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Thalassemia minor (Tm), the ß-thalassemia carrier state, is followed by favorable lipidemic profile and seems to protect against myocardial infarction mainly in men. However, the cardiovascular risk factor (CRF) and metabolic profile of these subjects has not been thoroughly addressed, although it is not known whether gender differences are involved. We evaluated CRFs, metabolic parameters and risk-prediction equations along with renal function and selected echocardiographic indices in 23,680 consecutive subjects, that is, 11,192 women and 12,488 men, with newly diagnosed hypertension according to the presence or absence of Tm. Of 23,680 patients, 548 (2.3%) had Tm. Compared with patients without Tm, Tm cases had similar gender distribution, age, body mass index and blood pressure. Besides having a better lipidemic profile, Tm patients were less frequently smokers (25% vs. 32%, P<0.001), had a lower prevalence of metabolic syndrome (26% vs. 39%, P<0.001) and lower HeartSCORE and INTERHEART scores (P<0.001). Tm patients also had lower levels of fibrinogen and plasminogen activator inhibitor-1 (P<0.001), lower serum creatinine and higher estimated glomerular filtration rate (P<0.001), lower prevalence of left ventricular hypertrophy (35% vs. 48%, P<0.001) and higher total and mid-wall fractional shortening (P=0.03 and <0.001, respectively). Most of these differences were consistent in both genders, whereas the HeartSCORE and the echo indices were significantly better in Tm only in women. Among patients with newly diagnosed hypertension, those with Tm have a better overall CRF and metabolic profile, beyond the well-known differences in serum lipids. Compared with men, women seem to be at least equally protected.

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Recent studies indicate that the pro-inflammatory action of aldosterone (ALDO) or the activation of mineralocorticoid receptors contribute to the increased risk of cardiovascular disease (CVD). The aim of the present study was to investigate the grade of the inflammatory activation, in relation to ALDO levels, in a large cohort of essential hypertensive patients. The study included 3770 consecutive essential hypertensive patients who attended our outpatient clinics. Patients were evaluated with medical history, repeated office blood pressure and 24-h ambulatory blood pressure monitoring (ABPM), physical examination and full laboratory assessment including ALDO in 24-h urine collection, plasma renin activity (PRA), high-sensitivity C-reactive protein (hsCRP), total fibrinogen, serum homocysteine (Hcy), serum amyloid A (SAA) and white blood cells (WBC) measurements in morning blood samples. Patients were divided according to PRA (high PRA >1 ng ml(-1) h(-1), low PRA <1 ng ml(-1) h(-1)) and ALDO levels (high ALDO >12 but <24 µg per 24 h, low ALDO <12 µg per 24 h) in four groups. The hsCRP (P<0.022) and SAA (P<0.001) levels increased in parallel with the ALDO metabolism. Similar differences were observed for Hcy (P<0.001), fibrinogen (P=0.001) and WBC (P<0.02). High ALDO levels within normal range are related to the presence of subclinical inflammation in essential hypertension. These data indicate that ALDO and PRA influence the process of subclinical inflammation involved in the increased risk of CVD.

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BACKGROUND AND AIM: Metabolic syndrome (MS) has been recently associated with an increased risk for the development of atrial fibrillation (AF) in the general population. Whether this relation is also apparent in patients with arterial hypertension remains to be clarified. In the present study we sought to investigate the independent association of the MS with the AF in a large cohort of hypertensive patients. MATERIAL AND METHODS: The study comprised 15,075 consecutive, non-diabetic patients with essential hypertension (age range: 40-95 years, 51.1% males). All subjects underwent a complete clinical and lipidemic profile assessment as well as a standard 12-lead ECG at drug free baseline. MS was diagnosed by using five different definitions, including the National Cholesterol Education Program Third Adult Treatment Panel (ATPIII) and the GISSI Score. RESULTS: The prevalence of the MS varied from 31.7% to 47.8% according to the each time definition used. In multiple logistic regression analysis, MS was associated with the presence of AF (odds ratio from 1.61 to 1.99, p < 0.001 for all), independenty of the definition used. All ATPIII MS components were found to be independently associated with an increased incidence of AF. The prevalence of AF increased progressively with the severity of the metabolic syndrome as assessed by the number of the metabolic syndrome components (p < 0.001). CONCLUSION: In non-diabetic patients with essential hypertension, the MS is directly and independently related to the AF prevalence.

