31: Valvular Disease

Degenerative valve disease is the most common form of valvular heart disease in the United States and as the population ages, clinicians will diagnose and manage more patients with this condition. Advances in surgical techniques have led to a greater number of older patients undergoing surgery for heart valve disease with improved morbidity and mortality risks. The decision to offer surgery to the older patient is complex. The patient’s preference is foremost consideration after detailed discussion of risks, benefits, and goals of care. A multidisciplinary team approach with input from the cardiac surgeon, anesthesiologist, primary care clinician and cardiologist is key to achieving desired outcomes.

Weighing the projected benefit of surgery with the natural course of untreated disease is crucial. The patient’s life-expectancy and quality of life regardless of the valve disease influence the potential benefit derived from surgery. Factors that should be weighed when considering surgery include a diagnosis of dementia, advanced cancer, severe pulmonary disease, significant frailty, symptomatic distress, and reluctance to undergo the procedure. Multivariable prognostic tools designed for older adults have been developed and validated and can provide clinicians more objectivity when estimating life expectancy (see Chapter 3, “Goals of Care & Consideration of Prognosis”).

When deciding whether surgical treatment is indicated in older patients with aortic stenosis (AS), mitral stenosis (MS), mitral regurgitation (MR), or aortic insufficiency (AI), the presence of limiting symptoms referable to the valve disease is the clearest rationale. In asymptomatic patients with severe AI or severe primary MR, the American Heart Association (AHA) and American College of Cardiology (ACC) guidelines recommend operation when the left ventricular (LV) dimension and ejection fraction reach specific parameters. The goal is to prevent further deterioration. Preventive operations such as these are justified in the older patient when the perioperative risks of stroke, acute renal failure, cognitive dysfunction, and other complications that affect quality of life are low relative to the desired benefit. In general, older patients are at increased risk for major complications following valve surgery (both aortic and mitral) including atrial fibrillation (AF), heart failure (HF), prolonged mechanical ventilation, worsened renal function, bleeding, and delirium. As a result, length of stay tends to be longer and convalescence slower.

In-hospital mortality rates associated with valve surgery range from 4% to 8% in all comers. Emergency operations, age >79 years, end-stage renal disease, and ≥2 previous cardiac operations are all strongly predictive of higher risk. Concomitant coronary artery bypass graft (CABG), low body weight, female gender, mitral valve surgery, combined valve surgeries, preoperative arrhythmias, hypertension, diabetes, and LV ejection fraction <30% are other variables predictive of in-hospital mortality following aortic and/or mitral valve surgery.

General Principles in Older Adults

The prevalence of AS increases with age, from 1.3% of 65–75-year-olds to 2.4% of 75–85-year-olds and 4% of those older than age 85 years. AS is the second most common indication for major cardiac surgery in older adults after coronary bypass surgery.

The most common cause of AS in the older adult is calcific valve disease. Aortic valve sclerosis represents an earlier stage of the disease. More than just a “wear-and-tear” process, evidence exists that calcific valve disease shares a common pathogenesis with atherosclerosis and common risk factors including age, male gender, hypertension, tobacco, lipoprotein (a), and low-density lipoprotein (LDL) cholesterol. Mechanical injury to the endothelium initiates the process that leads to lipid deposition, inflammation, neoangiogenesis, calcification, and sclerosis.

Prevention

There are no effective strategies to prevent AS. The evidence supporting use of statins to delay AS progression is inconsistent. Statins are not currently recommended for the prevention or treatment of AS in the absence of other indications, such as coronary disease.

The renin-angiotensin system is thought to play a role in the pathogenesis of calcific aortic valve (AV) disease as in atherosclerosis, however, evidence that angiotensin-converting enzyme (ACE) inhibitors modify AS progression is lacking.

