Evaluation of dental demands and needs of people experiencing homelessness in the city of Rome, Italy.

OBJECTIVE: Poor oral health and oral diseases are common among people experiencing homelessness. The aim of this study was to evaluate the dental demands and needs of a population of homeless persons in the city of Rome, Italy. PATIENTS AND METHODS: The clinical records of 165 homeless patients admitted between October 2020 and October 2021 to the dental service of the Primary Care Services of the Eleemosynaria Apostolica, Vatican City, were retrospectively reviewed. The service employed dentists to evaluate dental needs and oral conditions in patients experiencing homelessness. The main dental and oral pathological conditions were noted. RESULTS: One hundred and sixty-five records of homeless patients were included in the study. The sample consisted in 138 males (76.97%) and 27 females (23.03%) with a mean age of 46.9 years (range 7-85 years). Acute tooth pain was reported by 132 (80%) patients, 42 (25.45%) had edentulism or missing teeth and 18 (10.91%) patients had oral lesions. Both dental and oral pathologies were intercepted and managed in secondary healthcare facilities. CONCLUSIONS: Given the specific peculiarities of this vulnerable population, it is important to implement strategies that facilitate the access of persons experiencing homelessness to dental evaluation with a preventive and curative perspective.

Long-term arterial patency after coronary reperfusion.

Coronary reocclusion is a frequent event after reperfusion and may be responsible for the deterioration of left ventricular function. It may occur early as well as in the chronic phase after hospital discharge. Current, evidence based, strategies to prevent reocclusion include antiplatelet and anticoagulant agents as well as the use of intracoronary stenting in those patients who are treated by PTCA. The combination of aspirin and ticlopidine adds on the results of stenting. Further treatments are currently investigated and may significantly improve the long-term coronary patency.

[Low-dose aspirin in the long-term treatment of the patient with ischemic heart disease]. / Aspirina a basse dosi nel trattamento a lungo termine del paziente con cardiopatia ischemica.

Coronary atherosclerosis is the process underlying virtually all the clinical manifestations of ischemic heart disease. When ulcer or fissure in the fibrous cap of the atheroma occur, platelet adhesion to subendothelium, aggregation and further platelet recruitment culminate in thrombus formation. These mechanisms are known to be responsible for most cases of acute events in patients with ischemic heart disease. Inside platelets, aspirin blocks the synthesis of thromboxane A2 by irreversibly inhibiting cyclooxygenase. Aspirin is recommended not only for treatment of patients with acute coronary syndromes (unstable angina, acute myocardial infarction), but also for secondary prevention of vascular events in chronic coronary syndromes. Aspirin prevents myocardial infarction in patients with chronic stable angina and reduces mortality, reinfarction and stroke in survivors of an acute myocardial infarction. Aspirin, alone or in combination with dipyridamole, prevents early and late occlusion of aortocoronary vein grafts. It is useful also in patients undergoing coronary angioplasty. Such benefits extend to all patients regardless of age, sex, history of hypertension or diabetes. Higher daily doses (900-1500 mg) are not more effective than lower doses (75-325 mg). Other antiplatelet drugs are not more effective than aspirin, which has the best risk-to-benefit and cost-to-benefit ratios. Ticlopidine is a reasonable alternative for use in preventing vascular events among patients intolerant to aspirin. Warfarin is an effective antithrombotic alternative to aspirin for secondary prevention after a myocardial infarction. However aspirin is easier to administer and follow-up when compared with warfarin. Warfarin should be preferred in high risk patients with left ventricular dysfunction with or without a mural thrombus, and those with associated atrial fibrillation.

[Chronic ischemic cardiopathy: antiplatelet agents and anticoagulants, new protocols for prevention and treatment]. / Cardiopatia ischemica cronica: antiaggreganti ed anticoagulanti, nuovi regimi di profilassi e terapia.

