Heart Failure



Heart Failure


Andrew M. Peterson

Melody D. Randle

Troy L. Randle



Heart failure (HF), one of the most serious consequences of cardiovascular disease, has rapidly become one of the most important health problems in cardiovascular medicine. Nearly 5 million Americans have HF today, with an incidence approaching 20 per 1,000 among persons older than age 65 (Go et al., 2013). At age 40, the lifetime risk of developing HF for both men and women is 1 in 5. The incidence of HF increases with age (Go et al., 2013). HF is more common in men than in women, due to the higher incidence of ischemic heart disease in men. Approximately 75% of all ambulatory patients with HF are age 60 or older (Go et al., 2013). As the population is aging, the number of people with HF will significantly increase in the future. In people diagnosed with HF, the mortality rates remain approximately 50% within 5 years of diagnosis (Go et al., 2013). Health care disparities place African Americans at highest risk for HF (Bahrami et al., 2008).

In the United States, HF incidence has largely remained stable over the past several decades, with more than 650,000 new HF cases diagnosed annually. HF incidence increases with age, rising from approximately 20 per 1,000 individuals 65 to 69 years of age to greater than 80 per 1,000 individuals among those 85 years of age or older. Approximately 5.1 million persons in the United States have clinically manifest HF, and the prevalence continues to rise, and 7% of all cardiac deaths are due to HF.

The economic impact of HF also is significant. The large number and often high complexity of hospitalizations for HF make this diagnosis very costly. The total cost of HF hospitalizations in the United States has been estimated at $8 billion. After hypertension, HF is the second most common indication for physician office visits. The estimated direct and indirect cost of HF in the United States for 2009 was $37.2 billion (Go et al., 2013). Consequently, improved quality of life is considered a worthy health care goal, and the therapeutic approach to HF is directed toward increasing the patient’s ability to maintain a positive quality of life with symptom-free activity and to enhance survival. Vasodilator therapy, especially with the angiotensin-converting enzyme (ACE) inhibitors, has made significant contributions toward achieving this goal.


CAUSES

The development of HF may be related to many etiologic variables. Coronary artery disease, hypertension, and idiopathic cardiomyopathy are the most frequently cited risk factors for HF. Acute conditions that may result in HF include acute myocardial infarction (MI), arrhythmias, pulmonary embolism, sepsis, and acute myocardial ischemia. Gradual development of HF may be caused by liver or renal disease, primary cardiomyopathy, cardiac valve disease, anemia, bacterial endocarditis, viral myocarditis, thyrotoxicosis, chemotherapy, excessive dietary sodium intake, and ethanol abuse.

Drugs also can worsen HF. Drugs that may cause fluid retention, such as nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, hormones, antihypertensives (e.g., hydralazine [Apresoline], nifedipine [Procardia XL]), sodium-containing drugs (e.g., carbenicillin disodium [Geopen]), and lithium (Eskalith, others), may cause congestion. Beta-blockers, antiarrhythmics (e.g., disopyramide [Norpace], flecainide [Tambocor], amiodarone [Cordarone], sotalol [Betapace]), tricyclic antidepressants, and certain calcium channel blockers (e.g., diltiazem [Cardizem], nifedipine, verapamil [Calan]) have negative inotropic effects and further decrease contractility in an already depressed heart. Direct cardiac toxins (e.g., amphetamines, cocaine, daunorubicin [DaunoXome], doxorubicin [Adriamycin], and ethanol) also can worsen or induce HF.





PATHOPHYSIOLOGY

HF is a pathophysiologic state in which abnormal myocardial function inhibits the ventricles from delivering adequate quantities of blood to metabolizing tissues at rest or during activity. It results not only from a decrease in intrinsic systolic contractility of the myocardium but also from alterations in the pulmonary and peripheral circulations (Braunwald, 2015). The cardiac dysfunction is either in ventricular contraction/ejection (systolic) or ventricular filling/relaxation (diastolic).

When the heart fails as a pump and cardiac output (the volume of blood pumped out of the ventricle per unit of time) decreases, a complex scheme of compensatory mechanisms to raise and maintain cardiac output occurs. These compensatory mechanisms include increased preload (volume and pressure or myocardial fiber length of the ventricle prior to contraction [end of diastole]), increased afterload (vascular resistance), ventricular hypertrophy (increased muscle mass), and dilatation, activation of the sympathetic nervous system (SNS), and activation of the renin-angiotensin-aldosterone system (RAAS).

