agents improve preoperative or postoperative cardiac output by reducing systemic vascular resistance and increasing systemic blood flow resulting from myocardial dysfunction and/or significant mitral valve insufficiency. Nitrates are peripheral and coronary vasodilators used in the management of angina pectoris, heart failure, and myocardial infarction. ACE inhibitors are beneficial in all stages of chronic heart failure. Pharmacologic effects result in a decrease in systemic vascular resistance, reducing blood pressure, preload, and afterload. Dyspnea and exercise tolerance are improved.

Nitroprusside (Nitropress)

 

Vasodilator of choice for severe, low-output, left-sided heart failure, providing that the arterial pressure is reasonably maintained. Rapidly acts and has a balanced effect, dilating both arterioles and veins. Because of an increase in stroke volume, considerable hemodynamic improvement without much hypotension may occur. In general, some decrease in blood pressure occurs, which may limit therapeutic effect. No PO equivalent is available.

Captopril (Capoten)

 

Angiotensin converting enzyme (ACE) inhibitors have a major role as a peripheral vasodilator in hypertension and CHF. They act on angiotensin-renin-aldosterone system by inhibition of ACE. Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. This is most beneficial when CHF is accompanied by high plasma renin activity that leads to increased sympathetic activity, aldosterone release, and peripheral vasoconstriction. Use of ACE inhibitors usually is reserved for long-term postoperative management, at which point, the severity of myocardial dysfunction and mitral valve insufficiency has improved significantly to allow the use of PO medications.

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Phosphodiesterase Enzyme Inhibitor

Milrinone

 

Bi-pyridine positive inotrope and vasodilator with little chronotropic activity. Different in mode of action from both digitalis glycosides and catecholamines. Selectively inhibits phosphodiesterase type III (PDE III) in cardiac and smooth vascular muscle, resulting in reduced afterload, reduced preload, and increased inotropy.

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Contributor Information and Disclosures
Author

Mary C Mancini, MD, PhD  Professor and Chief of Cardiothoracic Surgery, Department of Surgery, Louisiana State University School of Medicine in Shreveport

Mary C Mancini, MD, PhD is a member of the following medical societies: American Association for Thoracic Surgery, American College of Surgeons, American Surgical Association, Phi Beta Kappa, Society of Thoracic Surgeons, and Southern Surgical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Howard S Weber, MD, FAAP, FACC, FSCAI  Professor, Assistant Chief, Section of Pediatric Cardiology, Penn State University School of Medicine; Director, Pediatric Catheterization Laboratory, Milton S Hershey Medical Center

Howard S Weber, MD, FAAP, FACC, FSCAI is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Specialty Editor Board

Paul M Seib, MD  Associate Professor of Pediatrics, University of Arkansas for Medical Sciences; Medical Director, Cardiac Catheterization Laboratory, Co-Medical Director, Cardiovascular Intensive Care Unit, Arkansas Children's Hospital

Paul M Seib, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, Arkansas Medical Society, International Society for Heart and Lung Transplantation, and Society for Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Alvin J Chin, MD  Professor of Pediatrics, University of Pennsylvania School of Medicine; Attending Physician, Cardiology Division, Children's Hospital of Philadelphia

Alvin J Chin, MD, is a member of the following medical societies: American Association for the Advancement of Science, American Heart Association, and Society for Developmental Biology

Disclosure: Nothing to disclose.

Gilbert Z Herzberg, MD  Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College; Consulting Staff, Department of Pediatrics, Sound Shore Medical Center

Gilbert Z Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Chief Editor

Steven R Neish, MD, SM  Director of Pediatric Cardiology Fellowship Program, Associate Professor, Department of Pediatrics, Baylor College of Medicine

Steven R Neish, MD, SM is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Heart Association

Disclosure: Nothing to disclose.

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Preoperative electrocardiogram in a 2-month-old infant with anomalous origin of the left coronary artery from the pulmonary artery demonstrating pathologic Q waves in leads I and aVL and diffuse ST-T wave changes consistent with an anterolateral infarction.
Electrocardiogram in 2-month-old infant with anomalous origin of the left coronary artery from the pulmonary artery 17 months following successful surgical revascularization, demonstrating complete resolution of the anterolateral infarction pattern and ST-T wave changes.
Two-dimensional echocardiographic image (parasternal short axis view) in a patient with anomalous origin of the left coronary artery arising from the pulmonary artery (ALCAPA). The left coronary artery (white arrow) appears to course towards the main pulmonary artery (MPA) just above the pulmonary valve and not to the aortic root (Ao). RV = Right ventricle.
Two-dimensional echocardiographic image with color flow mapping (parasternal short axis view) in the same patient with anomalous origin of the left coronary artery arising from the pulmonary artery (ALCAPA). The addition of color flow mapping to the 2-dimensional image demonstrates abnormal flow reversal within the left coronary artery (white arrows) towards the main pulmonary artery (MPA) just above the pulmonary valve. RV = Right ventricle. Ao = Aortic root.
Doppler interrogation of the abnormal color flow jet is depicted, demonstrating abnormal flow within the main pulmonary artery towards the transducer in diastole, which represents runoff from the anomalous left coronary artery (large white arrowhead). Small white arrow: Normal antegrade main pulmonary artery flow in systole. MPA = Main pulmonary artery.
Aortogram in a patient with suspected anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA). Frontal (left panel) and lateral (right panel) images demonstrating an enlarged right coronary artery (small white arrow), which fills a small left coronary system (solid arrow head) via collaterals with eventual faint opacification of the main pulmonary artery (not demonstrated in this frame).
Main pulmonary artery angiogram demonstrating the technique of stop flow angiography. There is retrograde opacification of the entire left coronary artery system, which originates from the distal main pulmonary artery (MPA), including the anterior descending (solid white arrowhead) and circumflex (small white arrow) branches. Left panel: Frontal image. Right panel: Lateral image.
 
 
 
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