The atherosclerotic process is negatively affected by all the components of the haemostatic system (vascular, platelets, blood coagulation, fibrinolysis). The diseased coronary tree is a high shear rate flow system which, in turn, implies a high number of platelet collisions at sites of vascular injury. This a distinctive feature of coronary thrombosis and illustrates the relevance of blood rheology in thrombosis development. It is appalling how the clinical benefit derived from a conceptually simple intervention such as the partial inhibition of platelet function or blood coagulation is actually discernible by a crude tool such as a clinical trial. Almost all the subgroups take advantage from the treatment and coronary as well as non-coronary events are prevented. Although strong arguments exist for the chronic use of oral anticoagulants in patients with previous myocardial infarction, antiplatelet regimens are more attractive because they do not require any particular skill and are unlikely to determine haemorrhagic complications. New strategies in the chronic antithrombotic treatment of patients with coronary atherosclerosis may involve the pharmacologic manipulation of GpIIb/IIIa (or other platelet integrins) as well as the direct blockade of thrombin. However it is the combination of different antithrombotic agents that appears most promising presently. The combined use of antiplatelet and anticoagulant drugs has already been shown to be effective in acute coronary syndromes and in patients with prosthetic heart valves. It is hoped that the same pattern will be confirmed also in the chronic phase of coronary artery disease by ongoing clinical trials.

Pharmacodynamic characteristics of low-molecular-weight dermatan sulphate after subcutaneous administration in acute myocardial infarction.

Sixteen patients (5 female and 11 male, mean age 59.1 years) who had had an acute myocardial infarction within the previous 7 days, were enrolled in an open pharmacodynamic study. Patients were randomly allocated to two treatment groups and given a single subcutaneous dose of 100 or 200 mg of a new low-molecular-weight dermatan sulphate. The drug pharmacodynamic profile was determined 1, 2, 4, 6, 8, 12 and 24 h after administration. The following coagulation and fibrinolysis tests were performed: activated partial thromboplastin time, thrombin time, activated factor X inhibition, Heptest (global clotting time), heparin cofactor II affinity, functional and antigenic plasminogen activator inhibitor and fibrin plate assay. Both Heptest and heparin cofactor II affinity were significantly increased (P < 0.001) in a dose-dependent manner. The XaI was enhanced, though to a lesser extent. None of the other coagulation or fibrinolysis tests showed significant changes at either dose. Systemic and local tolerance were always very good.

Neurocirculatory asthenia: a reassessment using modern psychosomatic criteria.

The purpose of this study was to assess the prevalence of mental illness and to evaluate the quality of life of patients with neurocirculatory asthenia. A consecutive series of 80 patients who satisfied the diagnostic criteria developed by Kannel et al. for neurocirculatory asthenia was included in this study. Patients underwent a psychiatric diagnostic research interview and extensive psychometric evaluation, with both observer and self-rated scales for depression, anxiety, phobic symptoms, quality of life and abnormal illness behavior. In 47 patients (59%), a psychiatric diagnosis (mainly an anxiety disorder) antedated the onset of neurocirculatory asthenia, which was thus defined as secondary, also because cardiorespiratory symptoms were part of the mental symptoms. In the remaining 33 patients (41%) neurocirculatory asthenia was the primary disorder. Patients with secondary neurocirculatory asthenia reported significantly higher levels of anxiety, depression, social phobia, abnormal illness behavior and an impaired quality of life compared with patients with primary neurocirculatory asthenia. This latter did not significantly differ in these variables (except for depression) from healthy control subjects matched for sociodemographic variables. At a 1-year follow-up, patients with primary neurocirculatory asthenia had a much better prognosis than those with secondary neurocirculatory asthenia. The results indicate the feasibility of the primary/secondary distinction based on the time of onset of mental and cardiorespiratory symptoms in neurocirculatory asthenia. Since only about one quarter of the patients were found to suffer from decreased energy and fatigue according to specified criteria, the terms neurocirculatory asthenia and effort syndrome should probably be discarded.

Benefit of adding low molecular weight heparin to the conventional treatment of stable angina pectoris. A double-blind, randomized, placebo-controlled trial.

