Peter De Leeuw

Prof. Peter De Leeuw

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Research Focus & Metrics

Academic Career Length

45Years (1982-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 January 2012 in Frontiers in Genetics
Verified
Journal Article
Open access
BVBernard J. van Varik
Bernard J. van Varik
RRRoger J. M. W. Rennenberg
Roger J. M. W. Rennenberg
CRChris PM Reutlingsperger
Chris PM Reutlingsperger
AKAbraham A. Kroon
Abraham A. Kroon
PLPeter De Leeuw
Peter De Leeuw
Leon SchurgersLeon Schurgers
Leon Schurgers
Vascular disease is still the leading cause of morbidity and mortality in the Western world, and the primary cause of myocardial infarction, stroke, and ischemia. The biology of vascular disease is complex and still poorly understood in terms of causes and consequences. Vascular function is determined by structural and functional properties of the arterial vascular wall. Arterial stiffness, that is a pathological alteration of the vascular wall, ultimately results in target-organ damage and increased mortality. Arterial remodeling is accelerated under conditions that adversely affect the balance between arterial function and structure such as hypertension, atherosclerosis, diabetes mellitus, chronic kidney disease, inflammatory disease, lifestyle aspects (smoking), drugs (vitamin K antagonists), and genetic abnormalities [e.g., pseudoxanthoma elasticum (PXE), Marfan's disease]. The aim of this review is to provide an overview of the complex mechanisms and different factors that underlie arterial remodeling, learning from single gene defect diseases like PXE, and PXE-like, Marfan's disease and Keutel syndrome in vascular remodeling.

1 March 2009 in JACC
Verified
Journal Article
Closed access
RKRoland van Kimmenade
Roland van Kimmenade
JJJames Januzzi
James Januzzi
JBJaap A. Bakker
Jaap A. Bakker
AHAlphonse J. Houben
Alphonse J. Houben
RRRoger Rennenberg
Roger Rennenberg
YPYigal M. Pinto
Yigal M. Pinto

1 September 2002 in Journal of the American Society of Nephrology
Verified
Journal Article
Open access
PDF file
PLPeter De Leeuw
Peter De Leeuw
LTLutgarde Thijs
Lutgarde Thijs
WBWillem H. Birkenhäger
Willem H. Birkenhäger
SVSophia M. Voyaki
Sophia M. Voyaki
AEAris D. Efstratopoulos
Aris D. Efstratopoulos
JSJan Albert Staessen
Jan Albert Staessen
Several reports suggest that markers of renal function such as serum creatinine, serum uric acid, and urinary excretion of protein may be related to cardiovascular complications and mortality. This study analyzed the data from the Syst-Eur trial, which was a randomized, placebo-controlled, double-blind intervention trial in elderly patients with isolated systolic hypertension. The purpose was to evaluate whether serum levels of creatinine and uric acid and urinary protein excretion at entry are related to subsequent morbidity and mortality. Incidence rates of total mortality, cardiovascular mortality, stroke (fatal as well as nonfatal), coronary events, and all cardiovascular endpoints were calculated for each quintile of serum creatinine or serum uric acid or for each category of protein excretion (none, trace, and overt). Crude and adjusted relative hazard rates were also determined for each 20 μM increase in serum creatinine, each 50 μM increase in serum uric acid, and for each protein excretion category. Even when adjusted for age, gender, and various other covariates, serum creatinine was significantly associated with a worse prognosis. There was an U-shaped relationship between serum uric acid and total mortality, but otherwise no obvious relationships were detected between serum uric acid levels and complications when appropriate adjustments were made for confounding variables. Proteinuria at entry was a significant predictor of total mortality and all cardiovascular endpoints. It is concluded that higher levels of serum creatinine and trace or overt proteinuria are associated with an increased number of cardiovascular events and with a higher mortality in patients with isolated systolic hypertension.

