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[Long-term course and complications of arterial hypertension after heart transplantation]
L A Bortolotto1, H B Silva, E A Bocchi
1Instituto do Coração do Hospital das Clínicas-FMUSP.
Insights
Arterial hypertension (AH) is common after cardiac transplantation (CT) with cyclosporine (CY) use, increasing in severity over time. This can lead to ventricular hypertrophy and impact transplant longevity.
Area of Science:
- Cardiology
- Immunology
- Nephrology
Context:
- Cardiac transplantation (CT) is a life-saving procedure for end-stage heart failure.
- Cyclosporine (CY) is a key immunosuppressant used post-CT.
- Arterial hypertension (AH) is a known complication after solid organ transplantation.
Purpose:
- To evaluate the progression of arterial hypertension (AH) and its consequences in patients undergoing cardiac transplantation (CT) while using cyclosporine (CY).
Summary:
- Post-CT, AH prevalence rose from 58.5% at 30 days to 93% at one year, with increasing severity.
- Serum creatinine levels rose significantly after one year, indicating potential renal impact.
- Echocardiography revealed left ventricle hypertrophy in 54% of patients, despite normal cardiac function, with two deaths linked to hypertensive complications.
Impact:
- Early and progressive AH post-CT on CY significantly increases vascular resistance.
- While not directly correlated with CY levels or nephrotoxicity, AH can impair renal function.
- Ventricular hypertrophy due to AH may compromise long-term transplant survival.
Purpose:
To evaluate the progression of arterial hypertension (AH) and its consequences, in patients submitted to cardiac transplantation (CT) in use of cyclosporine (CY).
Methods:
In 65 patients submitted to orthotopic CT, we evaluated blood pressure, serum creatinine and blood levels of CY before, 15 and 30 days, and 6, 12, 24, 48 and 60 months after CT; in 20 patients we analyzed cardiac index and systemic vascular resistance pre-CT, 15 and 30 days, 6 and 12 months after CT; in 33 patients, we studied anatomic and functional modifications by echocardiography, 24 +/- 13 months after CT.
Results:
Thirty days after CT, AH was present in 58.5% (50% mild), and after one year, 93% of patients were hypertensives (85% moderate-to-severe), remaining unchanged during the rest of follow-up. The serum creatinine progressively increased, reaching values significantly higher than those pre-CT after one year, persisting with a mild increment until 60 months. Echocardiography showed left ventricle hypertrophy in 54% of patients, all of which had normal function. Two patients died as a direct consequence of hypertensive complications.
Conclusion:
AH in patients submitted to CT on CY use occurs early, increases in prevalence and severity during the follow-up and is mediated by an increase in vascular resistance. Also, the AH does not correlate to CY blood levels or nefrotoxicity, but it can impair renal function and compromise longevity of transplantation by inducing ventricular hypertrophy.