This study was the first to examine the effect of tobacco policies in prisons on the health of inmates. Kentucky has two types of tobacco policies in its 16 state prisons: indoor smoke-free policies, where smoking is allowed outdoors and tobacco-free policies, in which no tobacco of any kind is allowed on the grounds of the prison. The smoking rate of inmates is three times higher than that of current smokers in the non-incarcerated population which results in high rates of tobacco-related health conditions such as heart disease and lung cancer. A literature review discussed the evolution of tobacco policies in prisons , the motivations for strengthening policies in prisons and the unintended consequences. Health outcomes in the non-incarcerated population on the benefits to cardiovascular and respiratory health following passage of smoke-free laws in public places were reviewed. No studies have been found on the health outcomes of inmates with varying degrees of smoke-free or tobacco-free policies. The first study was a time series analysis comparing the frequency of medication refills for asthma and/or COPD before and after a tobacco-free policy was implemented. Short-acting inhaler refills decreased in the first few months following the tobacco-free policy date but returned to baseline within 12 to 15 months. Rapid turnover of inmates, minimum security status of the prisons, and possible loosening of enforcement may have been related to the gradual increase in use. The second study was a survival analysis on the time to an inmate’s first acute myocardial infarction (AMI) with tobacco policy status (tobacco-free or smoke-free) of the prison as the primary predictor variable. Controlling for the multiple movements over time, facilities, co-morbidities, past smoking history, age and race, there was a 2.87 hazard for AMI for time spent in a smoke-free (indoors) prison compared to a tobaccofree prison. This finding may be due to the fact that tobacco is considered contraband after prisons become tobacco-free and inmates risk disciplinary action by smuggling or using tobacco in the prison, thereby reducing secondhand smoke for non-smokers and probably reducing the consumption of current smokers.

Referred pain is frequently associated with misdiagnosis and unnecessary therapy directed to the pain location instead of its origin. When craniofacial pain is the sole symptom of myocardial ischemia, failure to recognize its cardiac source can endanger the patient. In particular, patients with acute myocardial infarction (AMI) who do not experience chest pain run a very high risk of misdiagnosis and death. Pain that is limited to the craniofacial region during myocardial ischemia has so far been described only in case reports and its overall prevalence is unknown. Experimental research in animals suggests a vagal involvement in the pathological mechanisms of cardiac pain referred to the face. The aim of this study was to gain knowledge about the prevalence, clinical characteristics and possible mechanisms of craniofacial pain of cardiac origin, in order to improve the clinician’s ability to make a correct diagnosis. It was hypothesized that the quality of craniofacial pain from cardiac versus dental origin would differ, implying a high diagnostic validity. It was also hypothesized that craniofacial pain can be the sole symptom of a prodromal (pre-infarction) angina episode and that this pain location would be especially associated with cardiac ischemia in the areas more densely innervated by vagal afferent fibres. The study group was comprised of consecutive patients who experienced craniofacial pain of a verified cardiac (n=326) or dental (n=359) origin. Demographic details on age, gender and pain characteristics (location, quality and intensity) were assessed in both groups. Cardiovascular risk factors, cardiac diagnosis and ECG signs of ischemia were also assessed in the cardiac pain group. Ethics approval and informed consent for each patient was obtained. Craniofacial pain was found to be the sole symptom of myocardial ischemia in 6% of patients and was the sole symptom of an AMI in 4% of patients; this craniofacial pain was more prevalent in women (p=0.031). In those patients without chest pain, it was the most frequent pain location and was the only symptom of prodromal angina in 5% of AMI patients. The craniofacial pain included the throat, the jaws, the temporomandibular joints/ears and the teeth, mainly bilaterally. The pain quality descriptors “pressure” and “burning” were statistically associated with pain of cardiac origin, while “throbbing” and “aching” were associated with an odontogenic cause (p<0.001). In myocardial ischemia patients, the occurrence of craniofacial pain was associated with an inferior localization of ischemia in the heart (p<0.001). In conclusion, this study showed that pain in the craniofacial region could be the sole symptom of cardiac ischemia and AMI, particularly in women. Craniofacial pain of cardiac origin was commonly bilateral, with the quality pain descriptors “pressure” and “burning”, and pain provocation with physical activity and pain relief at rest. The association between the presence of craniofacial pain and inferior wall ischemia suggests a vagal involvement in the mechanisms of cardiac pain referred to the craniofacial region. Since the possibility of misdiagnosis and death in this group of patients is high, awareness of this clinical presentation needs to be brought to the attention of researchers, clinicians and the general public.

