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Background —It is still unclear whether substantial regression of hypertensive left ventricular hypertrophy (LVH) and normalization of chamber geometry are associated with improved left ventricular (LV) myocardial function. Methods and Results —Midwall mechanics were evaluated in 152 patients undergoing 1 year of effective antihypertensive treatment. Two-dimensionally directed M-mode echocardiography was performed as follows: (1) after a 4-week placebo “run-in” period, (2) after 1 year of treatment with 20 mg/d lisinopril (alone or associated with 12.5 to 25 mg/d hydrochlorothiazide), and (3) after a final 1-month placebo period to allow blood pressure (24-hour average ambulatory monitoring) to return to pretreatment levels. Treatment-induced reductions in blood pressure (from 149±16/95±11 to 131±12/83±10 mm Hg, P 2 , P 2 , P P P Conclusions —Regression of concentric LVH is associated with an improvement of midwall systolic function, which is more dependent on the normalization of LV geometry than on the reduction in LV systolic stress.

Objectives. First, to evaluate the prevalence of left ventricular (LV) hypertrophy, LV concentric remodelling and microalbuminuria in a selected sample of treated hypertensive patients with effective and prolonged clinic blood pressure (BP) control (BP < 140/90 mmHg). Second, to compare the prevalence of these markers of organ damage in patients with and without ambulatory BP (ABP) control, defined as average daytime BP < 132/85 mmHg). Design and methods. Fifty-eight consecutive hypertensive patients who attended our hypertension outpatient clinic over a period of 3 months and were regularly followed up by the same medical team were included in the study. Obesity, diabetes mellitus, history or signs of cardiovascular or renal complications and major noncardiovascular diseases were the exclusion criteria from the study. Each patient underwent 24 h ABP monitoring, echocardiography and 24 h urine collection for albumin measurement. Results. The prevalence of LV hypertrophy (LV mass index > 125 g/m2 in both sexes), LV concentric remodelling (relative wall thickness > 0.45) and microalbuminuria (urinary albumin excretion < 300 mg/24 h) in this selected group of patients (32 men, 26 women; mean age 53 ± 9 years; mean clinic BP 122 ± 9/78 ± 6 mmHg) was markedly low (6.9, 8.6 and 5.1%, respectively). The 26 patients with effective ABP control (group I) were similar to the 32 patients without effective ABP control (group II) in age, gender, body surface area, clinic BP, smoking habit, glucose, cholesterol and creatinine plasma levels. Prevalence of LV hypertrophy, LV concentric remodelling and microalbuminuria was lower in group I than in group II (0 versus 12.9% P < 0.01, 7.7 versus 9.4% NS, 3.8 versus 6.2% NS, respectively). Conclusions. This study demonstrates that nonobese, nondiabetic hypertensive patients with an effective clinic BP control have a very low prevalence of target organ damage and that LVH is present only in individuals with insufficient ABP control

Abstract —This study assessed whether 2 common surrogate measures of the “white-coat effect,” namely the clinic-daytime and the clinic-home differences in blood pressure (BP), were attenuated by long-term antihypertensive treatment and whether this attenuation is relevant to the treatment-induced regression of left ventricular hypertrophy, thus having clinical significance. We considered data from 206 patients with essential hypertension (aged 20 to 65 years) who had a diastolic BP between 95 and 115 mm Hg and echocardiographic evidence of left ventricular hypertrophy. In each patient, clinic BP, 24-hour ambulatory BP, and left ventricular mass index were assessed at baseline, after 3 and 12 months of treatment with an angiotensin-converting enzyme inhibitor, and after a final 4-week placebo run-off period. At baseline, the clinic-daytime differences in systolic and diastolic BP were 12.1±15.4 and 6.8±10.1 mm Hg, respectively; the corresponding values for the clinic-home differences were 5.7±10.6 and 2.9±6.1 mm Hg, respectively. These differences were reduced by 57.6% and 77.1% ( P P

Aim: The aim of the present study was to evaluate (1) the prevalence and patterns of left ventricular hypertrophy (LVH) and (2) the impact of blood pressure (BP) control, assessed by clinical and 24-hour ambulatory BP monitoring (ABPM) criteria on the persistence of LVH in a representative sample of treated patients attending our Hypertension Clinic. Methods: One hundred consecutive essential hypertensives (61 m/39 f, age 56± 9 years) regularly followed up by the same medical team (average period 52 months, 12–156 months) were included in the study and underwent 24-hour ABPM and complete echocardiographic examination. Results: Twenty-eight of the 100 patients were found to have LVH [left ventricular mass index (LVMI) >125 g/m2 in men and >110 g/m2 in women]; LVH was eccentric in 20 patients and concentric in the remaining 8. LVMI did not correlate with clinical BP values but only with ABPM values (mean 24 h systolic r = 0.34, p Conclusions: The results of this study suggest that the eccentric type of LVH is the prevalent pattern in chronically treated patients. The persistence of LVH is significantly dependent on BP levels achieved during treatment; indeed the prevalence of LVH is very low in patients with an optimal BP control, whereas it is elevated (37%) in uncontrolled patients.

Objectives. First, to evaluate the prevalence of clinic blood pressure (BP) control (BP ≤ 140/90 mmHg) in a representative sample of treated hypertensive patients followed in our hypertension clinic. Second, to assess in a subgroup of these patients: (a) the proportion of BP control with both clinic blood pressure (CBP ≤ 140/90 mmHg) and daytime ambulatory blood pressure (ABP) (≤ 132/85 mmHg) criteria, and (b) the prevalence of echocardiographic left ventricular hypertrophy (LVH) (left ventricular mass index, LVMI > 125 g/m2 in men and > 110 g/m2 in women). Design and methods. Seven hundred consecutive hypertensive patients who attended our hypertension centre clinic during a period of 6 months and who had regularly been followed up by the same medical team were included in the study. BP was taken in the clinic by a doctor using a mercury sphygmomanometer with the participants seated. Seventy-four patients with similar demographic and clinical characteristics to the entire population of participants underwent complete echocardiographic examination and 24 h ABP monitoring. Results. During follow-up, 352 of the treated patients had clinic BP ≤ 140/90 mmHg, 198 ≤ 160/95 mmHg and 150 > 160/95 mmHg, indicating that BP control was satisfactory in 50.3%, borderline in 28.3% and unsatisfactory in 21.4% of the cases. In the subgroup of 74 patients, the proportion of individuals with satisfactory clinic BP control (CBP ≤ 140/90 mmHg) was higher (50.0 versus 33.6%) than with satisfactory ABP control (daytime ABP values ≤ 132/85 mmHg). LVH was found in 21 of the 74 patients (28.3%): 12 of them had unsatisfactory CBP control and 19 had unsatisfactory ABP control. LVMI did not correlate with CBP values but only with ABP values (mean 24 h systolic r = 0.47, diastolic r = 0.40, P < 0.001; mean daytime systolic r = 0.45, mean daytime diastolic r = 0.39, P < 0.001; mean night-time systolic r = 0.38, mean night-time diastolic r = 0.38, P < 0.001). Conclusion. This study demonstrates that hypertensive patients managed in a hypertension centre clinic have satisfactory CBP control in 50% of cases, but this rate seems to over-estimate the effective BP control during daily life. A large fraction of patients show persistence of LVH and this evidence of organ damage almost entirely concerns individuals with poor ABP control.

