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Biomedical subjects

R Laureano

Publications and source records attributed to R Laureano.

9 recordsLinked to original sources
PubMed1996

[Hypertension, hyperpotassemia and normal glomerular filtration (Gordon's syndrome): a case report].

We describe a case of a 26 year old patient affected by a rare syndrome characterized by hyperkalemia, arterial hypertension and normal glomerular filtration rate (Gordon's syndrome), probably due to a renal tubular defect in the reabsorption of sodium or chloride. The patient, who had hyperkalemia since the age of 4 years, was referred to our Centre because of hypertension not well controlled with antihypertensive treatment. After drug therapy wash-out, we confirmed the existence of hypertension (180/100 mm Hg; ambulatory BP monitoring: 24-h mean BP = 151/91 mm Hg; 7 am-11 pm = 157/95; 11 pm-7 am: 133/82) and blood and urine tests showed hyperkalemia (6.6 mEq/L), hyperchloremia (115 mEq/L), mild metabolic acidosis (pH = 7.35, HCO3 = 19 mEq/L), low levels of plasma renin activity ( < 0.2 ng/ml/h), slight increase of plasma (1.08 nM/L) and daily urine aldosterone (129 nM) and normal serum creatinine (1.1 mg/dl) and glomerular filtration rate (91 ml/min). These data allowed to exclude the presence of renal failure and hyporeninemic hypoaldosteronism, which are the most common diseases with hypertension and hyperkalemia, and suggested the diagnosis of Gordon's syndrome. After 1 month of treatment with chlorthalidone (12.5 mg o.i.d) we observed the normalization of BP (130/80 mm Hg; ambulatory BP monitoring: 24-h BP: 132/76 mm), serum potassium (5,1 mEq/L) and the other blood and urine tests. These results were confirmed 6 months later and at present the patient has good clinical conditions.

Adult↗
PubMed1995

[The use of ambulatory pressure monitoring for evaluating antihypertensive treatment in clinical practice].

OBJECTIVE: To describe the clinical experience of our Centre in the assessment of antihypertensive therapy with 24-hour ambulatory blood pressure monitoring (ABPM). DESIGN AND PATIENTS: We retrospectively studied all the 241 out-patients on antihypertensive therapy submitted to ABPM (SpaceLabs 90207, USA) between March 1992 and March 1993 for clinical purposes. We evaluated: 1) the clinical indications for the test; 2) the modifications of drug treatment suggested by the ABPM results; 3) the referring physicians' acceptance of these suggestions; 4) the changes of office BP measured before and 3-6 months after ABPM. RESULTS: 1) The indications for ABPM were: resistant or poorly controlled hypertension (n = 170-71%); suspected "white coat effect" (n = 51-21%); assessment of symptoms (n = 20-8%). 2) The analysis of ABPM suggested to modify drug treatment in 51% of the patients; a "white-coat effect" was found in 18% of the patients. 3) The ABPM suggestions about treatment were accepted by the referring physicians in 89% of the patients. 4) Office BP decreased from 163 +/- 18/99 +/- 9 mm Hg (before ABPM) to 151 +/- 13/91 +/- 7 (3-6 months after ABPM), (p < 0.001). CONCLUSIONS: The use of ABPM in our Centre, which is based on specific clinical indications, provided indications to modify the drug treatment in a high percentage of patients.

Aged↗
PubMed1994

Fosinopril in the treatment of hypertension: effects on 24h ambulatory blood pressure and on blood pressure response to exercise.

This study evaluated the effects of medium-term once daily administration of fosinopril (20 mg) on BP profile and on BP response to exercise in patients with mild to moderate hypertension. Twenty patients (14 males and 6 females; 25-57 years of age), after a six week drug wash-out phase, underwent 24h ambulatory BP monitoring (ABPM) (Spacelabs 90207) and, the day after, maximal bicycle exercise testing. Patients then received a once daily treatment with fosinopril and ABPM and exercise testing were repeated 45-60 days later. Fosinopril decreased average 24h SBP and DBP (-13.5 mmHg and -9.7 mmHg, respectively, P < 0.002); a significant BP reduction was observed both in day and in nighttime, without alteration in diurnal BP profile. The antihypertensive effect was still evident 24h after dosing. Trough to peak ratio was 0.58 +/- 0.16. Fosinopril induced a reduction of SBP and DBP during exercise testing (-20 and -11 mmHg at baseline; -17 and -8 mmHg at peak exercise; -24 and -14 mmHg at the sixth minute of recovery; P < 0.002), with a slight prolongation of exercise time (+46 seconds, P = 0.041). These results indicate that fosinopril at a once daily dose of 20 mg provides a sustained 24h BP reduction associated with BP reduction during physical exercise. These effects have been obtained without altering diurnal BP profile, without excessive hypotension at the time of maximal antihypertensive effect and with a slight improvement of exercise tolerance.

Adult↗
PubMed1986

Enhanced peripheral vasoconstrictor response and increased thromboxane A2 synthesis after the cold pressor test in patients with angina at rest.