Despite several investigations and interventions aimed at decreasing the time from symptom onset to medical care seeking in acute myocardial infarction patients, the delay time is still too long for best treatment outcomes. In this thesis, investigations aimed at improving our understanding of the factors influencing delay time are evaluated, as well as attitudes to medical care seeking in patients, relatives and the general public. Additionally, an evaluation was performed to examine whether health-related quality of life had any influence on delay time and re-admissions. Participating patients, relatives and representatives of the general public were generally knowledgeable about acute myocardial infarction (AMI) and its symptomatology. The majority of participants knew about the importance of receiving fast treatment when an AMI occurs. Despite people’s knowledge, several patients and relatives felt uncertain of symptom origin and how to act at symptom onset. Patients commonly consulted an additional person when symptoms did not disappear. However, people appeared to act more appropriately if someone else had chest pain compared to self-experienced symptoms. In patients who had suffered from more than one AMI, poor total health status increased the risk of delaying for more than two hours, but no independent association was found between total health status and re-admissions within the first year post-AMI.

Philosophiae Doctor - PhD (Chemistry) / Electrochemiluminescence (ECL) is a light-emitting process generated by electrochemical redox reactions and has been widely used as an analytical tool, especially in the field of biosensing, that is, immunoassays and DNA-probe assays. Thus, the scope of this work was to develop a simple, sensitive ECL immunosensor for cardiac injury and to study and present insights into newly fabricated platforms for bioanalytical applications by using ECL as detection mechanism. / 2021-08-31

Introdução: Embora estatinas sejam benéficas após o infarto agudo do miocárdio (IAM), pouco se sabe sobre seus efeitos quando usadas previamente ao evento. Objetivo: Avaliar o efeito do uso prévio de atorvastatina sobre a função cardiovascular, inflamação e GLUT4 no coração de ratos após IAM (oclusão artéria coronária). Métodos: Ratos Wistar-Kyoto, machos, foram tratados com atorvastatina (20mg/kg) ou veículo (gavagem), 14 dias antes do IAM ou cirurgia sham e avaliação ecocardiográfica 48h pós-IAM (Protocolo A) ou + 7 dias de atorvastatina após IAM e avaliação ecocardiográfica 7 dias pós-IAM (Protocolo B), divididos 16/grupo: C (sham+veículo), I (IAM+veículo), CAt (sham+atorvastatina) e IAt (IAM+atorvastatina). Foram avaliados parâmetros funcionais ecocardiográficos, marcadores inflamatórios plasmáticos e GLUT4 no coração (Western blot). Resultados: A área de infarto foi ~50% nos grupos I e IAt. No protocolo A, a fração de encurtamento foi ~60% maior no grupo IAt vs. I (C:50,9±3,9; CAt:47,9±4,0; I:20,7±3,4; IAt:33,4±3,5 %; p=0,036), o que não ocorreu no protocolo B. A fração de ejeção apresentou redução nos animais após IAM (Protocolo A: ~37%; B: ~30%) e a atorvastatina não melhorou este índice. Houve aumento de GLUT4 (miocárdio, membrana plasmática) pelo IAM 48h pós-IAM: C:35,7±6,0; CAt:32,2±10,9; I:49,8±9,8; IAt:54,1±6,3 UA/g tecido; p<0,001, sem benefício pela atorvastatina, e redução 7 dias pós-IAM: C:50,2±4,4; CAt:52,3±3,1; I:39,0±7,9; IAt:26,4±11,0 UA/g tecido; p<0,001, com prejuízo pela atorvastatina (redução de 32% na membrana plasmática). O IAM determinou aumento de marcadores inflamatórios no plasma, não revertido pelo uso de atorvastatina. Conclusão: Atorvastatina prévia ao IAM melhora a contratilidade no miocárdio precocemente independente do GLUT4 cardíaco, efeito que não foi mantido quando da avaliação mais tardia. / Background: Although statins are beneficial after acute myocardial infarction (AMI), its effects when used prior to this event remains unclear. Aim: To evaluate the effect of prior use of atorvastatin on cardiovascular function, inflammatory state and GLUT4 expression in the rat heart after myocardial infarction (coronary artery