Objective To investigate the association between increased left ventricular mass and the intima-media thickening of carotid arteries in hypertensive patients and the simultaneous involvement of the heart and the conductance vessels by the hypertensive process. Methods Because no data are available concerning the ultrasonographic characteristics of large arteries in athletes with physiological increases in left ventricular mass, we measured the intima-media thickness (IMT) of the common carotid artery (CCA) in 14 normotensive subjects (group I, aged 22 +/- 4 years), in 14 borderline hypertensives (group II, aged 24 +/- 6 years) and in 14 Japanese wrestling players (group III, aged 23 +/- 4 years). The IMT of the posterior wall of the CCA was measured at 5, 10 and 20mm caudally to the bifurcation and the measurements were averaged. Left ventricular diameters and thicknesses of the interventricular septum and posterior wall were obtained from two-dimensionally guided M-mode tracings and measured according to the Penn convention. Left ventricular mass was calculated by the formula of Devereux. Left ventricular filling was measured by a pulsed Doppler technique. Results Both systolic and diastolic blood pressure values were significantly higher in group II (145 +/- 7/91 +/- 5 mmHg) than they were in group I (116 +/- 11/75 +/- 5 mmHg) and in group III (120 +/- 8/78 +/- 6 mmHg). In athletes and hypertensives both the left ventricular mass index and the IMT of the CCA were significantly greater than they were in control subjects (80 +/- 12 g/m2 and 0.45 +/- 0.05 mm in group I; 106 +/- 15 g/m2 and 0.57 +/- 0.08 mm in group II; and 122 +/- 17 g/m2 and 0.55 +/- 0.05 mm in group III). The mitral early:late peak flow velocity ratio was significantly lower in group II (1.9 +/- 0.58) than it was in the other two groups (2.3 +/- 0.66 in group I and 2.6 +/- 0.64 in group III). Conclusions The results of our study suggest that both hypertension and physical training can induce parallel changes in cardiac and in arterial walls, and that physiological left ventricular hypertrophy in athletes is accompanied by a normal diastolic filling pattern in contrast to the pathological pattern found in hypertensives. Further investigation is required to explore possible differences in carotid structure and function between these two conditions.

The aim of this study was to measure intima-media thickness (IMT) of the common carotid artery (CCA) in patients with hypertrophic cardiomyopathy (HCM) and in hypertensive patients with left ventricular hypertrophy (LVH). We studied 73 subjects: 20 normotensive healthy subjects as control group (I); 20 patients with essential hypertension without LVH (II); 20 hypertensives with LVH (III), and 13 normotensive patients with HCM (IV). Each subject underwent a complete echocardiographic and vascular ultrasonographic study in order to assess left ventricular parameters and the IMT at the level of the CCA. Left ventricular mass index (LVMI) was significantly higher in groups III and IV than in groups I and II (156 +/- 18 and 157 +/- 31 vs. 94 +/- 14 and 98 +/- 10 g/m2, respectively, p < 0.01), while IMT was significantly greater in group III but not in the others [0.88 +/- 0.04 vs. 0.61 +/- 0.03 (I), 0.64 +/- 0.03 (II) and 0.61 +/- 0.04 (IV) mm, p < 0.01]. The correlation between LVMI and IMT was statistically significant within all the hypertensive patients (r = 0.48, p < 0.01) but not in the HCM group (r = 0.17, p = NS). The hypertensive patients with LVH showed structural alterations (related to hemodynamic and humoral factors) both at cardiac and vascular level while in patients with HCM the cardiac alterations (due to a genetic disorder) were not associated with changes at the level of the large arteries.

In professional athletes with marked cardiac hypertrophy, reflex influences originating from cardiopulmonary receptors are impaired. To determine whether the reflex is restored after termination of physical training and regression of cardiac hypertrophy 8 former athletes (age 31 +/- 6 years, mean +/- SD) who stopped agonistic activity for 5 +/- 1 years were compared with 15 sedentary subjects (27 +/- 7 years) and 19 active professional athletes (22 +/- 7 years). Cardiopulmonary receptor stimulation and deactivation were obtained by increasing and reducing left ventricular end-diastolic diameter (echocardiography) through leg raising and nonhypotensive lower body negative pressure, respectively. Left ventricular mass index (echocardiography) was markedly and significantly (p less than 0.01) greater in athletes (135 +/- 6 g/m2) than in former athletes (105 +/- 4 g/m2) whose value was similar to that of sedentary subjects (98 +/- 4 g/m2). The reduction in forearm vascular resistance and plasma norepinephrine induced by increasing left ventricular end-diastolic diameter was 24 and 23% less in athletes than in former athletes whose responses were similar to those of sedentary subjects. This was the case also for the responses induced by reducing left ventricular end-diastolic diameter. In contrast, the hemodynamic responses to cold pressor test were similar in the 3 groups. It is concluded that the impairment of the cardiopulmonary reflex observed in athletes is largely reversible when physical training is terminated. This may be due to regression of left ventricular hypertrophy.

