Mitral valve regurgitation
| Classification according to ICD-10 | |
|---|---|
| I34.0 | Mitral valve regurgitation (non-rheumatic) |
| I05.1 | Rheumatic mitral regurgitation |
| Q23.3 | Congenital mitral regurgitation |
| ICD-10 online (WHO version 2019) | |
During systole, blood flows "backwards" (arrow) through the mitral valve from the left ventricle into the left atrium.
1 Mitral valve
2 Left ventricle
3 Left atrium
4 Aorta
Mitral regurgitation (also mitral regurgitation , abbr .: MI; not to be confused with MI = myocardial infarction ) is the medical one in humans and at least some species more common heart valve defects . It is an inability to close or a "leak" of the heart's mitral valve , which during the ejection phase ( systole ) leads to a backflow of blood from the left ventricle into the left atrium (cf. structure of the heart ).
Mild forms of mitral regurgitation are detected quite often during an ultrasound scan of the heart ( echocardiography ) and are usually harmless. Severe forms require precise clarification, as surgical treatment is useful under certain conditions .
In the past, mitral regurgitation was mostly the result of rheumatic fever , but this has become rare outside of developing countries as a result of more rigorous treatment of bacterial infections . In the industrialized countries today the main causes are coronary heart disease , cardiomyopathies and the mitral valve prolapse syndrome . Mitral regurgitation also occurs as a single congenital heart defect or occurs more frequently in conjunction with other congenital heart defects or as a result of other congenital diseases of the connective tissue .
Acute severe mitral regurgitation as a complication of a myocardial infarction or heart valve inflammation is a rare, but usually dramatic, clinical picture which requires intensive medical treatment and can often only be managed through emergency valve surgery.
Epidemiology
While it is one of the most commonly diagnosed valve defects in humans, the incidence of mitral regurgitation can only be estimated. There are only a few well-founded statistics on the basis of larger studies on healthy people. However, the following information allows an estimate of the magnitude to be expected:
- 8.6% of Turkish children with healthy heart aged 0–18 years showed mitral regurgitation by echocardiography.
- Mitral regurgitation is the most common damage to the heart among rheumatic heart diseases in children and adolescents in developing countries.
- A prospective study in Great Britain found a prevalence of 1.82% in children and adolescents aged 3–18 years . None of the sick children were younger than 7 years. Other studies (USA) found a prevalence of 2.4% in children and adolescents aged 0-14 years with otherwise healthy hearts
- Almost a fifth of the 3,589 total people examined in the Framingham Study had mitral regurgitation. There was no difference between the sexes: In 19% of the men and 19.1% of the women, echocardiography showed at least one slight insufficiency of the valve.
- Various studies have shown mitral regurgitation in 11–59% of all patients who have had a heart attack .
- In 89% of patients over 70 years of age with heart failure ( ejection fraction <40%), mitral regurgitation was found, which reached a significant level in 20% (severity III or IV).
- With 31% of all heart valve operations, mitral regurgitation is the second most common heart valve defect in Germany.
- A Japanese study on 211 healthy volunteers aged 6–49 years showed a prevalence of mitral regurgitation of 38–45% in each age group examined, regardless of severity and physiological versus pathological.
Pathophysiology
The mitral valve works like a valve between the left atrium and the left ventricle of the heart. It opens during the filling phase of the ventricle ( diastole ) and thus enables blood to flow in from the atrium. At the beginning of the ejection phase ( systole ), the sudden increase in pressure in the ventricle closes the valve and thus “seals” the atrium. In this way, there is only a pressure of around 8 mmHg (11 mbar ) in the atrium , while at the same time the systolic pressure of around 120 mmHg (160 mbar) in the ventricle drives the blood on its usual route into the main artery ( aorta ).
With mild mitral regurgitation, these physiological processes are only slightly changed. Neither the size of the leak ( regurgitation opening ) nor the amount of blood flowing back (regurgitation volume, pendulum volume, reflux volume) reach significant proportions, so that the pressures in the left atrium and in the pulmonary veins remain as normal as the pumping capacity of the heart.
In severe mitral regurgitation, however, the regurgitation opening is more than 40 mm² and the regurgitation volume is more than 60 ml , which can lead to serious and sometimes life-threatening changes, especially with low heart rates, reduced contractility and high peripheral and pulmonary vascular resistance.
In the acute stage, with the left ventricle and left atrium of normal size, there is a considerable increase in pressure in the atrium and thus also in the pulmonary veins. This can be up to 100 mmHg (130 mbar), which leads to immediate pulmonary edema if the pulmonary vessels are normal . In addition, the then predominant return flow of blood can result in an inadequate ejection capacity into the aorta and thus an insufficient blood supply to all organs.