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The aim of this study was to determine cardiovascular (CV) risk factors (RFs) and target organ damage clustering in 21280 Greek hypertensives stratified by gender and age. Glycemic and lipid profile were determined, left ventricular mass index, estimated gromerular filtration rate (eGFR), 10-years CV risk according to Framingham risk score (FRS) and HeartScore (HS) were calculated. Only 10.2% of patients had no concomitant RFs, 53.1% had one (48.8% dyslipidemia, 3.4% smoking, 0.9% diabetes), 32.9% had two (26% dyslipidemia and smoking, 6.6% dyslipidemia and diabetes, 0.3% smoking and diabetes) and 3.7% had all four traditional RFs. Obesity was present in 30%, metabolic syndrome in 38%, low eGFR in 24% and left ventricular hypertrophy in 49%. Mean FRS risk was 35% for males, 24.1% for females whereas in high risk (>20%) were 68.7 and 50.7%, respectively (P<0.0001). Mean HS risk was 8.4% for males, 6.2% for females whereas in high risk (>5%) were 48.6 and 36.2%, respectively (P<0.0001). Age was correlated to pulse pressure, eGFR, left ventricular mass index and CV risk (P<0.0001). Ageing increased the risk difference between genders for total (P=0.001) but not for fatal events (P=nonsignificant). In conclusion, as RFs cluster in hypertensives, CV risk calculation should guide treatment decisions.

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The aim of this study was to evaluate any possible association of homocysteine with arterial stiffness indices in patients with essential arterial hypertension (AH), isolated office hypertension (IOH) and normotensive controls. The final cohort comprised 231 normotensives (NTs, 119 males), 480 patients with IOH (196 males) and 1188 patients with essential AH (713 males). All patients were screened for plasma homocysteine levels and lipidaemic profile and underwent aortic compliance and wave reflection assessment by using carotid-femoral pulse wave velocity (PWVc-f) and aortic augmentation index corrected for heart rate (AIx) accordingly. In the total population, stepwise multiple linear regression analysis showed that homocysteine levels remained a significant determinant of PWV (beta (SE): 0.056 (0.007), P<0.001) and AIx (beta (SE): 0.236 (0.052), P<0.001) independently of the traditional factors affecting arterial stiffness and wave reflection. When the three groups were examined separately, homocysteine levels remained an independent determinant of PWFc-f in all groups (NT: beta (SE): 0.070 (0.022), P=0.002; IOH: beta (SE): 0.109 (0.015), P<0.001; AH: beta (SE): 0.040 (0.009), P<0.001). However, homocysteine levels remained an independent determinant of AIx only in the IOH and AH, but not in the NT group (IOH: beta (SE): 0.302 (0.124), P=0.015; AH: beta (SE): 0.183 (0.057), P=0.001; NT: beta (SE): 0.308 (0.240), P=0.200). This study points to an independent relationship between circulating homocysteine levels, aortic compliance and wave reflection.

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The purpose of the present study was to investigate whether there is a relationship between anemia and day-night blood pressure variations in essential hypertensive patients. We found that anemic hypertensives had significantly elevated nocturnal BP, and decreased mean 24-h BP and daytime BP.

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Pulse pressure (PP) is emerging as a major pressure predictor of cardiac disease. The study comprised 10 185 untreated patients with essential hypertension. A total of 5395 men and 4790 women 56+/-13 years old, with uncomplicated essential hypertension, after a 15-day washout period and after 6 months of antihypertensive monotherapy were included. All patients included in the final cohort were responders and had normalized their blood pressure. PP was decreased least with diuretics (-5 mm Hg) and most with angiotensin II receptor blockers (ARBs) and calcium antagonists (-15 mm Hg), followed by angiotensin-converting enzyme inhibitors (ACEI) (-12 mm Hg) alpha- and beta-blockers (-10 and -9 mm Hg), differentiating among antihypertensive classes (P<0.001). The magnitude of PP fall was related to the degree of left ventricular (LV) mass reduction (P<0.001), seen best with ARBs (r=0.42) and least with ACEIs (r=0.18). Of the antihypertensive medications used in everyday practice, PP decrease may be achieved best with ARBs and calcium antagonists, whereas diuretics confer poor response. PP was decreased least with diuretics (-5 mm Hg) and most with ARBs and calcium channel blockers (-15 mm Hg), followed by ACEI (-12 mm Hg) alpha- and beta-blockers (-10 and -9 mm Hg), differentiating among antihypertensive classes (P<0.001). Of the antihypertensive medications used in everyday practice, PP decrease may be achieved best with ARBs and calcium antagonists.