Clinical Findings

Symptoms & Signs

AS is a progressive disease with a prolonged asymptomatic phase and a shorter symptomatic phase. Symptoms usually manifest in the sixth decade or later. The classic triad of symptoms associated with severe AS includes exertional angina, lightheadedness or syncope, and dyspnea or orthopnea. However, AS in the older adult is often occult until it reaches an advanced stage because sedentary older persons may experience few symptoms or may attribute their symptoms to another disease or to old age (see Chapter 7, “Atypical Presentations of Illness in Older Adults”).

Significant AS is almost invariably associated with a grade II or greater systolic ejection murmur that is usually harsh and best heard in the right second intercostal space with radiation to the carotid arteries. The murmur may be difficult to hear in obese patients and in those with increased chest diameter because of chronic lung disease, whereas in others it may be heard best at the apex. Murmurs that peak in late systole tend to be associated with more severe AS, but the intensity of the murmur often diminishes in patients with severe LV failure. Other physical findings include an LV heave, S₄ gallop, and reduced intensity or absence of the A₂ component of the second heart sound. Classically, the carotid upstroke is delayed in patients with severe AS, but this finding may be masked in older patients with stiff, noncompliant vessels.

Special Tests

Electrocardiography and radiography—

The electrocardiogram (ECG) often demonstrates LV hypertrophy, and the chest radiograph frequently reveals LV prominence.

Echocardiography—

Echocardiography is the noninvasive procedure of choice for diagnosing AS. Typical echocardiographic features include a moderately or severely thickened and calcified valve with restricted opening. Doppler examination measures mean and peak velocities across the valve and allows for calculation of the effective aortic valve area. Table 31–1 classifies AS severity.

Cardiac catheterization—

Because approximately 50% of older patients with severe AS have obstructive coronary artery disease (CAD), cardiac catheterization with coronary angiography is indicated for all patients in whom aortic valve replacement (AVR) is being considered. Catheterization can also provide definitive information about the severity of AS when the echocardiogram is nondiagnostic.

Differential Diagnosis

The symptoms of AS may mimic many other cardiac and noncardiac diseases, including CAD, HF, arrhythmia, and chronic lung disease. Likewise, the physical findings, ECG, and chest radiograph are often nonspecific. Consequently, the clinician must maintain a high index of suspicion in patients with symptoms possibly attributable to AS in association with a systolic ejection murmur.

Treatment

There is no effective medical therapy for severe AS. Because AS is generally a disease of older age, hypertension is a frequent comorbidity and contributes to the load on the LV. There are no clear recommendations for antihypertensive therapy in these patients. When used, vasodilators, including nitrates and ACE inhibitors, should be administered at a low dose and titrated cautiously in patients with moderate to severe AS because of the risk of hypotension.

Once symptoms develop, patients with severe AS should be referred for AVR because the prognosis is poor in the absence of definitive therapy. AVR is the procedure of choice for patients with severe symptomatic AS, and the results of valve replacement are excellent in properly selected candidates. Table 31–2 lists other class I indications for AV surgery. In patients older than 75 years, most cardiac surgeons will implant a bioprosthetic valve, which has acceptable durability in this group and obviates the need for long-term anticoagulation.

Age alone should not be a contraindication to surgery because several series have shown that older patients who underwent AVR for AS had quality-of-life outcomes during late follow up comparable to an age-matched general population.

AVR for symptomatic AS is associated with a 30-day survival of 86% to 94% in 75–85-year-old patients; 1-year survival of 85% to 89%; and 5-year survival of 60% to 69%. Factors predictive of operative mortality in octogenarians are urgent procedure, concurrent CABG, New York Heart Association (NYHA) class IV HF, and prior percutaneous aortic valvuloplasty. In a group of octogenarians who underwent isolated AVR, nearly 75% survived at 5 years: 81% enjoyed favorable NYHA functional classes, 91% were free of angina, and 68% were living at home.

