Valvular Heart Disease
Adult-Gerontology Acute Care Practice Guidelines
Definition
A.Damage or defect in one of the four heart valves: Mitral, aortic, tricuspid, or pulmonary.
B.Two most common abnormalities: Regurgitation and stenosis of the aortic and mitral valves.
1.Regurgitation or insufficiency: Occurs when the valve leaflets do not close tightly; blood leaks backward into the respective chamber instead of flowing forward through the proper circulatory path.
2.Stenosis: Occurs because of stiffening and narrowing of the valve leaflets.
a.This prevents the valve from opening properly; the result is not enough blood flowing through the valve and circulatory path, which leads to an outflow-type obstruction during systole.
b.Mitral stenosis (MS) results in an increase in left atrial, pulmonary artery, and right ventricular pressures.
c.Mitral regurgitation (MR) leads to a backflow (or reversal) of blood from the left ventricle to the left atrium during systole; it can be primary or secondary and acute or chronic.
i.Acute MR: Typically occurs because of endocarditis or myocardial infarction (MI) with structural cardiac damage (papillary muscle rupture, chordae rupture).
ii.Chronic MR: Can be primary or secondary.
iii.Causes of primary MR: Mitral valve prolapse (MVP; subtype of MR where the mitral valve leaflets close improperly and bulge into the left atrium during systole), rheumatic heart disease, MI with resultant structural cardiac damage, or endocarditis.
iv.Causes of secondary MR: Left ventricular dysfunction.
Incidence
A.Globally, the prevalence of valvular heart disease (VHD) is estimated at 2.5%.
B.Prevalence of VHD increases in individuals older than 65 years of age, particularly in those with aortic stenosis (AS) or MR. More than 33% of those older than age 75 have moderate to severe VHD.
C.AS is the leading cause of clinically significant VHD in geriatric patients (prevalence of 2%–9%).
D.Acute aortic regurgitation (AR) is a rare and life-threatening condition. Chronic AR is common in geriatric patients (prevalence of 20%–30% in geriatric patients).
E.MS is more common in females as compared to males and usually occurs because of rheumatic heart disease (97%).
1.MS caused by rheumatic heart disease typically presents in the fourth or fifth decade but can occur in individuals older than age 65 years.
2.Only 60% of patients with MS secondary to rheumatic heart disease can recall a previous history of the infection.
3.Among geriatric patients with non-rheumatic heart disease-related MS, the etiology is typically because of age-related calcifications that narrow the valve.
F.MR occurs equally in males and females, with a prevalence of 2%.
1.Most common cause of MR is MVP.
2.MVP can be spontaneous or genetically linked.
Pathogenesis
A.Stenosis.
1.Senile AS or MS.
a.Exact mechanism is still not entirely understood; it is thought to be secondary to a buildup of calcifications within the valve.
b.Very similar to the process of atherosclerosis.
c.Increase in lipids, inflammation, and calcification of the valve.
2.Bicuspid AS: Secondary to an inherited congenital condition where two (of the normally structured three) leaflets of the aortic valve are fused together.
a.This improper fusion of the two valve leaflets results in a bicuspid aortic valve instead of a tricuspid-shaped valve.
b.Result is an increase in calcification formation and outflow obstruction.
3.Rheumatic heart disease-related AS or MS: Can affect the aortic or mitral valves via fusion of the leaflets to create narrowing and outflow obstruction.
B.Regurgitation.
1.Acute MR: Results in increase in preload and decrease in afterload.
a.This causes an increase in end-diastolic volume (EDV) and decrease in end-systolic volume (ESV).
b.Thus, stroke volume and left atrial pressures are increased.
2.Chronic MR: Slow deterioration of the valve allows the left atrium and left ventricle to adjust (dilate) to the increased backflow of blood.
a.Left atrial pressure is usually normal or slightly elevated; end-diastolic pressure is also within an acceptable range.
b.Over time, the left ventricle will continue to dilate, further damaging the mitral valve leaflets and worsening the MR.
