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Biomedical subjects

Jean-Jacques Mourad

Publications and source records attributed to Jean-Jacques Mourad.

6 recordsLinked to original sources
PubMed2003

Aspirin alters arterial function in patients with chronic heart failure treated with ACE inhibitors: a dose-mediated deleterious effect.

BACKGROUND: By inhibiting prostaglandin synthesis, aspirin can interfere with both arterial functional and angiotensin-converting enzyme inhibitor (ACEI) properties and be deleterious in chronic heart failure (CHF). AIM: Our aim was to prospectively evaluate the effect of aspirin on arterial functional properties in CHF patients treated with ACEIs. METHODS AND RESULTS: Over three consecutive treatment periods of 7 days, 18 patients received placebo, followed by aspirin 100 mg/day, and then aspirin 325 mg/day. Single blind prospective assessment of reflected wave and time reflection by radial applanation tonometry; pulse wave velocity; blood pressure; thromboxane B2 (TxB2) and prostaglandins in plasma and urine was performed. Aspirin 325 mg/day induced a significant increase in augmentation index of reflected wave (P<0.0001 and P=0.0013 vs. placebo and aspirin 100 mg, respectively) and a significant decrease in reflected wave traveling times (P=0.0007 vs. placebo). Aspirin 100 mg/day produced a similar, though non-significant, trend in these parameters compared with placebo. Both aspirin treatments produced a statistically significant decrease in serum TxB2 (P<0.0001) but did not have an effect on the metabolite of prostaglandin I2 (P=0.136). CONCLUSION: This study demonstrates the existence of a dose-mediated deleterious effect of aspirin upon arterial functional properties in CHF patients treated with ACEI.

Adult↗
PubMed2002

[Arterial pulse pressure].

A WELL IDENTIFIED RISK FACTOR: Other than systolic, diastolic and mean pressure, arterial pulse pressure (or differential pressure) is an independent factor of cardiovascular and notably coronary risk. The role of this factor is now clearly quantified in untreated hypertensive patients, but also in treated apparently controlled patients, and in patients with normal blood pressure. Demonstration of the deleterious role of an increase in pulse pressure was also made in populations at high risk of events such as heart failure, post-infarction or in hemodialyzed patients. FROM A THERAPEUTIC POINT OF VIEW: Antihypertensive treatments have inconstant efficacy on pulse pressure and new therapeutic routes appear promising. However, in the absence of available proof that a strategy axed on the decrease in pulse pressure improves cardiovascular prognosis, current recommendations do not yet include pulse pressure levels in therapeutic strategies. AN EFFICIENT MARKER: Whilst awaiting further data, the measurement of pulse pressure, because of its pertinence and simplicity, provides the practitioner with one of the most efficient markers for screening persons at high risk of cardiovascular and particularly coronary risk.

Antihypertensive Agents↗
PubMed2002

Who is fooling us?

Explore the source record for details and available documents.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2002

Aortic pulse pressure and extent of coronary artery disease in percutaneous transluminal coronary angioplasty candidates.

BACKGROUND: Pulse pressure and aortic stiffness are both predictors of coronary artery disease. Whether these parameters are directly related to coronary structural alterations has never been studied. METHODS: From September 1999 to September 2000, the following data were collected from 99 eligible patients: invasive intra-aortic systolic and diastolic blood pressures (BP), extent of coronary artery disease, cardiovascular risk factors, and the incidence of angiographically documented restenosis after coronary angioplasty. RESULTS: In the study population, independent determinants of aortic pulse pressure were age, gender, aortic mean BP, heart rate, and extent of coronary artery disease (r2 = 0.57, P < .0001). In univariate analysis, invasive aortic, but not noninvasive brachial, mean pressure (P = .017) and pulse pressure (P = .027) were significantly associated to the extent of coronary artery disease. In a multiple regression analysis, only male gender (P = .013) and the level of aortic pulse pressure (P = .023) were independently associated with the extent of coronary heart disease. Restenosis was angiographically documented in 11 patients (11%). There was a borderline significant association of restenosis to aortic mean BP (P = .05) and to a past history of multiple previous angioplasties (P = .03). CONCLUSIONS: In this study, aortic pulse pressure was a significant risk factor for the extent of coronary artery disease. There was only a borderline significant association of restenosis to the steady, but not pulsatile, component of aortic BP in the stent era.

Aged↗
PubMed2002

Age-related increase of pulse pressure and gene polymorphisms in essential hypertension: a preliminary study.

Genes may modulate the changes of blood pressure (BP) with age; this possibility has never been studied for the age-related increase of pulse pressure (PP), although in older populations, PP is considered the stronger mechanical factor predicting cardiovascular mortality. In humans, the presence of the mutant allele C of the angiotensin II (Ang II) AT(1)-receptor or of the mutant allele T of the eNOS G(298) T gene polymorphisms is associated with enhanced contractile properties of conduit arteries in response to vasoconstrictive agents. In this study, we evaluated, in subjects with untreated essential hypertension, whether the presence of these mutant alleles or their combination might influence the age-related increase of PP. Three main findings emerged from the study and were particularly observed in women: 1) the presence of the C and/or of the T mutant alleles or their combination were associated with a steeper slope of the age versus PP curve, compared with subjects without the mutant allele; 2) the slope was more significantly enhanced when the two mutant alleles were associated in the same genotype; and 3) no comparable age- and gender-related changes in systolic, diastolic or mean BP were found according to this genetic classification. In subjects with essential hypertension, genes may modulate the age-mediated increase of PP. This finding gives new insights in the interactions between genes, mechanical factors and cardiovascular risk.

Aging↗