If the acute stage is over or if the mitral regurgitation develops over a longer period of time, a number of chronic adaptation processes ( compensation mechanisms ) occur in the heart and in the pulmonary vessels. First of all, the sustained pressure and volume load on the atrium leads to its enlargement ( dilatation, dilatio cordis ), whereby the atrial volume can often increase three to fourfold within months and years. This dilation also reduces the pressure-increasing effect of the regurgitation volume in the pulmonary circulation over time . In addition, the volume load also causes the left ventricle to enlarge, which now has to promote the regurgitation volume in addition to the amount of blood actually required with each heartbeat. On the one hand, this dilation can also increase the stroke volume via the Frank Starling mechanism , but on the other hand it leads into a vicious circle if, with the expansion of the ventricle, the geometry of the mitral valve is also disturbed and its insufficiency is increased in this way.
Classification and nomenclature
The classification of mitral valve insufficiencies is not carried out uniformly due to constant new considerations and findings, so that the nomenclature derived from it can be misleading in individual cases. In the last decade, the distinction between functional and organic mitral regurgitation has gained in importance. Mitral valve regurgitation is referred to as organic (or valvular ) if changes in the valve itself have been identified as the cause. Functional (or secondary ) mitral regurgitation, on the other hand, is a result of changes in the surrounding structures, mainly the left ventricle. The valve leaflets and the cordae, i.e. the holding threads of the leaflets, are completely normal. Due to the enlargement of the left ventricle as part of a heart failure , the valve leaflets can no longer close completely and the blood flows in systole from the left ventricle back into the left atrium. This further reduces the left ventricular ejection fraction (and thus the cardiac output) and worsens the prognosis of heart failure.
A slight leak in the mitral valve that has no disease value can be detected with the help of sensitive examination methods in up to 90% of all adults with healthy heart. It is often referred to as physiological mitral regurgitation or minimal mitral regurgitation . In childhood and adolescence, the differentiation is made by the time of regurgitation (backflow): Genuine mitral regurgitation is viewed as backflow after valve closure, the return flow during valve closure as physiological. The problem with this classification is that the return flow during the valve closure of the mitral valve can also have a disease value.
“Real” mitral insufficiencies are usually divided into degrees of severity, whereby nowadays mostly three (mild, moderate and severe) and occasionally four (grade I to grade IV) manifestations are differentiated. According to Reinhard Larsen, a regurgitation fraction (proportion of the pendulum volume in the total stroke volume) of less than 0.3 (30%) is considered to be mild, from 0.3 to 0.6 of moderate and more than 0.6 of severe insufficiency .
causes
1 Diastole : both mitral leaflets wide open
2 Early systole: beginning valve
closure 3 The posterior leaflet prolapses into the left atrium
4 Beginning of valve opening
The acquired mitral regurgitation (as in the cleavage of the anterior mitral valve at thoracic trauma , degenerative calcification or inflammatory destruction of the mitral ring, wherein Sehnenfadenruptur different origin and dysfunction of the papillary muscles), and rheumatic mitral regurgitation (flaps damage as a result of rheumatic fever ) are in the industrialized countries now rare, still common in developing countries. Are in the foreground today
- the postinfarzielle mitral insufficiency after myocardial infarction ,
- the ischemic mitral regurgitation due to circulatory disorders of the heart muscle,
- the relative mitral regurgitation as a result of an enlargement of the left ventricle and
- The mitral regurgitation in Prolapssyndrom in connection with a mostly congenital mitral valve prolapse .
Furthermore, bacterial and non-bacterial endocarditis (for example due to lupus erythematosus visceralis) can lead to destruction or scarred shrinkage of valve tissue and thus to mitral regurgitation. Another special case is the occurrence as a result of systolic suction of the (septal) mitral valve leaflet near the heart septum due to a special form of cardiomyopathy ( HOCM ).
The congenital mitral regurgitation is either isolated as a result of a split in the anterior ( anterior ) mitral leaflet or in the case of a misalignment ( dysplasia ) of the mitral leaflet, or more often as a so-called "complex vitium" in connection with other heart defects such as a transposition of the great arteries , a corrected transposition , a Double outlet right ventricle , atrial septal defect, or a ventricular septal defect were observed. Accessory tendon threads ( Chordae tendinae ) can shift the mitral valve cusps towards the ventricle and thus cause mitral regurgitation.
Mitral regurgitation also occurs as a result of congenital diseases of the connective tissue such as Marfan syndrome and Ehlers-Danlos syndrome . Congenital metabolic diseases ( Hurler's disease , mucopolysaccharidosis I ) can also lead to mitral insufficiency. Another syndrome with congenital mitral regurgitation is Forney-Robinson-Pascoe syndrome .
