Treatments differ according to the type of<unk>  present. The majority of treatment is aimed at preserving heart function and treating heart failure symptoms. Light chain (AL-CM) Treatment: Since the cause of this subtype of<unk>  is the excessive production of free light chains, the major goal of treatment is the reduction in concentration of light chains. For light-chain<unk> , the use of FLC assays and NT-proBNP levels can be used to monitor the progression of<unk>  and any response to treatments. One of the major routes to decrease the production of these excess light chains is to kill the abnormal cells that are producing them. Chemotherapeutic agents such as melphalan or bortezomib can be used to kill off the abnormal cell line that is producing the free light chains. Following chemotherapy, a bone marrow transplant can be utilized to restore the normal cell lines. There are newer medications (ixazomib, carfilzomib, daratumumab, elotuzumab) under research for the treatment of multiple myeloma that can help 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<unk>  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<unk>  including methods to suppress transthyretin production, stabilize amyloid fibrils, and medications that can destroy already existing fibrils. For familial<unk> , 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<unk> . In 2012, Craig Lewis, a 55 year old Texan, presented at the Texas Heart Institute with a severe case of<unk> . He was given an experiment 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<unk> .
Cardiac amyloidosis
Amyloid cardiomyopathy
Viral cardiomyopathy
Diabetic cardiomyopathy
HIV associated cardiomyopathy
Alcoholic cardiomyopathy
Coxsackievirus-induced cardiomyopathy
Dilated cardiomyopathy