Reduced left ventricular ejection fraction (LVEF) <30% and low-gradient severe AS from LV systolic dysfunction and low transvalvular flow are factors associated with worse postoperative outcomes. A subgroup of patients, mostly older women, who develop excessive LV hypertrophy in response to AS are also at higher risk for operative mortality.

Aortic balloon valvotomy, a procedure where a balloon is placed across a stenotic AV and inflated, frequently results in a moderate reduction in transvalvular gradient and early symptom improvement. However, it is not recommended in older adults because of frequent acute complications, and restenosis occurs within 6–12 months in most patients.

Many older patients with severe symptomatic AS are considered inoperable because of high surgical risk. Transcatheter aortic valve replacement (TAVR) is an intervention that may be an alternative. TAVR is performed by following a balloon aortic valvotomy with deployment of a stented bioprosthetic valve into the aortic annulus transfemorally or through an alternative approach. When compared with standard care in older patients who are deemed unsuitable for surgery, TAVR was associated with lower 30-day all-cause mortality despite higher rates of strokes and vascular complications at 30 days. Furthermore, TAVR was associated with reduced severity of symptoms at 1 year. In high-risk patients who nevertheless were candidates for surgical treatment, TAVR and surgical AVR were associated with similar 1-year mortality rate, approximately 25%. TAVR patients had fewer ICU and total hospitalization days. They also had a more rapid improvement in NYHA class, a difference that was significant at 1 and 6 months, but not at 1 or 2 years. At 2 years, all-cause mortality was similar in both groups, approximately 34%. Strokes occurred more frequently in the TAVR group at 30 days, but did not differ significantly between the groups during the 2-year follow-up. Paravalvular regurgitation, which was associated with late mortality, was more frequent following TAVR.

Prognosis

Onset of symptoms secondary to AS heralds increased mortality risk. The average survival after the onset of angina or syncope is 3 years, 2 years after onset of dyspnea, and 1.5–2 years following onset of HF. In a more recent study, the 2-year survival rate after onset of symptoms was approximately 50%. HF was the cause of death in 50% to 60% and sudden cardiac death (SCD) in 15% to 20% of patients. SCD is rare in asymptomatic patients and is almost always preceded by symptoms. After AVR, survival is similar to that for persons of comparable age in the general population.

General Principles in Older Adults

The prevalence of trace or greater AI in the Framingham Heart Study is 13% in men, 8.5% in women, and increases with age. Pure AI is uncommon in the older adult population; the majority with aortic valve disease have combined AS and AI. Hypertension is the most common cause of nonvalvular chronic AI. The most prevalent valvular cause is calcific valve disease.

Older patients develop symptoms or LV dysfunction earlier and suffer worse operative mortality. Concomitant CAD complicates the evaluation of symptoms, LV dysfunction, and indication for surgery.

Prevention

Therapies directed at preventing the various disorders that cause chronic AI may reduce its prevalence.

Clinical Findings

Symptoms & Signs

Patients with mild or moderate chronic AI are usually asymptomatic, and those with chronic severe AI report progressive exercise intolerance, shortness of breath, orthopnea, and fatigue.

In patients with mild-to-moderate chronic AI, a short, early diastolic decrescendo murmur is often the only physical finding. In those with chronic severe AI, the diastolic murmur becomes louder, occasionally reaching grade V or VI, and longer, often persisting throughout diastole with presystolic accentuation. The LV apical impulse is often diffuse and displaced laterally and inferiorly. An S₃ gallop is often present and may be palpable. Blood pressure is characterized by a widened pulse pressure and especially by a low diastolic pressure. Peripheral manifestations of severe chronic AI include bounding pulses, head bobbing, Quincke pulses (capillary pulsations), and femoral bruits with light compression of the artery.

Special Tests

Chest radiography—

In patients with acute severe AI, the chest radiograph reveals pulmonary edema, often in association with a normal cardiac silhouette. In patients with chronic severe AI, the heart size is usually markedly increased.

