Prosthetic Heart Valves Follow-up

Updated: Feb 18, 2015
  • Author: Eric M Kardon, MD, FACEP; Chief Editor: Richard A Lange, MD, MBA  more...
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Follow-up

Further Outpatient Care

Following valve replacement, every patient should undergo a history, physical examination, and appropriate testing at the first postoperative visit (2-4 wk after hospital discharge). An echocardiographic examination should be performed at this time. Thereafter, follow-up visits are recommended annually, or earlier (with echocardiography) if new symptoms develop that are attributable to a potential valvular dysfunction. In patients with a bioprosthetic valve, annual echocardiograms may be considered after the first 5 years in the absence of any changes in clinical status. [9]

Patients with postoperative LV dysfunction should be treated with standard therapy for systolic heart failure, even if improved or asymptomatic. [9]

Although the risk of thromboembolic events is lower in patients with a bioprosthetic valve than in those with a mechanical prosthesis, low-dose aspirin (75-100 mg/d) is indicated in patients without thromboembolic risk factors (eg, atrial fibrillation, previous thromboembolism, hypercoagulable condition). Although the risk of early embolic events is relatively low in patients treated with aspirin only, the addition of warfarin at hospital discharge reduces the incidence of early embolic events, but that benefit is balanced by an increased risk of repeat hospitalization for bleeding. [23] For patients with risk factors, warfarin is indicated to achieve an international normalized ratio (INR) of 2.0 to 3.0, whether after AVR or MR. Alternatively, aspirin in a dose of 75-325 mg per day is indicated in patients who are unable to take warfarin.

All patients with prosthetic valves should receive antibiotic prophylaxis against infective endocarditis prior to dental procedures.

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Transfer

Initiate arrangements for transfer to a center with cardiac surgical capabilities in patients presenting with moderate-to-severe hemodynamic compromise if these services are not readily available.

The mortality rate in patients with acute prosthetic valvular failure is related directly to the delay of surgical correction.

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Deterrence/Prevention

Provide antibiotic prophylaxis to patients undergoing procedures that may result in bacteremia. The following list, although not exhaustive, includes most inpatient and outpatient procedures performed in the ED that may result in bacteremia and, therefore, may lead to prosthetic valve endocarditis (PVE) [24] :

  • Dental and oral procedures

  • Respiratory procedures, particularly those which involve disruption of the respiratory mucosal surface, or when a known infection is present. If a known infection caused by Staphylococcus aureus is present, prophylaxis with an antistaphylococcal penicillin, cephalosporin, or vancomycin should be given. In cases of known or suspected methicillin-resistant Staphylococcus aureus, prophylaxis with vancomycin should be given.

  • Sclerotherapy of bleeding esophageal varices

  • Routine prophylaxis for gastrointestinal or genitourinary procedures is no longer recommended, unless in the presence of a known infection [25] : Urethral catheterization in the presence of a suspected urinary tract infectio; vaginal delivery in the presence of infection

  • Incision and drainage of infected tissues

  • For dental, oral, or upper respiratory tract procedures, use amoxicillin 2 g PO 30-60 minutes before the procedure. If the patient is unable to take PO medication, use ampicillin 2 g IM/IV OR cefazolin 1 g IM/IV, OR ceftriaxone 1 g IM/IV 30-60 minutes before the procedure. For penicillin-allergic patients, use clindamycin 600 mg PO/IM/IV OR azithromycin 500 mg PO OR clarithromycin 500 mg PO OR cephalexin 2 g PO 30-60 minutes before the procedure. (These are all single-dose regimens.) Do not use cephalexin in patients with a documented significant allergy to penicillin unless there is documentation that the patient can tolerate cephalosporins.

  • Further guidelines on the prevention, diagnosis, and treatment of infective endocarditis are available from the American Heart Association and the European Society of Cardiology. [24, 26]

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Complications

Complications of prosthetic valves include primary valve failure, prosthetic valve endocarditis (PVE), prosthetic valve thrombosis, thromboembolism, and mechanical hemolytic anemia. In addition, anticoagulant-related hemorrhage may occur.

Primary valve failure may occur abruptly from the tearing or breakage of components or from a thrombus suddenly impinging on leaflet mobility. More commonly, valve failure presents gradually from calcifications or thrombus formation. Bioprostheses are less thrombogenic than mechanical valves, but this advantage is balanced by their diminished durability when compared with mechanical valves. Primary valve failure occurs in 3-4% of patients with bioprostheses within 5 years of implantation and in up to 35% of patients within 15 years. In contrast, it is anticipated that most mechanical valves will remain functional for 20-30 years.

When the mitral valve fails acutely, rapid left atrial volume overload causes increased left atrial pressure. Pulmonary venous congestion and, ultimately, pulmonary edema ensue. Cardiac output is decreased, because a portion of the LV output is regurgitated into the left atrium. The compensatory mechanism of increased sympathetic tone increases the heart rate and the systemic vascular resistance (SVR). This may worsen the situation by decreasing diastolic filling time and impeding LV outflow, thereby increasing the regurgitation.

Acute failure of a prosthetic aortic valve causes a rapidly progressive LV volume overload. Increased LV diastolic pressure results in pulmonary congestion and edema. The cardiac output is reduced substantially. The compensatory mechanism of an increased heart rate and a positive inotropic state, mediated by increased sympathetic tone, partly helps to maintain output. However, this is hampered by an increase in SVR, which impedes forward flow. Increased systolic wall tension causes a rise in myocardial oxygen consumption. Myocardial ischemia may follow acute aortic regurgitation, even in the absence of coronary artery disease.

Stenosis or incompetence of prosthetic valves may develop as a result of a tear or perforation of the valve cusp, valvular thrombosis, pannus formation, valve calcification, or stiffening of the leaflets.

PVE occurs in 2-4% of patients. The incidence is 3% in the first postoperative year, then 0.5% for subsequent years. The incidence is higher in mitral valves. Mechanical and biological valves are equally susceptible. PVE occurring within 60 days of implantation (early PVE) usually is due to perioperative contamination or hematogenous spread. PVE occurring after 60 days (late PVE) usually is caused by hematogenous spread. Glomerulonephritis, CHF, mycotic aneurysms, and metastatic abscesses may complicate PVE.

Bioprosthetic valve endocarditis usually causes leaflet tears or perforations. Valve stenosis is more common with bioprosthetic valves than with mechanical valves. Ring abscess, purulent pericarditis, and myocardial abscesses are much less frequent in bioprosthetic valve endocarditis.

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