Although initially beneficial for increasing cardiac output, these compensatory mechanisms are ultimately associated with further pump dysfunction. In effect, the consequence of activating the compensatory systems is worsening HF. This is often referred to as the vicious cycle of HF (Figure 22.1). Without therapeutic intervention, some of the compensatory mechanisms continue to be activated, ultimately resulting in a reduced cardiac output and a worsening of the patient’s symptoms. An understanding of the compensatory mechanisms makes it clear why one goal in treating HF is to interrupt this vicious cycle and why various drugs are used in managing patients with HF.






FIGURE 22.1 Vicious circle of heart failure.


DIAGNOSTIC CRITERIA

The signs and symptoms of HF are useful in diagnosing and assessing a patient’s clinical response to therapy. The clinical manifestations of HF are in part due to pulmonary or systemic venous congestion and edema. When the left ventricle malfunctions, congestion initially occurs proximally in the lungs. When the right ventricle functions inadequately, congestion in the supplying systemic venous circulation results in peripheral edema, liver congestion, and other indicators of right HF (Box 22.1). Both pulmonary and systemic congestion eventually develop in most patients with left HF. In fact, the chief cause of right HF is left HF.

Depressed ventricular function may be confirmed by echocardiography, radionuclide ventriculography, magnetic resonance imaging, or cardiac catheterization. Abnormalities in the electrocardiogram (ECG) are common and include arrhythmias, conduction delays, left ventricular (LV) hypertrophy, and nonspecific ST-T changes, which typically reflect the underlying etiology. Laboratory findings from liver function or other tests disclose such abnormalities as elevated blood urea nitrogen (BUN) and creatinine levels, hyponatremia, and elevated serum enzymes of hepatic origin. The circumstances in which the symptoms of HF occur are also particularly important in determining the severity of disease in a particular patient.

The New York Heart Association (NYHA) classifies the functional incapacity of patients with cardiac disease into four levels depending on the degree of effort needed to elicit symptoms (Table 22.1):



  • Class I: Patients may have symptoms of HF only at levels that would produce symptoms in normal people.




BOX 22.1
Clinical Manifestations of Heart Failure



















Left Ventricular Failure—Pulmonary Congestion


Symptoms:

Cough, dyspnea, dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, nocturia


Signs:

Cardiomegaly, S3 heart sound, bibasilar rales, signs of pulmonary edema, tachycardia, increased respiratory rate


Right Ventricular Failure—Systemic Congestion


Symptoms:

Peripheral pitting edema, abdominal pain, anorexia, bloating, constipation, nausea, vomiting


Signs:

Hepatomegaly, distention of the jugular veins, hepatojugular reflex, signs of portal hypertension, ascites, splenomegaly


Decreased Cardiac Output

Peripheral cyanosis, fatigue, decreased tissue perfusion, decrease in metabolism and renal elimination of drugs, decreased appetite, angina, increased risk for thromboembolism








TABLE 22.1 NYHA Functional Classification/ACCF/AHA Stages of HF































Class

Definition

Class

Definition


None


A

At high risk for HF without structural heart disease or symptoms of HF


I

No limitation of physical activity. Ordinary physical activity does not cause undue fatigue or dyspnea.

B

Structural heart disease but without signs or symptoms of HF


II

Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue or dyspnea

C

Structural heart disease with prior or current symptoms of HF


III

Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue or dyspnea


IV

Unable to carry on any physical activity without symptoms.


Symptoms are present even at rest. If any physical activity is undertaken, symptoms are increased.

D

Refractory HF requiring specialized interventions




  • Class II: Patients may have symptoms of HF on ordinary exertion.


  • Class III: Patients may have symptoms of HF on less than ordinary exertion.


  • Class IV: Patients may have symptoms of HF at rest.

