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Biomedical subjects

M L Muiesan

Publications and source records attributed to M L Muiesan.

At least 55 records · Page 3Linked to original sources
PubMed1996

Angiotensin II type 1 receptor A/C1166 polymorphism. Relationships with blood pressure and cardiovascular structure.

The angiotensin II type 1 (AT1) receptor has a key role in mediating the vasoconstrictor and growth-promoting effects of angiotensin II. It has been reported that a polymorphism of the AT1 receptor gene (an A/C transversion at position 1166) may be associated with cardiovascular phenotypes, such as arterial blood pressure and aortic stiffness, that underlie a condition of increased cardiovascular risk. We examined a sample of 212 subjects randomly selected from a general population in northern Italy to investigate the role of AT1 receptor gene polymorphism, in the regulation of blood pressure and cardiovascular growth. We measured blood pressure (both clinic and 24-hour ambulatory recording), left ventricular mass (echocardiography), and carotid artery wall thickness (B-mode ultrasound); we assessed the AT1 receptor genotype by polymerase chain reaction and allele-specific oligonucleotide hybridization. Blood pressure values were lower in CC homozygotes than in heterozygotes and AA homozygotes; the difference was statistically significant for clinic measurements (mean difference for mean blood pressure, -6.6 mm Hg, P = .01; 95% confidence interval, -1.6 to -11.7 mm Hg) but not for ambulatory blood pressure measurements. CC homozygotes also presented a lower incidence of a positive family history of hypertension (P = .027). No statistically significant differences among AT1 receptor A/C1166 genotypes were observed for left ventricular mass or carotid artery wall thickness. We conclude that the present study does not support a major role of the AT1 receptor gene A/C1166 polymorphism as a marker of conditions associated with increased cardiovascular risk.

Blood Pressure↗
PubMed1996

Cardiovascular characteristics in normotensive subjects with or without family history of hypertension.

The aim of our study was to evaluate whether initial changes of cardiovascular structure and/or function can be detected in young normotensive subjects with (F+) and without (F-) family history of hypertension. Thirty-two subjects (19 F+, 10 males and 9 females, age range 17-32 years; 13 F-, 6 males and 7 females, age range 19-33 years) were studied. In each subject 24 hours ambulatory blood pressure monitoring, a M-mode, 2d guided and pulsed doppler echocardiogram and postischemic forearm strain gauge plethysmography were performed. The two groups of subjects did not differ for causal systolic and diastolic BP and 24 hours systolic and diastolic ambulatory monitored blood pressure. No differences in LV end-diastolic and end-systolic diameters, as well as in LV wall thickness, and in LV mass index were observed. Systolic functional parameters were also similar in the two groups. In F+ subjects peak early filling velocity was reduced in respect to F- (p < 0.01), peak late filling velocity integral was increased (p < 0.05) and the ratio of peak E/peak A integrals was decreased (p < 0.05). No difference was observed for postischemic forearm blood flow and minimal vascular resistance, taken as an index of arteriolar structural changes as well as intima-media thickness of carotid arteries. In conclusion in this study F+ and F- had similar BP values, LV mass and min VR; differences previously observed in LV mass between F+ and F- may have been due to the presence of different basal levels of BP; in F+ LV diastolic filling, although still in the normal range, shifted early toward the pattern of LV filling usually observed in hypertensive patients.

Adult↗
PubMed1996

Influence of ACE inhibition on left ventricular hypertrophy.

Further studies are needed to assess the true clinical impact, in terms of reduced morbidity and mortality, of reversed LVH in hypertensive patients. However, the initial results strongly indicate that either a lack of decrease or an increase in left ventricular mass after antihypertensive treatment is associated with a higher risk of cardiovascular events, the latter being significantly reduced and almost normalised by a complete reversal of LVH.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Persistence of left ventricular hypertrophy is a stronger indicator of cardiovascular events than baseline left ventricular mass or systolic performance: 10 years of follow-up.

