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Biomedical subjects

B Chamontin

Publications and source records attributed to B Chamontin.

100 records · Page 6Linked to original sources
PubMedDate not supplied

[Long-term development of blood pressure profile in hypertensive hemodialysis patients].

OBJECTIVE: The prognostic value of nocturnal blood pressure (BP) in hemodialysis patients has been well established. The aim of this study was to evaluate the long-term outcome of ambulatory BP in hypertensive hemodialysis patients. DESIGN AND METHODS: Medical records of all hemodialysis patients seen for uncontrolled hypertension between 1993 and 1999 and who underwent an ambulatory blood pressure measurements (ABPM) were retrospectively studied. Uncontrolled hypertension was defined as office BP = 140/90 mmHg and 24 h ABP = 125/80 mmHg. Patients who underwent a second ABPM after an interval of at least 1 year were included in the study. Demographic characteristics, medical history, cardiovascular risk factors and treatments were recorded for each patient. A t-test (bilateral) was used to compare BP. RESULTS: 26 patients were included (545 +/- 18.9 years; 14 men). 7 had previous history of cardiovascular disease and 2 were diabetic. At the end of the follow-up (29 +/- 12.8 months), 9 patients (36%) had 24 h BP < 125/80 mmHg. A significant decrease in diurnal and nocturnal BP was observed (p < 0.05). No significant change was observed for office systolic BP and predialytic BP. CONCLUSION: Our data show that a long-term decrease in nocturnal BP can be obtained in hypertensive patients on hemodialysis. With respect to the prognostic value of this criteria, randomised trials could be carried out to determine whether nocturnal BP is superior to office BP as a target for antihypertensive therapy in this population.

Adult↗
PubMedDate not supplied

[Blood pressure control in hypertensive patients with stable coronary heart disease].

OBJECTIVE: To evaluate systolic blood pressure (SBP) control in hypertensive patients with a stable coronary heart disease (CHD) in general practice in France. METHODS: A survey was conducted in a sample of 206 general practitionners (GP) representative of the French medical population, in 2003 [LHYCORNE survey]. Each GP had to include 3 hypertensive patients, >18 years old, BP > or = 140/90 mmHg and/or treated for hypertension, and with evidence of CHD documented by myocardial infarction (MI) or angina pectoris (AP) [diagnosis previously established by a cardiologist]. Three office BP measurements were performed, the last two recorded. BP levels were considered as controlled by treatement if they were < 140/90 mmHg. RESULTS: 595 patients were included, 75% men mean age 66 years, 25% women mean age 73 years. All patients had a CHD: MI 46%, AP 54%; 533 (90%) had more than 2 cardiovascular risk factors: hyperlipidemia (411; 69%), smokers (375; 63%), diabetes (158; 27%). Mean BP was 140.7 +/- 14/80.8 +/- 9.7 mmHg; 553 (93%) of these hypertensive patients were treated, and 239 (40%) were considered as having a controlled SBP at the treshold of 140 mmHg: 47% in patients with previous MI and 38% with AP (p < 0.001). Diastolic BP (DBP) was <90 mmHg in 480 (81%) and pulse pressure was >65 mmHg in 202 (34%); 313 (53%) patients received a combination of three drugs or more; 354 (60%) had a beta-blocker, 260 (44%) a calcium channel blocker, 237 (40%) an ACE inhibitor, 287 (48%) other antihypertensive drugs (246 diuretics, 41%); 502 (84%) received antiplatelet therapy, 403 (68%) statins. CONCLUSION: This survey shows that systolic BP is not at goal in 6/10 hypertensive patients with stable CHD suggesting there is a place for a more effective combination therapy according to evidence-based medicine.

Adult↗
PubMedDate not supplied

[Renal insufficiency and treatment of persistent cardiac insufficiency with converting enzyme inhibitor].

The purpose of this retrospective study was to consider impaired renal function in patients with severe congestive heart failure after converting enzyme inhibition and to emphasize the characteristics of this population. The study concerned 26 patients (pts), 72.5 +/- 8.1 years old, with a severe congestive heart failure (NYHA Class IV). Before treatment serum creatinine was slightly increased and the introduction of angiotensin converting enzyme inhibitor (ACEI) - Captopril 58.9 +/- 17.3 mg/j or enalapril 9.2 +/- 4.4 mg - impaired renal function from 132.0 +/- 50.7 mumol/l to 183.5 +/- 139.3 mumol/l (n = 26; p less than 0.05). Patients were separated in 3 groups: in group I; 15 pts, serum creatinine remained unchanged under ACEI in despite of the significant decrease of blood pressure (BP); from 140.7 +/- 24.0/82.5 +/- 13.4 to 120.3 +/- 12.8/71.8 +/- 8.7 mmHg (p less than 0.01). The cause of heart failure was an ischemic heart disease (IHD) in 15 patients (chi 2 test, p less than 0.05), a dilated cardiomyopathy in 4 pts and an aortic or mitral valvular regurgitation in 2 pts. In contrast renal function was significantly impaired in group II; serum creatinine increased from 120.8 +/- 25.2 to 189.0 +/- 80.7 mumol/l under ACEI. BP remained unchanged 136.9 +/- 29.0/78.1 +/- 4.9 and 118.7 +/- 13.6/75.6 +/- 7.6 mmHg respectively before and after treatment. There was 4 pts with dilated cardiomyopathy, 4 pts with mitral or aortic valvular regurgitation and only one with IHD. The introduction of an ACEI in two pts--group III--with severe tricuspid regurgitation induced an acute and reversal renal failure (serum creatinine at 600 mumol/l).

