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The objective of this study on patients with suspected Acute Coronary Disease (ACS) was to verify with the risk stratification any differences between patients in which the AHA/ACC guidelines were not systematically applied and the same patients in which, retrospectively, the AHA/ACC guidelines were adhered to.Retrospective examination was carried out in our Emergency Department at Rome Policlinico Umberto I on 206 patients (age range 21-88, median age 56.6 +/- 18.9 years) (54.3% males) with symptoms compatible with ACS. All the patients underwent "triage" using code green or code yellow and were sub-divided into 7 subgroups based on degree of risk for death or non-fatal myocardial infarction (MI) at 30 days, (labelled A to G, with A representing highest risk and G the least at-risk) in accordance with the ACC/AHA guidelines. Each patient was then examined for: fi nal outcome, admittance and discharge from hospital, refusal of admittance, death.Of the 206 patients, 48 were judged improperly (23.3%) Of these, 13 were assigned code green rather than code yellow and 11 were assigned code yellow instead of code green. By risk stratification in accordance with the AHA/ACC guidelines, 128 patients (62.1%) belonging to subgroups A,B,C and D should have required hospitalization. Seventy eight patients belonging to subgroups E,F and G should have been sent for observation at the Chest Pain Unit (CPU), 54 from this group would have been potentially discharged after 6-12 hours of negative clinical observation. Actually, hospitalization was requested for 132 patients (64%) of whom 78 accepted, 50 declined and 4 were deceased before admission; 74 patients (35.9%) were discharged after brief observation. Risk stratification for 30 day mortality or non fatal MI emphasizes that 8 of the patients hospitalized should have been treated at the CPU (unwarranted hospitalization). Twenty four of the 50 patients who declined hospitalization should have benefited by brief observation at the Chest pain Unit. Twenty eight of the 78 patients examined in the Emergency Department and later discharged should have been hospitalized (wrong discharge).This study, even if limited by time restriction, provides enough evidence in support of the effectiveness of the ACC/AHA guidelines to determine subgroups and to correctly determine groups according to level of risk, thus limiting unwarranted hospitalizations and wrong discharges.

Obstructive sleep apnea syndrome (OSAS) is a syndrome in which the principal symptom is apnea during sleep. Hypoxia in OSAS is a stress condition, which when prolonged in time, could alter hypothalamo-hypophysial-suprarenal control and the cortisol cicadian rhythm. We studied 28 patients with OSAS (30-60 years old), 20 female and 8 male. We calculated the OSAS class according to the Simmons classification. Twenty of the 28 patients maintained unmodified cortisol circadian rhythms, while 8 had cortisol levels more elevated in late and nocturnal hours. Holter monitoring showed arterial hypertension in 8 of the 28 patients (the same patients with cortisol circadian rhythm alteration). Our data seem to indicate that when the OSAS patients lack cortisol circadian rhythm they are having arterial hypertension.

Many endoscopists sometimes prefer to perform endoscopies without anaesthetic support, using only benzodiazepines. Endogenous opioid peptides are believed to play an important role in the modulation of pain within the endogenous analgesic system. A group of 40 patients undergoing diagnostic and therapeutic Endoscopic Retrograde Cholangiography and Pancreatography (ERCP) was recruited. Patients were divided into 2 groups according to Visual Analog Scale: pain 1-5 (Group A) and pain 6-10 (Group B). The beta-endorphin baseline values were significantly different between patients of Group A and Group B. Our data show that patients with levels of beta-endorphin over 8 pmol/L were less sensitive to pain, so that they become candidates for a traditional utilization of the benzodiazepines. However in the patients with beta-end levels less of 8 pmol/L should be suitable an anaesthetic as propofol because strong pain might provoke neurohumoral reflexes, cardiovascular alterations, and even a heart attack.

Met-enkephalin plasma levels were evaluated in 20 cardioischemic diabetic patients. All the patients had ECG ischemic signs. Ten patients with diabetic autonomic neuropathy, experienced no pain during myocarial ischemia. Met-enkephalin levels in the diabetic patients with silent myiocardial ischemia were significantly lower compared to those in the symptomatic patients. This demonstrates that the absence of myocardial ischemic pain in neuropathic diabetic patients is not accounted for by met-enkephalin action.

