Osvaldo Robiolo

MITRAL INSUFFICIENCY

Mitral regurgitation can be defined as the failure of the valve apparatus of the same name to make the left chambers independent from each other during ventricular systole, thus allowing blood regurgitation from the left ventricle to the left atrium. This alteration may be secondary to anatomical and functional disorders of the mitral valve apparatus.

The mitral valve apparatus is made up of the valve leaflets, an antero-internal or septal and a postero-external or mural leaflet, the valve annulus, the chordae tendineae, and the muscular pillars. but physiologically, in addition, the status, size, and contractility of the left ventricle and atrium are important for the good outcome of valve function.

Certain peculiarities must be remembered regarding the anatomy:

1. the endocardium that lines the posterior leaflet is directly continuous with that of the left atrium;
2. the one that covers the anterior leaf also does it, but the valvular connective tissue inserts itself in the fibrous annulus that supports the aortic valve. In this way, a dilation of the left atrium will pull the posteroexternal leaflet, exaggerating its functional deficit, but it will not do so with the anterior leaflet due to its connective support;
3. the antero-internal or septal blade separates the left ventricular inlet tract from its outflow tract or subaortic region. During systolic expulsion, the tangential passage of the systolic "jet" towards the aortic valve generates forces by Venturi effect that reduce the load on said valve.

Physiology and pathophysiology of mitral valve closure

Mitral valve closure is more complex than it appears. It begins before left ventricular systole. After atrial systole, which produces an active passage of volume to a partially filled left ventricle, the leaflets rise and approach. During the isometric contraction of the left ventricle, the leaves join each other due to a decrease in chordal tension secondary to the change in the shape of the left ventricular cavity. The pressure continues to rise within the left ventricle and the blades coaptate further. When the expulsion occurs, the active contraction of the pillars and the reduction in the size of the cavity support the tension on the chords and leaflets. These coaptate even more and bend towards the left atrium, taking the shape of an inflated parachute, but without prolapse into the left atrium. The mitral valve annulus, having muscle fibers in its outer two thirds of circumference, contracts, reducing the area of ​​the orifice. The arch bridge shape gives great strength to the valve apparatus to withstand the high systolic pressure without giving up. Even so, and due to what is expressed in the anatomical considerations, the posterior leaflet is subjected to greater tension overload than the anteroseptal leaflet.

The functional anatomical status of the left ventricle is extremely important. A dilated left ventricle will misalign the direction of the support forces provided by the pillars that, from being almost perpendicular to the valve orifice, become tangential due to the lateral distance of the pillars. Likewise, if the parietal insertion area of ​​a pillar in the left ventricle does not contract, or if it pulses paradoxically, the pillar will not be able to carry out its characteristic action of slowing the ascent of the valve leaves.

A dilated left atrium will pull on the posterior leaflet exaggerating the pre-existing insufficiency.

The severity of systolic regurgitation depends on the magnitude of the valve lesion, regulated by three factors: a) speed of installation of the defect; b) state of the left atrium, and c) state of the left ventricle.

1. Quick installation of the defect . If this occurs abruptly, as in infective endocarditis with rupture of the chordae tendineae, or in acute myocardial infarction with necrosis of a papillary muscle, the left chambers cannot adapt to the defect, and serious pulmonary venocapillary hypertension occurs. On the other hand, if the lesion develops progressively, as in rheumatic endocarditis or in ischemic papillary muscle dysfunction, adaptation can be carried out and the symptoms are less even with larger defects.
2. Status of the left atrium . The size and tonicity of the left atrium is important, as a normal-sized, tonic atrium cannot accept sudden flow transfers without severely increasing its pressure (acute injuries). In chronic mitral regurgitation, the dilated left atrium dampens the rise in pressure and prevents it from moving into the pulmonary capillary.
   On the other hand, in the first case the systolic regurgitation will be slowed down during the mesosystole by hypertension in the left atrium; this does not happen in the second case, in which the regurgitation within a hypotonic and dilated left atrium may be holosystolic.
3. Status of the left ventricle . This cavity must accept the transfer of regurgitated flow to the left atrium, therefore it must have an adequate size and acceptable contractility. In chronic mitral regurgitation, the slowness with which the defect sets in allows the left chambers to progressively adapt to the new situation. The hemodynamic picture is marked by two primary alterations: 1) the retrograde effects of the regurgitation jet, and 2) the fall in the antegrade systolic volume.

The regurgitation jet, proportional to the defect, is propelled from the left ventricle to the left atrium and will cause little pressure increase in the latter, so its transfer to pulmonary veins and capillaries will be of medium magnitude. If there is a left ventricle capable of accepting diastolic flow from the left atrium, there will be no diastolic hypertension in this chamber and therefore no pulmonary venocapillary hypertension. The contractile compromise of that chamber can progressively alter this condition and cause a rise, in advanced cases, in the median pressure in the left atrium and the pulmonary capillaries.

Antegrade systolic output falls in direct proportion to the severity of the regurgitation, generating alterations in the morphology of the arterial pulse and symptoms of low peripheral minute volume.

The severity of mitral regurgitation can be classified as mild (regurgitant fraction: 30% of the stroke volume of the left ventricle), moderate (dc 30 to 50%) and severe (more than 50%).

The left atrium and left ventricle will show signs of volume overload with growth, predominantly dilatation, of both chambers.

Chronic dilation of the atrial myocardium and atrial fibrosis due to rheumatic cardiomyopathy (in cases of this etiology) lead to increased automatism with the appearance of arrhythmias, the most common of which is atrial fibrillation.

When there is pulmonary hypertension due to increased capillary pressure, the pulmonary arterioles can add a functional vasoconstriction factor first and concentric hypertrophy later, with enlargement of the right chambers and signs of failure of the same. In the natural history of the defect, this usually happens in remote evolution.

In acute mitral regurgitation, the rapid installation of the defect does not allow adaptation of the left atrium and left ventricle, so regurgitation produces a severe increase in pressure in the left atrium and pulmonary capillary with serious conditions, such as acute edema lung. The transfer of volume from the left ventricle to the left atrium is not great for the same reason hypertension in the left atrium that opposes reflux. Low peripheral minute volume signs are minor or absent.

Because the left atrium was previously of normal size, atrial fibrillation is infrequent, so sinus rhythm persists.

The growth of the left chambers is minimal and the heart characteristically small.

Chronic mitral regurgitation

The most common causes of chronic mitral regurgitation are rheumatic endocarditis (sequela) and mitral valve prolapse; It is frequently followed by the sequelae of ischemic heart disease and bacterial endocarditis, and cardiomyopathies. In left ventricular dilation due to different etiologies (more frequently cardiomyopathies), mitral regurgitation is a secondary phenomenon. Congenital etiology is rare and is generally associated with other structural defects. The various causes are listed in Table 5-1.

Symptoms and signs

Symptoms. They appear in a variable period of time after the episodes of rheumatic fever, in general years, although unlike mitral stenosis they can settle early, months after the acute picture. A history of one or more episodes of acute carditis is more common in mitral regurgitation than in mitral stenosis.

Most symptom-based diagnoses are made in the third decade of life. Such manifestations are: 1) symptoms resulting from pulmonary venulocapillary hypertension, 2) symptoms resulting from a fall in antegrade stroke volume, 3) arrhythmias, and 4) others.

1. Exertional dyspnea, with progressive disability over years, rarely acute pulmonary edema and nocturnal cough, and very rarely hemoptoic sputum, are expressions of pulmonary venulocapillary hypertension. These symptoms, unlike what happens in mitral stenosis, are not as severe and constant, since they depend on the adaptation and cushioning capacity of the left atrium (size and tone), and that of the left ventricle in terms of its contractility and ability to accept excess diastolic volume offered by the left atrium.
2. Fatigability with exercise, and muscle pain or cramps in severe cases, reflect peripheral tissue hypoperfusion due to a drop in stroke volume by regurgitating part of the ventricular ejection into the left atrium.
3. Palpitations in the form of vigorous beats at the level of the left ventricular impulse during exercise result from the hyperdynamic of the ventricular chamber due to its diastolic overload and subsequent dilation.

Palpitations in crisis, generally associated with increased signs of pulmonary venocapillary hypertension and a fall in minute volume, result from supraventricular arrhythmias, generally paroxysmal atrial fibrillation that sooner or later settles in cases of medium or severe severity.

The distant evolution in the natural history of valvular disease frequently presents the signs and symptoms resulting from right heart failure due to pulmonary hypertension, with jugular engorgement, hepatomegaly, and edema.

Occasionally, and less frequently than in mitral stenosis (there is no severe ecstasy in the left atrium), fragments of endoatrial thrombosis break off, producing peripheral embolism.

