Anomalous Left Coronary Artery From the Pulmonary Artery Medication

Updated: Aug 10, 2020
  • Author: Mary C Mancini, MD, PhD, MMM; Chief Editor: Syamasundar Rao Patnana, MD  more...
  • Print

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.



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.


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.


Phosphodiesterase Enzyme Inhibitor


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.