All concepts, explanations, trials, and studies have been re-written in plain English and may contain errors. I am not a doctor ----------------------------------------------------------- NOTE: You can make the print bigger with the font button on your browser! (It's usually a big "A") ----------------------------------------------------------- NON-DRUG THERAPY Non-drug measures to manage CHF are as important as medications. Efforts should be made to lower the risk of new injury to the heart. This includes stopping smoking, stopping use of alcohol, reducing weight in obese patients, and diet changes to control high cholesterol and diabetes. A low sodium diet is a must, restricting fluid intake to no more than 2 liters per day helps, and daily weighing to spot fluid retention early is critical. Other measures include flu shots and pneumonia shots. Doctors should avoid prescribing anti- arrhythmic drugs to CHFers if possible, especially class I anti-arrhythmic drugs. Except for amlodipine, calcium channel blockers and NSAIDs should be entirely avoided. Flexible diuretic use with the patient taking increased doses whenever his weight increases more than 2 to 3 lbs in a 24 hour period works well. Physical condition should be improved with moderate exercise as tolerated. DRUG THERAPY Patients with advanced CHF should take an ACE inhibitor, a beta-blocker, digoxin, a diuretic, and spironolactone if possible. ACE inhibitors are still the mainstay of CHF treatment, regardless of how severe the CHF is or isn't. Dose should be increased as tolerated to the doses used in large clinical trials (target dose). Reasons to lower dose or stop the drug include cough (after lung congestion has been ruled out), severe low blood pressure or worsening kidney function. ARBs should be used if an ACE inhibitor is not tolerated because of cough. There is no data yet showing that ACE inhibitor plus ARB is better than ACE inhibitor alone. However, in patients taking both an ACE inhibitor and a beta-blocker, adding an ARB may be *harmful*. With the exception of severely decompensated class 4 CHFers, beta-blockers should be used. Beta-blockers are difficult to start and maintain in class 3b to class 4 patients. However, beta-blockers improve survival. Raising dose depends on patient response. When raising the dose of an ACE inhibitor or ARB, and a beta-blocker, low blood pressure often limits progress. The ATLAS trial compared low dose versus high dose lisinopril. It showed only an 8% relative lowering of mortality in the high-dose group. Various beta-blocker trials have shown a 34% reduction in all-cause mortality when added to an ACE inhibitor. So it seems wise to keep patients on both an ACE inhibitor and beta-blocker, even if only low doses of each are tolerated. Digoxin has proven useful in CHF. The RADIANCE trial showed that patients with more severe CHF are more likely to benefit from digoxin. Digoxin blood level should be kept between 0.5 and 1.0 ng/mL. Diuretics have not been proven to improve mortality in CHF but are essential to controlling congestion and edema. Loop diuretics like Lasix, Bumex or torsemide are usually used. Torsemide (Demadex) may be the best diuretic for those with chronic CHF, especially in patients with high right-side filling pressure. Occasionally ethacrynic acid is used. Spironolactone is now part of standard CHF therapy. The RALES trial showed a 32% *relative* reduction in combined heart-related death and hospitalization with spironolactone use at 25mg daily. Using hydralazine and nitrates improves survival, but this combination was not as effective as ACE inhibitors in the VHeFT 2 trial. The combination is still useful in patients who cannot tolerate ACE inhibitors and ARBs. (Jon's note: In 2005, it was shown that African-American [black] patients benefit MORE from hydralazine plus nitrates than from ACE inhibitor!) The only calcium channel blocker that should be tried in CHF patients is amlodipine. Amlodipine is reserved for CHF patients with angina. Used with hydralazine and nitrates, amlodipine may also be used to further lower afterload in the rare patient with high blood pressure despite the other meds. IV DRUGS Inotropes are drugs that make the heart beat more forcefully. IV inotropes like dobutamine, dopamine, and milrinone are controversial. The debate is over the higher risk of death reported with their use. IV inotropes in current use fall into 2 classes. Dobutamine and dopamine are b-adrenergic blocker. Dobutamine is the most widely used inotrope in this class. It improves heart function and also relaxes blood vessels; this lowers preload AND afterload. It is generally used at 2 to 20 micrograms/kg/minute. Tolerance can occur. Potential side effects include tachycardia, arrhythmia, and increased demand for oxygen by the heart. The inotropic effect of dopamine is weak because it acts indirectly. Tolerance occurs much more quickly with dopamine. It is primarily used to get rid of fluid by its action on receptors in the kidney's blood vessels. It is used at low doses of 1 to 3 micrograms/kg/ minute. The other class of IV inotropes is phosphodiesterase-III inhibitors. These drugs also relax the blood vessels. Milrinone is the most widely used drug in this class although its high cost limits its use in some places. Milrinone is usually given as a continuous infusion at 0.375 to 0.75 micrograms/kg per minute. In acute cases, an infusion of 50 micrograms/kg over 10 minutes may be used. Since milrinone does not increase the heart's oxygen demand, it is preferred for patients with ischemic cardiomyopathy. Milrinone is a better choice for treating acute decompensation in patients taking beta-blockers. The FDA has approved IV inotropes for: 1) short-term in-hospital support for CHF patients. 