The natural history of mitral valve disease is aggravated by some circumstances: pregnancy, pulmonary thromboembolism, and paroxysmal atrial fibrillation, while bacterial endocarditis accentuates existing lesions or adds new ones.

The life prognosis from the onset of symptoms, in moderate or severe injuries and not mediating surgical treatment, is 15 to 30 years.

Signs . The general condition will depend on the presence of heart failure and its severity.

The arterial pulse is of rapid rise and fall, in the shape of an isosceles triangle, but of small magnitude. Its cause is the rapid decompression of the left ventricle by having two expulsion routes. The expulsive period is shortened in severe injuries.

The semiological examination of the neck reveals a poorly palpable aortic beat in the suprasternal fossa and absence of jugular engorgement if there is no involvement of the right cavities. The venous pulse retains its waves in the absence of atrial fibrillation or presents its own, if it is present.

The left ventricular impulse is displaced out and down by enlargement of the left ventricle. It is commonly found in the 5th or 6th intercostal space outside the hemiclavicular line or close to the anterior axillary line. It is localized, impulsive, muscular and with an increased surface area. Protodiastolic vibrations equivalent to R3 can be palpated. In certain cases it is possible to palpate a sagittal pseudobeat produced by the systolic expansion of a giant left atrium.

Auscultation reveals alterations in R1 and R2, presence of other sounds (R3) and murmurs.

R1 is characteristically hypophonic, absent on auscultation and difficult to register on phonocardiography. This is due to a very severe valve alteration. It can preserve its phonesis in cases of less compromise of the leaflets with mobility of the anterior leaf.

The R2 is permanently and constantly unfolded but not fixed in severe injuries. This is due to the advancement of the aortic component (A2) with respect to the pulmonary component (P2) by shortening the expulsion of the left ventricle.
In general, the phonesis of P2 is increased.

R3 is characteristically present at the end of the fast full period in moderate and severe injuries. It is produced by the abrupt deceleration of the early diastolic ventricular filling that abruptly bursts into the left ventricle.

The classic systolic murmur is of the regurgitate type; It begins with R1 (which it contributes to canceling) and has a variable duration depending on the severity of the injury; generally holosystolic, high frequency, steam jet, invades the early diastole in very severe lesions.

It is auscultated with a closed collector and the zone of maximum auscultation is the mitral area; radiates well to armpit. Moderate lesions with tonic or non-dilated atria produce rhomboidal (pseudo-ejective) or decreasing Rl-type murmurs that release end-systole.

After R3, a short mid-diastolic rumble is heard in severe lesions, which may come from stenosis of the subvalvular apparatus or from excessive diastolic fullness.

Never, in the absence of added mitral stenosis, a presystolic reinforcement of the aforementioned roll is auscultated.

Study methodology

Chest radiology . He shows left ventricular and atrial enlargement, moderate venocapillary hypertension, and dilation of the pulmonary mid-arch. It is important to remember the displacement of the esophagus with contrast in the right anterior oblique position and the elevation of the left bronchus in the left anterior oblique due to enlargement of the left atrium.

Electrocardiogram . Most often, the rhythm is atrial fibrillation, so left atrial overload cannot be seen. If the rhythm is sinus, the P is widened, with a double spine, in DI, DII, aVL, V5 and V6, and with a slow negative phase in VI.

The AQRS axis is deviated to the left and there are signs of left ventricular enlargement: deep S in VI and V2, and high R in V5 and V6.

Echocardiography and color Doppler : classic echocardiography - M-mode and two-dimensional - and color echo-Doppler have amply demonstrated their usefulness in all valvular heart disease.

In mitral regurgitation, M-mode and two-dimensional echocardiography inform about the causes and mechanisms that provoke it, such as rheumatic disease, ischemic heart disease, cardiomyopathies, endocarditis and prolapse of its leaflets, as well as the size of the cavities heart disease, its evolutionary modifications and ventricular function.

Color Doppler assesses the degree of insufficiency, regurgitant volume and regurgitant fraction, as well as the area of ​​the regurgitant orifice, thus allowing a quantitative estimate of the severity of valvular disease: if the regurgitant volume is less than 30, it is stated that insufficiency is mild; if it is estimated between 30 and 59, it will be moderate; and if it is equal to or greater than 60, the regurgitation will be considered severe.

Transesophageal echocardiography is recommended in cases where the transthoracic method casts doubt on the severity or mechanisms of regurgitation, as well as the status of ventricular function.

Special studies. Cardiac catheterization makes it possible to measure the pressures in the heart's chambers (large V wave in the left atrium), and by means of a contrasted study, cinematographic images are obtained that demonstrate the regurgitation of the left ventricle to the left atrium, together with their respective sizes and conditions of contractility.

Mild mitral regurgitation can be tolerated for decades with or without relevant symptoms. Moderate injuries produce symptoms that progressively incapacitate the patient over the years, and the average life span is around 50-60 years. Severe mitral regurgitation is seriously disabling in the third decade of life, and in the absence of surgical correction, the life prognosis does not exceed 40 years.

Circumstances or conditions such as pulmonary embolism, infective endocarditis, pregnancy, pulmonary infections, and high-frequency arrhythmias cast a shadow over the prognosis and can cause death.

Acute mitral regurgitation

It is an easily differentiable clinical syndrome from that of chronic mitral regurgitation. Its causes and mechanisms of production are various (table 5-2); Of these, the most notable are the rupture of the chordae tendineae or the papillary muscle, the chordal detachment and the destruction of a valve. In terms of incidence, bacterial endocarditis, by affecting the valve apparatus by various mechanisms, occupies a preponderant place. Ischemic heart disease with structural alteration and necrosis of the papillary muscle during acute infarction and chordal rupture in mitral valve prolapse are also frequent.

Symptoms and signs

Symptoms . Acute mitral regurgitation syndrome has common features, regardless of the etiology.

In general, it triggers, unlike chronic mitral regurgitation, severe and acute pictures, clinically standing out severe venocapillary hypertension with dyspnea at rest, paroxysmal dyspnea or acute lung edema. The drop in minute volume with its characteristic symptoms completes the picture. Typically the heart rate remains sinus, if it was previously. The condition often leads to the death of the patient within hours or days, especially if it is a complication of an acute myocardial infarction; if it is due to infective endocarditis, it is progressively installed, accentuating previous valvular lesions or adding new ones.

The cardiac chambers are of normal size and the left atrium, small and tonic, transmits all the tension rise that systolic regurgitation produces within it towards the pulmonary capillary. As in chronic mitral regurgitation, there is no damping of the retrograde transfer of pressures to the left atrium.

This means that rarely, and except in the case of serious injuries, regurgitation is stopped in the meso or end-systole due to the increase in tension in the left atrium. The V wave of the atrial and pulmonary capillary pulse is of great magnitude. The powerful atrial systole that is triggered by the hypertension of the left atrium produces a large a wave. The heart remains small.

Signs. The patient is tachypneic and is usually unable to assume a decubitus position. Cold and viscous sweating is frequent due to the fall in systemic ejection flow and arterial hypotension.

The arterial pulse is small in magnitude, rising and falling rapidly. The left ventricular impulse is not displaced and can be hyperdynamic. A presystolic impulse (atrial systole) is palpated in the mitral area.

Auscultation reveals the presence of an R4 in the mitral area due to strong atrial systole, which markedly increases the end-diastolic pressure of the left ventricle. The Rl is of normal intensity. A high-frequency protomesosystolic murmur (closed collector) and other times a rhomboid mid-systolic murmur are heard.

The unfolded R2 has the hyperphonetic pulmonary component (P2) in the second left intercostal space. There is no R3 since there is no important protodiastolic filling of the left ventricle, since the transfer of flow from the left ventricle to the left atrium is not significant due to the brake imposed by the atony of the latter cavity.

Study methodology

Chest radiology . The lung fields show the classic signs of pulmonary venocapillary hypertension. The cardiac silhouette does not show significant enlargement if it was previously normal.

Electrocardiogram . The rhythm is sinus. The P wave is the characteristic of left atrial enlargement. The left ventricle shows no signs of growth in the first days.

The severe picture, left to its natural evolution, leads to the death of the patient in hours or days. If it exceeds the first week of evolution, the prognosis improves and an acceptable adaptation can be achieved by the cardiac chambers.

Mitral valve prolapse

It is the most common heart valve disease in youth and middle age (10% of the population, according to some statistics). It constitutes a special group of chronic mitral regurgitation that differs from the classic ones due to its characteristics. In recent years it has been learned to recognize it and its pathophysiology has been understood. Its anatomical basis can be related to different alterations of the mitral valve apparatus: dilation and calcification of the annulus; tendinous chords that are too long or lax, papillary muscles with implantation anomalies, ventricular wall with contractile alteration, asymmetric hypertrophy of the interventricular septum and, in the classic form, leaflets with myxomatous degeneration of their connective tissue, which makes them lax, redundant and embossed.

