Aortic Stenosis

Echocardiography is the most efficient technique to evaluate the degree of stenosis, LV hypertrophy, and LV function in patients with aortic valve stenosis.¹² The American College of Cardiology/American Heart Association Task Force on Practice Guidelines has graded the degree of aortic stenosis as mild (effective valve area >1.5 cm²), moderate (area >1 to 1.5 cm²), or severe (area ≤1 cm²).¹³ When stenosis is severe and cardiac output is normal, the mean transvalvular pressure gradient is generally greater than 50 mm Hg. Symptomatic patients (dyspnea, angina, or palpitations) with severe stenosis are candidates for surgery (class 1 recommendation), as are asymptomatic patients with reduced ventricular function (left ventricular ejection fraction [LVEF] <50%) or patients undergoing any other cardiac surgery (CABG, mitral valve, or thoracic aorta). When cardiac output is reduced, transvalvular gradient is reduced (low flow/low output), and estimation of the severity of the stenosis may require advanced diagnostic tools such as stress test, echocardiography, or pressure measurement in the cath lab. An accurate estimation of the degree of stenosis is essential in those patients with low cardiac output who, despite being at high risk for surgery, do better than with medical treatment if correctly diagnosed.¹⁴

Management of patients with coronary artery disease who will have CABG and are incidentally diagnosed with mild to moderate aortic stenosis during workup is controversial. For asymptomatic patients with mild aortic stenosis (mean gradient between 30 and 50 mm Hg) who require CABG, it may be reasonable to replace the valve (class IIa recommendation). For patients with lower mean gradient, leaving the native valve is advised unless there is a risk of rapid progression, such as important calcification (class IIb).¹⁵ In very high risk patients, transcatheter aortic valve implantation (TAVI) is presently in its evaluation phase.¹⁶

Aortic Regurgitation

Chronic aortic regurgitation is usually well tolerated, and pure regurgitation is not considered for surgery unless severe (i.e., regurgitant volume >60 mL per beat or regurgitant orifice >0.3 cm²) in a symptomatic patient at rest (class I) or on exercise testing (class I) or in an asymptomatic patient with LV dysfunction (LVEF <50%) (class I) or with LV enlargement (end-systolic diameter >55 mm or end-diastolic diameter >75 mm) (class IIa).¹³ Symptomatic patients with mild aortic regurgitation should be investigated for other causes (ischemic cardiomyopathy). Regurgitation due to cusp lesions such as calcifications or destruction due to endocarditis are indications for valve replacement, except perhaps in very experienced hands in which repair is sometimes performed. Regurgitation due to annular enlargement with none or very little cusp lesion is now usually repaired with good results.^17,18 In the latter, annular enlargement is often concomitant with ascending aortic enlargement, and the aorta is replaced by a valve conduit if repair is not feasible or by a straight Dacron tube, with the native valve resuspended.¹⁹

Mitral Stenosis

Moderate or severe mitral stenosis (mitral valve area ≤1.5 cm²) in symptomatic patients is usually treated with percutaneous mitral balloon valvuloplasty, except when there is concomitant moderate to severe mitral regurgitation, left atrial thrombus, or the valve is not suitable for a percutaneous approach (echo score > 8); in the latter case, mitral valve replacement is performed.

Mitral Regurgitation

Mitral regurgitation is responsible for pulmonary hypertension, left atrial enlargement with atrial fibrillation, and excessive workload on the heart, leading to dyspnea. Much work has been done on the mechanisms and causes of mitral regurgitation, pioneered by Carpentier and colleagues in the early 1980s; advances include the development of repair techniques other than systematic valve replacement. In experienced hands, more than 90% of regurgitant valves are repaired, avoiding problems associated with prosthetic valves (degeneration, need for anticoagulation, prosthetic valve infection). The lower morbidity related to valve repair has broadened the indication for mitral valve surgery to asymptomatic patients with no ventricular dysfunction and no pulmonary hypertension or atrial fibrillation, if the regurgitant surface is more than 40 mm. In those patients, repair is mandatory, whereas in patients with any of the aforementioned complications of regurgitation, replacement is an option.^20,21 Recently, minimally invasive approaches through a 5-cm thoracotomy have been successfully applied to mitral repair and are gaining wide acceptance.^22,23

