**4. Outcomes after aortic valve replacement**

The Ad Hoc Liaison Committee for Standardizing Definitions of Prosthetic Heart Valve Morbidity of the American Association of Thoracic Surgery and the Society of Thoracic Surgeons published guidelines during years, which are now widely used in reporting outcomes after valve surgery. They presented a list of developing specific valve-related events during patients remaining lifetime. These valve-related events are:


**Structural valvular deterioration** - Any change in function or deterioration (a decrease of one New York Heart Association functional class or more) of an operated valve due to an intrinsic abnormality, which causes stenosis or regurgitation. Changes intrinsic to the valve include wear, fracture, poppet escape, calcification, leaflet tear stent creep and su‐ ture line disruption of the components of the operated valve. The definition excludes changes due to infection or thrombosis. *Mechanical prostheses* are extremely resistant to ma‐ terial fatigue or structural valve deterioration. This is characteristic of mechanical valves whether they are aortic or mitral valves.[16] Because of the long-term durability of me‐ chanical prostheses a valve replacement rate is less than 2% over 25 years. The most com‐ mon reasons for reimplantation are pre- and postoperative endocarditis, paravalvular leak and valve thrombosis.[17] *Bioprosthetic valves* are not as durable, have a shorter lifespan and are more susceptible to calcification than human and mechanical valves.[13] Biopros‐ theses have a significantly higher rate of reoperation due to structural valve deterioration. In large series, freedom from reoperation is > 90% at 10 years, but < 70 % at 15 years. [17,18,19] There is an important predisposition for premature bioprosthetic structural valve deterioration in younger patients, especially those under the age of 40 years.[17]

during extended follow-up. However, as seen in other studies, LV mass regression after stentless valve implantation was not different from stented aortic bioprostheses.[3,14]

(a) (b) (c)

**Figure 3.** Biological prosthesis: a) stented porcine bioprosthesis, b) pericardial bovine bioprosthesis and c) stentless

The Ad Hoc Liaison Committee for Standardizing Definitions of Prosthetic Heart Valve Morbidity of the American Association of Thoracic Surgery and the Society of Thoracic Surgeons published guidelines during years, which are now widely used in reporting outcomes after valve surgery. They presented a list of developing specific valve-related events

**Structural valvular deterioration** - Any change in function or deterioration (a decrease of one New York Heart Association functional class or more) of an operated valve due to an intrinsic abnormality, which causes stenosis or regurgitation. Changes intrinsic to the valve include wear, fracture, poppet escape, calcification, leaflet tear stent creep and su‐ ture line disruption of the components of the operated valve. The definition excludes changes due to infection or thrombosis. *Mechanical prostheses* are extremely resistant to ma‐ terial fatigue or structural valve deterioration. This is characteristic of mechanical valves

porcine bioprosthesis

368 Calcific Aortic Valve Disease

**4. Outcomes after aortic valve replacement**

**1.** Structural valvular deterioration

**2.** Nonstructural dysfunction

**5.** Valvular endocarditis and

**6.** Bleeding events.[7, 15]

**3.** Valve thrombosis

**4.** Embolism

during patients remaining lifetime. These valve-related events are:

**Nonstructural dysfunction** - Any abnormality that is not intrinsic to the valve per se, which causes stenosis or regurgitation. Examples for this include entrapment of pannus, tissue or suture; paravalvular leak; inappropriate sizing or positioning; residual leak and clinically important hemolytic anemia. This definition also excludes changes due to infection and thrombosis. Subvalvular pannus formation is rare with *mechanical bileaflet valves.*[20] Panus overgrowth and prosthetic structural degeneration interfering with normal valve opening and closure may cause hemolysis severe enough for reoperation. Paravalvular leak is an operative complication and it is related to operative technique and to endocarditis.[21]

**Valve thrombosis** – Any thrombus, in the absence of infection, which is attached to or near an operated valve that occludes part of the blood flow path or that interferes with function of the valve. The incidence of prosthesis thrombosis is < 0.2 % per year and it occurs more often in *mechanical prostheses.*[22] It is most commonly due to inadequate anticoagulation or noncom‐ pliance. Freedom from valve thrombosis at 20 years is > 97 %.[23,24]

**Embolism** – Any embolic event that occurs, in the absence of infection, after the immediate peri-operative period. This could be either a neurologic or peripheral embolic event. A neurologic event includes any new, temporary or permanent focal or global neurologic deficit. A peripheral embolic event is due to an embolus that produces symptoms from obstruction of a peripheral (non-cerebral) artery. The incidence of thromboembolic events between biopros‐ theses and mechanical prostheses are the same.[25] This is a continuous risk factor that is present through the life of patients with *mechanical valve prosthesis*, so they must maintain therapeutic anticoagulant levels. The embolic risk is highest in the first few months, before the ring and valve components have fully endothelialized.[26] Acceptable thromboembolic rates range between 0.8 and 2.3 % per patient-year.[21,22,25] 50 % of these events are neurologic, 40 % are transient and 10 % are peripheral.[21]

