RESUMO
The use of increasingly complex cardiac implantable electronic devices (CIEDs) has increased exponentially in recent years. One of the most serious complications in terms of mortality, morbidity and financial burden is represented by infections involving these devices. They may affect only the generator pocket or be generalised with lead-related endocarditis. Modifiable and non-modifiable risk factors have been identified and they can be associated with patient or procedure characteristics or with the type of CIED. Pocket and systemic infections require a precise evaluation and a specialised treatment which in most cases involves the removal of all the components of the device and a personalised antimicrobial therapy. CIED retention is usually limited to cases where infection is unlikely or is limited to the skin incision site. Optimal re-implantation timing depends on the type of infection and on the results of microbiological tests. Preventive strategies, in the end, include antibiotic prophylaxis before CIED implantation, the possibility to use antibacterial envelopes and the prevention of hematomas. The aim of this review is to investigate the pathogenesis, stratification, diagnostic tools and management of CIED infections.
RESUMO
Despite improvements in the treatment and prevention of risk factors (i.e. dyslipidemia), cardiovascular disease (CVD) remains one of the leading causes of morbidity and mortality in countries with a high degree of socio-economic development. As a matter of fact, in the last decades, several trials and meta-analysis highlighted the impact of treatments targeted to lowering cholesterol levels (particularly LDL-cholesterol) on outcomes of patients affected by CVD, both in terms of primary and secondary prevention. The main international CVD guidelines recommend lifestyle modifications and optimal lipid-lowering therapy in individuals with established CVD. The aim of the present document is to describe the dimension of the problem and the available therapies, offering a practical pharmacological flow-chart useful for accurate monitoring and intensive treatment of dyslipidemias in this patient population.
Assuntos
Doenças Cardiovasculares/prevenção & controle , Dislipidemias/terapia , Prevenção Secundária , Doenças Cardiovasculares/etiologia , Árvores de Decisões , Dislipidemias/complicações , Humanos , Guias de Prática Clínica como AssuntoRESUMO
BACKGROUND: Fractional Flow Reserve (FFR) is currently indicated as a first line strategy for the functional assessment of intermediate coronary stenoses. However, the protocol for inducing hyperemia still lacks standardization. Intracoronary adenosine boli, with a progressive increase to high-dosage, have been proposed as a sensitive and accurate strategy for the classification of coronary stenoses, although being potentially affected by the achievement of plateau of the effect and by a less prolonged and stable hyperemia as compared to intravenous administration. Therefore, the aim of the present study was to define the conditioning parameters and assess the impact of increasing-dose intracoronary adenosine on peak hyperemia duration in patients undergoing FFR for intermediate coronary stenoses. METHODS: FFR was assessed in patients with intermediate (40 to 70%) lesions by pressure-recording guidewire (Prime Wire, Volcano), after induction of hyperemia with intracoronary boli of adenosine (from 60 to 1440⯵g, with dose doubling at each step). Hyperemic duration was defined as the time for the variation form minimum FFR⯱â¯0.02 and time to recovery till baseline values. RESULTS: We included 87 patients, undergoing FFR evaluation of 101 lesions. Mean peak hyperemia duration and time to recovery significantly increased with adenosine doses escalation (pâ¯=â¯0.02 and pâ¯<â¯0.001). Peak hyperemia duration and time to recovery with 1440⯵g adenosine were 14.5⯱â¯12.6â¯s and 45.2⯱â¯30.7â¯s, respectively. Hyperemia duration was not related to Quantitative Coronary Angiography (QCA) parameters or FFR values. In fact, a similar increase in the time of hyperemic peak was noted when comparing patients with positive or negative FFR (pbetweenâ¯=â¯0.87) or patients with lesions < or ≥20â¯mm (pbetweenâ¯=â¯0.92) and lesions involving left main coronary or proximal left anterior descending artery (LAD) (pbetweenâ¯=â¯0.07). A linear relationship was observed between time to recovery and FFR variations, with a greater time to baseline required in patients with FFRâ¯≤â¯0.80 (pâ¯=â¯0.003) and in lesionsâ¯≥â¯20â¯mm (pâ¯=â¯0.006), but not in LAD/LM lesions (pâ¯=â¯0.55). CONCLUSIONS: The present study shows a progressive raise in the duration of peak hyperemia and time to recovery, after the administration of increasing doses of intracoronary adenosine for the assessment of FFR. Therefore, considering the potential advantages of a high-dose adenosine protocol, allowing a more prolonged hyperemia and a more precise and reliable measurement of FFR, further larger studies with such FFR strategy should certainly be advocated to confirm its safety and benefits, before its routinely use recommendation.
