Impaired circadian heart rate variability in Parkinson's disease: a time-domain analysis in ambulatory setting.

BACKGROUND: Heart rate variability (HRV) decreases in Parkinson's disease (PD) and it can be considered a marker for cardiovascular dysautonomia. The purpose of this pilot study is to evaluate long-term time-domain analysis of HRV of PD patients and compare the results with those of matched healthy individuals. METHODS: Idiopathic PD patients without comorbidity impairing HRV, and age-matched healthy individuals were recruited in a pilot study. A long-term time domain analysis of HRV using 24-h ambulatory ECG was performed. RESULTS: Overall, 18 PD patients fulfilling inclusion criteria completed the evaluation (mean age was 55.6 ± 8.8, disease duration: 5.0 ± 4.7). Mean SCOPA-AUT score was 10.1 ± 7.3. Patients were on Hoehn & Yahr stage 1-2 and mean Levodopa Equivalent Dose (LED) was 311 ± 239.9. Mean of the 5-min standard deviation (SD) of R-R intervals distribution (SDNN) for all 5 min segments of the entire recording (ISDNN) was significantly lower in patients compared to controls. ISDNN was significantly different between Parkinson's disease patients and healthy controls. CONCLUSIONS: In our population characterized by mild to moderate disease severity, time-domain assessment of HRV seemed to be a potential tool to characterize cardiovascular dysautonomia. Decrease of ISDNN in PD may reflect an autonomic derangement extending all day and night long.

Arterial stiffness indexes and serum cytokine levels in seronegative spondyloarthritis: relationships between stiffness markers and metabolic and immunoinflammatory variables.

OBJECTIVE: The aim of this study was to investigate the relationship between immunoinflammatory markers and indexes of arterial stiffness in patients with seronegative spondyloarthritis (SpA). METHOD: We enrolled consecutive patients with inflammatory seronegative SpA referred to a rheumatology outpatient clinic. Control subjects were patients admitted in the same period for any cause other than chronic inflammatory disease or acute cardiovascular and cerebrovascular events. Carotid-femoral pulse wave velocity (PWV) was measured and the aortic pressure waveform was used to calculate the augmentation index (Aix). We also evaluated plasma levels of C-reactive protein (CRP), interleukin (IL)-1ß, tumour necrosis factor (TNF)-α, and interleukin (IL)-6 as markers of immunoinflammatory activation. RESULTS: This study enrolled 53 patients with SpA and 55 control subjects. After adjustment for blood glucose, cholesterol, and triglyceride levels, and systolic (SBP) and diastolic blood pressure (DBP), patients with seronegative SpA showed higher mean PWV and Aix compared to controls. Moreover, in patients with seronegative SpA, we observed higher mean plasma levels of IL-6, IL-1ß, and TNF-α in subjects with mean PWV > 8 m/s in comparison with those with PWV < 8 m/s. Multivariate analysis revealed a significant association between PWV > 8 m/s and male gender, age, diabetes, hypertension, low density lipoprotein cholesterol (LDL-C) > 120 mg/dL, total cholesterol (TC) > 200 mg/dL, coronary artery disease (CAD), microalbuminuria, carotid plaque, and plasma levels of IL-6, IL-1ß, and TNF-α. CONCLUSIONS: These findings emphasize the role of inflammatory variables and metabolic factors in indexes of high arterial stiffness. Thus, an inflammatory-metabolic background may influence the pathogenesis of increased arterial stiffness in seronegative inflammatory arthritis.

Obesity and iron deficiency anemia as risk factors for asymptomatic bacteriuria.

