Timing of surgery for AS
Timing of surgery for AS
http://www.acc.org/clinical/guidelines/valvular/jac5929fla16.htm
Kevin - I agree w/ Mara that determining the time of surgery is what you pay your cardiologist for... but just in case you want to make sure s/he is on the job, the above link provides some (hopefully useful) info regarding your question.
Some excerpts below discuss some of the key determinants for pulling the trigger on surgery for aortic stenosis (I believe that's your condition in question?):
-valve area
-trans-valvular pressure gradient
-anatomic changes to the heart
-status of left ventricular function
-symptoms
-trade-offs between surgical risks and benefits
There's no crystal clear right answer, but general consensus among experts on what the key decision criteria are.
Aortic Stenosis
a. Grading the Degree of Stenosis. The aortic valve area must be reduced to one fourth its normal size before significant changes in the circulation occur. Because the orifice area of the normal adult valve is ~3.0 to 4.0 cm2, an area >0.75 to 1.0 cm2 is usually not considered severe AS (44,45). Historically, the definition of severe AS is based on the hydraulic orifice-area formulae developed by Gorlin and Gorlin, which indicate that large pressure gradients accompany only modest increments in flow when the valve area is <0.75 cm2 (46). However, in large patients, a valve area of 1.0 cm2 may be severely stenotic, whereas a valve area of 0.7 cm2 may be adequate for a smaller patient.
On the basis of a variety of hemodynamic and natural history data, in these guidelines we graded the degree of AS as mild (area >1.5 cm2), moderate (area >1.0 to 1.5 cm2), or severe (area <1.0 cm2) (46a). When stenosis is severe and cardiac output is normal, the mean transvalvular pressure gradient is generally >50 mm Hg. Some patients with severe AS remain asymptomatic, whereas others with only moderate stenosis develop symptoms. Therapeutic decisions, particularly those related to corrective surgery, are based largely on the presence or absence of symptoms. Thus, the absolute valve area (or transvalvular pressure gradient) is not usually the primary determinant of the need for aortic valve replacement (AVR).
(Regarding myocardial hypertrophy)
The development of concentric hypertrophy appears to be an appropriate and beneficial adaptation to compensate for high intracavitary pressures. Unfortunately, this adaptation often carries adverse consequences. The hypertrophied heart may have reduced coronary blood flow per gram of muscle and also exhibit a limited coronary vasodilator reserve, even in the absence of epicardial CAD (61,62). The hemodynamic stress of exercise or tachycardia can produce a maldistribution of coronary blood flow and subendocardial ischemia, which can contribute to systolic or diastolic dysfunction of the left ventricle.
(progression of condition)
Eventually, symptoms of angina, syncope, or heart failure develop after a long latent period, and the outlook changes dramatically. After the onset of symptoms, average survival is less than 2 to 3 years (85-90). Thus, the development of symptoms identifies a critical point in the natural history of AS. Management decisions are based largely on these natural history data; many clinicians treat asymptomatic patients conservatively, whereas corrective surgery is generally recommended in patients with symptoms thought to be due to AS.
(indications for surgery)
6. Indications for Aortic Valve Replacement. In the vast majority of adults, AVR is the only effective treatment for severe AS. However, younger patients may be candidates for valvotomy (see section VI.A. of these guidelines). Although there is some lack of agreement about the optimal timing of surgery, particularly in asymptomatic patients, it is possible to develop rational guidelines for most patients. Particular consideration should be given to the natural history of symptomatic and asymptomatic patients and to operative risks and outcomes after surgery.
a. Symptomatic Patients. Patients with angina, dyspnea, or syncope exhibit symptomatic improvement and an increase in survival after AVR (86,112-116). These salutary results of surgery are partly dependent on the state of LV function. The outcome is similar in patients with normal LV function and in those with moderate depression of contractile function. The depressed ejection fraction in many of the patients in this latter group is caused by excessive afterload (afterload mismatch [52]), and LV function improves after AVR in such patients. If LV dysfunction is not caused by afterload mismatch, then improvement in LV function and resolution of symptoms may not be complete after valve replacement (116). Survival is still improved in this setting (112), with the possible exception of patients with severe LV dysfunction caused by CAD (116). Therefore, in the absence of serious comorbid conditions, AVR is indicated in virtually all symptomatic patients with severe AS. However, patients with severe LV dysfunction, particularly those with so-called low gradient AS, create a difficult management decision (117) (see above). AVR should not be performed in such patients if they do not have anatomically severe AS. In patients who do have severe AS, even those with a low transvalvular pressure gradient, AVR results in hemodynamic improvement and better functional status.
b. Asymptomatic Patients. Many clinicians are reluctant to proceed with AVR in an asymptomatic patient (118), whereas others are concerned about following a patient with severe AS. Although insertion of a prosthetic aortic valve is associated with low perioperative morbidity and mortality, long-term morbidity and mortality can be appreciable for mechanical and bioprosthetic valves. Significant complications occur at the rate of at least 2% to 3% per year, and death due directly to the prosthesis occurs at the rate of ~1% per year (119-124). Thus, even if surgical mortality can be minimized, the combined risk of surgery and the late complications of a prosthesis exceed the possibility of preventing sudden death and prolonging survival in all asymptomatic patients, as discussed previously. Despite these considerations, some difference of opinion persists among clinicians regarding the indications for corrective surgery in asymptomatic patients. Some argue that irreversible myocardial depression and/or fibrosis may develop during a prolonged asymptomatic stage and that this may preclude an optimal outcome. Such irreversibility has not been proved, but this concept has been used to support early surgery (114,125). Still others attempt to identify patients who may be at especially high risk of sudden death without surgery, although data supporting this approach are limited. Patients in this subgroup include those who have an abnormal response to exercise (eg, hypotension), those with LV systolic dysfunction or marked/excessive LV hypertrophy, or those with evidence of very severe AS. However, it should be recognized that such "high-risk" patients are rarely asymptomatic.
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Hope this helps.
Bill