2) short-term support during major diagnostic or surgical procedures. 3) maintenance therapy in patients waiting for transplant or LVAD. Patients with weak heart function regardless of congestion may benefit from IV inotropes. The OPTIME-CHF trial did not show reduced hospital stays in 60 days of therapy, so there is no reason to routinely use inotropes in patients hospitalized with CHF. Except as a bridge to transplant or LVAD, chronic IV inotrope use is palliative (just to relieve symptoms) in patients with end-stage HF. Such use should begin in the hospital. Patients receiving intermittent IV inotropes should try weaning off the drug every 6 months to see if their heart function has improved. ANTI-ARRHYTHMIC DRUGS Ventricular arrhythmias are common in patients with advanced CHF. Most anti-arrhythmic drugs have unwelcome side effects in CHF patients. If an anti- arrhythmic drug is called for, type-1 anti-arrhythmic drugs should be avoided. The results of the STAT-CHF trial showed amiodarone to reduce ventricular arrhythmias in patients who did not have symptoms - but mortality did not improve. ULTRAFILTRATION Ultrafiltration may be used to successfully control severe fluid retention. It may make a patient more responsive to diuretic use. Various methods may be used, including dialysis. Continuous venovenous hemofiltration has been used most successfully in patients with severely decompensated CHF. SPECIALISTS The continued increase in CHF has created specialized clinics for heart failure. Along with aggressive drug treatment in such clincis, patient education is repeatedly stressed. Many of these CHF clinics have access to new, investigational meds and devices. KEY POINTS Managing advanced CHF requires a partnership between the patient and the doctor, with the patient needing to understand the disease process and preventive measures as much as possible. Not following CHF treatment guidelines when treating patients who have mild CHF leads to advancing disease and worsening symptoms. Patients should take both an ACE inhibitor and a beta-blocker, even if only low doses of each are tolerated. DISCUSSION Q: Should patients with advanced CHF be forbidden to drink even a small amount of alcohol? A: In anyone suspected of having alcoholic cardiomyopathy, alcohol should be absolutely forbidden. In patients with non-ischemic but not alcoholic cardiomyopathy, I counsel them that alcohol MIGHT have a toxic effect even at low levels. Why take the chance? Q: Is the problem with using NSAIDs in patients with advanced CHF due to kidney effects or do NSAIDs have a cardio-toxic effect? A: Most of the problem with NSAIDs has to do with prostaglandin inhibition and its effect on the kidney. NSAIDs can cause patients to retain more fluid. I've seen many CHF patients prescribed an NSAID for arthritis by another doctor and then end up in the hospital. If you have patients with arthritis who need NSAIDs, you MUST use these drugs cautiously. Q: Is this also a problem with the newer cyclooxy- genase-2 inhibitors (super-aspirins)? A: Yes. Q: What might the combination of ACE inhibitors and ARBs be better than just one or the other? A: The theory is that using both drugs more completely blocks angiotensin II at the receptor level. We know that ACE inhibitors alone do not completely block angiotensin II, so if you block its effects at 2 different levels you might get better results. (Recently, a study showed that if yu take a beta-blocker AND an ACE inhibitor, you probably should NOT take an ARB.) Q: Would you explain the advantage of increased bradykinin production linked to ACE inhibitor use? A: ACE inhibitors increase levels of bradykinin, which is a vasodilator that might help a weak heart pump better by reducing afterload. Whether higher levels of bradykinin actually improve survival is unknown. Q: You discussed the importance of raising ACE inhibitor dose in CHF patients to the doses used in trials. What are the blood pressure levels below which you get uncomfortable even if the patient does not have any ill effects (symptoms)? A: In an outpatient with dilated cardiomyopathy and clear coronary arteries, I think a systolic pressure of 80 mmHg and a diastolic pressure of 50 mmHg are fine. I am comfortable going even lower in an inpatient. In a patient with ischemic heart disease, I feel comfortable with a systolic pressure in the mid-90s and a diastolic pressure down to 60 mmHg. Q: In what situations would you favor the use of milrinone over dobutamine? A: Milrinone is a better pulmonary vasodilator than dobutamine so you get more bang for your buck by using milrinone in a patient with both right and left heart failure, and/or pulmonary hypertension. Second, in a CHF patient on a beta-blocker admitted with decompensated CHF, milrinone would work faster than dobutamine. Finally, studies have shown that milrinone does not increase the heart's oxygen demand. So in someone with severe coronary disease, milrinone might be a better drug. Title: Management of Advanced Heart Failure Authors: Adrian Van Bakel, Geoffrey Chidsey Source: Clinical Cornerstone 3(2):25-35, 2000