Four reasons are currently known that can induce prolapse of the mitral leaflets towards the left atrium during ventricular systole: 1) primary valve prolapse, where there is an abnormality of the leaflets, chordae tendineae or annulus, without recognizable systemic disease; 2) secondary to systemic diseases such as Marfan and Ehlers-Danlos syndromes and elastic pseudoxanthoma or, as described by some researchers, by damage to the leaflets during acute rheumatic fever; 3) hearts with a small left ventricular cavity and normal anatomy of the mitral apparatus with atrial septal defect, anorexia nervosa and hypovolemia, and 4) significant displacement of the mitral leaflets towards the left atrium on echocardiographic image, with normal heart and mitral apparatus. These people do not have mitral valve prolapse.

In all cases, the mechanism is identical: systolic shortening of ventricular diameters reaches a critical level in mesosistole, at which point the valve apparatus yields in one or both leaflets (they fall towards the left atrium) and regurgitation occurs. This is contributed by the level reached by intraventricular pressure,
which increases the mitral containment effort. Therefore, anything that further reduces ventricular volume (Valsalva maneuver, orthostatism, expiration, drugs) and / or simultaneously increases its pressure (isometric effort, drugs), will exaggerate regurgitation and advance its production towards protosystole.

Mitral regurgitation due to prolapse is hemodynamically insignificant with few exceptions; it occurs in the meso and telesystole and can be identified semiologically.

When the prolapse is due to myxomatous degeneration, it can have a family incidence. It is not exceptional in children and is associated with congenital heart disease (eg, atrial septal defect).

Symptoms and signs

Symptoms . The patient has few symptoms, and the most common are palpitations (caused by frequent extrasystolic arrhythmias) and chest pain, of a poorly clarified etiology (increased tension on the papillary muscle, coronary abnormalities, etc.).

Generally, the patient consults for these nonspecific symptoms; or in a routine examination, typical stetoacoustic elements of the syndrome are listened to.

Signs . R1 and R2 heart sounds are normal and there is no R3 or R4.

In mesosystole, and coinciding with the greater valve containment effort, the valve prolapses and generates a high-frequency, generally moderate-intensity mid-systolic click or click.

Various maneuvers that shorten the diameters of the left ventricle (Valsalva, orthostatism, expiration, nitrites), advance the production of prolapse in systole and, therefore, click and murmur, which can move to protosystole. Maneuvers that dilate the left ventricle (bradycardia, supine position, etc.) produce opposite changes.

Maneuvers or drugs that increase intraventricular diastolic pressure (isometric effort, catecholamines) will increase regurgitation and therefore the intensity of the murmur.

The rest of the physical exam is not altered. The heart is of normal size.

Study methodology

The ECG may show ventricular repolarization disorders, especially in the diaphragmatic wall (DII, Dili, and aVF), with T wave inversion. Ventricular extrasystoles are common. Two-dimensional echocardiography and echo-Doppler are the most useful non-invasive test for the diagnosis of mitral prolapse and to estimate the presence or absence of mitral regurgitation. They are also indicated to assess the compensatory ventricular response in asymptomatic patients with physical signs of prolapse.

On the echocardiogram, the presence of systolic displacement of one or both mitral leaflets in the parasternal long axis recording, particularly when they coapte in the atrial side of the mitral annulus plane, indicates a high possibility of mitral valve prolapse. The diagnosis is even more certain when the thickening of the leaflets is greater than 5 mm. There are also structural changes such as leaflet redundancy, annular dilation, and cord elongation.

The prognosis is very good except in 1–3% of cases, which can die suddenly from ventricular arrhythmias.

Possible complications (infrequent) are infective endocarditis, tendon cord rupture, and progression to severe forms of mitral regurgitation.

TRICUSPID INSUFFICIENCY

Tricuspid regurgitation is the systolic regurgitation of blood from the right ventricle into the right atrium. It can be organic or functional. The organic form is a rare condition whose causes can be acquired, as in rheumatic fever, bacterial endocarditis, carcinoid syndrome, endomyocardiopathies, etc., or congenital, such as fibroelastosis, Ebstein's disease, etc.

Right ventricular dilation with tricuspid regurgitation is a common consequence of pulmonary artery hypertension. The right ventricle is a volume pump that is not well suited to pushing blood against increased resistance. This resistance can be elevated by disease of the pulmonary artery or lung parenchyma, by hypertension in the left atrium, mitral stenosis, or left ventricular failure. In these cases the right ventricle and the tricuspid valve are considerably dilated.

The magnitude or severity of organic tricuspid regurgitation is regulated by the severity of the valve disease, by the state of the right atrium and ventricle, and by the acuteness with which the condition occurs.

In functional tricuspid regurgitation, there are two possibilities that guide the extent of regurgitation:

a) when tricuspid regurgitation is secondary to pathologies that have hypertrophied the right ventricle and it dilates, a very important tricuspid regurgitation occurs because it comes from a chamber capable of developing systemic pressures, so that in these cases the clinical signs are very accented;

b) when functional tricuspid regurgitation is secondary to causes that dilate the right ventricle, the clinical signs of said regurgitation are less pronounced, since they originate in very dilated chambers that act as shock absorbers.

Functional tricuspid regurgitation characteristically varies with right ventricular adequacy. It decreases a lot and its signs are modified with the medical treatment of heart failure.

Pathophysiology

The consequence of tricuspid regurgitation is the rise in right atrial pressure during ventricular systole, the diastolic period of the right atrium, in which its pressure normally drops.

If a pressure curve of the right atrium is recorded, an atriogram is observed in the form of a cv wave, with deep y wave and diastolic "Deep".

This curve is known as the ventriculized atrial curve or sustained peak systolic curve. The right ventricular pressure depends on the cause of the tricuspid regurgitation; it is elevated in functional tricuspid regurgitation and secondary to left valve disease or pulmonary hyper-resistance, and less in isolated organic tricuspid regurgitation.

The elevation of the mean pressure of the right atrium produces an increase in the systemic venous pressure.

Symptoms and signs

Symptoms . They are highly variable and depend on the type of tricuspid regurgitation. The organic form of the young is due to rheumatic fever (along with mitral valve disease) or bacterial endocarditis in drug addicts. Functional tricuspid regurgitation is manifested by a wide range of symptoms.

When tricuspid regurgitation is produced, and if it is dominant, there is a sensation of venous beats in the neck and heaviness in the right hypochondrium and epigastrium. There may be fatigue and weakness due to low minute volume.

Signs . Tricuspid regurgitation is recognized by a holosystolic murmur in the lower part of the left sternal border, which changes in intensity during inspiration, increased by increased venous return. In cases of severe regurgitation, a positive liver beat is detected during systole. The sagittal beat is frequently present.

Atrial fibrillation accompanies 80–95% of patients with tricuspid regurgitation. This fibrillation is believed to increase tricuspid regurgitation, as atrial systole contributes to better valve closure.

The positive venous pulse is one of the fundamental symptoms, and it becomes a positive, visible and palpable monophasic. Edema and ascites complete the picture of systemic venous hypertension.

Study methodology

Chest radiology . It shows an engorged superior vena cava with enlargement of the right atrium and ventricle, depending on the functional or organic type of valvular disease.

Electrocardiogram . The signs of tricuspid regurgitation are: a) incomplete right bundle branch block, b) low-voltage waves in LV and potential jump in V2, and c) atrial fibrillation.

Echocardiography : tricuspid disease is studied with precision by echocardiography and is used: a) for the etiological diagnosis; b) to rule out the existence of vegetations of infectious origin, and c) to assess the presence of insufficiency, very common in the normal population - its character is mild - and more so in any other form of heart disease. This high prevalence allows the calculation of the systolic pressure in the right ventricle, which in the absence of pulmonary stenosis is the same as the systolic pressure of the pulmonary artery. The Doppler echo will allow to establish the degree of severity of the regurgitation. Cardiac catheterization. The recording of the pressures in the right atrium and the right ventricle, with arterialization of the atrial curve, indicates the magnitude of the alteration.

AORTIC STENOSIS

Left ventricular outflow tract obstruction may be located above, below, or at the level of the aortic valve. Although valve stenosis is by far the most common, the remainder are not without clinical significance.

Aortic stenosis represents 25% of the cases of valvular heart disease diagnosed in adults, and 80% of these patients are male.

The origin may be rheumatic. During the acute process, fusion of the valve commissures occurs and the structure becomes a bicuspid valve, which clearly limits the mobility of these leaflets. Over time, this fibrous region often tends to calcify, possibly contributing to the permanent trauma caused by the passage of flow through this stenosed region. In certain cases, the calcification can spread over the interventricular septum, affecting the atrioventricular node and causing blockages at that level.

