{"id":1467,"date":"2012-07-01T13:55:26","date_gmt":"2012-07-01T13:55:26","guid":{"rendered":"http:\/\/phosdev.com\/todaysveterinarypractice\/?p=1467"},"modified":"2022-02-18T17:28:01","modified_gmt":"2022-02-18T17:28:01","slug":"an-everyday-approach-to-canine-degenerative-mitral-valve-disease","status":"publish","type":"post","link":"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/cardiology\/an-everyday-approach-to-canine-degenerative-mitral-valve-disease\/","title":{"rendered":"An Everyday Approach to Canine Degenerative Mitral Valve Disease"},"content":{"rendered":"

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Mark A. Oyama, DVM, Diplomate ACVIM (Cardiology)<\/em><\/p>\n

Degenerative mitral valve disease (DMVD) is a common canine cardiac disease; approximately 30% of dogs over age 10 possess the characteristic left-sided systolic murmur of DMVD and resulting mitral regurgitation (MR).1 <\/sup>DMVD is most common in small breeds, with some breeds being highly predisposed. For example, virtually all Cavalier King Charles spaniels will develop DMVD during the course of their lifetimes.<\/p>\n

Developing a standardized approach to patients with DMVD can help the clinician concentrate on the most important diagnostic aspects of disease as well as provide useful information about monitoring and prognosis. This overview will focus on the role of the physical examination and thoracic radiographs and how information from these tests can aid in the everyday diagnosis and management of DMVD.<\/p>\n

Diagnosis of Degenerative Mitral Valve Disease in Dogs<\/span><\/h2>\n

Diagnosis of DMVD is one of the easiest clinical aspects of the disease. A presumptive diagnosis can be made on the basis of patient signalment and physical examination, wherein the hallmark finding is an adult small-breed dog with a left-sided systolic murmur. In these instances, it is reasonable to assume that the source of the murmur is MR and hence, DMVD is present. Once a diagnosis has been made, the next question is: what is the severity of DMVD?<\/p>\n

Assessing Severity of DMVD<\/span><\/h2>\n

Pathophysiology<\/span><\/strong><\/h3>\n

As DMVD worsens, the valve leaflets degenerate, resulting in worsening MR. The reduction in forward cardiac output triggers activation of several neurohormonal pathways, including the renin\u2013angiotensin\u2013aldosterone system and sympathetic nervous system. For instance, reduction in renal perfusion results in renin release from the macula densa, which results in downstream production of angiotensin II via angiotensin-converting enzyme (ACE).<\/p>\n

Angiotensin II and its related molecule aldosterone act to conserve sodium and water and expand plasma volume. In this way, cardiac output is maintained and there is an increase in cardiac stroke volume and, over time, ventricular size. Thus, the degree of volume retention and subsequent eccentric cardiac hypertrophy is a marker of MR severity.<\/p>\n

Thoracic Radiography<\/span><\/strong><\/h3>\n

Measuring heart size is extremely useful in assessing severity of DMVD (Figure<\/strong>). Thoracic radiography is a relatively simple and cost-efficient tool for assessing heart size and identifying the presence of pulmonary venous distention or edema.<\/p>\n

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Measurement systems, such as the vertebral heart size (VHS) system, are useful in reducing inter-observer variability and tracking longitudinal changes in a patient’s heart size. The VHS technique has been well-described.2<\/sup>\u00a0Normal VHS size in dogs is < 10.7; severe heart enlargement and hence, severe DMVD, is usually considered to be > 12.<\/p>\n

I recommend performing baseline thoracic radiographs to assess heart size on every dog with a newly discovered murmur. Baseline radiographs establish the initial degree of disease severity and assess rate of disease progression during subsequent follow-up (recheck radiographs should be performed 6\u201312 months after initial detection and are often repeated every 3\u201312 months depending on rate of progression).<\/p>\n

Electrocardiography & Echocardiography<\/span><\/strong><\/h3>\n

The value of electrocardiography (ECG) and echocardiography (echo) in the diagnosis and monitoring of DMVD varies from case to case. Clearly, ECG is the gold standard for assessment of arrhythmias, but ECG criteria for heart enlargement (eg, increased R wave amplitude indicating left ventricular enlargement) are relatively insensitive.<\/p>\n

Echo is the gold standard for assessment of cardiac structure and function, but in most cases of DMVD, especially those that are relatively mild, the information obtained by echo rarely adds to what was already known from the physical examination and thoracic radiographs. While echo is helpful in some cases to detect concurrent cardiac disease, such as tricuspid regurgitation or pulmonary hypertension, lack of echo should not affect the ability to make an initial assessment of disease severity based on radiographic heart size.<\/p>\n

In most cases of DMVD, appropriate diagnostic, monitoring, and therapeutic decisions can be made without echo provided that radiographs are performed.<\/p>\n

Monitoring Progression of DMVD<\/span><\/strong><\/h2>\n

It is reassuring to remember that most dogs with DMVD will not develop enough MR to cause congestive heart failure or clinical signs.3<\/sup>\u00a0The preclinical course of disease can be many years and only a minority of dogs will progress to the point of heart failure.<\/p>\n

Classifying Patients<\/span><\/strong><\/h3>\n

By performing longitudinal examinations of heart size, clinicians can gradually stratify dogs into (1) those that have slowly progressive disease and are unlikely to develop signs versus (2) those with more rapidly progressing disease that are at risk for future heart failure. In general, it is very uncommon for dogs to develop congestive heart failure with VHS < 11.5.<\/p>\n

High-Risk Patients<\/span><\/strong><\/h3>\n

Once VHS\u00a0><\/span>\u00a011.5, both absolute VHS and rate of increase in VHS are linked to risk of heart failure. In these patients, more frequent rechecks and increased owner vigilance for subtle signs of early heart failure, such as mild increase in respiratory rate or effort while at rest, decreased activity tolerance, or lethargy, is recommended. Previous studies4<\/sup>\u00a0have shown that a rate of VHS increase > 0.25 vertebra over a 3-month period suggests that risk for heart failure is high.<\/p>\n

Slowing Progression of DMVD<\/span><\/strong><\/h2>\n

Unfortunately, there are no proven interventions that slow the rate of DMVD progression or significantly delay the onset of heart failure in preclinical DMVD.<\/p>\n

Role of Ace Inhibitors<\/span><\/strong><\/h3>\n

While 2 large studies5,6<\/sup>\u00a0failed to demonstrate that ACE inhibitors significantly affected the primary endpoint of first-onset heart failure, the majority of cardiologists and members of the consensus panel on DMVD recommend ACE inhibitors prior to onset of heart failure, after cardiac enlargement is detected.7<\/sup>\u00a0In contrast, most cardiologists do not advocate use of furosemide prior to onset of congestive heart failure.<\/p>\n

Monitoring & Prompt Therapy<\/span><\/strong><\/h3>\n

Other medications are being assessed in ongoing clinical trials, but until these trials are completed, I recommend that dogs at high risk for heart failure are simply monitored more closely, both by the clinician and owner. Detection of subtle signs of heart failure as previously mentioned followed by prompt initiation of conventional therapy can prevent development of severe and life-threatening heart failure that requires emergency visits, intravenous treatment, and prolonged hospitalization.<\/p>\n

Treatment of DMVD<\/span><\/h2>\n

Clinical Signs<\/span><\/strong><\/h3>\n

In dogs with severe DMVD, progressive MR and chronic neurohormonal activation ultimately leads to congestion in the form of pulmonary edema. Dogs often present for respiratory signs, ranging from:<\/p>\n