According to a study by Eagle et al, for patients 50-59 years old theres an operative mortality rate of 1.8% while patients older than 80, the risk is 8.3%. Other factors which increase mortality are: female gender, re-operation, dysfunction of Left ventricle and left main disease. In most cases, CABG relieves angina, but in some patients it reoccurs in a later stage of their lives. Around 60% of patient will be angina free, 10 years after their operation. Myocardial infarction is rare 5 years after a CABG, but its prevalence increases with time. Also, the risk of sudden death is low for CABG patients. Quality of life is also high for at least 5 years, then starts to decline.The beneficial effects of CABG are clear at cardiac level. LV function is improved and malfunctioning segments of the heart (dyskinetic-moving inefficiently or even akinetic-not moving) can show signs of improvement. Both systolic and diastolic functions are improved and keep improving for up to 5 years in some cases. LV function, and myocardial perfusion, during exercise also improves after CABG.
Other
Symptoms, whether connected or not to GS, have been reported in a subset of those affected: fatigue (feeling tired all the time), difficulty maintaining concentration, unusual patterns of anxiety, loss of appetite, nausea, abdominal pain, loss of weight, itching (with no rash), and others, such as humor change or depression. But scientific studies found no clear pattern of adverse symptoms related to the elevated levels of unconjugated bilirubin in adults. However, other substances glucuronidized by the affected enzymes in those with Gilberts syndrome could theoretically, at their toxic levels, cause these symptoms. Consequently, debate exists about whether GS should be classified as a disease. However, Gilbert syndrome has been linked to an increased risk of gallstones. Cause
Mutations in the UGT1A1 gene lead to Gilbert Syndrome. The gene provides instructions for making the bilirubin uridine diphosphate glucuronosyltransferase (bilirubin-UGT) enzyme, which can be found in the liver cells and responsible for the removal of bilirubin from the body.The bilirubin-UGT enzyme performs a chemical reaction called glucuronidation. Glucuronic acid is transferred to unconjugated bilirubin, which is a yellowish pigment made when your body breaks down old red blood cells, and then being converted to conjugated bilirubin during the reaction. Conjugated bilirubin passes from the liver into the intestines with bile. Its then excreted in stool. People with Gilbert syndrome have approximately 30 percent of normal bilirubin-UGT enzyme function, which contributes to a lower rate of glucuronidation of unconjugated bilirubin. This toxic substance then accumulates in the body, causing mild hyperbilirubinemia.