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Hypertension following orthotopic cardiac transplantation
Insights
Hypertension is a common complication after heart transplantation, often resistant to treatment. Cyclosporine use contributes to kidney damage and persistent high blood pressure, suggesting ACE inhibitors may help in later stages.
Area of Science:
- Cardiology
- Nephrology
- Immunology
Background:
- Hypertension frequently develops after cardiac transplantation, independent of pre-existing conditions.
- This de novo hypertension presents unique challenges due to the denervated heart's altered blood pressure regulation.
Purpose of the Study:
- To investigate the multifactorial etiology of post-cardiac transplantation hypertension.
- To evaluate the role of immunosuppressive therapy, particularly cyclosporine, in hypertension development and persistence.
- To assess therapeutic strategies for managing hypertension in this patient population.
Main Methods:
- Analysis of factors contributing to acute and chronic hypertension post-transplantation.
- Evaluation of renal function impairment and its correlation with plasma renin activity and angiotensin II.
- Assessment of the efficacy of different antihypertensive drug classes, including diuretics, vasodilators, and ACE inhibitors.
Main Results:
- Acute hypertension is linked to volume expansion and increased systemic vascular resistance.
- Cyclosporine use is a major factor in persistent hypertension and progressive renal dysfunction.
- Renal alterations correlate with increased plasma renin activity and angiotensin II, potentially exacerbating hypertension.
Conclusions:
- Managing post-transplant hypertension requires addressing multifactorial causes, including immunosuppression-induced renal damage.
- Adjusting cyclosporine dosage and considering combination therapy may mitigate renal and hypertensive complications.
- ACE inhibitors show promise for later-stage management as plasma renin activity increases, though careful monitoring is essential.
Abstract:
It seems established that hypertension, to some degree, is a frequent consequence of cardiac transplantation. The hypertension occurs de novo and is not related to whether hypertension was present in association with the heart disease that led to the need for transplantation. The etiology of this hypertension is multifactorial and varies depending on the time that has ensued after transplantation. Acutely, it is primarily a problem related to intravascular volume expansion and persistently increased systemic vascular resistance. Although it may be modest in severity, it seems to be particularly resistant to therapy with most antihypertensive drugs. Moreover, the total "hyperbaric impact" of the hypertension is rendered greater because the blood pressure and heart rate in these patients with denervated hearts fails to show the usual 10 to 15 percent fall when recumbent/asleep at night, which occurs in normotensive individuals and in most with hypertension of other etiologies. The major factor in the persistence of the hypertension through the later stages post-transplantation appears to be the cyclosporine that is used as an immunosuppressive. Although cyclosporine has been the major contributor to reduced rejection in these individuals, and to their increasingly prolonged survival, it inevitably produces slowly progressive impairment of renal function. The damage to the kidney is reflected both in tubular as well as glomerular and vascular damage, with a steady fall in glomerular filtration and a rise in creatinine. From our studies it appears that the renal alterations are associated with a gradual rise in plasma renin activity and angiotensin II, which perhaps further damages the kidney and causes persistence of the increased systemic vascular resistance. The use of lower doses of cyclosporine during the ischemic phase in the kidney that immediately follows surgery and of reduced doses over time, often with azathioprine added, seems to minimize the renal damage, or at least to stabilize it and to slow progression of the renal dysfunction and hypertension. Treatment of the hypertension with conventional drugs has definite but limited value. Diuretics and vasodilators have been the mainstay of our approach during the early phases of the hypertension but our recent data indicate that ACE inhibitors may become relatively specific in management during the later phases of the post-transplantation period as PRA levels rise in response to vascular damage by cyclosporine. ACE inhibitors have inherent dangers that require careful monitoring.(ABSTRACT TRUNCATED AT 400 WORDS)