occlusion). Methods: Wistar-Kyoto male rats were treated with atorvastatin (20mg/kg) or vehicle (gavage), 14 days before the AMI or sham surgery, and echocardiographic evaluation 48 hours after AMI (protocol A) or atorvastatin + 7 days after AMI and echocardiography 7 days after AMI (Protocol B), allocated 16/grupo: C (sham + vehicle), I (AMI + vehicle), CAt (sham + atorvastatin) and IAt (AMI + atorvastatin). Functional echocardiographic parameters, plasma inflammatory markers and GLUT4 in the heart (Western blot) were measured. Results: Infarcted area was ~50% in groups I and IAt. In protocol A, left ventricular fractional shortening was ~60% higher in the IAt vs. I (C: 50.9 ± 3.9; CAt: 47.9 ± 4.0; I: 20.7 ± 3.4; IAt: 33.4 ± 3.5%, p=0.036), which not occur in protocol B. Ejection fraction was reduced in the animals after acute myocardial infarction (Protocol A: ~37%, B: ~30%) and atorvastatin did not improve this parameter. There was an increase of GLUT4 (plasma membrane) in the Protocol A (C: 35.7 ± 6.0; CAt: 32.2 ± 10.9, I: 49.8 ± 9.8; IAt: 54.1 ± 6.3 AU/g tissue, p<0.001) with no benefit by atorvastatin, and reduction in the Protocolo B (C: 50.2 ± 4.4; CAt: 52.3 ± 3.1; I: 39, 0 ± 7.9; IAt: 26.4 ± 11.0 AU/g tissue, p<0.001), damage by atorvastatin (32% reduction in the plasma membrane). The AMI resulted in an increase of inflammatory markers in plasma, not reversed by the use of atorvastatin. Conclusion: Atorvastatin prior to AMI improves myocardial contractility in early heart independent of GLUT4, an effect that was not maintained when evaluating later.

Introdução: A inflamação e o estresse oxidativo estão associados à progressão do infarto agudo do miocárdio (IAM) para a insuficiência cardíaca (IC). Logo, o tratamento com metilprednisolona, um conhecido glicocorticoide com propriedades anti-inflamatórias e antioxidantes, tem o potencial de mitigar a piora da função do ventrículo esquerdo após o IAM. Entretanto, a utilização de glicocorticoides após o IAM tem apresentado resultados contraditórios que podem ser decorrentes da maneira como são aplicados. Objetivo: Verificar a influência do período de administração de acetato de metilprednisolona sobre a função cardíaca de ratos após o infarto agudo do miocárdio. Materiais e Métodos: No experimento 1, foram utilizados 29 ratos Wistar machos divididos em 3 grupos: Sham (n=14), infartado tratado com salina logo após o IAM (IAM0 n=7) e infartado tratado 7 dias pós-IAM (IAM7 n=8). A função cardíaca foi avaliada 2 e 56 dias pós-IAM pelo exame de ecocardiografia. No experimento 2 foram utilizados 45 ratos Wistar machos divididos em 4 grupos: Sham (Sham, n=13); infartado (IAM, n=14); infartado e tratado com metilprednisolona no dia da indução do infarto (IAM+M0, n=7); infartado e tratado com metilprednisolona no 7º dia após a cirurgia (IAM+M7, n=7). A cirurgia do IAM foi realizada pela oclusão da artéria coronária descendente anterior esquerda. Uma dose única de acetato de metilprednisolona (40mg/kg,i.m.) foi aplicada nos animais dos grupos IAM+M. A função cardíaca foi avaliada pela ecocardiografia e pelo cateterismo ventricular 56 dias após a indução do infarto. Dados morfométricos e de estresse oxidativo do coração foram avaliados No experimento 3, foram utilizados 16 ratos Wistar machos, sendo divididos em 2 grupos: grupo controle tratado com salina no dia 0 (C, n=5) e grupo tratado com acetato de metilprednisolona (40mg/kg. i.m.) no dia 0. A coleta de sangue ocorreu uma vez por semana durante oito semanas, para avaliação de parâmetros do soro. A função cardíaca foi avaliada pelo cateterismo ventricular 56 dias o início da administração farmacológica. Dados morfométricos e de estresse oxidativo do coração foram avaliados. Parecer CEUA/UFRGS: 30797. Resultados: Os grupos IAM e IAM+M0 e IAM+M7 apresentaram área de infarto de 50,4%, 54,8% e 55,1%, respectivamente. A fração de encurtamento e a mudança de área fracional do ventrículo esquerdo diminuíram significativamente (37% e 39%) no grupo IAM em relação ao Sham. O tratamento iniciado no 7º dia promoveu um declínio adicional na mudança da área fracional (66%) quando comparado ao IAM. Tais