Aortic stenosis is a narrowing or obstruction of the aortic valve. With the aging of the United States population, diseases in the elderly are a major interest among health care professionals. Valvular aortic stenosis (AS) is no exception; senile degenerative aortic stenosis is now the leading indication for aortic valve replacement (AVR). The favorable long-term outcome following aortic valve surgery and the relatively low operative risk emphasize the importance of an accurate and timely diagnosis.
Stenotic aortic valve (macroscopic appearance).
The pathophysiologic mechanisms responsible for symptoms (ie, angina, syncope, congestive heart failure) in patients with aortic stenosis include an increase in left ventricular (LV) afterload, progressive LV hypertrophy, and a decrease in systemic and coronary flow as consequences of valve obstruction.
In adults with aortic stenosis, LV outflow obstruction increases gradually over a long period of time, during which time the patient is asymptomatic. This progressive outflow obstruction results in increased LV mass by parallel replication of sarcomeres producing concentric hypertrophy, which is a compensatory mechanism to normalize LV wall stress. Inadequate development of hypertrophy, depression of myocardial contractility, or a combination of these factors may lead to impairment of LV performance (so-called afterload mismatch) and congestive heart failure (CHF) symptoms. Indeed, wall thickness appears to be a critical determinant of ventricular performance in patients with aortic stenosis. If afterload mismatch occurs, the LV ejection fraction, cardiac output, stroke volume, and transvalvular pressure gradient decline.
In most patients with aortic stenosis, LV systolic function is preserved and cardiac output is maintained for many years despite an elevated LV systolic pressure. Despite the fact that cardiac output at rest is normal, it often fails to increase appropriately during exercise, which may result in exercise-induced syncope or near syncope.
In the patient with aortic stenosis, diastolic dysfunction may occur as a consequence of impaired LV relaxation and/or decreased LV compliance, as a result of increased afterload, LV hypertrophy, or myocardial ischemia. LV hypertrophy often regresses following relief of valvular obstruction. However, in some individuals, extensive myocardial fibrosis develops, which may not disappear despite regression of hypertrophy.
In patients with severe aortic stenosis, atrial contraction plays a particularly important role in diastolic filling of the LV. Thus, development of atrial fibrillation in aortic stenosis is often catastrophic to the maintenance of normal forward stroke volume.
Increased LV mass, increased LV systolic pressure, and prolongation of the systolic ejection phase all elevate the myocardial oxygen requirement, especially in the subendocardial region. Coronary blood flow at rest is increased but normal when corrected for LV mass; however, coronary flow reserve is often reduced. Myocardial perfusion is also compromised by the relative decline in myocardial capillary density and by a reduced diastolic transmyocardial (coronary) perfusion gradient due to elevated LV diastolic pressure. Therefore, the subendocardium is susceptible to underperfusion, which results in myocardial ischemia.
Aortic sclerosis (considered a precursor of calcific degenerative aortic stenosis) increases in incidence with age and is present in 29% of individuals older than 65 years and in 37% of individuals older than 75 years. In elderly persons, the prevalence of aortic stenosis is between 2% and 9%.
Patients with severe aortic stenosis may be asymptomatic for many years despite the presence of severe LV outflow tract obstruction. Such patients have a survival similar to those without aortic stenosis. With the appearance of symptoms, however, their survival is reduced; onset of angina is associated with an average survival of 5 years, syncope with an average survival of 2-3 years, and congestive heart failure with an average survival of 1.5-2 years.
Among symptomatic patients with medically treated moderate-to-severe aortic stenosis, mortality rates from the onset of symptoms are approximately 25% at 1 year and 50% at 2 years. More than 50% of deaths are sudden.
Asymptomatic patients, even with critical aortic stenosis, have an excellent prognosis regarding survival, with an expected death rate of less than 1% per year; only 4% of sudden cardiac deaths in severe aortic stenosis occur in asymptomatic patients.