The American College of Cardiology/American Heart Association (ACC/AHA) has developed a classification system that categorizes the progression of HF and is intended to complement the NYHA classification (Table 22.1):



  • Stage A: Patients who are at high risk for developing HF but have no structural heart disease


  • Stage B: Patients with structural heart disease who have never had symptoms of HF


  • Stage C: Patients with past or current symptoms of HF associated with underlying structural heart disease


  • Stage D: Patients with end-stage disease who require specialized treatment strategies, such as mechanical circulatory support, continuous IV inotrope infusions, cardiac transplantation, or hospice care


INITIATING DRUG THERAPY

In the past, digitalis, glycosides, and diuretics were the mainstays of therapy for HF. However, the concept of HF has changed dramatically from a narrow focus on the weakened heart to a broadened view of the systemic pathophysiologic state, with peripheral as well as myocardial factors playing important roles. Individualization of pharmacologic therapy is a cornerstone of care and now based on the stage of HF. The goals of therapy are to improve the quality of life, decrease mortality, and reduce the compensatory mechanisms causing the symptoms. Three general approaches are used:



  • An underlying cause of HF is treated if possible (e.g., surgical correction of structural abnormalities/valvular heart disease or medical treatment of conditions such as hypertension, diabetes mellitus, or dyslipidemia).


  • Precipitating factors that produce or worsen HF are identified and minimized (e.g., fever, anemia, arrhythmias, medication noncompliance, or drugs).


  • After these two steps, drug therapy to control the HF and improve survival becomes important.

Nonpharmacologic management techniques should be used along with pharmacologic therapy in patients with HF. In the past, reduced activities and bed rest were considered a standard part of the care of patients with HF. However, it has been determined that short periods of bed rest result in reduced exercise tolerance and aerobic capacity. There is insufficient evidence to recommend a specific type of training program or the routine use of supervised rehabilitation programs. Although most patients should not participate in heavy labor or exhausting sports, aerobic activity should be encouraged (except during periods of acute decompensation). For example, according to the Agency for Healthcare Research and Quality (AHRQ), regular exercise (e.g., walking or cycling) is recommended for patients with stable class I to III disease.



Goals of Drug Therapy

Pharmacologic management of patients with HF is critical in reducing symptoms and decreasing mortality. In most cases, drug therapy is long term and consists of ACE inhibitors and beta blockers for class I indications. Diuretics, aldosterone antagonists, hydralazine, nitrates, digoxin (Lanoxin), and others medications are also used. Table 22.2 provides an overview of drugs used to treat HF.

In patients with a history and reduced ejection fraction (EF), ACE inhibitors (ACE-I) or angiotensin receptor blockers (ARBs) should be used to prevent HF. In patients with an MI and reduced EF, beta-blockers should be used to prevent HF and a statin also given.


Angiotensin-Converting Enzyme Inhibitors (ACE-I)

Patients who have HF resulting from LV systolic dysfunction and who have an LV EF less than 35% to 40% should be given a trial of ACE inhibitors, unless they cannot tolerate treatment with these drugs. The ACE inhibitors may be considered therapy in the subset of patients who present with fatigue or mild dyspnea on exertion and who do not have any other signs or symptoms of volume overload. In patients with evidence for, or a prior history of, fluid retention, ACE inhibitors are usually used together with diuretics. (See section on Selecting the Most Appropriate Agent.) ACE inhibitors are also recommended for use in patients with LV systolic dysfunction who have no symptoms of HF. The clinical and mortality benefits of the ACE inhibitors have been shown in numerous uncontrolled and controlled, randomized clinical trials.

ACE inhibitors (ACE-I) have a positive effect on cardiac function (i.e., reduced preload and afterload, increased cardiac index, and EF) and the signs and symptoms of HF (e.g., dyspnea, fatigue, orthopnea, and peripheral edema). As a result, exercise capacity is increased, NYHA functional classification is significantly improved, and morbidity and mortality rates in patients with HF, including those who have suffered an MI, are reduced because these drugs can attenuate ventricular dilation and remodeling.

Captopril (Capoten), enalapril (Vasotec), fosinopril (Monopril), lisinopril (Zestril), quinapril (Accupril), trandolapril (Mavik), ramipril (Altace), and perindopril (Aceon) are the ACE inhibitors currently indicated for treating HF (see Table 22.2). The ACE inhibitors that are approved for use in patients with LV dysfunction, and have been shown to prolong survival, are enalapril, captopril, and lisinopril. Quinapril and fosinopril are labeled for symptom reduction in HF, but data are lacking as to their effect on mortality rates.


Mechanism of Action

“Balanced” vasodilators, including the ACE inhibitors and angiotensin II receptor blockers, cause vasodilation on both the venous and arterial sides of the heart and therefore provide the hemodynamic and clinical benefits of both preload and after-load reduction.