3.Acute AR: Increased volume in the left ventricle during diastole; the ventricle does not have sufficient time to dilate appropriately to accommodate the sudden increase in fluid.
a.EDV increases quickly, which this causes an elevation in pulmonary artery pressures, affecting coronary and pulmonary circulation.
b.With this increase in volume and pressures, patients develop symptoms consistent with pulmonary congestion (i.e., dyspnea).
4.Chronic AR: Results in slow progressing fluid overload within the left ventricle.
a.This condition causes the left ventricle to dilate over time, resulting in left ventricular hypertrophy.
b.Initially, the hypertrophy helps mitigate the increased pressure and volume that occurs within the left ventricle.
c.In early phase, cardiac contractility (or ejection fraction [EF]) remains normal via compensation mechanisms.
d.As the disease progresses and the ventricle continues to dilate, it reaches maximal stretch capacity; beyond this threshold there is an increase in end-diastolic pressures and decrease in perfusion of the coronary system.
e.As the left ventricle structure and function worsens, the EF decreases and symptoms (i.e., dyspnea) ensue.
Predisposing Factors
A.Recent MI with resultant structural damage of valve leaflets, chordae, and papillary muscles.
B.Most common risk factors for MR: MVP, rheumatic heart disease, infective endocarditis, known coronary artery disease (CAD), and cardiomyopathies. Note the following:
1.Rheumatic heart disease most commonly causes regurgitation of the mitral valve followed by the aortic valve (rarely affects tricuspid or pulmonary valves).
2.Infective endocarditis can technically affect any valve—it most commonly targets the tricuspid but also affects the aortic and mitral valves.
C.Possible cause of MS: Age-related degenerative changes or more rare etiologies, including congenital malformations and intracardiac tumors (myxoma).
D.AS: Age-related changes, bicuspid aortic valves, and rheumatic heart disease.
E.Advanced hypertension (HTN) and atherosclerosis, which can affect valvular function.
F.Conditions that can lead to VHD: Autoimmune and connective tissue processes such as systemic lupus erythematous and Marfan’s syndrome.
G.Other conditions that increase risk: Tobacco use, insulin resistance/diabetes mellitus (DM), obesity, and a family history of VHD.
H.Acute aortic dissection, which can result in acute life-threatening AR.
Subjective Data
A.Common complaints/symptoms.
1.AS: Angina, syncope, and findings associated with heart failure (i.e., fatigue, orthopnea, paroxysmal nocturnal dyspnea, shortness of breath, decreased exercise tolerance, dyspnea on exertion).
2.AR.
a.Acute AR: Dramatic presentation of cardiogenic shock (secondary to infective endocarditis or aortic dissection).
b.Chronic AR: Palpitations, angina, heart failure presentation (dyspnea on exertion, peripheral edema, fatigue, paroxysmal nocturnal dyspnea).
3.MS.
a.Often presents with new-onset atrial fibrillation (i.e., fatigue, chest discomfort, palpitations, lightheadedness, dizziness).
b.Rarely presents with Ortner’s syndrome: Occurs with MS where there is compression of the left recurrent laryngeal nerve due to an enlarged left atrium; results in hoarseness.
4.MR: New-onset atrial fibrillation (similar to MS), anxiety, chest discomfort, dyspnea, fatigue, and/or signs of volume overload consistent with heart failure.
B.History of the present illness.
1.Obtain information regarding specific symptom: Onset, provoking/palliative, quality, severity, radiation (if applicable), and timing.
2.Review patient’s past medical history: Particularly, recent MIs, known CAD, HTN, or HLD; congenital cardiac abnormalities, previous rheumatic fever, connective tissue disorders, cardiomyopathies, or congestive heart failure (CHF).
3.Determine if the patient ever had a previous cardiac evaluation, especially an echocardiogram, or learned about a heart murmur.
4.Understand that patient scenarios will vary based on the valve affected, type of dysfunction (stenosis or regurgitation), and underlying etiology.
C.Family and social history.
