Medication Summary
Vasodilator therapy may be considered under the previously described conditions. Many classes of vasodilators have been studied, with long-term hydralazine or nifedipine therapy being associated with higher EF and less LV dilation in smaller trials. Results with enalapril and quinapril have been less consistent. [4]
Historically, beta-blocker therapy has been discouraged in patients with severe AR because heart rate reduction could prolong diastole, thus worsening AR. However, beta-blockers have been shown to produce beneficial neuroendocrine alterations in patients with heart failure. An observational study suggested that beta-blocker therapy is associated with a significant survival benefit in patients with severe AR, [45] spurring hope that further investigation will confirm this finding and allow its translation into a clinically meaningful recommendation.
Angiotensin-Converting Enzyme (ACE) Inhibitors
Class Summary
These agents are competitive inhibitors of angiotensin-converting enzyme (ACE). They reduce angiotensin II levels, decreasing aldosterone secretion.
Captopril
Captopril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. It is rapidly absorbed, but bioavailability is significantly reduced with food intake. Captopril achieves a peak concentration in 1 hour and has a short half-life. The drug is cleared by the kidney; impaired renal function requires reduction of the dosage. Captopril is absorbed well orally.
Give captopril at least 1 hour before meals. If it is added to water, use it within 15 minutes. The dose can be low initially, then titrated upward as needed and as tolerated by the patient.
Enalapril (Vasotec)
Enalapril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. The drug helps to control blood pressure and proteinuria. Enalapril decreases the pulmonary-to-systemic flow ratio in the catheterization laboratory and increases systemic blood flow in patients with relatively low pulmonary vascular resistance.
Enalapril has a favorable clinical effect when administered over a long period. Because it helps to prevent potassium loss in the distal tubules, enalapril reduces the amount of oral potassium supplementation needed by the patient.
Lisinopril (Prinivil, Zestril)
Lisinopril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.
Benazepril (Lotensin)
Benazepril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.
Fosinopril
Fosinopril is a competitive ACE inhibitor. It prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. It decreases intraglomerular pressure and glomerular protein filtration by decreasing efferent arteriolar constriction.
Quinapril (Accupril)
Quinapril is a competitive ACE inhibitor. It reduces angiotensin II levels, decreasing aldosterone secretion.
Ramipril (Altace)
Ramipril partially inhibits both tissue and circulating ACE activity, thereby reducing the formation of angiotensin II in the tissue and plasma. Ramipril has an antihypertensive effect, even in patients with low-renin hypertension.
Angiotensin Receptor Blockers (ARBs)
Class Summary
ARBs inhibit angiotensin II binding to type 1 angiotensin II receptors. These agents are also available in numerous combinations with diuretics.
Losartan (Cozaar)
Losartan inhibits the vasoconstrictor and aldosterone-secreting effects of angiotensin II by blocking the binding of angiotensin II to receptors.
Valsartan (Diovan)
Valsartan inhibits the vasoconstrictor and aldosterone-secreting effects of angiotensin II by blocking the binding of angiotensin II to receptors.
Azilsartan (Edarbi)
Azilsartan inhibits the vasoconstrictor and aldosterone-secreting effects of angiotensin II by blocking the binding of angiotensin II to receptors.
Candesartan (Atacand)
Candesartan inhibits the vasoconstrictor and aldosterone-secreting effects of angiotensin II by blocking the binding of angiotensin II to receptors.
Eprosartan (Teveten)
Eprosartan inhibits the vasoconstrictor and aldosterone-secreting effects of angiotensin II by blocking the binding of angiotensin II to receptors.
Irbesartan (Avapro)
Irbesartan inhibits the vasoconstrictor and aldosterone-secreting effects of angiotensin II by blocking the binding of angiotensin II to receptors.
Olmesartan (Benicar)
Olmesartan inhibits the vasoconstrictor and aldosterone-secreting effects of angiotensin II by blocking the binding of angiotensin II to receptors.
Telmisartan (Micardis)
Telmisartan inhibits the vasoconstrictor and aldosterone-secreting effects of angiotensin II by blocking the binding of angiotensin II to receptors.
Calcium channel blockers
Class Summary
Calcium channel blockers inhibit the movement of calcium ions across the cell membrane, depressing impulse formation (automaticity) and conduction velocity.
Nifedipine (Procardia, Adalat, Nifedical)
Produces significant fall in arterial pressure, reduces LV volume and mass, increases EF, and delays need for AVR in asymptomatic patients with severe AR and normal LV systolic function. Effective vasodilator therapy requires adjustment of dosage to decrease arterial pressure.
Diltiazem (Cardizem, Dilacor, Cartia XT, Tiazac)
During depolarization, diltiazem inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium. It produces vasodilation but causes less reflex tachycardia than nifedipine does. Diltiazem may be useful if patients develop excessive hypotension with nifedipine.