A special form of mitral regurgitation with regard to the cause is caused by cardiotoxic drugs. The primary damage to the heart is cardiomyopathy , for example from chemotherapy for cancer diseases using anthracyclines such as doxorubicin or daunorubicin . With echocardiography, mitral regurgitation can often be diagnosed as the first sign of myocardial damage: 11.6% of children and adolescents treated with anthracyclines develop mitral regurgitation (untreated 1.8%) without clinical symptoms. All subjects had normal left ventricular function at the time of the examination; however, in the course of the disease, 4 out of 34 patients showed manifest left heart failure (5–27 months after diagnosis of mitral regurgitation). Also mediastinal irradiation , for example as part of the therapy of Hodgkin's disease can lead to mitral regurgitation.
A syndromic form is macrothrombocytopenia with mitral valve regurgitation .
Clinical picture
Symptoms and clinical signs
Lighter forms are not noticed by the person concerned. The typical symptoms of severe mitral regurgitation are easy exhaustion ("performance kink") and shortness of breath ( dyspnoea ). Cardiac arrhythmias, which are more common in mitral regurgitation, can manifest themselves in the form of palpitations or palpitations .
The most important and groundbreaking finding during the physical examination is a high-frequency band-shaped, "pouring" systolic (decrescendo) sound that is audible immediately after the 1st heart sound , which is usually attenuated depending on the severity of the valve insufficiency , and which is usually loudest above the apex of the heart and is carried forward into the left armpit . The 2nd heart sound to the left of the sternum is often louder. A third heart sound can also be heard. In the case of percussion, the cardiac attenuation widened to the left. In addition, left ventricular dilatation may occasionally in a leftward shift of the outside and widespread, in which palpation palpable heart apex , pulmonary rales and pulmonary congestion at a jugular vein congestion and edema are detected in secondary right heart failure.
In children and adolescents, symptoms of mitral regurgitation do not differ from symptoms in adulthood. The symptoms of mitral regurgitation are more severe and appear more quickly the younger the child is. In small children and newborns, the symptoms of developmental delay or stagnation in growth should be emphasized: Despite sufficient food intake, children with significant mitral regurgitation do not gain weight, and the expected increase in size does not occur. Furthermore, frequent infections of the lower airways (especially left-sided pneumonia or obstructive bronchitis ) are a possible indication of mitral regurgitation, since the left main bronchus is narrowed by the enlarged left atrium and thus the ventilation of the left lung is reduced. Otherwise, the severity of mitral regurgitation also correlates with the severity of the symptoms in children.
Technical findings
In addition to the physical examination, today only an ultrasound examination of the heart ( echocardiography ) is usually required ( replacing the earlier phonocardiography ), in cases of doubt also in the form of transesophageal echocardiography ("Schluckecho", abbr. TEE). Further examination procedures are only required in special cases or before a planned operation to exclude concomitant diseases. The diagnosis of mitral regurgitation in children does not differ from that in adults. TEE is very difficult to perform in toddlers, infants and newborns.
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| Severe MI | Legend |
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1 Left atrium (LA) - 2 MI-Jet LV Left ventricle - RV Right ventricle - RA Right atrium |
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Echocardiography
Echocardiography is indispensable as a standard procedure: It allows the diagnosis to be confirmed, the severity and probable cause to be determined, and the course to be assessed. As a result of the improved display quality of the ultrasound images, TEE is now only required in less than five percent of patients.
The color Doppler echocardiography (see fig.) Shows the presence of mitral regurgitation as a color cloud (usually shown in blue ) in the left atrium, which is referred to as the insufficiency jet or regurgitation jet . The width and extent of this color cloud already allow a rough estimate of the severity of the insufficiency. In addition, the underlying mechanism (ring dilatation, incomplete valve closure, endocarditis, prolapse , flail leaflet , “unclear”) and the localization of any valve changes can usually be documented during echocardiography .
The size and pumping function of the left ventricle can also be reliably determined with the help of echocardiography. These important parameters of the heart function are important for the assessment of severe mitral regurgitation, as they provide information about the optimal time for a valve operation.
| light | moderate | heavy | |
| Atrium size | ≤ 4.0 cm | > 4.0 cm | > 4.0 cm |
| Jet plane | <4.0 cm² | 4.0-8.0 cm² | > 8.0 cm² |
| Jet area / atrium size | <0.2 | 0.2-0.4 | > 0.4 |
| Jet length / atrial length | < 1 / 3 | 1 / 3 - 2 / 3 | > 2 / 3 |
| proximal jet width | <0.3 cm | 0.3-0.69 cm | ≥ 0.7 cm |
| Regurgitation volume | <30 ml | 30-59 ml | ≥ 60 ml |
| Regurgitation opening | <0.2 cm² | 0.2-0.39 cm² | ≥ 0.4 cm² |
| Echocardiographic severity assessment | |||
The determination of the severity of mitral regurgitation with the help of echocardiography has increased considerably in reliability over the past 20 years. As a rule, various parameters are measured today, which were initially controversial. The severity is then assessed in an overview of the values determined. In the case of organic insufficiencies, especially in mitral valve prolapse, the extent of the proximal convergence method is regularly overestimated.
