Abstract

Hypertension developing in 65-85% of previously normotensive cyclosporin-treated patients reflects an unusual hemodynamic transition from peripheral vasodilation to systemic and renal vasoconstriction. Circadian BP patterns after liver transplant (Tx) are characterized by loss of normal nocturnal BP decrease, which is thought to be associated with rapid development of hypertensive and end-organ damage including left ventricular hypertrophy and impaired diastolic function.

The aim of this study was to follow-up prospectively BP and to detect early cardiac deterioration in liver graft recipients.

Design and methods: Office BP, 24-h ABPM, and echocardiography were obtained in 18 patients (mean age 46.7 ± 12.33 years, 14 M, 4 F) with end-stage liver disease pre-, 6 weeks and 8.21 (± 3.67) months post-Tx (at their last follow-up).

Results: (See Table)

Pre-TXPost-TX (last FU)p
Office SBP, mmHg114.7 ± 13.17128.4 ± 15.250.001
Office DBP, mmHg68.4 ± 8.8480.3 ± 8.790.001
Hypertension* (%)3 (16.7%)14 (77.8%)0.001
24-h ABPM SBP, mmHg119.6 ± 9.70133.8 ± 19.020.001
24-h ABPM DBP, mmHg86.4 ± 7.2799.2 ± 13.830.001
LVPw, mm9.38 ± 0.7449.13 ± 1.553n.s.
IVS, mm9.50 ± 0.7569.25 ± 1.488n.s.
LVID, mm51.5 ± 5.2450.3 ± 6.59n.s.
IVRT, ms86.1 ± 16.4590.8 ± 14.54n.s.
E/A1.31 ± 0.5231.09 ± 0.564n.s.
CO, L/min6.24 ± 1.6935.56 ± 1.665n.s.
Pre-TXPost-TX (last FU)p
Office SBP, mmHg114.7 ± 13.17128.4 ± 15.250.001
Office DBP, mmHg68.4 ± 8.8480.3 ± 8.790.001
Hypertension* (%)3 (16.7%)14 (77.8%)0.001
24-h ABPM SBP, mmHg119.6 ± 9.70133.8 ± 19.020.001
24-h ABPM DBP, mmHg86.4 ± 7.2799.2 ± 13.830.001
LVPw, mm9.38 ± 0.7449.13 ± 1.553n.s.
IVS, mm9.50 ± 0.7569.25 ± 1.488n.s.
LVID, mm51.5 ± 5.2450.3 ± 6.59n.s.
IVRT, ms86.1 ± 16.4590.8 ± 14.54n.s.
E/A1.31 ± 0.5231.09 ± 0.564n.s.
CO, L/min6.24 ± 1.6935.56 ± 1.665n.s.
Pre-TXPost-TX (last FU)p
Office SBP, mmHg114.7 ± 13.17128.4 ± 15.250.001
Office DBP, mmHg68.4 ± 8.8480.3 ± 8.790.001
Hypertension* (%)3 (16.7%)14 (77.8%)0.001
24-h ABPM SBP, mmHg119.6 ± 9.70133.8 ± 19.020.001
24-h ABPM DBP, mmHg86.4 ± 7.2799.2 ± 13.830.001
LVPw, mm9.38 ± 0.7449.13 ± 1.553n.s.
IVS, mm9.50 ± 0.7569.25 ± 1.488n.s.
LVID, mm51.5 ± 5.2450.3 ± 6.59n.s.
IVRT, ms86.1 ± 16.4590.8 ± 14.54n.s.
E/A1.31 ± 0.5231.09 ± 0.564n.s.
CO, L/min6.24 ± 1.6935.56 ± 1.665n.s.
Pre-TXPost-TX (last FU)p
Office SBP, mmHg114.7 ± 13.17128.4 ± 15.250.001
Office DBP, mmHg68.4 ± 8.8480.3 ± 8.790.001
Hypertension* (%)3 (16.7%)14 (77.8%)0.001
24-h ABPM SBP, mmHg119.6 ± 9.70133.8 ± 19.020.001
24-h ABPM DBP, mmHg86.4 ± 7.2799.2 ± 13.830.001
LVPw, mm9.38 ± 0.7449.13 ± 1.553n.s.
IVS, mm9.50 ± 0.7569.25 ± 1.488n.s.
LVID, mm51.5 ± 5.2450.3 ± 6.59n.s.
IVRT, ms86.1 ± 16.4590.8 ± 14.54n.s.
E/A1.31 ± 0.5231.09 ± 0.564n.s.
CO, L/min6.24 ± 1.6935.56 ± 1.665n.s.

*Defined as mean of three office BP readings equal or greater than 140/90 mmHg, or taking antihypertensive medication.

There was a significant increase in both office and ABPM values post-Tx. The circadian variation was totally suppressed six weeks post-Tx and remained so throughout follow-up. Despite a significant increase in BP, no cardiac involvement was seen.

Conclusion: Rapidly developing hypertension, characterized by loss of nocturnal fall, was not associated with early cardiac changes in our liver Tx recipients.

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