Activation of the RAAS is an important compensatory mechanism in HF (Figure 22.2). ACE catalyzes the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor and stimulant of aldosterone secretion. ACE inhibitors are uniquely effective in managing HF by interrupting stimulation of the RAAS, inhibiting the contributions of this system to the downward spiral of HF. The pharmacodynamic properties of ACE inhibitors involve specific competitive binding to the active site of ACE.

Angiotensin II interacts with at least two known membrane receptors, type 1 and type 2 (AT1 and AT2). By blocking formation of angiotensin II, ACE inhibitors indirectly produce vasodilation and a decrease in systemic vascular resistance (LV afterload). In addition, because angiotensin II stimulates aldosterone secretion by the adrenal cortex and provides negative feedback for plasma renin, inhibition of angiotensin II may lead to decreased aldosterone and increased renin activity. This prevents aldosterone-mediated sodium and water retention and may produce a small increase in serum potassium levels. The reduction in volume expansion due to ACE inhibition decreases ventricular end-diastolic volume (i.e., preload). Because ACE (kininase II) is involved in the breakdown of bradykinin, a vasodilator, a decrease in kininase II activity by an ACE inhibitor could increase bradykinin as well as prostaglandin production, either of which can lead to vasodilation.

ACE inhibitors produce vasodilation, inhibit fluid accumulation, and increase blood flow to vital organs, such as the brain, kidney, and heart, without precipitating reflex tachycardia. The hemodynamic effects of ACE inhibitors in HF include decreased preload, afterload, and mean arterial pressure, as well as increased cardiac output. EF is also improved. Clinical benefits to patients with HF include improvement in exercise duration, NYHA functional class, dyspnea/fatigue focal index, and signs and symptoms of HF, as well as increased survival.


Dosage

ACE inhibitors should be initiated at low doses followed by gradual dosage increases if the lower doses have been well tolerated. Renal function and serum potassium should be assessed within 1 to 2 weeks of starting therapy and periodically thereafter, especially in patients with preexisting hypotension, hyponatremia, diabetes, or azotemia, or if they are receiving potassium supplementation. Doses should be titrated as tolerated by the patient to the target doses shown in clinical trials to decrease morbidity and mortality (e.g., 150 mg/d in divided doses of captopril; 20 mg/d of enalapril or lisinopril). The doses of ACE inhibitors can be increased to these effective doses unless the patient cannot tolerate high doses. The practitioner should provide the following information to patients taking ACE inhibitors:



  • Adverse effects may occur early in therapy but do not usually prevent long-term use of the drug.


  • Symptomatic improvement may not be seen for several weeks or months.










    TABLE 22.2 Overview of Selected Agents Used to Treat Heart Failure



































































































































































































    Generic (Trade) Name and Dosage

    Selected Adverse Events

    Contraindications

    Special Considerations


    Selected Angiotensin-Converting Enzyme Inhibitors


    captopril (Capoten)

    Common: cough; hypotension, particularly with a diuretic or volume depletion; hyperkalemia, loss of taste, leukopenia; angioedema, neutropenia, and agranulocytosis in <1% of patients; rash in >10% of patients

    Contraindicated in pregnancy


    Avoid in patients with bilateral renal artery stenosis or unilateral stenosis.

    Renal impairment related to ACE inhibitors is seen as an increase in serum creatinine and azotemia, usually in the beginning of therapy.


    Monitor BUN, creatinine, and K levels when starting.

    Start: 6.25 mg or 12.5 mg tid


    Therapeutic range: 25-100 mg tid


    enalapril (Vasotec)

    Same as above

    Same as above

    Same as above


    Use only 2.5 mg/d in patient with impaired renal function or hyponatremia.

    Start: 2.5 mg qd or bid


    Range: 5-20 mg qd or bid daily


    fosinopril (Monopril)

    Same as above

    Same as above

    Same as above


    Use only 5 mg/d in patient with impaired renal function or hyponatremia.

    Start: 10 mg qd


    Range: 10-40 mg qd


    lisinopril (Zestril, Prinivil)

    Same as above

    Same as above

    Same as above


    Use only 2.5 mg/d in patient with impaired renal function or hyponatremia.

    Start: 5 mg qd


    Range: 5-20 mg qd


    quinapril (Accupril)

    Same as above

    Same as above

    Same as above


    Use only 2.5 mg/d in patient with impaired renal function or hyponatremia.

