Frequency of left ventricular hypertrophy in non-valvular atrial fibrillation

Left ventricular hypertrophy (LVH) is significantly related to adverse clinical outcomes in patients at high risk of cardiovascular events. In patients with atrial fibrillation (AF), data on LVH, that is, prevalence and determinants, are inconsistent mainly because of different definitions and heterogeneity of study populations. We determined echocardiographic-based LVH prevalence and clinical factors independently associated with its development in a prospective cohort of patients with non-valvular (NV) AF. From the "Atrial Fibrillation Registry for Ankle-brachial Index Prevalence Assessment: Collaborative Italian Study" (ARAPACIS) population, 1,184 patients with NVAF (mean age 72 \ub1 11 years; 56% men) with complete data to define LVH were selected. ARAPACIS is a multicenter, observational, prospective, longitudinal on-going study designed to estimate prevalence of peripheral artery disease in patients with NVAF. We found a high prevalence of LVH (52%) in patients with NVAF. Compared to those without LVH, patients with AF with LVH were older and had a higher prevalence of hypertension, diabetes, and previous myocardial infarction (MI). A higher prevalence of ankle-brachial index 640.90 was seen in patients with LVH (22 vs 17%, p = 0.0392). Patients with LVH were at significantly higher thromboembolic risk, with CHA2DS2-VASc 652 seen in 93% of LVH and in 73% of patients without LVH (p <0.05). Women with LVH had a higher prevalence of concentric hypertrophy than men (46% vs 29%, p = 0.0003). Logistic regression analysis demonstrated that female gender (odds ratio [OR] 2.80, p <0.0001), age (OR 1.03 per year, p <0.001), hypertension (OR 2.30, p <0.001), diabetes (OR 1.62, p = 0.004), and previous MI (OR 1.96, p = 0.001) were independently associated with LVH. In conclusion, patients with NVAF have a high prevalence of LVH, which is related to female gender, older age, hypertension, and previous MI. These patients are at high thromboembolic risk and deserve a holistic approach to cardiovascular prevention

Association of kidney disease measures with risk of renal function worsening in patients with type 1 diabetes

Background: Albuminuria has been classically considered a marker of kidney damage progression in diabetic patients and it is routinely assessed to monitor kidney function. However, the role of a mild GFR reduction on the development of stage 653 CKD has been less explored in type 1 diabetes mellitus (T1DM) patients. Aim of the present study was to evaluate the prognostic role of kidney disease measures, namely albuminuria and reduced GFR, on the development of stage 653 CKD in a large cohort of patients affected by T1DM. Methods: A total of 4284 patients affected by T1DM followed-up at 76 diabetes centers participating to the Italian Association of Clinical Diabetologists (Associazione Medici Diabetologi, AMD) initiative constitutes the study population. Urinary albumin excretion (ACR) and estimated GFR (eGFR) were retrieved and analyzed. The incidence of stage 653 CKD (eGFR < 60 mL/min/1.73 m2) or eGFR reduction > 30% from baseline was evaluated. Results: The mean estimated GFR was 98 \ub1 17 mL/min/1.73m2 and the proportion of patients with albuminuria was 15.3% (n = 654) at baseline. About 8% (n = 337) of patients developed one of the two renal endpoints during the 4-year follow-up period. Age, albuminuria (micro or macro) and baseline eGFR < 90 ml/min/m2 were independent risk factors for stage 653 CKD and renal function worsening. When compared to patients with eGFR > 90 ml/min/1.73m2 and normoalbuminuria, those with albuminuria at baseline had a 1.69 greater risk of reaching stage 3 CKD, while patients with mild eGFR reduction (i.e. eGFR between 90 and 60 mL/min/1.73 m2) show a 3.81 greater risk that rose to 8.24 for those patients with albuminuria and mild eGFR reduction at baseline. Conclusions: Albuminuria and eGFR reduction represent independent risk factors for incident stage 653 CKD in T1DM patients. The simultaneous occurrence of reduced eGFR and albuminuria have a synergistic effect on renal function worsening

High plasma endothelin-1 levels in hypertensive patients with low-renin essential hypertension

Endothelin-1 (ET-1) is a potent vasoconstrictor peptide derived from endothelial cells and may be important in the control of systemic blood pressure (BP) and local brood flow. Immunoreactive ET-1 plasma levels may be normal or elevated in human arterial hypertension, although the exact pathophysiological role of ET-1 remains to be established. The aim of our study was to determine the relationship between the components of the renin-angiotensin-aldosterone system and plasma ET-1 levels in patients with law, normal or high-renin essential hypertension. The study groups included 13 patients with low-renin essential hypertension (average age 43.5 +/- 16.2 years), 16 patients with normal-renin essential hypertension (46.5 +/- 13.4 years), 11 patients with high-renin essential hypertension (40.7 +/- 13.8 years) and 12 healthy subjects (43.1 +/- 11.4 years). Our results demonstrated that the mean ET-1 Values of all patients with essential hypertension were 10.4 +/- 3.4 pg/ml; there was not a statistical correlation between plasma renin activity (PRA) and the ET-1 levels of hypertensives; instead there was a statistically significant correlation between plasma ET-1 and plasma aldosterone (PA) (r = 0.393; P < 0.026). In particular mean plasma ET-1 values in patients with low-renin essential hypertension (12.6 +/- 2.1 pg/ml) were significantly higher (ANOVA = 0.000, P < 0.05) than those of normotensive subjects (7.7 +/- 1.7 pg/ml), patients with normal-renin essential hypertension (8.5 +/- 2.8 pg/ml), and patients with high-renin essential hypertension (9.9 +/- 3.8 pg/ml), respectively. There was a statistical correlation between PA and ET-1 levels in patients with low-renin essential hypertension (r = 0.619, P < 0.024). Our study demonstrated that there was an increase of circulating ET-1 revels in patients with low-renin essential hypertension and ET-1 plasma levels correlated with PA. The results suggest that ET-1 may play an important role in this particular form of human essential hypertension