parâmetros foram semelhantes entre os grupos IAM e IAM+M0. Observamos um aumento de 69% na pressão diastólica final do ventrículo esquerdo (PDFVE) no grupo IAM quando comparado ao grupo Sham. O tratamento com acetato de metilprednisolona, independentemente do tempo de administração, foi capaz de atenuar a PDFVE apenas os grupos IAM e IAM+M7 apresentaram congestão pulmonar. Conclusão: Nossos resultados demonstram que o tratamento com metilprednisolona iniciado logo após o infarto agudo do miocárdio impede ou reverte o aumento da PDFVE e a congestão pulmonar. O tratamento realizado no 7º dia após o IAM também foi eficaz em atenuar a PDFVE, porém não reverteu a congestão pulmonar. Portanto, concluímos que o tratamento iniciado precocemente apresenta potencial em mitigar a transição do IAM para a insuficiência cardíaca. / Introduction: Inflammation and oxidative stress are associated with the progression of acute myocardial infarction (AMI) to heart failure (HF). Therefore, treatment with methylprednisolone, a known glucocorticoid with anti-inflammatory and antioxidant properties, has the potential to mitigate the worsening of left ventricular function after AMI. However, the use of glucocorticoids after AMI has presented contradictory results that may be due to the way they are applied. Aim: To verify the influence of the period of administration of methylprednisolone acetate on the cardiac function of rats after acute myocardial infarction. Materials and Methods: In the experiment 1, 29 male Wistar rats were divided into 3 groups: Sham (n = 14), infarcted treated with saline immediately after AMI (AMI0 n = 7) and infarcted treated 7 days after AMI n = 8). Cardiac function was assessed 2 and 56 days post AMI by echocardiography. In the experiment 2, 45 male Wistar rats were divided into 4 groups: Sham (Sham, n = 13); infarcted (AMI, n = 14); infarcted and treated with methylprednisolone on the day of infarction induction (AMI+M0, n = 7); infarcted and treated with methylprednisolone on the 7th day after surgery (AMI+M7, n = 7). The AMI surgery was performed by occlusion of the left anterior descending coronary artery. A single dose of methylprednisolone acetate (40 mg / kg, i.m.) was applied to animals in the AMI-M groups. Cardiac function was assessed by echocardiography and ventricular catheterization 56 days after infarction induction. Morphometric and oxidative stress of the heart were evaluated. In the experiment 3, 16 male Wistar rats were divided into 2 groups: control group treated with saline at day 0 (C, n = 5) and group treated with methylprednisolone acetate (40mg / kg, im) at day 0 Blood collection occurred once a week for eight weeks for evaluation of serum parameters. Cardiac function was assessed by ventricular catheterization 56 days after initiation of pharmacological administration. Morphometric data and oxidative stress of the heart were evaluated. CEUA / UFRGS opinion: 30797. Results: The AMI and AMI+M0 and AMI+M7 groups presented an infarct area of 50.4%, 54.8% and 55.1%, respectively. The fraction of shortening and the change in fractional area of the left ventricle decreased significantly (37% and 39%) in the AMI group in relation to Sham. The treatment started on day 7 promoted an additional decline in the fractional area change (66%) when compared to AMI. These parameters were similar between the AMI and AMI + M0 groups. We observed a 69% increase in left ventricular end-diastolic pressure (LVEDP) in the AMI group when compared to the Sham group. Treatment with methylprednisolone acetate, irrespective of the time of administration, was able to attenuate LVDEP only the AMI and AMI+M7 groups presented pulmonary congestion. Conclusion: Our results demonstrate that treatment with methylprednisolone initiated shortly after acute myocardial infarction prevents or reverses the increase in LVEDP and pulmonary congestion. Treatment on the 7th day after AMI was also effective in attenuating LVEDP, but did not reverse pulmonary congestion. Therefore, we conclude that the treatment started early has the potential to mitigate the transition from AMI to heart failure.

