Prevalence of oral and maxillofacial lesions in children and adolescents at a regional Brazilian oral pathology service: a retrospective study and the relevant literature review.

PURPOSE: This study assessed the prevalence of maxillofacial lesions in children, i.e., 0-9 years, and adolescents, i.e., 10-19 years, in a Brazilian Oral Pathology Service and compared results with available literature. METHODS: Clinical and histopathological records from January 2007 to August 2020 were analysed and a literature review investigating maxillofacial lesions in paediatric populations was also performed. RESULTS: Overall, "reactive salivary gland lesions" and "reactive connective tissue lesions" were the most prevalent group of soft tissue lesions, affecting children and adolescents equally. From these, mucocele and pyogenic granuloma were the most prevalent histological diagnoses, respectively, regardless of age. These findings were consistent with the 32 studies included. Considering intraosseous lesions, "odontogenic cysts" and "periapical inflammatory lesions" were the most prevalent groups, with no relevant differences between age groups, except for the odontogenic keratocyst, which was more prevalent in adolescents. Moreover, several odontogenic tumours, such as ameloblastic fibroma and odontogenic myxoma, were significantly more prevalent in children. CONCLUSION: Most maxillofacial lesions presented a similar prevalence between children and adolescents. Reactive salivary gland lesions and reactive connective tissue lesions were the prevailing diagnostic categories, regardless of age. Some odontogenic tumours and the odontogenic keratocyst showed significantly different frequencies across these age groups.

Pre-hospital fibrinolysis in the management of patients with ST elevation acute coronary syndrome: review of the evidence, implementation and future directions.

Time to reperfusion is among the strongest predictors of clinical outcome in patients who present with ST elevation acute myocardial infarction. When time to access is equivalent, primary percutaneous coronary intervention has demonstrated superior outcomes to fibrinolysis. However, where significant delays exist in accessing percutaneous intervention, fibrinolysis has an important role. The potential for fibrinolysis delivery in the pre-hospital setting means that delays to primary percutaneous intervention need to be considered from the time that the patient becomes eligible for fibrinolysis in the field. This can be particularly challenging in patients with symptom duration ofless than two hours, as some evidence suggests fibrinolysis may be particularly beneficial in this early phase. Additionally, access to primary percutaneous intervention provided by an experienced operator, in a timely manner at any time of the day or night, is not an available option in many healthcare settings. This review focuses on the current evidence and practice of pre-hospital fibrinolysis and assesses potential roles for this therapy in the future.

Anti-Platelet Therapy for Acute Coronary Syndrome: A Review of Currently Available Agents and What the Future Holds.

Dual anti-platelet therapy remains a cornerstone in the management of patients suffering from acute coronary syndromes (ACS). The combination of aspirin and clopidogrel has been shown to result in significant reductions in cardiovascular end points including recurrent infarction and death in several randomised control trial of patients with ACS. However, many patients still experience ischaemic events on the combination of aspirin and clopidogrel. Aspirin is a relatively weak anti platelet agent. Clopidogrel is a pro drug that required activation by hepatic metabolism and hence its onset of action is delayed; there is genetic variation in the clinical response to the drug, the platelet inhibition is irreversible and no intravenous form is available. Consequently new anti-platelet agents have been developed to address the short falls of this combination therapy. This paper discusses existing anti-platelet regimes and focuses on novel antiplatelet agents that are currently under clinical evaluation.

High-dose tirofiban with enoxaparin and inflammatory markers in high-risk percutaneous intervention.

