Managing chronic valvular disease (Proceedings)
CDVD is the most common cause of cardiac disability in dogs. The disease process is best described as myxomatous degeneration of the heart valves wherein the integrity of the valves is compromised often resulting in valvular insufficiencies.
CDVD is the most common cause of cardiac disability in dogs. The disease process is best described as myxomatous degeneration of the heart valves wherein the integrity of the valves is compromised often resulting in valvular insufficiencies. In a necropsy study performed by JW Buchanan the mitral valve alone was affected in 62% of cases, the mitral and tricuspid valve in 33%, mitral and aortic valves in 3%, mitral, tricuspid and aortic in 1% and tricuspid valve alone in 1%. Small breed dogs such as toy and miniature Poodles, miniature Schnauzers, Pomeranians, Chihuahuas, cocker spaniels, Pekingese, fox terriers, and Boston terriers appear predisposed to the development of CDVD while males are more frequently affected than females (1.5:1.0).
During the initial stages of the disease there is no valvular insufficiency so there is no hemodynamic change or murmur ausculted, and the patients are entirely asymptomatic. A systolic click, possibly from mitral valve prolapse, is sometimes ausculted in these patients. As the lesions progress and the valves become incompetent, a systolic murmur results at the affected valve site and atrial pressure begins to rise. In the compensated patient, left atrial enlargement and eccentric hypertrophy of the left ventricle maintain normal cardiac output for an indefinite period of time, often months to years. Eventually, left atrial and pulmonary venous pressures rise resulting in pulmonary venous congestion and pulmonary edema.
History and clinical signs
Most of the early signs of mitral regurgitation result from pulmonary congestion and owners seek treatment for their dog after noticing coughing or respiratory distress. Coughing is a common but nonspecific sign of developing heart failure in dogs. Many older, small breed dogs cough because of chronic bronchitis or from a collapsing trachea. When due to heart failure, coughing is usually accompanied by an elevated respiratory rate (tachypnea) and increased respiratory effort (dyspnea). Some dogs with congestive heart failure become restless at night, are unable to sleep and may experience orthopnea, that is, they have more difficulty breathing lying down than sitting or standing.
Some dogs with CDVD develop signs of right heart failure due to degeneration of the tricuspid valve, as a consequence of pulmonary hypertension, or a combination of these disorders. Regardless of the cause, the development of abdominal distension and ascites is usually accompanied by signs of low output heart failure and a decline in the severity of pulmonary congestion. Generalized muscle weakness and progressive exercise intolerance become evident when forward output is impaired by severe valvular regurgitation, pulmonary hypertension, and/or declining myocardial contractility. Syncope tends to occur primarily when cardiac output declines precipitously.
Cardiac auscultation by a skilled examiner is the most practical and economical diagnostic method for detecting mitral regurgitation. The classic murmur of mitral regurgitation is holosystolic, constant in intensity (plateau-shaped), of mixed frequency, and loudest at the left apex. A soft, grade 1/6, systolic murmur over the mitral area is the first clinical sign of CDVD. A mid or late systolic click or a click-murmur can sometimes be auscultated prior to the development of a holosystolic murmur. There is a strong relationship between murmur intensity, heart size, the severity of regurgitation, and NYHA class of heart failure. Dogs with a murmur of grade 3/6 or less and a clearly audible second heart sound are likely to have mild disease. With the development of more severe disease, the murmur becomes louder, the second heart sound becomes softer or inaudible, and a gallop heart sound may be auscultated. The murmur of mitral regurgitation is usually best heard at the left fifth intercostal space, but dorsal, cranial, caudal, or rightward radiation of the murmur is common. It is particularly difficult to determine whether murmurs heard over the tricuspid valve area originate from that valve or if they are referred from an incompetent mitral valve. Cardiac arrhythmias can be readily identified as they interrupt the predominating cadence of the heart, create abnormal pauses in the rhythm, and alter the intensity of both murmurs and transient heart sounds.
Electrocardiograms are frequently normal in dogs with mitral regurgitation even when cardiomegaly can be demonstrated on radiographs or an echocardiogram. P wave prolongation (> 0.04 sec in dogs) may be present due to left atrial enlargement. Left ventricular enlargement is suggested by prolongation of the QRS complex (> 0.05 - 0.06 sec in dogs) or by increased R wave amplitude in leads II, III, and aVF (R wave > 2.5 mV in small dogs and > 3.0 mv in large dogs). The mean electrical axis is usually normal.
Sinus arrhythmia or sinus tachycardia predominates in animals with mitral regurgitation. Premature ventricular and supraventricular beats are the most common rhythm disturbances recorded in dogs with mitral regurgitation. Atrial fibrillation develops in a small but substantial number of dogs with severe CDVD. The onset of atrial fibrillation is usually accompanied by marked clinical deterioration.
