Observations on seven cases of mitral insufficiency in the horse

Observations on seven cases of mitral insufficiency are described. Three of the horses had recent histories of cardiac failure and formed a separate group in which there were marked haemodynamic changes which varied in relation to heart rate but were associated with pulmonary hypertension, elevated right ventricular pressure and low peak left ventricular pressure. In the other four horses the heart appeared to be compensating at rest but to be unable to cope with severe exertion. On auscultation, a widespread pansystolic murmur and a prominent third heart sound were characteristic of the left ventricular volume overload. Microscopic changes were found in one left papillary muscle. The possibility that changes in the position of the papillary muscles consequent upon left ventricular dilatation may lead to or exaggerate mitral valve eversion is discussed.     

Mitral valvular insufficiency associated with ruptured chordae tendineae in three foals

Mitral valvular insufficiency associated with ruptured chordae tendineae was diagnosed in 3 foals with signs of congestive heart failure, which were believed to be secondary to the development of pulmonary hypertension associated with the valvular insufficiency. The septal leaflet of the mitral valve was affected in all 3 foals, and foal 2 also had ruptured chordae tendineae associated with the caudal mitral valve leaflet. Bacterial endocarditis and myocardial necrosis were associated with the ruptured chordae tendineae in foals 3 and 2, respectively. Idiopathic rupture was considered in foal 1. Two-dimensional echocardiography demonstrated a flail mitral valve leaflet in foals 2 and 3 and a ruptured chorda tendineae in foal 3. The ruptured chorda tendineae in foal 1 was not visualized with M-mode echocardiography.     

Identification of surface morphologic changes in the mitral valve leaflets and chordae tendineae of dogs with myxomatous degeneration

OBJECTIVE: To describe structural changes in the left atrioventricular (mitral) valve complex of dogs with endocardiosis by use of scanning electron microscopy. ANIMALS: 5 clinically normal dogs and 4 dogs with mitral valve endocardiosis. PROCEDURE: The mitral valve complex from each dog was fixed and prepared for examination via scanning electron microscopy. Findings in valves from clinically normal and affected dogs were compared to identify surface changes associated with endocardiosis. RESULTS: Compared with findings in valves from clinically normal dogs, endocardiosis-affected mitral valve complexes had several morphologic abnormalities. Tissue swelling on the edge of valve leaflets, chordae tendineae, and the chordal-papillary muscle junction was evident. Damage to the valve complex endothelium was unevenly distributed; in some areas, denudation of endothelial cells had exposed the basement membrane or subendothelial valve collagen matrix. This damage was most noticeable on the leaflet edges and extended more to the ventricular aspect of the valve than the atrial side. Cell loss also extended to the chordae tendineae but was less apparent at the chordal-papillary muscle junction. The remaining endothelial cells on affected valves were arranged in less-ordered rows and had more plasmalemmal microappendages, compared with cells on unaffected valves. CONCLUSIONS AND CLINICAL RELEVANCE: Morphologic changes associated with mitral valve endocardiosis in dogs were similar to those observed in humans with mitral valve prolapse. In dogs with mitral valve endocardiosis, gross changes in the valve complex may affect hemodynamics in the heart; alterations in the leaflet and chordal endothelium may contribute to pathogenesis of this disease.     

Long‐term outcome in dogs undergoing mitral valve repair with suture annuloplasty and chordae tendinae replacement

Mitral valve repair under cardiopulmonary bypass was performed in three dogs with clinical signs associated with mitral regurgitation that were not controlled by medication. Mitral valve repair comprised circumferential annuloplasty and chordal replacement with expanded polytetrafluoroethylene. One dog died 2 years after surgery because of severe mitral regurgitation resulting from partial circumferential suture detachment. The others survived for over 5 years, but mild mitral valve stenosis persisted in one. The replaced chordae did not rupture in any dog. Mitral valve repair appears to be an effective treatment for mitral regurgitation in dogs. Chordal replacement with expanded polytetrafluoroethylene is a feasible technique, demonstrating long‐term durability in dogs. However, mitral annuloplasty techniques need improvement.     