Since the advent of the Doppler color flow echocardiography, the presence of a small degree of insufficiency of the cardiac valves has been detected with relative frequency in structurally and functionally normal hearts. Data about this so-called 'physiological' regurgitation are presently available only in normotensive subjects and athletes. We therefore studied the prevalence of this phenomenon in a group of patients with essential hypertension compared to a population of normotensive subjects. To this purpose, a Doppler color flow echocardiography study was performed in 130 essential hypertensive patients (72M/58F: age 44.2 ± 13.5 years; BP 154.3 ± 12.8/98.3 ± 7.1 mm Hg) without any evidence of left ventricular hypertrophy or cardiopathy and in 100 normal subjects (59M/41F; age 41.2 ± 14.8 years; BP 119.1 ± 8.1/79.2 ± 8.1 mm Hg). We conclude that in patients with essential hypertension the physiological regurgitant jets are present in one or more cardiac valves; moreover, the regurgitation of the mitral and aortic valve is found with more frequency than in the normotensive control group (36.1 vs. 27.0% and 17.7 vs. 11.0%, respectively). These data suggest that the increased afterload of the left ventricle may play an important role in the pathogenesis of even minor degree of insufficiency of the cardiac valves. As this finding does not appear to have a pathological relevance, the main clinical implication of this study is that it is not advisable to create a jatrogenic heart disease in the hypertensive patients routinely screened by the echo-Doppler technique. © 1992 S. Karger AG, Basel.

The aim of this study was to evaluate the diastolic function in athletes and in young borderline hypertensives with mild left ventricular hypertrophy. Left ventricular filling was assessed by echo Doppler measurement of transmitral flow velocity in 18 soccer players (age 22 +/- 4 years, left ventricular mass index, LVMI 136 +/- 12 g/m2), in 15 borderline hypertensives (age 21 +/- 3 years, LVMI 137 +/- 9 g/m2), and 20 normotensive subjects (age 22 +/- 4 years, LVMI 93 +/- 10 g/m2) as reference group. We found that left ventricular filling profile was similar in borderline hypertensives, in athletes and in normotensive subjects. These findings suggest that, at least in the early stage, mild cardiac hypertrophy secondary to borderline blood pressure elevation is characterized by indexes of diastolic function not different from those found in athletes with physiological hypertrophy.

Background: The cardiac effects of hypertension include a variety of structural changes such as increases in left ventricular mass (LVM) and left atrium (LA) size. Although data on hypertension-induced left ventricular changes are extensive, relatively little information is available on LA size from large-scale studies. Objective: We sought to assess the prevalence of LA enlargement in a large selected hypertensive population and to determine the relations of LA size to several biologic variables including left ventricular hypertrophy (LVH) and metabolic disturbances. Methods: A total of 2500 untreated and treated uncomplicated essential hypertensives consecutively attending, for the first time, our hospital out-patient hypertension clinic and included in the Evaluation of Target Organ Damage in Hypertension, an observational ongoing registry of hypertension-related target organ damage (TOD), were considered for this analysis. All patients underwent extensive clinical, laboratory and ultrasonographic investigations searching for cardiac (and extracardiac) TOD. The LA was considered enlarged when its anteroposterior diameter exceeded 3.7 cm in women and 4.1 cm in men. LVH was defined according to two different criteria: ≥ 125 g/m2 in men and ≥ 110 g/m2 in women; or ≥ 51 g/m2.7 in men and ≥47 g/m2.7 in women. Results: Enlarged LA diameter was present in 24.5% of women and in 21.5% of men. Compared with 1925 patients with normal LA size, the 575 patients with enlarged LA were older, more frequently overweight, had higher systolic blood pressure and included a greater proportion of subjects under antihypertensive treatment, with diabetes and metabolic syndrome. Both LA size and prevalence of LA enlargement differed significantly in relation to left ventricular geometry and LVM, being greater in patients with concentric or eccentric LVH than in those with left ventricular concentric remodeling or normal geometry. The prevalence of LA enlargement was similar in patients with concentric and eccentric LVH. According to a logistic regression analysis, overweight, LVH, fasting blood glucose > 7.0 mmol/l and metabolic syndrome were the main independent predictors of LA enlargement in the overall population as well as in both untreated and treated hypertensive subgroups. Conclusions: Our study suggests that: LA enlargement is a common echocardiographic finding in selected essential hypertensive patients with different left ventricular geometric patterns; LA size and LA enlargement is related to LVM rather than the type of LVH; and, in addition to LVH, overweight, high fasting glucose and metabolic syndrome are associated with LA dimensions. © 2005 Lippincott Williams & Wilkins.

Objective: Target organ damage (TOD) in chronically treated hypertensives is related to effective blood pressure (BP) control. The aim of this study was to evaluate the prevalence of cardiac and extracardiac TOD in patients with refractory hypertension (RH) compared with well-controlled treated hypertensives (C). Methods: Fifty-four consecutive patients with RH (57 ± 10 years), selected according to WHO/ISH guidelines definition, and 51 essential hypertensives (55 ± 10 years) with satisfactory BP control obtained by association therapy, underwent the following procedures: (1) clinic BP measurement; (2) blood sampling for routine chemistry examinations; (3) 24 h urine collection for microalbuminuria; (4) non-mydriatic retinography; (5) echocardiogram; (6) carotid ultrasonogram. In order to exclude 'office resistance' (defined as clinic BP > 140/90 mmHg and average 24 h BP ≤ 125/79 mmHg), all patients with RH were subjected to 24-hour ambulatory BP monitoring. Results: Both groups were similar for age, gender, body surface area, smoking habit and duration of hypertension, glucose, creatinine and lipid levels. By definition, clinic BP was significantly higher in RH than C (161 ± 19/96 ± 9 versus 127 ± 6/80 ± 5 mmHg, respectively, P < 0.01). The increased prevalence of left ventricular hypertrophy (LVH) and carotid intima-media (IM) thickening (40 versus 12%, P < 0.01, according to a non-gender-specific partition value of 125 g/m2; and 36 versus 14%, P < 0.01, according to IM thickness ≥ 1.0 mm, respectively); a higher prevalence of carotid plaques (65 versus 32%, P < 0.05), a more advanced retinal involvement (grade II and III, 73 and 5% versus 38 and 0%, P < 0.01) and a greater albumin urinary excretion (22 ± 32 mg/24 h versus 11 ± 13 mg/24 h, P < 0.01) were found in RH compared to C. Conclusions: Our study suggests that RH is a clinical condition associated with a high prevalence of TOD at cardiac, macro- and microvascular level and consequently with high absolute cardiovascular risk, which needs a particularly intensive therapeutic approach aimed to normalize BP levels and to induce TOD regression. © 2001 Lippincott Williams & Wilkins.