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OBJECTIVES: Increased QT dispersion has been considered as predisposing to ventricular arrhythmias in hypertrophic cardiomyopathy, congestive heart failure, and coronary artery disease. An increased QT dispersion has also been found in hypertensive patients with left ventricular hypertrophy (LVH). The data on the effect of LVH regression on QT dispersion are limited. METHODS AND RESULTS: To assess the relation of LVH regression and QT dispersion decrease, 68 patients (42 men and 26 women, mean age 56.3+/-9.5 years) with uncomplicated essential hypertension were studied. All underwent full electrocardiographic and echocardiographic studies at baseline and after 6 months of monotherapy, 29 with angiotensin-converting enzyme inhibitors and 39 with calcium antagonists. QT dispersion was calculated by subtracting the shortest QT from the longest QT, in absolute value (QTmax - QTmin). It was also corrected with Bazett's formula (QTc dispersion). Left ventricular mass index was assessed according to the Devereux formula. After treatment, LVH decreased with both angiotensin-converting enzyme inhibitors (from 155 to 130 g/m2, P < .001) and calcium antagonists (156 to 133/92/m2, P < .001). QT dispersion decreased both after angiotensin-converting enzyme inhibitor treatment (from 82 to 63 ms) and calcium antagonist treatment (from 77 to 63 ms, both P < .001 ). There was a significant correlation of QT dispersion and left ventricular mass after therapy (r = 0.36, P < .005). There was a correlation of the degree of LVH and QT dispersion decrease (r = 0.27, P < .05). CONCLUSIONS: It is concluded that LVH regression influences AQT favorably. Its prognostic value has yet to be determined.

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OBJECTIVES: This study sought to determine whether the natural decrease in sex hormones that occurs during menopause in hypertensive women plays a role in aortic root stiffness. BACKGROUND: The effect of menopause-induced sex hormone deprivation on aortic root function is not known; however, it is of special interest in hypertensive subjects, whose aortic elastic properties are already compromized. METHODS: Eighteen women with essential hypertension were followed-up for 3 years, during which time they went through menopause (group A) and were compared with 22 age-matched hypertensive women with normal menses (group B) and 20 hypertensive men (group C). Blind echocardiographic tracings and simultaneous blood pressure measurements were obtained after at least 30 medication-free days, both at baseline and 3.5 years later. RESULTS: Aortic root function tended to be aggravated in both groups B and C, but not significantly so, with no between-group differences (p = NS), whereas it deteriorated in group A. Thus, in menopausal hypertensive subjects, aortic root systolodiastolic percent change decreased (from 6.7% to 4.9%, p < 0.0001 [p = 0.002 vs. group B; p = 0.006 vs. group C]); cross-sectional compliance decreased (from 18 to 13 cm2/mm Hg, p < 0.0001 [p = 0.002 vs. group B; p = 0.03 vs. group C]); Peterson's elastic modulus increased (from 1.2 to 1.9 dynes/cm2, p = 0.0006 [p = 0.003 vs. group B; p = 0.005 vs. group C]); aortic stiffiness index increased (from 7.0 to 10.8, p = 0.0008 [p = 0.004 vs. group B; p = 0.007 vs. group C]); and aortic root distensibility decreased (from 1.8 to 1.2 dynes/cm2, p < 0.0001 [p = 0.0003 vs. group B; p = 0.007 vs. group C]). Serum lipids did not change significantly in any group (p = NS). CONCLUSIONS: In hypertensive women, the effect of menopause on the elastic properties of the aortic root is abrupt and devastating.

