Introduction to Feline Hypertrophic Cardiomyopathy

Maigan Espinili Maruquin


It is important to be aware that some of the diseases your pets may have are actually inherited. In cats, there are myocardial diseases that can be breed- related.

The most common myocardial disease in cats is Hypertrophic cardiomyopathy (HCM), wherein abnormal thickening of the walls of the left ventricle (LV) is observed [1]. First time described in cats in 1977 [2], it has been reported to have a prevalence of around 14.7% in apparently healthy cats [3-5]. In humans, the HCM is considered a genetic disease [6-8], whereas occurrences of the disease were observed in mix- breeds [9], Persian [10], and American shorthair cats [11], while an HCM caused by mutation was identified in Maine coon [12] and ragdoll [13].

The HCM are diagnosed at mean of 5-7 years, although all ages can get the disease [6]. On the other hand, some cat breeds including Maine Coons [14]; Sphynx [15], and Ragdoll [16] were reported on earlier onset of under 2 years old [3]. Cats that are diagnosed with HCM are also recorded to develop congestive heart failure (CHF), arterial thromboembolism (ATE), or sudden cardiac death (SCD) [1, 17, 18].


Clinical Presentation

When cats visit the clinics, routine veterinary examinations are conducted, and during auscultation, signs like arrhythmias, gallop sounds, or murmurs can be detected [6, 19, 20]. Respiratory distress is a manifestation of heart failure in diseased cats, whereas, some cats display hypothermia and pre-renal azotemia. On the other hand, the murmurs in cats may vary in intensity form moment to moment, and are commonly associated with dynamic and labile phenomena [6].



Fig. 1. Approach to the asymptomatic cat with suspected heart disease. BP, blood pressure; PCV, packed cell volume; T4, thyroxine [1]

The feline HCM are primarily diagnosed on echocardiographic examination, which recognizes basic patterns that are intuitive [21], with ventricular wall thickness that is equal to or exceed 6 mm [6, 22]. Respiratory distress is reported to display left atrial enlargement. However, echocardiographic examination has limitations [1] and there is no definitive, gold-standard to diagnose HCM, unless there is a hypothetical and flawless molecular or genetic testing [6]. The LV wall thickness has no exact value allowable, and body weight can affect its thickness [1].


An increase of cTn-I in plasma concentration indicates its sensitivity and specificity as a biomarker to provide myocardial damage severity and prognosis information. On the other hand, the N-terminal pro B-type natriuretic peptide (NT-proBNP) assay may provide ongoing myocardial stress, however, full cardiac evaluation shall be performed to detect its cause of elevation [1].


Myocyte enlargement and interstitial fibrosis were observed, along with disorganized spatial arrangement of myocytes in histopathological examination [3, 23]


Genetic testing for single point mutation that affects MYBPC3 in Maine coon cats (A31P) [12] and ragdolls (R820W) [13] are commercially available. Autosomal dominant inheritance were reported in both breeds [1].


Therapy and Management

For asymptomatic cats with HCM, diltiazem or beta-blockers were reported to improve physical condition. Meanwhile, Diltiazem is administered at three times a day as a licensed formulation in UK to manage cases of HCM [21].

In a study conducted by Rishniw, M. and P.D. Pion in 2011, participatiing clinicians used furosemide for evident CHF, and most of them also used and ACEIs, while for cases with substantial dynamic LVOT obstruction, β-blockers were used by most [24]. Altering the progression of HCM in the pre- or subclinical stage is an approach that is ideal in the absence of safe and efficient therapy [1].




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