[Left ventricular hypertrophy in systemic arterial hypertension. 1987].
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Biomedical subjects
Publications and source records attributed to L Corea.
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The aim of our study was to assess the frequency of important problems in the ultrasonic estimate of septal thickness as a consequence of multiple endocardial lines inside the septum in echocardiographic tracings of otherwise good technical quality. We performed an echocardiographic study in a population composed of 311 subjects (131 essential hypertensive subjects and 180 normotensive healthy controls) by using M-mode echocardiography under two-dimensional control, according to the recommendations of the American Society of Echocardiography. We observed the presence of one or more continuous lines inside the septum, each of them simulating an endocardial border and thus producing the appearance of two or more superimposed septal thicknesses differing by 2 mm or more in greater than 50% of the subjects (54% normotensive and 56% hypertensive). Furthermore, within the group of subjects with multiple septal lines, we found the disappearance of at least one of the farthest linear echoes, with resulting septal thinning of almost 2 mm in 58% of the normotensive and 61% of the hypertensive subjects. These findings suggest the need for caution when interpreting echocardiographic measurements of left ventricular septal thickness. We suggest that in the presence of multiple lines inside the septum, the echocardiographic examination should be continued up to the appearance of the thinnest septal image, possibly devoid of multiple lines inside the septum.
In this study we compared the antihypertensive efficacy and tolerability of captopril at 25 mg twice daily, hydrochlorothiazide (HCTZ), 12.5 mg twice daily and placebo in a multicentre, double-blind, randomized study that included 152 essential hypertensive patients (77 males, 75 females, 87 WHO stage I, 65 WHO stage II, aged 69 +/- 4 years, mean +/- s.d.). Supine and standing blood pressure were similarly reduced by captopril and HCTZ (P less than 0.01 for both compared with placebo). The heart rate did not change. Captopril (25-30 mg twice daily) and HCTZ (12.5 mg twice daily), alone or in combination, maintained their antihypertensive effect during a 24-week single-blind follow-up study. During the follow-up, diastolic blood pressure remained less than 100 mmHg in seven essential hypertensives on placebo, in 45 on captopril and in 25 on HCTZ. Side effects were observed in seven essential hypertensives during placebo (treatment withdrawn in two), in eight during HCTZ and in three during captopril. Serum potassium was reduced (P less than 0.05) and uric acid was increased (P less than 0.01) only during HCTZ. We conclude that captopril and HCTZ have similar antihypertensive efficacy in the elderly; however, captopril appears to be better tolerated.
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The short- and long-term effects of two calcium channel blocking drugs, verapamil and nifedipine, on blood pressure, heart rate, plasma catecholamines, plasma renin activity, plasma volume and cardiac performance (echocardiography) were studied in essential hypertensive patients and in normal subjects. Verapamil, 160 mg orally, reduced blood pressure within 60 minutes in 22 hypertensive patients, but not in 12 normotensive subjects. Nifedipine, 10 mg sublingually, reduced blood pressure within 15 minutes in 19 hypertensive patients, but not in 7 normotensive subjects. Plasma noradrenaline was significantly increased both in normal subjects and in hypertensive patients only after nifedipine was administered. Verapamil (80 mg three times a day) first, and nifedipine (10 mg three times a day) thereafter, or vice versa, were given to 12 hospitalized hypertensive patients on a fixed sodium and potassium intake; the drugs produced similar blood pressure reductions, but heart rate and plasma catecholamines were increased only after nifedipine (p less than 0.05). Neither drug affected plasma volume, aldosterone or plasma renin activity. Long-term ambulatory treatment with verapamil (80 or 160 mg three times a day for 2 to 4 months) or nifedipine (10 mg three times a day for 2 months) produced changes in all variables that were similar to those observed in the hospital (controlled) study. Shortening fraction was significantly increased after nifedipine (p less than 0.05) but no change was observed after verapamil. In conclusion, blood pressure is effectively reduced by both verapamil and nifedipine; an appreciable adrenergic stimulation may be caused by nifedipine, but usually not by verapamil, and fluid retention, renin release or myocardial depression is not observed during verapamil or nifedipine treatment.
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Twenty-seven mild to moderate essential hypertensive patients were treated with captopril alone or combined with hydrochlorothiazide and left ventricular echocardiographic changes were evaluated after 1, 3 and 6 months. The left ventricular mass decreased slightly after 3 months, together with mean wall stress and total peripheral resistance, while the cardiac performance, as measured by fractional shortening and cardiac output, was unaffected. A high degree of individual variability was observed, and only 9 out of 20 patients examined after 3 months had a consistent reduction in left ventricular mass. The effect of captopril on the isomyosin composition was also evaluated in 4 normotensive rats after 12 weeks of drug administration. No interference with the physiological pattern was observed and no modifications of the biochemical and structural properties of the myocardium were detected.
