Mark D. Kittleson

Background: Some dogs with severe mitral valve regurgitation can have chronic cough, but its cause is unclear. Many of these dogs exhibit left principal (synonym mainstem) bronchial collapse or compression. Some clinicians believe that an enlarged heart, particularly the dilated left atrium, compresses the left principal bronchus, while others argue that a healthy bronchus cannot be compressed and that the cough is due to concurrent airway disease, such as bronchomalacia. In this study, we aimed to investigate the correlation between chronic cough and radiographic signs of bronchial narrowing in dogs with cardiomegaly secondary to primary mitral valve regurgitation. Methods: Four radiologists independently evaluated 51 sets of thoracic radiographs from client-owned dogs with cardiomegaly due to severe mitral valve regurgitation, including 26 sets of radiographs belonging to dogs with chronic (>8 weeks) cough and 25 without cough. The presence or absence of bronchial narrowing was assessed while the radiologists were blinded to patient characteristics and each other’s findings. Results: Interobserver variability was high, and the radiologists could not reliably predict which dogs had a chronic cough. Dogs with left atrial enlargement and airway narrowing sometimes coughed and sometimes did not. Likewise, some dogs with left atrial enlargement but no signs of airway compression or collapse coughed, and some did not. It was impossible to distinguish the groups based on these features. Conclusions: Bronchial compression by an enlarged heart and left atrium is an unlikely cause of chronic cough in dogs with severe primary mitral valve regurgitation.

Practical relevance: Although feline hypertrophic cardiomyopathy (HCM) occurs more commonly, dilated cardiomyopathy (DCM), restrictive cardiomyopathy (RCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), left ventricular noncompaction (LVNC) and cardiomyopathy – nonspecific phenotype (NCM; formerly unclassified cardiomyopathy) are all recognized in domestic cats. Patient group: Any adult domestic cat, of either sex and of any breed, can be affected. Diagnostics: The non-HCM cardiomyopathies are rarely suspected in subclinically affected cats, so most are first identified when a cat presents with signs of heart failure or systemic thromboembolic disease. The definitive clinical confirmatory test for these other feline cardiomyopathies is echocardiography. Key findings: ‘Cardiomyopathy – nonspecific phenotype’ is a catch-all term that groups hearts with myocardial changes that either do not meet the criteria for any one type of cardiomyopathy (HCM, RCM, DCM, ARVC, LVNC) or meet the echocardiography criteria for more than one type. RCM is characterized by diastolic dysfunction due to fibrosis that results in a restrictive transmitral flow pattern on Doppler echocardiography and usually marked left or biatrial enlargement. DCM is characterized by decreased myocardial contractility and is rare in cats. When it occurs, it is seldom due to taurine deficiency. However, since taurine-deficient DCM is usually reversible, a diet history should be obtained, whole blood and plasma taurine levels should be measured and taurine should be supplemented in the diet if the diet is not commercially manufactured. ARVC should be suspected in adult cats with severe right heart enlargement and right heart failure (ascites and/or pleural effusion), especially if arrhythmia is present. Feline LVNC is rare; its significance continues to be explored. Treatment of the consequences of these cardiomyopathies (management of heart failure, thromboprophylaxis, treatment of systemic arterial thromboembolism) is the same as for HCM. Conclusions: While these other cardiomyopathies are less prevalent than HCM in cats, their clinical and radiographic presentation is often indistinguishable from HCM. Echocardiography is usually the only ante-mortem method to determine which type of cardiomyopathy is present. However, since treatment and prognosis are often similar for the feline cardiomyopathies, distinguishing among the cardiomyopathies is often not essential for determining appropriate therapy. Areas of uncertainty: The feline cardiomyopathies do not always fit into one distinct category. Interrelationships among cardiomyopathies in cats may exist and understanding these relationships in the future might provide critical insights regarding treatment and prognosis.

Practical relevance: Hypertrophic cardiomyopathy (HCM) is the most common form of feline cardiomyopathy observed clinically and may affect up to approximately 15% of the domestic cat population, primarily as a subclinical disease. Fortunately, severe HCM, leading to heart failure or arterial thromboembolism (ATE), only occurs in a small proportion of these cats. Patient group: Domestic cats of any age from 3 months upward, of either sex and of any breed, can be affected. A higher prevalence in male and domestic shorthair cats has been reported. Diagnostics: Subclinical feline HCM may or may not produce a heart murmur or gallop sound. Substantial left atrial enlargement can often be identified radiographically in cats with severe HCM. Biomarkers should not be relied on solely to diagnose the disease. While severe feline HCM can usually be diagnosed via echocardiography alone, feline HCM with mild to moderate left ventricular (LV) wall thickening is a diagnosis of exclusion, which means there is no definitive test for HCM in these cats and so other disorders that can cause mild to moderate LV wall thickening (eg, hyperthyroidism, systemic hypertension, acromegaly, dehydration) need to be ruled out. Key findings: While a genetic cause of HCM has been identified in two breeds and is suspected in another, for most cats the cause is unknown. Systolic anterior motion of the mitral valve (SAM) is the most common cause of dynamic left ventricular outflow tract obstruction (DLVOTO) and, in turn, the most common cause of a heart murmur with feline HCM. While severe DLVOTO is probably clinically significant and so should be treated, lesser degrees probably are not. Furthermore, since SAM can likely be induced in most cats with HCM, the distinction between HCM without obstruction and HCM with obstruction (HOCM) is of limited importance in cats. Diastolic dysfunction, and its consequences of abnormally increased atrial pressure leading to signs of heart failure, and sluggish atrial blood flow leading to ATE, is the primary abnormality that causes clinical signs and death in affected cats. Treatment (eg, loop diuretics) is aimed at controlling heart failure. Preventive treatment (eg, antithrombotic drugs) is aimed at reducing the risk of complications (eg, ATE). Conclusions: Most cats with HCM show no overt clinical signs and live a normal or near-normal life despite this disease. However, a substantial minority of cats develop overt clinical signs referable to heart failure or ATE that require treatment. For most cats with clinical signs caused by HCM, the long-term prognosis is poor to grave despite therapy. Areas of uncertainty: Genetic mutations (variants) that cause HCM have been identified in a few breeds, but, despite valiant efforts, the cause of HCM in the vast majority of cats remains unknown. No treatment currently exists that reverses or even slows the cardiomyopathic process in HCM, again despite valiant efforts. The search goes on.