Aortic stenosis can also be of congenital origin. In some of these cases the fusion of a commissure that transforms the valve into a clamshell with an eccentric orifice is observed; in others, the valve is completely devoid of commissures and has only a dome-shaped cusp. Thickening and subsequent calcification of this valve is common in adult patients. The valve can be congenitally bicuspid without stenosis in childhood; but the functional alteration of this structure causes, over time, thickening and subsequent calcification and stenosis in adulthood.

In elderly people, with calcification and aortic valve degeneration, a variable degree of valve stenosis can be found, with or without commissure fusion, which can be clinically of variable importance.

It is the most common cause of aortic narrowing in people over 60 years of age.

Pathophysiology

Left ventricular outflow obstruction caused by valve stenosis is the fundamental cause of the condition. Faced with this obstacle, the left ventricle is forced to increase its pressure in order to maintain the systemic flow at normal levels. This causes the appearance of a pressure gradient between said cavity and the aorta that will depend fundamentally on two factors: the degree of valve stenosis and the magnitude of the minute volume expelled.

Faced with this pressure overload, the left ventricle undergoes marked hypertrophy, mainly in a concentric manner, that is, increasing the thickness of its walls at the expense of a reduction in the ventricular cavity. This causes a significant decrease in the compliance of the walls, evidenced by an increase in end-diastolic pressure, without this signifying ventricular failure in this case. Faced with this condition, the atrium must manifestly force its systolic contraction, which is evidenced by an increase in the "a" wave in the pressure curve of said cavity. This causes a certain stretching of the myocardial fiber that favors ventricular contraction.

This action of the left atrium tends to be of utmost importance for ventricular performance; so much so that the absence of atrial activity, as happens for example when said cavity fibrillates, often causes decompensation of the left ventricle.

The expulsion volume and the minute volume remain within normal limits if the patient is at rest, but the required increase as needed is not produced during exercise.

When the left ventricle goes into failure, the minute volume at rest falls, the end-diastolic pressure increases very clearly, and therefore the mean pressure of the left atrium and pulmonary veins does, giving rise to venocapillary hypertension.

The increase in both the thickness and the tension of the left ventricular wall significantly increases the demand for 02, which, together with the other hemodynamic alterations, are responsible for the signs and symptoms of this valvular disease, which will be more or less accentuated depending on the magnitude of the injury and its evolutionary degree.

Symptoms and signs

Symptoms . As long as the left ventricle can maintain a normal minute volume, these patients can remain asymptomatic for a long time. They generally begin to manifest symptoms around adulthood, although the diagnosis of valvular heart disease can be quite early.

Exertional dyspnea, angina pectoris, and syncope are the three main symptoms of this valvular disease.

Dyspnea is the manifestation that the left ventricle has given way, since, despite its hypertrophy, it is no longer efficient against stenosis; This causes a greater increase in end-diastolic pressure that affects the left atrium and pulmonary veins and can lead to acute pulmonary edema, due to this venocapillary hypertension.

Angina pectoris is very common in patients with aortic stenosis. It generally occurs with exertion and its characteristics are indistinguishable from that caused by coronary disease, although in the case of valvular disease, nitroglycerin is less efficient in relieving pain.

Several are the factors that intervene in the production of angina pectoris: a) there is a marked increase in the requirement of 02 by the myocardium due to the increase in the tension of the ventricular wall;

b) given the significant hypertrophy, there is a decrease in the ratio of capillaries per gram of myocardium; c) a relatively decreased aortic pressure during diastole, associated with a reduction in diastolic time, a period during which coronary flow is more important, and an accentuated intramural pressure during systole, s or factors that influence considerably, and d) the association with coronary atherosclerosis.

Angina pectoris is frequently associated with syncope.

Syncope is the sudden loss of consciousness, usually after exertion, sometimes with seizures, that appears in about a third of patients with severe aortic stenosis.

Its cause is the impossibility of increasing the minute volume by the left ventricle according to the requirements of the moment, which, associated with a decrease in peripheral resistance due to vasodilation caused by exercise, causes a sharp drop in blood pressure and ende of cerebral flow. In some cases, it can be attributed to a reflex-type peripheral vasodilation, due to the marked increase in left ventricular pressure.

Less frequently, the origin of syncope are arrhythmias, for example, an atrio-ventricular block due to the extension of calcification found at the level of the aortic valve, which is unusual, or arrhythmias that are generated by electrical instability; whatever the case, they can lead to sudden death.

Given that a considerable number of patients with aortic stenosis have another added valve disease, especially mitral stenosis, it is necessary to emphasize that in such cases the classic symptoms lose magnitude and their appearance is delayed, due to the low minute volume with which the left ventricle is managed.

Signs . Blood pressure is within lower normal limits with a decreased differential.

The arterial pulse presents typical characteristics. It is not very wide, of slow ascent, with delay or absence of the dicrotic incision. It is the classic parvus and tardus pulse.

The venous pulse will not show alterations except in preterm cases, in which the repercussion on the right cavities (marked pulmonary hypertension) can lead to tricuspid regurgitation or a giant "a" wave.

Precordial palpation allows finding a left ventricular impulse not very displaced, but with special characteristics: sustained and localized due to the concentric hypertrophy of the left ventricle.
Over the aortic area, a significant systolic thrill can be felt that spreads to the neck.

On auscultation, a first normal noise is found followed by a click or systolic ejection sound that is preferentially heard over the 3 ° -4Q left intercostal space, produced by the stressing of the injured aortic valves at the beginning of systole and possibly also by vibrations of the dilated adjacent aortic wall. It is absent in cases of significant calcification of the valve.
Immediately after the ejection sound, a high-frequency systolic ejection murmur is heard, with a focus of greater intensity in the aortic area, which spreads to the other sources, but preferably towards the neck vessels. Like all ejection puffs, it is diamond-shaped and ends with R2.

R2 is generally diminished in intensity, rarely split, and in extreme cases it is possible to observe reverse splitting (second aortic sound after the pulmonary one) due to a very significant spread of the left ventricular systolic period.

In severe cases, an R4 can be auscultated, evidence of a significant atrial systole, which struggles against a greatly increased end-diastolic pressure of the left ventricle.

Study methodology

Chest radiology . In compensated aortic stenoses, a normal-sized cardiac image is found; in some cases, the tip of the heart is slightly below the diaphragm, which is consistent with concentric left ventricular hypertrophy. The most significant finding is the aortic dilation at the level of the ascending aorta, which protrudes over the right edge of the cardiac image (poststenotic dilation).

It is frequent, and therefore necessary, to always look for the existence of calcifications at the level of the valve, which can generally be observed by televised fluoroscopy.

In advanced cases, a left ventricular dilation is found; this is generally associated with different degrees of venocapillary hypertension, observable in the pulmonary fields.

Electrocardiogram . Signs of left ventricular overload can be observed, that is, deviation of the electrical axis of the QRS to the left, high Rs with inverted T in left precordials and deep S in right precordials.

Echocardiogram: echocardiography and its variants confirm the presence of aortic stenosis and determine the size and function of the left ventricle. Thus it allows to reveal the hypertrophy of the ventricular walls, including the septum. The aortic valve loses its normal echocardiographic configuration, which is replaced by dense and multiple echoes corresponding to calcification. The eccentricity of the diastolic echo line suggests the existence of a bicuspid valve. The dilation of the ventricle, which can be accurately measured, is accompanied by a reduction in the movement of its walls. The Doppler technique makes it possible to determine the pressure gradient between the left ventricle and the aorta, the jet velocity, the valve area, and the valve area index. So,

It is important to note that this method is extremely useful also for the evolutionary control of asymptomatic patients who are carriers of severe aortic stenosis (annual control), moderate (every one or two years) and mild (every 3 to 5 years).

Hemodynamic study . It consists preferably in the study of the left chambers of the heart, although in certain circumstances it may be necessary to assess the state of the right chambers, especially in advanced cases with signs and symptoms of pulmonary hypertension.

The study consists of retrograde catheterization of the aorta and passing through the valve to the left ventricle. Taking the pressure in both cavities allows the determination of the pressure gradient, since, together with the determination of the minute volume, it gives a very approximate idea of ​​the magnitude of the injury.

In addition, a left ventriculography is performed, which shows the size of the cavity and the thickness of the wall, rules out the existence of added mitral regurgitation, and allows us to observe the characteristics of this valve and the aorta, although the latter may It can be better appreciated by means of an aortography, injecting contrast substance over the valve plane.

In these patients, it is also essential to perform a coronary angiography, in order to assess or rule out atherosclerotic lesions that could be associated.

Supra-aortic stenosis

It is a congenital familial heart disease that consists of a narrowing of the ascending aorta, above the coronary artery.

