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Biomedical subjects

A A Paleologos

Publications and source records attributed to A A Paleologos.

7 recordsLinked to original sources
PubMed1998

Significance of blood pressure levels achieved with felodipine anti-hypertensive treatment on cardiovascular structure and function changes.

One of the targets of anti-hypertensive treatment is cardiovascular structural and functional improvements, while the level of blood pressure (BP) under treatment is related to patient morbidity and mortality. The aim of this study was to evaluate the relation of BP achieved after felodipine monotherapy to the degree of cardiovascular changes. Six hundred patients with essential hypertension were studied and grouped according to diastolic BP (DBP) levels after 6 months of therapy: 90-94 (n = 86), 85-89 (n = 186), 80-84 (n = 180) and < 80 mm Hg (n = 148). Overall BP fell from 175/103 to 137/83 mm Hg with a concomitant moderate reflex tachycardia (3.3%). Left ventricular (LV) dimensions decreased to a degree (-0.4 and -0.8%, P < 0.0001), with the greatest decrease in patients with lower DBP levels under treatment (P < 0.0001). LV systolic function improved to a modest degree (0.8%, P < 0.0001), depending on DBP fall (P < 0.0001), as did cardiac output (2.4%, P < 0.0001). LV systolic wall stress and total peripheral resistance fell (-18% and -14%, P < 0.0001) in relation to DBP drop (P < 0.0001), as did aortic root distensibility (55%, P < 0.0001). It is concluded that the degree of cardiovascular structure and function improvements are directly related to the DBP levels achieved under felodipine anti-hypertensive therapy.

Aged↗
PubMed1995

Myocardial trophic effects of blood pressure in children with insulin-dependent diabetes mellitus.

To evaluate the effect of blood pressure (BP) on the left ventricular mass index (LVMI), 66 children with IDDM 13 +/- 3 years of age were studied and compared with 58 healthy age-matched siblings. The 24 h BP recordings disclosed that children with diabetes had higher DBP (68 vs. 65 mm Hg, P = 0.002), especially at night (60 vs. 55 mm Hg, P = 0.00007), with a minimisation of the normal nocturnal hypotension (-9.9 vs. -12.4 mm Hg, P = 0.04). Their LVMI was higher (79 vs. 71 g/m2, P = 0.02); it was independent of BP values and variability (P = NS), but it was positively correlated with heart rate (r = -0.46, P = 0.0005). In the control group, LVMI was significantly correlated with the mean SBP (r = 0.46, P = 0.0005); with its variability (r = 0.32, P = 0.02) and, to a lower extent, with heart rate (r = -0.29, P = 0.03). It is concluded that in children with diabetes mellitus the participation of BP in myocardial hypertrophy is not so obvious, although the BP load is increased. The increase of the LVMI occurs early in life and before the onset of hypertension.

Adolescent↗
PubMed1992

Comparison of ketanserin and celiprolol on regression of left ventricular hypertrophy in older hypertensive patients.

The effects of ketanserin, a specific serotonin2-receptor agonist, and celiprolol, a new, highly cardioselective beta 1 blocker with partial beta 2 agonist activity and peripheral vasodilating properties, on left ventricular (LV) structure and function were assessed in 60 older hypertensive patients (greater than 55 years) with clinical LV hypertrophy (LV mass index greater than 130 g/m2). The patients were studied using echocardiography after 1 month of placebo treatment, and 6 and 18 months of monotherapy with active drug. Ketanserin and celiprolol lowered blood pressure to normal levels. Heart rate did not change with ketanserin and fell moderately (-5%) with celiprolol (p less than .001). Regression of LV hypertrophy was achieved with the use of either medication (p less than .0001), although the magnitude of reduction in LV mass was greater with celiprolol at both 6 months (-10% vs -5%, p = .001) and 18 months (-13% vs -7%, p = .002). While LV volume did not change with either drug, celiprolol tended to decrease it, resulting in a 5% reduction in cardiac index (p = .01), which was associated with mild bradycardia. Ketanserin did not change LV ejection fraction, whereas celiprolol caused a slight (1.5%) long-term improvement (p = .003). Systolic wall stress and total peripheral resistance decreased with both agents (p less than .01), with no between-group differences. In conclusion, anti-hypertensive treatment of older persons with ketanserin or celiprolol achieves regression of LV hypertrophy without associated deleterious effects on LV function.

Adrenergic beta-Antagonists↗
PubMed1992

Differentiation of beta-blocker effects on serum lipids and apolipoproteins in hypertensive patients with normolipidaemic or dyslipidaemic profiles.

