Heart Failure and Valvular Heart Disease

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Chapter 27 Heart Failure and Valvular Heart Disease

Martin M. LeWinter, MD , Neil Agrawal, MD

1 What are the causes of cardiomyopathy resulting in the syndrome of heart failure (HF)?

image Reduced ejection fraction (HFREF, systolic HF, dilated cardiomyopathy): impaired contraction and/or loss of cardiomyocytes. Multiple causes but approximately 65% ischemic.

image Normal or preserved ejection fraction (HFNEF, diastolic HF): abnormal relaxation and/or increased stiffness of the left ventricle (LV), most commonly associated with hypertension, type 2 diabetes mellitus, and aging. Comorbidities (e.g., chronic obstructive pulmonary disease, stroke, obstructive sleep apnea) are very common.

image Restrictive cardiomyopathy: markedly decreased LV compliance leading to impaired diastolic filling. The usual cause is infiltrative disease.

image Hypertrophic cardiomyopathy: LV hypertrophy usually with asymmetric septal thickening and often outflow tract systolic pressure gradient. The mechanisms of HF are complex, but the presumed cause is sarcomeric protein mutations.

image Right ventricular (RV) failure: Most common causes are LV failure, obstructive sleep apnea, pulmonary hypertension, and RV myocardial infarction (MI).

2 What are the causes of HFREF besides ischemic heart disease or MI?

See Table 27-1.

Table 27-1 Causes of HFREF

Type Cause
Myocarditis Infectious (viral) or inflammatory (e.g., systemic lupus erythematosus) giant cell (may require transplant)
Toxins EtOH, cocaine, cancer chemotherapy, radiation
Stress-induced cardiomyopathy Catecholamine surge from stress, apical ballooning (takotsubo syndrome)
Genetic Idiopathic, familial (multiple mutations)
Valvular disease Aortic, mitral (see valvular disease section)
Other Peripartum, sustained tachycardia, HTN, DM, endocrine or nutritional, acidosis, sepsis

DM, Diabetes mellitus; EtOH, ethyl alcohol; HTN, hypertension.

3 How do we classify HF by functional status or stage?

See Table 27-2.

Table 27-2 Classifying Heart Failure by Functional Status/Stage

NYHA Functional Classification
Class I (mild) No limitation of physical activity
Class II (mild) Slight limitation of physical activity
Class III (moderate) Marked limitation of physical activity
Class IV (severe) Unable to carry out any physical activity without discomfort, symptoms at rest
ACC-AHA Staging System
Stage A Patients at high risk for development of HF in the future but no functional or structural heart disease
Stage B Structural heart disease but no symptoms
Stage C Previous or current symptoms of HF in the context of underlying structural heart disease, adequately managed with medical treatment
Stage D Advanced disease requiring hospital-based support, heart transplantation or mechanical support, or palliative care

ACC, American College of Cardiology; AHA, American Heart Association; NYHA, New York Heart Association.

4 What is the role of brain natriuretic peptide in the diagnosis of HF?

image Not required to diagnose HF

image Helpful when diagnostic uncertainty exists and for prognosis

image Lower in HFNEF than in HFREF

image Lower in obese patients

5 How is acute decompensated HF treated?

Treatment is based on systemic perfusion and evidence of vascular congestion. See Table 27-3.

Table 27-3 Systemic Perfusion and Congestion

image

Congestion: dyspnea, orthopnea, crackles, elevated venous pressure, ascites, peripheral edema

Impaired perfusion: reduced pulse pressure, cold extremities, altered mentation

The numbers in Table 27-3 can be defined as follows:

1. Normal and requires no intervention.

2. Pump failure without pulmonary edema. Usually represents end-stage HF. Patients require inotropic support: dobutamine (β1-adrenergic agonist), milrinone (phosphodiesterase inhibitor), mechanical support (intraaortic balloon pump [IABP], LV assist device); consider cardiac transplantation.