Echocardiography is also the diagnostic tool of choice for children. In contrast to adulthood, the severity classification based on echocardiographically determined parameters is not validated comparably well .
Other procedures
Other examination methods are only required to identify any complications or to prepare for surgery immediately. For example, an ECG and, if necessary, a long-term ECG can be helpful for diagnosing accompanying cardiac arrhythmias and an X-ray of the thoracic organs for the question of possible pulmonary congestion.
With the cardiac catheter examination , the mitral regurgitation is also diagnosed and quantified, but the examination is only necessary in older patients before a planned heart valve operation in order to carry out a bypass operation at the same time if an accompanying coronary heart disease is involved .
course
The course of mitral regurgitation is extremely variable and can only rarely be foreseen. Even severe mitral regurgitation can remain completely "stable" (unchanged) for many years, and this is even the rule for minor insufficiencies. Regular check-ups, for example at annual intervals, can provide information about the individual progress. Particular attention is paid to the severity of the insufficiency, the size and pumping function of the left ventricle and other signs of an impending overload of the heart in order to recognize impending deterioration at an early stage. These “progress parameters” are important pointers for optimal therapy planning .
In children, especially young children and newborns, mitral regurgitation is more severe and faster than in adults or adolescents. In most cases, congestive heart failure results in young children within three years of being diagnosed with mitral regurgitation.
Prophylaxis and therapy
As a general rule, all patients with “real” (not just “physiological”) mitral regurgitation have an increased risk of developing bacterial endocarditis . For this reason, the medical societies have been recommending consistent endocarditis prophylaxis for decades before all interventions such as colonoscopy and tooth extraction , in which bacteria can get into the bloodstream. While European and German guidelines provide for this recommendation, it has been limited by the American Heart Association (AHA) since April 2007 to high-risk patients with an artificial heart valve or who have had endocarditis.
In addition, no therapy is required for mild mitral regurgitation. However, normal blood pressure values should be maintained, as high blood pressure increases the pressure difference between the left ventricle and the left atrium and thus the regurgitation volume and the pressure load on the atrium.
In childhood, regular check-ups by means of echocardiography at intervals of 6 to 12 months are indicated.
Medical therapy
In severe mitral regurgitation with signs of heart failure , therapy is based on the principles of heart failure therapy, whereby the improvement of contractility (through digitalis ), the reduction of the preload (through diuretics and nitrates) and the lowering of the afterload or the peripheral vascular resistance (through vasodilators such as ACE inhibitors, prazosin and nitroprusside) are in the foreground. Whether long-term drug therapy with ACE inhibitors improves the prognosis even in symptom-free patients without heart failure is still controversial. If cardiac arrhythmias such as atrial fibrillation are present at the same time , the use of antiarrhythmics may be necessary.
In the case of a given indication, such as non- valvular atrial fibrillation (depending on the CHA2DS2-VASc score and the HAS-BLED score), anticoagulants (such as phenprocoumon or warfarin ) are used to prevent thrombus formation within the (enlarged) left atrium and especially here of the left atrial appendage. The new oral anticoagulants such as rivaroxaban (Xarelto), dabigatran (Pradaxa), apixaban (Eliquis) and edoxaban (Lixiana) are gradually replacing vitamin K antagonists such as phenprocoumon or warfarin due to the lower bleeding complications associated with stroke prophylaxis.
In acute severe mitral regurgitation, treatment usually has to be carried out in the intensive care unit . In this case, the aim of drug therapy is to reduce the regurgitation volume in order to increase forward flow on the one hand and to reduce pulmonary congestion on the other. In patients with normal blood pressure, this goal can be achieved with nitroprusside sodium ; in the case of low blood pressure, the additional administration of catecholamines such as dobutamine is useful. These patients often also benefit from the use of the intra-aortic balloon pump , which can help stabilize the preparatory phase for the necessary valve surgery.
In children, the mild forms of mitral regurgitation are also treated with medication. The start of drug therapy depends on the severity itself and the course of the echocardiographic controls. The primary therapeutic goal is to reduce the afterload. As in adults, mainly ACE inhibitors are used; In addition, diuretics and digitalis -Präparate ( digoxin , digitoxin ) was used.
Operative therapy
The indication for heart valve surgery should be examined in all patients with severe mitral regurgitation . Either
- a reconstruction of the heart valve carried out in the sense of an open operation ,
- an artificial heart valve inserted or
- a minimally invasive percutaneous mitral valve reconstruction, in which a clip is placed on the natural valve using a catheter-assisted procedure.
