Acta Veterinaria Scandinavica 2008, 50:22 http://www.actavetscand.com/content/50/1/22 HCM have been identified [1,4], primary HCM may be a more appropriate name. The hypertrophy associated with HCM ranges from local- ized and mild thickening, involving any part of a particu- lar wall segment, to diffuse and pronounced hypertrophy of the entire chamber [5,6]. With moderate to severe hypertrophy, end-systolic cavity obliteration is often seen at the level of the papillary muscles. As isolated regions of the basal, middle or apical parts of the ventricular walls can be affected, it is necessary that the echocardiographic examination is performed from the right parasternal long- axis view as well as the short-axis view. Because M-mode echocardiograms obtained from the standard view for measuring the left ventricular dimensions, just below the mitral valve leaflets, can miss localized hypertrophy, assessment of ventricular dimensions should be made from both two-dimensional (2D), sweeping from base to apex, and from M-mode [1-3]. There is a wide morphologic spectrum of HCM and no pattern of hypertrophy can be considered typical. This makes the diagnosis of mildly affected cats, often seen in screening programs, difficult. In these cases the cardiolo- gist may have the delicate task to decide if a cat with find- ings in agreement with less pronounced signs of HCM, like SAM, moderate hypertrophy of the papillary muscles or left ventricular wall of between 5,0 and 6,0 mm, should be considered being affected, and what recommendations should be given to the owner concerning breeding. Systolic anterior motion (SAM) of the mitral valve is com- monly identified in cats with HCM, and can be seen before hypertrophy of the left ventricular wall is evident [1]. SAM is reported to produce dynamic obstruction to left ventricular outflow tract, as well as mitral regurgita- tion [1,2,5]. Narrowing of the left ventricular outflow tract by hypertrophy of the interventricular septum contributes to dynamic obstruction of the left ventricular outflow tract. Cats with SAM often have a systolic heart murmur, best heard over sternum or left apex [2]. There is evidence suggesting that HCM in certain cat breeds, i.e. American shorthairs [4], Persians [7,8] and Maine coon cats [1] is heritable. A heritable basis for HCM in pigs [9] and pointer dogs [10] is also suspected. Because there is evidence that HCM is heritable in some cats, breeders are increasingly interested in identifying affected cats. Data from a family of Maine coon cats with familial HCM suggest that the disease is inherited in a simple auto- somal dominant pattern with complete penetrance.[1]. The aim of the study was to assess the prevalence of myo- cardial hypertrophy in a population of Maine coon cats. Methods Cats over the age of 8 months, owned by breeders listed on the website of Maine coon cat breeders in Sweden, liv- ing in Stockholm, as defined by area code number, by feb- ruary 2001 were invited to participate in the study. Nine out of ten invited breeders accepted the invitation, and 42 out of 45 possible cats participated in the examinations. Out of these cats, 30 were closely related (mother, father, daughter, son, sister, brother, half sister or half brother) to one or more of the other cats examined in this study. Exclusion criteria consisted of echocardiographic signs of heart disease, other than HCM. None of the invited cats was excluded from the study. Clinical examination Body weight and gender were registered, as was informa- tion on whether the cats were castrated or pregnant. Any knowledge of HCM among ancestors was noted. All cats were examined clinically, and any heart murmur auscul- tated was located and graded on a scale of I-VI [11]. Other causes for concentric left ventricular hypertrophy, such as hyperthyroidism, systemic arterial hypertension or hyper- somatotropism were not investigated. Echocardiography Two dimensional (2D) and M-mode echocardiography was performed using an Aloka SSD-2200 with a multifre- quence, phased array transducer ranging from 2 to 5 MHz. All echocardiographic examinations were performed by one cardiologist (SG), who was unaware of the cats indi- vidual family history at the time of examination. All meas- urements were made directly on the screen. ECG was simultaneously recorded. The cats were unsedated and gently restrained in right lateral recumbency and the examination was performed from the dependant side of the thorax. Standard right parasternal long-axis and short- axis views were used and echocardiographic examinations analyzed according to the recommendations of the Amer- ican Society of Echocardiography [12] and the Echocardi- ographic Committee of the speciality of cardiology, American College of Veterinary Internal Medicine [13]. Measurements of diastolic left ventricular dimensions were made from short axis view on M-mode and in case of local hypertrophy seen on 2D, measurements were made from 2D long axis and short axis view as well. The greatest dimension of these images was used. Presence of papillary muscle hypertrophy, end-systolic cavity obliteration was subjectively evaluated from 2D short axis view, and systo- lic anterior motion (SAM) of the septal mitral valve leaflet was evaluated from 2D long axis view [1]. Definite diagnosis of primary HCM was based on echoc- cardiographic demonstration of concentric hypertrophy of the left ventricle, when a region of the left ventricular wall or the entire wall of the left ventricle was ≥ 6 mm Page 2 of 6 (page number not for citation purposes)