Objective: To evaluate in a selected population of patients with a recent diagnosis of hypertension whether a reduced nocturnal fall in blood pressure, confirmed by two 24 h ambulatory blood pressure monitoring (ABPM) sessions is associated with more prominent target organ damage (TOD). Methods: The study was structured in two phases: in the first, 141 consecutive, recently diagnosed, never-treated essential hypertensives underwent 24 h ABPM twice within 3 weeks; in the second phase, 118 of these patients showing reproducible dipping or non-dipping patterns underwent the following procedures: (1) routine blood chemistry, (2) 24 h urinary collection for microalbuminuria, (3) amydriatic photography of ocular fundi, (4) echocardiography and (5) carotid ultrasonography. Results: The 92 patients with (>10%) night-time fall in systolic blood pressure (SBP) and diastolic blood pressure (DBP) (dippers) in both monitoring sessions were similar for age, gender, body surface area, smoking habit, clinic BP, 24 h and 48 h BP to the 26 patients with a ≤10% nocturnal fall (non-dippers) in both sessions. The prevalence of left ventricular hypertrophy (LVH) (defined by two criteria: (1) LV mass index ≥ 125 g/m2 in both genders; (2) LV mass index ≥ 120 and 100 g/m2 in men and women, respectively) and that of carotid intima-media (IM) thickening (IM thickness ≥ 0.8 mm) were significantly higher in non-dippers than in dippers (23 versus 5%, P < 0.01; 50 versus 22%, P < 0.05; and 38 versus 18%, P < 0.05, respectively). There were no differences among the two groups in the prevalence of retinal changes and microalbuminuria. The strength of the association of LV mass index with night-time BP was slightly but significantly greater than that with daytime BP. Conclusions: This study suggests that a blunted reduction in nocturnal BP, persisting over time, may play a pivotal role in the development of some expressions of TOD, such as LVH and IM thickening, during the early phase of essential hypertension, despite similar clinic BP, 24 h and 48 h BP levels observed in non-dippers and dippers

xObjective The Plaque Hypertension Lipid Lowering Italian Study (PHYLLIS), is the first study in patients with hypertension (diastolic blood pressure (DBP) 95-115 mmHg; systolic blood pressure (SBP) 150-210 mmHg), moderate hypercholesterolaemia (LDL-cholesterol 4.14-5.17 mmol/l (160-200 mg/dl) and initial carotid artery alterations (maximum intima-media thickness (IMT) T-max greater than or equal to 1.3 mm). The primary objective of PHYLLIS is investigating whether in these patients administration of an angiotensin converting enzyme inhibitor, fosinopril, and a statin, pravastatin, is more effective than administration of a diuretic and a lipid-lowering diet in retarding or regressing alterations in carotid IMT. While the study is in progress, baseline data are here reported to clarify the association of various risk factors with carotid IMT in these medium-high risk hypertensive patients. Methods Patients numbering 508 have been randomized to PHYLLIS by 13 peripheral units, in Italy. Age was (mean +/- SD) 58.4 +/- 6.7 years, males were 40.2%, current smokers 16.5%, means +/- SD of serum total, low-density lipoprotein (LDL), high-density lipoprotein (HDL) cholesterol and triglycerides concentrations were 6.79 +/- 0.67, 4.69 +/- 0.51, 1.37 +/- 0.38, 1.59 +/- 0.64 mmol/l (262.4 +/- 25.8, 181.3 +/- 19.8, 53.0 +/- 14.6, 141.0 +/- 56.7 mg/dl) Means +/- SD of clinic sitting SBP/DBP were 159.8 +/- 9.0/98.3 +/- 4.2 mmHg. 483 of the 508 patients also had 24 h ambulatory BP monitoring, edited and read at a centralized unit (mean +/- SD 24 h SBP/DBP averages 136.3 +/- 14.1/84.0 +/- 10.0 mmHg). Quantitative B-mode ultrasound (Biosound 2000 II 5A, Biosound, Indianapolis, Indiana, USA) recordings of carotid arteries were taken by certified sonographers in the peripheral units and tracings were all read at a central unit. CBMmax (mean IMT of eight sites at common carotids and bifurcations) was 1.21 +/- 0.17; M-max (mean of 12 sites also including internal carotids) 1.16 +/- 0.17, and T-max (single maximum) 1.85 +/- 0.48 mm. Results Ambulatory SEP and pulse pressure (PP) (24 h, daytime, night-time averages) and their variability indices (24 h SD) were always significantly correlated with CBMmax and M-max (P0.01-0.001), and the correlations remained significant after adjustment for age, gender and smoking. No measurement of DBP was ever associated with any IMT measurement. Likewise, no lipid variable was found associated with any IMT measurement. Conclusions Baseline data from PHYLLIS indicate that in this population of hypertensive patients with moderate hypercholesterolaemia, SEP and PP are with age among the most significant factors associated with carotid artery alterations. However, the narrow range of inclusion LDL-cholesterol and DBP values may have obscured an additional role of these variables. (C) 2001 Lippincott Williams & Wilkins.

Background: Pilot educational meetings were conducted to (1) verify the support of hypertensive patients in this initiative; (2) test the knowledge of patients regularly followed-up in our Hypertension Centre Outpatient Clinic concerning problems related to hypertension; (3) improve patients knowledge about hypertension through a formal teaching session, (4) compare the knowledge of these patients with that of a control group. Methods: An invitation to participate in an educational program on hypertension was extended to 210 consecutive patients (group I) followed-up in the outpatient clinic of our Hypertension Centre. Each meeting included four sessions: (1) an interactive phase with electronic devices aimed at evaluating the degree of information about hypertension by means of multiple-choice questionnaires, (2) a traditional teaching session, (3) an interactive phase to assess the compliance to treatment, and (4) a general discussion session. The control group (II) included 144 hypertensive patients referred for the first time to our Hypertension Centre. Before the initial visit the patients were asked to answer a questionnaire identical to that provided to group I during the meetings. Results: The meetings were attended by 183 out of the 210 patients in group I (participation rate = 87%). The answers to the questions were corrected as a percentage ranging from 73.7 to 95.6 in group I and from 43.9 to 74.7 in group II (p < 0.01). The provision of more detailed information about problems in hypertension was associated with better compliance to treatment and blood pressure control. (BP under treatment 138 ± 14/83 ± 7 mmHg in group I, 152 ± 15/91 ± 11 mmHg in group II; (p < 0.01). Conclusions: Our data indicate that this type of educational approach is appreciated by patients (participation rate 87%) and that the level of knowledge about hypertension and compliance to treatment are greater in selected patients than in control patients.