It is usually associated with an alteration in the metabolism of vitamin D (idiopathic hypercalcemia) giving a typical syndrome with mental retardation, branch stenosis of the pulmonary artery (and even of the pulmonary valve) and a characteristic (pixie) face, with a very overhang, epicanthic folds in the eyes, accentuated bridge of the nose, strabismus and dental anomalies.

Very frequently it is also accompanied by subaortic stenosis and diffuse myocardial alterations, for which it is actually a true syndrome.

The clinical findings are similar to those of valvular aortic stenosis, except that the aortic component of the 2nd sound is accentuated and the click or ejection sound is frequently absent. In addition, continuous murmurs caused by multiple stenoses of branches of the pulmonary artery can be heard; they are found throughout the chest and especially below the armpits.

Cardiac catheterization allows a definitive diagnosis to be made by showing the existence of a pressure gradient above the aortic valve. Angiocardiography, in turn, reliably reveals the injury.

Idiopathic hypertrophic subaortic stenosis

Hypertrophic cardiomyopathy is a disease characterized by muscular hypertrophy of the left ventricular wall, which is not typically accompanied by dilation. The process is not preceded by known hypertensive vascular or aortic valve disease.

It is transmitted by inheritance in an autosomal dominant way with varied penetration capacity, which is evidenced with great variation of degrees in the clinical manifestations.

It is characterized by myocardial hypertrophy different from that observed in arterial hypertension. It presents great variations in the different regions of the left ventricle. In general, the thickening occurs in the ventricular septum and shows a significant difference from what is observed in the free wall. Hypertrophy of the cardiac apex or free ventricular wall occurs with some frequency. The pathological anatomy shows a lack of organization of myocardial cells with variable fibrosis, as well as abnormalities in the small intramural coronary arteries.

In addition to hypertrophy, there is a gradient in the outflow tract in 25% of patients that manifests as diastolic dysfunction due to the stiffness of the hypertrophied ventricular wall. This determines an increased diastolic filling pressure despite a hyperdynamic left ventricle. This pressure gradient associated with the narrow subaortic area was successively called hypertrophic idiopathic subaortic stenosis, hypertrophic obstructive heart disease, etc.

The gradient in the outflow tract is produced by a systolic movement of the anterior mitral leaflet against the hypertrophic septum.

This is always present when obstruction develops in hypertrophic cardiomyopathy.

The pressure gradient develops successively due to an increase in ventricular contractility, with a reduction in its stroke volume and an increase in ejection velocity, which brings the anterior leaflet against the septum as its compliance is reduced. Also, the decrease in the volume of the ventricle or preload contributes to decrease the lumen of the outflow tract. There is a decrease in aortic impedance, as well as pressure or afterload, which increases the flow in the subaortic area and also contributes to reducing the stroke volume of the ventricle.

Symptoms and signs

The presentation is changeable and dynamic, varying from exam to exam. The patient may be completely asymptomatic and be detected in the evaluation of the family group or may consult for dyspnea, palpitations, fatigue, according to the degree of obstruction. It can debut with a sudden death.

On physical examination, he presents a double or triple left ventricular impulse with a rapidly increasing arterial pulse.

The first noise does not decrease in intensity, but on the contrary, it appears normal or increased. The absence of a click is characteristic, although in 7% of cases it can be found.

The rude ejection mid-systolic murmur is located in the 4th left intercostal space with a short irradiation towards the base, and does not spread to the neck. During the first part of the systolic expulsion, as there is no obstruction in the left ventricular outflow path, there is no gradient between the ventricle and the aorta and therefore the expulsion is silent. During mesosystole, there is obstruction by the septum and the anterior leaf of the mitral valve; this reduces the expulsion and creates a gradient between the ventricle and the aorta, generating alterations of the murmur. In the final part of systole, when ventricular pressure begins to decrease, there is a gradient with minimal or no expulsion, and therefore there is no murmur. The shape is crescendo-decrescendo, diamond.

There are three factors to take into account: a) myocardial contractility: anything that increases the contractile power of the myocardium increases obstruction; b) left ventricular volume: anything that increases left ventricular volume decreases the degree of obstruction, and c) left ventricular systolic distension pressure. The distention pressure of the left ventricular outflow tract is the force capable of keeping the walls of that tract apart. This depends on the peripheral resistance. If this is increased, the degree of obstruction decreases (Tables 5-3 and 5-4).

The inverted doubling of the second sound, as well as the respiratory paradoxical behavior, demonstrates a lengthening of the ventricular systole. The fourth noise is one of the constant elements of auscultation. Along with the aortic murmur, there may be a murmur of mitral regurgitation.

Study methodology

1. Interrogation and clinical examination: of great importance for the data it provides.
2. Electrocardiogram: left ventricular hypertrophy, wide and thick Q waves and in all leads. Arrhythmias
3. Chest X-ray: normal or increased cardiac silhouette.
4. Echocardiogram: demonstrates hypertrophy as well as mitral valve movement. The ventricular cavity is small with a vigorous posterior wall, and the mobility of the interventricular septum is reduced.
5. Hemodynamic study: very useful to define it.
6. Radioisotopic scintigraphy with thallium 201: reveals perfusion defects.

PULMONARY VALVULAR STENOSIS

Obstruction to the outflow of the right ventricle is always of congenital origin except in the rare cases in which it is part of the carcinoid syndrome, and can present at the supravalvular, subvalvular or valvular level.

Isolated pulmonary valvular stenosis accounts for 8% of all congenital heart disease and is the most common form of obstruction. It can also be associated with other malformations, as occurs in Noonan syndrome (hypertelorism, low implantation of the ears and hair at the level of the neck, and mental retardation).

The pulmonary sigmoid valve presents as a carp-shaped diaphragm with one or two raphes that extend into the pulmonary annulus and do not divide the valve into the leaflets that usually compose it. The valve is made up of fibrous tissue and rarely undergoes significant calcification.

It is mobile toward the pulmonary artery and into the pulmonary infundibulum during systole and diastole, respectively, and has an eccentric orifice whose size depends on the magnitude of the stenosis.

The condition occurs in equal proportions in men and women.

Pathophysiology

The consequence of pulmonary valvular stenosis is the work or systolic overload of the right ventricle. This is transformed into a pressure chamber presenting a marked hypertrophy, which extends to the right atrium according to the severity of the stenosis. The obstacle to flow generates a pressure gradient between the right ventricle and the pulmonary artery, the greater the greater the stenosis. The hypertrophic myocardium can suffer the consequences of ischemia.

Symptoms and signs

Symptoms . In cases where pulmonary valvular stenosis is not extreme, there are generally no symptoms from birth until many years later, depending on the severity of the stenosis.

When symptoms appear, the patient presents dyspnea on exertion, due to decreased pulmonary flow (dyspnea due to pulmonary ischemia).

Signs . When valvular pulmonary stenosis is very important, there is moderate cyanosis due to right-to-left shunts, which occur at the atrial level through the patent foramen ovale.

Valvular pulmonary stenosis is accompanied by a rounded facies, at full moon, with normal weight-bearing development.

The presence of a large "a" wave presystolic positive jugular venous pulse indicates a powerful right atrial systole due to significant valvular pulmonary stenosis.

Precordial palpation detects an intense pulmonary systolic thrill, a left ventricular impulse with characteristics of the right muscle (located downward and diffuse), and a sagittal beat that is all the more important the greater the right hypertrophy.

The fundamental auscultatory elements are: a) the protosystolic pulmonary ejection click or sound, b) a pulmonary ejection systolic murmur, and c) the behavior of R2.

a) The pulmonary protosystolic ejection sound identifies the valve level of the stenosis. It occurs in 75% of cases and may not exist in very mild pulmonary valvular stenosis or in extreme forms. It is an intense valve click, audible in the lung area and in the precordial area up to the tip area, which decreases its intensity on inspiration and increases it on expiration.

b) The pulmonary systolic murmur is a "diamond" or a "rhombus", typically ejection, with maximum auscultation in the lung area, radiating towards the left clavicle, and whose length indicates the severity of the stenosis. In mild valvular pulmonary stenosis, the murmur has its maximum vibrations before mesosystole; when it is more closed, it reaches mesosystole, while in closed forms it is in end-systole, the later the more closed the stenosis.

c) The audibility of R2 in the lung area depends on the length of the murmur and the transvalvular gradient. An R2 with physiological unfolding or permanent unfolding, not fixed, with normophonetic pulmonary R2, is typical of mild or moderate valvular pulmonary stenosis.

An R2 that cannot be heard in the pulmonary area (or a pulmonary R2 with hypophonic characteristics) indicates a severe valvular pulmonary stenosis

d) Severe valvular pulmonary stenosis is accompanied by a right R4.