Evaluation of techniques and outcomes of mitral valve repair in dogs

OBJECTIVE: To describe surgical techniques for and assess outcome of treatment of mitral regurgitation in dogs. DESIGN: Uncontrolled prospective study. ANIMALS: 18 dogs with naturally occurring mitral regurgitation. PROCEDURE: All dogs weighed > 5 kg (11 lb) and had severe mitral regurgitation, congestive heart failure (CHF), and no serious noncardiac disease. Left ventricular volume indices, left atrial size, and degree of mitral regurgitation were determined echocardiographically before and after surgery. Repair techniques included circumferential annuloplasty, placement of artificial chordae, chordal fenestration and papillary muscle splitting, and edge-to-edge repair. Factors predictive for surgery survival and resolution of CHF were determined. RESULTS: 12 dogs survived surgery. Factors predictive for surgery survival included weight > 10 kg (22 lb) and CHF of less than 6 months' duration. In 9 dogs, CHF resolved for a median period of 1 year (range, 4 months to 3 years) after surgery. One dog had stable CHF at 12 months. One dog died as a result of progressive CHF; another was euthanatized for a noncardiac reason. Left ventricular diastolic volume index was 226.9 +/- 117.7 cm3/m2 before surgery and 134.9 +/- 70.4 cm3/m2 at 6 months after surgery (n = 10). Factors predictive for resolution of CHF included left ventricular diastolic volume index < 250 cm3/m2 and systolic volume index < 70 cm3/m2. CONCLUSION AND CLINICAL RELEVANCE: Mitral valve repair may resolve CHF in dogs with severe mitral regurgitation, particularly in dogs that weigh > 10 kg and are treated within 6 months of the onset of CHF.     

Clinical, echocardiographic, and Doppler imaging characteristics of mitral valve stenosis in two dogs.

Mitral stenosis was diagnosed noninvasively by echocardiography and Doppler imaging in 2 Bull Terriers. Two-dimensional echocardiography revealed severe atrial and moderate left ventricular dilatation; severely reduced mitral valve opening excursion; doming of the cranial mitral valve leaflet into the left ventricle during diastole; thickened, nodular cranial mitral valve leaflets; and reduced mitral valve orifice. M-mode echocardiographic findings additionally indicated greatly diminished mitral valve E to F slope and abnormal caudal mitral valve leaflet motion. Color flow Doppler imaging revealed bright bursts of color with aliasing originating from the stenotic mitral valve orifice, extending into the left atrium during systole, and into the left atrium during diastole. Spectral Doppler recordings revealed transvalvular mitral valve gradients and prolonged pressure half-times. Necropsy performed on 1 dog revealed extremely thickened, nodular, and stiff mitral valves with short, thickened, and fused chordae tendineae. The diagnosis of mitral valve stenosis was easily facilitated with diagnostic ultrasonography.     

Effect of age and training on murmurs of atrioventricular valvular regurgitation in young thoroughbreds

Cardiac auscultation was carried out on 111 Thoroughbred horses age 2-5 years to test the hypothesis that athletic training might influence the development of atrioventricular (AV) valve regurgitation in young Thoroughbreds. Murmurs of valvular regurgitation were identified and graded on a 1-6 scale. There were 2 sources of auscultation data: 1) 55 2-year-old horses that were examined by auscultation before training commenced and 9 months later when at race fitness; 2) 56 horses age 2-5 years that were examined on one occasion only (25 2-year-olds, 23 3-year-olds, five 4-year-olds and five 5-year olds). All horses in the second data set were in full training and racing regularly at the time of the examination. To conclude the study, 35 horses were selected randomly from both groups of horses and examined with colour-flow Doppler echocardiography. The aim of the final part of the study was to check specificity and sensitivity of auscultation for detection of AV valve murmurs and therefore validate the auscultation findings. Prior to training, the prevalence in 2-year-old racehorses of murmurs of mitral regurgitation and tricuspid regurgitation was 7.3% (4/55) and 12.7% (7/55), respectively. After training, the prevalence proportions increased to 21.8% (12/55) and 25.5% (14/55). After training, one horse developed a murmur characteristic of aortic regurgitation. The differences in murmur prevalence were statistically significant for mitral and tricuspid regurgitation (paired t test results: mitral regurgitation, P = 0.019; tricuspid regurgitation, P = 0.007), as were the differences in mean murmur grade (P = 0.018 and P = 0.0006, respectively). There were no significant effects of age on the prevalence of valvular regurgitation in 56 horses examined at race fitness. Auscultation was a specific (specificity 100%) and reasonably sensitive method for detection of murmurs of mitral and tricuspid regurgitation (mitral regurgitation: positive predictive value 100%, negative predictive value 84%, tricuspid regurgitation: positive predictive value 100%, negative predictive value 65%). These data suggest that the prevalence and grade of murmurs of mitral and tricuspid valvular regurgitation increase in 2-year-old Thoroughbreds after 9 months of athletic training. Whereas the effects of age and growth on the prevalence of murmurs cannot be ruled out from these data, this study suggests that there is an influence of athletic training on the development of atrioventricular valvular regurgitation in flat-racing Thoroughbreds.     