Introdução: A inflamação e o estresse oxidativo estão associados à progressão do infarto agudo do miocárdio (IAM) para a insuficiência cardíaca (IC). Logo, o tratamento com metilprednisolona, um conhecido glicocorticoide com propriedades anti-inflamatórias e antioxidantes, tem o potencial de mitigar a piora da função do ventrículo esquerdo após o IAM. Entretanto, a utilização de glicocorticoides após o IAM tem apresentado resultados contraditórios que podem ser decorrentes da maneira como são aplicados. Objetivo: Verificar a influência do período de administração de acetato de metilprednisolona sobre a função cardíaca de ratos após o infarto agudo do miocárdio. Materiais e Métodos: No experimento 1, foram utilizados 29 ratos Wistar machos divididos em 3 grupos: Sham (n=14), infartado tratado com salina logo após o IAM (IAM0 n=7) e infartado tratado 7 dias pós-IAM (IAM7 n=8). A função cardíaca foi avaliada 2 e 56 dias pós-IAM pelo exame de ecocardiografia. No experimento 2 foram utilizados 45 ratos Wistar machos divididos em 4 grupos: Sham (Sham, n=13); infartado (IAM, n=14); infartado e tratado com metilprednisolona no dia da indução do infarto (IAM+M0, n=7); infartado e tratado com metilprednisolona no 7º dia após a cirurgia (IAM+M7, n=7). A cirurgia do IAM foi realizada pela oclusão da artéria coronária descendente anterior esquerda. Uma dose única de acetato de metilprednisolona (40mg/kg,i.m.) foi aplicada nos animais dos grupos IAM+M. A função cardíaca foi avaliada pela ecocardiografia e pelo cateterismo ventricular 56 dias após a indução do infarto. Dados morfométricos e de estresse oxidativo do coração foram avaliados No experimento 3, foram utilizados 16 ratos Wistar machos, sendo divididos em 2 grupos: grupo controle tratado com salina no dia 0 (C, n=5) e grupo tratado com acetato de metilprednisolona (40mg/kg. i.m.) no dia 0. A coleta de sangue ocorreu uma vez por semana durante oito semanas, para avaliação de parâmetros do soro. A função cardíaca foi avaliada pelo cateterismo ventricular 56 dias o início da administração farmacológica. Dados morfométricos e de estresse oxidativo do coração foram avaliados. Parecer CEUA/UFRGS: 30797. Resultados: Os grupos IAM e IAM+M0 e IAM+M7 apresentaram área de infarto de 50,4%, 54,8% e 55,1%, respectivamente. A fração de encurtamento e a mudança de área fracional do ventrículo esquerdo diminuíram significativamente (37% e 39%) no grupo IAM em relação ao Sham. O tratamento iniciado no 7º dia promoveu um declínio adicional na mudança da área fracional (66%) quando comparado ao IAM. Tais parâmetros foram semelhantes entre os grupos IAM e IAM+M0. Observamos um aumento de 69% na pressão diastólica final do ventrículo esquerdo (PDFVE) no grupo IAM quando comparado ao grupo Sham. O tratamento com acetato de metilprednisolona, independentemente do tempo de administração, foi capaz de atenuar a PDFVE apenas os grupos IAM e IAM+M7 apresentaram congestão pulmonar. Conclusão: Nossos resultados demonstram que o tratamento com metilprednisolona iniciado logo após o infarto agudo do miocárdio impede ou reverte o aumento da PDFVE e a congestão pulmonar. O tratamento realizado no 7º dia após o IAM também foi eficaz em atenuar a PDFVE, porém não reverteu a congestão pulmonar. Portanto, concluímos que o tratamento iniciado precocemente apresenta potencial em mitigar a transição