Background Decision about the management of hypertensive patients should not be based on the level of blood pressure alone, but also on the presence of other risk factors, target organ damage (TOD) and cardiovascular and renal disease. Objective To evaluate the impact of echocardiography and carotid ultrasonography in a more precise stratification of absolute cardiovascular risk. Methods Never-treated essential hypertensives (n = 141; 73 men, 68 women, mean age 46 +/- 11 years) referred for the first time to our out-patient clinic were included in the study. They underwent the following procedures: (1) family and personal medical history, (2) clinical blood pressure (BP) measurement, (3) routine blood chemistry and urine analysis, (4) electrocardiogram, (5) echocardiogram, (6) carotid ultrasonogram. Risk was stratified according to the criteria suggested by the 1999 WHO/ISH guidelines. TOD was initially evaluated by routine procedures only, and subsequently reassessed by using data on cardiac and vascular structure obtained by ultrasound examinations (left ventricular hypertrophy (LVH) as left ventricular mass index (LVMI) > 134 g/m2 in men and > 110 g/m2 in women; carotid plaque as focal thickening > 1.3 mm). Results According to the first classification 20% were low-risk patients, 50% medium-risk, 22% high-risk and 8% very-high-risk patients. A marked change in risk stratification was obtained when TOD was assessed by adding ultrasound examinations: low-risk patients 18%, medium-risk 28%, high-risk 45%, very-high-risk patients 9%. Conclusions The detection of TOD by ultrasound techniques allowed a much more accurate identification of high-risk patients, who represented a very large fraction (45%) of the patient population seen at our hypertension clinic. In particular, a large proportion of patients classified as at moderate risk by routine investigations were instead found to be at high risk when ultrasound examinations were added. The results of this study suggest that cardiovascular risk stratification only based on simple routine work-up can often underestimate overall risk, thus leading to a potentially inadequate therapeutic management especially of low-medium risk patients.

Background: Hypertensive patients with left ventricular hypertrophy (LVH) need a prompter and more intensive pharmacological treatment than subjects without evidence of cardiac involvement. So the detection of LVH plays an important role for decision-making in hypertensives. Objective: To evaluate the impact of different echocardiographic criteria to define LVH in a more precise stratification of absolute cardiovascular risk in hypertensives without target organ damage (TOD) as assessed by routine investigations. Methods: A total of 100 never treated patients with grade 1 and 2 essential hypertension (53 men, 47 women, age 44 ± 12 years) referred for the first time to our outpatient clinic were included in the study. They underwent the following procedures: (1) family and personal medical history, (2) clinic blood pressure (BP) measurement, (3) routine blood chemistry and urine analysis, (4) electrocardiogram, (5) echocardiogram. Risk was stratified according to the criteria suggested by the 1999 WHO-ISH guidelines. TOD was initially evaluated by routine procedures only, and subsequently reassessed by using six different echocardiographic criteria to recognise LVH: (a) left ventricular mass index (LVMI)

Background: Left ventricular hypertrophy (LVH) and increased carotid intima-media thickness (IMT) represent independent risk factors for cardiovascular disease. Objective: To evaluate the prevalence of echocardiographic LVH and common carotid artery (CCA) intima-media (IM) thickening by different criteria in a large sample of hypertensive patients referred to our Hypertension Clinic. Methods: Echocardiograms and ultrasonographic carotid examinations have been performed in 640 consecutive hypertensives referred to our outpatient's hypertension unit. LVH was diagnosed using six different criteria, when left ventricular mass index (LVMI) exceeded (a)100 g/m2 in women and 120 g/m2 in men, (b) 110 g/m2 in women and 125 g/m2 men, (c) 110 g/m2 in women and 134 g/m2 in men, (d) 125 g/m2 in both sexes, (e) 47 g/h2.7 in women and 51 g/h2.7 in men, (f) 105 g/h in women and 126 g/h in men. Thickening of CCA IM was identified using three partition values; when IMT was (a) ≥0.8 mm; (b) ≥0.9 mm; (c) ≥ 1.0 mm in both sexes. Results: Echocardiographic and ultrasonographic examinations of sufficient quality to be analysed were obtained in 611 patients (95.2%). Prevalence of LVH ranged from 18.6% (d) to 42.2% (f) and was significantly higher in men than in women by criteria (d) and (e), but slightly higher in women when using criteria (a) and (c). Eccentric hypertrophy was the most frequent type of LVH independently of the criteria used. Prevalence of IM thickening ranged from 14.7% (c) to 44.2% (a). Significant correlations between left ventricular mass (LVM)/body surface area, LVM/height and LVM/height2.7, and carotid IM thickness were found (r = 0.41; p < 0.0001; r = 0.31; p < 0.0001; r= 0.30; p < 0.0001, respectively). Conclusion: The prevalence of LVH and CCA IM thickening in hypertensive patients is markedly dependent on the partition values used to define these markers of target organ damage. Considering the pivotal role of LVH and CCA IM thickening in assessing the global cardiovascular risk profile in hypertensives, improved standardization in defining LVH and carotid IM thickening is needed

Objective. To evaluate in a selected population of subjects with a recent diagnosis of hypertension whether a blunted nocturnal fall in blood pressure is associated with more advanced cardiac and vascular damage. Methods. One hundred and eleven recently diagnosed and never-treated patients with mild essential hypertension underwent 24-h ambulatory blood pressure monitoring (ABPM), echocardiography and carotid ultrasonography. Results. The 78 patients with normal (> 10%) night-time fall in systolic blood pressure (SBP) and diastolic blood pressure (DBP) (dippers) were similar to the 33 patients with a small (≤ 10%) fall (non-dippers) for age, sex, body surface area, smoking habit, clinic and 24-h blood pressure. There were no differences between dippers and non-dippers in left ventricular mass index (104 versus 105 g/m2), common carotid internal diameter (5.8 versus 5.9 mm), intima-media thickness (0.66 versus 0.64 mm) and carotid plaques prevalence (25 versus 29%). Furthermore, no differences were found in the correlation of daytime and night-time SBP and DBP with left ventricular mass and carotid wall thickness. When the 77 men and 34 women were analysed separately, similar results were obtained. Conclusion. These results suggest that a blunted reduction in night-time blood pressure does not play a major role in the development of cardiovascular changes during the early phase of essential hypertension.

