Title: Endovascular Stent-Grafts for the Treatment of Abdominal Aortic Aneurysms: NICE Technology Appraisal Guidance
Topic: Cardiovascular Surgery
Date Posted: 12/9/2009
Author(s): Hay N, McCracken F, Richardson J, George E, Barnett D.
Citation: Heart 2009;95:1798-800.
Clinical Trial: No
Perspective: The top 10 points to remember about the NICE guidance on the use of stent-grafts to treat abdominal aortic aneurysms (AAAs) are:
1. Endovascular aneurysm repair (EVAR) is recommended as a treatment option in patients with infrarenal AAAs for whom repair is considered appropriate.
2. Decisions as to whether to pursue EVAR or open AAA repair should be made jointly by the patient and his/her clinician.
3. Aneurysm size and morphology, patient age, life expectancy and fitness, and long- and short-term benefits and risks of the procedures should figure into the decision about which route of AAA repair is appropriate.
4. EVAR should only be performed in centers of excellence by clinical teams experienced in the management of patients with AAAs.
5. EVAR was not recommended for ruptured AAAs, except in the context of research.
6. EVAR has lower medium-term reduced rates of operative and aneurysm mortality.
7. EVAR, however, is not associated with a reduction in all-cause mortality long-term. In addition, EVAR is associated with increased rates of complications and reinterventions compared with open repair.
8. As most reports comparing open repair and EVAR use older devices, the appraisal committee suggested that the benefits of EVAR were likely greater than that seen in randomized control trials.
9. Assuming an endograft cost of 5000 pounds, the committee concluded that there was little or no difference in the initial procedure costs between EVAR and open repair.
10. In determining the fitness for surgery, which impacts cost-effectiveness, the group agreed that decisions over recommending EVAR versus open repair should be made on an individual basis, jointly between the patient and his/her clinician. Gilbert Upchurch, Jr., M.D.
Title: Mitral-Valve Repair for Mitral-Valve Prolapse
Topic: Cardiovascular Surgery
Date Posted: 12/9/2009
Author(s): Verma S, Mesana TG.
Citation: N Engl J Med 2009;361:2261-2269.
Clinical Trial: No
Perspective: This summary describes a case of a patient presenting with myxomatous degeneration of the mitral valve and severe mitral regurgitation (MR), and then discusses the clinical problem and the benefits and risks of mitral valve repair. Ten points to remember are:
1. ‘Mitral valve prolapse’ (myxomatous degeneration of the mitral valve) is the most common cause of MR in developed countries, with a prevalence of ~2.5%. There is a heterogeneous natural history of disease. In some patients, MR does not progress to severe, and life expectancy is normal; whereas in other patients (estimated at 5-10%), MR progresses to severe, with associated adverse outcomes.
2. The mitral valve apparatus is comprised of mitral leaflets, annulus, chordae tendinae, papillary muscles, and the associated left ventricular (LV) myocardium. The posterior mitral valve has three scallops. One terminology refers to the posterior scallops as P1, P2, and P3 (from anterolateral to posteromedial). MR can be caused by malcoaptation of myxomatous, prolapsing leaflets, potentially exacerbated by mitral annular dilation. (Although not discussed, MR also can be caused by partial flail of a leaflet, typically associated with rupture of one or more chordae.)
3. When present, chronic severe MR leads to volume overload of the LV, with LV dilation, hypertrophy, neurohumeral activation, and heart failure. Elevation of left atrial pressure leads to left atrial enlargement, atrial fibrillation, pulmonary venous congestion, and pulmonary hypertension.
4. There are no randomized trials comparing medical therapy with surgery for MR caused by mitral valve prolapse. However, some (but not all) observational studies suggest that survival is superior with early surgical intervention.
5. Mitral valve surgery can take the form of mitral valve replacement (with a mechanical or a tissue prosthesis) or mitral valve repair. There are no randomized trials comparing mitral valve repair and mitral valve replacement for MR caused by mitral valve prolapse. However, most (but not all) observational studies suggest that outcomes (including survival) are superior with mitral valve repair.
6. Surgical intervention generally is recommended for chronic severe MR and the presence of any symptoms, LV systolic dysfunction (in this review defined as an ejection fraction <60%, but based on American College of Cardiology [ACC]/American Heart Association [AHA] guidelines the threshold is ≤60%), significant LV enlargement (in this review defined as a systolic diameter >40 mm, but based on ACC/AHA guidelines the threshold is ≥40 mm), pulmonary arterial hypertension, or new atrial fibrillation. When surgery is indicated, current ACC/AHA and European Society of Cardiology (ESC) guidelines recommend preferential use of repair over replacement. If valve replacement is performed, subvalvular chordal attachments should be preserved.
7. There is debate regarding the use of ‘prophylactic’ mitral valve repair, used to treat chronic severe MR in an asymptomatic patient with none of the usual indications for surgery (see #6, above). ACC/AHA guidelines recommend prophylactic mitral valve repair if the likelihood of successful repair is >90%; the ESC guidelines recommend a more conservative approach.
8. Mitral valve repair is a specialized technique that should be carried out by an experienced repair surgeon. Individual and institutional experience is crucial; and high volumes are associated with both greater likelihood of valve repair rather than replacement, and lower procedural mortality.
9. Surgical valve repair can include resection of redundant or flail posterior segment(s); ‘sliding plasty’ to decrease posterior leaflet height; and chordal transposition, the use of artificial chordae, and edge-to-edge repair for anterior leaflet pathology.
10. Adverse outcomes associated with surgery include death, requirement for prolonged ventilatory support, renal insufficiency, stroke, thromboembolism, and late recurrence of MR sometimes requiring reoperation. David S. Bach, M.D., F.A.C.C.
Title: The Yield of Risk Stratification for Sudden Cardiac Death in Hypertrophic Cardiomyopathy Myosin-Binding Protein C Gene Mutation Carriers: Focus on Predictive Screening
Topic: Heart Failure/Transplant
Date Posted: 12/21/2009
Author(s): Christiaans I, Birnie E, van Langen IM, et al.
Citation: Eur Heart J 2009;Dec. 16:[Epub ahead of print].
Clinical Trial: No
Study Question: What is the value of risk stratification with genetic screening and clinical evaluations in patients with MYBPC3 gene mutations?
Methods: Two hundred and thirty-five mutation carriers were evaluated for the presence of hypertrophic cardiomyopathy (HCM) and risk factors. A clinical diagnosis of HCM was made in 53 carriers (22.6%).
Results: Disease penetrance was variable for all types of MYBPC3 gene mutations, and women were affected less often than men (15% and 32%, respectively; p = 0.003). One risk factor was present in 87 carriers and 9 had two or more risk factors. Twenty-five carriers (11%) with one or more risk factors and manifest HCM could be at risk for sudden cardiac death (SCD).
Conclusions: At first evaluation, one-quarter of asymptomatic carriers were diagnosed with HCM. Risk factors for SCD were frequently present, and 11% of carriers could be at risk for SCD. The authors concluded that predictive genetic testing in HCM families and frequent cardiac evaluation for the presence of HCM and risk factors for SCD are justified until advanced age.
Perspective: Close clinical follow-up is indicated in relatives of patients with HCM. Knowledge of the mutation status may aid in follow-up if a likely causative mutation is identified. Most mutation carriers in the current study had the same Dutch founder mutation. However, because of the uncertainty of mutation causality in a diverse population and incomplete penetrance of mutation carriers, the added value of genetic testing remains unclear. Clinical outcomes data in HCM families managed with and without genetic screening would be necessary to address this question. Daniel T. Eitzman, M.D., F.A.C.C.