Most mitral valves successfully repaired suffer from structural abnormalities and are identified as organic mitral regurgitation. Functional mitral regurgitation is the term used when the valve has no anatomic defect but is incompetent secondary to LV dysfunction, annulus dilation, or papillary muscle dysfunction. In some cases, CABG alone may improve LV function and reduce mitral regurgitation. Some advocate the use of ring annuloplasty or ventricular reduction surgery, but results are less convincing than in structural disorders.²⁴

In long-standing mitral regurgitation, chronic right ventricular overload causes tricuspid regurgitation and atrial enlargement, promoting atrial fibrillation. Tricuspid regurgitation and atrial fibrillation also have to be assessed during the intervention, with a tricuspid annuloplasty and lesions made to the atria to stop reentrant circuits causing the arrhythmia.^25,26

Ascending Aorta

Dilation of the ascending aorta is associated with hypertension, atherosclerotic disease, and structural (bicuspid aortic diseases)²⁷ and genetic factors that arise with entities such as Marfan or Ehlers-Danlos syndromes. When reaching threshold values²⁸ or when rapidly enlarging, dilated ascending aortas present a risk of rupture and dissection, prompt surgery is indicated.²⁹ In patients with structural arterial wall abnormalities, surgery is warranted when the largest diameter is 45 mm, while in general population 55 mm is the cutoff value for surgery.³⁰

Dissection of the ascending aorta presents in almost every patient with pain, cardiac tamponade, or acute or poorly tolerated aortic regurgitation requiring urgent surgical correction.

Axillary cannulation and selective cerebral perfusion have permitted more thorough repair of aneurysm and dissection of the ascending aorta, prolonging in the aortic arch. Actual development is directed towards one-step treatment of the entire thoracic aorta.³¹

Miscellaneous

Besides the indications discussed, some less frequent conditions can be encountered, which are usually referred to centers with specific expertise. Surgery for terminal heart failure, long dominated by heart transplantation, is nowadays (mainly because of organ shortage) a field of active research for the ideal mechanical substitute to be used as a bridge to transplantation or as a definitive organ substitute (destination therapy).

Large pulmonary emboli unresponsive to thrombolysis can be surgically removed from the pulmonary arteries, as can the organized fibrotic material found in chronic thromboembolic disease. Isolated tricuspid disease, rhythm restoring surgery, and adult congenital surgery are other indications.

Bleeding and Cardiac Tamponade

Hemostasis is deeply altered after cardiac surgery under CPB.³² Problems include decreased platelet numbers and function and activation of the coagulation and fibrinolytic cascade. All these factors, associated with cytokine activation and kallikrein stimulation of neutrophils, lead to a propensity for patients to bleed after the procedure.

Besides careful surgical techniques, diffuse bleeding can be prevented.³³ Patients should be rapidly rewarmed at 37°C, since hypothermia inhibits coagulation and alters platelet function. Arterial hypertension should be aggressively treated in the first 24 hours with short-acting drugs. Even if transfusion affects long-term outcome,^34–36 one should not be afraid to transfuse blood components: packed red blood cells, platelets, and plasma are to be given in a bleeding patient even before coagulation results are available. Correction of fluid deficits with crystalloid or colloid infusion induces some degree of hemodilution, contributing to altered hemostasis. If the patient is bleeding, correcting hemostasis according to lab results actually corrects a past situation, so blood components must be given on an empirical basis. When the coagulation tests are available, specific measures are taken; prolonged partial thromboplastin time (PTT) should be treated with a protamine supplement first, before fresh frozen plasma (FFP) is considered. Whereas prolonged prothrombin time is treated with FFP and cryoprecipitate, low platelet count should be corrected by platelet transfusion. A normal platelet count does not exclude platelet dysfunction, so a platelet transfusion may be indicated even in the presence of a normal platelet count if the patient had been treated by antiplatelet agents, is uremic, or is suspected of von Willebrand disease. In the latter patients, the use of desmopressin is warranted. The use of aprotinin, once commonly given to reduce bleeding in cardiac surgery, has been abandoned in view of its serious side effects.

