Valvular Diseases Flashcards
What is echocardiography? How does it work?
Echocardiography is the first line exam done to diagnosed cardiovascular diseases. It is a fast, safe and practical exam that uses ultrasound to examine the heart, asses the cardiac function and structure. The main limit is that it is expert dependent.
Echocardiographic imaging relies on the reflection of ultrasound waves from structures within the cardiovascular system.
In an echo image the black part is blood as it is less reflective while the grey is the tissue. Different frequencies can be used to increase or decrease resolution as they are directly proportional, also different wavelength have different penetration power.
What are some echo approaches?
1.Transthoracic : it is the most common, used in 95% of cases. You put the probe in specific points called views or windows: parasternal, apical, subcostal, suprasternal. You can get different pictures of the heart depending on these points.
- Transesophageal : done by introducing a transesophageal probe in the esophagus to get very close to the heart, useful to study posterior stuctures (not well visible in the transthoracic) : left atrium, left atrial appendage, pulmonary veins, interatrial septum, mitral valve. It is usully a second level exam, so you do transthoracic and then if you need some clarifications or in case you cannot conclude a diagnosis, you can use it. It is usually used directly in case of thrombi in LA, because the transthoracic is unuseful.
- Intracardiac : it is not a standard approach. The probe is introduced in the femoral vein up to the RA. It is mainly used to monitor percutaneous procedures.
- Epicardial : it is performed only in the OR, less common. Used to check results of an intervention when the transesophageal approach cannot be used.
What are the different echo modalities?
- 2D echo : Gives a snapshot in time of a cross-section of tissue, if these sections are produced in quick succession and displayed on a screen, they can show real-time imaging of heart chambers, valves and blood vessels. Can evaluate different parts of the LV wall by different views, long axis, two chamber and four chamber view.
- M-mode : Transmission and reception of US signal along only one line, giving higher sensitivity. Can be used to measure diameter and thickness of myocardial wall.
- Doppler : It is used to evaluate the velocity of flow, it uses the reflection of US by moving RBC. The Doppler phenomenon is used to derived velocity information from frequency shifts.
- Continuous wave Doppler : uses two crystal one transmitting continuously and the other receiving continuously. Does not localize precise flow signal but can measure peak and mean velocity.
- Pulsed wave Doppler : used single crystal to calculate velocity in a single point like assessing diastolic function of LV. - Color Doppler : It allows us to study the direction of the flow. BART convention, blue is away and red is towards. Very useful in diagnosis of regurgitations.
How are valvular disease classified?
They are classified based on type of defect :
• Stenosis : the orifice of the valve is narrowed, therefore it does not allow the normal passage of blood.
• Insufficiency : there is a leak of blood into the wrong chamber, as the valve is not able to stop the backflow.
• Mixed Valvular Disease : there is a combination of stenosis and insufficiency.
Classified also based on number of valves affected :
• Single Valve Disease: one valve is pathologically modified. For example, the aortic valve alone can be affected causing either aortic stenosis or insufficiency.
• Multivalvular Disease: more than one valve is pathologically modified. For example, both the aortic and the mitral valves are affected.
Epidemiology and etiology of valvular diseases?
Their prevalence is 2.5 % of the general population. The most frequent valvular disease is aortic stenosis with a mea age of 70. The second most frequent valvulopathy is mitral regurgitation followed by aortic reguargitation. The least frequent is mitral stenosis.
Degenerative etiology is the most common etiology of aortic stenosis, aortic regurgitation, and mitral regurgitation. While rheumatic etiology is the most common in mitral stenosis.
What is wiggers diagram?
It is a diagram that represents the relationship between pressure and volume in the different cardiac chambers during the cardiac cycle. It represents the ventricular, aortic and atrial pressure and volume.
What are the three cusps of the aortic valve?
Right Coronary Cusp (R), located below the right coronary sinus from which the right coronary artery originates.
Left Coronary Cusp (L), located below the left coronary sinus from which the left coronary artery originates.
Non Coronary Cusp (N), located below the non coronary sinus from which no artery originates.
What is the commissure?
The commissure is the point where each cusp meets the other. This anatomical structure is important because it is the point in which the inflammatory process starts in case of rheumatic disease.
What is the free edge structure?
During systole, the three cusps coarct together at this level.
What is the mitroaortic continuity?
It is the fibrous sheet located between the non coronary and the left coronary leaflet of the aortic valve and the anterior leaflet of the mitral valve. This structure is important because in aortic endocarditis a common complication if the formation of an infective abscess of this structure.
What is the etiology of aortic stenosis?
In younger patients the main cause is a bicuspid configuration, which affects 2% of the population. This conformation is more subject to degeneration compared to the normal tricuspid configuration. In 6% of patients with bicuspid aortic valve there is the coexistence of another congenital defect which is the coarctation of the aorta which is a restriction at the level of the isthmus.
To sum up : in the case of middle aged patients (within their 4th or 5th decades of life) we should think about a bicuspid or rheumatic disease. In old patients (within their 7th or 8th decades of life) we should think about a degenerative disease with a phenotypic tricuspid valve. However, a bicuspid valve is also possible.
What are the mechanisms of aortic stenosis?
In both tricuspid and bicuspid aortic stenosis the degenerative process is the same. The cusps fuse together in a so called raphe and calcify. This creates a rigid valve and impairs normal movement.