3. Adequate perfusion with volume overload and increased filling pressures. The treatment focus is intravenous loop diuretics (most commonly furosemide) or bedside ultrafiltration. Reduction of preload with intravenous vasodilators (morphine sulfate, nitroglycerin or nitroprusside, angiotensin-converting enzyme inhibitors [ACEIs]) is another option.

4. Volume overload with pump failure. These patients require inotropes, vasodilators, diuretics, and consideration of mechanical support.

Notes:

image Ultrafiltration can remove large amounts of volume rapidly and is usually reserved for patients in whom an adequate response to IV diuretics is not achieved.

image Nesiritide is an alternative vasodilator therapy in patients whose blood pressure is normal and who continue to have dyspnea because of volume overload despite the use of intravenous loop diuretics.

6 How is diastolic dysfunction diagnosed?

An elevated LV end-diastolic or pulmonary capillary wedge pressure in a patient with a normal LV EF and end-diastolic volume by echocardiography establishes the presence of diastolic dysfunction. Various two-dimensional echocardiographic-Doppler parameters are also used, including increased ratio of early transmitral flow velocity to early diastolic velocity of the mitral valve annulus (E/E′), left atrial enlargement, and concentric LV hypertrophy.

Aortic stenosis

7 What are the causes of aortic stenosis (AS)?

image Supravalvular (rarest)

image Subvalvular (discrete, tunnel)

image Valvular

image Congenital

image Age 1 to 30 years, unicuspid

image Age 40 to 60 years, bicuspid

image Rheumatic

image Senile degenerative (> 70 years) → most common in United States

8 What is the pathophysiology of AS?

An increase in afterload caused by LV outflow obstruction causes concentric hypertrophy and increased wall thickness. By Laplace’s law, the increased wall thickness normalizes systolic wall stress and maintains shortening (EF). These structural changes are associated with diastolic dysfunction (impaired relaxation, reduced chamber compliance), which increases LV filling pressures and, in turn, increases pressures in the pulmonary circulation. In a minority of patients, the ability to hypertrophy is exhausted, EF decreases, and the LV dilates.

9 What is the classic triad of symptoms of AS, and what is its significance?

1. Increase in afterload

2. Decrease in subendocardial blood flow

3. Progressive hypertrophy with diastolic dysfunction

This triad leads to the symptoms of dyspnea (HF), angina, and dizziness or syncope. The appearance of these symptoms directly correlates with mortality. Fifty percent of patients are dead 5 years after presentation with syncope, 3 years after presentation with angina, and 2 years after presentation with HF. The rate of progression of disease by valve gradient and area is another important predictor of mortality.

10 How is the severity of AS graded with use of echocardiographic-Doppler methods?

See Table 27-4.

Table 27-4 Grading Aortic Stenosis with Use of Echocardiographic-Doppler Methods

Severity Mean gradient (mm Hg) Valve area (cm2)
Mild < 25 > 1.5
Moderate 25-40 1.0-1.5
Severe > 40 < 1.0

11 How is AS medically managed in the critically ill patient?

The only definitive treatment for AS is surgical valve replacement. Critically ill patients with adequate blood pressure can sometimes be managed with vasodilators, in particular nitroprusside. In carefully selected patients, nitroprusside increases cardiac index and stroke volume and reduces mean and diastolic arterial pressure and systemic vascular resistance. Vasodilator therapy should not be used without careful hemodynamic monitoring with a flow-directed pulmonary artery catheter. Excessive vasodilation causing systemic hypotension can cause severe deterioration by decreasing coronary perfusion. In some patients, dobutamine can be considered as an alternative.

12 When should aortic valvuloplasty and percutaneous valve implantation be considered?

In carefully selected patients, balloon valvuloplasty can be used as a bridge to surgery for patients who are hemodynamically unstable. The procedure can also be used as palliation in patients with multiple comorbidities who are poor operative candidates. However, balloon valvuloplasty has a high rate of early restenosis and poor long-term survival, which prevent it from being a definitive treatment. Recently, interest has been great in transarterial aortic valve implantation, in which a replacement valve is inserted within the stenotic aortic valve with use of percutaneous techniques. This is currently not widely available but may well be a routine option in the future.