In principle, valve reconstruction is preferred because it leads to less impairment of the heart function and does not require permanent inhibition of blood clotting ( anticoagulation ) if the sinus rhythm is preserved . However, it is not possible in particular in the case of severely shrunk, calcified or even destroyed valve leaflets, so that then only valve replacement is possible. The chances of valve reconstruction can be reliably estimated beforehand with the help of echocardiography; in individual cases, the need for an artificial valve only becomes clear during the operation.
The minimally invasive, catheter-supported mitral sail clipping is particularly suitable for patients who have a significantly increased risk of surgery due to age or secondary diseases. It is a percutaneous mitral valve reconstruction in which the lumen that is too large is made into two small ones. It looks like turning a 0 into an 8 through the clip. The patient now has two small valve opening areas instead of one large one on his mitral valve. Your sum is less than the KÖF before the intervention. Several clips can be placed next to each other for severely ill patients. Intraoperative measurements using echocardiography ensure that there is no stenosis despite the reduced valve opening area . The reflux ( i.e. regurgitation ) becomes smaller; the cardiac output is größer.Die largest study ever to Mitralsegel clipping ( coapt ) showed at Clip patients significantly reduced risk of death and improve quality of life.
A valve operation is useful if the symptoms clearly caused by the mitral regurgitation cannot be eliminated by medication, as long as the pumping function of the left ventricle is not severely restricted ( ejection fraction [EF]> 30%).
In asymptomatic patients (without symptoms) with severe mitral regurgitation, surgery is recommended if there is evidence of cardiac overload. This is the case with restricted pumping function (EF <60%) or significant enlargement (end systolic diameter [LVESD]> 45 mm or LVESD index> 26 mm / m²) of the left ventricle, also with evidence of pulmonary hypertension (systolic pulmonary artery pressure> 50 mmHg (67 mbar ) at rest or> 60 mmHg (80 mbar ) during exercise). In the case of a reconstructable mitral valve, the indication is given more generously, because the expected improvement through the operation is to be assessed higher.
In cases of doubt, the stress hemodynamics, i.e. the changes in the pressure values and the heart's pumping function under physical stress, can be helpful for the initial assessment of the indication for surgery. An American study from 2013 now indicates that early surgical treatment of the mitral valve can lower the rate of heart failure diseases and extend the life of those affected.
Postoperatively, patients with a reconstructed valve can usually be considered "heart healthy" after a few weeks. If there are no other diseases, their resilience is not significantly impaired and special cardiac therapy is not required. Patients with an artificial heart valve often need permanent blood coagulation inhibition ( anticoagulation ) through medication such as Marcumar ® . With them, the heart function is occasionally measurably restricted under load, depending on the diameter of the valve prosthesis used. With an otherwise normal heart function, however, this deviation is so small that no restrictions can be felt in everyday life.
Special features in children
As the mitral regurgitation progresses more rapidly, children often require surgical therapy. Compared to adulthood, it suffers from special problems. On the one hand, the use of valve prostheses in children before they reach their final height during puberty is always associated with the need for one or more repeated operations to adapt the prosthesis size to the size of the heart. This is not possible indefinitely. On the other hand, the mandatory use of anticoagulant drugs in the presence of a valve prosthesis in childhood before puberty causes significant difficulties with regard to bleeding complications. Small children in particular only adhere to the rules of conduct to avoid bleeding complications to a limited extent when taking anticoagulants for a long time. Since the anticoagulation must be carried out over long periods of time when using a valve prosthesis at a young age, the indication for the use of a valve prosthesis is made as cautious as possible. Nevertheless, in children with mitral regurgitation that requires surgery in the long term, heart valve replacement can be expected in many cases. The short- and medium-term prognosis after a surgical valve replacement is good in children. The long-term prognosis of a mechanical or bioprosthetic valve replacement is only moderate, with corresponding morbidity and mortality rates , due to the frequent occurrence of cardiac arrhythmias requiring treatment and left ventricular insufficiency .
Therefore, whenever possible, valve reconstruction without the use of a prosthesis is attempted first ( annuloplasty , valvuloplasty ). There are currently no reliable and unambiguous criteria for the use of a valve prosthesis in childhood.
forecast
Due to the very different course of mitral regurgitation, the prognosis of the patients is also very different. It is now assumed that people with mild mitral regurgitation without any other heart disease have a normal life expectancy.
Patients who were indicated for surgery according to current guidelines had an 8-year survival rate of 89%. Figures from 1980 to 1989 show a clear dependence of the prognosis on the pumping function of the left ventricle before the operation: The 10-year survival rate of those patients with normal ventricular function (EF ≥ 60%) was 72% and thus corresponded to the survival rate Peers without heart surgery, while it was significantly lower at 32% for an EF of less than 50% and 53% for an EF between 50 and 60%.
Sudden deaths are rare in patients with mitral regurgitation; they occur in patients with a torn tendon thread with a frequency of 0.8%, but with simultaneous atrial fibrillation with a probability of 4.8% per year.