Although the obstruction tends to progress more rapidly in patients with degenerative calcific aortic valve disease than in those with congenital or rheumatic disease, predicting the rate of progression in individual patients is not possible. Therefore, careful clinical follow-up is mandatory in all patients with moderate-to-severe aortic stenosis. Catheterization and echocardiographic studies suggest that, on average, the valve area declines 0.1-0.3 cm2 per year; the systolic pressure gradient across the valve can increase by as much as 10-15 mm Hg per year. A more rapid rate of progression is observed in elderly patients with coronary artery disease (CAD) and chronic renal insufficiency.
No racial predilection is associated with congenital or acquired aortic stenosis.
Severe aortic stenosis is rare in infancy, occurring in 0.33% of live births and is due to a unicuspid or bicuspid valve. Most patients with a congenitally bicuspid aortic valve who develop symptoms do not do so until middle age or later. Patients with rheumatic aortic stenosis typically present with symptoms after the sixth decade of life, and those with senile degenerative aortic stenosis may not manifest symptoms until their mid 70s to early 80s.
In aortic stenosis, a long latent period exists during which time the LV outflow obstruction and the pressure load on the myocardium gradually increase while patients remain asymptomatic.
The classic symptom triad of aortic stenosis includes angina pectoris, syncope, and heart failure, which most commonly manifest after the sixth decade of life.
Some patients remain asymptomatic, but others develop exertional chest pain, effort dizziness or lightheadedness, easy fatigueability, and progressive inability to exercise.
Exertional dyspnea is the most common initial complaint, even with normal LV systolic function, and it often relates to abnormal LV diastolic function.
Angina pectoris occurs in approximately two thirds of patients with critical aortic stenosis, of which 50% have significant coronary artery disease. Because angina commonly is precipitated by exertion and relieved by rest, it simulates symptoms of coronary artery disease. Angina results from a concomitant increased oxygen requirement by the hypertrophic myocardium and diminished oxygen delivery secondary to diminished coronary flow reserve, decreased diastolic perfusion pressure and relative subendocardial myocardial ischemia. Of course, angina also can result from coexistent coronary artery disease.
The cause of syncope is multifactorial. It often occurs upon exertion when systemic vasodilatation causes the arterial systolic blood pressure to decline in the presence of a fixed forward stroke volume. It also may be caused by atrial or ventricular tachyarrhythmias.
Syncope at rest may be due to transient ventricular tachycardia, atrial fibrillation, or atrioventricular block, with the latter due to extension of the calcification of the valve into the conduction system. Another cause of syncope is abnormal vasodepressor reflexes caused by increased LV intracavitary pressure (vasodepressor syncope).
Congestive heart failure symptoms (ie, paroxysmal nocturnal dyspnea, orthopnea, dyspnea on exertion, and shortness of breath) may be due to systolic dysfunction from afterload mismatch, ischemia, or a separate cardiomyopathic process. Alternatively, diastolic dysfunction from LV hypertrophy or ischemia may also result in congestive heart failure symptoms.
In patients in whom the aortic valve obstruction remains unrelieved, the onset of symptoms predicts a poor outcome with medical therapy; the approximate time interval from the onset of symptoms to death is 2 years for congestive heart failure, 3 years for syncope, and 5 years for angina.
Gastrointestinal bleeding due to angiodysplasia or other vascular malformations is present at a higher than expected frequency in patients with calcific aortic stenosis; it usually resolves following aortic valve surgery.
The risk of infective endocarditis is higher in younger patients with mild valvular deformity than in older patients with degenerated calcified aortic valves, but it can occur in either. It can occur at any age with hospital-acquired Staphylococcus aureus bacteremia, which frequently results in aortic valve replacement.
Calcific aortic stenosis rarely may cause emboli of calcium to various organs, including the heart, kidney, and brain.
Sudden cardiac death is rare and usually occurs in symptomatic patients.
In severe aortic stenosis, the carotid arterial pulse is typically diminished and rises slowly (pulsus parvus et tardus); however, in elderly individuals with rigid carotid vessels, this may not be present. A lag time may be present between the apical impulse and the carotid impulse. Systolic hypertension can coexist with aortic stenosis, but a systolic blood pressure higher than 200 mm Hg is rare in patients with critical aortic stenosis.