    Start: 5 mg bid


    Range: 20-40 bid


    ramipril (Altace)

    Same as above

    Same as above

    Same as above

    Start: 1.25 mg twice daily


    Range: 1.25-5 mg twice daily


    trandolapril (Mavik)

    Same as above

    Same as above

    Same as above

    Start: 0.5-1 mg daily


    Target dose: 4 mg


    Selected Thiazide and Thiazide-like Diuretics


    chlorthalidone (Hygroton) 12.5-50 mg qd

    Hyperuricemia, hypokalemia, hypomagnesemia, hyperglycemia, hyponatremia, hypercalcemia, hypercholesterolemia, hypertriglyceridemia, pancreatitis, rashes and other allergic reactions

    High doses are relatively contraindicated in patients with hyperlipidemia, gout, and diabetes.

    Thiazide diuretics preferred in patients with CrCl >30 mL/min


    hydrochlorothiazide (HydroDIURIL, Microzide) 12.5-50 mg qd

    Same as chlorthalidone

    Same as chlorthalidone

    Same as chlorthalidone


    metolazone (Zaroxolyn) 2.5-10 mg qd

    Less or no hypercholesterolemia

    Same as chlorthalidone

    Same as chlorthalidone


    Loop Diuretics


    bumetanide (Bumex) 0.5-5 mg qd-bid

    Dehydration, circulatory collapse, hypokalemia, hyponatremia, hypomagnesemia, hyperglycemia, metabolic alkalosis, hyperuricemia (short duration of action, no hypercalcemia)

    High doses are relatively contraindicated in patients with hyperlipidemia, gout, and diabetes.

    Effective in patients with CrCl <30 mL/min


    Monitor BUN, creatinine, and K levels when starting and with dosage changes.


    ethacrynic acid (Edecrin) 25-100 mg bid-tid

    Same as bumetanide (only nonsulfonamide diuretic, ototoxicity)

    Same as bumetanide

    Same as bumetanide


    furosemide (Lasix) 20-320 mg bid-tid

    Same as bumetanide

    Same as bumetanide

    Same as bumetanide


    torsemide (Demadex) 5-20 mg qd-bid

    Short duration of action, no hypercalcemia

    Same as bumetanide

    Same as bumetanide


    Potassium-Sparing Diuretics


    amiloride (Midamor) 5-20 mg qd-bid

    Hyperkalemia, GI disturbances, rash

    High doses are relatively contraindicated in patients with hyperlipidemia, gout, and diabetes.

    Same as bumetanide


    spironolactone (Aldactone) 12.5-100 mg qd-bid

    Hyperkalemia, GI disturbances, rash, gynecomastia

    Same as amiloride

    Spironolactone ideal in patients with heart failure


    triamterene (Dyrenium) 50-150 mg qd-bid

    Hyperkalemia, GI disturbances, nephrolithiasis

    Same as amiloride

    Same as bumetanide


    Other Agents


    digitalis/digoxin (Lanoxin) 0.25 mg qd

    Ventricular tachycardia, paroxysmal atrial tachycardia, fatigue, anorexia, nausea

    Allergy, ventricular tachycardia, ventricular fibrillation, heart block, sick sinus syndrome, idiopathic hypertrophic subaortic stenosis, acute MI, renal insufficiency, electrolyte abnormalities


    Use with caution in pregnancy and lactation.

    Check potassium levels before starting. Check serum levels once a year.


    hydralazine (Apresoline) 25-75 mg tid

    Postural hypotension, tachycardia

    Coronary artery disease, aortic stenosis

    Advise patient to avoid rapid changes in position.


    Patient can be started on 10 mg tid if elderly, with severe heart failure, or hypotensive.


    isosorbide dinitrate (ISDN) (Isordil) 10-40 mg tid

    Headache, dizziness, tachycardia, retrosternal discomfort, blurred vision, rash, flushing

    Hypersensitivity to nitrates, closed-angle glaucoma, early MI, head trauma, pregnancy (category C)

    Advise patient to avoid rapid changes in position.


    Beta-Blockers


    bisoprolol (Zebeta)

    Bradycardia, congestive heart failure, atrioventricular block, postural hypotension, vertigo, fatigue, depression, bronchospasm, impotence, insomnia, decreased exercise tolerance, impaired peripheral circulation, generalized edema, sinusitis

    Sinus bradycardia, second- or third-degree heart block, asthma, liver abnormalities

    Advise patient to avoid abrupt cessation of therapy. Observe for signs of dizziness for 1 h when dose is increased.

