Aortic Valve Disease


Article Author:
Peter Wenn


Article Editor:
Roman Zeltser


Editors In Chief:
David Wood
Andrew Wilt
Hajira Basit


Managing Editors:
Avais Raja
Orawan Chaigasame
Khalid Alsayouri
Kyle Blair
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Abbey Smiley
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beenish Sohail
Hajira Basit
Phillip Hynes
Sandeep Sekhon


Updated:
11/5/2019 3:42:41 PM

Introduction

There are two primary pathologies of the aortic valve; the valve can either be stenotic or insufficient (aka regurgitant). When the valve leaflets become stiff, it leads to a reduced orifice and the pressure gradient across the valve increases, sometimes leading to decreased anterograde flow during systole; this can lead to a number of clinical consequences usually beginning with left ventricular hypertrophy which can later include dilation, decreased cardiac output, arrhythmias, ischemia, etc. Aortic insufficiency occurs due to inadequate closure of the aortic valve during diastole leading to retrograde flow of blood from the aorta into the left ventricle. The consequences of this are an increase in left ventricular end diastolic volume and wall stress.

Etiology

There are two common causes of aortic stenosis (AS), calcified (age-related) aortic stenosis and congenital bicuspid aortic valves. Rarely aortic stenosis and/or aortic regurgitation can be a result of rheumatic heart disease, although this is more commonly a disease of the mitral valve and generally seen in developing countries. Calcified aortic stenosis is by far the most common etiology and is believed to occur via progressive endothelial damage over many years.

 Aortic regurgitation can occur in a chronic or acute setting. Causes of acute aortic regurgitation include type A aortic dissection extending to the valve or damage to leaflets from infectious or noninfectious endocarditis. The same pathologies most commonly cause chronic aortic regurgitation in developing countries as aortic stenosis; calcific disease, congenital bicuspid valve issues, and Marfan syndrome. Other less common etiologies include complications following percutaneous aortic balloon valvuloplasties and transcatheter aortic valve replacements (TAVR) as well as a slew of inflammatory disorders including but not limited to systemic lupus erythematosus, rheumatoid arthritis, and Takayasu arteritis. The most prevalent etiology of chronic aortic regurgitation in developing countries is rheumatic heart disease.[1][2]

Epidemiology

Aortic stenosis is a condition more prevalent in the elderly population (fifth through eighth decades). According to a prospective population-based study, the incidence of aortic stenosis was 0.2% during the fifth decade of life, 1.3% during the sixth, 3.9% during the seventh and 9.8% during the eight. When comparing the subset of patients with congenital anatomic malformations of the aortic valve to those patients with normal anatomy in those who underwent surgery for isolated aortic stenosis, the fraction of abnormal valves decreased with increasing age. In post surgery patients less than 50 years of age, two-thirds were found to have a bicuspid valve while one-third had unicuspid, ages 50 to 70 saw two-thirds of patients with bicuspid, but one-third had normal tricuspid anatomy, and in patients, greater than 70 years of age 60% had tricuspid valve, and 40% had bicuspid.

Aortic regurgitation has an estimated prevalence of 4.9%, also increasing with age until the sixth decade when incidence begins to decrease. This number, however, may be artificially low because up to 75% of aortic stenosis patients may have some degree of regurgitation that goes unreported.[3][4]

Pathophysiology

Narrowing of the valve in aortic stenosis occurs due to the fusion of the leaflets or calcifications that cause the valve to have decreased mobility and obstruct the orifice. Calcified aortic stenosis occurs via progressive endothelial damage that can cause inflammation and infiltration of macrophages and other inflammatory cells initially. This inflammation and damage lead to profibrotic factors that establish a collagen matrix which not unlike bone formation later becomes calcified. The most common consequences of aortic stenosis stem from decreased anterograde flow from the left ventricle into the aorta, leading to a back up of blood in the left ventricle and increased left ventricular pressures. This backflow can cause symptoms of heart failure beginning with left atrial dilation and mitral regurgitation, and eventually leading to pulmonary edema and right-sided heart failure. A healthy aortic valve measures 3 to 4 cm; symptoms generally do not precipitate until the valve area has decreased to less than 1.0 cm. The more severely stenotic the valve becomes, the more difficult it becomes to maintain adequate cardiac output. The left ventricle undergoes hypertrophy and remodeling, which can lead to increased left ventricular oxygen demand; this coupled with decreased cardiac output can lead to ischemia and arrhythmias as well as decreased cerebral perfusion.