In a multicenter, randomized, double-blind study, 108 hypertensive patients were treated with either chlorthalidone 25 mg or slow-release metoprolol 200 mg both given once daily over 4 weeks. Blood pressure and heart rate at rest and at the peak of an isometric exercise test (30% of maximal voluntary contraction for 3 min) were recorded at random and at the end of the study. Both treatments induced a significant (p less than 0.01) blood pressure reduction at rest and at the peak exercise, 50.0% of patients on chlorthalidone and 59.2% on metoprolol, respectively, having a lying diastolic blood pressure less than 95 mmHg. A weak but significant (p less than 0.001) positive correlation was found between age and change in systolic and diastolic blood pressure after chlorthalidone. Such a relationship was absent in the metoprolol group, where a significant (p less than 0.01) positive correlation was found between diastolic pressure rise from rest to the peak exercise at randomization, and the reduction in resting diastolic pressure at the end of the study. Treatments were well tolerated, only a decrease (p less than 0.05) in serum potassium (from 4.4 to 4.0 mEq/l) in the chlorthalidone group was observed. Results suggest that age may influence the antihypertensive response to chlorthalidone, while diastolic pressure rise in isometric exercise may predict the degree of pressure response to sustained beta-adrenergic blockade with metoprolol.
The relations between some pressure and humoral factors, and some echocardiographic indexes of left ventricular (LV) hypertrophy were studied in 64 patients with essential hypertension. Fifty-seven percent of these patients showed echocardiographic evidence of LV hypertrophy (LV mass greater than 215 g). Multivariate stepwise regression analysis showed that only mean blood pressure (BP) and circulating norepinephrine (NE) levels were significantly related to LV mass index in the group of patients with LV hypertrophy. However, mean BP was the only factor related to LV mass index in the subgroup of patients with LV hypertrophy and plasma NE within the normal laboratory range, whereas NE was the sole factor related to LV mass index in the subgroup with LV hypertrophy and abnormally elevated NE levels (greater than mean + 2 standard deviations of the normal laboratory range). Correlation of LV mass index vs NE was -0.35 (not significant) in the former group of patients and 0.89 (p less than 0.01) in the latter group. NE showed no relation with the echocardiographic variables in the hypertensive patients without LV hypertrophy; in this group, diastolic BP was the only factor related to LV mass index. Circulating NE levels were slightly higher in patients with LV hypertrophy (213 +/- 68 ng/liter) than in those without LV hypertrophy (187 +/- 46 ng/liter), but differences were not significant when adjusting NE for age. Plasma renin activity was not dissimilar in the absence or presence of hypertrophy. In conclusion, our findings suggest that NE might be associated with pressure factors in regulating LV hypertrophy development only in a subgroup of hypertensive patients characterized by echocardiographic LV hypertrophy and abnormally elevated circulating NE levels.
The relative chronotropic and inotropic activity of preferential beta 1- and beta 2-adrenoceptor stimulation was investigated in seven healthy male subjects in a randomized within-subject, single-blind study. Two doses of beta 1-selective agonist prenalterol (1 mg/hr or 2 mg/hr) and of beta 2-selective agonist salbutamol (300 micrograms/hr or 600 micrograms/hr) were infused intravenously in four separate sessions, with intervals of at least 48 hr between sessions. At each session cuff blood pressure and heart rate (HR) were measured and some hemodynamic information on the inotropic state were derived by echocardiography. Both prenalterol and salbutamol induced increases in HR, but tachycardia was greater after salbutamol, whereas the positive inotropic response to beta-stimulation was greater after prenalterol. At comparable HR rises (prenalterol, from 66.0 +/- 5.5 to 72.2 +/- 4 bpm; salbutamol, from 64.6 +/- 6 to 70.0 +/- 7 bpm), inotropic response seemed to be greater after prenalterol than after salbutamol (systolic blood pressure [SBP]: 133.5 +/- 8 and 120.7 +/- 8 mm Hg; mean velocity of circumferential fiber shortening [Vcf]: 1.54 +/- 0.13 and 1.31 +/- 0.12 c/s; ejection fraction [EF]: 72.4% +/- 5% and 69.5% +/- 4%; stroke index: 47.4 +/- 4 and 41.7 +/- 3 ml/m2). In presence of a chronotropic effect (HR from 64.6 +/- 6 to 70.0 +/- 7 bpm), the low salbutamol dose did not induce any changes in the indices of inotropism (SBP: from 119.2 +/- 6 to 120.7 +/- 8 mm Hg; mean Vcf: from 1.28 +/- 0.11 to 1.31 +/- 0.12 c/s; EF: from 68.1% +/- 5% to 69.5% +/- 4%; stroke index: from 40.2 +/- 3 to 41.7 +/- 3 ml/m2.(ABSTRACT TRUNCATED AT 250 WORDS)