1.Gather information regarding family history of VHD (especially bicuspid aortic valves or MVP), HTN, hyperlipidemia, CHF, arrhythmias (i.e., atrial fibrillation), or connective tissue disorders.
2.Obtain social history information, especially regarding tobacco use, alcohol use, and illegal substance use (very important to document any intravenous drug use due to high risk of infective endocarditis).
D.Review of systems.
1.General: Fatigue, malaise, fevers, chills, weight changes, and appetite changes.
2.Skin/Nails: Painful red-purple nodules on hands/feet (Osler nodes of infective endocarditis) and painless red areas on palms/soles (Janeway lesions of infective endocarditis).
3.Head, ear, eyes, nose, and throat (HEENT): Hoarseness.
4.Cardiac: Chest discomfort, palpitations, racing heartbeat, decreased exercise tolerance, peripheral edema, and uncomfortable awareness of heartbeat (associated with AR).
5.Pulmonary: Cough, shortness of breath, dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, and hemoptysis (rare but associated with MS).
6.Gastrointestinal: Increasing abdominal girth.
7.Neurological: Lightheadedness, dizziness, syncope, and near-syncope.
8.Psychological: Anxiety.
Physical Examination
A.Vital signs: Assess pulse rate and rhythm, blood pressure (BP), respirations, temperature, and oxygen saturation.
1.Possible tachycardia or bradycardia.
2.Possible irregularly irregular pulse (consistent with atrial fibrillation).
3.Possible hyperthermia (concern for infection) or hypothermia (in geriatric patients with infections who cannot mount fevers).
4.Decreased oxygen saturation (concern for signs of CHF).
5.Possible HTN (acute or long-standing) or hypotension (concern for cardiogenic shock).
6.Widened pulse pressure (associated with AR).
7.Mayne sign: Decrease in BP with arm elevation (associated with AR).
8.Hill sign: Higher BP in lower as compared to upper extremity (associated with AR).
B.General survey: Determine if patient is in acute distress, or asymptomatic.
C.Skin/Nails: Assess for Osler nodes and Janeway lesions.
D.Head: Possible evidence of head bobbing with each heartbeat (de Musset sign of AR).
E.Neck.
1.Consider possible jugular venous distention (JVD; concern for CHF).
2.Evaluate carotids.
a.Pulsus parvus et tardus (associated with AS) where there is a weakened and delayed pulse with late carotid upstroke.
b.Brisk carotid upstroke (associated with MR).
F.Pulmonary: Possible rales or crackles (sign of increased fluid accumulation).
G.Gastrointestinal: Possible ascites or hepatomegaly (concern for worsening heart failure).
H.Cardiac.
1.Inspect for lifts/heaves (concern for ventricular enlargement).
2.Palpate for thrills (grade IV to VI murmurs) and the point of maximum impulse (PMI; if displaced, concern for ventricular hypertrophy).
3.Auscultate for S1, S2, and evidence of extra heart sounds (S3 and S4) and murmurs.
a.AS: Harsh late-peaking crescendo-decrescendo systolic murmur that radiates to carotids and best heard over right second intercostal space (ICS), can also have paradoxical splitting of second heart sound.
b.Aortic regurgitation: PMI often displaced toward axilla, possible S3, diastolic low-pitched rumbling murmur best heard at left sternal border; can also hear an Austin Flint murmur (severe AR: Low-pitched, rumbling, mid-diastolic murmur; heard best at apex).
c.MS: Loud first heart sound, positive high-pitched opening snap after A2 heart sound; nonradiating mid-diastolic murmur best heard at apex.
d.MR: Decreased S1, wide splitting of S2, high-pitched holosystolic (can be early systole in acute MR) best heard at cardiac apex and radiates to left axilla.
i.MVP: If concern for MVP (associated with MR): Murmur is usually in late systole and associated with the hallmark mid-systolic click that precedes that MR murmur.
I.Peripheral vascular: Possible bounding peripheral pulses (water hammer pulse associated with AR), possible peripheral edema.