Practical relevance: The feline cardiomyopathies are the most prevalent type of heart disease in adult domestic cats. Several forms have been identified (see Parts 2 and 3), with hypertrophic cardiomyopathy (HCM) being the most common. Clinically the cardiomyopathies are often indistinguishable. Cats with subclinical cardiomyopathy may or may not have characteristic physical examination findings (eg, heart murmur, gallop sound), or radiographic cardiomegaly. Cats with severe disease may develop signs of heart failure (eg, dyspnea, tachypnea) or systemic arterial thromboembolism (ATE; eg, pain and paralysis). Sudden death is possible. Treatment usually does not alter the progression from subclinical to clinical disease and often the treatment approach, once clinical signs are apparent, is the same regardless of the type of cardiomyopathy. However, differentiating cardiomyopathy from normal variation may be important prognostically. Patient group: Domestic cats of any age from 3 months upward, of either sex and of any breed, can be affected. Mixed-breed cats are most commonly affected but certain breeds are disproportionately prone to developing HCM. Diagnostics: Subclinical feline cardiomyopathies may be suspected based on physical examination findings, thoracic radiographs and cardiac biomarker results but often the disease is clinically silent. The definitive clinical confirmatory test is echocardiography. Left heart failure (pulmonary edema and/or pleural effusion) is most commonly diagnosed radiographically, but point-of-care ultrasound and amino terminal pro-B-type natriuretic peptide (NT-proBNP) biomarker testing can also be useful, especially when the stress of taking radiographs is best avoided. Key findings: Knowledge of pathophysiological mechanisms helps the practitioner identify the feline cardiomyopathies and understand how these diseases progress and how they manifest clinically (heart failure, ATE). Existing diagnostic tests have strengths and limitations, and being aware of these can help a practitioner deliver optimal recommendations regarding referral. Conclusions: Several types of feline cardiomyopathies exist in both subclinical (mild to severe disease) and clinical (severe disease) phases. Heart failure and ATE are the most common clinical manifestations of severe cardiomyopathy and are therapeutic targets regardless of the type of cardiomyopathy. The long-term prognosis is often guarded or poor once overt clinical manifestations are present. Areas of uncertainty: Some cats with presumed cardiomyopathy do not have echocardiographic features that fit the classic cardiomyopathies (cardiomyopathy – nonspecific phenotype). Although no definitive treatment is usually available, understanding how cardiomyopathies evolve remains worthy of investigation.

Background Cough in the geriatric small breed dog with myxomatous mitral valve degeneration (MMVD), a large left atrium, and absence of heart failure often is attributed to compression of the left mainstem bronchus by the left atrium. Studies investigating this syndrome are lacking in dogs. Hypothesis Airway collapse is independent of left atrial enlargement. Animals A total of 16 dogs presenting with chronic cough in the absence of congestive heart failure. Group 1 dogs (n = 10) had moderate-to-severe left atrial enlargement based on an echocardiographically calculated left atrial:aortic surface area [LA:Ao(a)] > 6. Group 2 dogs (n = 6) had no to mild left atrial enlargement [LA:Ao(a) ≤ 6]. Methods Dogs were prospectively evaluated. CBC, biochemistry, urinalysis, cervical and thoracic radiographs, fluoroscopy, echocardiography, and bronchoscopy were performed. Bronchoscopic abnormalities were compared between groups using Fisher's Exact Test. P < .05 was considered significant. Results Fluoroscopy identified airway collapse in both groups. Bronchoscopic evidence of airway collapse >50% was observed in multiple bronchi with no difference between groups. All dogs had inflammation on airway cytology with respiratory infection in 1 dog in group 2. Left atrial size was interpreted radiographically as enlarged in 9 of 10 group 1 dog and in 2 of 6 group 2 dogs. VHS was above normal in both groups of dogs regardless of echocardiographic evidence of cardiomegaly. Conclusions Results failed to identify an association between left atrial enlargement and airway collapse in dogs with MMVD, but did suggest that airway inflammation is common in dogs with airway collapse.