Acquired mitral stenosis in a cat with hypertrophic cardiomyopathy

A seven-year-old castrated male domestic shorthair cat was diagnosed with hypertrophic cardiomyopathy (HCM) and suspected mitral stenosis (MS) based on electrocardiography, thoracic radiographs and echocardiographic findings. Post-mortem examination of the heart revealed morphological features consistent with HCM. In addition, there was marked fibrous deposition on the surfaces of the chordae tendineae extending to both mitral valve leaflets, which caused total chordal fusion into pillars of fibrous tissue and fusion of the commissures. The present case indicates that acquired MS can occur in association with HCM in the cat.     

Echocardiographic evaluation of equine aortic insufficiency

Echocardiographic evaluation of 23 horses with aortic insufficiency was performed, using M-mode (n = 23) and 2-dimensional real-time echocardiography (n = 14 of 23). Echocardiograms were evaluated for abnormalities of aortic and mitral valves and alterations in motion of these valves. Changes in left ventricular chamber size and function, as well as aortic root size, were evaluated. The presence of other cardiac disease was also evaluated. Horses with aortic insufficiency had significant increases (P less than 0.01) in mean values of left ventricular chamber size, aortic root diameter, and shortening fraction. Left ventricular free wall thickness also was significantly decreased (P less than 0.01). Valvular abnormalities were seen echocardiographically in all 23 horses. Eighteen horses with aortic insufficiency had thickened valves, whereas two horses had lesions associated with vegetative endocarditis. High-frequency vibrations of the septal leaflet of the mitral valve were noticed in all horses, whereas similar vibrations of the aortic valve were seen in six horses. The presence of a bounding arterial pulse correlated significantly (P less than 0.05) with increased left ventricular chamber size at end diastole and shortening fraction, indicating a marked left ventricular volume overload. A reliable diagnosis of aortic insufficiency can be made with the detection of bounding arterial pulses in concert with a holodiastolic decrescendo grade II to V/V murmur with maximal intensity over the aortic valve area, radiating toward the left cardiac apex.     

Left ventricular volume determination in the horse by two-dimensional echocardiography: an in vitro study

This study was designed to evaluate the accuracy of two-dimensional echocardiography (2DE) in determining the left ventricular volume (LVV) of the horse in vitro. After examining the shape of the left ventricular silicon rubber casts of four equine hearts, two modified Simpson's rule methods (Model A and Model B) as combinations of conical shapes and one biplane area-length method as a single cone (Model C) were chosen for volume calculations. One long axis and three short axis planes were used for linear and area 2DE measurements, respectively. The ventricular length (L) was calculated from the chordal length (CL) by using a linear regression equation (L = 5.54 + 1.83 CL) obtained by anatomical measurement of these two parameters on 40 normal hearts. The LVV was calculated in 15 formalin-fixed hearts from 2DE measurements with the three geometric models. Left ventricular casts were then made using silicon rubber, and their volumes were determined by water displacement. The calculated volumes were plotted against cast volumes with linear regression analysis. All calculated LVVs correlated well with the cast LVVs (R = 0.921 to 0.957; P less than 0.001). The highest correlation was provided by Model A which best represented the shape of the left ventricle. This model consisted of a truncated cone bordered by the area at the level of the mitral valve and by the area at the level of the chordae tendineae, plus a cone the base of which was the area at the level of the papillary muscles. The results demonstrate the applicability of 2DE for equine LVV determinations in vitro, similar to other species.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pulmonary artery wedge pressure measurement in healthy warmblood horses and in warmblood horses with mitral valve insufficiencies of various degrees during standardised treadmill exercise

In 12 healthy warmblood horses and 10 horses with mitral valve insufficiencies (MVI) of various degrees heart rate and pulmonary artery wedge pressure (PWP) was measured at rest and during standardised exercise on a high speed treadmill. There was a significant increase in PWP with each change in speed of the treadmill (p < 0.01). The PWP of horses with mild mitral valve regurgitation under working conditions was not significantly different compared to the healthy horses. The horses with moderate mitral valve regurgitation showed a significant higher pulmonary artery wedge pressure at rest and during exercise compared to the healthy horses (p < 0.01) at rest and during treadmill velocity. The tendencies were seen that mild mitral valve regurgitation results only in mild hemodynamic changes during exercise, while moderate MVI have an important influence on haemodynamics.     