do IAM para a insuficiência cardíaca. / Introduction: Inflammation and oxidative stress are associated with the progression of acute myocardial infarction (AMI) to heart failure (HF). Therefore, treatment with methylprednisolone, a known glucocorticoid with anti-inflammatory and antioxidant properties, has the potential to mitigate the worsening of left ventricular function after AMI. However, the use of glucocorticoids after AMI has presented contradictory results that may be due to the way they are applied. Aim: To verify the influence of the period of administration of methylprednisolone acetate on the cardiac function of rats after acute myocardial infarction. Materials and Methods: In the experiment 1, 29 male Wistar rats were divided into 3 groups: Sham (n = 14), infarcted treated with saline immediately after AMI (AMI0 n = 7) and infarcted treated 7 days after AMI n = 8). Cardiac function was assessed 2 and 56 days post AMI by echocardiography. In the experiment 2, 45 male Wistar rats were divided into 4 groups: Sham (Sham, n = 13); infarcted (AMI, n = 14); infarcted and treated with methylprednisolone on the day of infarction induction (AMI+M0, n = 7); infarcted and treated with methylprednisolone on the 7th day after surgery (AMI+M7, n = 7). The AMI surgery was performed by occlusion of the left anterior descending coronary artery. A single dose of methylprednisolone acetate (40 mg / kg, i.m.) was applied to animals in the AMI-M groups. Cardiac function was assessed by echocardiography and ventricular catheterization 56 days after infarction induction. Morphometric and oxidative stress of the heart were evaluated. In the experiment 3, 16 male Wistar rats were divided into 2 groups: control group treated with saline at day 0 (C, n = 5) and group treated with methylprednisolone acetate (40mg / kg, im) at day 0 Blood collection occurred once a week for eight weeks for evaluation of serum parameters. Cardiac function was assessed by ventricular catheterization 56 days after initiation of pharmacological administration. Morphometric data and oxidative stress of the heart were evaluated. CEUA / UFRGS opinion: 30797. Results: The AMI and AMI+M0 and AMI+M7 groups presented an infarct area of 50.4%, 54.8% and 55.1%, respectively. The fraction of shortening and the change in fractional area of the left ventricle decreased significantly (37% and 39%) in the AMI group in relation to Sham. The treatment started on day 7 promoted an additional decline in the fractional area change (66%) when compared to AMI. These parameters were similar between the AMI and AMI + M0 groups. We observed a 69% increase in left ventricular end-diastolic pressure (LVEDP) in the AMI group when compared to the Sham group. Treatment with methylprednisolone acetate, irrespective of the time of administration, was able to attenuate LVDEP only the AMI and AMI+M7 groups presented pulmonary congestion. Conclusion: Our results demonstrate that treatment with methylprednisolone initiated shortly after acute myocardial infarction prevents or reverses the increase in LVEDP and pulmonary congestion. Treatment on the 7th day after AMI was also effective in attenuating LVEDP, but did not reverse pulmonary congestion. Therefore, we conclude that the treatment started early has the potential to mitigate the transition from AMI to heart failure.