1 May 2017 in Hypertension
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Journal Article
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PLPeter De Leeuw
Peter De Leeuw
JBJohn D. Bisognano
John D. Bisognano
GBGeorge L. Bakris
George L. Bakris
MNMitra K. Nadim
Mitra K. Nadim
HHHermann Haller
Hermann Haller
AKAbraham A. Kroon
Abraham A. Kroon
Baroreflex activation therapy is a novel technique for treating patients with resistant hypertension. Although short-term studies have demonstrated that it lowers blood pressure, long-term results have not yet been reported. The aim of the present study is to assess the long-term efficacy and safety of baroreflex activation therapy. Long-term follow-up data were analyzed from all patients who had been included in 1 of the 3 trials that focused on treatment-resistant hypertensive patients. Altogether, 383 patients were available for analysis: 143 of these had completed 5 years of follow-up and 48 patients had completed 6 years of follow-up. In the entire cohort, office systolic blood pressure fell from 179±24 mm Hg to 144±28 mm Hg ( P <0.0001), whereas office diastolic pressure dropped from 103±16 mm Hg to 85±18 mm Hg ( P <0.0001). Heart rate fell from 74±15 beats per minute to 71±13 beats per minute ( P <0.02). The effect of baroreflex activation therapy is greater than average in patients with signs of heart failure and less than average in patients with isolated systolic hypertension. In ≈25% of patients, it was possible to reduce the number of medications from a median of 6 to a median of 3. Temporary side effects, related to either the surgical procedure or the cardiovascular instability, do occur, but they do not require specific measures and resolve over time. After a follow-up of 6 years, baroreflex activation therapy maintains its efficacy for persistent reduction of office blood pressure in patients with resistant hypertension without major safety issues.

13 December 2004 in Archives of internal medicine (1960)
Verified
Journal Article
Open access
PDF file
PLPeter De Leeuw
Peter De Leeuw
LRLuis M. Ruilope
Luis M. Ruilope
CPChristopher R. Palmer
Christopher R. Palmer
MBMorris J. Brown
Morris J. Brown
ACAlain Castaigne
Alain Castaigne
GWGilbert Wagener
Gilbert Wagener
Evidence is accumulating that the kidney contributes to the development of cardiac and cerebral complications. Recent data indicate that, besides microalbuminuria, serum creatinine level also acts as a marker of risk.1,2 Interestingly, the predictive power of serum creatinine is already demonstrable with relatively normal values.2,3 In hypertensive populations, relationships have been found between serum creatinine level and cardiovascular events, but in most of the studies either the type of treatment was not accounted for or patients were at relatively low risk. Consequently, only limited information is available regarding the effect of renal function on cardiovascular prognosis in patients who are already at high risk. We have addressed this question using the results from the Intervention as a Goal in Hypertension Treatment (INSIGHT) trial. The INSIGHT trial was a large, prospective, double-blind, randomized, controlled trial that compared the effects of nifedipine gastrointestinal therapeutic system (GITS) with a diuretic combination (hydrochlorothiazide and amiloride hydrochloride) on cardiovascular outcome in hypertensive patients with additional cardiovascular risk factors. The main results of this trial have been described elsewhere.4 In the present study, we report on the evolution of renal function during treatment and on the post hoc analysis of the relationship between renal function at baseline and cardiovascular complications. As markers of renal function, serum creatinine, creatinine clearance, serum uric acid, and proteinuria were used.

1 September 2000 in Hypertension
Verified
Journal Article
Closed access
PDF file
WSWilko Spiering
Wilko Spiering
AKAbraham A. Kroon
Abraham A. Kroon
MFMonique M. J. J. Fuss-Lejeune
Monique M. J. J. Fuss-Lejeune
MDMat J. A. P. Daemen
Mat J. A. P. Daemen
PLPeter De Leeuw
Peter De Leeuw
—Several investigations have shown heterogeneity in the functional responses to angiotensin II (Ang II) in patients with essential hypertension. The present study was initiated to evaluate ...