Study methodology

Chest radiology . It shows the hypertrophy of the right ventricle with a protruding lower left arch, very convex and separated from the left hemidiaphragm. The arch of the right atrium may be somewhat protruding. The left middle arch, corresponding to the pulmonary artery, is highly protruding (poststenotic dilation), as are the right and left pulmonary branches. The pulmonary maculature is normal, and there is no pulmonary hypoflux as long as the right ventricle maintains good contractility.

Electrocardiogram . It is an important element to assess the severity of the condition, since its modifications are parallel to the growth of the right ventricle and atrium:

1. Very mild pulmonary valvular stenosis is characterized by a normal ECG.
2. Moderate pulmonary valvular stenosis shows incomplete right bundle branch block with rSr 'type QRS in the LV and slight deviation to the right of the AQRS.
3. Severe valvular pulmonary stenosis is modeled on right ventricular systolic overload, with rsR or QR wave in LV and RS in V2 and V3, and high and accumulated P wave in D2, D3 and aVF.
4. Very severe pulmonary valvular stenosis shows a high R wave in all the precordials (from VI to V6) and ST with negative slope, right P wave and AQRS frankly to the right.

Echocardiogram : shows the dilated pulmonary trunk and thickened valve. The Doppler technique is the method of choice for estimating the severity of the transvalvular gradient and monitoring its evolution. Pulmonary stenosis will be considered severe when the jet velocity is greater than 4 m / s or the mean gradient exceeds 60 mm Hg.

Cardiac catheterization . When valvular pulmonary stenosis is moderate to severe, cardiac catheterization should be performed, regardless of the age of the patient.

The magnitude of the gradient between the right ventricle and the pulmonary artery measures the severity of the stenosis. A gradient above 50 mm Hg is significant. The magnitude of the elevation of the systolic pressure of the right ventricle and its end-diastolic pressure also indicate the stenotic severity. Right ventriculography shows the stenotic valve diaphragm, the size of the cavity and the existence of an infundibular stenosis acquired due to hypertrophy of said ventricle.

MITRAL STENOSIS

Mitral valve stenosis consists of a reduction in the mitral area from its normal size of 5 cm2 as a result of abnormalities in the structure of the valve leaves and the subvalvular apparatus that prevent adequate diastolic opening, producing an obstacle to left atrioventricular flow .

Mitral stenosis is almost always secondary to a rheumatic disease of the mitral apparatus, rarely corresponds to a congenital anomaly, and even more rarely is secondary to inflammatory processes of the mitral apparatus, in malignant carcinoid syndrome or as part of the endomyocardial fibroelastosis of hypereosinophilic syndrome . Rheumatic mitral stenosis occurs more frequently in women, in a 4: 1 ratio.

Acute rheumatic fever with rheumatic endocarditis causes deformation of the mitral valve apparatus, leading to a progressive degree of sclerosis, fibrosis, and calcification. The resulting valve deformation is the cause of the difficulty in diastolic opening. The left atrium suffers an overload of work (systodiastolic), with consecutive atrial hypertrophy. If the atrial myocardium has suffered rheumatic inflammatory insult, the left atrium may be markedly dilated.

The incidence of acquired mitral stenosis has decreased in recent years, possibly as a consequence of a decrease in rheumatic fever. It is one of the most frequent rheumatic valve diseases; it constitutes half of all valvular heart disease and is two to three times more common than pure rheumatic MR. It is also more common than rheumatic mitral disease (stenosis and regurgitation).

Another cause of impediment to atrioventricular flow can be due to an obstructive element in the left atrium when there is an atrial tumor (myxoma) or a thrombosis in said chamber. In these cases, it can be considered that there is an atrioventricular flow alteration similar to that of mitral valve stenosis, and with which a differential diagnosis should be made.

Pathophysiology

Mitral stenosis creates a diastolic gradient between the left atrium and the left ventricle due to difficulty in atrial emptying during diastole; the greater this gradient, the greater its hemodynamic impact.

The main factor that determines the severity of mitral stenosis is the area of ​​the narrowed orifice; if it is taken into account that the normal mitral valve area is 5 cm2, any reduction in it constitutes anatomic mitral stenosis. However, from a hemodynamic and clinical point of view, there is significant mitral stenosis when the mitral area is below 2 cm2.

In addition to the valve area, valve mobility and the anatomical state of the subvalvular apparatus are very important. The severity of mitral stenosis results from the interplay of these factors. Thus, it is considered:

1. Mild mitral stenosis : when the mitral area is greater than 1.5 cm2, with good valve mobility and unaltered subvalvular apparatus.
2. Moderate mitral stenosis : mitral area between 1.0 and 1.5 cm2, with varying degrees of valvular alteration and moderate subvalvular stenosis.
3. Severe mitral stenosis : mitral area smaller than 1.0 cm2, with significant alteration of the valve leaves and the subvalvular apparatus, accompanied by fusion and shortening, constituting a funnel-shaped mitral subvalvular stenosis with loss of valve mobility.

In addition to the valvular factor, the hemodynamic impact of mitral stenosis depends on the following elements:

1. Heart rate . The higher the heart rate, the greater its repercussion due to shortening of diastole and impediment to atrial emptying.
2. Minute volume . The minute volume that passes through the stenosed mitral orifice determines variations in the mean pressure of the left atrium, in a relationship that is directly proportional.
3. Atrial factor . The more hypertrophic the left atrium, the higher the mean atrial pressure and the greater its hemodynamic repercussion, creating more pulmonary venocapillary hypertension.
   The reverse occurs when atrial dilation predominates.
   The atrial content can also influence, since when there is a thrombosis in this cavity the flow is reduced.
   Finally, the ear work is important. Atrial fibrillation influences the mean atrial pressure, since, when atrial systole is abolished, this pressure falls, provided that the ventricular rate is not increased. Atrial paroxysmal dysthymia increase mean atrial pressure.
4. Pulmonary factors and their impact on the right heart . Increased mean pressure in the left atrium causes chronic pulmonary venocapillary hypertension; the more important this is, the greater the severity of mitral stenosis.
   Therefore, the alteration of the structures located behind the left atrium affects the pulmonary capillary pressure. The consequences of this situation are the following:
   1. Modifications occur in the alveolocapillary barrier, in order to protect the alveoli, which prevent or restrict alveolar transudation.
   2. the anatomical state of the pulmonary veins, the degree of pulmonary arterial resistance, the sufficiency of the right ventricle, and the presence of tricuspid regurgitation tend to decrease the flow through the mitral stenosis, reducing its hemodynamic degree. As all these factors affect the right ventricle, we can summarize it by saying that:
   3. when pulmonary arteriolar resistance is normal, right ventricular overload is a direct consequence of the magnitude of mitral stenosis; there is postcapillary pulmonary arterial hypertension and the "venocapillary" stage of increased work of the right ventricle is constituted;
   4. when there is pulmonary arteriolar hyperresistance, the overload depends on its magnitude; it is the pulmonary arterial hyperresistance stage of mitral stenosis and the flow to the left atrium is very limited. In this stage, compensatory right ventricular hypertrophy occurs, and during this stage, said ventricle is sufficient in its contractile action. When the latter is lost, heart failure appears; It is the third stage of right ventricular failure that initially progresses without great ventricular dilation, and finally reaches its final stage of right ventricular failure with tricuspid failure.
5. Mitral postvalvular factor . Left ventricular myocardial alterations (ischemic heart disease) and the concomitance of aortic valve disease (stenosis) or systemic arterial hypertension can aggravate mitral stenosis, due to the elevation of the left ventricular end diastolic pressure, which makes it difficult to flow after mitral valve.

Symptoms and signs

Symptoms . Breathlessness . It is the most common symptom (80%). The intensity depends on the magnitude or severity of the mitral stenosis. In general, it is a progressive dyspnea on exertion, always caused by pulmonary venocapillary hypertension. Due to the pulmonary changes already mentioned, the patient with mitral stenosis is prepared to endure significant venocapillary hypertensions without as much dyspnoea repercussion as would be expected.

All factors that tend to increase left atrial pressure (heart disease that overload the left ventricle, tachycardia, atrial fibrillation with high ventricular rate, etc.) aggravate dyspnea.

The appearance of paroxysmal nocturnal dyspnea is important to assess the severity of the condition and its meaning varies depending on whether it occurs in isolation and related to a large cardiac work overload or whether it is repetitive and unrelated to said overload. Thus, when the patient does not present with great prior dyspnea, paroxysmal nocturnal dyspnea may occur after violent exercise and is not indicative of great severity. In contrast, the spontaneous appearance of paroxysmal nocturnal dyspnea, unrelated to exertion or significant derangement, is significant as a sign of severe chronic pulmonary venocapillary hypertension.

Hemoptysis . It very frequently accompanies mitral stenosis, and after dyspnea it is the most frequent manifestation. It can vary between frank hemoptysis and hemoptoic sputum.

