[Trazodone Contramid® in clinical practice: personalizing antidepressant intervention]

This paper examines the use of Trazodone Contramid® in major depressive disorder (MDD), with a focus on practical guidance regarding real world challenges. The paper includes clinical case reports, developed for didactic reasons, which detail the practical management with Trazodone Contramid® of patients with MDD and either insomnia or anxiety or dementia or isolated (ipo)manic symptoms, which often fulfill the criteria for a diagnosis of MDD with with anxious distress or MDD with mixed features, according to the new DSM-5 classification

Variations of peripheral markers of serotoninergic system in selected vascular patients

BACKGROUND AND AIM: Serotonin (5-HT), a decarboxylated derivative of tryptophan, is synthesized in the enterochromaffin cells and released into blood stream to be incorporated into platelets. At the site of endothelial lesions, platelets aggregate and secrete 5-HT that presents several vascular actions involved in thrombosis and atherogenesis. In fact, 5-HT may induce vasoconstriction in the presence of endothelial injury, aggregation of platelets, and mitogenesis of arterial smooth muscle cells and endothelial cells. It may also contribute to the vascular inflammation associated with atherogenesis by increasing the synthesis of Interleukin-6 in vascular smooth muscle cells. We evaluated serotonin levels in plasma and platelets of patients with unstable angina and ischemic stroke, to identify an association between serotonin and atherosclerosis of coronary and cerebral arteries. METHODS AND RESULTS: Twenty patients (14 men, 6 women, mean age 69 +/- 10 years) with unstable angina and 15 patients (7 men, 8 women, mean age 81 +/- 10 years) with ischemic stroke were included in the study. Twenty-four healthy subjects matched for age and sex constituted the control group. Blood samples were drawn in the morning to determine plasma and platelet concentrations of serotonin. In patients with unstable angina serotonin levels in platelets were significantly lower (p < 0.001) than those observed in controls, while serotonin concentrations in plasma did not significantly differ from those found in controls. In patients affected by stroke serotonin levels in plasma and in platelets did not significantly differ from those found in normal subjects. CONCLUSIONS: Our findings may contribute to the knowledge to different mechanisms involved in the pathogenesis of cardiac and cerebral ischemia

QTc interval prolongation during infusion with dipyridamole or adenosine

The aim of our study was to discover whether there was a relationship between the QTc interval prolongation on the standard 12-lead electrocardiogram (ECG) and provoked myocardial ischemia. Since the increase of adenosine plasma levels, obtained either with adenosine or dipyridamole (an adenosine reuptake inhibitor) infusion, has been used to test the coronary artery reserve in patients affected by coronary artery disease, the QTc interval modifications during dipyridamole or adenosine echocardiographic stress test were evaluated. Twenty-five patients admitted to our Institute for evaluation of chest pain of suspected myocardial origin underwent an echocardiographic dipyridamole stress test (0.84 mg/kg over 10 min) after discontinuation of antianginal treatment. Of these patients, 10 underwent an echocardiographic adenosine stress test (scalar doses of 50, 75, 100, 140 μg/kg/min) after 48–72 h. The Bazett formula was used to evaluate the QTc interval. After dipyridamole and adenosine administration, a significant prolongation of the QTc interval was observed only in those patients who had positive test results. Our data suggested that QTc interval prolongation during pharmacological stress tests might be considered a marker of myocardial ischemia

Peripheral neuropathy associated with ischemic vascular disease of the lower limbs

This paper deals with the possible identification of somatic and autonomic nerve damage in patients with peripheral obliterative arterial disease (POAD) at different stages of the disease, with a well-reproducible technique like electroneurographic evaluation of nerve conduction. In 64 patients with intermittent claudication, 19 patients with pain at rest, and 7 patients with trophic ulcers, electroneurographic evaluation of motor (tibial and peroneal) and sensory (superficial peroneal and sural) nerve conduction was performed. The median nerve (motor and sensory) was used as control. A severe impairment of sural and superficial peroneal nerve velocities was evident in many claudicant patients and in all patients with pain at rest and trophic ulcers, with a progression in the conduction abnormalities in advanced stages of the disease. Motor nerve conduction showed only minor reductions in patients with claudication and pain at rest, although some of them did show very poor velocity values. In 21 patients with intermittent claudication and sensory nerve abnormalities, the autonomic fibers activity, evaluated by the skin sympathetic response (SSR) test, was significantly depressed, thus suggesting an involvement of the local autonomic system in the ischemic disease. A correlation exists between the severity of the somatic nerve damage and the stage of the vascular insufficiency. However, in the group of claudicant patients, the evidence of similar ischemic threshold (claudication distance) may be associated with a marked difference in the amount of somatic nerve damage. The somatic and autonomic nerve alterations may play a relevant role in the progression of the disease toward critical limb ischemi

Plasma levels of asymmetric dimethylarginine (ADMA) in Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarct and Leukoencephalopathy (CADASIL)

BACKGROUND: Asymmetric dimethylarginine (ADMA) is a marker of endothelial dysfunction and a new independent risk factor for adverse cerebrovascular events in small vessel disease. Conversely, L-arginine (LARG) may have a protective role. METHODS: To assess ADMA, LARG levels and LARG/ADMA ratio in 16 patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) and normal controls, and to look for possible correlations with white matter changes. Plasma levels of ADMA and LARG were assayed by high-performance liquid chromatography in all subjects. The overall T(1) and T(2) lesion load was obtained from brain MRI of patients with CADASIL. RESULTS: ADMA plasma concentrations (1.5 +/- 2.0 microM) were significantly higher (p < 0.05) in CADASIL patients than in controls (0.35 +/- 0.075 microM). Analyzing only CADASIL subjects, an inverse borderline-significant correlation was found between LARG/ADMA (190 +/- 20) and T(2)-weighted lesion volumes (57.9 +/- 46.5; r = -0.578, p = 0.024). CONCLUSION: Our results may indicate the possible coexistence of endothelial dysfunction in CADASIL patients, broadening the range of potentially pathogenetic mechanisms in this disease and providing insights for future therapeutic strategies