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246  Section 3  Cardiovascular Disease

            implications. In  particular, when  the RAAS becomes   enlarge and there is a sudden increase of left atrial pres-
  VetBooks.ir  activated in dogs with natural occurring MMVD has   sure with development of acute pulmonary edema.
            been the source of much controversy. Some studies sug-
            gest that the RAAS might be activated relatively early in
            the history of the disease, whereas other studies suggest   Epidemiology
            otherwise. Further complicating the picture is the obser-  Myxomatous mitral valve disease is the most common
            vation that in dogs, alternative pathways for angiotensin   heart disease in dogs and the most frequent cause of con-
            II production, such as the chymase pathway, may be par-  gestive heart failure in this species. MMVD in dogs
            ticularly active. Moreover, it is possible that release of     represents 75% of all cardiovascular disease in this spe-
            natriuretic hormones from the dilated left atrium   cies. The prevalence of the disease varies with age and
            and  ventricle might balance RAAS and sympathetic   whether the study is based on necropsy, echocardio-
            activation.                                       graphic or clinical findings. The prevalence of MMVD
             Moderate to severe mitral valve regurgitation leads to   has  also  been correlated  with breed. In  some breeds,
            left ventricular volume overload, left atrial and left ven-  such as the CKCS, the prevalence of the disease in ani-
            tricular enlargement. Mitral valve insufficiency due to   mals older than 10 years is greater than 90%. Males are
            MMVD represents a unique hemodynamic condition    also reported to develop the disease at a younger age
            with increased preload and decreased afterload. This is   than females. Although the disease is more commonly
            because a significant volume of left ventricular preload is   diagnosed in small‐breed dogs, it can occur in large‐
            ejected into the left atrium at the beginning of systole.   breed dogs.
            Because the left atrium is a low‐pressure chamber, there
            is no increase in cardiac work. This is likely the reason   History and Clinical Signs
            why  many  dogs  with  severe  mitral  valve  regurgitation
            can tolerate this situation for a long time without pre-  Myxomatous mitral valve disease is a chronic disease in
            senting clinical signs.                           which the clinical presentation is variable. Some patients
             Left ventricular eccentric hypertrophy, decreased   remain asymptomatic for all their lives, whereas others
            afterload, and increased sympathetic activation produce   develop life‐threating pulmonary edema and chronic
            hyperkinetic left ventricular function. Therefore, the   congestive heart failure (CHF). Most dogs with mild to
            recognition of normal values for fractional shortening or   moderate MMVD are generally free of clinical signs.
            ejection fraction during an echocardiographic exam in   The presence of clinical signs is generally related to the
            dogs with left ventricular enlargement suggests the pres-  severity of the disease. Dogs with pulmonary edema have
            ence of a systolic dysfunction. Systolic dysfunction has   tachypnea and dyspnea. It has been reported that the
            been recognized to play an important role in disease pro-  normal respiratory rate at rest for dogs should be less
            gression and it is independent of clinical status. It has   than 30 breaths per minute. Accordingly, an increased
            been hypothesized that systolic dysfunction in dogs with   respiratory rate at rest might represent the first clinical
            MMVD is the consequence of inadequate hypertrophy.   sign of worsening of the disease. Dogs with pulmonary
            Wall stress imposed by pure volume overload might not   edema are often anxious and have difficulties sleeping.
            be a very potent stimulus for cardiac hypertrophy, and   They often cannot lie in lateral recumbency and prefer a
            experimental canine models of MMVD systolic dysfunc-  sternal position (orthopnea). Weight loss is common in
            tion were associated with inadequate left ventricular   dogs with advanced stages of MMVD and CHF. Patients
            hypertrophy. Systolic dysfunction is more apparent in   that develop right‐sided heart failure have abdominal
            large‐breed dogs affected by MMVD.                distension due to ascites. Syncope  is occasionally
             Left atrial function also plays an important role in the   reported in dogs with MMVD. Arrhythmias, pulmonary
            pathophysiology of the disease. Slowly progressing mitral   hypertension, vasovagal syncope, and coughing can
            valve regurgitation is associated with a progressive dila-  cause syncope in these patients.
            tion of the left atrium. If left atrial compliance is main-  Cough  represents  the  most  common  complaint  for
            tained, filling pressure is also maintained close to normal   dogs affected by MMVD, especially in small breeds. It
            limits. Accordingly, patients with severe mitral regurgi-  should be stressed that cough is a general clinical sign of
            tation do not develop pulmonary edema. However,   respiratory disease and its presence in a dog with a mur-
            chronic dilation of the left atrium is associated with left   mur is not an indicator for starting treatment for CHF.
            atrial hypertrophy and remodeling that, with time,   Old small‐breed dogs are commonly affected by tracheo-
            decreases compliance and leads to development of pul-  bronchial disease and by MMVD. In these patients, the
            monary edema. In dogs with rupture of a major chorda   cough is often the result of their primary respiratory dis-
            tendinea, there is an acute worsening of mitral regurgita-  ease and not heart disease. A recent study has shown
            tion. In this condition, the left atrium has no time to   that cough was not associated with the presence of active
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