Chronic Valvular Heart Disease in Dogs

Chapter 177


Chronic Valvular Heart Disease in Dogs




Chronic valvular heart disease (CVHD) is the most common acquired heart disease in dogs, with an overall cumulative incidence of more than 40%. CVHD often results in congestive heart failure (CHF). Cardiac disease is an important cause of morbidity and mortality in dogs, responsible for approximately 10% of all canine deaths and with a higher incidence in some breeds of dogs such as the cavalier King Charles spaniel. The mitral valve most commonly is affected in CVHD, but concurrent tricuspid valve disease often is noted. Most veterinarians are very familiar with CVHD; thus the goal of this chapter is to discuss and highlight some important concepts about this disorder, consider frequently discussed topics, and review recent developments in diagnosis and therapy.



Etiology, Pathology, and Pathophysiology


The cause of CVHD currently is unknown, although a genetic tendency to develop the disease has been proven in the cavalier King Charles spaniel and suspected in other breeds. As the field of canine cardiac genetics continues to develop, it is likely that specific genes causing or contributing to the development of CVHD will be identified. In addition, poorly defined environmental and epigenetic factors likely play a role in the rate of onset or severity of the disease.


Advanced myxomatous degeneration leads to grossly thickened and shortened valve leaflets with curled, nodular margins (Figure 177-1). Valvular hemorrhage and calcification may be seen. There is fibrosis of the valves, loss of collagen fibers, and an accumulation of acid-staining glycosaminoglycans within affected valves. Chordae tendineae often are affected and may become thickened, stretched, or ruptured, which allows portions of the diseased valve leaflets to bulge or prolapse into the atrial chamber. Electron microscopy has documented great variation in endothelial cell size and morphology of affected valves, with focal loss of the endothelial layer, collagen exposure, and activation of valvular interstitial cells. It is not clear which of these findings is a result of the disease and which might be a cause or contributor to disease progression. CVHD historically has been considered a noninflammatory, myxomatous degeneration of the atrioventricular valve, but there is growing interest in the role that serotonin or other inflammatory mediators may play in accelerating the pathologic development of the disease. There is one report of elevated C-reactive protein concentrations in the serum of affected dogs, which suggests a possible role of low-grade systemic inflammation in the progression of the disease (Rush et al, 2006). Another study evaluating genomic expression patterns in the valves of dogs with CVHD confirmed activation of several pathways involved in cell signaling, inflammation, and extracellular matrix activation, with several inflammatory cytokines and serotonin–transforming growth factor-β pathways identified as contributory to the development of the degenerative process in the valve (Oyama and Chittur, 2006). Increased serum serotonin levels have been found in dogs with CVHD, and increased autocrine production of serotonin, as well as up-regulation of the serotonin receptor 5HT-R2β, has been detected in affected valves. Increased serotonin signaling or decreased clearance can activate mitogenic pathways in valvular interstitial cells, resulting in their transformation to a more active myofibroblast phenotype. These activated interstitial cells are believed to play a role in pathologic valve remodeling via increased deposition of glycosaminoglycans, collagen turnover, and expression of transforming growth factor-β1 and other signaling molecules (Oyama and Levy, 2010). Further research into the role that serotonin pathways play in the pathogenesis of the valvular remodeling accompanying CVHD is ongoing.



In addition to valvular abnormalities, many dogs with CVHD have histopathologic lesions in the myocardium, including small foci of myocardial fibrosis and necrosis, as well as more widespread intramural coronary arteriosclerosis (Falk et al, 2006). The role that arteriosclerosis, myocardial fibrosis, and microinfarction resulting from occlusion of these arteriosclerotic lesions might play in the progression toward ventricular dilation, systolic dysfunction, and CHF is not well understood at this time, but these lesions seem to offer possible alternative avenues for investigation as treatment or interventional opportunities.