Left atrial enlargement is the earliest and most consistent radiographic feature of mitral regurgitation. In the dorsoventral projection, the enlarged left auricle is initially recognized as a slight bulge protruding from the left cranial border of the heart, from the 1 to 3 o'clock position using the clock face analogy. The entire left border of the heart becomes more convex, and the left atrial bulge may be obscured from view as the left ventricle enlarges. The enlarged cardiac silhouette eventually occupies a greater proportion of the thorax. The posterior border of the heart becomes rounded and may be displaced to either the left or right of midline. It is not possible to distinguish pure left ventricular enlargement from biventricular enlargement on routine thoracic radiographs. As the left atrium dilates further, the main-stem bronchi assume a more obtuse angle, and the body of the atrium may become visible as a dense mass superimposed on the caudal portion of the cardiac silhouette.
In the lateral projection, left atrial enlargement causes the ventral deflection of the terminal trachea to disappear. The left main-stem bronchus is elevated by the enlarging left atrium and becomes visible dorsal to its counterpart on the right. Enlargement of the left atrium and ventricle causes the caudal border of the heart to flatten and then become more convex than normal. The dorsoventral and craniocaudal dimensions of the heart increase. Again, it is not possible to distinguish how much the left and right ventricles contribute to the obviously enlarged cardiac silhouette.
Thoracic radiographs are the most sensitive and readily available clinical indicator of pulmonary hemodynamics available to the veterinary practitioner. As left-sided congestive heart failure develops, the evaluation of good quality radiographs permits the visualization of early changes in the pulmonary veins and the interstitium of the lung. As pulmonary venous pressures rise, the pulmonary veins distend and become more evident centrally and in the peripheral lung fields. The dilated veins become more dense and larger than the pulmonary arteries. Further elevations of venous pressure result in the development of radiographically detectable interstitial edema. Fluid accumulation in perivascular lymphatics and the interstitium causes the margins of pulmonary vessels to loose their crisp definition. Fluid accumulates in a similar fashion in the walls of the bronchi and bronchioles causing peribronchiolar cuffing. The overall increase in pulmonary fluid content results in decreased radiolucency of the lung and a loss of contrast between the parenchyma and bronchovascular structures. These changes are often most apparent in the hilar regions of the lungs or in the right caudal lung lobes. In dogs, alveolar pulmonary edema, characterized by the appearance of indistinct fluffy densities, air alveolograms and air bronchograms, develops initially in the hilar region or in the right caudal lung lobe.
1. M-mode and two-dimensional echocardiography: Most abnormalities detected by M-mode and 2-dimensional echocardiography reflect changes caused by volume overload of the left heart and are not specific for mitral regurgitation. These changes include an enlarged left atrial dimension, increased left atrial to aortic ratio, an increased ventricular diastolic dimension, exaggerated septal motion and left ventricular wall motion, excessive mitral valve amplitudes of motion and a steep E to F slope. The identification of mitral regurgitation by finding a separation between the mitral leaflets during systole is unreliable. Structural abnormalities of the degenerative mitral valve identifiable by two-dimensional echocardiography include thickened valve leaflets, mitral valve prolapse (inclusive of tip protrusion into the left atrium), and flail leaflets caused by chordal rupture.
2. Ventricular performance: Echocardiographic estimates of left ventricular contractility should be interpreted cautiously in dogs with mitral regurgitation. The ejection phase indices including fractional shortening of the left ventricle, ejection fraction, and mean velocity of circumferential shortening (mean Vcf) are inaccurate measures of contractility in dogs with mitral regurgitation. The values obtained from dogs with mitral regurgitation are often normal or greater than normal as the left ventricle rapidly decompresses into the low pressure left atrium. End-systolic volume indices provide more accurate estimates of myocardial contractility in dogs with mitral regurgitation.
3. Detection of regurgitant flow: Mitral regurgitation produces a high velocity, systolic jet of turbulent blood flow in the left atrium that can usually be detected by pulsed, continuous wave, or color flow Doppler echocardiography. In most cases, mitral regurgitant flow continues throughout systole at a velocity of 5 to 6 meters per second. Flow velocity is a function of the pressure difference between the left ventricle and left atrium.
At this time early institution of therapy, prior to the onset of heart failure and in the absence of significant cardiomegaly, is not advised. Management of congestive heart failure entails the use of diuretics to control congestion, angiotensin converting enzyme inhibitors to blunt activation of the renin angiotensin system, and positive inotropes (digoxin or pimobendan) to increase systolic performance. Pimobendan may have the additional benefit of reducing afterload. Detailed notes on these medications can be found in the section "Therapy of new onset and refractory heart failure".
Selected recent references
Oyama MA. Neurohormonal activation in canine degenerative mitral valve disease: implications on pathophysiology and treatment. J Small Anim Pract. 2009 Sep;50 Suppl 1:3-11.
Häggström J, Höglund K, Borgarelli M. An update on treatment and prognostic indicators in canine myxomatous mitral valve disease. J Small Anim Pract. 2009 Sep;50 Suppl 1:25-33.
Hansson K, Häggström J, Kvart C, Lord P. Reader performance in radiographic diagnosis of signs of mitral regurgitation in cavalier King Charles spaniels. J Small Anim Pract. 2009 Sep;50 Suppl 1:44-53.
Häggström J, Boswood A, O'Grady M, 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 J Vet Intern Med. 2008 Sep-Oct;22(5):1124-35.