Amlodipine (Norvasc)
Amlodipine has a longer duration of action than nifedipine or diltiazem and requires less frequent dosing. Experience with this agent in pulmonary hypertension is not as extensive as that with other agents. Amlodipine has fewer effects on conduction and infrequently causes atrioventricular (AV) block.
Cardiovascular, Other
Class Summary
The effects of digoxin include an increase in the force and velocity of myocardial systolic contraction (positive inotropic action), a slowing of the heart rate, and a decrease in conduction velocity through the atrioventricular (AV) node (vagomimetic effect). The use of this drug in patients with heart failure has been associated with 25% reduction in the frequency of hospitalization for heart failure. However, digoxin use is not associated with a mortality benefit.
Digoxin (Lanoxin)
The effects of digoxin include an increase in the force and velocity of myocardial systolic contraction (positive inotropic action), a slowing of the heart rate, and a decrease in conduction velocity through the atrioventricular (AV) node (vagomimetic effect). The use of this drug in patients with heart failure has been associated with 25% reduction in the frequency of hospitalization for heart failure. However, digoxin use is not associated with a mortality benefit.
Diuretics
Class Summary
Diuretics increase urine flow. These agents are ion-transport inhibitors that decrease the reabsorption of sodium at different sites in the nephron. Diuretics have major clinical uses in managing disorders involving abnormal fluid retention (edema) or in treating hypertension, in which their diuretic action causes decreased blood volume.
Furosemide (Lasix)
Like torsemide and bumetanide, furosemide is a potent loop diuretic. Compared with all other classes of diuretics, loop diuretics have the highest efficacy in mobilizing sodium and chloride from the body, inhibiting the Na+, K+, and Cl- cotransport in the ascending limb of the loop of Henle.
Furosemide and other loop diuretics are indicated in the treatment of edema associated with CHF, cirrhosis of the liver, and renal disease, including nephrotic syndrome. They may be used alone or with other antihypertensive agents to treat hypertension.
Bumetanide
Bumetanide increases the excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle. This agent does not appear to act in the distal renal tubule.
Adrenergic Agonists
Class Summary
These agents act directly on alpha- and beta-receptors, producing effects similar to those that occur following stimulation of sympathetic nerves or the release of the hormone epinephrine from the adrenal medulla.
Dobutamine (Dobutrex)
Dobutamine is a synthetic direct-acting catecholamine and beta-receptor agonist. It increases cardiac contractility and output in CHF. At therapeutic doses, it is mainly an inotropic agent, while producing comparatively mild chronotropic and vasodilative effects. As compared with other sympathomimetic drugs, dobutamine does not significantly increase myocardial oxygen demands, which is its major advantage compared with other direct-acting catecholamines.
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Aortic regurgitation. Color Doppler echocardiogram.
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Aortic regurgitation. Doppler echocardiographic signals may be reviewed to evaluate the severity of disease.
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Aortic regurgitation. Two-dimensional (2D) color Doppler echocardiography.
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Aortic regurgitation. Aortic-root angiography shows regurgitation of contrast material into the left ventricle (LV).
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Aortic regurgitation. Chest radiograph in a patient with aortic dissection and acute aortic regurgitation shows a cardiac silhouette of essentially normal dimension.
Tables
LVESD (mm) |
LVEDD (mm) |
Dimensions |
Clinical Evaluation |
Echocardiogram |
< 45 |
< 60 |
Stable |
6-12 months |
12 months |
< 45 |
< 60 |
Increasing |
3 months |
3 months |
45-50 |
60-70 |
Stable |
6 months |
12 months |
45-50 |
60-70 |
Increasing |
3 months |
3 months |
50-55 |
70-75 |
Stable |
6 months |
6 months |
50-55 |
70-75 |
Increasing |
3 months |
3 months |
>55 |
>75 |
|
Surgery recommended |
|
Aortic valve replacement (AVR) indications Note: STS guidelines recommend “valve replacement or valve repair” |
AHA/ACC (2014) [4] |
ESC/EACTS (2012) [43] |
STS (2013) [9] |
Symptomatic severe AR |
Class I |
Class I |
Class I |
Asymptomatic chronic severe AR and left ventricular ejection fraction (LVEF) ≤50% |
Class I |
Class I |
Class I |
Severe AR when undergoing other cardiac surgery |
Class I |
Class I |
Class I |
Asymptomatic severe AR with normal LVEF (≥50%) but with severe LV dilation (LVESD >50mm) |
Class IIa-Reasonable |
Class IIa-Reasonable |
Class IIa-Reasonable |
Moderate AR when undergoing other cardiac surgery |
Class IIa-Reasonable |
Class IIb-Consider |
|
Asymptomatic severe AR and normal LVEF (≥50%) but with progressive severe LV dilation (LVEDD >65 mm) if surgical risk is low |
Class IIb-Consider |
Class IIa-Reasonable |
Class IIb-Consider |
Not indicated for asymptomatic patients with mild, moderate, or severe AR and normal LV systolic function at rest when the degree of LV dilation is not moderate or severe |
Class III |
