to decrease the production of free light chains. new data suggests that orthotopic heart transplant followed by melphalan and stem cell transplant produces results similar to non cardiac amyloidosis indicated heart transplant. to treat complications, medications can be prescribed including midodrine for autonomic neuropathy, amiodarone for patients with atrial fibrillation to prevent arrhythmias, and warfarin used after a cardioembolic episode. beta-blockers should be avoided due to the usual symptom of hypotension. familial (attrm-cm) treatment: in recent years there have been developments in the treatment of familial/transthyretin cardiac amyloidosis including methods to suppress transthyretin production, stabilize amyloid fibrils, and medications that can destroy already existing fibrils. for familial amyloidosis, ace-inhibitors and beta-blockers can be prescribed if there is no autonomic neuropathy. suppression of transthyretin production: liver transplantation and medications that decreases the activity of the transthyretin genes (patisiran and inotersen). in patients with familial transthyretin mutations, liver transplantation can provide the body with a source of normal transthyretin. by changing the source of transthyretin from the original liver that contains the mutated transthyretin to a healthy liver, there will be no more production of the abnormal protein. however, liver transplant does not reverse the disease. the goal of liver transplant is to prevent additional amyloid deposition and prevent new symptoms/complications from happening. these medications bind to the mrna of transthyretin and prevent the production of the transthyretin protein, thus decreasing the overall amount of transthyretin that can accumulate in the body. stabilization of abnormal transthyretin: there are medications that can stabilize the normally folded transthyretin, preventing misfolding and subsequent amyloid deposition. these medications include tafamidis, the nsaid diflunisal, and ag10. tafamidis is a medication that binds to transthyretin and keeps it in its normal shape, stopping it from aggregating into amyloid fibrils. diflunisal and ag10 work in a similar manner to tafamidis in their ability to bind to and stabilize transthyretin. destruction of existing amyloid fibrils: there are multiple medications that show amyloid destroying properties, doxycycline, tauro-ursodeoxy-cholic acid (tudca), and monoclonal antibodies. the use of pacemakers (both right ventricular pacing and biventricular pacing) or implantable cardioverter defibrillators remains questionable in cardiac amyloidosis. in 2012, craig lewis, a 55 year old texan, presented at the texas heart institute with a severe case of amyloidosis. he was given an experimental continuous-flow artificial heart transplant which saved his life. lewis died 5 weeks later of liver failure after slipping into a coma due to the amyloidosis. prognosis overall prognosis is dependent on the extent of cardiac dysfunction. worse outcomes have been seen when echocardiography shows left ventricular wall thickness, poor systolic function and severe diastolic dysfunction. light chain (al-cm) prognosis: for light-chain amyloidosis early detection leads to best possibility of therapies prolonging the period of remission. well treated light chain cardiac amyloidosis has a 4-year survival rate of around 90%. in patients that undergo stem cell transplant the average survival time increases to 10 years. staging systems have been developed to stratify severity of the disease, including the mayo biomarker stage, which utilizes various biomarkers such as troponin i, troponin t, bnp, and nt-probnp, and free light chain concentrations. familial (attrm-cm) prognosis: due to the extensive number of variables involved in this subtype, prognosis varies depending on the specific type of familial cardiac amyloidosis. variables involve mutant vs wild type transthyretin mutation and age of onset of symptoms. in comparison to light chain amyloidosis, the familial subtype is slower to progress and has a more favorable prognosis. however, the val 122lle mutation (most common cause of familial cardiac amyloidosis) has a 4-year survival rate of 16% with an average length of 26 months. a delay in recognition plays a major factor in this reduced survival rate.