Peripheral vascular resistance (PVR) and thromboxane A2(TxA2) synthesis after the cold pressor test were investigated in different subsets of patients with angina (10 with stable effort angina, 36 with resting angina [24 in an active phase and 12 in an inactive phase], and five with Prinzmetal's variant angina) and in 41 control subjects of equivalent age and risk factors. Left ventricular end-diastolic pressure, ejection fraction, extent of coronary angiographic lesions, and baseline PVR were not significantly different among the various patient groups. In all patient groups, except those with variant angina, the cold pressor test resulted in a higher increase in PVR than in the control subjects (p less than .001 for all groups). In patients with variant angina the vasoconstrictor response was increased only in proximity (about 1 hr) to ischemic attacks. In patients with active resting angina the vasoconstrictor response was on the average four times longer than that in patients with effort angina and with inactive resting angina (p less than .001). This exaggerated vasoconstrictor response was associated with elevated TxA2 resting levels in plasma and with increased TxA2 synthesis after the cold pressor test. A linear relationship was found between the area of the vascular response and the area of TxA2 production after the cold pressor test in patients with active resting angina (r = .87, p less than .001). The increased TxA2 synthesis and the inappropriate increase of peripheral vascular response to sympathetic stimulation revert back to normal in the inactive phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1985

Abnormal cardiocoronary thromboxane A2 production in patients with unstable angina.

Thromboxane B2 (TXB2), the stable metabolite of thromboxane A2 (TXA2), was measured in the coronary sinus and in aortic blood before and after cold pressor test (CPT) in 21 patients suffering from ischemic heart disease (7 affected by stable effort angina and 14 by unstable angina) and in 12 patients not suffering from myocardial ischemia (control group) during coronary angiography. Aspirin (10 mg/kg intravenously) was administered before catheterization in order to prevent platelet and leukocyte TXA2 formation. Control subjects and patients with effort angina had TXB2 resting levels lower than unstable angina patients without a transcardiac gradient which, on the contrary, was found in unstable angina patients. Only in these patients CPT resulted in a significant TXB2 increase more marked in the coronary sinus (from 50.0 +/- 18.9 pg/ml to 73.0 +/- 35.1 pg/ml, p less than 0.001) than in the aorta (from 33.4 +/- 17.1 pg/ml to 42.6 +/- 24.0 pg/ml, p less than 0.05), so that the transcardiac TXB2 gradient significantly increased. In all but two unstable angina patients, TXB2 elevation was not associated with a fall of cardiac lactate extraction. The resting and CPT-induced TXB2 gradients were unrelated to the presence and severity of coronary angiographic lesions. These results indicate that unstable angina patients show an abnormal cardiocoronary capacity to synthesize TXA2, which seems not to be elicited by the occurrence of myocardial ischemia.

Adult↗
PubMed1982

Platelet aggregation and thromboxane A2 production after adrenergic stimulation in young healthy humans.

The effects of adrenergic stimulation on platelet aggregation (platelet aggregation ratio; PAR), beta-thromboglobulin (beta-TG) release and plasma thromboxane B2 (TxB2) levels were investigated in 25 healthy young volunteers. Adrenergic stimulation induced by cold application was checked by evaluating the changes in the calculated vascular resistance in the forearm. A prompt increase in platelet aggregates and plasma beta-TG and TxB2 concentrations was observed after adrenergic stimulation. PAR changed from resting values of 0.97 +/- 0.05 to 0.75 +/- 0.08 (p less than 0.001) at the end of cold application. At the same time, beta-TG plasma concentration increased from 32.09 +/- 19.64 to 135.48 +/- 37.97 ng/ml (p less than 0.001) and TxB2 plasma levels changed from 0.49 +/- 0.24 to 0.99 +/- 0.39 pmol/ml (p less than 0.001). TxB2 levels, but not PAR and beta-TG concentration came back to the resting values at the end of the observation period (10 min). Aspirin, as the lysine acetylsalicylate equivalent to 5 mg/kg i.v. of acetylsalicylic acid, although able to completely inhibit platelet cyclooxygenase failed to inhibit the plasma TxB2 increase induced by adrenergic stimulation. This strongly suggests that the increase in plasma TxB2 following adrenergic stimulation is of extraplatelet origin. Also beta-TG and PAR changes were not affected by aspirin administration.

Adolescent↗
PubMed1981

Platelet aggregation testing.

The authors review the methods currently used for platelet aggregation testing, which are mainly grouped in two classes: 1. methods measuring the sensitivity of platelets to aggregating agents and to mechanical stimulation in vitro and 2. methods measuring the spontaneous tendency of platelets to aggregate in vivo. Their advantages, their pitfalls and their potential usefulness are reported. The platelet behavior as assessed by the available methods is not strictly related to the true platelet behavior in circulating blood. Therefore much criticism is requested in the interpretation of the results obtained for a given group of subjects with a given method and any unallowed extrapolation must be avoided.

Adenosine Diphosphate↗