OBJECTIVE: Left ventricular hypertrophy (LVH) and depressed left ventricular performance have been shown to be associated to an adverse prognosis in hypertensive patients. It has not been established, however, whether, during chronic antihypertensive treatment, the increased cardiovascular risk is more strictly related to the presence of LVH or of a low left ventricular performance. DESIGN AND METHODS: A total of 215 patients with uncomplicated hypertension (129 males, 86 females; age range 18-70 years, mean +/- SD 45 +/- 11) underwent an echocardiographic evaluation of left ventricular anatomy and function. In 151 patients (87 males, 64 females; age range 18-70 years, mean 45 +/- 10.4) the echocardiogram was repeated on average 10 +/- 1 years after the initial study. The presence of LVH (left ventricular mass index > 134 g/m2 in males and 110 g/m2 in females) and the midwall left ventricular shortening/end-systolic stress relationship were prospectively analysed as predictors of cardiovascular non-fatal events (n = 23) in patients who were seen at follow-up. RESULTS: The incidence of non-fatal cardiovascular events was greater in patients with LVH (n = 17, P < 0.0001) and in those with a lower midwall performance (n = 14, P < 0.01) at baseline. At follow-up, the incidence of non-fatal cardiovascular events was significantly greater in patients without a reduction in the left ventricular mass index, after adjusting for traditional risk factors (relative risk 3.52 versus 1.38 in patients with persistence and regression of LVH, respectively; P < 0.01). The baseline midwall fractional shortening was lower in patients with both persistence or regression of LVH (analysis of variance, P < 0.0001) than in patients with a normal left ventricular mass index. In logistic analysis, the left ventricular mass index at follow-up and age were independent determinants of non-fatal cardiovascular events (P < 0.001); without the left ventricular mass index at follow-up, this analysis showed that age, systolic blood pressure at follow-up and baseline midwall fractional shortening were independent determinants of non-fatal cardiovascular events. CONCLUSIONS: Our results suggest that lack of regression of LVH is a stronger indicator of cardiovascular risk than a depressed baseline midwall left ventricular performance.

Adolescent↗
PubMed1995

Angiotensin-converting enzyme I/D polymorphism and arterial wall thickness in a general population. The Vobarno Study.

BACKGROUND: It has been reported that the D allele of an insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme (ACE) gene is associated with conditions of increased cardiovascular risk, including left ventricular hypertrophy. METHODS AND RESULTS: Considering that a genetically determined overactivity of the renin-angiotensin system may influence cardiac as well as vascular growth, we investigated possible relations between ACE I/D genotype and carotid artery wall thickness (B-mode ultrasound) in 199 subjects, 50 to 64 years old, sampled from the general population of Vobarno, a small town in northern Italy. ACE DD genotype was associated with significantly higher common carotid artery intima-media thickness (P = .003). The occurrence of carotid atherosclerotic plaques was similar in the different genotypes. There was no association of the ACE I/D genotype with blood pressure values (either casual of 24-hour ambulatory monitored). CONCLUSIONS: ACE DD genotype may be considered a risk factor for the development of common carotid intima-media thickening in our study population.

Alleles↗
PubMed1995

Arterial spontaneous rhythmic contractile activity in humans and rats: spectral analysis and regulatory mechanisms.

OBJECTIVE: Many experimental observations have demonstrated the presence of spontaneous cyclic vasomotor activity (CVA) in large and small arteries. This study aimed to evaluate the characteristics of spontaneous CVA in rat and human resistance arteries, and to investigate its possible interference with the evaluation of sympathetic activity by means of spectral analysis of blood pressure in vivo. DESIGN AND RESULTS: In study 1 we examined small mesenteric arteries of spontaneously hypertensive rats and Wistar-Kyoto rats, as well as small omental arteries of normotensive subjects and hypertensive patients (Mulvany and Halpern technique). CVA was enhanced by the agonists of nitric oxide release, and was abolished by the inhibitors of nitric oxide or cyclic GMP synthesis. A potassium channel, which is barium- and zinc-sensitive and tetraethylammonium-insensitive, seems to play a crucial role in the genesis of CVA. In rats and in humans the frequency of CVA fell exactly in the frequency band ('low frequencies') of power spectral analysis of blood pressure usually considered to be an 'index of sympathetic activity'. In study 2, a power spectral analysis of blood pressure variability before and after intra-arterial infusion of noradrenaline or acetylcholine was performed in 18 patients with mild-to-moderate hypertension. The absolute and normalized spectral power of the low-frequency systolic blood pressure peak increased remarkably after noradrenaline and acetylcholine infusion, while its central frequency shifted from 0.10 Hz to approximately 0.06 Hz, exactly the frequency of CVA observed in vitro. CONCLUSIONS: A potassium channel appears to be involved in the genesis of CVA. Also, CVA might contribute to the blood pressure variability independently of the autonomic nervous system activity, and thus probably plays a role in the genesis of the low-frequency peak in the rat and in humans.

