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Gene Transfer for Ischemic Heart Failure in a Preclinical Model
Published on: May 15, 2011
[The effect of carvedilol on apoptosis gene PDCD5 expression in chronic heart failure patients]
Yan Wu1, Xiao-Yun Nie, Da-Yi Hu
1People's Hospital, Peking University, Beijing 100044, China.
Insights
Serum PDCD5 antibody levels are elevated in chronic ischemic heart failure patients. Carvedilol treatment significantly reduced these antibody levels and improved cardiac function, indicating its therapeutic potential.
Area of Science:
- Cardiology
- Immunology
- Molecular Biology
Background:
- Chronic ischemic heart failure is associated with complex pathophysiological changes, including apoptosis.
- The role of programmed cell death protein 5 (PDCD5) and its antibody in heart failure pathogenesis requires further elucidation.
- Understanding the impact of therapeutic interventions on apoptotic markers is crucial for managing heart failure.
Purpose of the Study:
- To investigate serum levels of PDCD5 antibody in patients with chronic ischemic heart failure.
- To evaluate the effect of carvedilol treatment on serum PDCD5 antibody titers and cardiac function parameters.
Main Methods:
- A cohort of 20 chronic ischemic heart failure patients (LVEF < 45%, NYHA II-III) received carvedilol for 6 months.
- Serum PDCD5 antibody levels were measured using ELISA before and after treatment.
- Comparisons were made with serum levels from 20 healthy individuals; cardiac function (LVEF, chamber dimensions) and NYHA class were assessed.
Main Results:
- Patients with chronic ischemic heart failure exhibited significantly higher serum PDCD5 antibody levels compared to healthy controls (P < 0.01).
- Carvedilol treatment led to a significant reduction in serum PDCD5 antibody levels (P < 0.05).
- Carvedilol therapy improved cardiac function, evidenced by increased LVEF (35.5% to 42.7%, P < 0.05) and decreased ventricular diameters, along with a slight improvement in NYHA class (P < 0.05).
Conclusions:
- Elevated serum PDCD5 antibody titers are associated with chronic ischemic heart failure, suggesting a role for apoptosis.
- Carvedilol treatment effectively reduces PDCD5 antibody levels in these patients.
- The observed improvements in cardiac function underscore carvedilol's therapeutic benefits in chronic ischemic heart failure.
Objective:
To observe the changes of serum PDCD5 antibody in chronic ischemic heart failure patients and the effect of carvedilol treatment.
Methods:
Twenty chronic ischemic heart failure patients, 11 males and 9 females, aged 58 +/- 13, with the left ventricular ejection fraction (LVEF) < 45% by echocardiography and New York Heart Association (NYHA) cardiac function classification II-III, were treated with carvedilol for 6 months with a target dosage of 50 mg/d. The serum PDCD5 antibody was tested by ELISA before and after carvedilol treatment and compared with those of 20 healthy persons.
Results:
The A value of PDCD5 antibody in the heart failure patients was 3.5 +/- 1.4, significantly higher that in than healthy persons (1.9 +/- 1.0, P < 0.01). After treatment of carvedilol, the A value of PDCD5 antibody in the heart failure patients decreased to 2.5 +/- 1.2 (P < 0.05). In 6 months maintenance treatment, 14 (70%) patients reached the dosage 50 mg/d, 4 (20%) reached 25 mg/d, and 2 (10%) reached 12.5 mg/d. Five patients (25%) had side effect such as dizziness, nausea and cough, one patient (5%) was hospitalized for 3 weeks because of heart failure, no patient died. After treatment of carvedilol, the NYHA degree increased by 0.3 (P < 0.05), LVEF increased from 35.5% +/- 7.8% to 42.7% +/- 9.6% (P < 0.05), left ventricular end-diastolic diameter decreased 5.3 mm (P < 0.05), and left ventricular end-systolic diameter decreased by 8.1 mm (P < 0.01).
Conclusion:
The titer of apoptosis gene PDCD5 antibody in the serum of chronic ischemic heart failure patients are higher, which shows apoptosis and treatment of carvedilol significantly decreases its titer.
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