Electrocardiography—

Electrocardiographic findings are nonspecific, but LV hypertrophy may be evident in patients with severe chronic AI. Table 31–3 classifies AI severity.

Echocardiography—

Transthoracic and transesophageal echocardiography, CT, and MRI are useful noninvasive techniques for evaluating AI. In most cases, transthoracic echocardiography is the initial procedure of choice. In mild-to-moderate chronic AI, the AI jet is visualized but the echocardiogram may be normal otherwise. In chronic severe AI, the left ventricle is usually dilated and there is a prominent AI jet. Echocardiography may also provide valuable insight into the cause of AI, such as infective endocarditis, flail aortic valve leaflet, or aortic root aneurysm or dissection.

Cardiac catheterization—

In most cases, cardiac catheterization is not necessary to diagnose and quantify AI. Older patients who require surgery for AI should first undergo coronary angiography.

Differential Diagnosis

Other causes of chronic HF must be considered in the differential diagnosis of severe chronic AI.

Complications

The course of chronic severe AI is insidious and gradually progressive over many years, ultimately leading to severe HF. In asymptomatic patients with normal LVEF, the annual rate of progression to symptoms and/or LV dysfunction is <6%, 1.2% to asymptomatic LV dysfunction, and <0.2% to SCD.

Asymptomatic patients with LV dysfunction develop symptoms that indicate need for AVR within 2–3 years and are at greater risk of death.

The onset of angina, dyspnea, or HF heralds greater mortality, with annual rates of 10% in patients with angina and 20% in those with HF. Severity of HF symptoms correlate with mortality risk.

The annual risk of aortic dissection or rupture is approximately 7% in patients with aortic diameter of ≥6 cm.

Treatment

Mild chronic AI requires no additional treatment. Serial clinical evaluation and echocardiography are recommended at 2–3-year intervals. Annual echocardiography is recommended for patients with moderate to severe AI and minimal ventricular dilation. When the degree of ventricular enlargement approaches surgical indication, echocardiography is recommended every 6 months.

Chronic vasodilator therapy is recommended in patients with severe AI who are symptomatic or have LV dysfunction but are deemed inappropriate for surgery. Vasodilators may prolong the compensated phase of asymptomatic patients who have an enlarged LV but normal systolic function. In the absence of hypertension, vasodilators are not indicated in asymptomatic patients with mild to moderate AI and normal systolic function. In the presence of hypertension, blood pressure (BP) control with vasodilator therapy in asymptomatic AI patients is recommended to reduce wall stress, although systolic hypertension associated with severe AI is often difficult to lower. The goal is generally to lower BP to <150/90 mm Hg.

β Blockers are thought to worsen AI by prolonging diastolic regurgitation. However, based on observational data that β-blocker use is associated with improved survival in patients with chronic severe AI independent of comorbid hypertension and CAD, the use of this class of antihypertensive is not contraindicated and possibly beneficial as long as heart rate is >70 beats/min.

Table 31–2 lists class I indications for surgical treatment of AI. Patients with symptoms that improve with medical therapy remain at risk for dying and surgery relieves symptoms, is relatively low risk, and associated with long-term survival similar to expected rate. Severity and duration of AI and LV dysfunction, degree of symptoms and functional impairment, and degree of aortic enlargement are factors that affect postoperative survival and LV function. In older adults, symptoms should guide clinicians in deciding whether or not to recommend AVR, particularly in octogenarians. Older patients usually receive bioprosthetic valves.

General Principles in Older Adults

Based on pooled data from U.S. population-based studies, the prevalence of MS is 0.2% in those >65 years old.

MS is an obstruction to the LV inflow caused by a structurally abnormal mitral valve (MV). Normal valve area is 4–6 cm². Transvalvular pressure gradient rises when the area is reduced to <2 cm² and symptoms develop when <1.5 cm². The pathophysiology of MS is associated with the volume of flow through the valve and the duration of diastole. Consequently, patients with severe MS decompensate from conditions that result in tachycardia and increased flow, such as exercise, anemia, AF, and infection.