Blood losses must be monitored as long as drains are in place. Reoperation must be considered if the bleeding rate exceeds 300 mL/h for 3 consecutive hours or 1000 mL/h during the first 4 to 5 hours after the procedure in adult patients. Early reexploration for bleeding is indicated in 0.5% to 5% of cardiac surgery patients, depending on institutional criteria. Early reoperation generally stops the bleeding even if no bleeding origin is found.

Cardiac tamponade may occur if excessive bleeding persists. To prevent it, chest drainage must be placed properly in the operating room, and aspiration must be applied early to avoid blood accumulation in the pericardium and pleural space. Hypotension and pulsus paradoxus are early signs of tamponade; suspicion should be high if the bleeding abruptly decreases, and transesophageal echo is mandatory to diagnose it. Tamponade can result from circumferential effusion or from a local hematoma compressing the left or right atrium. Delayed cardiac tamponade may also occur within days after cardiac surgery. If required, drainage is performed via a reopening of the incision below the xiphoid process.

Myocardial Dysfunction After Cardiac Surgery

Most cardiac interventions are done under cardiac arrest; the heart is isolated from the circulation and hence not perfused for some time, causing ischemia-reperfusion injury. Schematically, there is an overload of intracellular calcium during ischemia and generation of reactive oxygen species during reperfusion. This cellular environment is responsible for various protein activation, leading to depressed cellular contractility (myocardial stunning), apoptosis, or cell necrosis. Various forms of myocardial protection have been developed to prevent myocardial injury, including intermittent cross-clamping, cold crystalloid, or cold or warm blood cardioplegia. While cold blood cardioplegia is the most used technique worldwide, it should be emphasized that there is no definitive evidence favoring one strategy over another.^37,38 Failing to protect the myocardium during surgery leads to 2% to 7% of diffuse ventricular failure. Although most patients will respond to inotropic support and recover global function after a few hours or a few days—depending on the extent of injury—patients with extensive apoptosis and necrosis evidenced as cardiac marker elevation will have a statistical survival impairment. Patients with preoperative cardiac dysfunction and diffuse coronary disease are more at risk for myocardial protection deficit. Segmental myocardial zones might be electively damaged in incomplete revascularization, technical failure to complete anastomoses, or distal disease impeding delivery of the cardioplegic solution. STEMI and NSTEMI may occur, requiring specific treatment, possibly including the need for coronary angiogram. Electrocardiographic (ECG) interpretation is difficult in the perioperative period, and biomarker assays are delayed.³⁹ Liberal use of echocardiography is advised to discern segmental ischemia from diffuse dysfunction; any other causes of low cardiac output will be diagnosed along.

Treatment involves preload, afterload, and rhythm optimization and administration of inotropic agents like dobutamine and levosimendan.⁴⁰ Should all these measures fail, the use of mechanical devices to support the circulation is indicated. All devices have advantages and risks. The first device generally considered is the intraaortic balloon pump (IABP). Contraindications include aortic regurgitation, dissecting thoracic aortic aneurysm, and synthetic thoracic aortic graft. At best, cardiac output may be increased by 20% by an IABP, depending on the extent of myocardial injury and preexisting myocardial function. If the IABP fails to increase cardiac output to a sufficient level, one should consider the insertion of an extracorporeal membrane oxygenation^41,42 and/or a ventricular assist device.^43,44 These supports generally require anticoagulation to avoid embolic complications and may induce severe hemorrhagic complications.