On the other hand in rheumatic disease the process is inflammatory. It starts from the commissure and spreads to the leaflets where it is called valvulitis. After the acute phase the healing process leaves fibrotic tissue in the commissures and causes a restriction.
There are different degrees of aortic stenosis related to the severity of the degenerative process.
What is the molecular and cellular mechanism behind aortic stenosis?
The process of degeneration in aortic stenosis is the same that occurs in atherosclerosis. An inflammatory process with endothelial injury on the leaflets and infiltration of cholesterol. The inflammatory reaction leads to a differentiation of the interstitial cells to osteoblast like cells with the deposition of micro and macro calcifications. This is the pathophysiological process that can lead to the calcification of the aortic valve.
What happens to the left ventricle during aortic stenosis?
During aortic stenosis, there is a remodelling of the left ventricle in terms of hypertrophy, but also a remodelling of the small intramyocardial vessels, because the hypertrophy can compress them during the systole. Moreover, the number of small vessels does not increase parallel to the increase in the left ventricular muscle, creating a mismatch between mass and vessels. On the other hand, the compression of the small vessels causes a micro vascular ischemia of the left ventricle, which is one of the main causes of left ventricular dysfunction and dilation in the late stage of aortic stenosis.
How are hemodynamics affected due to aortic stenosis?
There is a gradient between LV and aortic pressure, due to the obstruction at the level of the aortic valve (the higher is the gradient, more severe is the stenosis). The aortic valve area progressively decreases, and the LV adapts through hypertrophy (the left ventricle increases its myocardial mass to pump more blood through the narrowed orifice). This early coping mechanism yields diastolic dysfunction due to decreased compliance. Late changes include systolic dysfunction, myocardial ischemia and fibrosis due to microvascular dysfunction and decreased contractility, with eventual atrial fibrillation due to diastolic dysfunction, mitral regurgitation coexisting with artic stenosis and ultimately can lead to heart failure.
How is aortic stenosis diagnosed and graded? What is aortic valve calcium score?
Diagnoses is done with echo. We should report 6 parameter for aortic stenosis : velocity of Doppler signals recorded in aortic valve, mean gradient, aortic valve area, LV function, stroke volume and EF.
To grade AS we use the echo parameters : aortic velocity, aortic valve area and mean gradient. A sign of severe aortic stenosis is when the area is less than 1 cm2, peak aortic velocity ≥4 m/s and the mean gradient is greater than 40 mmHG.
When we are not able to grade the severity of AS, we can perform a CT scan to evaluate the presence of calcium (because not in all patients echo has a good performance) The more the calcium the more severe the stenosis.
What are the symptoms associated to aortic stenosis?
Chest pain (angina), reduced coronary flow, increased demand (high afterload), syncope/dizziness, fixed cardiac output, vasodepressor response, dyspnea on exertion and rest and impaired exercise tolerance.
Other signs include diastolic and systole dysfunction.
Angina is due to a decrease in perfusion because of stenosis or microvascular dysfunction. Indeed, 25-30% of patients with critical stenosis (especially when it is degenerative) present with associated epicardial coronary artery disease. It is possible to have stenosis in concomitance with CAD because the mechanisms of stenosis and atherosclerosis are the same.
What are some physical findings in patients with aortic stenosis?
The typical aortic murmur is a diamond shaped systolic crescendo decrescendo murmur (lub-whoosh-dub). The main site of auscultation is the right second intercostal space. Intensity does not predict severity. The murmur radiates to the carotids, mostly the right carotid ( important for DDX with HCM).
ECG in aortic stenosis? Sokolow index?
The ECG shows LV hypertrophy with ischemic ST alteration mimicking subendocardial ischemia.There is also alteration in repolarization in patients with severe LV hypertrophy.
SOKOLOW INDEX : A classical approach to define LVH, and it calculates the sum of QRS voltage of S wave in V1 or V2 and R wave in V5 or V6 : if it is greater than 35 mm it indicates hypertrophy. Putting together all this information you can give a diagnosis, grade the severity and stratify the prognosis.
What are the ESC guidelines for aortic stenosis?
There is no medication for valvulopathies. The only therapy is surgery. There is indication for surgery in asymptomatic patients ONLY when the patients present with severe aortic stenosis and LV dysfunction.
There are two therapeutic options: standard surgical aortic valve replacement for patients younger than 50yo with low risk. The other option is TAVI (transcatheter aortic valvular implantation) and it is for patients older than 75yo and patients with high or very high surgical risk (which cannot be operated, such as patients with previous radiation therapy).
What are the different types of secondary mitral regurgitation?
Atrial functional MR : characterized by remodeling of the LA, dysfunction of the mitral annulus w/ regurgitation but normal LV function. Etiology is 6%-7% AF, up to 53% in HFpEF.
Ventricular MR : characterized by systolic LV dysfunction, dilated LV secondary to DCM or ischemic cardiomyopathies due to MI.
Anatomic variability of the tricuspid valve?
Type I→ three leaflets: anterior, septal and posterior. (54%)
Type II→ three leaflets: one septal and two mural leaflets, meaning that it is possible to separate the anterior leaflet from the posterior one.
Type III→ four leaflets. This variant happens in case of indentations or clefts and has an impact on the pathophysiology of tricuspid regurgitation and on the evaluation of percutaneous catheter
intervention.
Type IV→ five leaflets.