AIM: The study assessed the benefit of high bolus dose tirofiban (HD-tirofiban) with enoxaparin compared with HD-tirofiban with unfractionated heparin (UFH). The study examined markers of platelet activation, thrombin generation and inflammation. MATERIALS AND METHODS: The study is a prospective single centre open-label trial of patients with high-risk acute coronary syndrome treated with percutaneous intervention (PCI) who were randomized to anticoagulation with UFH or enoxaparin with HD-tirofiban (25 microg kg(-1) bolus). This study measured a panel of platelet activation markers, inflammatory biomarkers and thrombus generation between the two groups. RESULT: Sixty patients undergoing high-risk PCI were enroled in the study. Platelet inhibition as assessed by whole blood aggregometry following HD-tirofiban infusion was similar in both the UFH and enoxaparin groups. CD40 ligand expression on platelets was significantly reduced following PCI with HD-tirofiban and either UFH or enoxaparin. Following PCI, there were significant reductions measured in other markers of platelet activation including PAC-1, P selectin, factor V/Va, platelet-monocyte aggregates and monocyte expression of Mac-1 as determined by analysis of venous blood samples using flow cytometry. Prothrombin fragment 1+2, D-dimer, von Willebrand factor and high sensitive C-reactive protein levels were significantly less post PCI in the enoxaparin group compared with those patients receiving UFH. CONCLUSION: The combination of HD tirofiban with enoxaparin resulted in an attenuated inflammatory response when compared with that of the combination of HD tirofiban with UFH.

Platelet-monocyte aggregates predict troponin rise after percutaneous coronary intervention and are inhibited by Abciximab.

BACKGROUND: Platelet-monocyte aggregates and other markers of platelet activation were investigated before and after percutaneous coronary intervention (PCI) with abciximab therapy. The study sought to assess the relationship between the level of platelet-monocyte aggregation and increases in cardiac troponin I post coronary intervention. METHODS: Blood samples were collected from 40 patients before PCI and 10 min after abciximab administration. These were tested for platelet activation markers by flow cytometry. Cardiac troponin I levels were assayed at baseline and at 24 h post PCI. RESULTS: Compared to healthy controls, patients with coronary artery disease had elevated markers of platelet activation including platelet-monocyte aggregates, P-selectin and PAC-1 (a marker specific for activated glycoprotein IIb/IIIa) prior to PCI. Increased levels of platelet-monocyte aggregates before PCI were associated with increased expression of P-selectin on the platelet surface. Abciximab therapy reduced platelet-monocyte aggregate levels but had no effect on P-selectin expression. The high levels of expression of activated glycoprotein IIb/IIIa (PAC-1) on platelets prior to PCI was reduced with abciximab therapy. Patients with higher levels of platelet-monocyte aggregates prior to PCI were more likely to develop an elevation of cardiac troponin I during the 24 h after PCI. CONCLUSIONS: Increased levels of platelet-monocyte aggregates may predict patients at risk for troponin elevation following PCI and identify those most likely to benefit from abciximab.

Failure of current public educational campaigns to impact on the initial response of patients with possible heart attack.

AIMS: The National Heart Foundation of Australia recognizes that the risk of lethal arrhythmias is greater very early after the onset of myocardial infarction and that the more promptly flow can be restored in the infarct-related artery the greater will be the benefits for survival and preservation of heart function. The Heart Foundation has therefore conducted several public media campaigns to encourage patients to seek help more promptly and evaluated their impact. METHODS: Since 1996, we have conducted four surveys of delays preceding admission of patients to coronary care units throughout Australia to assess the impact of the Heart Foundation's media campaigns. Data were collected on 1665 patients who presented to 73 hospitals; information on patient delay was available for 1178 of them. RESULTS: There were no significant differences in patient delay (median 1.5-2.0 h) in the four surveys from 1996 to 2002, nor when patients were categorized by age, sex, presenting diagnosis or history of previous myocardial infarction or coronary revascularization by percutaneous or surgical techniques. CONCLUSION: New approaches are needed to reduce patient-related delay after the onset of symptoms suggesting possible myocardial infarction.

Actinomycin-eluting stent for coronary revascularization: a randomized feasibility and safety study: the ACTION trial.