In developed nations, rheumatic fever has become rare, although it still accounts for the majority of MS cases. Degenerative etiology is common in developed countries. Mitral annular calcification (MAC) is a degenerative process characterized by the deposition of calcium along the valve annulus. It is reported to be more prevalent in older women and can cause functional MS by impairing the annular dilatation that normally occurs during diastole.

Prevention

Rheumatic MS can be prevented by prompt identification and treatment of group A β-hemolytic streptococcal infections. No interventions have been shown to prevent or delay the development of MAC.

Clinical Findings

Symptoms & Signs

The latency period from rheumatic fever episode to symptoms is 2–4 decades in developed countries and the mean age of presentation is in the fifth to sixth decades. Classic symptoms include exertional fatigue, a gradual decline in exercise tolerance, hemoptysis, dyspnea, and orthopnea.

Rheumatic MS is characterized by an opening snap in early diastole followed by a mid-diastolic rumbling murmur. The murmur is low pitched, best heard at the apex in left lateral decubitus position, and intensified by tachycardia. An earlier opening snap and longer duration of the diastolic murmur are associated with more severe stenosis. All of these features may be absent in patients with MS because of MAC. Additional findings associated with MS may include evidence for pulmonary hypertension (RV heave, augmented P2) and evidence for biventricular failure (pulmonary rales, elevated jugular vein pulse [JVP], and peripheral edema).

Special Tests

Chest radiography—

The chest radiograph may demonstrate calcification in the region of the MV, evidence for left atrial or right ventricular enlargement, and increased vascular markings in the lower lung fields.

Electrocardiography—

The ECG demonstrates left atrial enlargement or AF; right axis deviation and signs of right ventricular hypertrophy may also be present.

Echocardiography—

Echocardiography is the diagnostic procedure of choice because it can reliably determine the presence of MS, assess disease severity, estimate left atrial size, and evaluate for rheumatic or calcific involvement of other valves. Transesophageal echocardiography allows better anatomic visualization, excludes left atrial clot, and is necessary before percutaneous mitral balloon valvotomy (PMBV). Table 31–4 classifies MS severity.

Cardiac catheterization—

In older patients with severe MS who are being considered for cardiac surgery, coronary angiography is indicated to evaluate for obstructive CAD.

Differential Diagnosis

Differential diagnosis includes other cardiac and pulmonary conditions that produce left- or right-sided HF, AF, or pulmonary hypertension.

Complications

In minimally symptomatic patients, 10-year survival is >80%. Once limiting symptoms develop, the 10-year survival drops to 0% to 15%, and is inversely proportional to symptom severity.

After onset of severe pulmonary hypertension, the average survival is 3 years. Increased pulmonary arterial resistance may protect from pulmonary edema and allow patients to be asymptomatic for a prolonged period. Eventually, pulmonary hypertension leads to impaired right ventricular function and adversely affects prognosis.

Atrial fibrillation complicates one-third of symptomatic MS cases and affects older patients more frequently. Because atrial contraction helps maintain LV filling, the onset of AF reduces cardiac output, precipitates symptoms, and increases the risk of embolism (approaches 20% per year in the absence of anticoagulation).

Among untreated patients with severe MS, 60% to 70% die from progressive HF, 20% to 30% from systemic embolism, and 10% from pulmonary embolism.

Treatment

Anticoagulation and rate control are indicated in AF (refer to Chapter 29, “Heart Failure & Heart Rhythm Disorders,” for a discussion of AF management). Anticoagulation is also indicated in the setting of sinus rhythm with the presence of a left atrial thrombus or a history of embolism. Maintenance of sinus rhythm has been shown to improve exercise capacity; however, maintenance is difficult to achieve, even after valvotomy, particularly if duration of AF is >1 year and atrial diameter remains >45 mm. Anticoagulation should be continued in patients with persistent AF after valvotomy. Salt restriction and diuretics are useful to manage vascular congestion. Vasodilator therapy has not been shown to be beneficial in the absence of LV systolic dysfunction.