Aged↗
PubMedDate not supplied

[Peripheral vasodilators: from the hemodynamic effect to clinical benefit].

Patients with chronic occlusive arterial disease of lower limbs have an excess mortality due to associated cardiovascular diseases or cancer. They also have an important morbidity with a high prevalence of coronary artery diseases and strokes. In this context, the only benefit of peripheral vasodilators devoid of any effect on morbidity and mortality, could be only on quality of life. Haemodynamic effects of these drugs have been evaluated by several reproducible techniques in order to measure the peripheral blood flow (plethysmography, 133Xe clearance, transcutaneous oxygen-pressure, electromagnetic debimetry). An increase in blood flow has been demonstrated in patients receiving pentoxifylline, naftidrofuryl, or blufomedil in phase II clinical trials using these different methods. No general haemodynamic effect has been observed with these drugs which were better denominated vaso-active drugs. However the most relevant criteria remained to confirm a clinical benefit, particularly on intermittent claudication. Number of positive clinical trials in patients with intermittent claudication have been published, but from a methodological point of view few of them were suitable and demonstrated a statistically significant benefit. Criticisms were mainly related to the type of trial (cross-over is not recommended because of the drug-period effect), the lack of 'intention to treat' analysis, the inhomogeneity of the compared groups (for example different percentages of diabetics and excess of drop-outs). In spite of an established haemodynamic effect and of a demonstrated benefit in claudicants, peripheral vasodilators appear to have a slight interest in the global care of patients with occlusive arterial disease of lower limbs mainly on functional symptoms.

Clinical Trials as Topic↗
PubMedDate not supplied

[Drug interactions with antihypertensive drugs].

Numerous of pharmacokinetic and pharmacodynamic interactions with antihypertensive drugs have to be considered. In this review, interactions are analysed in the major organ sites of these interactions and in cardiovascular target sites of arterial hypertension, with respect to the major antihypertensive drugs. Many antihypertensive drugs are metabolized in the liver (calcium antagonists, liposoluble beta-blockers, and some ACE-inhibitors) via the cytochrome-oxidase system. Phenytoin, barbiturates, and rifampin can accelerate the breakdown of these drugs; conversely, cimetidine, which inhibits oxidase system, can increase antihypertensive drug levels, resulted in greater therapeutic effect. Hepatic blood flow can be modified by propranolol and nifedipine with opposite effects. When combined with nifedipine the breakdown of propranolol is accelerated because of an increase of hepatic blood flow. In the kidney, some anti-hypertensive agents interact with other cardiovascular drugs by competing for renal clearance; calcium antagonists alter the renal clearance of digoxin, but the mechanism remains unclear. In vascular muscle cells, excess vasodilatation or vasoconstriction can be observed. The combination of an alpha 1-blocking agent with a dihydropyridine can induce hypotension, which is sometimes severe. Non-steroidal antiinflammatory drugs (NSAIDs) are able to lessen the antihypertensive effects of beta-blockers, diuretics and ACE-inhibitors, via vascular prostaglandin inhibition. The cardiac pharmacodynamic interactions of beta-blockers and calcium antagonists, verapamil and diltiazem, at the sino-atrial node, atrio-ventricular node, conduction system and myocardium are well established and must be avoided. The main interactions with beta-blockers concern calcium antagonists, class I antiarrhythmic drugs and NSAIDs.(ABSTRACT TRUNCATED AT 250 WORDS)

Antihypertensive Agents↗
PubMedDate not supplied

[Arterial hypertension and insulin resistance].

Insulin resistance manifested by hyperinsulinism is an important risk factor for the development of cardiovascular diseases. When associated with characteristic disorders of the lipid metabolism and arterial hypertension it is regarded today as a metabolic syndrome X. To detect hyperinsulinism in patients with arterial hypertension in everyday practice, it is advisable to determine the rations "circumference of the waist, circumference of the hips", while its abnormal values necessitate a carbohydrate challenge. Hyperinsulinism in AH patients should be born in mind when devising therapeutic measures, the mainstay of which is dietary therapy, with Calcium antagonists and inhibitors of the converting enzyme being used as hypotensive agents.

Antihypertensive Agents↗