[Serum activity of angiotensin-converting enzyme and osteocalcin levels in hyperthyroidism

This study was carried out in order to investigate serum changes of osteocalcin (BGP) and angiotensin converting enzyme (SACE) activity in a group of patients with hyperthyroidism. We studied 20 hyperthyroid patients (F 14, M 6; age mean 37.5 +/- 16.8 years) and 13 control subjects (F 11, M 2; age mean 40.3 +/- 7.5 years). In both patients and controls we measured: FT3, FT4, T3, T4, TSH, BGP, SACE. Finally, in patients with hyperthyroidism a TRH test and functional investigations were also performed. We observed that mean SACE levels were significantly increased in hyperthyroid patients (32.06 +/- 10.3 nmol/ml/min) in respect to control subjects (14.66 +/- 3.88 nmol/ml/min) (p = 2.02 E-6). Similarly serum BGP levels were significantly increased in hyperthyroid patients (5.94 +/- 2.55 ng/ml) than in control subjects (2.89 +/- 1.58 ng/ml) (p = 5.66 E-4). There was a significant linear correlation between SACE and T4 levels (r = 0.48; p < 0.05), between serum BGP and T4 (r = 0.50; p < 0.02) and furthermore between SACE and BGP (r = 0.57; p < 0.01). In conclusion both serum BGP and SACE levels are increased in patients with hyperthyroidism and are directly correlated between than and with indexes of thyroid function; therefore, they may be regarded as peripheral indexes of hyperthyroidism

Response of serum angiotensin converting enzyme, plasma renin activity and plasma aldosterone to conventional dialysis in patients on chronic haemodialysis

The aim of this study was to examine serum angiotensin converting enzyme (SACE) activity and the renin-angiotensin-aldosterone system in patients on chronic haemodialysis during one routine dialysis session. Fourteen patients (8 men and 6 women; mean age 51.9 ± 17 years) with end stage renal disease, receiving regular haemodialysis treatment for an average of 6 months, were studied. The patients were dialysed for 4 hours three times a week using cellulose membranes (cuprophan). After an overnight fast blood samples were taken from the patients before and after the haemodialysis session. Serum and plasma were separated and stored at -20°C until assayed for SACE, plasma renin activity (PRA) and plasma aldosterone (PA). For comparison, SACE, PRA and PA were also measured in 8 patients after renal allotransplantation and on treatment with cyclosporin A (5 men, 3 women; mean age 38.9 ± 12.3 years) and in 19 healthy subjects (13 men, 6 women; mean age 38.9 ± 12.3 years). SACE levels in patients with chronic renal failure and on haemodialysis (17.55 ± 9.03 nmol/ml/min) and in patients with renal transplantation (18.12 ± 3.92) were significantly higher than those of the healthy subjects (9.27 ± 1.67) (p < 0.0001, respectively). At the end of the dialysis session SACE levels in patients with chronic renal failure (14.9 ± 7.19) did not increase in respect to pre-dialysis levels (17.55 ± 9.03; p = 0.132). PRA and PA values increased after the dialysis session (p < 0.026 and p < 0.044, respectively). Correlation of SACE with PRA and PA was not demonstrated before or after the dialysis session. In patients with chronic renal failure and on haemodialysis our findings suggest that a disarrangement exists between the circulatory components of the renin-angiotensin-aldosterone system before and after the dialysis session

Angiotensin-converting enzyme activity in stools of healthy subjects and patients with celiac disease

Angiotensin-converting enzyme (ACE) is a dipeptidylcarboxypeptidase that occurs in three types of cells: endothelial, epithelial, and neuroepithelial. ACE activity is present in plasma, urine, and vascular endothelium. High levels of ACE are found in the brush border of human small bowel. The aim of this study was to evaluate ACE activity in human stools and to find a correlation with the intestinal loss of epithelial cells. Fifteen healthy subjects (HS) (8 males, 7 females; age range 6-56 years), 20 patients with celiac disease (CD) (11 males, 9 females; age range 15-53 years), and 18 patients with CD in remission after a gluten-free diet (CD-GFD) (8 males, 10 females; age range 14-54 years) were enrolled in the study. The fecal ACE activity was measured in all groups. Fecal samples were kept at -20 degrees C for a subsequent test. In HS, fecal ACE activity was 21.03 +/- 16.17 nmol/min/100 g (mean +/- SD). In patients with CD with subtotal mucosa atrophy, ACE activity was significantly higher (113 +/- 88.94) than in HS and CD on GFD (36.65 +/- 23.9). We have demonstrated ACE activity in human stools. ACE activity in stools seems to derive from the microvilli of the intestinal mucosa, thus suggesting the potential usefulness of ACE determination as an index of enterocyte damage