Acetylcholine↗
PubMed1995

Association of change in left ventricular mass with prognosis during long-term antihypertensive treatment.

OBJECTIVE: The aim of the present study was to assess the prognostic value of changes in left ventricular hypertrophy in hypertensive patients with time. DESIGN: Two hundred and fifteen uncomplicated hypertensive patients underwent a high-quality baseline echocardiogram for left ventricular anatomy evaluation and in 151 of those patients the echocardiographic examination was repeated 10 +/- 1.4 years after the initial study. METHODS: Left ventricular mass index changes were evaluated, in relation to the incidence of non-fatal cardiovascular events, adjusted for traditional cardiovascular risk factors. RESULTS: According to the presence or absence of left ventricular hypertrophy (left ventricular mass index > 134 g/m2 in men and > 110 g/m2 in women) at baseline and at the end of follow-up study, patients were divided into four groups: with normal left ventricular mass at both examinations (n = 78), with regression of left ventricular hypertrophy (n = 32), with persistence of left ventricular hypertrophy (n = 34) and with hypertrophy development (n = 7). After adjustment for traditional cardiovascular risk factors, the cumulative incidence of non-fatal cardiovascular events was significantly higher in the group of patients without regression of left ventricular hypertrophy. Cox survival analysis showed the presence of left ventricular hypertrophy at the end of follow-up study to be the most important factor related to cardiovascular events. CONCLUSIONS: The present findings strongly indicate that the lack of decrease or the increase of left ventricular mass after antihypertensive treatment can be associated with a higher risk for cardiovascular events, which is significantly reduced and almost normalized by complete regression of left ventricular hypertrophy.

Adolescent↗
PubMed1995

Relationship between sympathetic nervous system activity, baroreflex and cardiovascular effects after acute nitric oxide synthesis inhibition in humans.

OBJECTIVE: To examine the cardiovascular effects of acute systemic nitric oxide synthesis inhibition in humans in relation to the possible involvement of changes in sympathetic nervous system activity or in the baroreceptor reflex. DESIGN: Placebo or NG-monomethyl-L-arginine (250 mg by intravenous infusion for 5 min) was administered to seven healthy male volunteers according to a random, double-blind sequence. METHODS: Blood pressure and heart rate were measured non-invasively using a Finapres device from 20 min before to 80 min after starting infusion; beat-to-beat variability of blood pressure, pulse interval and systolic blood pressure and pulse interval covariation were assessed by means of spectral and sequence analysis methods. Under basal conditions and 15 min and 60 min after infusion, we measured stroke volume and indices of cardiac systolic and diastolic function by echocardiography, forearm blood flow by strain-gauge venous occlusion plethysmography, and plasma catecholamine levels. RESULTS: Compared with placebo, administration of NG-monomethyl-L-arginine caused a transient increase in blood pressure and reduction in heart rate. Stroke volume and indices of cardiac function did not change significantly, whereas cardiac index and forearm blood flow were significantly reduced after 15 min. Spectral analysis of blood pressure and pulse interval showed a significant reduction of power spectral density in the low frequencies (0.03-0.15 Hz) that persisted 60 min after infusion. The plasma noradrenaline level was significantly reduced after 15 min. No change in baroreflex engagement or sensitivity was detected by the cross-spectral or the sequence method. CONCLUSIONS: Acute systemic nitric oxide synthesis inhibition transiently increases blood pressure and reduces heart rate and cardiac index. The acute hypertensive response to NG-monomethyl-L-arginine is dependent neither on sympathetic nervous system activity, which is probably reduced as a consequence of baroreceptor reflex activation, nor on baroreceptor reflex sensitivity, which is not impaired.

Adult↗
PubMed1995

ACE inhibitor ramipril is more effective than the beta-blocker atenolol in reducing left ventricular mass in hypertension. Results of the RACE (ramipril cardioprotective evaluation) study on behalf of the RACE study group.