Percutaneous mitral balloon valvotomy (PMBV) involves placing a balloon across the valve and inflating it under pressure to split the fused commissures. While PMBV is the mainstay of treatment for MS in younger patients, most older adults are not suitable candidates for the procedure due to unfavorable valve morphology, such as calcified leaflets or commissures, fusion of subvalvular apparatus, or concomitant moderate or severe mitral regurgitation. Nonetheless, among older patients without contraindications, PMBV can be performed safely with salutary effects on symptoms. PMBV may also be considered as a palliative option in selected older adults who are not candidates for surgical treatment. Long-term outcomes after PMBV are less favorable in older compared to younger patients. In one study, 87% of those <40 years compared to 19% of those >70 years were in NYHA class I or II at 5-year follow-up, and mortality rates were 0% and 59%, respectively.

In patients with severe MS who are not candidates for open commissurotomy or PMBV, MV replacement offers the only viable therapeutic option. As with aortic valve replacement, mitral valve surgery in older patients is associated with increased morbidity and mortality. In the older patients with comorbid medical problems or pulmonary hypertension at systemic levels, perioperative mortality may be up to 10–20%.

General Principles in Older Adults

The prevalence of mild or greater severity MR in the Framingham Heart Study is 19%. It is the most common valvular disorder in the older adult population and is the second most common reason for valve surgery in this population after AS.

Causes and mechanisms are distinct in MR; a specific cause can lead to MR through different mechanisms. The mechanisms are classified as primary and secondary. Primary MR results from intrinsic valve abnormalities causing incomplete coaptation of leaflets, backflow, and LV volume overload. Causes of primary MR include degenerative processes (eg, MV prolapse and annular calcification), ischemia (eg, chordal rupture), rheumatic fever, or endocarditis. In contrast, the valve structure is normal in secondary MR; LV remodeling secondary to myocardial infarction or other causes of dilated cardiomyopathy results in papillary muscle and leaflet displacement. Frequent causes of MR in older adults are degenerative processes, ischemia, and cardiomyopathy.

Prevention

Therapies directed at preventing the various disorders that cause acute or chronic MR may reduce the prevalence of this condition.

Clinical Findings

Symptoms & Signs

Chronic mild or moderate MR is usually asymptomatic, and chronic severe MR is often well tolerated as long as LV function is preserved. Once LV dysfunction develops, patients with severe chronic MR typically experience symptoms and signs of left-sided HF, including exertional dyspnea, orthopnea, an S₃ gallop, and pulmonary rales. As the disease progresses, signs of right-sided HF including elevated jugular venous pressure and peripheral edema, may ensue.

Chronic MR is characterized by an apical holosystolic murmur radiating to the axilla, back, or across the precordium. In patients with MV prolapse, a midsystolic click may be heard, followed by the MR murmur. In patients with severe chronic MR, the apical impulse is usually laterally displaced, and an S₃ gallop may be present.

Special Tests

Chest radiography—

The most common finding is cardiomegaly from LV and left atrial enlargements. Annular calcification may be seen. In the absence of pulmonary hypertension, the right ventricle size is normal.

Electrocardiography—

In chronic severe MR, the ECG reveals left atrial enlargement or AF; in advanced stages there may be evidence of right ventricle hypertrophy.