Progressive valvular thickening leads to poor leaflet coaptation and worsening valvular regurgitation with progressive dilation and eccentric hypertrophy of the atria and ventricles. As the regurgitant fraction increases, forward cardiac output may diminish, and compensatory neurohumoral pathways are activated (e.g., adrenergic activation, enhanced renin-angiotensin-aldosterone system activity) in an attempt to restore blood pressure and maintain tissue perfusion. As long as the dilated left atrium remains sufficiently compliant to accept the regurgitant blood volume, CHF does not develop, although coughing may occur due to left main-stem bronchial compression. Increased left ventricular filling pressure eventually precipitates CHF as the volume of regurgitated blood becomes overwhelming; chordal rupture suddenly increases the regurgitant fraction; and the limits of left atrial or ventricular compliance are exceeded, or the left ventricular myocardium starts to fail. Atrial rhythm disturbances, including atrial fibrillation, also can contribute to cardiac dysfunction and precipitation of CHF. The onset of decompensated CHF typically is manifested by the development of pulmonary edema in mitral valve disease. Chronic left-sided heart failure often leads to postcapillary pulmonary hypertension (PHTN), which further strains the right side of the heart and leads to signs of right-sided CHF with accumulation of ascitic fluid and possibly pleural effusion. In some dogs, there is evidence of severe PHTN beyond that explained simply by elevated pulmonary venous pressures.




Clinical Presentations in Chronic Valvular Disease


Most dogs are first diagnosed with CVHD based on the finding of a cardiac murmur in the absence of any signs of cardiac decompensation. The period between first detection of a murmur and onset of clinical signs generally is years. As the disease advances, many dogs develop a cough as the first sign of CVHD, caused by either early CHF or left atrial enlargement leading to main-stem bronchial compression. Panting, dyspnea, exercise intolerance, weight loss, weakness, and syncope are additional causes for a visit to a veterinarian. Specific triggers that cause a sharp increase in fluid retention or decrease in cardiac performance may precipitate CHF. These include increased dietary intake of salty foods, vigorous exercise or exertion in the previous 48 hours, recent onset of a rapid tachyarrhythmia, overzealous fluid therapy, general anesthesia, and potentially glucocorticoid administration.



Evaluation of Asymptomatic Dogs with a Heart Murmur


Many dogs with CVHD have an audible murmur for years before the onset of cardiac decompensation and CHF (see Table 177-1 for the American College of Cardiology/American Heart Association [ACC/AHA] staging classification). An extra systolic sound known as a midsystolic click is often detected before the onset of this murmur and has been associated with mitral or tricuspid valve prolapse; this is a sign of early CVHD. With rare exceptions, clinically significant CVHD is accompanied by a holosystolic murmur of medium to loud intensity. Point of maximal murmur intensity is over the left apex with radiation dorsally and to the right in most cases. In most dogs the intensity of the murmur is correlated roughly with the severity of mitral regurgitation (MR) as long as arterial blood pressure is normal. Thus in dogs with soft murmurs of MR the volume of regurgitation is unlikely to result in clinical signs; however, once a loud murmur is present, one cannot readily predict the onset of CHF in a given dog.



When a murmur is auscultated in a dog without clinical signs, baseline testing can be offered to the owner and often is helpful for comparison at subsequent examinations (see Table 177-2 for American College of Veterinary Internal Medicine [ACVIM] consensus recommendations on diagnostic testing). At a minimum the client should be clearly informed of the presence of the murmur and the fact that the disease ultimately may progress to CHF. Baseline testing ideally should include thoracic radiography to assess for cardiomegaly and optimally echocardiography to confirm the diagnosis and help assess cardiac size and function. A baseline B-type natriuretic peptide or N-terminal prohormone B-type natriuretic peptide (NT-proBNP) level also may be helpful in disease staging, and an NT-proBNP concentration above 1500 pmol/L indicates a higher chance of cardiac decompensation in the next 6 to 12 months. A blood pressure measurement is indicated to exclude systemic hypertension, which might accelerate progression of MR. If hypertension is identified, an underlying cause such as renal or adrenal disease should be sought. Baseline laboratory evaluation should include, at a minimum, assessment of hematocrit, total solids, serum creatinine level, and urinalysis. However, a complete blood count, full serum chemistry analysis, urinalysis, and possible urine protein : creatinine ratio are recommended in hypertensive animals or dogs with other signs of systemic disease.




