If the diagnosed individual has no relatives that are at risk, then genetic testing is not required. Genetic testing is not intended for risk assessment or treatment decisions. Evidence only supports clinical testing in predicting the progression and risk of developing complications of HCM.For individuals suspected of having HCM:

Genetic testing is not recommended for determining other causes of left ventricular hypertrophy (such as "athletes heart", hypertension, and cardiac amyloidosis). HCM may be differentiated from other hypertrophy-causing conditions using clinical history and clinical testing. Treatment
Asymptomatic people
A significant number of people with hypertrophic cardiomyopathy do not have any symptoms and will have a normal life expectancy, although they should avoid particularly strenuous activities or competitive athletics. Asymptomatic people should be screened for risk factors for sudden cardiac death. In people with resting or inducible outflow obstructions, situations that will cause dehydration or vasodilation (such as the use of vasodilatory or diuretic blood pressure medications) should be avoided. Septal reduction therapy is not recommended in asymptomatic people. Medications
The primary goal of medications is to relieve symptoms such as chest pain, shortness of breath, and palpitations. Beta blockers are considered first-line agents, as they can slow down the heart rate and decrease the likelihood of ectopic beats. For people who cannot tolerate beta blockers, nondihydropyridine calcium channel blockers such as verapamil can be used, but are potentially harmful in people who also have low blood pressure or severe shortness of breath at rest.
Additional implicated genes include: SMAD4, BMPR1A, PTEN, GREM1, and MUTYH. The only validated genetic cause of SPS is RNF43. However, most individuals with SPS do not have a germline mutation in any of the associated genes, including RNF43. As the underlying genetic risks for SPS are not fully understood, genetic testing is not recommended. Both autosomal dominant and autosomal recessive patterns of inheritance have been reported, as well as sporadic. Individuals with SPS have serrated polyps, which include hyperplastic polyps, traditional serrated adenomas, and sessile serrated polyps. In addition to serrated polyps, adenomas are often identified. Diagnosis
The diagnosis of serrated polyposis syndrome is achieved when either one of two criteria are met: ≥5 serrated lesions/polyps proximal to the rectum (all ≥ 5 mm in size, with two lesions ≥10 mm), or >20 serrated lesions/polyps of any size distributed throughout the large bowel with 5 proximal to the rectum. Any serrated polyp is counted towards the diagnosis, including sessile serrated lesions, hyperplastic polyps, and traditional serrated adenomas. In addition, the cumulative number of serrated lesions is cumulative over time and includes multiple colonoscopies. The diagnosis of SPS is often overlooked, and requires lifelong tracking of cumulative serrated polyps. Treatment
Colonoscopy is the mainstay of treatment for SPS, which allows for the identification of polyps and removal. Polyp removal is recommended to prevent the development of colorectal cancer. If polyps are relatively few, then removal may be achieved with colonoscopy. After polyps are removed, repeat colonoscopy is recommended in 1 to 3 year intervals.