Mitral valve regurgitation in animals
In dogs and cats, mitral valve regurgitation is one of the most common acquired heart diseases; in dogs, organic mitral valve regurgitation due to a degenerative change in the basic collagen structure of the valve (so-called mitral valve endocardiosis ) is even the most frequently diagnosed heart disease, accounting for almost 40 percent. In addition, the clinical picture occurs regularly as an accompanying symptom of cardiomyopathy in dogs and cats and can be the trigger for serious complications such as atrial fibrillation in dogs and thromboembolism in cats.
dogs
Especially representatives of smaller breeds of dogs are susceptible to chronic degenerative mitral valve diseases. Breeds that are often affected by this include Cavalier King Charles Spaniels , Poodles , Chihuahua , Pekingese , Fox Terriers and Cocker Spaniels . The prevalence of the disease within a dog population is around 10% in five to eight year old animals and increases with age, so that by the age of 13, 30 to 35% of the animals are affected. No data are available for the frequency of occurrence as a secondary clinical picture in cardiomyopathies, but valve insufficiency is often determined by the disease-related expansion of the valve's suspension apparatus. In rare cases, the mitral valve is infected by bacteria, which also result in valve insufficiency.
The most common signs of impaired cardiac ability are: decreased performance, cough, nocturnal restlessness and dyspnoea . In auscultation , holosystolic heart murmurs of constant intensity can be heard in various volumes (grade 1 to grade 6) in most cases. The loudest noise ( punctum maximum ) of the mitral valve is in the 5th intercostal space at the apex of the heart. In the X-ray image an enlarged heart is often observed. The left atrium can in this case in the form of a triangle ( "Mitralisdreieck") according kaudo- dorsal emerge. The often noticeable bend between the windpipe and the spine can have given way to a parallel course; in some cases the atrium can even compress the windpipe and, as a result of the mechanical irritation caused by this, intensify the coughing symptoms. In advanced cases, pulmonary edema is present. The electrocardiogram is often not very specific; there are sometimes indications of an enlarged atrium (extended P-wave, over 0.04 seconds) or an enlarged main chamber (QRS complex longer than 0.06 seconds). In addition, atrial or ventricular extrasystoles can develop , and in some cases atrial fibrillation is observed. This symptom is common in dogs with functional mitral regurgitation due to dilated cardiomyopathy. With echocardiography , mitral valve regurgitation can be easily identified using a Doppler examination. In addition, the following effects occur: enlarged main chamber due to the volume overload, often hypercontractility due to compensation mechanisms, significantly enlarged atrium.
Depending on the severity of the disease, there are different forms. In addition to dogs with or without symptoms for years, the disease can get worse and worse within a few months. The NYHA classification or the ISACHC classification is used as a measure for this . Medicinal therapy usually only starts when the first clinical symptoms appear (see above).
If the mitral valve is severely ill, the blood can flow back under high pressure and overload the atrial wall at the point where the jet hits it so much that it ruptures . In addition, the clinical picture can be acutely aggravated by the fact that the tendon threads tear that fix the valve during the heart contraction , so that a valve prolapse occurs.
The currently common therapy for mitral valve regurgitation is based, depending on the severity of the disease, on the use of pimobendan , ACE inhibitors and dehydrating drugs . In contrast to humans, the surgical treatment of degenerative valve diseases has not yet caught on because, in addition to high financial and technical expenditure, a high surgical mortality rate has been observed in the animals treated in this way.
Other animal species
In cats mitral regurgitation are less frequently observed than in the dog. Here they are mostly associated with diseases of the heart muscle as functional valve insufficiency. A relatively frequent special case is a leak as a consequence of functional aortic stenosis due to a thickening of the heart muscle in the outflow area of the left ventricle. In rare cases, cats develop organic mitral valve disease as a result of endocardial fibrosis .
Horses are another species that are regularly affected by mitral valve regurgitation. It is estimated that 45% of all horses with a systolic heart murmur have mitral valve regurgitation, the cause of which often appears to be endocardiosis . It is believed that between 3 and 4% of all horses are affected by diseases of the mitral valve.
In rabbits , the occurrence of the disease is also described.
literature
- BG Baylen: Congenital mitral insufficiency. In: HD Allen, HP Gutgesell, EB Clark (Eds.): Moss and Adams' Heart Disease in Infants, Children, and Adolescents Including the Fetus and Young Adult. 6th edition. November 2000. Lippincott Williams & Wilkins Publishers, ISBN 0-683-30742-8 .
- RO Bonow, E. Braunwald: Mitral Regurgitation. In: DP Zipes et al. (Ed.): Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 7th edition. WB Saunders Company, Philadelphia 2004, ISBN 1-4160-0014-3 .
- RO Bonow et al .: ACC / AHA Guidelines for the Management of Patients With Valvular Heart Disease. In: J Am Coll Cardiol . 2006 48, pp. E1 – e148. Guidelines of the US professional societies online (English) .