Pulsus alternans can occur with the onset of LV dysfunction. The jugular venous pulse may show prominent a waves reflecting reduced RV compliance consequent to hypertrophy of the interventricular septum.
At the apex, a precordial a wave often is visible and palpable. A hyperdynamic LV is unusual and suggests concomitant aortic regurgitation or mitral regurgitation. A systolic "thrill" may be present at the second right intercostal space or at the suprasternal notch. The thrill is best felt while the patient is leaning forward. On occasion, it can be transmitted to the carotids.
S1 is usually normal or soft.
The aortic component of the second heart sound, A2, is usually diminished or absent because the aortic valve is calcified and immobile and/or aortic ejection is prolonged and it is obscured by the prolonged systolic ejection murmur. The presence of a normal or A2 speaks against the presence of severe aortic stenosis. Paradoxical splitting of the S2 also occurs because of late closure of A2. P2 may also be accentuated when LV failure leads to secondary pulmonary hypertension.
The presence of an ejection sound (eg, ejection click) is dependent on the mobility of the valve cusps and disappears when they become immobile and severely calcified. Thus, an ejection click is common in children and young adults with congenital aortic stenosis but rare in elderly individuals with acquired calcific aortic stenosis. This sound occurs approximately 40-60 milliseconds after the onset of S1 and is frequently heard best along the mid to lower left sternal border; it is often well transmitted to the apex and may be confused with a split S1.
A prominent S4 is usually present due to forceful atrial contraction into a hypertrophied left ventricle. The presence of an S4 in a young patient with aortic stenosis indicates significant aortic stenosis, but with aortic stenosis in an elderly person, this is not necessarily true.
The classic crescendo-decrescendo systolic murmur of aortic stenosis is best heard at the second intercostal space in the right upper sternal border; it is harsh at the base and radiates to one or both carotid arteries. However, it may be more prominent at the apex in elderly persons with calcific aortic stenosis due to radiation of the high-frequency components of the murmur to the apex (Gallavardin phenomenon) leading to its misinterpretation as a murmur of mitral regurgitation. Accentuation of the aortic stenosis murmur following a long R-R interval (as in atrial fibrillation or following a premature beat) distinguishes it from the mitral regurgitation murmur, which usually does not change.
The intensity of the systolic murmur does not correspond to the severity of aortic stenosis, rather, the timing of the peak and the length or duration of the murmur corresponds to the severity of aortic stenosis. The more severe the stenosis, the longer the duration of the murmur and the more likely it peaks at mid-to-late systole.
The murmur of valvular aortic stenosis is augmented upon squatting or following a premature beat; the murmur intensity is reduced during Valsalva strain, which is contrary to what occurs with hypertrophic obstructive cardiomyopathy where a Valsalva maneuver increases the intensity of the murmur.
When the left ventricle fails and cardiac output falls, the aortic stenosis murmur becomes softer and may be barely audible. Atrial fibrillation with short R-R intervals can also decrease the murmur intensity or make it appear absent.
Rarely, RV failure with systemic venous congestion, hepatomegaly, and edema precede LV failure. This is probably due to the bulging of the interventricular septum into the right ventricle, with impedance in filling, elevated jugular venous pressure, and a prominent a wave (Bernheim effect).
Most cases of aortic stenosis are due to the obstruction at the valvular level. Common causes are summarized in Table 1. Valvular aortic stenosis can be either congenital or acquired.
Congenital valvular aortic stenosis
Congenitally unicuspid, bicuspid, tricuspid, or even quadricuspid valves may be the cause of aortic stenosis. In neonates and infants younger than 1 year, a unicuspid valve can produce severe obstruction and is the most common anomaly in infants with fatal valvular aortic stenosis.
In patients younger than 15 years, unicuspid valves are most frequent in cases of symptomatic aortic stenosis.