Echocardiography—

Echocardiographic findings depend on the cause, chronicity, and severity of MR. A regurgitant MR jet is invariably present, and color Doppler techniques permit a qualitative assessment of MR severity. The preload is increased and afterload is reduced in MR resulting in a greater than normal LVEF. LV function may be hyperdynamic (eg, acute severe MR resulting from chordal rupture), normal (eg, moderate chronic MR), or impaired (eg, MR resulting from ischemic or dilated cardiomyopathy). The left atrial size is often normal in acute MR but becomes progressively dilated in severe chronic MR. The MV may appear structurally normal or there may be evidence of myxomatous degeneration, rheumatic involvement, endocarditis, or a flail leaflet. For patients in whom the cause or severity of MR remains in doubt after transthoracic echocardiography, the transesophageal approach provides excellent visualization of MV anatomy and function. Serial measurements of LV size and ejection fraction by echocardiography play a crucial role in management and timing of surgery.

Cardiac catheterization—

Cardiac catheterization with left ventriculography is also helpful in assessing MR severity and determining LV function. However, the role of catheterization is principally limited to evaluating hemodynamics, pulmonary pressures, and coronary anatomy in patients with severe MR who are being considered for MV surgery. Table 31–5 classifies MR severity.

Differential Diagnosis

The differential diagnosis of MR includes numerous other conditions that may result in the clinical findings of left- or right-sided HF. Often, multiple such chronic conditions coexist in older patients, and it may be difficult to determine the extent to which the patient’s symptoms are a result of MR or other causes.

Treatment

The mechanism of chronic MR influences outcomes with medical therapy. No medical therapy has been shown to delay the need for surgery in primary chronic MR with degenerative causes. Vasodilators are used in acute MR to increase forward flow, however, there are no conclusive studies of ACE inhibitors, angiotensin receptor blockers (ARBs), or other vasodilators for primary chronic MR, and they are not recommended for nonhypertensive asymptomatic patients.

Optimal medical therapy of systolic dysfunction HF reduces secondary MR (see Chapter 29, “Heart Failure & Heart Rhythm Disorders”).

Chronic MR is the second most common indication for valve surgery in older adults. See Table 31–2 for ACC/AHA class I recommendations for surgery. Although surgery is recommended for young patients with asymptomatic MR and early LV dysfunction, the presence of symptoms is often the recommended surgical indication in octogenarians. However, MV surgery before onset of LV dysfunction has been associated with greater freedom from cardiovascular mortality and hospitalization in octogenarians with isolated, nonischemic, nonrheumatic MR disease. Observational evidence also exists that 7-year mortality is excellent and no different between younger and older patients with LVEF >40% who had surgery while in NYHA class I or II. Delay in surgery likely contributes to poor outcomes from MV surgery in the older adult population. Older patients with severe LV dysfunction or markedly dilated left ventricles respond poorly to surgery and should be managed medically.

The mechanism of chronic MR guides decision about surgical treatment. For primary MR, MV repair is the primary treatment to prevent LV dysfunction and should occur before LVEF decreases to <60% or left ventricular end-systolic diameter (LVESD) increases to ≥40 mm. Surgical treatment is less straightforward in secondary MR, which is primarily a ventricular, rather than a valve, problem. Outcome of surgery for secondary disease remains suboptimal with high operative and long-term mortality, recurrent MR, and HF rates.

Observational studies suggest that MV repair is preferred over replacement as treatment of primary MR because it:

1. preserves the native valve without prosthesis and in the absence of AF, obviates chronic anticoagulation,

2. preserves LV geometry and function, reducing risk of HF, and

3. is associated with improved survival.

Mitral repair also is associated with lower postoperative stroke and shorter ICU and hospital stay in patients age 75 years and older. However, because of unfavorable valve morphology and the concomitant need for other cardiac surgery, MV repair may be a more complicated procedure in older adults.

MV replacement is associated with worse short- and long-term mortality in patients with secondary ischemic MR. The benefit of any MV surgery for octogenarians with severe secondary ischemic MR is questionable; in one study fewer than half of patients who underwent either type of MV surgery were alive in 1 year.