OBJECTIVES: To compare the effect of the angiotensin converting enzyme (ACE) inhibitor ramipril with that of the beta-blocker atenolol on reversal of left ventricular hypertrophy, on blood pressure and on other echocardiographic parameters. DESIGN: The study was conducted in accord with the PROBE (prospective randomized open blinded endpoint) design. Randomized treatment either with ramipril or with atenolol was continued for 6 months, and echocardiograms were recorded before and after 3 and 6 months of treatment. The echo tracings were blindly evaluated in a single reading centre. METHODS: M-mode, two-dimensional guided echocardiography was used to measure left ventricular wall thicknesses and dimensions, from which left ventricular mass was calculated, according to the Penn convention. RESULTS: Of 193 patients at 16 centres, 111 had echocardiograms that could be quantitatively evaluated. The primary analysis of the study was performed using data from those patients. In addition, echocardiograms of 88 patients were analysed on an 'according to protocol' basis (patients with preset values of left ventricular mass). Systolic and diastolic blood pressures were significantly reduced both by ramipril and by atenolol without any significant difference between the two drug treatments. The heart rate was significantly reduced by atenolol only. Both the 'primary' and the 'according to protocol' analyses showed that the left ventricular mass was significantly reduced by ramipril only. Comparison between treatments according to a multivariate analysis demonstrated a significantly greater reduction in left ventricular mass during ramipril than during atenolol treatment. CONCLUSIONS: The present study is the first of suitably large size in which a direct comparison of the effects of an ACE inhibitor and a beta-blocker on echocardiographic left ventricular mass has been performed. It has demonstrated that ramipril is more effective than atenolol in reversing left ventricular hypertrophy in essential hypertensive patients.

Adrenergic beta-Antagonists↗
PubMed1995

Effects of low and high doses of fosinopril on the structure and function of resistance arteries.

It has been suggested that angiotensin-converting enzyme inhibitors may induce a significant regression of cardiovascular hypertrophy not only through blood pressure reduction but also as a possible consequence of growth factor inhibition. The aim of this study was to evaluate the effects of the angiotensin-converting enzyme inhibitor fosinopril, given either at a hypotensive high dose or a nonhypotensive low dose, on structural and functional alterations of mesenteric resistance arteries and on cardiac mass in spontaneously hypertensive rats (SHR) and control Wistar-Kyoto rats. Fosinopril was administered in the drinking water from 6 to 12 weeks of age. Rats were killed at 12 weeks, and the ratio of heart weight to body weight was measured. Mesenteric arterioles were dissected and mounted on a micromyograph (Mulvany's technique). Vascular morphology (media-lumen ratio, media thickness) and endothelial function (response to acetylcholine) were then assessed. During the 6 weeks of treatment, systolic pressure in SHR treated with high-dose fosinopril was significantly lower compared with that in untreated SHR, whereas no difference was observed with low-dose fosinopril. In SHR treated with both high-dose and low-dose fosinopril, a statistically significant reduction of vascular structural alterations, in terms of both media-lumen ratio and media thickness, was observed. The ratio of heart weight to body weight was reduced only in SHR treated with high-dose fosinopril. An improvement in the endothelium-dependent relaxation to acetylcholine was observed in SHR treated with high-dose fosinopril compared with untreated SHR, whereas in SHR treated with low-dose fosinopril no improvement in endothelial function was detected.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1995

Media: lumen ratio in human small resistance arteries is related to forearm minimal vascular resistance.

BACKGROUND: For the evaluation in humans of structural alterations in resistance arteries, most studies have used an indirect index, the measurement of minimal vascular resistance (mean blood pressure divided by maximal postischaemic blood flow) in suitable vascular beds. A sensitive and specific micromyographic technique was recently made available for the study of human small resistance arteries. Whether a correlation really exists between results obtained with the two techniques has not yet been investigated. OBJECTIVE: To evaluate both forearm minimal vascular resistance and media:lumen ratio of omental or subcutaneous small arteries in normotensive subjects and hypertensive patients. DESIGN AND METHODS: Thirty-four individuals were included in the study (age range 35-74 years; 24 hypertensive, 10 normotensive). Twenty-five had elective abdominal surgery and nine hypertensive patients had a gluteal biopsy. Omental and subcutaneous small arteries were dissected and mounted on a wire micromyograph (Mulvany's technique), and media:lumen ratio and media thickness were measured. The dose-response curve to noradrenaline was constructed at cumulative concentrations from 3 x 10(-9) to 3 x 10(-5) mol/l. Venous occlusion plethysmography was used to measure blood flow in the forearm, and minimal vascular resistance was calculated from mean blood pressure and postischaemic maximal blood flow (13 min ischaemia plus exercise). RESULTS: A statistically significant correlation was found between media:lumen ratio and minimal vascular resistance (r = 0.74, P < 0.001) as well as between media:lumen ratio and systolic (r = 0.44, P < 0.01) and diastolic (r = 0.38, P < 0.05) blood pressures. Similar correlations were observed between media thickness and systolic and diastolic blood pressures. Small arteries from hypertensive patients had a significantly increased reactivity to noradrenaline (by analysis of variance) compared with those from normotensive subjects, in terms of wall tension but not of active media stress. CONCLUSIONS: The present study demonstrated that the media:lumen ratio of small resistance vessels is significantly related to forearm minimal vascular resistance, suggesting that direct and indirect evaluations of vascular morphology will give similar results.