In adults, congenital aortic stenosis is usually due to a bicuspid valve. It does not cause significant narrowing of the aortic orifice during childhood. The altered architecture of the bicuspid aortic valve induces turbulent flow with continuous trauma to the leaflets, ultimately resulting in fibrosis, increased rigidity and calcification of the leaflets, and narrowing of the aortic orifice in adulthood.
Congenitally malformed tricuspid aortic valves with unequally sized cusps and commissural fusion can also cause turbulent flow leading to fibrosis and, ultimately, to calcification and stenosis. Clinical manifestations of congenital aortic stenosis in adults usually occur after the fourth decade of life.
Acquired valvular aortic stenosis
The main causes of acquired aortic stenosis include rheumatic heart disease and senile degenerative calcification.
In rheumatic aortic stenosis, the underlying process includes progressive fibrosis of the valve leaflets with varying degrees of commissural fusion, often with retraction of the leaflet edges and, in certain cases, calcification. As a consequence, the rheumatic valve often is regurgitant and stenotic. Coexistent mitral valve disease is common.
Degenerative (senile) calcific aortic stenosis involves progressive calcification of the leaflet bodies resulting in limitation of the normal cusp opening during systole. This represents a consequence of long-standing hemodynamic stress on the valve and is currently the most frequent cause of aortic stenosis requiring aortic valve replacement. It usually occurs in individuals older than 75 years. Cellular aging and degeneration have been implicated. Diabetes mellitus and hypercholesterolemia are risk factors for the development of this lesion. The calcification may also involve the mitral annulus or extend into the conduction system, resulting in atrioventricular or intraventricular conduction defects.
The available data suggest that the development and progression of calcific aortic stenosis are due to an active disease process at the cellular and molecular level that shows many similarities with atherosclerosis, ranging from endothelial dysfunction to, ultimately, calcification.
Calcific aortic valve disease is associated with older age, male sex, serum LDL and Lp(a) levels, systemic arterial hypertension, diabetes mellitus, and smoking.
Other infrequent causes of aortic stenosis include obstructive vegetations, homozygous type II hypercholesterolemia, Paget disease, Fabry disease, ochronosis, and irradiation.
Table 1. Common Reasons of Aortic Stenosis Requiring Surgery
Open table in new windowAge <70 years (n=324)
Bicuspid AV (50%)
Age >70 years (n=322)
Abu Zubair meriwayatkan dari Jabir bin Abdullah bahwa Nabi Muhammad SAW bersabda:
"Setiap penyakit ada obatnya. Jika obat yang tepat diberikan dengan izin Allah, penyakit itu akan sembuh".
(HR. Muslim, Ahmad dan Hakim).
Sabtu, 15 Maret 2008
Diposkan oleh FX di 06.00