**Valvular endocarditis** – Any infection involving an operated valve diagnosed by customary clinical criteria. It is rare case with prophylactic antibiotics. Around 60 % of events occur early and are associated with staphylococci. The mortality for this event is high. Freedom from endocarditis with mechanical prosthesis is 97 to 98 % at 20 to 25 years. A number of studies have reported a higher incidence of valvular endocarditis after *mechanical valve* replacement in comparison with the biologic valve replacement during the initial few months after implantation. *Bioprostheses* are less susceptible to early infection, which is often restricted to the leaflets, making cure with antibiotics more likely but increasing the chances of late failure due to degeneration of the cusps.[27,28,29]

**Bleeding event** – Formerly classified as anti-coagulant hemorrhage, a bleeding event is an episode of major internal or external bleeding that causes death, hospitalization, and perma‐ nent injury or requires transfusion. This definition applies to all patients, irrespective of anticoagulation status. *Mechanical valves* are durability but anticoagulation is key of long-term success. International Normalized Ratio (INR) is the standard to which anticoagulation levels should be targeted. Level of INR should be individual for each person. Complications occur during fluctuations in the INR and less during steady-state levels, be they high or low.[30,31] When levels of INR increase, bleeding episodes become more common, and when levels of INR decrease thromboembolic episodes become more common. Some studies showed that around 40 % of the bleeding episodes occurred in the first year after surgery, when levels of INR are more likely to fluctuate. Many studies suggested that in the early postoperative period slowly raise the level of INR to therapeutic levels is needed, to prevent bleeding events. [21,32,33] According to ACC and ACH after mechanical AVR, the goal of antithrombotic therapy is usually to achieve an INR of 2.5 to 3.5 for the first 3 months after surgery and 2.0 to 3.0 beyond that time. At that level of anticoagulation, the risk of significant hemorrhage appears to be 1% to 2% per year.7 Low-dose aspirin is also indicated in addition to warfarin to result in a lower incidence of thromboembolic event, with a low possibility for bleeding.[34] Older patients are at higher risk for thromboembolic event because of the greater number of risk factors that accumulate with aging.[30] Anticoagulation-related hemorrhage (ARH) is the most common valve-related event. More often it will occur during fluctuations in INR, which happens most often early after valve replacement.[21,22] The most common places for ARH are gastrointestinal tract and central nervous system.[21] Acceptable ARH rates range from 1.0 to 2.5% per patient-year in long term reports.[21,22,25,35] It is very dangerous complication, because mortality more often occurs in relation to bleeding events than in relation to throm‐ boembolic events.[21]

**5. Factors affecting long-term outcome after AVR**

**◦** Higher pre-operative NYHA functional class

**◦** Longer cardiopulmonary bypass time

**◦** Previous myocardial infarction

**◦** Previous aortic valve surgery **◦** Coronary artery disease (CAD)

**◦** Pure aortic regurgitation

**◦** Hypertension

**◦** Renal failure **•** Surgery-related

**•** Morphological

**6. Patient selection**

**◦** Diabetes mellitus

**◦** Pre-operative atrial fibrillation and non-sinus rhythm

**◦** Left ventricular structure and functional abnormality

Older patients have a lot of comorbiditis and they are at higher risk for valve-related events. Atrial fibrillation is one of the risk factor for thromboembolism, because of that INR levels must be higher (INR 2.5 to 3.5) than regular.[30,34] The majority of patients undergoing AVR have other cardiac lesions, most commonly CAD, and more complex pathology has been associated with increased risk. Combined myocardial revascularization and AVR increases cross-clamp time and has the potential to increase perioperative myocardial infarction and

to severity of CAD and AS, the multivariate factors for late postoperative mortality include low ejection fraction, severity of LV dysfunction, age greater than 70 years (especially in

Propter selection of patients for valve replacement can bring us excellent long-term results,

In addition

Surgical Valve Replacement (Bioprosthetic VS Mechanical)

http://dx.doi.org/10.5772/53687

371

early postoperative mortality compared with patients undergoing isolated AVR.7

women), and presence of NYHA functional class IV symptoms.[36]

long-term survival and low incidence of valve-related complications.

**•** Demographic **◦** Older age **◦** Male sex

**•** Clinical

**Operative mortality** – Operative mortality is defined as all-cause mortality within 30 days of operation. According to the Society of Thoracic Surgeons mortality for isolated AVR is 4.3% and for AVR with concomitant coronary artery disease is 8%.[36] Many factors have been associated with an increased risk of operative mortality in isolated AVR. Some of these risk factors are age, female gender, diabetes, renal failure, and emergency status, previous operation, advanced preoperative NYHA class, lower cardiac index, concomitant coronary artery bypass grafting and longer aortic crossclamp and cardiopulmonary bypass time respectively.[37] In the absence of major comorbidities and preserved ejection fraction, isolated AVR can be performed with an expected mortality of less than 2%.[38]

Several studies have evaluated independent risk factors for operative mortality after AVR. Five variables predictive of increased mortality risk after AVR are common to each of these analyses: preoperative renal failure, urgency of AVR, preoperative heart failure, presence of CAD or recent MI, and redo cardiac operation. Other factors independently associated with operative mortality from the individual studies include preoperative atrial fibrillation, active endocarditis, preoperative stroke, advanced age, lower body surface area, multiple valve procedures, and hypertension. [39, 40]