OBJECTIVES: We sought to demonstrate the safety and performance of the actinomycin D-coated Multilink-Tetra stent(Guidant Corp., Santa Clara, California) in the treatment of patients with single de novo native coronary lesions. BACKGROUND: Drug-eluting stents (DES) releasing sirolimus or paclitaxel dramatically reduce restenosis. The anti-proliferative drug, actinomycin D, which is highly effective in reducing neointimal proliferation in preclinical studies, was selected for clinical evaluation. METHODS: The multi-center, single-blind, three-arm ACTinomycin-eluting stent Improves Outcomes by reducing Neointimal hyperplasia (ACTION) trial randomized 360 patients to receive a DES (2.5 or 10 microg/cm(2) of actinomycin D) or metallic stent (MS). The primary end points were major adverse cardiac events (MACE) at 30 days, diameter stenosis by angiography, tissue effects, and neointimal volume by intravascular ultrasound (IVUS) at six months. When early monitoring revealed an increased rate of repeat revascularization, the protocol was amended to allow for additional follow-up for DES patients. Angiographic control of MS patients was no longer mandatory. RESULTS: The biased selection of DES patients undergoing IVUS follow-up invalidated the interpretation of the IVUS findings. The in-stent late lumen loss and that at the proximal and distal edges were higher in both DES groups than in the MS group and resulted in higher six-month and one-year MACE (34.8% and 43.1% vs. 13.5%), driven exclusively by target vessel revascularization without excess death or myocardial infarction. CONCLUSIONS: The results of the ACTION trial indicate that all anti-proliferative drugs will not uniformly show a drug class effect in the prevention of restenosis.

Actinomycin-eluting stent for coronary revascularization: a randomized / feasibility and safety study: the ACTION trial

OBJECTIVES: We sought to demonstrate the safety and formance of the actinomycin D-coated Multilink-Tetra stent(Guidant Corp., Santa Clara,California) in the treatment of patients with single de novo native coronary lesions. BACKGROUND: Drug-eluting stents (DES) releasing sirolimus or paclitaxel dramatically reduce restenosis. The anti-proliferative drug, actinomycin D, which is highly effective in reducing neointimal proliferation in preclinical studies, was selected for clinical evaluation. METHODS: The multi-center, single-blind,three-arm ACTinomycin-eluting stent Improves Outcomes by reducing Neointimal hyperplasia (ACTION) trial randomized 360 patients to receive a DES (2.5 or 10 microg/cm(2) of actinomycin D) or metallic stent (MS). The primary end points were major adverse cardiac events (MACE) at 30days, diameter stenosis by angiography, tissue effects, and neointimal volume by intravascular ultrasound (IVUS) at six months. When early monitoring revealed an increased rate of repeat revascularization, the protocol was amended to allow for additional follow-up for DES patients. Angiographic control of MS patients was no longer mandatory. RESULTS: The biased selection of DES patients undergoing IVUS follow-up invalidated the interpretation of the IVUS findings. The in-stent late lumen loss and that at the proximal and distal edges were higher in both DES groups than in the MS group and resulted in higher six-month and one-year MACE (34.8% and 43.1% vs. 13.5%), driven exclusively by target vessel revascularization without excess death or myocardial infarction...

Five-year angiographic patency of radial artery bypass grafts.

BACKGROUND: Little information exists regarding mid-term and long-term patency of radial artery grafts. METHODS AND RESULTS: We performed restudy coronary angiography at 5.2+/-0.4 years after surgery on 50 asymptomatic patients who had undergone coronary artery bypass graft surgery, using at least 1 radial artery graft, to determine both graft patency and presence of narrowing. We examined preoperative clinical or angiographic variables that might predict graft occlusion. Radial artery graft patency was 89%, with 91% of grafts free of narrowing. Preoperative New York Heart Association anginal class < or =2, target vessel proximal stenosis < or =70%, and small target vessel supply territory were predictive of graft occlusion. CONCLUSIONS: At 5 years after surgery, radial artery grafts have disease-free patency rates that are similar to other graft types.

Use of an accelerated chest pain assessment protocol in patients at intermediate risk of adverse cardiac events.

OBJECTIVE: To determine the feasibility, safety and effectiveness of a structured clinical pathway for stratification and management of patients presenting with chest pain and classified as having intermediate risk of adverse cardiac outcomes in the subsequent six months. DESIGN: Prospective clinical audit. PARTICIPANTS AND SETTING: 630 consecutive patients who presented to the emergency department of a metropolitan tertiary care hospital between January 2000 and June 2001 with chest pain and intermediate-risk features. INTERVENTION: Use of the Accelerated Chest Pain Assessment Protocol (ACPAP), as advocated by the "Management of unstable angina guidelines--2000" from the National Heart Foundation and the Cardiac Society of Australia and New Zealand. MAIN OUTCOME MEASURE: Adverse cardiac events during six-month follow-up. RESULTS: 409 patients (65%) were reclassified as low risk and discharged at a mean of 14 hours after assessment in the chest pain unit. None had missed myocardial infarctions, while three (1%) had cardiac events at six months (all elective revascularisation procedures, with no readmissions with acute coronary syndromes). Another 110 patients (17%) were reclassified as high risk, and 21 (19%) of these had cardiac events (mainly revascularisations) by six months. Patients who were unable to exercise or had non-diagnostic exercise stress test results (equivocal risk) had an intermediate cardiac event rate (8%). CONCLUSIONS: This study validates use of ACPAP. The protocol eliminated missed myocardial infarction; allowed early, safe discharge of low-risk patients; and led to early identification and management of high-risk patients.