Mitral stenosis

13 What are the causes of mitral stenosis (MS)?

image Rheumatic disease (worldwide)

image Congenital

image Other: calcification related to aging and/or end-stage renal disease, obstructive left atrial myxoma, carcinoid heart disease

14 How does MS affect cardiac function and hemodynamics?

As the mitral valve orifice narrows, the left atrial pressure rises and a diastolic pressure gradient develops between the left atrium (LA) and the LV. The latter is required to maintain forward flow. The increased LA pressure is transmitted backward, in turn increasing pressure in the pulmonary veins, capillaries, pulmonary artery, and RV. In the lungs, this results in congestion and symptoms of HF. Over time, the increased LA pressure and secondary increases in pulmonary artery pressure may result in RV overload with high filling pressures.

15 How is mitral stenosis graded with use of echocardiographic-Doppler methods?

See Table 27-5.

Table 27-5 Grading Mitral Stenosis with Use of Echocardiographic Doppler Methods

Severity Mean gradient (mm Hg) Mitral valve area (cm2)
Mild < 5 > 1.5
Moderate 5-10 1.0-1.5
Severe > 10 < 1.0

16 How are critically ill patients with MS managed?

The most common cause of decompensation in patients with MS is a rapid heart rate associated with atrial fibrillation. If tachycardia is present, this should be the focus of treatment through the use of β-blockers or calcium channel antagonists such as diltiazem. Direct current cardioversion for atrial fibrillation often has a role but is usually contraindicated in the acute setting in patients who have not been receiving prior anticoagulant therapy. Diuretics should also be used if necessary to reduce circulatory congestion. Vasodilators and positive inotropic agents generally have no role. Patients with MS, even if critically ill, are candidates for percutaneous mitral balloon valvotomy.

17 What are the indications for percutaneous mitral balloon valvotomy for MS?

This is the preferred treatment for patients with moderate to severe MS who continue to have significant symptoms on medical management; who have pliable, noncalcified mitral valve leaflets; and who do not have moderate or worse mitral regurgitation. Contraindications to valvotomy include left atrial thrombus and more than moderate mitral regurgitation.

Aortic regurgitation

18 What are the causes of aortic regurgitation (AR)?

See Table 27-6.

Table 27-6 Causes of Aortic Regurgitation

Valvular disease Aortic disease
Rheumatic —
Bicuspid Type A aortic dissection
Endocarditis (bacterial or marantic) Marfan
Degenerative or calcified Degenerative
Vasculitis Inflammatory (syphilis, Reiter syndrome)

19 What is the pathophysiology of AR?

AR represents combined volume and pressure overload. Regurgitant flow in diastole increases the end-diastolic pressure and volume. This initiates LV hypertrophy with both increased wall thickness and further increases in diastolic volume. This combination initially helps to maintain stroke volume. Approximately 50% of patients in whom severe AR is diagnosed progress to HF. Tachycardia reduces diastolic filling time and decreases the regurgitant fraction. In contrast, bradycardia does the opposite and is often poorly tolerated in patients with AR.

20 What is the management of acute, severe AR in the critical care setting?

Most acute, severe AR will require surgical intervention, depending on the cause (e.g., endocarditis, valve vs. aortic disease). The first line of medical management in patients with normal blood pressure is diuretics and nitroprusside to reduce LV filling pressure, decrease the regurgitant fraction, and improve forward flow. Care must be taken not to cause excessive hypotension. The LV is typically hyperdynamic and does not require inotropic support. Pressors in general are contraindicated because they increase arterial load and promote a higher regurgitant fraction. AR is also a contraindication for use of an IABP. When AR is stabilized, treatment consists of vasodilators such as hydralazine, nifedipine, and ACEIs.