Aortic regurgitation leads to retrograde flow of blood from the aorta into the left ventricle, an increase in left ventricular volume and dilation of the chamber. Initially, this leads to an increase in cardiac output and is maintainable for a prolonged period. However, this increase in cardiac output leads to distention and increased pressure in peripheral arteries, causing increased peripheral systolic pressure. Eventually, this causes worsening of the regurgitation which can give rise to a rapid decrease in peripheral systolic pressure and in severe disease cardiovascular collapse (this phenomenon is what causes the characteristic wide pulse pressure in severe aortic regurgitation).[5][6][7]

History and Physical

An in-depth history and thorough physical exam are essential, and commonly, the first line of diagnosis for aortic valvulopathy. Symptoms of aortic stenosis or regurgitation often are not present or are too mild for the patient to notice until the pathology has become severe. Due to this, a careful cardiac physical exam is essential for early detection.

For aortic stenosis, a systolic ejection murmur can often be heard best over the right sternal border at the second intercostal space. This murmur will peak early during systole when the disease is mild, and as severity increases will peak later, it also tends to radiate to the carotid arteries along with a slowly rising carotid upstroke. Auscultation often reveals a sustained apical impulse as well. In severe disease states, a thrill can sometimes be palpated over the carotid arteries and aortic area. Additional physical exam findings due to complications and sequelae of aortic stenosis include those associated with heart failure and left ventricle remodeling, such as third and fourth heart sounds, pulmonary crackles, jugular venous distention, and pedal edema.

Aortic regurgitation when acute and/or severe can be suspected when the patient has a wide pulse pressure and a low pitched early diastolic murmur is auscultated again over the right sternal border at the second intercostal space. Accentuated P2 may also be noticed due to elevated pressures in the pulmonary vasculature. Chronic aortic regurgitation may illicit a blowing diastolic decrescendo murmur with a positive correlation between duration of murmur and severity of the disease. Often auscultation of a laterally and inferiorly displaced apical impulse is present and sustained. Often there is the phenomenon of Corrigan pulse (water hammer), a bounding and forceful pulse that rapidly increases and collapses. Other less common physical exam findings include de Musset sign, which is subtle head bobbing with a pulse as well as Quincke sign and Muller sign (pulsations on the fingernails and uvula respectively). Similar physical exam findings to aortic stenosis can also be seen late in disease progression. Acute aortic regurgitation will present differently depending on the etiology. If a patient presents with tearing severe chest pain along with physical exam findings such as variation in blood pressure between the right and left extremities, consider aortic dissection as a cause. If the patient presented with a history of streptococcal infection along with fevers, swollen and tender joints, skin nodules, new onset of rash then rheumatic heart disease would be high on the differential.

Chronic aortic regurgitation and late in disease progression of aortic stenosis symptoms generally fall into two categories; heart failure and decreased coronary and systemic perfusion. Overtime increased pressures in the left ventricle lead to congestive heart failure; patients may complain of pedal edema, shortness of breath, orthopnea, paroxysmal nocturnal dyspnea, and exertional dyspnea. Patients may state that they require additional pillows at night to sleep because lying flat causes them to be short of breath. Additionally, patients may complain that they have decreased exercise tolerance, the number of city blocks they can walk before feeling short of breath or lightheaded decreasing. In severe disease states, patients may present with syncope or may also complain of anginal symptoms.[8][9]

Evaluation

Diagnosis is first suspected based off either patient subjective history or incidental finding on physical exam. Once there is suspicion of valvular disease, a 2D echocardiogram with doppler study would be the gold standard test. There are three major parameters measured to evaluate the competency of the aortic valve during an echocardiogram; the aortic jet velocity, mean aortic valve pressure gradient and the aortic valve area. These values are used in conjunction with the presence or absence of symptoms to determine the severity of the aortic disease. Other existing comorbidities and/or sequela can be investigated using imaging such as cardiac CT or MRI, stress testing, blood cultures for suspected endocarditis or rheumatic disease.[10]