The Holy Al-Qur'an (English version)
- Surah 1 - Al Fatiha THE OPENING
- Surah 2 - Al Baqarah THE HEIFER
- Surah 3 - Ali 'Imran - THE FAMILY OF 'IMRAN
- Surah 4 - Al-Nisa' THE WOMEN
- Surah 5 - Al Ma'idah THE REPAST
- Surah 6 - Al An'am THE CATTLE
- Surah 7 - Al A'raf THE HEIGHTS
- Surah 8 - Al Anfal THE SPOILS OF WAR
- Surah 9 - Al Tawbah THE REPENTANCE
- Surah 10 - Yunus JONAH
- Surah 11 - Hud THE PROPHET HUD
- Surah 12 - Yusuf JOSEPH
- Surah 13 - Al Ra'd THE THUNDER
- Surah 14 - Ibrahim ABRAHAM
- Surah 15 - Al Hijr THE ROCKY TRACT
- Surah 16 - Al Nahl BEES
- Surah 17 - Al Isra' THE NIGHT JOURNEY
- Surah 18 - Al Kahf THE CAVE
- Surah 19 - Maryam MARY
- Surah 20 - TA HA
- Surah 21 - Al Anbiya THE PROPHETS
- Surah 22 - Al Hajj THE PILGRIMAGE
- Surah 23 - Al Mu'minun THE BELIEVERS
- Surah 24 - Al Nur THE LIGHT
- Surah 25 - Al Furqan THE CRITERION
- Surah 26 - Al Shu'ara' THE POETS
- Surah 27 - Al Naml THE ANTS
- Surah 28 - Al Qasas THE NARRATIONS
- Surah 29 - Al 'Ankabut THE SPIDER
- Surah 30 - Al Rum THE ROMANS
- Surah 31 - Luqman LUQMAN
- Surah 32 - Al Sajdah THE PROSTRATION
- Surah 33 - Al Ahzab THE CONFEDERATES
- Surah 34 - Saba' SHEBA
- Surah 35 - Fatir THE ORIGINATOR OF CREATION
- Surah 36 - Ya Sin YA SIN
- Surah 37 - Al Saffat THOSE RANGED IN RANKS
- Surah 38 - Sad SAD
- Surah 39 - Al Zumar CROWDS
- Surah 40 - Ghafir FORGIVER
- Surah 41 - Fussilat EXPOUNDED
- Surah 42 - Al Shura CONSULTATION
- Surah 43 - Al Zukhruf THE GOLD ADORNMENTS
- Surah 44 - Al Dukhan THE SMOKE
- Surah 45 - Al Jathiyah THE KNEELING DOWN
- Surah 46 - Al Ahqaf WINDING SAND-TRACTS
- Surah 47 - Muhammad MUHAMMAD
- Surah 48 - Al Fath THE VICTORY
- Surah 49 - Al Hujurat THE CHAMBERS
- Surah 50 - Qaf QAF
- Surah 51 - Al Dhariyat THE WINDS THAT SCATTER
- Surah 52 - Al Tur THE MOUNT
- Surah 53 - Al Najm THE STAR
- Surah 54 - Al Qamar THE MOON
- Surah 55 - Al Rahman THE MOST GRACIOUS
- Surah 56 - Al Waq'iah THE INEVITABLE
- Surah 57 - Al Hadid IRON
- Surah 58 - Al Mujadilah THE WOMAN WHO PLEADS
- Surah 59 - Al Hashr THE MUSTERING
- Surah 60 - Al Mumtahinah THAT WHICH EXAMINES
- Surah 61 - Al Saff THE BATTLE ARRAY
- Surah 62 - Al Jumu'ah FRIDAY
- Surah 63 - Al Munafiqun THE HYPOCRITES
- Surah 64 - Al Taghabun THE MUTUAL LOSS AND GAIN
- Surah 65 - Al Talaq DIVORCE
- Surah 66 - Al Tahrim PROHIBITION
- Surah 67 - Al Mulk THE DOMINION
- Surah 68 - Al Qalam THE PEN
- Surah 69 - Al Haqqah THE SURE REALITY
- Surah 70 - Al Ma'arij THE WAYS OF ASCENT
- Surah 71 - Nuh NOAH
- Surah 72 - Al Jinn THE SPIRITS
- Surah 73 - Al Muzzammil THE ENFOLDED ONE
- Surah 74 - Al Muddaththir THE ONE WRAPPED UP
- Surah 75 - Al Qiyamah THE RESURRECTION
- Surah 76 - Al Insan MAN
- Surah 77 - Al Mursalat THOSE SENT FORTH
- Surah 78 - Al Naba' THE GREAT NEWS
- Surah 79 - Al Nazi'at THOSE WHO TEAR OUT
- Surah 80 - 'Abasa HE FROWNED
- Surah 81 - Al Takwir THE FOLDING UP
- Surah 82 - Al Infitar THE CLEAVING ASUNDER
- Surah 83 - Al Mutaffifin THE DEALERS IN FRAUD
