Essentials of Diagnosis
Exertional dyspnea or fatigue, orthopnea, peripheral edema.
Holosystolic murmur at the apex radiating to the axilla.
Echocardiography demonstrates MR, increased left atrial size, and progressive ventricular dilation.
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.
Therapies directed at preventing the various disorders that cause acute or chronic MR may reduce the prevalence of this condition.
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.
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.
In chronic severe MR, the ECG reveals left atrial enlargement or AF; in advanced stages there may be evidence of right ventricle hypertrophy.
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 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.
Table 31–5.Classification of MR severity. ||Download (.pdf) Table 31–5. Classification of MR severity.
|MR Severity ||Regurgitant Volume (mL/beat) ||Regurgitant Fraction (%) ||Regurgitant Orifice Area (cm2) |
|Mild ||<30 ||<30 ||<0.20 |
|Moderate ||30–59 ||30–49 ||0.20–0.39 |
|Severe ||≥60 ||≥50 ||≥0.40 |
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.
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:
preserves the native valve without prosthesis and in the absence of AF, obviates chronic anticoagulation,
preserves LV geometry and function, reducing risk of HF, and
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.
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:
Only a very few cases of IE is prevented by antibiotic prophylaxis, even if it is 100% effective.
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.
Dental procedures that involve manipulation of gingival, periapical region of teeth, or oral mucosa perforation warrant prophylaxis in the highest-risk persons listed above.
IE prophylaxis prior to genitourinary or gastrointestinal procedures is not recommended.
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