Acta Veterinaria Scandinavica 2008, 50:22 http://www.actavetscand.com/content/50/1/22 Our study has a number of limitations. The number of cats and breeders is too small to estimate the prevalence of HCM in the whole population of Swedish Maine coon cats, and reference values for Maine coon cats in general. There is a possibility that cats in Sweden have differences in genotype and phenotype compared to other popula- tions. Because our study was designed as a prebreeding program of supposedly healthy cats, we did not initially investigate other possible causes for concentric myocar- dial hypertrophy in these cats. However, in February 2007, five years after initial examination, we invited the owners of the four cats with left ventricular wall dimen- sions of 6 mm or more, to a follow up examination. We then had the opportunity to examine two cats, then 10 and 13 yars old, They had until then not showed any signs of cardiac disease, and we could at the reexamination, by blood samples and measuring of systemic blood pressure, eliminate systemic hypertension, hyperthyroidism and renal failure as causes of myocardial hypertrophy. The probe used was a multifrequence probe 2–5 MHz. A probe with higher frequency would have given more detailed information that to some degree may have influ- enced the outcome of the examinations. A genetic test for a specific mutation in the myosin bind- ing protein C gene, found among Maine coon cats with familial HCM, is now available [28,29], which has led to cats being genetically screened. The value of this test in Maine coon cats outside that colony and in the general cat population has not yet been evaluated. There are indica- tions that other genes may cause HCM in cats, which indi- cates that echocardiographic screening of the general cat population is still important. Conclusion Irrespective of the reference values used, the prevalence of echocardiographic findings consistent with HCM in this population of asymptomatic cats was high. Using a reference value of ≥ 6 mm for the left ventricular wall, we found that in the present study 4 (9,5%) cats were definitively diagnosed with HCM, and two additional cats with SAM were suspected of having the disease, which added together makes 14,3% of this population. The most interesting result of our study is that it suggests that the left ventricular wall thickness of a normal cat is 5,0 mm or less. Using this value as reference, 5 (11,9%) more cats with a left ventricular wall thickness of more than 5,0 mm but less than 6,0 mm can be suspected of being affected with HCM. In that case a total of 11 (26,2%) cats will be considered abnormal. By echocardiography, we are however unable to detect cats that carry mutant genes, but have mild or no echocar- diographic changes. Hopefully, it will in the future be pos- sible to identify all specific mutations causing HCM carriers by analysis of blood samples, but until then more studies about normal reference values and diagnostic cri- teria for HCM are needed. Competing interests The authors declare that they have no competing interests. Authors' contributions SG participated in the design of the study, carried out the clinical and echocardiographical examinations and drafted the manuscript. AT participated in the design of the study, participated in the examinations of the cats and helped to revise the man- uscript. JH participated in the design of the study, performed the statistical analysis and interpretation of data and helped to revise the manuscript. References 1. 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