Evaluation of Dogs with Signs of Cardiac Dysfunction


Once heart failure develops, a range of clinical presentations are possible, related to the degree and duration of valvular dysfunction. In an acute setting clinical signs usually are pulmonary or behavioral and may include cough, tachypnea, retching or gagging, nocturnal dyspnea, orthopnea or reluctance to settle down, and sometimes either excessive clinginess or social isolation. Less commonly, abdominal distention from ascites may be present, or the client may detect a “racing heart.” Exertional collapse or syncope may be the initial sign of heart disease and can occur as a result of significant arrhythmias, secondary to low cardiac output, in association with a vasovagal reflex (neurocardiogenic) response, or following a coughing spell (tussive syncope). In our experience syncope can be seen at the time of the initial presentation of heart failure, and syncope in this setting likely has a reflex-mediated or vasovagal component. Moderate to severe PHTN also has been associated with syncope in dogs with CVHD. Some dogs exhibit decreased exercise tolerance and weight loss for weeks to months before the onset of CHF, but these are often overlooked and rarely are the cause of a trip to a veterinarian.



Physical Examination


Pulmonary auscultation may reveal loud bronchovesicular sounds that can progress to pulmonary crackles with the onset of alveolar edema. The latter may be particularly prominent over the hilar or caudal lung fields on inspiration. Hepatomegaly and ascites may be evident in dogs with right-sided CHF from advanced tricuspid regurgitation (TR) or mitral disease with postcapillary PHTN. Jugular venous distention is commonly appreciated in dogs with ascites. Often the femoral pulses are easily palpated and prominent, even at the time of onset of CHF. Irregularities in pulse rate and strength may be noted in association with an arrhythmia. In animals with CHF the heart rate usually is elevated or in the upper-normal range, and sinus arrhythmia typically is absent, although this is variable. The ventricular apex beat is hyperdynamic and is progressively shifted caudally from the fifth intercostal space with increasing disease severity. If present, a precordial thrill also is palpable over the left apex. A louder murmur or more pronounced thrill on the right hemithorax typically indicates concurrent TR and PHTN. There may be a left ventricular heave or apical thrust. There may be other abnormalities since most CVHD patients are geriatric; therefore a complete physical examination is warranted.



Thoracic Radiography


Thoracic radiographs are essential to the management of CVHD. The earliest characteristic findings on thoracic radiographs are mild left ventricular enlargement and left atrial enlargement, which may be best noted as an auricular prominence on the dorsoventral view at the 2- to 3-o’clock position. Left atrial and left ventricular enlargement elevate the trachea and carina on the lateral radiographic projection, with a decrease in the angle between the trachea and the thoracic spine. The left main-stem bronchus may become elevated and compressed in cases of moderate to severe left atrial enlargement. There is straightening of the caudal cardiac border and loss of the caudal cardiac waist. Pulmonary venous dilation occurs; this finding may be best appreciated in the cranial lung fields in the lateral view. Distended pulmonary veins (and arteries in severe cases) also can be identified in the caudal lung fields on the dorsoventral or ventrodorsal projections. Early pulmonary edema is seen as a diffuse increase in interstitial density in the hilar or caudal lung fields, progressing to perihilar densities with air bronchograms corresponding to alveolar edema. Cardiogenic pulmonary edema appears to have a propensity for the right caudal lung fields in some dogs, and this finding may be noted on the dorsoventral view. With TR and right-sided or biventricular CHF, the cranial aspect of the trachea may be elevated, the caudal vena cava increases in size, and small-volume pleural effusion may be noted.


Not only is radiographic evaluation useful for monitoring cardiac chamber size and documenting CHF, but it also serves to guide therapy and exclude other disorders. Pneumonia can develop in an older dog with CVHD and CHF; thus, in a patient with new signs or a poor response to therapy, infection or another problem such as lung cancer should be considered. Chronic bronchitis also is common in many dogs with CVHD and occasionally can be recognized by the presence of severe bronchial patterns or bronchiectasis. The rate of increase in vertebral heart score has been shown to accelerate in the 6 to 12 months before the onset of CHF; thus sequential monitoring of radiographs may be helpful in predicting impending heart failure (Figure 177-2).


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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Chronic Valvular Heart Disease in Dogs

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