Mechanisms of atherothrombosis in chronic obstructive pulmonary disease

Patients affected by chronic obstructive pulmonary disease (COPD) have an increased risk of atherothrombotic acute events, independent of smoking and other cardiovascular risk factors. As a consequence, myocardial ischemia is a relevant cause of death in these patients. We reviewed studies concerning the potential mechanisms of atherothrombosis in COPD. Bronchial inflammation spreads to the systemic circulation and is known to play a key role in plaque formation and rupture. In fact, C-reactive protein blood levels increase in COPD and provide independent prognostic information. Systemic inflammation is the first cause of the hypercoagulable state commonly observed in COPD. Furthermore, hypoxia is supposed to activate platelets, thus accounting for the increased urinary excretion of platelet-derived thromboxane in COPD. The potential metabolic risk in COPD is still debated, in that recent studies do not support an association between COPD and diabetes mellitus. Finally, oxidative stress contributes to the pathogenesis of COPD and may promote oxidation of low-density-lipoproteins with foam cells formation. Retrospective observations suggest that inhaled corticosteroids may reduce atherothrombotic mortality by attenuating systemic inflammation, but this benefit needs confirmation in ongoing randomized controlled trials. Physicians approaching COPD patients should always be aware of the systemic vascular implications of this disease

Aging changes complexity of heart rate dynamics assessed by entropy and Lyapunov exponent analysis

In recent years, many research groups are trying to quantify the physiological signals of an individual, proposing new models to assess the complex dynamics of biological control systems. Indeed, life coincides with the good handling of the structures in the organism and of physiological control mechanisms, while disease and death coincide with the loss of structure and of coordinated functions. The homeodynamic systems which normally govern health are the same that cause pathological events when activated inadequately, or rather, when the balance between order and chaos of the elementary physiological processes is no longer effectively controlled in relation to any type of stress, both external and internal to the body. In a complex system, loss or alteration of communication between physiological signals means pathology. In this paper a signal analysis method based on Entropy (E), Lyapunov exponent (1), Median Absolute Deviation (MAD), Multiscale Entropy (MSE), is proposed to estimate the complexity of long-range temporal correlation heart rate (HR) time series for an elderly person and a young person both healthy. These new methods could improve overall understanding of the physiological system of the human organism, by adopting new models and experimental paradigms, such as those of fractality and entropy, who have the ability to direct from an organ medicine to a modern systemic medicine

Portal vein thrombosis in liver cirrhosis

Portal vein thrombosis (PVT) is observed in 10-20% of patients with liver cirrhosis, which is responsible for 20% of all PVT cases. The main pathogenic factor of PVT in cirrhosis is the obstacle to portal flow, but acquired and inherited clotting abnormalities may play a role. The formation of collateral veins allows many patients to remain asymptomatic and prevents the onset of clinical complications also in patients with totally occlusive PVT. Gastrointestinal bleeding, thrombosis of superior mesenteric vein and refractory ascites are typical manifestations of PVT. Instrumental diagnosis can be obtained by colour-doppler ultrasonography. Future studies should verify whether asymptomatic PVT worsens liver failure, or if its life-threatening complications reduce survival in patients with cirrhosis. Moreover, randomized controlled trials should clarify the potential effectiveness of anticoagulant therapy in the treatment of PVT

Evaluation of D-dimer and factor VIII in cirrhotic patients with asymptomatic portal venous thrombosis

D-dimer and factor VIII levels raise in advanced cirrhosis. We investigated the behavior and the diagnostic usefulness of D-dimer and factor VIII in cirrhotic patients with asymptomatic portal venous thrombosis. Factor VIII coagulant and D-dimer values were measured in 136 consecutive outpatients with stable cirrhosis divided according to Child-Pugh (CP) classification, who underwent color/power ultrasonography to detect portal thrombosis. Portal thrombosis was found in 33 patients (24.2%). In patients without thrombosis, factor VIII was significantly higher in CP class C compared with class A and B. Conversely, class C patients with portal thrombosis had lower factor VIII levels than those without thrombosis. In both groups, D-dimer was significantly increased in class C compared with class A and B. In class C, thrombotic patients showed higher D-dimer values than did patients without thrombosis. In class C, a D-dimer value >= 0.55 mu g/mL provided a sensitivity and a negative predictive value for portal thrombosis of 100%, and a factor VIII coagulant level <= 80% showed a specificity and a negative predictive value of 76% and 84%, respectively. In class B, a D-dimer value <= 0.225 mu g/mL had a sensitivity of 89% and a negative predictive value of 82%. In conclusion, our study shows that factor VIII values increase in severe cirrhosis but significantly decrease in the presence of concomitant portal thrombosis, likely because of consumption during thrombosis; D-dimer is enhanced by both liver failure and portal thrombosis; in severe cirrhosis, normal D-dimer and factor VIII values may safely exclude the presence of asymptomatic portal thrombosis