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Using echocardiographic and Doppler methodology, we evaluated the effects of celiprolol 200-400 mg/day and metoprolol 100-200 mg/day, given for one year, on haemodynamics, left ventricular structure and function, and aortic root distensibility in 40 hypertensive patients. Total peripheral resistance was unchanged with metoprolol (-1.7%) but decreased with celiprolol (-11.2%), a significant difference between the two treatments (P = 0.01). Left ventricular mass index was reduced by 5.7% in those patients receiving metoprolol and by 11.8% in those receiving celiprolol (P < 0.001). Cardiac index fell significantly with metoprolol and marginally with celiprolol (-13.9% vs. 5.9%, P = 0.003). Left ventricular diastolic function-as shown by the transmitral early to late peak filling velocity ratio-was not altered with metoprolol, but a significant increase (17%, P = 0.2) was seen with celiprolol. Both metoprolol and celiprolol increased aortic root distensibility, with celiprolol having a significantly greater effect (80% vs. 30%, P < 0.01). We conclude that, in comparison to metoprolol, long term antihypertensive therapy with celiprolol improves left ventricular diastolic and aortic root function, whilst reducing total peripheral resistance and left ventricular hypertrophy.

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Blood pressure (BP) changes during the menstrual cycle (MC) have not been studied in hypertensive women in relationship to changes in sex hormone levels and plasma renin activity (PRA). We therefore carried out 24 h ambulatory BP recordings and hormonal measurements in 34 hypertensive and 27 matched normotensive women during the follicular ovulatory and luteal phases of the menstrual cycle. Plasma renin activity was similar in the two groups and rose significantly during the luteal phase only in the hypertensives (P < .01). There were no differences in plasma estradiol or progesterone between the normotensives and hypertensives, but testosterone was higher in the hypertensives during the ovulatory (P < .01) and luteal (P < .001) phases. Blood pressure did not change in the normotensives throughout the cycle, but it increased in the hypertensives during ovulation (P < .01). When patients were divided according to mean menstrual cycle PRA, only those with relatively low PRA (< 2 ng/mL/h) had a significant BP rise during ovulation and it primarily occurred at night (P < .05). The results demonstrate that premenopausal hypertensive women have increased testosterone during ovulation and increased testosterone and PRA during the luteal phase of the cycle. Like normotensives, hypertensives with relatively high PRA exhibit no change in BP during the cycle, whereas those with relatively low PRA have a nighttime increase in BP during ovulation.

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To assess left ventricular (LV) structural and functional changes, 45 hypertensive patients were studied by echocardiography after 2 weeks of placebo and 6 months of isradipine monotherapy. Although LV cavity size did not change, LV wall thickness decreased dramatically (P < .0001), producing a significant decrease in LV mass index (from 158 g/m2 to 136 g/m2; P < .0001). In addition, LV fractional shortening (FS) did not change (1.2%; P = NS) whereas the cardiac index increased (6.4%; P = .0007) due to a modest tachycardia accompanied by a reduction in total peripheral resistance (-22.1%; P < .0001). The magnitude of the reduction of LV mass was related to the degree of FS increase (r = -0.70; P < .0001), an indication of beneficial LV remodeling. It can be concluded that isradipine antihypertensive therapy leads to regression of LV hypertrophy without depression of LV pump function.

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

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

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

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A prospective angiographic study of the coronary collateral circulation was performed in 600 consecutive patients found to have significant coronary arterial disease at cardiac catheterization. As the number of diseased coronary vessels increased the evidence of collaterals rose significantly (P = 0.00002) and the intensity of the collateral circulation increased (P = 0.05). For totally occluded lesions the collateral incidence was 70.4%, independent of the particular vessel involved. For stenoses greater than 90% collateral frequency and intensity were significantly greater for lesions of the right coronary artery than of the left anterior descending and the left circumflex arteries. The distribution of the coronary collateral circulation is described quantitatively according to the site of the lesion. Finally, a coronary collateral circulation occurred more frequently (P less than 0.000 001) and excepting Grade I, the intensity of the coronary collateral circulation was significantly greater in patients with a history of acute myocardial infarction.

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