Age, concomitant CAD, other valvular lesions, symptom severity, comorbidities, LV size, and LV function also influence operative outcomes following MV replacement. In 31,688 patients who underwent MV replacement alone or with concomitant CABG or tricuspid surgery, operative mortality increased from 4% in those aged <50 years to 17% in those aged >80 years and major operative complications increased from 13.5% to 35.5%, respectively. The volume of procedures performed in the institution is also a determinant of operative mortality in older adults, being as high as 20% in low-volume centers (<100 valve replacements/year).

Improvement in surgical techniques in recent years has yielded better outcomes in all age groups although it remains worse in the oldest group. Overall operative mortality declined from 16% in 1980 to 3% in 1995. Improvement in cardiac output and length of hospitalization were also observed in all age groups during this period. One reason proposed for the improvement in outcomes is the more frequent performance of MV repair. Patients older than 75 years who underwent MR surgery had more severe disease with NYHA class III or IV symptoms and more comorbidities, but experienced similar restoration in life expectancy compared with younger patients when adjusted to expected survival.

Percutaneously placed clips (MitraClip) that approximate the leaflets are now approved as treatment of MR. This procedure has been used to treat MR of primary degenerative and secondary functional causes. Commonly cited contraindications to the procedure are active endocarditis, MS, rheumatic valve disease, and leaflet anatomy that does not allow both leaflets to be grasped. Mean age of participants in published clinical trials ranged from 67 to 73 years. Short- and mid-term safety and efficacy as measured by in-hospital/procedural mortality, reduction in MR severity to ≤2+ at discharge and 12 months, and improvement in NYHA class appear favorable. Five- to 10-year durability of the clip is currently undetermined. The option of subsequent MV surgery is preserved in patients who had previously undergone this intervention.

Quality of life is frequently considered a better indicator of surgical success in older adults than survival. Two hundred twenty-five patients ≥70 years who underwent surgery for primary MR were surveyed at 3 years. Of those surveyed, 91% were alive, but greater than half had suboptimal quality-of-life scores. Increased age, preoperative AF, diabetes, renal disease, residual MR, and pulmonary hypertension predicted less-favorable scores.

Wall motion abnormalities often contribute to secondary MR. In selected patients with severe HF, LVEF <35%, and left bundle branch block and QRS duration ≥150 ms, cardiac resynchronization therapy (CRT) may improve MR, cardiac output, symptoms, and reverse remodeling long-term. One-year survival with improvement in NYHA class and without HF hospitalization in older persons who received CRT was comparable with patients younger than 75 years old. In addition, there was significant reduction in the presence of grade 2 or greater MR in both groups.

Prognosis

Complications of chronic severe MR include progressive LV failure eventually leading to AF, pulmonary hypertension, and death. Determinants of 5-year adverse events (death, congestive heart failure, new AF) in asymptomatic persons with primary MR are an effective regurgitant orifice >0.4 cm², increased age, diabetes mellitus, LV size, and LV function.

Patients with severe MR from flail leaflet frequently develop symptoms, LV dysfunction, or AF in 2–3 years, and mortality rate is estimated at 6% to 7% per year.

In older patients with secondary MR associated with systolic dysfunction HF, the degree of MR is independently and directly associated with 1-year mortality.

Prevention of Infective Endocarditis

High-velocity flow through abnormal heart valves is associated with damage to endothelium causing platelet-fibrin deposition which may serve as nidus for infective endocarditis (IE). The 2007 American Heart Association guidelines for prevention of infectious endocarditis include the following points:

1. Only a very few cases of IE is prevented by antibiotic prophylaxis, even if it is 100% effective.

2. Prophylaxis is reasonable for dental procedures in setting of valvular conditions at highest risk for adverse outcome from IE, namely, the presence of prosthetic heart valve, a history of IE, presence of cardiac valvulopathy after cardiac transplantation, and certain patients with congenital heart disease.

3. Dental procedures that involve manipulation of gingival, periapical region of teeth, or oral mucosa perforation warrant prophylaxis in the highest-risk persons listed above.

4. IE prophylaxis prior to genitourinary or gastrointestinal procedures is not recommended.