VIP Class Notes (Cynthia) (W)

Writing

The patient was consciously tired after labor in January 2017 with the slight edema of the both lower extremities, then relieved after rest. In February 2017, the conscious edema of both lower extremities was aggravated. Echocardiography and cardiac MRI showed hypertrophic cardiomyopathy which was highly suspected as myocardial amyloidosis was possible, but the patient refused to conduct myocardial biopsy. Regular follow-up clinics were followed up, and the symptoms were aggravated repeatedly. The patient was admitted to the department of Cardiology in January, February, and May of 2018. During the hospitalization in May 2018, the creatinine was high. There was no abnormality in immunoglobulin and hematuria immunofixation. Perfect bone penetration to exclude the blood system leads to amyloidosis. On August 2, 2018, he was treated with an emergency heart failure and furosemide injection was pushed. On August 13, 2018, he was admitted to the Department of Nephrology for renal puncture. The pathological results suggest that there is no basis for amyloidosis. Therefore, this hospitalization is mainly for the treatment of heart failure, and cedilan (deslanoside injection 400ug once). After the patient’s regular outpatient follow-up, there was still edema, the diuretic effect gradually deteriorated, and the body weight increased significantly. (2018.10.29 NT-proBNP 6413pg/ml)
On December 4, 2018, the patient entered the trial randomly.
On April 10, 2019, patients were informed of genetic testing. The results showed that the highly suspected pathogenic mutation TTR gene heterozygous missense mutation (Grade B) with amyloidosis supports the diagnosis of clinical myocardial amyloidosis.
The consideration from Principle investigator (Rational), why this patient was selected.
From September 2017, the patient regularly came to visit the PI for clinic follow-up, PI diagnosis of patients may be restrictive cardiomyopathy, highly suspected myocardial amyloidosis, repeated recommendations for genetic testing and myocardial biopsy, but patients always refused. In August 2018, the results of renal wear did not find a myocardial amyloid basis. In December 2018 decided to screen patients into the study.

The patient feels tired after light exercise/activities on January 2017 with slight edema at the lower extremities/calves, edema relieve after some rest. On February 2017, the patient felt that the edema of both lower extremities/calves was aggravated. Echocardiography and cardiac MRI showed that hypertrophic cardiomyopathy is one of the cause while myocardial amyloidosis is also a high possible suspect as the cause of the edema. But the patient refused to conduct myocardial biopsy test. Regular check-ups at the clinic, the results showed the conditions were aggravated repeatedly. The patient was admitted to the department of Cardiology in January, February, and May of 2018. During the hospitalization in May 2018, the creatinine was high. There was no abnormality in immunoglobulin and hematuria immunofixation. Perfect bone penetration to exclude the blood system leads to amyloidosis. On August 2, 2018, he was suffered from a heart failure and was given furosemide injection at the emergency department. On August 13, 2018, he was admitted to the Department of Nephrology for renal puncture. The pathological results suggested that there is no evidence to support the diagnosis for amyloidosis. Therefore, this hospitalization is mainly for the heart failure treatment, patient was given cedilan (deslanoside injection 400ug once). After the patient’s regular outpatient follow-up, there was still edema, the diuretic effect gradually deteriorated, and the body weight increased significantly. (2018.10.29 NT-proBNP 6413pg/ml)
On December 4, 2018, the patient entered the trial randomly.
On April 10, 2019, we found out that patient took a genetic test. The results showed that pathogenic mutation TTR gene heterozygous missense mutation (Grade B)  supports the diagnosis with amyloidosis of clinical myocardial amyloidosis is the highly suspected cause. 
Following are the Principle Investigator’s opinion :
From September 2017, the patient regularly came to visit the PI for regular check-ups. PI concluded that the patient may be suffering from restrictive cardiomyopathy, highly suspected myocardial amyloidosis, repeated recommendations for genetic testing and myocardial biopsy. But patient always refused to undergo any test or biopsy. In August 2018, the results of renal wear did not find a myocardial amyloid basis. In December 2018 PI went through all of patients results, and there is no evidence that patient has this sickness.