Limits to sustained energy intake. IV. Effect of variation in food quality on lactating mice Mus musculus.

Observations were made on 30 MF1 mice with their litters. The animals were fed either normal pelleted mouse food (SDS BP Nutrition Ltd) containing 13.4 kJ x g(-1) digestible energy or a specially formulated diet that provided 25% less digestible energy (9.75 kJ x g(-1)) but equivalent amounts of protein and essential minerals and vitamins per gram as the normal diet. Half the animals were switched to the low-energy diet during early pregnancy and half after parturition. The food intake of the two groups increased enormously following parturition, reaching an asymptote over the last few days of lactation. In both groups, the asymptotic food intake exceeded that previously observed across 71 litters of this strain of mice fed the normal diet throughout pregnancy and lactation; the intake of the group fed the low-energy diet from early lactation significantly exceeded that of the mice switched to the low-energy diet after parturition. The increased intakes of the experimental groups were, however, insufficient to offset the lower digestible energy content of the food during lactation. The body mass of the mothers at the end of lactation did not differ between the two experimental groups and the controls. Offspring mass at weaning was inversely related to litter size, but also did not differ between the three groups; pup mortality did not differ between the experimental and control groups. Behavioural observations showed that during both the dark and light phases the general activity of the mother declined enormously from early pregnancy to late lactation. In the dark phase, the time spent in general activity was replaced by time spent both feeding and resting (suckling young), but in the light phase it was replaced only by feeding. At peak lactation, the mice fed for 30-50% of the dark phase and for 30-40% of the light phase. The data indicate that a previously observed asymptote in food intake during peak lactation at 23 g x day(-1) is unlikely to be a limit mediated centrally by the alimentary tract. A higher central limit may exist, at 26.9 g x day(-1), but this is unlikely to reflect the time available for feeding. The data are consistent with limits on sustainable daily energy intake being mediated by the performance of the mammary glands. Animals appeared to accommodate the demands for milk production within a constrained total energy budget by compensating their behaviour, most notably by reductions in the time spent in 'general activity'.

Sociodemographic characteristics, care, feeding practices, and growth of cohorts of children born to HIV-1 seropositive and seronegative mothers in Nairobi, Kenya.

UNLABELLED: OBJECTIVES To compare sociodemographic profiles, child care, child feeding practices and growth indices of children born to HIV-1 seropositive and seronegative mothers. METHODS: A cohort study of 234 children (seropositive and seronegative) born to HIV-1 seropositive mothers and 139 children born to seronegative mothers in Pumwani Maternity Hospital which serves a low-income population in Nairobi, Kenya from December 1991 and January 1994. RESULTS: With few exceptions, at the time of their birth children in all three cohorts had parents with similar characteristics, lived in similar housing in similar geographical areas, had their mothers as their primary care givers, had similar feeding practices and similar growth status and patterns. However, the HIV-1 seropositive mothers were slightly younger (23.8 years vs. 25.0 years, P < 0.01), if married they were less likely to be their husband's first wife (79% vs. 91%, P = 0.02) and more likely to have a one-room house (75% vs. 63%, P = 0.04). All three cohorts had mean Z-scores in length-for-age and in weight-for-height within the normal range (>/= 2.0 Z-scores) from birth to 21 months with the exception of the length-for-age of the seropositive children at the 18-month visit. In all cohorts length-for-age became more compromised than weight-for-length, dropping to about -1.45 Z-score by 21 months; in contrast, weight-for-length dropped to about -0.5 Z-score by this age. The only statistically significant differences in growth indices among the three cohorts were between the two cohorts of seronegative children: those with seronegative mothers were less compromised in length-for-age at 1.5 months (mean Z-score = -0.19 vs. -0.48, P < 0.05) and more compromised in weight-for-length at 6 months (mean Z-score = 0.10 vs. 0.45, P < 0.05) and at 18 months (mean Z-score = -0.73 vs. -0.16, P < 0.05). 27-34% were exclusively breastfed at 1.5 months; 52-61% consumed solid foods in addition to breast milk by 2.5 months. CONCLUSIONS: Low-income HIV-1 seropositive- and seronegative-born children were from families with similar characteristics and similar housing environments. Similar growth patterns in the cohorts suggest that the challenging environment and the choice of weaning foods had an impact on all three cohorts. The aggressive care given the children with HIV-1 seropositive mothers and their children may have reduced the progression and impact of HIV-1 disease on the growth of the seropositive children. Further research is needed to corroborate our findings to be certain that our results are not affected by loss to follow-up bias: we lost the same proportion in all three cohorts but cannot verify that the children we lost had the same growth patterns as those who remained in the study.