Introdução: Embora estatinas sejam benéficas após o infarto agudo do miocárdio (IAM), pouco se sabe sobre seus efeitos quando usadas previamente ao evento. Objetivo: Avaliar o efeito do uso prévio de atorvastatina sobre a função cardiovascular, inflamação e GLUT4 no coração de ratos após IAM (oclusão artéria coronária). Métodos: Ratos Wistar-Kyoto, machos, foram tratados com atorvastatina (20mg/kg) ou veículo (gavagem), 14 dias antes do IAM ou cirurgia sham e avaliação ecocardiográfica 48h pós-IAM (Protocolo A) ou + 7 dias de atorvastatina após IAM e avaliação ecocardiográfica 7 dias pós-IAM (Protocolo B), divididos 16/grupo: C (sham+veículo), I (IAM+veículo), CAt (sham+atorvastatina) e IAt (IAM+atorvastatina). Foram avaliados parâmetros funcionais ecocardiográficos, marcadores inflamatórios plasmáticos e GLUT4 no coração (Western blot). Resultados: A área de infarto foi ~50% nos grupos I e IAt. No protocolo A, a fração de encurtamento foi ~60% maior no grupo IAt vs. I (C:50,9±3,9; CAt:47,9±4,0; I:20,7±3,4; IAt:33,4±3,5 %; p=0,036), o que não ocorreu no protocolo B. A fração de ejeção apresentou redução nos animais após IAM (Protocolo A: ~37%; B: ~30%) e a atorvastatina não melhorou este índice. Houve aumento de GLUT4 (miocárdio, membrana plasmática) pelo IAM 48h pós-IAM: C:35,7±6,0; CAt:32,2±10,9; I:49,8±9,8; IAt:54,1±6,3 UA/g tecido; p<0,001, sem benefício pela atorvastatina, e redução 7 dias pós-IAM: C:50,2±4,4; CAt:52,3±3,1; I:39,0±7,9; IAt:26,4±11,0 UA/g tecido; p<0,001, com prejuízo pela atorvastatina (redução de 32% na membrana plasmática). O IAM determinou aumento de marcadores inflamatórios no plasma, não revertido pelo uso de atorvastatina. Conclusão: Atorvastatina prévia ao IAM melhora a contratilidade no miocárdio precocemente independente do GLUT4 cardíaco, efeito que não foi mantido quando da avaliação mais tardia. / Background: Although statins are beneficial after acute myocardial infarction (AMI), its effects when used prior to this event remains unclear. Aim: To evaluate the effect of prior use of atorvastatin on cardiovascular function, inflammatory state and GLUT4 expression in the rat heart after myocardial infarction (coronary artery occlusion). Methods: Wistar-Kyoto male rats were treated with atorvastatin (20mg/kg) or vehicle (gavage), 14 days before the AMI or sham surgery, and echocardiographic evaluation 48 hours after AMI (protocol A) or atorvastatin + 7 days after AMI and echocardiography 7 days after AMI (Protocol B), allocated 16/grupo: C (sham + vehicle), I (AMI + vehicle), CAt (sham + atorvastatin) and IAt (AMI + atorvastatin). Functional echocardiographic parameters, plasma inflammatory markers and GLUT4 in the heart (Western blot) were measured. Results: Infarcted area was ~50% in groups I and IAt. In protocol A, left ventricular fractional shortening was ~60% higher in the IAt vs. I (C: 50.9 ± 3.9; CAt: 47.9 ± 4.0; I: 20.7 ± 3.4; IAt: 33.4 ± 3.5%, p=0.036), which not occur in protocol B. Ejection fraction was reduced in the animals after acute myocardial infarction (Protocol A: ~37%, B: ~30%) and atorvastatin did not improve this parameter. There was an increase of GLUT4 (plasma membrane) in the Protocol A (C: 35.7 ± 6.0; CAt: 32.2 ± 10.9, I: 49.8 ± 9.8; IAt: 54.1 ± 6.3 AU/g tissue, p<0.001) with no benefit by atorvastatin, and reduction in the Protocolo B (C: 50.2 ± 4.4; CAt: 52.3 ± 3.1; I: 39, 0 ± 7.9; IAt: 26.4 ± 11.0 AU/g tissue, p<0.001), damage by atorvastatin (32% reduction in the plasma membrane). The AMI resulted in an increase of inflammatory markers in plasma, not reversed by the use of atorvastatin. Conclusion: Atorvastatin prior to AMI improves myocardial contractility in early heart independent of GLUT4, an effect that was not maintained when evaluating later.