21 What are the indications for surgery in AR?

Patients with prosthetic valve failure, aortic dissection, and most forms of acute, severe AR should be considered for emergent surgical intervention. Patients with HF, symptoms provoked by stress testing, EF < 55%, or end-systolic dimension by echocardiography > 55 mm should in general have surgical intervention. With EF < 50%, the 10-year survival after surgery is at best 56%. In the setting of endocarditis, surgical intervention should be balanced with antibiotic sterilization. Active infection is not a contraindication for valve replacement in critically ill patients.

Mitral regurgitation

22 What are the causes of mitral regurgitation (MR)?

image Degenerative (mitral prolapse and/or chordal rupture): 65%

image Functional (dilated cardiomyopathy, LV and annular dilatation), ischemia of the posterior LV wall or the medial papillary muscle: 27%

image Rheumatic (in United States): 1%

image Other (endocarditis): 5%

23 What is the pathophysiology of MR?

The mitral apparatus (leaflets, chordae tendineae, papillary muscles, and underlying LV walls) works in a coordinated fashion to maintain valve competence. In acute, severe MR, there are increased LV filling and decreased afterload, which increase EF and total stroke volume (SV). Forward SV is often reduced. The LV and LA chambers enlarge and become more compliant via rearrangement of myocardial fibers (eccentric remodeling). This allows an increase in total and forward SV. Eventually, the ventricle cannot meet the demands of worsening MR and volume overload through hypertrophy. Further dilation occurs, which is associated with an increased end-systolic volume and eventually a decrease in EF.

24 How is acute, severe MR managed?

In a patient with normal blood pressure, the goal of medical management is to pharmacologically reduce MR. This can be done by reducing systemic vascular resistance with arterial dilators such as nitroprusside and/or unloading the LV with diuretics. Acute MR often responds well to vasodilators alone. In the patient whose condition is unstable or who has hypotension, nitroprusside should be used in conjunction with an inotrope such as dobutamine or an IABP. Almost all patients with severe MR will eventually require surgical treatment.

25 What are the indications for surgery in MR?

image Symptoms of HF, even if mild

image LV dysfunction (EF < 50%, end-systolic dimension > 40 mm)

image Severe, nonfunctional MR

Note: EF < 25% is usually prohibitive for surgery because of high operative mortality.

Key Points Heart Failure and Valvular Diseaseimage

1. The causes of cardiomyopathy

image Systolic failure (reduced EF)
image Diastolic failure (normal or preserved EF)
image Restrictive cardiomyopathy
image Hypertrophic cardiomyopathy
image RV failure

2. Treatment of acute decompensated HF

image Dry-cold → Inotropes
image Wet-warm → Vasodilators or diuretics
image Wet-cold → Inotropes, vasodilators, diuretics

3. AS and mortality

image Syncope → 50% mortality after 5 years
image Angina → 50% mortality after 3 years
image Congestive HF → 50% mortality after 2 years

4. Treatment of AS in the critically ill

image Valve replacement
image Systolic blood pressure control

5. The pathophysiology of AR

image Volume and pressure overload

Bibliography

1 Bonow RO, Carabello BA, Chatterjee K, et al: 2008 Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons.J Am Coll Cardiol 52:e1-e142, 2008.

2 Carabello B.A. The current therapy for mitral regurgitation. J Am Coll Cardiol. 2008;52:319–326.

3 Carabello B.A. Contemporary aortic valve therapy. Methodist DeBakey Cardiovasc J. 2010;6:33–39.

4 Felker G.M., Thompson R.E., Hare J.M., et al. Underlying causes and long-term survival in patients with initially undiagnosed cardiomyopathy. N Engl J Med. 2000;342:1077.

5 Hunt SA, Abraham WT, Chin MH, et al: 2009 focused update incorporated into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation. Circulation 119:e391, 2009.

6 Nohria A., Mielniczuk L.M., Stevenson L.W. Evaluation and monitoring of patients with acute heart failure syndromes. Am J Cardiol. 2005;96:32G–40G.

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