The study was designed to evaluate whether the increase in left ventricular (LV) mass in essential hypertensives (H) is associated with a proportional increase in diameter of the left coronary artery (LCA) trunk. Twenty-six hypertensives, 14 with left ventricular hypertrophy (LVH) (left ventricular mass index [LVMI] >134 g/m2 in men and >110 g/m2 in women) and 12 without LVH, and 10 normotensive controls (C) underwent clinical laboratory and echocardiographic transthoracic examination. LV dimensions were measured according to the Penn convention and LV mass calculated by the formula of Devereux. The LCA main trunk was visualized by two-dimension short axis view at the level of the great vessels section, and the diameter measured as intima-intima distance at end-diastole. Hypertensives with and without LVH and C had similar age, sex, and body surface area distribution. LVMI was, by definition, significantly higher in H with LVH than in H without LVH and in C (144 ± 21, 113 ± 13, and 98 ± 10 g/m2, P < .01), whereas the diameter of the LCA trunk was similar in all groups (0.48 ± 0.1, 0.48, and 0.46 cm, respectively). There was no significant correlation between LVMI and LCA diameter in H (r = 0.21, P = not significant). The diameter of LCA trunk was significantly correlated only with BSA (r = 0.5, P < .01), LV end-systolic and end-diastolic diameters (r = 0.5 and r = 0.4, P < .05). Our data suggest that in H the increase in LVM is not associated with a concomitant increase of epicardial coronary artery diameter, and this finding may account in part for the impairment of coronary blood flow reserve in LVH. Am J Hypertens 1999;12:1163-1168 © 1999 American Journal of Hypertension, Ltd.

Left ventricular hypertrophy (LVH) in humans is a common adaptive process induced by different physiological and pathological stimuli.

Aim. Left ventricular concentric remodelling defines a modified left ventricular geometry in the presence of a normal left ventricular mass; it is an early and frequent adaptation in arterial hypertension. The present study was designed to evaluate the extent of carotid structural changes in essential hypertensives with left ventricular remodelling. Patients and methods. Two groups of hypertensive patients, who had never previously received antihypertensive treatment, 14 with left ventricular concentric remodelling (group I, relative wall thickness 0.48 ± 0.02) and 48 with normal left ventricular geometry (group II, relative wall thickness 0.37 ± 0.04) underwent clinical and laboratory examination, echocardiography, carotid artery ultrasonography and 24 h ambulatory blood pressure monitoring (ABPM). The left ventricular dimensions and mass were obtained according to the Penn convention. The intima-media thickness (IMT) of the posterior wall of both common carotid arteries was measured 5, 10 and 20 mm caudally to the bulb and the average value was used for analysis. Results. In both groups age (group I 44 ± 9 years; group II 40 ± 9 years), body surface area (group I 1.85 ± 0.2 m2; group II 1.80 ± 0.2 m2), duration of hypertension (group I 4.4 ± 4; group II 3.8 ± 3.9 years), metabolic parameters and smoking habits were similar. Both clinic and 24 h ABPM values were higher in group I (clinic 157 ± 12/102 ± 5; 24 h ABPM 145 ± 10/95 ± 7 mmHg) than they were in group II (clinic 146 ± 11/97 ± 5; 24 h ABPM = 134 ± 10/87 ± 8 mmHg, P < 0.01). The left ventricular mass index (LVMI) and IMT were found to be slightly but significantly greater in group I than they were in group II (LVMI 106 ± 7 versus 98 ± 12 g/m2, P < 0.05; IMT 0.68 ± 0.13 Versus 0.61 ± 0.10 mm, P < 0.05). A significant correlation was found between LVMI and common carotid IMT in the whole group of hypertensive patients (r = 0.43, P < 0.01). Conclusions. Our results indicate that left ventricular concentric remodelling does not represent the only early cardiovascular change in arterial hypertension but rather is associated often with carotid intima-media thickening

Whether antihypertensive agents exert an antiatherosclerotic effect by blood pressure reduction or independently of their antihypertensive effect is clinically relevant. Animal studies have generally shown that the calcium antagonist verapamil has a preventive rather than a therapeutic antiatherosclerotic effect, which is independent of its antihypertensive effect. However, doses used in animal studies were much higher than those administered to humans and, in animals, the time of administration of verapamil coincided with the application of atherogenic stimulus. Human studies have given controversial results. Verapamil appears to effectively reduce the restenosis rate after coronary angioplasty. However, in patients with coronary stenosis who were undergoing bypass surgery, results were conflicting: a retrospective study provided positive results, while a prospective study gave negative results. An ongoing study investigating the effect of verapamil on the carotid arteries of hypertensive patients could help clarify the relationship between blood pressure reduction and the progression, regression or development of carotid lesions.

OBJECTIVE Physical training induces multiple changes in the cardiovascular system which allow an increased performance along with increased oxygen consumption. The present study was designed to investigate whether the changes include an increase in arterial compliance. METHODS AND DESIGN In six normotensive right-handed hammer-throwers (aged 21.3 +/- 1.8 years, mean +/- SE) we measured radial artery diameter continuously via a new non-invasive echo-tracking device, and beat-to-beat blood pressure. Arterial compliance was calculated by an arctangent model. In each subject measurements were made from both the left and the right arm. The data were compared with those obtained in six age-matched normotensive controls. RESULTS Compared to the controls, the hammer-throwers had similar blood pressure, a lower heart rate and plasma norepinephrine and a higher left ventricular mass index and radial artery diameter. In the athletes, right radial artery compliance was significantly greater than either right or left radial artery compliance in the sedentary subjects (+61 and 63%, P < 0.05). It was also significantly greater than contralateral radial artery compliance (+53 +/- 8%, P < 0.05). CONCLUSIONS Physical training is accompanied by an increase in arterial compliance. In our hammer-throwers this increase was mainly evident in the more highly trained arm, suggesting that local mechanisms are involved in this phenomenon.

