Similar to the other subtypes of cardiac amyloidosis, a biopsy is required for diagnosis. However, formal diagnosis of Senile cardiac amyloidosis is a diagnosis of exclusion. Biopsy with histological evaluation can rule out Light chain and Familial subtypes, leaving the diagnosis of Senile. This type is often misdiagnosed, however, greater use of cardiac magnetic resonance has increased the rate of diagnosis The severity of the disease tends to be less than the Light chain and Familial variants. This is due to the amount of time that it takes to accumulate the amyloid depositions being longer in the Senile variant. Symptoms and signs
Symptoms of cardiac amyloidosis are a combination of heart failure and amyloid deposition in various other organs. Amyloid deposition in the heart causes restrictive diastolic heart failure that progresses to systolic heart failure.Cardiac manifestations include:

Dyspnea on exertion
Peripheral edema and ascites
Pericardial effusion
Arrhythmias (secondary to disruption of the normal electrical system of the heart)
Atrial arrhythmias (such as atrial fibrillation)
First/second degree heart blocks
Syncope
Elevated neck veins and jugular venous pressure
Myocardial ischemia/Angina (secondary to amyloid deposition in the small arteries of the heart)Myocardial oxygen demand is increased in patients with cardiac amyloidosis, regardless of changes to coronary perfusion.For patients with light-chain amyloidosis, there can be depositions of amyloid into numerous different organs. Deposition of amyloid into other organs makes the diagnosis of cardiac amyloidosis difficult as these extracardiac manifestations mask the diagnosis.
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.