BACKGROUND: Patients with chronic coronary artery disease exhibit a dysfunctioning endothelium, which may be responsible for exercise-induced platelet activation and expression of a procoagulant moiety. In this study, we evaluated the therapeutic efficacy of a low molecular weight heparin (Parnaparin) in patients with stable angina pectoris. METHODS AND RESULTS: According to a double-blind, randomized, placebo-controlled trial, 29 patients with stable exercise-induced angina pectoris and angiographically proven coronary artery disease received a single daily subcutaneous injection of Parnaparin or placebo on top of aspirin and conventional antianginal medication over 3 months. Patients randomized to Parnaparin showed a significant decrease in the fibrinogen level (P = .035) and an improvement in both the time to 1-mm ST segment depression (P = .008) and the peak ST segment depression (P = .015). The Canadian Cardiovascular Society class for angina pectoris was also improved by Parnaparin (P = .016). Parnaparin did not affect ADP and collagen-induced platelet aggregation, whereas thrombin-induced aggregation was reduced (P = .0001). The bleeding time was slightly prolonged, but this was not associated with any significant bleeding. CONCLUSIONS: Patients with stable angina pectoris may be treated with Parnaparin in addition to aspirin and conventional antianginal medication. Side effects are negligible, and compliance is excellent.

Comparison of efficacy of low molecular weight heparin (parnaparin) with that of unfractionated heparin in the presence of activated platelets in healthy subjects.

Arterial thrombosis is typically platelet-rich. In this study, it is shown that heparin levels resulting in the usual activated partial thromboplastin time therapeutic range provide only a small anticoagulant effect in the presence of activated platelets. Thrombin inhibition is also negligible when heparin is added to platelet-rich plasma. Aspirin improves the anticoagulant effect of heparin in these circumstances, but the degree of anticoagulation is still considerably lower than that observed in platelet-poor plasma. A low molecular weight heparin (parnaparin) is more active in the presence of activated platelets (such as may occur in acute coronary syndromes) regardless of whether aspirin is used concomitantly.

Spontaneous superoxide generation by polymorphonuclear leukocytes isolated from patients with stable angina after physical exercise.

The activation of circulating polymorphonuclear leukocytes was determined in terms of O2.- generation and elastase release in patients with stable angina (n = 12) and in control subjects (n = 8) after maximal physical exercise and after a 15-min recovery. There was no spontaneous O2.- formation under basal conditions in both groups of patients. On the contrary, there was significant formation of O2.- (p < 0.001) from patients with stable angina measured directly after exercise, along with a slight spontaneous O2.- formation in control subjects (p < 0.05). After recovery, the spontaneous polymorphonuclear leukocyte-O2.- formation decreased but was still present in the patients with stable angina, while in the healthy subjects these values returned to resting levels. The activation of polymorphonuclear leukocytes with phorbol 12-myristate 13-acetate enhanced O2.- formation both in healthy subjects and in patients with stable angina, with a lesser effect in the latter. Moreover, no differences were observed in polymorphonuclear leukocyte-stimulated O2.- formation during the protocol, both in the angina stable patients and healthy subjects. No changes were found in plasma elastase levels among stable angina patients nor in control subjects as a consequence of exercise or recovery. This study indicates there is an early activation of circulating polymorphonuclear leukocytes in terms of O2.- production in stable angina patients during maximal exercise, which is still present after a 15-min recovery. Such activation occurs without elastase release. However, in healthy subjects maximal exercise resulted in very little increase in neutrophil activation.

Effects of two dosages of subcutaneous low molecular weight heparin (Parnaparin) and of unfractionated heparin on fibrin formation and lipolysis in acute myocardial infarction.

Although low molecular weight heparins (LMWH) have been extensively investigated for the prophylaxis and treatment of venous thromboembolism in surgical environments, few data in acute myocardial infarction are available in the literature. In this study two dosages of a new LMWH, Parnaparin, and unfractionated heparin (UF) were investigated in 50 pts with acute myocardial infarction. 20 pts received UF (15.000 units, three subcutaneous injections, Group 1), 20 pts received Parnaparin (6.400 units, single injection, Group 2) and 10 pts received a higher dose of Parnaparin (12.800 units, single injection, Group 3). Similar fibrinopeptide A (FpA) levels were observed in Group 1 and Group 2. In Group 3 the dosage of Parnaparin resulted in a significant prolongation of the APTT and in lower FpA levels. Fibrin formation was decreased by Parnaparin in a concentration-dependent way, according to both the anti-Xa activity and the APTT ratio. Parnaparin did not result in a significant increase in free fatty acid concentration, in comparison with UF. Thus, Parnaparin may offer the advantage of a single subcutaneous injection in patients with acute myocardial infarction.

