Related Experiment Videos
Cardiovascular adaptation to cyclosporine-induced hypertension
H O Ventura1, C J Lavie, F H Messerli
1Department of Internal Medicine, Ochsner Medical Institutions, New Orleans, LA 70112.
Insights
Cyclosporine-induced hypertension in heart transplant patients shows higher systemic vascular resistance and lower cardiac output compared to essential hypertension. This leads to more severe heart muscle thickening and impaired function.
Area of Science:
- Cardiology
- Nephrology
- Immunology
Background:
- Arterial hypertension is a common complication following heart transplantation, often linked to immunosuppressive drugs like cyclosporine.
- Understanding the cardiovascular adaptations to this specific type of hypertension is crucial for patient management.
Purpose of the Study:
- To investigate the hemodynamic and echocardiographic differences between cyclosporine-induced hypertension in heart transplant recipients and essential hypertension.
- To characterize the cardiac adaptation to hypertension in heart transplant patients.
Main Methods:
- A comparative study involving 25 hypertensive cardiac transplant recipients, 25 patients with essential hypertension, and 25 normotensive controls.
- Hemodynamic and echocardiographic parameters were measured and compared between groups matched for key physiological variables.
Main Results:
- Hypertensive cardiac transplant recipients exhibited higher systemic vascular resistance and lower cardiac output and stroke volume index compared to essential hypertension patients.
- Both hypertensive groups showed increased posterior wall thickness and left ventricular mass index versus controls.
- Cardiac transplant hypertension was associated with more severe left ventricular hypertrophy and a lower ejection fraction than essential hypertension.
Conclusions:
- Cyclosporine-induced hypertension in heart transplant recipients is characterized by elevated systemic vascular resistance, reduced cardiac output, and impaired left ventricular systolic performance.
- Cardiac adaptation to this hypertension involves more severe concentric left ventricular hypertrophy compared to essential hypertension.
- These findings highlight distinct cardiovascular changes in transplant-related hypertension.
Abstract:
Arterial hypertension is a complication of cyclosporine therapy in heart transplant recipients. We studied cardiovascular adaptation to cyclosporine-induced hypertension by determining haemodynamic and echocardiographic indexes in 25 cardiac transplant recipients matched by mean arterial pressure, age, sex, height and weight to 25 patients with established essential hypertension. Twenty-five normotensive subjects matched by age, sex and body habitus were used as controls. Systemic vascular resistance was 15% higher (P = 0.07) and cardiac and stroke volume indices were 20% and 25% lower (P < 0.01), respectively, in the hypertensive cardiac transplant recipients compared with patients with essential hypertension. Patients with essential hypertension and hypertensive cardiac transplant recipients had greater posterior wall thickness and left ventricular mass index than normotensive subjects (P < 0.01); however, hypertensive cardiac transplant recipients had a greater left ventricular mass (245 +/- 7 vs. 223 +/- 8 g, P < 0.05) than patients with markedly established essential hypertension. Left ventricular ejection fraction was significantly lower in hypertensive cardiac transplant recipients when compared with either normotensives or patients with established essential hypertension. These results indicate that established essential and cardiac transplant hypertension are associated with markedly increased systemic vascular resistance. However, after heart transplantation, hypertension is associated with higher systemic vascular resistance, lower cardiac output, stroke volume and stroke work compared with patients with established essential hypertension at the same level of mean arterial pressure. The cardiac adaptation to cyclosporine-induced hypertension has more severe concentric left ventricular hypertrophy and impaired left ventricular systolic performance.(ABSTRACT TRUNCATED AT 250 WORDS)