The aim of this study has been to analyze the acute and chronic effects of oral verapamil on diastolic function indices, derived from Doppler echocardiography, and left-ventricular (LV) dimensions and mass, assessed by M-mode echocardiography, in hypertensive patients without LV hypertrophy. 12 patients with essential hypertension were studied in basal conditions and (1) after a single oral administration of verapamil 160 mg and placebo in a double-blind protocol and (2) over chronic treatment (12 months) with verapamil 240 mg/day. At baseline, the ratio between early and atrial-induced transmitral velocities (E/A ratio) was lower in patients than in 12 age-matched normal subjects (1.08 +/- 0.2 vs. 1.51 +/- 0.3, p less than 0.01). Acute verapamil administration significantly decreased arterial blood pressure (162 +/- 26/101 +/- 8 to 142 +/- 12/88 +/- 7 mm Hg, p less than 0.01 after 2 h) and increased the E/A ratio to 1.26 +/- 0.3 (p less than 0.05) after 3 h. No change in ventricular dimensions and heart rate was observed. After chronic therapy, we found a further increase in the E/A ratio in 10 responder patients (1.49 +/- 0.3, p less than 0.01). The LV mass index, that was higher than in normal subjects before the treatment (118 +/- 16 vs. 91 +/- 11 g/m2, p less than 0.01), was significantly reduced (100 +/- 17 g/m2, p less than 0.05 vs. basal, nonsignificant vs. normal subjects). Our results demonstrate that acute administration of verapamil only partially improves the abnormal indices of diastolic function in hypertensive patients, whereas chronic treatment, by reducing LV mass indices and blood pressure to normal values, can completely normalize the indices of LV diastolic filling.

Cardiopulmonary receptor control of the circulation is impaired in a variety of diseases having cardiac hypertrophy as a common feature. Whether this also occurs in the so-called "physiological" cardiac hypertrophy of the athlete, however, is unknown. We studied nine sedentary healthy subjects and 19 age-matched professional runners or hammer throwers who had trained at least 2 hours per day, 5 days per week for 7 years. The left ventricular mass index (echocardiography) was 99 +/- 7.4 and 135 +/- 5.9 g/m2 in the two groups, respectively. Cardiopulmonary receptor stimulation and deactivation were obtained by increasing and reducing left ventricular end-diastolic diameter for 5 minutes by leg raising and lower body negative pressure, keeping both stimuli at a level not affecting blood pressure and heart rate. In the sedentary healthy subjects, forearm vascular resistance (the ratio between mean arterial pressure and forearm blood flow) and plasma norepinephrine fell during leg raising (forearm vascular resistance, -7 +/- 1.7 units; norepinephrine, -57.4 +/- 1.4 pg/ml) and increased during lower, body negative pressure (forearm vascular resistance, 20 +/- 5.3 units; norepinephrine, 97.7 +/- 21.5 pg/ml). For similar or greater alterations in left ventricular end-diastolic diameter, the correspondent changes observed in the professional runners or hammer throwers were -5.3 +/- 1.3 units (forearm vascular resistance), -35.4 +/- 9.6 pg/ml (norepinephrine), 9.1 +/- 1.4 units (forearm vascular resistance), and 30.9 +/- 6.9 pg/ml (norepinephrine). This represented an attenuation of 25%, 38%, 55%, and 68%, respectively (p less than 0.01), of the control response.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiopulmonary receptors modulate renin release in several animals species. However, their involvement in reflex control of this humoral substance in humans is controversial. Furthermore, no information is available on the alteration of this control in hypertension. We studied the modulation of plasma renin activity (radioimmunoassay) in 12 normotensive subjects and in 12 age-matched subjects with untreated hypertension of mild or moderate degree. Cardiopulmonary receptors were stimulated by increasing central venous pressure (right atrial catheter) and cardiac volume (echocardiographic measurement) through passive leg raising and deactivated by reducing central venous pressure and cardiac volume through lower body negative pressure. The stimuli were maintained for 20 to 30 minutes, and their degree was set to avoid changes in blood pressure (indirect or direct measurements) and heart rate, thus avoiding involvement of arterial baroreceptors. In normotensive subjects, deactivation of cardiopulmonary receptors induced a progressive rise in plasma renin activity and stimulation of cardiopulmonary receptors induced a progressive fall. The reflex gain (ratio between plasma renin activity and central venous pressure or cardiac volume changes) was similar for deactivation and stimulation. During cardiopulmonary receptor deactivation, the gain corresponded to that obtained by dividing the increase in plasma renin by the reduction in central venous pressure induced by tilting. Cardiopulmonary receptor deactivation and stimulation also induced clear-cut changes in plasma renin activity in hypertensive subjects, but the percent magnitude of the reflex plasma renin activity excursion was less than that in normotensive subjects. These observations indicate that cardiopulmonary receptors modulate plasma renin activity in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

The structure and function of the right ventricle in arterial hypertension have been the subject of only a few reports. The present study evaluated the functional and structural changes in both left and right ventricles. Doppler and standard echocardiography were performed in 58 hypertensive patients (33 without and 25 with left ventricular hypertrophy). We concluded that right ventricular wall thickness is significantly increased in hypertensive patients compared with normotensive subjects, and that there is a significant, direct correlation between right and left ventricular thickness. Abnormalities in right and left ventricular filling, characterized by a reduction in early and an increase in late diastolic flow velocity, occur in hypertensive patients, and there is a direct correlation between late mitral and tricuspidal flow velocities and left and right ventricular thickness.

This study examined the effects of ageing on the cardiopulmonary receptor regulation of vasomotor tone in skeletal muscle and renin release by the kidney. To this end, the changes in forearm vascular resistance (mean arterial pressure divided by plethysmographically measured forearm blood flow), plasma noradrenaline concentration and plasma renin activity were measured in eight young (23 +/- 2 years, mean +/- s.e.m.) and seven elderly healthy subjects (69 +/- 2 years) during manoeuvres which altered cardiopulmonary receptor activity. The cardiopulmonary receptors were stimulated by increasing central venous pressure through passive leg-raising and deactivated by reducing central venous pressure through non-hypotensive (-15 mmHg) and hypotensive (-40 mmHg) levels of lower body negative pressure. During either manoeuvre, central venous pressure changed by the same amount in both groups, but the reflex changes in forearm vascular resistance, plasma noradrenaline and plasma renin activity were significantly less in elderly subjects. Since the increase in forearm vascular resistance induced by a cold pressor test was comparable in young and elderly subjects, a non-specific depression of cardiovascular responsiveness to neural stimuli can be excluded. Thus, healthy normotensive elderly subjects show an impairment of both vascular and neurohumoral influences exerted by cardiopulmonary receptors. This may be involved in the decreased ability of the elderly to cope with gravity challenges.