Echocardiographic features of accessory mitral valve tissue presenting left ventricular outflow tract obstruction in a dog

In a 3-year-old Samoyed, aortic bulging was found on radiography during a general check-up. On echocardiography, turbulent flow was found in left ventricular outflow tract (LVOT) with high velocity (6.1 m/s). A linear structure was attached to the interventricular septum and connected to the chordae tendineae reaching the papillary muscle. A part of the structure moved during cardiac cycle, similar to mitral motion. This dog was diagnosed with LVOT obstruction caused by accessory mitral valve tissue (AMVT). This is the first report of AMVT in veterinary medicine. AMVT should be considered as a possible cause of LVOT obstruction in dogs.     

Changes in platelet life span in dogs with mitral valve regurgitation

Platelet life span was measured in dogs with experimentally-induced mitral regurgitation (MR) by using an in vitro whole-blood biotinylation technique to evaluate the effects of shear stress induced by MR. Mitral regurgitation was created in healthy dogs by ablation of the mitral valve chordae tendineae. Mitral regurgitation was identified by auscultation and postoperative color Doppler echocardiography. Platelets were biotinylated. and derivatized blood was reinfused into the dogs. Biotinylated platelet disappearance was measured over time to determine platelet life span. Pre- and postablation platelet life span was compared in each dog. Platelet life span was shorter in dogs with experimentally induced MR. Shear stress from MR was postulated to shorten platelet life span. Alternations in platelet function and life span may contribute to the progression of cardiovascular disease in dogs with MR. Further studies are required to determine if platelet dysfunction is related to disease progression in these patients.     

Influence of detomidine on echocardiographic function parameters and cardiac hemodynamics in horses with and without heart murmur

30 warmblood horses were examined before and after sedation with 20 micrograms/kg BW detomidine, to determine changes of cardiac function parameters, using B-mode, M-mode and Doppler echocardiography. 15 horses showed a heart murmur, but no clinical signs of cardiac heart failure, 15 horses had neither a heart murmur nor other signs of cardiac disease. After sedation with detomidine we could recognise a significant increase of end-diastolic left atrium diameter, an increase of end-systolic left ventricular diameter and aortic root diameter. The end-systolic thickness of papillary muscle and interventricular septum showed a decrease. Fractional shortening and amplitude of left ventricular wall motion was decreased after sedation. The mitral valve echogram revealed a presystolic valve closure and an inflection in the Ac slope (B-notch) in xy horses before sedation. Both increased after sedation with detomidine. Doppler echocardiography showed a decrease of blood flow velocity and velocity time integral (VTI) in the left and right ventricular outflow tract after sedation. Regurgitant flow signals were intensified following sedation in xy horses, especially at the mitral valve.     

Prevalence and clinical importance of heart murmurs in racehorses

OBJECTIVE: To determine the prevalence of various types of heart murmurs in Thoroughbred racehorses and assess their association with performance by echocardiography and review of the horses' race records for the preceding 2 years. DESIGN: Clinical and retrospective study. ANIMALS: 846 Thoroughbred racehorses. PROCEDURE: Cardiac auscultations were performed by 3 individuals; for 30 horses, Doppler echocardiographic examinations were also performed. Statistical analyses of race records for 753 horses were performed to assess association of heart murmurs with performance. RESULTS: Heart murmurs were detected by cardiac auscultation in 686 of 846 (81.1%) horses. Systolic murmurs over the heart base were most common; 365 (43.1%) horses had systolic murmurs that were loudest over the pulmonary valve area, and 232 (27.4%) horses had systolic murmurs that were loudest over the aortic valve area. Systolic murmurs over the tricuspid valve area were detected in 241 (28.5%) horses, whereas systolic murmurs over the mitral valve area were detected in only 32 (3.8%) horses. Diastolic murmurs were much less common than systolic murmurs. Review of race records did not reveal a significant association between murmurs and performance. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that heart murmurs are a common finding in racehorses; most of these heart murmurs do not appear to be clinically important.     