J.Neurological: Mental status examination (if positive mental status changes) and complete neurological examination if concern for associated syncope/near-syncope.
Diagnostic Tests
A.MS.
1.Routine laboratory studies: Complete blood count, electrolytes, renal function, and liver function.
2.Chest x-ray: Can see left atrial enlargement, prominent pulmonary vasculature, and interstitial edema (Kerley A and B lines).
3.ECG: If severe MS, signs of left atrial enlargement, atrial fibrillation, and right ventricular hypertrophy.
4.Transthoracic echocardiogram (TTE) to assess overall cardiac function, left ventricular dysfunction, and degree of stenosis.
a.Mild: Valve area greater than 1.5 cm².
b.Moderate: Valve area of 1.0 to 1.5 cm².
c.Severe: Valve area less than 1.0 cm².
d.Consider transesophageal echocardiogram (TEE) if TTE does not produce quality images; there is question of a left atrial thrombus or prior to surgical intervention.
5.Cardiac catheterization is not routine, but can be considered in several circumstances.
a.If discrepancy between physical examination and echocardiogram results.
b.Patients with severe underlying lung disease and pulmonary HTN who require further evaluation.
c.Geriatric patients with severe MS to rule out comorbid CAD.
B.AS.
1.Routine laboratory studies: Complete blood count, electrolytes, cardiac biomarkers, renal function, and liver function.
2.ECG: Could be normal, possible left ventricular hypertrophy pattern, and possible atrial fibrillation.
3.TTE.
a.Follow recommendations of American Heart Association (AHA) for evaluation of grade 3 AS murmurs via TTE.
b.Consider stress echocardiogram in asymptomatic patients with severe AS to determine need for clinical intervention.
c.Perhaps consider TEE if concern for bicuspid aortic valve.
4.Cardiac catheterization.
a.Use if discrepancy between patient presentation and echocardiogram results.
b.Consider in patients older than 35 years of age with AS requiring surgical intervention to evaluate for CAD.
5.Exercise stress testing: Absolutely contraindicated in severe symptomatic AS (can be considered in those with asymptomatic severe AS under strict surveillance of cardiologist).
6.CT angiography: Can be used in patients for whom transcatheter aortic valve replacement (TAVR) is being considered.
7.Chest x-ray: Findings vary based on severity of AS.
a.In severe AS: May appreciate aortic valve calcifications, left atrial enlargement, right-sided heart enlargement, and pulmonary congestion.
C.AR: Evaluation is based on clinical scenario and suspected underlying etiology.
1.Laboratory studies.
a.For infective endocarditis: Complete blood count, electrolytes, renal function, kidney function, blood cultures, lactate levels, prothrombin time (PT)/partial thromboplastin time (PTT), and international normalized ratio (INR).
b.For connective tissue disorders: Consider serologic tests (antinuclear antibody [ANA], Anti-dsDNA).
2.TTE: Assess valve structure and degree of dysfunction, overall left ventricular function, EF percentage, size of aortic root, and presence of vegetations (TEE may be required if + vegetation on TTE).
3.Cardiac catheterization: Obtain if surgical intervention is a consideration, especially if concern for underlying CAD.
D.MR.
1.Chest x-ray: Possible left ventricular enlargement and increased pulmonary venous congestion (if concomitant CHF).
2.TTE.
a.The American College of Cardiology (ACC) and American Heart Association (AHA) recommend TTEs for several reasons.
i.Evaluate left ventricular size and function.
ii.Determine right ventricle and left atrial size, pulmonary artery pressure, and severity of MR.
iii.Monitor EF of symptomatic patients with moderate-to-severe MR.
iv.Determine etiology of MR.
v.Monitor EF and left ventricular size and function if patient has change in clinical status.
vi.Evaluate MR integrity and left ventricular function in patients with mitral valve repair or replacement.
b.Consider TEE if TTE is nondiagnostic or prior to surgical repair/replacement.
Differential Diagnosis
A.MS.
B.MR.
C.MVP.
D.AS.
E.AR.