To evaluate the differential effects of beta-blockers on serum lipids and apolipoproteins in normolipidaemic and dyslipidaemic hypertensives, 330 patients with mild to moderate essential hypertension were studied 1 month after placebo therapy and 6 months after monotherapy with propranolol (n = 53), atenolol (n = 66), metoprolol (n = 58), pindolol (n = 53), or celiprolol (n = 100). Serum total cholesterol, triglycerides, high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), and apolipoproteins (Apo) A1 and B were measured at baseline and study end. A total of 136 (41.2%) patients were considered normolipidaemic (pretreatment LDL-C < 160 mg.dl-1) and 194 (58.8%) were considered dyslipidaemic (LDL-C > 160 mg.dl-1). Changes in total cholesterol differed between normolipidaemics and dyslipidaemics with propranolol (+13% in normolipidaemics vs -0.5% in dyslipidaemics, P < 0.001), atenolol (+7% vs -2%, P = 0.01), metoprolol (+9% vs -4%, P0.0006), pindolol (+8% vs -9%, P < 0.001), and celiprolol (-1% vs -13%, P = 0.002). HDL-C differed less, with propranolol (-18% vs -13%), atenolol (-6% vs -2%), metoprolol (-2% vs -6%), pindolol (+4% vs +1%), and celiprolol (+9% vs +4%); none of these changes between normolipidaemic and dyslipidaemic patients were statistically significant. LDL-C changes differed the most, with propranolol (+35% vs -1%, P < 0.0001), atenolol (+15% vs -4%, P = 0.001), metoprolol (+12% vs -6%, P = 0.004), pindolol (+12% vs -13%, P < 0.0001), and celiprolol (+3% vs -16%, P = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1991

Dyslipidemic effects of cigarette smoking on beta-blocker-induced serum lipid changes in systemic hypertension.

To assess the effects of beta blockers on lipids and apolipoproteins in cigarette smokers and nonsmokers, 330 patients with systemic hypertension received 1 month of placebo and 6 months of beta-blocker monotherapy. Serum total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and apolipoproteins A1 and B were measured. Total cholesterol increased with propranolol (smokers vs nonsmokers, 8 vs 2%); increased for smokers and decreased for nonsmokers with atenolol (8 vs -3%), metoprolol (6 vs -1%) and pindolol (7 vs -6%); and decreased for both groups with celiprolol (-3 vs -10%). HDL cholesterol decreased with propranolol (smokers vs nonsmokers, -8 vs -18%), atenolol (-7 vs -2%) and metoprolol (-12 vs -1%); increased for smokers and decreased for nonsmokers with pindolol (11 vs -2%); and increased for both groups with celiprolol (5 vs 6%). Similar trends were observed with LDL cholesterol and the total/HDL cholesterol ratio. It is concluded that early noncardioselective beta blockers such as propranolol have significant dyslipidemic effects in both smokers and nonsmokers. Cardioselective drugs such as atenolol and metoprolol, or drugs with partial agonist activity such as pindolol, have variable effects. Celiprolol, a new, highly cardioselective beta 1 blocker with partial beta 2 agonist activity and vasodilatory properties, has favorable effects on lipids and minimizes the dyslipidemic effects associated with smoking.

Adrenergic beta-Antagonists↗
PubMed1990

Left ventricular hypertrophy regression and function changes with ketanserin in elderly hypertensives.

Ketanserin is a serotonin antagonist with age-related antihypertensive efficacy. Its effects on left ventricular (LV) function and hypertrophy have not been adequately reported. We studied noninvasively 54 elderly hypertensives before and 6 months after ketanserin monotherapy. Mean blood pressure was controlled (174/101 to 145/86 mmHg, p less than 0.0001) with no heart rate changes. LV dimensions and volumes remained unchanged, as did all LV ejection indices, thus preserving LV output (p = ns). Total peripheral resistances fell (from means of 1986 to 1615 dynes, cm.s-5, p less than 0.0001), as did LV systolic wall stresses. Mean LV mass was reduced (248 to 237 g, p less than 0.0001), mainly due to interventricular septum thinning (11.8 to 11.1 mm, p less than 0.0001), resulting in a decrease in mean LV cross-sectional area (21.3 to 20.5 cm2, p less than 0.0001) and mass/volume ratio (2.14 to 2.01 p = 0.0001). Thus, LV hypertrophy regression did not affect contractility (LV mass index relation to stress/end-systolic volume index, r = -0.558 before and r = -0.564 after ketanserin therapy). It is concluded that ketanserin is an effective antihypertensive agent in the elderly that reduces LV hypertrophy indices and maintains cardiac output, with no concomitant burdening on LV hemodynamics.

Aged↗