De novo hypertension after liver transplantation.

Textor, Stephen C.

doi:10.1161/01.hyp.22.2.257

Cited by 58 publications

(28 citation statements)

References 94 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…[1][2][3][10][11][12]18 Earlier re- ports suggested a lower incidence of posttransplant hypertension with tacrolimus, although this may have reflected, in part, a shorter period of observation. 10,11,18 The mechanisms of early posttransplant hypertension appear to differ between cyclosporine and tacrolimus.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3] Several reports have suggested that the incidence of hypertension in patients treated with tacrolimus (also called FK 506) is lower than that in patients treated with cyclosporine within the first year or two after kidney transplantation, [4][5][6] up to 3 years after heart transplantation, [7][8][9] and during the first year after liver transplantation. [10][11][12] We have observed, however, that the prevalence of hypertension in tacrolimus-treated patients increases in the second year after liver transplantation and may approach that observed in patients treated with cyclosporine.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Late hypertension after liver transplantation: A comparison of cyclosporine and tacrolimus (FK 506)

et al. 1998

View full text Add to dashboard Cite

Hypertension frequently develops early after liver transplantation when cyclosporine-based immunosuppression is used. However, initial experience with tacrolimus has suggested that its use leads to a lower early incidence of hypertension. In this study, the blood pressure status of patients treated with cyclosporine (n ‫؍‬ 131) and those treated with tacrolimus (n ‫؍‬ 28) was compared 24 months after liver transplantation. At this time interval, the prevalence of hypertension in the cyclosporine and tacrolimus groups were 82% and 64%, respectively (P F .05). For those patients who were hypertensive by 24 months, onset was delayed in the tacrolimus group compared with the cyclosporine group: 40% versus 71% and 73% versus 93% at 1 and 12 months, respectively (P F .05). Within the cyclosporine group, patients with hypertension were heavier than those with normal blood pressure, 84.7 ؎ 1.8 versus 73.4 ؎ 4.0 kg, respectively (P F .05). Within the tacrolimus group, hypertensive patients had lower glomerular filtration rates and higher renal vascular resistances compared with normotensive patients, 74 ؎ 12 versus 47 ؎ 6 mL/min and 15,711 ؎ 2,445 versus 28,830 ؎ 4,310 dyne/s/cm 5 / m 2 , respectively (P F .05). There were no withingroup differences for age, gender, pretransplant history of hypertension, family history of hypertension, graft function, or daily doses of prednisone, cyclosporine, or tacrolimus. These results indicate that, compared with cyclosporine, the onset of hypertension after liver transplantation is delayed and less prevalent with tacrolimus. Additionally, hypertension is associated with increased body weight in cyclosporine-treated patients and with more severe renal dysfunction in patients receiving tacrolimus. The relationships of these findings to the development of posttransplant hypertension requires further study. Copyright 1998 by the American Association for the Study of Liver DiseasesH ypertension frequently occurs early after liver transplantation when immunosuppression with cyclosporine plus prednisone is used, amounting to a prevalence of 75% to 85% by 24 months. 1-3 Several reports have suggested that the incidence of hypertension in patients treated with tacrolimus (also called FK 506) is lower than that in patients treated with cyclosporine within the first year or two after kidney transplantation, 4-6 up to 3 years after heart transplantation, 7-9 and during the first year after liver transplantation. [10][11][12] We have observed, however, that the prevalence of hypertension in tacrolimus-treated patients increases in the second year after liver transplantation and may approach that observed in patients treated with cyclosporine. 3 We examined the development of hypertension in patients treated with cyclosporine or tacrolimus and followed up for 24 months after liver transplantation. The goals of this study were to assess the prevalence of hypertension in these two patient groups and to compare clinical and laboratory characteristics that might be associated with the development of...

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Late hypertension after liver transplantation: A comparison of cyclosporine and tacrolimus (FK 506)

et al. 1998

View full text Add to dashboard Cite

show abstract

“…Concentrations of nitrite and nitrate were determined in serum samples stored frozen at Ϫ80°C. Before analysis, serum of these samples was deproteinized with 35% sulfosalicylic acid and the supernatants neutralized with NH 4 Cl buffer and NaOH. Concentrations of nitrite and nitrate were quantitated colorimetrically in supernatants after reaction with the Griess reagent.…”

mentioning

confidence: 99%

Selective impairment of endothelium-mediated vasodilation in liver transplant recipients with cyclosporin A -induced hypertension