F.Pulmonic stenosis.
G.Acute coronary syndrome.
H.Tricuspid stenosis.
I.Tricuspid regurgitation.
J.Infective endocarditis.
Evaluation and Management Plan
A.General plan.
1.Determine etiology of given VHD and treat accordingly.
2.Monitor patients for symptoms of worsening VHD.
3.Evaluate patients for determination of management: Medical versus surgical (open approach vs. percutaneous approach, such as TAVR).
4.Manage symptoms associated with given VHD (i.e., CHF).
5.Treat underlying comorbidities that contribute to worsen VHD (i.e., HTN, HLD, DM).
B.Patient/family teaching points.
1.Explain underlying etiology and specific type of VHD.
2.Discuss course of therapy: Medical versus surgical and importance of ongoing monitoring.
3.Emphasize importance of compliance with follow-up appointments and medications.
a.If utilizing anticoagulation agents: Ensure patients understand not to discontinue drugs prior to any procedures without consulting cardiologist.
b.If clinically indicated: Educate regarding preinvasive procedure prophylactic antibiotics.
4.Geriatric patients: Consider involving family members to help determine best course of treatment.
5.For patients at high risk for endocarditis, discuss use of preprocedure prophylactic antibiotics.
6.Ensure understanding regarding reasons for urgent return to ED such as hemodynamic
instability, new or worsening chest discomfort, palpitations, new or worsening difficulty breathing, syncope/near-syncope, or mental status changes.
C.Management of specific valvular diseases.
1.AR.
a.Surgical intervention via valve replacement: If angina, evidence of CHF, or ventricular failure.
b.Medical management: Typically reserved for patients who are not surgical candidates (due to comorbidities) because conservative management of symptomatic patients is rarely successful.
i.There is conflicting evidence with regard to use of medical management for asymptomatic patients with AR.
ii.With medications: Goal is to reduce afterload via vasodilators such as calcium channel blockers or ACE inhibitors); beta-blockers are not first-line drugs (due to bradycardia) but could benefit patients with significant left ventricular dysfunction.
2.AS.
a.According to AHA, there is no acceptable medical management to alleviate AS.
b.Available medical therapy is only used to alleviate symptoms and manage comorbidities (diuretics are not indicated due to the possibility of a decrease in cardiac output).
i.Beta-blockers (help with HTN and CAD).
ii.ACE inhibitors (help with HTN, DM, and left ventricular fibrosis).
c.Once patients are symptomatic, considerations should be made for surgery.
i.If patient is not a candidate for open (traditional) aortic valve replacement (AVR), consider TAVR.
3.MS.
a.Medical management may be useful, although it cannot ameliorate the narrowing of the mitral valve.
b.Several classes of medications can be used to assist with symptoms.
i.Beta-blockers: Decrease heart rate and improve dyspnea on exertion.
ii.Diuretics: Decrease pulmonary edema.
c.Symptomatic patients will require surgical intervention. There are several options.
i.Percutaneous mitral valvuloplasty: Typically used in younger patients and those with mild MS (contraindicated in moderate to severe disease).
ii.Surgical procedures: Open repair with commissurotomy or valve replacement with mechanical or bioprosthetic valve (considered high-risk procedures; mortality >20% in geriatric population with multiple comorbidities).
4.MR.
a.Asymptomatic patients with normal BPs and no left ventricular dysfunction do not require treatment.
b.Medical therapy can be used for symptom management (i.e., vasodilators and diuretics to manage BP).
c.Symptomatic patients should be considered for surgical repair/replacement.
i.If possible, valve repair is preferred to replacement: Eliminates requirement of long-term anticoagulation, improves symptoms, and increases postoperative survival rates.
ii.Surgical management indicated if NYHA class II to IV CHF, severe MR regardless of cardiac size and function, or asymptomatic patients with MR and atrial fibrillation, pulmonary HTN, or left ventricular dysfunction.
iii.Various percutaneous options are in the development process.
D.Additional pharmacologic considerations.