- FA Flachkampf, WG Daniel: Mitral insufficiency. In: Internist. Volume 47, 2006, pp. 275-286.
- Reinhard Larsen: Anesthesia and intensive medicine in cardiac, thoracic and vascular surgery. (1st edition 1986) 5th edition. Springer, Berlin / Heidelberg / New York a. a. 1999, ISBN 3-540-65024-5 , pp. 235-245.
- Klaus Holldack, Klaus Gahl: Auscultation and percussion. Inspection and palpation. Thieme, Stuttgart 1955; 10th, revised edition ibid. 1986, ISBN 3-13-352410-0 , pp. 157-163, 170-172 and 178 f.
- WN Nelson, CG Couto et al .: Internal Medicine of Small Animals. 1st edition. Urban & Fischer, Munich / Jena 2006, ISBN 3-437-57040-4 .
- SH Rahimtoola, M. Enriquez-Sarano, HV Schaff, RL Frye: Mitral valve disease. In: V. Fuster, RW Alexander, RA O'Rourke (eds.): Hurst's The Heart. 10th edition. McGraw-Hill Professional, New York 2000, ISBN 0-07-135694-0 .
- J. Seeburger et al .: Percutaneous and surgical therapy of mitral valve regurgitation . In: Dtsch Arztebl Int . No. 108 (48) , 2011, pp. 816-821 ( review article ).
Web links
- Mitral regurgitation: diagnosis, therapy . ( Memento from August 17, 2011 in the Internet Archive ) University of Essen
Individual evidence
- ↑ C. Ayabakan et al .: The Doppler echocardiographic assessment of valvular regurgitation in normal children. In: Turk J Pediatr. (2003); 45, pp. 102-107. PMID 12921295 .
- ↑ KC Bahadur et al .: Prevalence of rheumatic and congenital heart disease in schoolchildren of Kathmandu valley in Nepal. In: Indian Heart J. 2003 Nov-Dec; 55 (6), pp. 615-618. PMID 14989511
- ^ JD Thomson et al .: Left sided valvar regurgitation in normal children and adolescents. In: Heart . 2000 Feb; 83 (2), pp. 185-187. PMID 10648494 .
- ^ A. Brand et al .: The prevalence of valvular regurgitation in children with structurally normal hearts: a color Doppler echocardiographic study. In: Am Heart J . 1992 Jan; 123 (1), pp. 177-180. PMID 1729823
- ↑ JP Singh et al .: Prevalence and clinical determinants of mitral, tricuspid, and aortic regurgitation (the Framingham Heart Study). In: Am J Cardiol. (1999); 83, pp. 897-902. PMID 10190406 .
- ↑ F. Bursi et al .: mitral regurgitation after myocardial infarction: a review. In: Am J Med. (2006); 119, pp. 103-112. PMID 16443408
- ^ G. Cioffi et al .: Functional mitral regurgitation predicts 1-year mortality in elderly patients with systolic chronic heart failure. In: European Journal of Heart Failure (2005); 7, pp. 1112-1117. PMID 15919238 .
- ↑ K. Yoshida et al .: Color Doppler evaluation of valvular regurgitation in normal subjects. In: Circulation . 1988 Oct; 78 (4), pp. 840-847. PMID 3262454 .
- ↑ Reinhard Larsen (1999), p. 243 ( Hemodynamic goals in mitral regurgitation ).
- ↑ T. Buck, R. Erbel: Advances in the diagnosis and therapy of mitral valve insufficiency. In: heart. (2006) Archive link ( Memento from September 27, 2007 in the Internet Archive )
- ^ Georg Goliasch, Philipp E. Bartko, Noemi Pavo, Stephanie Neuhold, Raphael Wurm: Refining the prognostic impact of functional mitral regurgitation in chronic heart failure . In: European Heart Journal . tape 39 , no. 1 , January 1, 2018, ISSN 1522-9645 , p. 39-46 , doi : 10.1093 / eurheartj / ehx402 , PMID 29020337 .
- ↑ Andrea Rossi, Frank L. Dini, Pompilio Faggiano, Eustachio Agricola, Mariantonietta Cicoira: Independent prognostic value of functional mitral regurgitation in patients with heart failure. A quantitative analysis of 1256 patients with ischaemic and non-ischaemic dilated cardiomyopathy . In: Heart (British Cardiac Society) . tape 97 , no. October 20 , 2011, ISSN 1468-201X , p. 1675-1680 , doi : 10.1136 / hrt.2011.225789 , PMID 21807656 .
- ↑ Reinhard Larsen: Anesthesia and intensive medicine in cardiac, thoracic and vascular surgery. (1st edition 1986) 5th edition. Springer, Berlin / Heidelberg / New York a. a. 1999, ISBN 3-540-65024-5 , pp. 235-245 ( mitral regurgitation ); here: p. 236.