Enhanced thrombolytic efficacy and reduction of infarct size by simultaneous infusion of streptokinase and heparin.

Because paradoxical increase in thrombin activity was reported after the administration of streptokinase in patients with acute myocardial infarction the velocity of reperfusion and degree of myocardial damage were studied when heparin was infused during rather than after streptokinase infusion. Thirty seven consecutive patients with acute myocardial infarction were randomised to receive intravenous heparin during (group 1, n = 18) or after (group 2, n = 19) streptokinase (1.5 megaunits over 60 minutes). Markers of reperfusion were monitored every 15 minutes for 3 hours. The serum concentration of creatine kinase was measured every 2 hours. The two groups were similar in terms of age and sex distribution, infarct site, time to treatment, and baseline myocardial ischaemia. Patients in group 1 had a significantly shorter mean (SD) reperfusion time (57 (35) minutes v 101 (47)). From 60 to 120 minutes after randomisation there were significant differences in ST segment elevation between the groups. Serum creatine kinase MB peaked earlier (8 (2) hours) in group 1 than in group 2 (10 (4) hours). The peak concentration was significantly lower in group 1 (87 (47) mU/ml) than in group 2 (134 (96) mU/ml) and infarcts were smaller (25.2 (9.8) gram equivalents/m2) in group 1 than in group 2 (35.1 (10.2) gram equivalents/m2). Simultaneous infusion of heparin and streptokinase speeds up the appearance of signs of reperfusion and reduces infarct size.

Comparative haemodynamic effects of transdermal vs intravenous nitroglycerin in acute myocardial infarction with elevated pulmonary artery wedge pressure.

The comparative haemodynamic effects of transdermal and intravenous nitroglycerin were evaluated in 16 patients with haemodynamic and radiographic left heart failure following a recent myocardial infarction. After the control period patients were randomized to transdermal (10 mg(24 h)-1) or intravenous (mean dose: 40 +/- 9 micrograms min-1) nitroglycerin. Haemodynamic parameters were recorded after 0.5,1,2,6,12,18 and 24 h during administration of the drug and 2 h after drug discontinuation. After the washout period the alternate system of nitroglycerin administration was adopted, according to a cross-over design. No differences were found in baseline measurements. Transdermal nitroglycerin reduced the pulmonary artery wedge pressure after 0.5 h (from 21 +/- 5 to 16 +/- 5 mmHg; P less than 0.05). The peak effect occurred at 2 h (12 +/- 5 mmHg). The improvement was sustained over 24 h. Transdermal nitroglycerin also significantly reduced mean pulmonary arterial and right atrial pressures (from 28 +/- 3 to 20 +/- 5 mmHg and from 6 +/- 3 to 2 +/- 2 mmHg at peak effect, respectively). Cardiac index increased from 2.5 +/- 0.6 to 2.8 +/- 0.8 l min-1 m-2 (P less than 0.05). There was no change in heart rate. Similar haemodynamic changes were observed after the intravenous infusion of nitroglycerin. Thus transdermal nitroglycerin is a safe and effective treatment of acute myocardial infarction with signs of left ventricular failure when an intravenous nitroglycerin infusion cannot be properly implemented.

Cardiac neurosis and psychopathology.

Psychiatric illness according to DSM-III-R criteria was investigated in 54 consecutive patients suffering from cardiac neurosis (neurocirculatory asthenia or Da Costa's syndrome). Thirty-seven of the 54 patients (68.5%) were found to suffer from a psychiatric disorder. Generalized anxiety disorder, social phobia and panic disorder accounted for most of the diagnoses. Panic disorder was frequently preceded by (and associated with) generalized anxiety, phobic avoidance and hypochondriasis. The results should alert the physician to inquire for symptoms of an anxiety disorder when a patient presents with cardiac neurosis.