Angiographic follow-up and clinical experience with the flexible Tantalum Cordis stent.

The Cordis stent is a flexible, highly radioopaque intracoronary stent engineered from a single Tantalum filament folded into a sinusoidal helical coil. It is premounted on a semicompliant balloon expandable stent delivery system. From September 1995-March 1996, 147 Cordis stents were deployed in 105 patients (aged 58+/-12 yr, 71% male). Clinical indications for stenting were unstable angina in 59 (55%), stable angina in 41 (38%), and acute myocardial infarction in 7 (7%). The target vessel was the right coronary artery in 45%, the left anterior descending in 31%, and the circumflex artery in 22%. One stent was deployed in a vein graft, and one stent was deployed in a left internal mammary artery graft. Stent deployment was achieved in all but one patient. Acute in-stent thrombosis occurred in 3 patients (2.9%). Two of these patients required urgent coronary artery bypass surgery. Subacute stent thrombosis occurred in 2 patients (1.9%). Minimum lumen diameter increased from 0.70+/-0.41 mm to 3.50+/-0.60 mm following stent placement. All patients received aspirin. Eighty-one patients (77%) received ticlopidine, and 4 patients (4%) received warfarin therapy. The mean hospital stay was 3.4+/-2.3 days. Six-month follow-up angiography was performed on 50 out of 55 eligible patients at one of the two institutions involved in this study. Computer-assisted quantitative coronary angiography defined a restenosis rate of 26%. Repeat revascularization was required in 8 patients (14.5%) at 6-mo follow-up. The Tantalum Cordis intracoronary stent is an effective and safe means of treating coronary lesions, even in patients with unstable ischemic syndromes. Acute and subacute rates of in-stent thrombosis were acceptable, and the long-term angiographic restenosis rates and need for repeat revascularization were favorable.

Multiple stent implantation in single coronary arteries: acute results and six-month angiographic follow-up.

A total of 147 stents were implanted (in overlapping manner in 76% of vessels) in a single coronary artery in 59 patients (60 vessels, 97 lesions, 2.45 stents/vessel) over a period of 18 mo using high pressure stent deployment without ultrasound guidance. The indications for stenting were suboptimal percutaneous transluminal coronary angioplasty (PTCA) result (45%), primary prevention of restenosis (44%), acute closure (10%), and restenosis after plain balloon angioplasty (1%). One patient required emergency coronary artery bypass grafting (CABG) (extensive dissection), and one required early intervention with plain balloon angioplasty and intracoronary urokinase for stent thrombosis. There were no deaths. Thirteen patients had recurrence of angina within 6 mo and angiograms were performed in all. These showed intrastent restenosis in nine (all had successful repeat plain balloon angioplasty), development of new disease in other vessels along with restenosis close to the stent in the target vessel in one (underwent elective CABG) and normal angiograms with widely patent stents in three. Forty-five patients (77%) remained free of recurrent angina and 25 of these had follow-up angiograms (56%) at a mean of 172 days, two showing restenosis. Thus, the restenosis rate per patient in the symptomatic group (angiographic follow-up in 100%) was 77% and in the asymptomatic group (angiographic follow-up in 56%) was 8%. The restenosis rate in the subgroup with bailout stenting (n = 6) was 20% (angiographic follow-up in 83%). The overall restenosis rate per patient was 32% (overall angiographic follow-up in 66%). During the 6-mo follow-up period, one patient underwent elective CABG (1.7%), one sustained a non-Q myocardial infarction (1.7%), nine had repeat PTCA to the target vessel (15.5%), and there were no deaths. The event-free survival rate was 77%. Multiple stent implantation aided by high pressure stent deployment without ultrasound guidance and with adjunctive optimal antiplatelet therapy without oral anticoagulation seems to be a useful and effective revascularisation strategy to deal with long lesions and acute dissections with a high procedural success rate. The restenosis rate is acceptable and is not appreciably high as reported in previous studies from the "warfarin era."