Adult↗
PubMed1995

[The organ damage in arterial hypertension].

The development of hypertension is associated with the presence of cardiovascular structural alterations. The principal target organs of hypertensive disease are the heart, brain, kidney and eye. Although left ventricular hypertrophy is an initially useful and well tolerated adaptive mechanism because it tends to reduce wall stress, it may subsequently lead to impaired cardiac function and even heart failure. Vascular structural alterations include reduced compliance, the appearance of atheromatous lesions in the large arteries, and hypertrophy or remodelling of small artery walls, and may be involved in the onset of retinal, renal and brain lesions. Technological progress now enables us to evaluate cardiovascular structural alterations early on as well as to monitor their natural history and the modifications induced by antihypertensive therapy. There is no question as to capacity of antihypertensive therapy to reduce the incidence of stroke, heart failure, renal failure and severe hypertensive retinopathy. Although a number of drugs are able to lower blood pressure, ACE-inhibitors and calcium entry blockers more effectively bring about the regression of left ventricular hypertrophy and, probably, also the retrocession of structural alterations in small resistance arteries; they seem to have a beneficial effect on structural alterations in large arteries as well. Although the regression of left ventricular hypertrophy could be associated with an improved prognosis, no data are available yet on the prognostic significance of the presence and regression of vascular structural alterations.

Cardiovascular System↗
PubMed1995

Effects of antihypertensive therapy with angiotensin converting enzyme inhibitors or calcium antagonists on spontaneous cyclic vasomotor activity in small resistance arteries of spontaneously hypertensive rats.

OBJECTIVE: Spontaneous cyclic vasomotor activity can occur in small resistance arteries in vitro after precontraction with a vasoconstrictor. Calcium and potassium channels and nitric oxide synthesis or release seem to be involved in the genesis of this vasomotor activity. We therefore investigated the effects of chronic antihypertensive therapy with calcium antagonists and angiotensin converting enzyme (ACE) inhibitors on the amplitude and frequency of cyclic vasomotor activity in vitro in spontaneously hypertensive rats (SHR). MATERIALS AND METHODS: SHR were treated with fosinopril at 25 mg/kg per day or lacidipine at 10 mg/kg per day or nitrendipine at 30 mg/kg per day, from the age of 4 to 12 weeks. Data were compared with those obtained in untreated SHR and Wistar-Kyoto (WKY) rats. Half the rats were killed at 13 weeks of age, and the remaining half were killed at 38 weeks of age. The mesenteric small resistance arteries were dissected, mounted on a micromyograph and then contracted submaximally with noradrenaline. Acetylcholine was then added to the organ bath. RESULTS: More than 50% of the vessels showed cyclic vasomotor activity. The frequency and amplitude of this activity were greater in SHR than WKY rats after noradrenaline and after acetylcholine. At 13 weeks of age (but not at 38 weeks of age), treatment with a calcium antagonist (either lacidipine or nitrendipine) significantly reduced the frequency and amplitude of the vasomotor activity, probably by interfering with calcium entry. No change was observed after fosinopril. CONCLUSIONS: Antihypertensive treatment with different drugs may affect cyclic vasomotor activity differently, probably by interfering with cellular mechanisms involved in its genesis. The effects of calcium antagonists on cyclic vasomotor activity are still present after short-term but not after long-term treatment withdrawal.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

Vascular structural and functional alterations before and after the development of hypertension in SHR.