1.Outpatient anticoagulation.
a.INR monitoring is recommended in patients with mechanical prosthetic valves.
b.Goal is INR of 2.0 to 3.0 in patients with mechanical AVR and no other risk of thromboembolism.
c.Goal is INR 2.5 to 3.5 in patients with a mechanical AVR, MVR, and additional risk factors for thromboembolisms (i.e., atrial fibrillation, previous thromboembolism).
d.Low-dose daily aspirin is recommended in addition to anticoagulation in patients with a mechanical valve prosthesis.
e.Low-dose daily aspirin can be used in patients with a bioprosthetic aortic or mitral valve.
f.Anticoagulation can be used for the first 3 months after bioprosthetic MVR or AVR or repair to achieve an INR of 2.5.
g.Can consider clopidogrel 75 mg daily for the first 6 months after TAVR in addition to daily lifelong aspirin.
2.Anticoagulation with bridging.
a.Continuation of anticoagulation with a therapeutic INR is recommended in patients with mechanical heart valves undergoing minor procedures (i.e., dental extractions or cataract removal) where bleeding is easily controlled.
b.Bridging anticoagulation with heparin is recommended for invasive procedures when the INR is subtherapeutic preoperatively in those with a mechanical AVR, any thromboembolism risk factor, older generation mechanical AVRs, or a mechanical MVR.
E.Discharge instructions.
1.Ensure patient receives all prescriptions prior to discharge.
2.Arrange timely follow-up appointments with cardiologist.
3.Educate patients about reasons to return to ED with regard to worsening symptoms of VHD.
4.Based on clinical scenario and degree of VHD, provide patients with information regarding physical activity restrictions.
Follow-Up
A.Patients require monitoring via history/physical examinations and echocardiography based on clinical scenario, degree of VHD, and overall cardiac status (i.e., EF and left ventricular function). In AS, for example:
1.If mild disease, echocardiograms every 3 to 5 years.
2.If moderate disease, echocardiograms every 1 to 2 years.
3.If severe disease, echocardiograms every 6 months to 1 year.
Consultation/Referral
A.Consult with cardiologist for VHD.
B.Consult with infectious disease specialist (if concern for underlying infective endocarditis).
C.Consult with rheumatologist (if concern for underlying connective tissue disorder).
D.Consult with cardiothoracic surgeon (if surgical repair is a consideration).
E.Consult with interventional cardiologist (if consideration for TAVR).
F.Refer to cardiac rehabilitation following invasive valve repair/replacement procedure.
Special/Geriatric Considerations
A.Antibiotic prophylaxis.
1.According to AHA, preinvasive procedure prophylactic antibiotics (against Streptococcus viridans) should be used in certain populations and scenarios with risk of infective endocarditis.
a.Prosthetic heart valve.
b.History of previous infective endocarditis.
c.Congenital heart disease (CHD) that is unrepaired and cyanotic, repaired CHD using prosthetic material/device for 6 months, or repaired CHD with a residual defect.
d.Cardiac transplant patients with VHD.
e.Recommended for patients with MVP or moderate to severe primary MR.
f.Procedures: Dental (if manipulation of gingiva, perforation of oral mucosa, or significant teeth manipulation) or respiratory (i.e., tonsillectomy, adenoidectomy). Amoxicillin (2 g 1-hour preprocedure), clindamycin (600 mg 1-hour preprocedure), or cephalexin (2 g 1-hour preprocedure) may be used.
B.Geriatric considerations.
1.Aortic valve disease is the most common type of VHD in this demographic.
2.If surgical intervention is a consideration, it is important to assess underlying CAD risk, cognitive status, and overall health status.
3.For elderly patients with severe AS who are not surgical candidates, consultation should be obtained for TAVR, which is minimally invasive.
4.If valve replacement procedure is indicated, it is necessary to assess risk versus benefit regarding use of anticoagulation.
5.It is important to remember that VHD symptoms in this population can be vague (i.e., fatigue and dyspnea) and difficult to differentiate from normal aging.
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