Comparison of Systolic Cardiac Function Before and After Treatment of Atrial Fibrillation in Horses With and Without Additional Cardiac Valve Insufficiencies

Clinical, electrocardiographic and echocardiographic examinations were conducted before therapy and 4 days after conversion to normal sinus rhythm in 15 horses with a history of atrial fibrillation of 2-6 months duration. Seven horses showed no other signs of cardiac disease. Four horses suffered additionally from mitral valve insufficiency, while six horses had aortic valve insufficiency, including two of the four horses with mitral valve insufficiency, but none had signs of congestive heart failure. Doppler echocardiographic estimates of various variables were made for assessment of systolic heart function. These included heart rate, stroke volume, cardiac output and cardiac output per kg of body weight (heart index). After conversion to normal sinus rhythm, the horses without heart valve insufficiency showed a statistically significantly decreased heart rate (-24%) and cardiac output (-3%), but an increase in stroke volume (+8.4%) and heart index (+9%). The horses with heart valve insufficiency experienced a statistically significant decrease in heart rate (-21%) after conversion to normal sinus rhythm, but showed an increase in all other variables. Cardiac output increased statistically significantly by 20%, stroke volume by 54% and heart index by 58%.     

Pathologic and clinical features of infectious endocarditis

Infectious endocarditis is a systemic disease associated with high morbidity and mortality. Clinical recognition and effective management is challenging, but insights can be gleaned from relevant pathologic features. Risk factors include subaortic stenosis, possibly certain other congenital anomalies, and bacteremia. Auscultation can provide clues regarding valvular involvment, particularly when a diastolic left basilar murmur of aortic valve regurgitation is present. Aortic valve vegetations and insufficiency may also alter femoral arterial pulse characteristics. Echocardiography may facilitate diagnosis, particularly with aortic valve lesions, but may not be able to distinguish between small mitral valve vegetations and early chronic degenerative valve disease. Vegetative lesions develop along edges of valve closure on the ventricular aspect of the aortic valve and the atrial surface of atrioventricular valves. They may extend across valve leaflet, from valves to adjacent left atrial endocardium, interventricular or interatrial septum, or chordae tendineae. Vegetations can be friable and frequently embolize to spleen, kidney, and left ventricle — often before clinical recognition of the disease. Valvular insufficiency develops as a consequence of valvular vegetations, necrosis, perforation, or rupture of the chordae tendineae. Histopathologic appearance varies with respect to duration of disease and antimicrobial therapy. These factors influence the amount of necrotic material, blood clot, fibrin, and inflammatory cells which make up the vegetations. Bacteria are not always identified in valvular lesions, especially following antibacterial therapy, but may be detected in other organs. Common sequellae include congestive heart failure, sepsis, arrhythmias, and systemic organ infarction.     

An Echocardiographic Study of Atrial Fibrillation in Horses: Before and After Conversion to Sinus Rhythm

Two-dimensional and M-mode echocardiograms were recorded from 41 horses before they were successfully treated for atrial fibrillation. In addition, these examinations were performed in a subgroup of 20 horses after treatment, and the results were compared with pretreatment values. Atrial fibrillation in this group of horses was associated with a reduction of mean left ventricular fractional shortening (mean 31 %± 5.24%), and 22 of the 41 horses were below the reference range. The remaining mean M-mode variables were within the normal reference range, although 12 horses had increased left ventricular lumen dimensions in systole, and 8 horses had decreased left ventricular ejection times. Abnormal motion of the mitral valve was present in all horses and was characterized by the absence of A peaks, which were replaced by small diastolic undulations in 55% of the horses. In horses 1 to 20, after conversion to sinus rhythm, the mean fractional shortening increased (35.34%± 5.4%, P = .004), but there were no significant differences in heart rate or left ventricular lumen diameters in systole or diastole. These results suggest that ventricular function may be compromised by the presence of atrial fibrillation. However, this improved after correction of the arrhythmia.     

Effects of the ACE inhibitor quinapril on echocardiographic variables in horses with mitral valve insufficiency

Twenty horses with mitral valve insufficiency, but without signs of congestive heart failure, and five horses without signs of heart disease were examined before and after medication with an angiotensin-converting enzyme (ACE) inhibitor. The examination included echocardiography assessment as well as heart catheterization. The echocardiographic examination included B-mode, M-mode, conventional and colour Doppler techniques. For 8 weeks, all horses were treated with Accupro 20 (active substance: Quinapril) at an oral dose rate of 120 mg/horse/day. A follow-up of the horses with mitral valve insufficiency after 8 weeks revealed a statistically significant increase in the stroke volume and the cardiac output as well as a decrease in regurgitation velocity time integral (VTI). The regurgitation blood velocity remained the same. The severity of mitral valve insufficiencies revealed a moderate improvement in five horses, from moderate to mild, after therapy. Significant changes of cardiac dimension (B-mode) and shortening fraction (M-mode) before and after treatment could not be observed. The owners' judgement of the horses' performance was that of a minor improvement. In the horses without clinical findings the results of examination before and after treatment remained the same.