et al. 1998

View full text Add to dashboard Cite

Arterial hypertension is commonly observed in orthotopic liver transplantation (OLT) recipients receiving cyclosporin A (CsA), but the precise pathogenetic mechanisms remain partially unknown. The aim of this study was to investigate endothelium-dependent and -independent dilation and adrenergic constriction of resistance vessels of OLT recipients treated with CsA. Vascular reactivity was examined in 22 OLT patients, 10 with and 12 without arterial hypertension, and in 10 control subjects by assessing the forearm blood flow response to the brachial artery infusion of increasing concentrations of methacholine chloride, sodium nitroprusside, and phenylephrine. In 10 OLT patients, the response to methacholine was also examined after acetylsalicylate. The ratio of serum nitrite and nitrate to serum creatinine was lower (P F .05) in OLT patients with hypertension than in nonhypertensive patients and controls. Basal forearm flow was similar in the three groups. Methacholine vasodilation was impaired in the hypertensive patients as shown by a lower maximum forearm vasodilator response and a shift in the dose response curve to methacholine to the right compared with the nonhypertensive OLT patients and the controls. The response to methacholine was not modified after salicylate. Forearm flow response to nitroprusside was similar in the three groups. No differences between the patients and the controls were found in the maximum forearm flow contraction in response to phenylephrine. An impairment in endothelium-dependent vasodilation could mediate arterial hypertension in OLT patients immunosuppressed with CsA. (HEPATOLOGY 1998;27:332-338.)Arterial hypertension is a side-effect commonly observed in patients with an allogeneic solid organ graft receiving an immunosuppressive regimen based on cyclosporin A (CsA). 1,2 Published reports show that between 60% and 85% of transplant recipients treated with CsA develop hypertension. 3 The precise pathogenetic pathways underlying CsA-induced hypertension remain partially unknown. This problem is further hindered by the frequent discrepancy between the results obtained in humans and in animal models, and the relative resistance of rats that receive CsA to develop systemic hypertension. These facts make it difficult to extrapolate data from the experimental to the human setting. 4 Recent lines of evidence point to a disturbance in the local mechanisms of vascular regulation as the most likely cause of hypertension after transplantation. In this regard, several studies that have focused on the effects of CsA on arachidonic acid metabolites and endothelium-dependent and -independent vasodilation suggest that the arterial hypertension developed during CsA therapy reflects a shift in favor of vasoconstriction through an impairment of vasodilating mechanisms. [5][6][7][8][9][10][11] These studies have been performed in animal models, in vessels from healthy humans incubated with CsA, or in vessels from CsA-treated patients. However, no study to date has investigated the pattern of reacti...

show abstract

“…In our study, we found significantly higher levels of diastolic arterial pressure at rest and at peak exercise in transplanted subjects relative to that in controls,and no differences of systolic arterial pressure between groups 6,7 . The etiology of this complication seems to be multifactorial, having as a common final route the elevation of systemic vascular resistance [63][64][65][66][67] . The reason for the attenuated pressure response at peak exercise has not been clarified 18 .…”

Section: Work Ratementioning

confidence: 99%

“…In this situation cardiac output was similar to the normal. Another explanation for the excessive ventilatory response could be muscular respiratory dysfunction consequent to hypoperfusion and muscular fatigue 67,70 . Kavanagh et al 71 reported significant improvement in the respiratory response during exercise following physical training.…”

Section: Work Ratementioning

confidence: 99%

Adaptation to exercise following cardiac transplantation

Af¹,

Ja²

2000

Arq. Bras. Cardiol.

View full text Add to dashboard Cite

Cardiac transplantation has been the treatment of choice for patients with terminal cardiac insufficiency, increasing survival time by more than 80% in the first year 1 and by more than 50% over ten years 2 . Following cardiac transplantation, the quality of life improves considerably, and many transplanted patients return to work becoming reintegrated into the community 3 . During regular activity, transplanted subjects have shown physical conditioning similar to that of healthy individuals 4-7 . Starling's axiom, "today's physiology will be tomorrow's medicine" 8 , emphasizes the need for knowledge about post-transplantation cardiovascular adaptations, to serve as the basis for clinical treatment and rehabilitation. The present article has the aim of discussing the state-of -the-art of this subject.Aerobic capacity -Aerobic capacity is the total amount of O 2 capable of being metabolized by an organism. Aerobic potency is the amount of 0 2 consumed per unit of time (VO 2 ). Maximal O 2 consumption (VO 2 max.) or maximal aerobic potency is the maximum VO 2 obtained in an endurance (of progressive loads) test, in which VO 2 reaches a maximal value without additional increase due to an additional work load. In tests in which the patient does not reach maximum oxygen consumption, as frequently occurs in cardiopathy patients and transplanted subjects, peak VO 2 is defined as the highest value of VO 2 obtained. Following cardiac transplantation, patients progress with a reduction of peak VO 2 9-15 of 30-50% [16][17][18][19][20][21][22] . In our study 6,7 , deficits were 32.4% and 25.7% at peak exercise and at the anaerobic threshold, respectively. Marzo et al 18 found a 35% reduction in the absolute values of the anaerobic threshold. Degré et al 23 reported an early and intense accumulation of lactate during exercise, attributed to increased production in active tissues and reduced clearance secondary to decreased blood flow in the liver and other inactive tissues. In our study 7 , VO 2 in light to moderate submaximal exercise (40 watt load) below the anaerobic threshold was 12.34 and 12.38ml/kg/ min, in transplanted and healthy subjects, respectively, without significant differences between these groups. Meyer et al 24 , working with a load of 50 watts, reported a VO 2 of 0.96 ±0.1 and 0.95±0.08 L/min -1 in transplanted and control subjects, respectively.The reduction of peak VO 2 is due to multiple factors, both central and peripheral. Chronotropic incompetence and alteration in diastolic function are central factors 21,22,25,26 . At the peripheral level, reduction of peripheral oxygen extraction occurs 17,21,22,[27][28][29] . An exaggerated neuroendocrine response 19 and reduced capacity of pulmonary diffusion 20,30 also seem to be involved in decreased tolerance to exercise.Heart Rate -Heart rate values at rest have been observed to be higher in transplanted compared with healthy individuals due to the absence of parasympathetic innervation and corresponding to the intrinsic frequency of the sinus node 17,23,[31...

show abstract

De novo hypertension after liver transplantation.

Cited by 58 publications

References 94 publications

Late hypertension after liver transplantation: A comparison of cyclosporine and tacrolimus (FK 506)

Late hypertension after liver transplantation: A comparison of cyclosporine and tacrolimus (FK 506)

Selective impairment of endothelium-mediated vasodilation in liver transplant recipients with cyclosporin A -induced hypertension

Adaptation to exercise following cardiac transplantation

Contact Info

Product

Resources

About