Treatment / Management

There is no medical management which can delay the progression of asymptomatic aortic valve disease. Management is a two-prong approach focusing on optimizing other cardiac comorbidities such as hypertension, coronary artery disease, left ventricular dysfunction, atrial fibrillation and other arrhythmias and vigilante serial evaluation to monitor for disease progression and early detection of symptoms. Patients with Stage B mild aortic valve disease should have echocardiograms every 3 to 5 years, moderate every 1 to 2 years. For patients with stage C1 severe asymptomatic disease, echocardiography is necessary every 6 to 12 months. Regardless of stage, the development of new symptoms will always warrant immediate evaluation.

Valve replacement for aortic stenosis is the recommendation for asymptomatic patients (evidenced by history and/or stress testing) with a high-gradient disease or asymptomatic patients with severe AS (C2) and a left ventricular ejection fraction less than 50%. Indications for valve replacement for stenotic patients include any patients with severe stenosis (C or D) who are undergoing other cardiac surgery. New guidelines also show that aortic valve replacement is reasonable in a subset of patients:

  • Asymptomatic (C1) with severe AS and decreased exercise tolerance or exercise fall in blood pressure
  • Symptomatic patients with low flow/low gradient and reduced LVEF (D2) but a low dose dobutamine stress study showing aortic velocity greater than 4 m/s (or mean pressure gradient greater than 40mm Hg) and a valve area less than 1cm2
  • Symptomatic patients with low flow/low gradient severe AS (D3) who are normotensive and have LVEF greater than 50%, if clinical, hemodynamic and anatomic data support valve obstruction as the most likely cause of symptoms
  • Moderate AS (B) who are undergoing other cardiac surgery; valve replacement may be a consideration for asymptomatic patients with severe AS (C1) and evidence of rapid disease progression with low surgical risk.

Valve replacement for the treatment of aortic regurgitation is indicated for symptomatic patients with severe AR regardless of LV systolic function (D), asymptomatic patients with chronic severe AR and evidence of LV systolic dysfunction (EF less than 50%; ie C2),  and patients with severe AR (C or D) while undergoing cardiac surgery for any other indication. Valve replacement is reasonable for:

  • Asymptomatic severe AR patients  and normal LV systolic function (EF greater than 50%) but severe dilation of the left ventricle (left ventricular end diastolic pressure greater than 50mm Hg; i.e., C2)
  • Moderate AR patients (B) who are undergoing other cardiac surgery
  • Asymptomatic patients with severe AR and normal LV systolic function (C1) but with evidence of progressive severe LV dilation (greater than 65 mm) if the surgical risk is low

Patients, whom life expectancy after the replacement is less than one year and/or quality of life is not expected to improve, would not be candidates for valve replacement. However, if life expectancy is greater than one year, and predictions include improvement in the quality of life, there are two methods for aortic valves replacement, surgical or transcatheter. Transcatheter aortic valve replacement is only indicated for aortic stenosis, not for aortic regurgitation. Electing one method over the other is determined by evaluating the morbidity and mortality risk of surgical valve replacement, often utilizing the Society of Thoracic Surgeons Predicted Risk of Mortality (STS-PROM). If the risk of serious complication or death is greater than 50% transcatheter aortic valve replacement (TAVR) is the preferred option. If the surgical risk is less than 50%, the consensus has been that SAVR is the preferred method. However, several studies are now showing that there is no difference in morbidity and mortality one year post-op between SAVR and TAVR and that TAVR is safe to use in any patient regardless of the risk level. There is one other procedure that sees occasional use for aortic stenosis patients, that is a balloon valvuloplasty.[11][12][13][14][15] This procedure involves balloon inflation in the valve orifice in an attempt to widen the valve, used only as a temporary bridge to valve replacement for hemodynamically unstable patients or for palliative/symptomatic relief in patients who are not surgical candidates. The indications for valve replacement will be addressed in the staging portion of this review.[15][16][17]

Differential Diagnosis

The differential diagnosis for patients presenting with aortic valve disease symptoms includes but is not limited to hypertrophic obstructive cardiomyopathy, restrictive/constrictive cardiomyopathies, congestive heart failure with reduced ejection fraction (HFrEF), coronary artery disease, atrial fibrillation/flutter, ischemic heart disease, pericardial effusion, and pulmonary hypertension. Non-cardiac disorders considered for inclusion in the differential are chronic obstructive pulmonary disease, restrictive lung diseases, symptomatic anemia, and hemoglobinopathies.