Community acquired pneumonia in the elderly: the Pneumonia in Italian Acute Care for Elderly units (PIACE) study protocol by the Italian Society of Hospital and Community Geriatrics (SIGOT)

Pneumonia is a frequent cause of hospital admission in elderly patients. Diagnosis of pneumonia in elderly persons with comorbidity may be challenging, due to atypical presentation and complex clinical scenarios. Community-acquired pneumonia (CAP) arises out-of-hospital in subjects without previous contact with the healthcare system. Healthcare associated pneumonia (HCAP) occurs in patients who have frequent contacts with the healthcare system and should be treated with empiric broad spectrum antibiotic therapy also covering multi-drug resistant (MDR) pathogens. Recent findings, however, have questioned this approach, because the worse prognosis of HCAP compared to CAP may better reflect increased level of comorbidity and frailty (poor functional status, older age) of HCAP patients, as well as poorer quality of hospital care provided to such patients, rather than pneumonia etiology by MDR pathogens. The Pneumonia in Italian Acute Care for Elderly units (PIACE) Study, promoted by the Società Italiana di Geriatria Ospedale e Territorio (SIGOT), is an observational prospective cohort study of patients consecutively admitted because of pneumonia to hospital acute care units of Geriatrics throughout Italy. Detailed information regarding clinical presentation, diagnosis, etiology, comprehensive geriatric assessment, antibiotic therapy, possible complications and comorbidities was recorded to identify factors potentially predicting in-hospital mortality (primary endpoint), 3-month mortality, length of hospital stay, postdischarge rate of institutionalization and other secondary endpoints. This paper describes the rationale and method of PIACE Study and reviews the main evidence on pneumonia in the elderly

Baroreflex sensitivity in the elderly with silent myocardial ischemia

In order to assess high-pressure barocepture sensitivity and parasympathetic function in elderly patients with silent myocardial ischemia, we selected 45 inpatients in our geriatric unit for a prospective cohort study of patients with coronary heart disease. All patients were over 65 years of age (37 men and 8 women) and had coronary heart disease, documented by an angiographic study and electrocardiographic evidence of myocardial ischemia during exercise stress testing, performed according to the Bruce protocol. The subjects were divided in three subgroups: group 1 (22 patients) with electrocardiographic and echocardiographic history of myocardial infarction but no angina chest pain during exercise testing; group 2 (13 patients) with no exercise induced chest pain; and group 3 (10 patients) with exercise-induced chest pain. Baroceptor sensitivity was assessed in all subjects, by evaluating heart rate changes expressed in RR interval on the basis of changes in the mean arterial pressure during intra venous infusion of stepwise doses (50-100 and 150 mu g) of phenylephrine hydrochloride. Heart rate changes were also evaluated during overshoot of the Valsalva maneuver (Valsalva max.), providing an index of parasympathetic activity. Our results showed that group two patients (only silent ischemia) had significantly (P> 0.001) greater baroceptor sensitivity than the other two groups (group 2; 15.2 +/- 1.9 ms/mmHg; group 1: 10.0 +/- 1.7 ms/mmHg; and group 3: 9.8 +/- 1.7 ms/mmHg). Group two also showed a significant positive correlation (r = 0.58: P < 0,05) between baroceptor sensitivity and end-diastolic pressure and a significant inverse correlation (r= -0.672; P<0.05) between baroceptor sensitivity and the ejection fraction. Group 2 patients had a significantly longer RR interval than group 1 (P < 0.05) and group 3 (P < 0.05): a significant positive correlation (r = 0.620; P < 0.05) between Valsalva max. and end-diastolic pressure; and a significant inverse correlation (I = 0.694; P < 0.05) between Valsalva max. and the ejection fraction. Valsalva max. and baroceptor sensitivity correlated significantly in all three groups (group 1, r = 0.707; P < 0.001; group 2, r = 0.94; P < 0.001; and group 3; r = 0.833; P < 0.05). In conclusion our data suggest that elderly patients with silent ischemia appear to have an increased capacity for evoking parasympathetic reflexes that could inhibit pain perception. (C) 1997 Elsevier Science Ireland Ltd