Atrial pacing (AP) procedure was carried out in 11 cardioischemic patients to reproduce tachycardia-induced myocardial ischemia. Six control subjects underwent the same procedure until the maximum pacing rate was reached. During the procedure, endothelin-1 (ET-1) and plasma lactate levels were measured in the coronary sinus and in the aortic root. In all the patients, atrial pacing provoked electrocardiographic signs and metabolic evidence of myocardial ischemia and a significant decrease (p0.001) in left ventricular ejection fraction. At AP-induced ischemia, coronary sinus (17.31 +/- 4.20 pg/mL) and arterial (9.60 +/- 3.31 pg/mL) ET-1 plasma levels were significantly different (p0.001) in the patients. On the contrary, at maximum pacing rate, no significant difference (p=0.186) emerged between coronary sinus (9.72 +/- 1.09 pg/mL) and arterial (8.95 +/- 0.75 pg/mL) plasma ET-1 levels in the control group. These results suggest that, in cardioischemic patients, tachycardia can induce the coronary endothelium to release significant amounts of ET-1.

Positivity for circulating intercellular adhesion molecule-1 (ICAM-1) in heart transplant recipients has been claimed to predict the development of coronary artery disease and risk of graft failure. Soluble ICAM-1 were evaluated in 32 heart transplant recipients. Five of these patients, who had undergone transplantation several years before, were positive for soluble ICAM-1 but did not present any clinical sign of graft rejection. Furthermore, although heart graft coronary disease was diagnosed in 15 of the 32 patients, they did not show significantly higher titres of soluble ICAM-1 compared to the remaining patients. These findings suggest that major caution is necessary when considering ICAM-1 positivity as a marker of graft disease.

In order to evaluate polymorphonuclear leukocyte (PMN) activity in diabetes mellitus, leukotriene B4 (LTB4) levels were measured in sixty patients, 31 affected with Type 1 diabetes mellitus and 29 affected with Type 2 diabetes mellitus. The LTB4 levels (12.1+/-0.2 pg/100 microl) in diabetic patients were higher compared to those of the control group (7.9+/-0.1 pg/100 microl) (P < 0.001), and remained significantly higher (P < 0.001) (12.8+/-0.2 pg/100 microl) than in the control group (11.0+/-0.2 pg/100 microl) after stimulation with calcium ionophore. A significant and positive correlation between glycated hemoglobin and LTB4 was demonstrated (P < 0.001, r = 0.80). This study demonstrates that in diabetic patients there is a PMN activation and that this activation is correlated to glycated hemoglobin level.

Calcitonin gene-related peptide (CGRP) is a 37 amino acid peptide displaying about 50% homology with amylin which is secreted from the pancreatic islets of Langerhans. The main form, the beta-CGRP, is produced by the enteric nervous system and perivascular nerves of the vasa-vasorum. It represents one of the most powerful vasodilator yet discovered but its role is not yet completely clarified. High levels of this peptide have been shown in patients affected with thyroid medullary carcinoma, phaemocromocytoma and lung carcinoma. Recently circulating levels of CGRP have been found in normal subjects. Endothelin-1 (ET-1), a potent vasoconstrictor peptide, isolated from porcine endothelial cells, is an important regulator of the vascular tone acting in physiological antagonism with atrial natriuretic hormone (ANH). With this study we intended to investigate the presence of any correlation between CGRP and ET-1 in normal subjects.For the study we considered 20 normal subjects (11 males and 9 females) aged 23 to 50.Plasma levels of CGRP and ET-1 were measured by radioimmunological Kit.A positive and significant correlation between calcitonin gene-related peptide and endothelin-1 was found.Our results confirms that CGRP and ET-1 have opposing actions on vessels and that they can act together in haemodinamic regulation.

Atrial natriuretic hormone (ANH) concentrations were measured in 16 patients affected with myotonic dystrophy (MyD) undergoing 24-hour Holter ECG and in 15 age-matched normal subjects. Although the MyD patients did not show overt left ventricular function impairment, their plasma ANH levels were found to be higher (183.76 ± 113.25 pg/ml) compared to those of the control subjects (39.73 ± 9.95 pg/ml, p < 0.001). Nine patients with arrhythmias and some echocardiographic alterations formed subgroup A. Seven patients without cardiac alterations formed subgroup B. No significant difference in ANH emerged between the two subgroups. This evidence suggests that high plasma ANH levels in MyD cannot always be related to overt or latent heart failure and to arrhythmias.

Endothelial cell injury in blood vessels of small arteries and capillaries is considered the primary event in the pathogenesis of systemic sclerosis (SSc). Because endothelin-1 (ET-1) is mainly released in the site of endothelial cell damage, thereby inducing a potent vasoconstriction, it was our intention to study ET-1 release in a group of SSc patients during a cold pressor test (CPT). Twelve SSc patients and a control group of 10 healthy subjects underwent CPT. Blood samples for ET-1 assay were collected at 90 and 180 seconds of exposure to cold stress. Heart rate and blood pressure were recorded at the same intervals. A capillaroscopic examination was performed in both groups before and after CPT. We observed significantly higher levels of plasma ET-1 in SSc patients compared with those of the control group at baseline (P=0.007) and at 90 (P=0.006) and 180 seconds (P=0.03) of CPT. During the test, the capillaroscopic examination showed a dramatic worsening of the vascular picture that was parallel to the increase in ET-1 plasma levels. This suggests that higher ET-1 plasma levels can have a part in the acute vascular reac tivity of SSc patients undergoing CPT.