Bronchitis and bronchial asthma . They express congestion of the bronchial and bronchiolar mucosa due to the hypertension of the bronchial veins that flow into the pulmonary veins. Night cough is an important early symptom.

Palpitations . They appear as a crisis of paroxysmal supraventricular tachycardia or flutter or paroxysmal atrial fibrillation. They are frequent and accentuate dyspnea, being indicative of left atrial hypertension. There may also be palpitations due to supraventricular extrasystoles.

Systemic embolisms . They occur in 9 to 14% of cases, most frequently in the brain and later in the viscera and limbs. They can be multiple embolisms and in 60% of cases they are recurrent.

They appear more frequently when atrial fibrillation has been installed and can be the first symptom of mitral stenosis, even before dyspnea.

Symptoms of low systemic stroke volume . They occur in severe mitral stenosis, or mitral stenosis with pulmonary arterial hypertension. They include fatigue, easy tiredness, dizziness, and anginal pain.

Left vocal cord paralysis . Bitonal voice and cough, as well as dysphagia, are symptoms due to dilation of the left atrium; they occur very rarely.

Signs . Mitral facies . These patients may occasionally present a yellowish-cyanotic facies on the cheekbones, where telangiectasia is observed. It is more common in women.

Radial pulse and blood pressure . Radial pulse width and blood pressure figures allow us to infer data on the severity of mitral stenosis. In cases with low minute volume, the radial pulse is small and the blood pressure is low.

Left ventricular impulse The more severe the stenosis is the more dependent on the right ventricle. Furthermore, it is a typical valve beat with a predominance of valve vibrations over muscular ones.

Sagittal beat . Mitral stenosis is the ideal condition for the production of this phenomenon, also called a low parasternal systolic positive precordial beat. The growth of the left atrium between the spinal column and the right ventricle supports the
hypertrophic right ventricle , which during systole propels the precordium in its lower parastemal portion.

Auscultatory signs . They constitute the fundamental element for the diagnosis of valvular disease.

The classic Duroziez rhythm in the mitral area is constituted by: a) increased intensity of R1, b) free systole, c) R2 A, d) mitral opening snap, e) mid-diastolic roll, and f) presystolic reinforcement.

The RIM appears intense, modified in its timbre and delayed. Increasing the intensity and modifying its timbre give it a "bright", "snapping" or "sailboat" characteristic, so important for the diagnosis of mitral stenosis.

It is, together with the mitral opening snap, the most constant element in the auscultation of mitral stenosis.

Exceptionally, it loses the indicated characteristics and becomes a low intensity R1, as occurs in mitral stenosis with great valvular calcification or complicated with pulmonary arteriolar hyper-resistance.

The mitral opening snap occurs from 0.04 to 0.12 sec from R2A.

It occurs at the end of the valve excursion in early diastole. The separation time between the R2A and the mitral opening snap (R2A-mitral opening snap interval) depends on the magnitude of the left atrial pressure and on valve compliance. In general, the higher the left atrial pressure, the lower the interval and vice versa, hence it constitutes a sign of the magnitude of the left atrial pressure and, indirectly, of the severity of the stenosis.

The diastolic roll begins after the mitral opening snap, in mesodiastole, and decreases during it as the left atrioventricular gradient is reduced; it is sharply increased at the end of diastole, in end diastole or presystole, due to left atrial systole, which produces an intense ejection murmur, called presystolic enhancement. This reinforcement is absent when there is atrial fibrillation.

Hemodynamic data can be inferred from the duration of the diastolic roll since, if it occupies the entire mesosystole, the gradient between the left atrium and the left ventricle is important; if, on the other hand, it is quickly exhausted, such a gradient will be small. In addition, there are other variations related to the state of the subvalvular apparatus, pulmonary hyper-resistance, etc.

Auscultatory phenomena are reinforced in the left lateral decubitus position.

Study methodology

Chest radiology . It allows recognizing characteristic changes in the size and shape of the heart and great vessels, and in the appearance of the lungs, which are quite significant in this disease.

In frontal position, the "mitral image" is made up of four arches on its left edge: a) the aorta, which appears smaller the younger the patient and the more severe the stenosis; b) protruding dilated pulmonary artery; c) appendage of the left atrium, whose magnitude of salience depends on the size of said cavity, and d) lower left arch formed by the right ventricle and which, therefore, is rounded, convex and with its lower tip separated from the left hemidiaphragm. This arc is the greater the more severe the valve disease.

The right border presents the arch of the right atrium, the more prominent the more right repercussion there is, and inside it, or exceeding it in its upper third, another arch corresponding to the left atrium. The arch of the ascending aorta is small and the superior vena cava can be visualized.

The separation of both bronchi can also be visualized by the upward growth of the left atrium.

In right anterior oblique (OAD) the displacement of the esophagus backwards (visualized with esophageal filling) due to the growth of the left atrium is notable and very important. The arches of the right ventricle and the pulmonary artery are protruding, while the arches of the left ventricle appear small.

In the left anterior oblique (LAA), the displacement of the left atrium of the left bronchus upwards and the arch of the right ventricle forward is notable.

The magnitude of all these changes is related to the magnitude of the mitral stenosis. In some circumstances, valve calcification may be better seen on LAA or OAD.

In mitral stenosis with normal pulmonary arteriolar resistance, images of pulmonary congestion due to chronic venocapillary hypertension appear, namely: a) enlarged and blurred pulmonary hila, due to interstitial edema, lymphatic stasis and dilation of parahilar bronchial veins, with little visible hilar arteries ; b) Kerley's lines, which are observed in the lung bases in its external portion and which are constituted by thickened interalveolar septa and engorged lymphatics; c) bibasal congestion in standing X-rays, d) parenchymal images of congestion that, over time, can present as a miliary-type dotted or hemosiderin nodules and even calcified; e) interlobar effusions or costodiaphragmatic sinuses.

The radiological findings are modified when pulmonary hyperresistance appears, acquiring the
characteristic image of this situation.

Electrocardiogram . In mitral stenosis with normal pulmonary resistance, the ECG is of little help for the diagnosis, being able to show only a wide mitral P wave, double spine, in Dl, D2, aVL, V4, V5 and V6, with diphasic P and wide negative component and nicked in VI. As valve disease causes right ventricular enlargement, electrocardiographic changes appear: deviation of the QRS axis to the right and signs of right ventricular systolic overload in the right precordial and aVF.

Echocardiogram: it is the most sensitive and specific bloodless method of diagnosing mitral stenosis. In diastole, the two leaves, anterior and posterior, do not separate properly and both are directed forward. On the other hand, the anterior leaf does not move backwards in the mesodiastole, as it normally does, reducing the EF slope. The thickening and calcification of the valve is reflected by the presence of multiple echoes in the anterior leaf or by a diffuse increase in all the echoes of the mitral leaf. It will be possible to assess whether there is left atrial dilation, as well as the degree of valve opening and even the detection of thrombi inside the left atrial appendage, although the transesophageal echocardiogram is more sensitive for the latter. The Doppler technique allows estimating the severity of the stenosis,

If the mean gradient is less than 5 mm Hg, the stenosis is considered mild; If it is between 5 and 10, it will be moderate, while if it exceeds 10 mm Hg, we will find ourselves facing severe stenosis. If we take the valve area, mitral stenosis will be serious if it is less than 1 cm2.

Cardiac catheterization and angiocardiography . This invasive method constitutes the best procedure to diagnose the severity of the stenosis, its right repercussion and the anatomical state of the valve and the subvalvular apparatus.

AORTIC INSUFFICIENCY

The most common etiology of aortic regurgitation is rheumatic.

The acute rheumatic process very quickly causes valve insufficiency due to inflammatory lesion, to later lead to a thickening of the leaflets, with retraction and distortion, which determine permanent insufficiency.

Aortic regurgitation can also occur in patients with congenital abnormalities; p. For example, in those with a mono, bi, or quadricuspid aortic valve, or in those with a VSD in the upper part of the septum, which allows a leaflet to prolapse through the defect.

On other occasions, the alteration is not at the level of the leaflets, but the aortic annulus, which dilates considerably and makes it impossible for the leaflets to close the orifice completely; this is what is found in cases of syphilitic aortic regurgitation or aneurysmal dilatations of the ascending aorta in patients with Marfan syndrome.

The picture of acute aortic regurgitation can also appear in bacterial endocarditis, which, by attacking either a valve slowly damaged by rheumatic fever, or a congenital bicuspid valve, or even, in less frequent cases, a healthy valve, causes the perforation of one or more of the valvar leaves.

The dissecting aneurysm of the aorta, when located in the ascending portion, and more rarely a very important thoracic trauma, can be the cause of aortic regurgitation.

This valvular disease is twice more common in men than in women, except when it is associated with mitral stenosis, which is frequent, in which the female sex predominates.