Interventional management of acute myocardial infarction (AMI).

The best way to limit infarct size and improve survival in patients with early heart attacks is to restore as quickly as possible patency in the infarct-related artery and blood flow to the threatened myocardium. The value of thrombolytic therapy and aspirin has been shown in large clinical trials. A regimen of accelerated recombinant tissue plasminogen activator is more effective than those using streptokinase. In older patients, there is a greater risk of haemorrhagic stroke; nevertheless, thrombolytic treatment saves more lives because the mortality of myocardial infarction (MI) is higher. Thrombolytic therapy fails to restore blood flow sufficiently rapidly or completely in nearly one-fifth of patients. Its efficacy, therefore, has been compared with immediate or direct angioplasty (PTCA). If it can be done promptly enough, PTCA is superior in preventing recurrent ischaemia and the combined outcome of death or non-fatal reinfarction, and is associated with a lesser risk of intracranial haemorrhage. It may also be cheaper because patients spend less time in hospital and fewer of them require late revascularisation. PTCA should be considered for patients with cardiogenic shock or for those in whom there is a contraindication to thrombolytic therapy. The benefits of prompt treatment have been reduced by excessive delay in reaching hospital and door-to-needle time. After fibrinolysis, coronary angiography and PTCA may be reserved for those with spontaneous angina or exercise-induced ischaemia.

Growth factors released into the coronary circulation after vascular injury promote proliferation of human vascular smooth muscle cells in culture.

OBJECTIVES: This study sought to 1) assess in vivo release of platelet-derived growth factor (PDGF) and basic fibroblast growth factor (bFGF) into the coronary circulation after vascular injury in human subjects; and 2) evaluate mitogenic effects of PDGF and bFGF on the patient's own vascular smooth muscle cells (VSMCs). BACKGROUND: Circumstantial evidence suggests involvement of PDGF and bFGF peptides in the neointimal response to vascular injury. To date, no study has shown biologically active growth factors within the coronary circulation after vascular injury in human subjects. METHODS: In 18 patients, plasma PDGF AB, platelet factor 4 (PF4) and beta-thromboglobulin (beta-TG) levels were measured in coronary sinus blood obtained before and up to 30 min after angioplasty. In five patients undergoing atherectomy, coronary sinus serum was added to cultured VSMCs derived from atherectomy tissue to assess the mitogenic potential of the serum. Mitogenicity attributable to PDGF and bFGF was determined using neutralizing antibodies to these factors. PDGF A, PDGF B and bFGF were localized within the atherectomy tissue using immunocytochemical analysis. RESULTS: Before angioplasty, PDGF AB, PF4 and beta-TG levels were elevated threefold in patients scheduled for angioplasty compared with those in control patients (p < 0.01). Within 5 min of angioplasty, PDGF AB levels increased twofold and returned toward preangioplasty levels at 30 min; PF4 and beta-TG levels remained elevated. Serum obtained at 30 min after atherectomy showed a sixfold increase in mitogenicity compared with preatherectomy serum (p = 0.01). This increase in mitogenicity was reduced by 20%, 40% and 65% in the presence of neutralizing antibodies to PDGF, bFGF and PDGF + bFGF, respectively. PDGF A, PDGF B and bFGF were visualized within the intima of the atherectomy tissue. CONCLUSIONS: The change in plasma PDGF level is consistent with first-phase release of PDGF after vascular injury. The increase in mitogenicity of serum suggests that PDGF and bFGF are biologically active.