Diuretics and Neurohormonal Medications

INTRODUCTION

In this chapter we review the medical management for mitral stenosis and mitral regurgitation. We go over the pathophysiology of the disease process to understand which medications may be most useful. We will review the medications that are helpful for use in both valve diseases and indications for initiation. The main medications we will discuss are β-blockers, angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers, nitrates and other after load reducers, as well as diuretics. We will review the preoperative treatment course for patients and medications that can be used to delay surgery or stabilize patients preoperatively. We hope this will be a valuable resource for understanding how to medically manage patients who have severe mitral valve disease.

MITRAL STENOSIS

Narrowing of the mitral valve impairs left atrial emptying which causes increased left atrial volume and pressure. This relationship between flow and pressure is quite profound when we consider that the pressure gradient for a given flow rate is a function of the square of the transvalvular flow rate. A doubling of flow rate would quadruple the pressure gradient. A 50% increase in flow would result in a 125% increase in pressure gradient. This causes increased back pressure into the pulmonary veins and ultimately pulmonary congestion. Given the relationship between heart rate and flow to the mitral valve gradient, reversible causes of increased heart rate and flow should be considered and treated if appropriate such as anemia, arrythmias, hyperthyroidism, or infection.

While medical therapy cannot relieve or alter the obstruction, it can help with decongestion to relieve symptoms. Narrowing of the mitral valve decreases left ventricular filling resulting in reduced cardiac output despite preserved left ventricular function. This increased back pressure causes elevation in pulmonary artery pressures which over time can be worsened by pulmonary artery vasoconstriction and changes of pulmonary artery hypertension that further elevate pulmonary pressures even out of proportion to left atrial pressure and results in right ventricular dysfunction.

Although pulmonary vasodilators address the pulmonary vasoconstriction and right ventricular dysfunction, increased flow to the left heart in advanced mitral stenosis can increase left atrial pressure and precipitate pulmonary edema. Thus, pulmonary vasodilators are contraindicated in the setting of significant mitral stenosis. Fortunately, pulmonary hypertension appears to improve over time at least partially after mechanical correction of mitral stenosis, with one study of 60 patients undergoing balloon valvuloplasty or surgical commissurotomy having an average decrease for pulmonary artery systolic pressure of 55 mm Hg preoperatively to 32 mm Hg 3-years postoperatively. Additionally, in contrast to mitral regurgitation, left ventricular (LV) filling is impaired, thus there is no role for afterload reduction as this can precipitate hypotension in an already underfilled ventricle.