We compared the ventilatory effects of prenalterol (beta 1-selective adrenoceptor agonist) with those of salbutamol (beta 2-selective adrenoceptor agonist) in 6 healthy volunteers. Two intravenous doses of prenalterol (1 mg/60 min, 2 mg/60 min) and of salbutamol (300 micrograms/60 min, 600 micrograms/60 min) were given in random order in 4 separate sessions of 60 minutes each. Pulmonary ventilation per minute (V'E) increased only on the high dose of salbutamol. Mouth occlusion pressure (P0.1) did not vary either on prenalterol or on salbutamol. Only the high dose of salbutamol induced (1) an increase in tidal volume (VT) without changes in respiratory rate (RR), (2) an increase in mean inspiratory flow (VT/Ti) without changes in the fraction of inspiratory time to total cycle duration (Ti/Ttot). During forced expiration, salbutamol elicited a small bronchodilating effect at the level of both large (FEV1, FEF25-75, FEF50) and small (FEV3, FEF75-85, FEF75) airways. Prenalterol induced a very small dilatation of the large airways, and a somewhat more pronounced effect at the level of the small airways. Neither the indexes of ventilatory pattern nor those of bronchial tone showed any statistical or biological differences between values on prenalterol and values on salbutamol. However, both the former and the latter indexes showed a trend to be higher on salbutamol than on prenalterol. Results suggest that salbutamol-induced increase in pulmonary ventilation per minute in subjects without bronchial obstruction is likely the result of a reduced bronchomotor tone at rest, leading to an increase in tidal volume because of the rise in the VT/Ti ratio.(ABSTRACT TRUNCATED AT 250 WORDS)
The long-term effects of metoprolol monotherapy, 100 mg b.i.d., for 16-18 months, were investigated in 8 previously untreated essentially hypertensive patients (resting blood pressure greater than 155/95 mmHg) and echocardiographic evidence of left ventricular hypertrophy (LVH) (left ventricular mass by Penn Cube formula greater than 215 g). Echocardiographic studies, according to the American Society of Echocardiography recording techniques and measurements criteria, were performed before starting treatment and at the end of follow-up. Metoprolol induced a decrease in systolic and diastolic blood pressure and heart rate, accompanied by a reduction of interventricular septum and posterior wall thickness (from 1.21 cm to 1.10 cm, and from 1.15 cm to 1.06 cm, respectively), left ventricular mass index and mean wall stress. All these changes were significant (p less than 0.01). Cardiac index decreased from 3017 ml/m2 to 2632 ml/m2 (p less than 0.01), mostly because of the reduction in the heart rate. In fact, stroke index, ejection fraction and fractional shortening all slightly increased during treatment in respect to pre-treatment values. Plasma renin activity fell from 1.45 ng/ml/h to 0.81 ng/ml/h (p less than 0.01), whereas both plasma noradrenaline and adrenaline concentration at rest did not change. Results indicate that in essentially hypertensive patients who have already developed LVH as a consequence of the hypertension, a long-term metoprolol therapy can successfully induce a reversal of LVH together with an effective blood pressure control, without noticeable adverse effects of changes in cardiac performance.
Systolic, diastolic and mean arterial pressure (SAP, DAP, MAP), heart rate (HR) and tension time index (TTI) were evaluated in 20 uncomplicated hypertensives and in 20 normotensives at rest and during isometric exercise, performed by handgrip (HG). In the hypertensive population the same parameters were evaluated also after two and six weeks of treatment with a beta-blocking agent, nadolol, given in a single daily dose. In all cases isometric exercise induced a significant increase of SAP, DAP, MAP, HR and TTI and this increase was more relevant in hypertensives than in controls. In the hypertensive population, nadolol was effective in lowering arterial pressure at rest, and significantly reduced the levels of SAP, DAP, MAP, HR and TTI reached at the end of the HG test. Moreover, the increments of the investigated parameters induced by isometric exercise were significantly reduced after nadolol. The results suggest that nadolol, unlike other beta-blocking agents, exerts a "protective" action against the hazardous increments of blood pressure which may occur in the daily life of hypertensive subjects during involuntary isometric exercises, and which could trigger dangerous cardiovascular complications.
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The aim of this study was to examine the interrelationships between age, plasma catecholamines, plasma renin activity (PRA) and blood pressure in essential hypertensive (EH) patients. PRA, plasma noradrenaline (NA) and adrenaline (A) were measured in 76 consecutive EH patients (WHO stages 1-2, aged 24-66 years) and in 28 normotensive subjects (aged 25-64 years) studied at rest in supine position after 5 days of normal fixed sodium and potassium intake. Both plasma NA and A were slightly but significantly higher in EH patients (p less than 0.05). While no relationship was found between the various parameters in normotensive subjects, in EH patients, particularly those at WHO stage 2, plasma NA was directly related to mean blood pressure (MBP) (p less than 0.001) and PRA (p less than 0.01). Plasma A was weakly related to MBP (p less than 0.05); PRA was inversely related to age (p less than 0.01) but no relationship was found between NA or A and age. Partial correlation analysis confirmed all these relationships. In fact, NA was related to MBP also considering constant PRA (p less than 0.001) or age (p less than 0.001), and NA was related to PRA also considering constant MBP (p less than 0.01) or age (p less than 0.001). Acute pharmacological alpha- and beta-blockade, with labetalol 100 mg i.v., induced a reduction of MBP which was directly related to basal plasma NA (p less than 0.001). These results support the view that in EH the sympathetic nervous system might be in part responsible for PRA levels and for the severity of hypertension.