BACKGROUND: Few studies examined the risk factors of asymptomatic bacteriuria, showing contradictory results. Our study aimed to examine the association between different clinical and laboratory parameters and asymptomatic bacteriuria in internal medicine patients. MATERIALS AND METHODS: 330 consecutive hospitalized subjects, asymptomatic for urinary tract infections (UTIs), underwent to microscopic examination of urine specimens. 100 subjects were positive for microscopic bacteriuria and were recruited into the study. At the quantitative urine culture 31 subjects of study population were positive while 69 subjects were negative for bacteriuria. RESULTS: The analysis of clinical characteristics showed that the two groups of subjects (positive and negative urine culture for bacteriuria) were significant different (p<0.05) about obesity (76.7% vs 42% respectively), metabolic syndrome (80.6% vs 44,9%), cholelithiasis (35.5% vs 13,2%) and iron deficiency anemia (80.6% vs 53,6%). The univariate analysis showed that only obesity, cholelithiasis and iron deficiency anemia were positively associated with positive urine culture for bacteriuria (Odds Ratios [OR]=3.79, p=0.0003; OR=2,65, p=0.0091; OR=2.63, p=0.0097; respectively). However, the multivariate analysis by logistic regression showed that only obesity and iron deficiency anemia, independently associated with positive urine culture for bacteriuria (OR=3.9695, p=0.0075; OR=3.1569, p=0.03420 respectively). CONCLUSIONS: This study shows that obesity and iron deficiency anemia are independent risk factors for asymptomatic bacteriuria.

Use of QT intervals for a more accurate diagnose of syncope and evaluation of syncope severity.

BACKGROUND: This study aimed to evaluate the use of QT intervals, their diagnostic predictive value in patients with syncope and their relationship with syncope severity. METHODS: One hundred and forty nine patients with a diagnosis of syncope were admitted to Internal Medicine departments at the University of Palermo, Italy, between 2006 and 2012, and 140 control subjects hospitalised for other causes were enrolled. QT maximum, QT minimum, QTpeak, QT corrected, QT dispersion and Tpeak-to-Tend interval were compared between two groups. The paper medical records were used for scoring with San Francisco Syncope Rule (SFSR), Evaluation of Guidelines in SYncope Study (EGSYS) score and Osservatorio Epidemiologico sulla Sincope nel Lazio (OESIL) risk score. RESULTS: Mean QTc (p < 0.0005), mean QTmax (p < 0.0005), mean QTdisp (p < 0.0005), mean QTpeak (p = 0.005) and mean TpTe (p = 0.018) were significantly longer in patients with syncope compared with control subjects. A QTc > 424.8 ms (sensibility: 81.88 - specificity: 57.86) showed the greatest predictive value for diagnosis of syncope. On the EGSYS score and on the OESIL score, QTc was significantly prolonged in high-risk patients compared with low-risk patients. On the San Francisco Syncope Rule, QTc and QTdisp were significantly prolonged in high-risk patients compared with low-risk patients. CONCLUSION: Mean QTc, mean QTdisp, mean TpTe, mean QTmax and mean QTpeak were significantly longer in patients with syncope compared with control subjects. Furthermore, prolonged QTc and QTdisp were associated with major severe syncope according to San Francisco Syncope Rule, EGSYS and OESIL risk scores.

Metabolic and anti-inflammatory effects of a home-based programme of aerobic physical exercise.