    Start: 5 mg daily


    Range: 5-20 mg daily


    carvedilol (Coreg) 3.125-50 mg bid

    Same as above

    Same as above

    Same as above


    metoprolol

    Same as above

    Same as above

    Same as above

    Start: 6.25 mg 2-3 times daily


    Range: 50-100 mg 2-3 times daily


    Selected Angiotensin Receptor Blockers


    losartan (Cozaar)

    Dyspnea, hypotension, hyperkalemia

    Angioedema secondary to ACE inhibition

    May be used in patients experiencing cough due to ACE inhibitor

    Start: 12.5 mg/d


    Range: 50-100 mg/d


    valsartan (Diovan)

    Same as above

    Same as above

    Same as above

    Start: 80 mg/d


    Range: 80-160 mg twice daily


    Other Agents


    dobutamine (Dobutrex)

    Elevated blood pressure, increased heart rate, angina, hypotension

    Idiopathic hypertrophic subaortic stenosis

    May increase insulin requirements

    2-5 mcg/kg/min intravenously


    ivabradine (Corlanor) 2.5-7.5 mg bid

    Bradycardia, HTN, atrial fibrillation, visual disturbances

    Severe hepatic impairment, sick sinus syndrome, SA block without pacemaker, resting HR <60, atrial fibrillation, BP <90/50

    Avoid grapefruit.




  • ACE inhibitors may reduce the risk of disease progression even if the patient’s symptoms have not responded favorably to treatment (Savarese et al., 2013).

Captopril, lisinopril, ramipril, and trandolapril have been shown to reduce mortality rates in patients who have had an MI and who have HF symptoms. The indications for these ACE inhibitors in this population vary slightly, and the dosing in patients after MI differs from the dosing for patients with chronic HF. Captopril is indicated to improve survival after MI in clinically stable patients with LV dysfunction manifested as an EF of 40% or less and to reduce the incidence of overt HF and subsequent hospitalizations for HF. Captopril may be initiated with a single dose of 6.25 mg. If the patient tolerates this dose, the dose should be titrated in increments to a maximum of 50 mg three times a day as long as tolerated (systolic blood pressure greater than 100 mm Hg). Other post-MI therapies (e.g., thrombolytics, aspirin, and beta-blockers) may be used concurrently.






FIGURE 22.2 The renin-angiotensin-aldosterone (RAA) syndrome.

Lisinopril has been shown to decrease mortality rates in both acute and post-MI patients. Lisinopril also is indicated for treating hemodynamically stable patients within 24 hours of an acute MI to improve survival. Patients should receive, as appropriate, the standard recommended treatments, such as thrombolytics, aspirin, and beta-blockers. The first 2.5-mg dose of lisinopril may be given to hemodynamically stable patients within 24 hours of the onset of symptoms of acute MI. The dose of lisinopril should be titrated as tolerated to a dose of 10 mg daily. Dosing should be continued for 6 weeks. At that time, the patient should be assessed for signs and symptoms of HF, and therapy should be continued if necessary. The dose should be decreased to 2.5 mg in patients with a low systolic blood pressure (below 120 mm Hg) when treatment is started or during the first 3 days after the MI. If hypotension occurs (systolic blood pressure below 100 mm Hg), a daily maintenance dose of 5 mg may be given with temporary reductions to 2.5 mg if needed. If prolonged hypotension occurs (systolic blood pressure below 90 mm Hg for at least 1 hour), lisinopril therapy should be discontinued. Patients who develop symptoms of HF should receive the usual effective dose of lisinopril for HF, with a goal of 20 mg/d.

Ramipril has also been approved for stable patients who have shown clinical signs of HF within the first few days after an acute MI. It is used to decrease the risk of death (principally
cardiovascular death) and to decrease the risks of HF-related hospitalization and progression to severe or resistant HF. The starting dose is 2.5 mg twice daily. A patient who becomes hypotensive at this dose may be switched to 1.25 mg twice daily, but all dosages should then be titrated, as tolerated, toward a target dose of 5 mg twice daily. In patients with a creatinine clearance less than 40 mL/min/1.73 m2 (serum creatinine level of less than 2.5 mg/dL), the dose should be decreased to 1.25 mg once daily. The dosage may be increased to 1.25 mg twice daily up to a maximum dose of 2.5 mg twice daily, depending on clinical response and tolerability.

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Nov 11, 2018 | Posted by in PHARMACY | Comments Off on Heart Failure

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