- ↑ a b G. D. Webb et al .: Congenital Heart Disease. In: DP Zipes et al. (Ed.): Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 7th edition. WB Saunders Company, Philadelphia 2004, ISBN 1-4160-0014-3 .
- ^ CD van Karnebeek et al .: Natural history of cardiovascular manifestations in Marfan syndrome. In: Arch Dis Child . 2001 Feb; 84 (2), pp. 129-137. PMID 11159287 .
- ↑ CF Wippermann et al .: Mitral and aortic regurgitation in 84 patients with mucopolysaccharidoses. In: Eur J Pediatr. 1995 Feb; 154 (2), pp. 98-101. PMID 7720756 .
- ↑ J. Allen et al .: Mitral regurgitation after anthracycline treatment for childhood malignancy. In: Heart. 2001 Apr; 85 (4), pp. 430-432. PMID 11250971 .
- ↑ MB Lund et al .: Increased risk of heart valve regurgitation after mediastinal radiation for Hodgkin's disease: an echocardiographic study. In: Heart. 1996 Jun; 75 (6), pp. 591-595. PMID 8697163 .
- ↑ JL Monin et al .: Functional assessment of mitral regurgitation by transthoracic echocardiography using standardized imaging planes, diagnostic accuracy and outcome implications. In: J Am Coll Cardiol. (2005); 46, pp. 302-309. PMID 16022959 .
- ^ W. Voelker: Structured data set for documentation of findings in echocardiography - version 2004. In: Zeitschrift für Kardiologie (2004); 93, p. 997. doi: 10.1007 / s00392-004-0151-8 .
- ↑ T. Buck et al .: Current recommendations for echocardiographic severity assessment of mitral valve regurgitation. In: heart. (2006); 31, pp. 30-37.
- ↑ G. Grossmann et al .: Value of the proximal flow convergence method for quantification of the regurgitant volume in mitral regurgitation. In: Z Kardiol. (2004); 93, pp. 944-953. doi: 10.1007 / s00392-004-0151-8 .
- ^ W. Wilson et al .: Prevention of Infective Endocarditis. Guidelines From the American Heart Association. A Guideline From the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group . In: Circulation. (2007) online ( Memento of the original from March 2, 2008 in the Internet Archive ) Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. . PMID 17446442
- ↑ Reinhard Larsen (1999), p. 240 f.
- ↑ Abbott Medical GmbH: The percutaneous mitral valve reconstruction.
- ↑ Rakesh M. Suri: Association Between Early Surgical Intervention vs Watchful Waiting and Outcomes for Mitral Regurgitation Due to Flail Mitral Valve Leaflets. In: JAMA. 310, 2013, p. 609, doi: 10.1001 / jama.2013.8643 .
- ^ I. Adatia et al .: Clinical course and hemodynamic observations after supraannular mitral valve replacement in infants and children. In: J Am Coll Cardiol. 1997; 29, pp. 1089-1094. PMID 9120164
- ↑ S. Chavaud et al .: Reconstruction surgery in congenital mitral valve insufficiency (Carpentier's techniques): long term results. J Thorac Cardiovasc Surg . 1998; 115, pp. 84-92. PMID 9451050 .
- ↑ AS Aharon et al .: Early and late results of mitral valve repair in children. In: J Thorac Cardiovas Surg. 1994; 107, pp. 1262-1270. PMID 8176970
- ↑ M. Enriquez-Sarano et al .: Echocardiographic prediction of survival after surgical correction of organic mitral regurgitation. In: Circulation. (1994); 90, pp. 830-837. PMID 8044955 .
- ^ JW Buchanan: Prevalence of Cardiovascular Disorders. In: RF Fox, D. Sisson, NS Moïse: Textbook of Canine an Feline Cardiology: Principles and Clinical Practice. 2nd Edition. Saunders, Philadelphia 1999, ISBN 0-7216-4044-3 .
- ^ J Häggström et al .: Effect of pimobendan or benazepril hydrochloride on survival times in dogs with congestive heart failure caused by naturally occurring myxomatous mitral valve disease: the QUEST study. In: J Vet Intern Med. 2008 Sep-Oct; 22 (5), pp. 1124-1135 PMID 18638016
- ↑ IMPROVE Study Group: Acute and short-term hemodynamic, echocardiographic and clinical effects of enalapril maleate in dogs with naturally acquired heart failure: results of the Invasive Prospective Multicenter Evaluation of Veterinary Enalapril study. In: J Vet Intern Med. 1995; 9, p. 234, PMID 8523320 .
- ↑ A. Michl: Clinical and further cardiological examinations in warm-blooded horses with heart valve insufficiency. Dissertation . Hanover 2001, pp. 20-21. d-nb.info