The time-course of the development of vascular and cardiac hypertrophy, as well as of arterial dysfunction, in human and experimental hypertension is still unclear. Moreover, the interrelationships between structural and functional vascular alterations are presently under debate. The aim of this study was to assess the arteriolar wall thickness and left ventricular mass as well as the vascular response to norepinephrine and acetylcholine in spontaneously hypertensive rats (SHR), before and after the development of hypertension, as compared to age-matched normotensive Wistar-Kyoto rats (WKY). Seventeen SHR (4 to 12 weeks old) and 17 WKY were included in the study. Blood pressure was measured noninvasively. After killing the animals, relative left ventricular mass (RLVM) was calculated, and mesenteric arcades were dissected and mounted on a micromyograph. Functional and structural characteristics of the vessels were measured: media thickness (MT), media/lumen ratio (M/L), and wall tension in response to norepinephrine and acetylcholine. At 4 weeks of age, no difference in blood pressure and RLVM between SHR and WKY was detected, but MT and M/L of mesenteric small resistance arteries were significantly greater in SHR. An increased response to norepinephrine was observed in terms of wall tension, but not of active media stress at the two higher norepinephrine concentrations. No difference in the dose-response curve to acetylcholine between SHR and WKY was observed. At 8 and 12 weeks of age systolic blood pressure was significantly higher in SHR; RLVM, MT, and M/L were also higher at this stage.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1994

Delayed development of hypertension after short-term nitrendipine treatment.

In this study we evaluated the delayed effects of a calcium entry blocker on blood pressure and on vascular structural and functional alterations in mesenteric resistance arteries of spontaneously hypertensive rats (SHR). The calcium entry blocker nitrendipine was administered (30 mg/kg per day) according to three different schedules: in one group of SHR from 4 to 8 weeks of age (n = 12), in a second group from 8 to 12 weeks of age (n = 12), and in a third group from 4 to 12 weeks of age (n = 12). Twelve untreated SHR and 12 untreated Wistar-Kyoto rats served as controls. Half the animals of each group were killed at 13 weeks, and the remaining were killed at 38 weeks. After death, relative left ventricular mass was calculated. Vascular morphology and function (responses to norepinephrine and acetylcholine) in mesenteric small arteries were then assessed using a micromyographic technique. Nitrendipine treatment delayed the development of hypertension and determined the regression of structural alterations of mesenteric resistance arteries in SHR. These favorable effects were maintained for several weeks after treatment withdrawal, provided that treatment was started at 4 weeks of age. Considering the functional alterations of mesenteric arteries in SHR (responses to norepinephrine and acetylcholine), nitrendipine treatment determined an improvement of both these dysfunctions as long as reductions of the media-to-lumen ratio and blood pressure, respectively, were maintained.

Animals↗
PubMed1994

Cardiovascular structural changes and calcium antagonist therapy in patients with hypertension.

Regression of cardiovascular structural changes is a main goal of antihypertensive treatment. Two recent meta-analyses of relatively small noncomparative studies have suggested that angiotensin-converting enzyme (ACE) inhibitors may be more effective than other classes of drugs in inducing regression of left ventricular hypertrophy (LVH). The effect of different antihypertensive drugs on arteriolar structural changes has not yet been properly investigated. The aim of this study was to evaluate the effect of 6 months of treatment with amlodipine (5-10 mg o.d.) or enalapril (10-20 mg o.d.) on blood pressure (BP) (ambulatory monitoring), heart rate (HR), LV mass and function (M-mode echo, two-dimensionally guided), forearm minimal vascular resistance (min VR = BP/max blood flow-venous occlusion plethysmography, taken as an index of vascular structural changes) in 24 hypertensive patients in a comparative single-blind, randomized study, with blind reading of echocardiograms and plethysmographic tracings. After 6 months of treatment with amlodipine 5-10 mg o.d., significant reductions in LV mass index (p = 0.004) and forearm min VR (p = 0.02) were observed. Before and during treatment, LV systolic function, both at rest and during stress (handgrip test), evaluated by fractional shortening as related to end-systolic stress, was in every case within 95% confidence limits calculated in normal subjects. Similar results were observed with enalapril. No significant differences were observed for Doppler indices of diastolic filling after 6 months of treatment with either drug. These results indicate that a significant regression of structural changes in the heart and in the small resistance vessels can be observed after long-term treatment with amlodipine in essential hypertensive patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