Assuntos
Adenosina/administração & dosagem , Angiografia Coronária/métodos , Estenose Coronária/diagnóstico , Reserva Fracionada de Fluxo Miocárdico/efeitos dos fármacos , Hiperemia/fisiopatologia , Idoso , Cateterismo Cardíaco , Estenose Coronária/fisiopatologia , Vasos Coronários , Relação Dose-Resposta a Droga , Feminino , Seguimentos , Humanos , Hiperemia/induzido quimicamente , Infusões Intra-Arteriais , Masculino , Estudos Retrospectivos , Índice de Gravidade de Doença , Vasodilatadores/administração & dosagemRESUMO
BACKGROUND: Residual high-on treatment platelet reactivity (HRPR) still represents a challenging matter in patients with coronary artery disease. Drug-to-drug interaction has been suggested between some statin and antiplatelet agents, despite their co-administration is mandatory in patients after an acute cardiovascular event or coronary stenting. Therefore, the aim of the current study was to investigate any impact of rosuvastatin or atorvastatin co-administration on platelet reactivity in patients receiving dual antiplatelet therapy (DAPT). METHODS: Our population is represented by patients on DAPT (ASA and either clopidogrel 75 mg or ticagrelor 90 mg b.i.d) after an ACS or percutaneous revascularization, and receiving rosuvastatin or atorvastatin. Platelet function was assessed by Multiplate Impedance Aggregometry (Roche Diagnostics AG). RESULTS: We included a total of 374 patients, 240 (64.2%) receiving atorvastatin, 134 (35.8%) rosuvastatin. Rosuvastatin treated patients were more often using beta-blockers (p = 0.05), diuretics (p = 0.04) and displayed higher HDL (p < 0.001) and lower LDL cholesterol (p < 0.001). The prevalence of HRPR for ASA was low, with no difference according to statin type (0.8% vs 1.5%, p = 0.62, adjusted OR[95%CI] = 2[0.23-16.6], p = 0.52). Concerning ADP-antagonists, in the 163 patients treated with clopidogrel, rosuvastatin co-administration was associated with a significantly increased rate of HRPR (55.6%vs 32%, p = 0.01, adjusted OR[95%CI] = 2.69[1.22-5.96], p = 0.015) with higher ADP-mediated platelet reactivity (p = 0.01) and TRAP-test results (p = 0.04). On the contrary, in the 211 ticagrelor treated patients, statin type did not affect mean platelet reactivity or the prevalence of HRPR with ticagrelor (10.5% vs 11.2%, p = 0.99, adjusted OR[95%CI] = 0.86[0.34-2.22], p = 0.76) CONCLUSIONS: Among patients receiving DAPT, rosuvastatin but not atorvastatin is associated with an increased rate of HRPR for clopidogrel, without any influence on the antiplatelet effect of ASA or ticagrelor. Therefore, cautiousness should be exerted for clopidogrel and rosuvastatin therapeutic association.
Assuntos
Adenosina/análogos & derivados , Aspirina/uso terapêutico , Atorvastatina/uso terapêutico , Inibidores da Agregação Plaquetária/uso terapêutico , Agregação Plaquetária/efeitos dos fármacos , Rosuvastatina Cálcica/uso terapêutico , Ticlopidina/análogos & derivados , Adenosina/efeitos adversos , Adenosina/uso terapêutico , Idoso , Aspirina/efeitos adversos , Atorvastatina/efeitos adversos , Distribuição de Qui-Quadrado , Clopidogrel , Interações Medicamentosas , Quimioterapia Combinada , Feminino , Humanos , Modelos Logísticos , Masculino , Pessoa de Meia-Idade , Análise Multivariada , Razão de Chances , Inibidores da Agregação Plaquetária/efeitos adversos , Testes de Função Plaquetária , Polimedicação , Medição de Risco , Fatores de Risco , Rosuvastatina Cálcica/efeitos adversos , Ticagrelor , Ticlopidina/efeitos adversos , Ticlopidina/uso terapêutico , Resultado do TratamentoRESUMO
BACKGROUND: Serum uric acid (SUA) elevation has been largely addressed in the past as a possible risk factor for cardiovascular disease. However, uric acid has not clearly emerged as independent risk factor for coronary artery disease. Several studies in literature have assessed sex-related differences in the association between elevated SUA levels and cardiovascular events with conflicting results. Therefore, aim of the current study was to evaluate the relationship between uric acid levels and the extent of coronary artery disease in male and female patients undergoing coronary angiography. METHODS: Our population is represented by 3520 consecutive patients undergoing coronary angiography from March 2007 to October 2012. Patients were divided according to Tertiles of SUA (Males, Group 1, ≤5.5 mg/dL-0.33 mmol/mol, n = 762, Group 2, 5.5-6.8 mg/dL-0.33-0.40 mmol/mol, n = 829 and Group 3 ≥6.8 mg/dL-0.40 mmol/mol, n = 851), (Females, Group 1, ≤4.8 mg/dL-0.28 mmol/mol, n = 349, Group 2, 4.8-6.3 mg/dL-0.28-0.37 mmol/mol, n = 359 and Group 3 ≥ 6.3 mg/dL-0.37 mmol/mol, n = 370). Fasting samples were collected for uric acid levels assessment. Coronary disease was defined for at least 1 vessel stenosis >50% as evaluated by QCA. Severe coronary disease was defined as three-vessel disease and/or left main disease. RESULTS: Among 3520 patients, we identified 2442 men (69.4%) and 1078 women (30.6%). Males had higher levels of uric acid than women (6.33 ± 1.7 vs 5.8 ± 1.9 - p < 0.001). The association between elevated uric acid (≥7 mg/dl or 0.42 mmol/l) and male gender was confirmed after correction for baseline confounding factors (Adjusted OR = 1.28 [1.01-1.62], p = 0.004). Males displayed a significantly higher prevalence and extent of CAD (p < 0.001) and more complex coronary lesions (p < 0.001). However, no significant relationship was observed between uric acid and CAD (Adjusted OR [95%CI] = 0.90 [0.76-1.06], p = 0.22) or severe CAD (Adjusted OR [95%CI] = 0.89 [0.79-1.01], p = 0.08). Among females, higher SUA levels were significantly associated with higher prevalence of severe CAD (p < 0.001) (Adjusted OR [95% CI] = 1.29 [1.03-1.62], p = 0.03). CONCLUSION: Our study showed that uric acid levels are significantly higher in men. However, high uric acid levels are associated with severe CAD only in women. Future large studies are certainly needed to confirm our findings and to evaluate the effects of SUA lowering therapies on cardiovascular prevention and outcome, especially in women.