Pathogenesis of ascites in patients affected by liver cirrhosis is still debated; humoral and haemodynamic factors can play a role. Plasmatic renin activity (PRA), plasmatic aldosterone (PA), atrial natriuretic peptide (ANP) plasma levels, blood Na, K, urea, urinary K and Na were evaluated in 14 patients affected by liver cirrhosis (11 males and 3 females, aged from 38 to 62 years), 8 of them with ascites. The results were compared with those obtained in a control group poised to age and sex to the experimental group. 4 out of 14 patients suffering from ascites unresponsive to medical treatment were submitted to peritoneal venous jugular shunt (PVGS) and blood samples for PRA, PA and ANP were withdrawn immediately before, 4, 8 hours following surgery. The patients affected by liver cirrhosis without ascites showed PRA and PA levels similar to those observed in the control group, while ANP plasma levels were significantly higher (50.6 + 9.6 vs. 39.7 + 9.5 Pg/ml) (p0.02). In patients with ascites ANP, PA and PRA levels were higher than those observed in non ascites patients (ANP = 147.8 + 97.3 vs. 50.6 + 9.6 pg/ml; PA = 20.6 + 2.7 vs 7.8 + 0.8 ng/dl; PRA = 4.48 + 0.5 vs 1.9 + 0.34 ng/ml/h). In patients submitted to PVGS, PA and PRA levels were reduced 4 and 8 hours following the surgery, while ANP levels showed significant increase. A natriuretic and diuretic response has been observed even in the absence of ANP plasma levels variations.(ABSTRACT TRUNCATED AT 250 WORDS)

The syndrome X is a clinical disease characterised by anginous pain with the absence of significant and angiographically visible stenosis of the coronary tree. D. P. M., a 61-year-old woman suffering from biliary lithiasis, underwent cholecystectomy. During the immediate postoperative period, the patient showed difficulty in regaining consciousness and there were electrocardiographic signs of extensive anterior ischemia; prior to the operation only a 1st degree atrio-ventricular block and a positive history of occasional precordial pain had been reported. On the 2nd postoperative day the patient complained of violent retrosternal pain irradiated to the left shoulder. Given that the signs of ischemia had regressed, various instrumental tests were performed: echocardiogram, cycloergometric test, dipyridamole test, cold pressure test, Holter's dynamic ECG, all of which were within the normal; moreover, selective coronarography did not reveal significant stenosis of the coronary tree. The patient was therefore diagnosed as suffering from syndrome X. In the light of the present case, the authors conclusion may be summarised as follows: the diagnosis of syndrome X, which is by definition not easy, may sometimes become critical, as in the present case, since rapid intervention would have enabled prophylactic therapy to be performed to combat surgical stress.

Met-enkephalin (Met-enk) has been demonstrated to modulate myocardial-ischemia mechanisms via the opioid receptors, but no studies are now available on Met-enk levels in the coronary circulation. In this experience Met-enk levels were evaluated in aortic root and in coronary sinus at baseline (T0), during PTCA induced transient ischemia (T1) and during reperfusion (T2). No significant differences were found at any time. Thus, it appears that there is no Met-enk extraction from the coronary circulation during provoked myocardial ischemia and no Met-enk release from the ischemic heart.

The decrease in active hormones that characterizes chronic adrenal insufficiency results in hypovolemia. In some patients, residual adrenal function, mineralocorticoid therapy, and concomitant heart or liver failure, or both, can paradoxically provoke edema. The case report that follows describes a patient with iatrogenically induced anasarca resulting from the unhappy confluence of usually appropriate therapy and coexisting medical conditions.

The authors treated acute flare-ups of chronic bronchitis with a combination of sulfadiazine (SDZ) and trimethoprim (TMP) (cotrimazine). They treated thirty patients for a week, with daily dosages of 900 mg SDZ and 300 mg TMP, in an open trial in comparison with ampicillin 2 g daily. The result of treatment (course and duration of the acute episode, fever, cough, dyspnoea, sputum amount and description, chest sounds, ESR, and WBC count), tested by suitable statistical methods, showed that cotrimazine had excellent therapeutic activity and was readily tolerated; over-all results compared closely with those obtained with ampicillin. In their concluding remarks the authors state that in addition to being effective in the morbid condition selected for trial, cotrimazine offers some advantages over similar combinations of TMP and other sulfonamides, both because of the intrinsic physicochemical and pharmacological properties of SDZ and because of its lower dosage in this combination.