Pathophysiology

The reflux of blood present in aortic regurgitation imposes a significant volume overload on the left ventricle.

At the beginning, the ventricle supports this overload by hypertrophying, but mainly by dilating, handling a considerable volume at the end of diastole, and without producing a very significant increase in the pressure at the end of diastole.

In the evolution of the process, there comes a time when said dilation is no longer compensatory; the volume of expulsion decreases, the ventricular diastolic volume increases even more, with a very significant increase in end-diastolic pressure and therefore in the pressure of the left atrium and pulmonary veins.

The facts vary in the case of acute aortic regurgitation; In these cases, the left ventricle does not have time to condition itself to the new regimen and enters failure early on without reaching a marked dilation.

Regurgitated volume depends on several factors: a) the diastolic pressure gradient existing between the aorta and the left ventricle; b) the level of the peripheral resistances; generally the patient with aortic regurgitation has diminished peripheral resistance; an increase in them will logically cause an increase in reflux from the aorta to the ventricle; and c) the duration of diastole; bradycardia will increase reflux.

In turn, the evolutionary behavior of aortic regurgitation will depend on: a) the size of the diastolic valve opening, which, although important, is not essential as an index of reflux, since there are numerous influencing factors, such as those mentioned above. the existence of added valvular heart disease, etc .; b) ventricular function, since in chronic aortic insufficiency the left ventricle adjusts to the new situation by dilating, and handles a large diastolic volume but without increasing its pressure; in the acute form, on the other hand, it rapidly goes into failure; c) of the peripheral resistance, very important with regard to the determination of the clinical signs and the evolution of the process. As already mentioned, there is peripheral vasodilation that allows a significant percentage of the left ventricular ejection flow to reach the peripheral circulation; d) the presence of other valve diseases, such as mitral or aortic stenosis, and e) the competence of the mitral valve; In cases of significant dilation of the left ventricle, mitral regurgitation may be caused by dysfunction of the papillary muscles, which, although it reduces the signs of aortic regurgitation by subtracting a percentage of flow to the aorta to direct it to the left atrium, aggravates the symptoms of pulmonary hypertension.

Symptoms and signs

Symptoms . The manifestations of severe chronic aortic regurgitation are established around 10 years after the first rheumatic process, for which the asymptomatic period is usually quite long.

Patients frequently consult due to the discomfort caused by the wide beats in the neck or abdomen, or due to palpitations caused by extrasystoles, or simply because of the uncomfortable perception of the heartbeat when lying on the left, produced by the cardiac enlargement.

Dyspnea in these patients implies a serious prognosis since it is evidence of a left ventricle that, despite its dilatation, cannot handle the large diastolic volume and increases its end-diastolic pressure, causing pulmonary hypertension.

Although less frequently than in aortic stenosis, these patients may develop angina pectoris on exertion. The increase in systolic pressure caused by the greater volume of expulsion, associated with the significant dilation, are, by Laplace's law, factors that increase the tension of the ventricular wall with the consequent increase in the demand for 02; this, together with the significant hypertrophy that the left ventricle also presents, plays a very significant role in determining angina pectoris. Furthermore, during diastole, which is when coronary blood supply is greatest, aortic pressure is decreased, which reduces the supply of blood to the myocardium; the suction effect on the coronary ostium (Venturi effect) also has an influence, which will be caused by reflux during diastole.

Signs . Arterial pulse . It is the typical jumping pulse, with a wide differential, of rapid ascent and descent; the classic water hammer pulse. The rapid rise is due to the increase in the left ventricular ejection volume and the decrease to the decrease in diastolic pressure. In cases of heart failure, these characteristics may diminish or disappear, which reappear once the patient is compensated again.

The capillary pulse, which is seen by gently compressing the tip of the patient's nails, reveals vasodilation and aortic reflux.

Blood pressure . There is a wide differential pressure with an increase in systolic and a decrease in diastolic.

The level of diastolic pressure is influenced not only by the level of peripheral resistance but also by that of ventricular diastolic pressure and their interactions; therefore, it is not valid to deduce the degree of aortic insufficiency on the basis of the arterial diastolic pressure.

The left ventricular impulse is highly displaced down and to the left. It is wide, prolonged, and hyperdynamic and is present even in asymptomatic patients as evidence of ventricular dilation (Bard's dome shock).

Auscultatory signs . A decreasing aspiration high-frequency diastolic murmur is heard, beginning immediately after R2; it is preferably located on the lower left border of the sternum and in severe cases in the mitral area. Given its characteristics, and especially in not very severe cases, it is difficult to auscultate, which is why it is recommended to place the patient in a sitting position, slightly bent forward and on expiration.

Dr. Proctor Harvey presented extensive experience based on numerous patients with aortic root dilation, in whom the diastolic murmur was most intense at the right sternal border.

Along with the diastolic murmur, a harsh systolic ejection murmur is heard in the first half of systole, clearly evident in the aortic focus, with transmission to the neck vessels, without thrill, due to the turbulent flow produced by the large ejection volume passes through an abnormal aortic valve and root. This does not represent an aortic stenosis. The first noise is normal and the second normal or more often decreased or absent.

It is also common to auscultate a third noise in the mitral focus. It is common to find, in cases of significant aortic regurgitation, the Austin Bint murmur, a soft diastolic roll caused by displacement of the anterior mitral leaf due to reflux, which leads to a narrowing of the mitral orifice. Although it can sometimes be confused with a true mitral stenosis murmur, it differs from it by the fact that it is accompanied by a normal or diminished first noise, by the absence of an opening click, and because it generally begins after a third noise .

Study methodology

Chest radiology . Posteroanterior plaques are characterized by a greatly enlarged cardiac image, even in asymptomatic patients, with a predominance of left ventricular dilation. The tip of the heart moves down and to the left, appearing below the image of the diaphragm. This is associated with a significant dilation of the aorta in its ascending part, which is observed protruding over the right lateral edge of the image. Pulmonary circulation depends on the evolutionary degree of the process.

Electrocardiogram . Signs of left ventricular overload are observed, with high R's in V5-V6, generally high and pointed T's (although they can be negative), and deep S's in VI-V2.

Echocardiogram Echocardiographic signs of aortic regurgitation are indirect. It allows estimating the cause of chronic insufficiency, valve morphology and the size of the aortic root, as well as estimating left ventricular hypertrophy and volume and systolic function. It is very useful for the follow-up and reevaluation of the severity of the condition and ventricular function and volumes, especially in asymptomatic cases.

The most characteristic image is the appearance of a diastolic vibration (fluter) in the anterior valve of the mitral valve, produced by the impact of the jet of regurgitated blood against said structure. It is a practically constant and independent sign of the importance of regurgitation. If it is an acute aortic regurgitation, the echocardiogram also shows the early closure of the mitral valve, secondary to the elevation of ventricular diastolic pressure. The increase in the dimensions of the ventricular cavity is due to volume overload and does not indicate ventricular failure if the contractile dynamics of the walls is preserved and the ejection fraction remains in the normal range.

Doppler is the most sensitive method for the diagnosis of aortic regurgitation, since it allows detecting minor degrees of regurgitation, sometimes inaudible. As in the case of mitral regurgitation, the quantification of valve incompetence is based on the path of the regurgitant jet, regurgitant fraction and the area of ​​the regurgitant orifice: if the regurgitant volume is equal to or greater than 60 ml / beat, the regurgitant fraction is equal to or greater than 50% of the volume and the regurgitant area is equal to or greater than 0.30 cm2, aortic insufficiency will be severe.

Hemodynamic study . It should be done in every patient with this pathology who has symptoms.

It consists of catheterization of the right and left chambers of the heart, recording the corresponding pressures, but mainly in the angiocardiographic study of the left ventricle and aorta.

The level of pressures in the aorta, and especially the end-diastolic pressure of the left ventricle, makes it possible to assess the evolutionary degree of the process, but it is through left ventriculography that the magnitude of ventricular dilation, its contractile capacity, and its ability to be inferred can be inferred. the existence or not of associated mitral regurgitation, while with an aortography performed from the valve plane it is possible to observe the characteristics of aortic reflux. In these cases, a coronary angiographic study should also be performed.

Chronic aortic regurgitation evolves slowly in a long asymptomatic patient. But once symptoms begin, especially of heart failure, the patient rapidly worsens in a marked way and even becomes very difficult to manage with clinical treatment, since the left ventricle, in most of these cases, no longer has almost reserves to face the hemodynamic situation that causes valvular disease.

Given the predisposition to bacterial endocarditis, this should be suspected in any patient who suddenly begins with symptoms.

In acute aortic regurgitation, on the other hand, the evolution is rapid; the patient enters heart failure almost immediately, without allowing time for ventricular dilation.