AIMS: Regular exercise demonstrated the ability to provide enormous benefits to many diseases, atherosclerotic-based, degenerative and neoplastic, but also to grant anti-inflammatory actions, assessed by various authors in different populations. Despite of these clear benefits, many patients are unable to attain long-term results through chronic physical activity for different causes. On this basis, the aim of our study was to assess the metabolic and anti-inflammatory effects of a home-based programme of fast walking in patients affected by metabolic syndrome (MS). MATERIALS AND METHODS: We enrolled 176 subjects with MS as stated by ATP III criteria. Patients were invited to walk for 1 h every day 5 days a week for 24 weeks. The walking velocity was required higher than the one retained 'comfortable' by the patient, previously assessed in the run-in visit. Monitoring of physical activity was carried out through an OMRON step counter type Walking Style II. All the subjects enrolled completed the training period. RESULTS: After the 24 weeks of intervention body mass index changed from 31.59 to 29.23 (p < 0.001); mean waist circumference passed from 105.19 to 100.06 cm (p < 0.001); mean fasting glucose changed from 119.76 to 114.32 mg/dl (p < 0.001); for diabetic population (n = 70) mean glicated haemoglobin levels changed from 7.38% to 6.86% (p < 0.001); total cholesterol levels from 192.15 to 185.78 mg/dl (p < 0.001); HDL cholesterol levels raised from 44.03 to 47.63 mg/dl (p < 0.001); triglycerides levels lowered from 148.29 to 135.20 mg/dl (p < 0.001); WBC changed from 7361.08 to 7022.56/mm(3) (p < 0.001); hs-CRP from 0.55 to 0.28 mg/dl (p < 0.001); fibrinogen serum levels lowered from 339.68 to 314.86 mg/dl (p < 0.001). CONCLUSIONS: A long-term home-based programme of aerobic physical activity improves metabolic asset and reduces systemic inflammation in sedentary people.

Effects of physical exercise on inflammatory markers of atherosclerosis.

It is well established that physically fit individuals have a reduced risk of developing CVD (cardiovascular disease) and other age-related chronic disorders. Regular exercise is an established therapeutic intervention with an enormous range of benefits. Chronic low-grade systemic inflammation may be involved in atherosclerosis, diabetes and in pathogenesis of several chronic pathological conditions; recent findings confirm that physical activity induces an increase in the systemic levels of a number of cytokines and chemokines with anti-inflammatory properties. The possibility that regular physical exercise exerts anti-inflammation activity, being the interaction between contracting muscle and the other tissues and the circulating cells mediated through signals transmitted by "myokines" produced with muscle contractions. To date the list of myokines includes IL-6, IL-8, and IL-15. During muscle contractions are also released IL-1 receptor antagonis and sTNF-R, molecules that contribute to provide anti-inflammatory actions. Nevertheless discrepancies, analysis of available researches seem to confirm the efficacy of regular physical training as a nonpharmacological therapy having target chronic low-grade inflammation. Given this, physical exercise could be considerate a useful weapon against local vascular and systemic inflammation in atherosclerosis. Several mechanisms explain the positive effect of chronic exercise, nevertheless, these mechanisms do not fully enlighten all pathways by which exercise can decrease inflammation and endothelial dysfunction, and hence modulate the progression of the underlying disease progress.

Effects of ACE-inhibitors and angiotensin receptor blockers on inflammation.

The role of inflammation in cardiovascular disease and in hypertensive disease above all, is complex. Several studies confirm that activation of renin-angiotensin-aldosterone system (RAAS), through increase in the production of angiotensin II (Ang II), is closely related to local vascular inflammation. Over the BP lowering effects of anti-hypertensive treatments, several ancillary effects for every class may be found, distinguishing the various drugs from one another. Given the pro-inflammatory effects of Ang II and aldosterone, agents that interfere with the components of RAAS, such as ACE inhibitors, Angiotensin Receptor Blockers (ARBs), and mineralocorticoid receptor antagonists (spironolactone or the more selective eplerenone), represent logical therapeutic tools to reduce vascular inflammation and cardiovascular risk, as suggested in large clinical trials in patients with hypertension and diabetes. Regarding ACE inhibitors, actually there is no convincing evidence indicating that ACEi's reduce plasma levels of major inflammatory markers in hypertension models. Lack of evidence concerns especially these inflammation markers, such as fibrinogen of CRP, which are less closely related to atherosclerotic disease and vascular damage and conversely are affected by several more aspecific factors. Results obtained by trials accomplished using ARBs seem to be more univocal to confirm, although to great extent, these is an anti-inflammatory effect of drugs blocking AT1 receptor. In order to strictly study the effects of blockage of RAAS on inflammation, future studies may explore different strategies by, for example, simultaneously acting on the ACE and the AT1 angiotensin receptors.