The cardiopulmonary reflex control of circulation (which, in man, depends largely on cardiac receptors) is impaired in hypertensive subjects who have left ventricular hypertrophy. To determine whether hypertension or cardiac hypertrophy per se is responsible for this, we studied nine sedentary normotensive subjects aged 23 +/- 1 years and nine age-matched normotensive weight-lifters with echocardiographic signs of left ventricular hypertrophy (left ventricular mass index for the weight-lifters: 134 +/- 7; for the sedentary subjects: 99 +/- 7 g/m2; P less than 0.01). Cardiac receptors were manipulated by increasing and decreasing the left ventricular end-diastolic diameter (LVEDD) by raising the leg and by reducing the lower-body negative pressure, respectively, and the reflex responses were assessed from the changes in forearm vascular resistance and plasma noradrenaline (high performance liquid chromatography assay). Forearm vascular resistance and the noradrenaline concentration were reduced by increasing the LVEDD, and were increased when the LVEDD was reduced. For a given change in the LVEDD, the responses were markedly less in the weight-lifters than in the non-athletes. In contrast, the haemodynamic effects of a cold pressor test were similar in both groups. Thus, the cardiopulmonary reflex is impaired in normotensive subjects in whom intense physiological training has led to an increase in left ventricular hypertrophy. This suggests that structural alteration of the heart per se is responsible for the phenomenon.

Arterial baroreflex is impaired in the normotensive elderly. However, no information is available on the effects of aging on another major reflex mechanism of cardiovascular control, i.e., cardiopulmonary reflex. Three groups of normotensive subjects divided according to age were evaluated during leg raising, which increased central venous pressure, and during lower body negative pressures, which reduced central venous pressure without altering blood pressure and heart rate. These maneuvers stimulated and deactivated cardiopulmonary receptors with only little involvement of arterial baroreceptors. During lower body negative pressures, central venous pressure decreased similarly in three groups, but reflex increases in forearm vascular resistance, plasma norepinephrine, and plasma renin activity were smaller in elderly than in middle-aged and young subjects. Furthermore, during leg raising, comparable increases in central venous pressure caused reflex vascular and humoral responses that were smaller in elderly than in middle-aged and young subjects. Elderly subjects had smaller changes in left ventricular diameter in response to changes in central venous pressure. Blood pressure and vascular responses to cold pressor test were similar in the three groups, excluding a hyporeactivity of older subjects to neural stimuli. Thus aging is associated with an impairment of the cardiopulmonary reflex. This may originate from an impaired ability of cardiac receptors to sense alterations in central blood volume because of an age-dependent reduction in cardiac compliance.

The finding of hypokalemia and of low plasma renin activity (PRA) in a hypertensive patient suggests a diagnosis of primary hypermineralocorticoidism. Medications containing compounds with mineralocorticoid-like activity (licorice, carbenexolone) may also cause the same syndrome. Recently, we carried out detailed studies on 10 patients with severe hypertension and hypokalemic alkalosis, suppressed PRA and low aldosterone levels. Plasma levels of cortisol and ACTH were suppressed in most of the cases. Measurement of deoxycorticosterone and corticosterone (and in some patient of 18-hydroxydeoxycorticosterone and 18-hydroxycorticosterone) was not significantly higher than normal. Therapeutic trials of dexamethasone and aminoglutethimide were ineffective. In contrast, spironolactone and amiloride treatment resulted in substantial but incomplete amelioration of both hypertension and hypokalemia. All of the patients share a common history of chronic rhinitis and habitual use of large doses of nasal spray containing 9α-fluoroprednisolone and vasoconstrictor agents. Withdrawal resulted in a complete remission of hypokalemia in one to two weeks in all patients. The hypertension and depressed levels of PRA, aldosterone and cortisol took longer to return to normal, varying from case to case; in all but one patient, the values returned to normal within two months. This report reveals another cause of factitious mineralocorticoid excess which may be considered in the differential diagnosis of hypokalemic hypertensive syndromes. © 1981.

Felodipine, a new dihydropyridine derivative with a selective action on vascular smooth muscle, was investigated in 2 short term studies in hypertensive patients. In the first study, oral administration of felodipine 12.5 mg three times daily in a preliminary tablet formulation for 3 days significantly reduced supine and upright blood pressure with only a slight increase in heart rate and no clinically relevant signs of sodium and water retention. By increasing each dose to 25 and 50 mg three times daily, there was a further, but quite moderate, decrease in blood pressure; however, this was accompanied by an increase in heart rate and a tendency towards a reduction of creatinine clearance and urinary sodium output. In the second study, a new oral formulation containing 10 mg felodipine, administered twice daily for 7 days, was effective in lowering blood pressure without a clinically relevant tachycardia. Following the first dose of felodipine, urinary sodium excretion was slightly increased while potassium excretion showed only minor changes. The new calcium antagonist, felodipine, lowers blood pressure without the clinically relevant adverse reactions commonly related to other direct vasodilator antihypertensive drugs.

Studies that have examined the cardiopulmonary receptor control of circulation in hypertension have produced conflicting results. In 10 normotensive subjects and in age-matched essential hypertensive subjects without (n = 10) or with left ventricular hypertrophy (n = 12), as well as in seven subjects of the latter group restudied after 1 year of treatment that induced regression of cardiac hypertrophy, we examined the cardiopulmonary reflex by increasing central venous pressure and stimulating cardiopulmonary receptors through passive leg raising and by reducing central venous pressure and deactivating cardiopulmonary receptors through nonhypotensive lower body negative pressure. Reflex responses were measured as changes in forearm vascular resistance (mean blood pressure divided by plethysmographically measured blood flow), plasma norepinephrine concentration, and plasma renin activity. In hypertensive subjects without left ventricular hypertrophy, stimulation and deactivation of cardiopulmonary receptors caused changes in forearm vascular resistance, norepinephrine concentration, and plasma renin activity that were modestly reduced as compared with those in normotensive subjects. However, all these changes were markedly reduced in hypertensive subjects with left ventricular hypertrophy. Following regression of left ventricular hypertrophy, the changes in vascular resistance, plasma norepinephrine, and plasma renin activity induced by cardiopulmonary receptor manipulation all improved markedly. These results demonstrate that cardiopulmonary receptor regulation of peripheral vascular resistance and of neurohumoral variables is impaired in essential hypertension and that the impairment is much more pronounced when this condition is associated with cardiac structural alterations. Therapeutic regression of these alterations, however, leads to a marked improvement of this reflex, with consequent favorable effects on circulatory homeostasis.