- Surah 84 - Al Inshiqaq THE RENDING ASUNDER
- Surah 85 - Al Buruj THE CONSTELLATIONS
- Surah 86 - Al Tariq THE NIGHT STAR
- Surah 87 - Al A'la THE MOST HIGH
- Surah 88 - Al Ghashiyah THE OVERWHELMING EVENT
- Surah 89 - Al Fajr THE DAWN
- Surah 90 - Al Balad THE CITY
- Surah 91 - Al Shams THE SUN
- Surah 92 - Al Layl THE NIGHT
- Surah 93 - Al Duha THE GLORIOUS MORNING LIGHT
- Surah 94 - Al Sharh THE EXPANSION OF THE BREAST
- Surah 95 - Al Tin THE FIG
- Surah 96 - Al Alaq THE CLINGING CLOT
- Surah 97 - Al Qadr THE NIGHT OF POWER
- Surah 98 - Al Bayyinah THE CLEAR EVIDENCE
- Surah 99 - Al Zalzalah THE EARTHQUAKE
- Surah 100 - Al 'Adiyat THOSE THAT RUN
- Surah 101 - Al Qari'ah THE GREAT CALAMITY
- Surah 102 - Al Takathur THE PILING UP
- Surah 103 - Al 'Asr TIME THROUGH THE AGES
- Surah 104 - Al Humazah THE SCANDALMONGER
- Surah 105 - Al Fil THE ELEPHANT
- Surah 106 - Quraysh THE TRIBE OF QURAYSH
- Surah 107 - Al Ma'un THE NEIGHBOURLY ASSISTANCE
- Surah 108 - Al Kawthar THE ABUNDANCE
- Surah 109 - Al Kafirun THOSE WHO REJECT FAITH
- Surah 110 - Al Nasr THE HELP
- Surah 111 - Al Masad THE PLAITED ROPE
- Surah 112 - Al Ikhlas THE PURITY OF FAITH
- Surah 113 - Al Falaq THE DAYBREAK
- Surah 114 - Al Nas MANKIND
- Acute Coronary Syndromes
- Angina Pectoris
- Anomalous Left Coronary Artery From the Pulmonary Artery
- Aortic Coarctation
- Aortic Dissection
- Aortic Regurgitation
- Aortic Stenosis
- Aortic Stenosis, Subaortic
- Aortic Stenosis, Supravalvar
- Ashman Phenomenon
- Atrial Fibrillation
- Atrial Flutter
- Atrial Myxoma
- Atrial Septal Defect
- Atrial Tachycardia
- Atrioventricular Block
- Atrioventricular Dissociation
- Atrioventricular Nodal Reentry Tachycardia (AVNRT)
- Benign Cardiac Tumors
- Brugada Syndrome
- Complications of Myocardial Infarction
- Coronary Artery Atherosclerosis
- Coronary Artery Vasospasm
- Digitalis Toxicity
- Dissection, Aortic
- Ebstein Anomaly
- Eisenmenger Syndrome
- First-Degree Atrioventricular Block
- HACEK Group Infections (Infective Endocarditis)
- Heart Failure - Decompensatio Cordis
- Holiday Heart Syndrome
- Hypertensive Heart Disease
- Junctional Rhythm
- Loeffler Endocarditis
- Long QT Syndrome
- Lutembacher Syndrome
- Mitral Regurgitation
- Mitral Stenosis
- Mitral Valve Prolapse
- Myocardial Infarction
- Myocardial Rupture
- Paroxysmal Supraventricular Tachycardia
- Patent Ductus Arteriosus
- Patent Foramen Ovale
- Pericardial Effusion
- Pericarditis Acute
- Pericarditis, Constrictive
- Pericarditis, Constrictive-Effusive
- Pulmonic Regurgitation
- Pulmonic Stenosis
- Right Ventricular Infarction
- Saphenous Vein Graft Aneurysms
- Second-Degree Atrioventricular Block
- Sinus of Valsalva Aneurysm
- Sudden Cardiac Death
- Tetralogy of Fallot
- Third-Degree Atrioventricular Block
- Torsade de Pointes
- Tricuspid Regurgitation
- Tricuspid Stenosis
- Unstable Angina
- Ventricular Fibrillation
- Ventricular Septal Defect
- Ventricular Tachycardia
- Wolff-Parkinson-White Syndrome