Pertinent Studies and Ongoing Trials

Transcatheter aortic valve implantation vs. surgical aortic valve replacement for the treatment of severe aortic stenosis: a meta-analysis of randomized trials showed reduced mortality with TAVR as compared to SAVR, with data being most significant in transfemoral TAVR.[18]

Staging

Chronic aortic disease is staged A to D. Stage A (at risk) is a patient with no change in hemodynamics of the valve and no symptoms but the presence of at least one risk factor; i.e., bicuspid valve, sclerotic valve, history of rheumatic fever, etc. Stage B (progressive) has mild hemodynamic changes with or without left ventricular dilation of early left ventricular diastolic dysfunction along with the presence of known risk factor, but the patient remains asymptomatic. Stage C1 (asymptomatic severe) includes severe hemodynamic changes on echocardiogram, presence of left ventricular diastolic dysfunction, without decrease left ventricular function and no symptoms in daily life (however symptoms may be precipitated with exercise stress testing). Stage C2 has the same hemodynamic parameters as C1 with the presence of depressed left ventricular ejection fraction (under 50%).  Stage D1 (symptomatic severe) is high gradient (Vmax less than 4m/s) with left diastolic dysfunction, left ventricular hypertrophy and potentially pulmonary hypertension accompanied by angina or heart failure symptoms on exertion. D2 (symptomatic severe) is low flow/gradient with reduced left ventricular ejection fraction (Vmax greater than 4m/s), decreased left ventricular ejection fraction (under 50%) and symptoms at rest. D3 (severely symptomatic ) is the last stage and characteristically presents with a low gradient with normal left ventricular ejection fraction (aka paradoxical low flow), ejection fraction less than 50% is present, but stroke volume is less than 35mL/min; consequence small left ventricular chamber and restrictive diastolic filling. Stage D3 aortic stenosis also has symptoms at rest.[19][20][21]

Prognosis

Prognosis is largely determined by time of onset to symptoms. Asymptomatic patients who do not progress to symptomatic have a longer life expectancy. Prognosis of patients with severe symptomatic aortic valve disease who do not undergo valve replacement is very poor, with survival at 3 years ranging from approximately 40 to 60%, whereas those who underwent valve replacement ranging from 80 to 90% survival.[22]

Enhancing Healthcare Team Outcomes

The difficulty with diagnosing and treating aortic stenosis lies with the vast array of nonspecific symptoms the patient may present with, creating a substantial differential. In patients with whom cardiac comorbidities do not exist, and patients do not regularly see a cardiologist the duty often falls on the primary care physician to perform a proper physical exam that includes auscultation of the heart as the first step in diagnosing asymptomatic aortic valve disease. If symptoms or physical exam findings warrant suspicion, it is vital to send the patient for an echocardiogram and consult a cardiologist for proper staging. A significant responsibility also falls on the patient to give a detailed history and description of symptoms and their progression. The sooner those symptoms are identified, and management initiated, the better the outcome for the patient’s long term survival.

Proper management of comorbidities by primary care physicians, nurses, and other specialists is essential in ensuring the patient is optimized for surgery if necessary.

In summary, caring for patients with aortic valve disease requires an interprofessional team approach, including physicians, specialists, specialty-trained nurses, and pharmacists, all collaborating across disciplines to achieve optimal patient results. [Level V]


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Aortic Valve Disease - Questions

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When is surgery required in a patient with aortic stenosis?



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You are examining a 67-year-old female with heart disease. She is a poor historian and other than telling you she has heart disease and shortness of breath, she is unable to provide any medical history. She has asked that you read her medical chart, which you apparently cannot find. You start off with the physical exam and observe that her pulse is characterized by two systolic peaks separated by a mid-systolic dip. You are most likely to observe such a pulse in a patient with what disorder?



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An 86-year-old female with a history of hypertension, obstructive sleep apnea, diabetes, and heart failure presents to the clinic for follow up. She had a surgical aortic valve replacement for severe symptomatic aortic stenosis 12 years ago. She complains that she is getting progressively short of breath with exertion. Her EKG shows left ventricular hypertrophy, which is unchanged when compared to previous EKGs. A repeat echocardiogram shows a left ventricular ejection fraction of 40% which was 50% six months earlier, a bioprosthetic aortic valve which is severely stenotic and evidence of mild mitral regurgitation. She has no history of coronary artery disease or peripheral artery disease. She has a 30-pack-year history of smoking but quit 15 years ago. She has a predicted risk of mortality of 18.06% by the society of thoracic surgeons (STS-PROM). Which of the following is the most appropriate therapeutic approach for this patient?



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A 70-year-old male with no history of cardiac symptoms has an echocardiogram performed to evaluate a systolic ejection murmur auscultated on physical exam and is found to have a stenotic aortic valve measuring 1.1 cm2 with a Vmax of 2.7 m/s and an ejection fraction of 55%. A stress test with echocardiogram is performed to evaluate the degree of aortic stenosis further. The gradient across the valve is unchanged. However, a drop in systolic blood pressure of 20 mmHg and anterior wall motion abnormality of the left ventricle along with ST-segment depression in anterior leads is observed. The patient is sent for cardiac catheterization to evaluate for coronary artery disease and is found to have greater than 90% occlusion of the ostial left anterior descending artery. He is scheduled for a coronary artery bypass graft. Which of the following is the most appropriate step in treating the patient’s aortic stenosis?



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A 61-year-old male is seen for the first time in the clinic complaining of chronic intermittent palpitations. EKG shows normal sinus rhythm at 82 bpm. The patient's current medications include tamsulosin and montelukast. An echocardiogram from 1 year ago was significant for a left ventricular ejection fraction (LVEF) of 65% to 70% with normal left ventricular diastolic and systolic function, and severe aortic stenosis. The patient is sent home with a Holter monitor for two weeks. When he returns for the results, it is noted that he had several episodes of paroxysmal atrial fibrillation. During these episodes, his heart rate ranged from 120 to160 bpm. Which of the following is the most appropriate option while considering anticoagulation for this patient?



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A 49-year-old African American male with a past medical history of hypertension and tobacco use presents to the emergency department complaining of left-sided tearing chest pain radiating to his back. The patient states that he ran out of his hypertensive medication approximately two weeks ago. The physical exam is pertinent for a patient in severe distress with a grade IV/VI diastolic decrescendo murmur heard best at the left 3rd intercostal space, which was not present at the previous outpatient visit one month ago. Vital signs are notable for a heart rate of 106/min, blood pressure 205/115 mmHg in the left arm, and 199/105 mmHg in the right arm. A bedside transthoracic echocardiogram is performed, showing a left ventricular ejection fraction of 55-60% and valvular heart diasease. Once hemodynamically stabilized, what is the definitive treatment plan for this patient?



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A 65-year-old female with a past medical history of type 2 diabetes presents to the hospital complaining of fevers and chills for the past three days. She also states that she has been dizzy intermittently during this time, with one syncopal episode occurring this morning, which prompted her to come to the emergency department. On physical exam, the patient is diaphoretic and oriented only to person. The patient's lungs are clear to auscultation with no signs of hypervolemia. Vital signs show a heart rate of 55 BPM, blood pressure of 92/60mmHg, afebrile, and oxygen saturation of 99% on room air. EKG is performed and shows a second-degree type 2 AV block. Initial blood cultures grow staph aureus. A transthoracic echocardiogram is performed and shows two large vegetations on the noncoronary cusp of the aortic valve. The patient is resuscitated with 3 liters IV bolus and started on IV vancomycin. What is the most appropriate subsequent treatment plan?



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Aortic Valve Disease - References

References

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