nÃo hà / O estudo tem por objetivo revisar o diagnÃstico de enfermagem (DE) Dor aguda em pacientes hospitalizados com infarto agudo do miocÃrdio (IAM). Estudo metodolÃgico de validaÃÃo de diagnÃsticos de enfermagem, desenvolvido em trÃs etapas fundamentadas no modelo de Hoskins (1989): anÃlise de conceito de dor aguda, validaÃÃo por especialistas e validaÃÃo clÃnica. Na primeira etapa utilizaram-se o modelo de Walker e Avant (2005) e a revisÃo integrativa conforme Whittemore; Knafl (2005) a partir da busca em periÃdicos indexados, por meio do acesso nas bases de dados CINHAL, SCOPUS e PUBMED, de estudos publicados sobre dor aguda no infarto agudo do miocÃrdio no perÃodo de 2006 a 2012. Para a busca nas bases de dados utilizou-se o vocabulÃrio MeSH â Medical Subject Headings of U.S National Library of Medicine e o DeCS â Descritores em CiÃncias da SaÃde em lÃngua inglesa e espanhola: acute pain; myocardial infarction e dolor agudo, el infarto miocardio. Para a busca nas trÃs bases de dados e cruzamento dos descritores utilizou-se o operador booliano âANDâ. Para ampliar a busca empregou-se o cruzamento: âacute painâ and âmyocardial infarctionâ. Aplicados os critÃrios de inclusÃo e exclusÃo, restaram 29 estudos. Encontraram-se quatro atributos crÃticos essenciais para a compreensÃo do conceito dor aguda no infarto agudo do miocÃrdio: qualidade (constrictiva, opressiva, pressÃo, aperto e peso, sensaÃÃo de esmagamento, tÃpica isquÃmica, dilacerante e triturante); localizaÃÃo (regiÃo retroesternal, subesternal, torÃcica, do lado esquerdo do peito, centro do esterno emeio do peito, peito direito); tempo e duraÃÃo (inÃcio sÃbito, prolongada com duraÃÃo de 15 a 30 minutos, recorrente e intermitente); irradiaÃÃo (pescoÃo, ombro esquerdo, mandÃbula, regiÃo interescapular, braÃo direito e esquerdo, costas, estÃmago, abdome, epigastro, pulso braquial e radial esquerdo). Foram identificadas 14 caracterÃsticas definidoras(CDs) na anÃlise de conceito, das quais oito encontraram correspondÃncia no DE Dor aguda da NANDA-I. Elaborou-se um instrumento com a definiÃÃo construÃda na anÃlise de conceito, a constante na NANDA-I e as 14 CDs e respectivas definiÃÃes conceituais e referÃncias empÃricas identificadas. Submeteu-se esse instrumento ao crivo de 22 especialistas em terminologias de enfermagem e/ou dor aguda e/ou infarto agudo do miocÃrdio. Dos especialistas (54,54%) optaram pela definiÃÃo resultante da anÃlise de conceito. ApÃs o julgamento, recomenda-se, alÃm das oito CDs identificadas na NANDA-I, o acrÃscimo de mais seis CDs ao DE Dor aguda identificadas na anÃlise de conceito: Dispneia; Fraqueza; Fadiga; NÃusea; VÃmito e Palidez. As 14 CDs analisadas e validadas por especialistas foram testadas na prÃtica clÃnica, por meio de um estudo transversal realizado com 125 pacientes com diagnÃstico de IAM. Os achados mostraram que Relato de dor aguda, Diaforese, Fadiga, Palidez e Fraqueza, sÃo bons indicadores da ocorrÃncia do diagnÃstico de enfermagem Dor aguda no infarto agudo do miocÃrdio. As CDs PressÃo sanguÃnea elevada, DistÃrbio do sono, FrequÃncia cardÃaca elevada, FrequÃncia respiratÃria elevada, DispnÃia, NÃusea, VÃmito, Ansiedade e Medo nÃo foram indicadores satisfatÃrios do diagnÃstico em estudo. Portanto, cinco CDs demonstraram-se conforme a anÃlise de conceito, validaÃÃo por especialistas e validaÃÃo clÃnica, apropriadas para avaliar o DE Dor aguda em pacientes com IAM. / The objective of the study was the nursing diagnosis validation (ND) of Acute Pain of patient with Acute Myocardial Infarction (AMI). Methodological study developed in three stages of nursing diagnosis validation, found by the Hoskins model (1989): concept analysis, validation by specialists and clinical validation. In the first stage were Walker and Avant model (2005) and Whittemore; Knafl (2005) integrative review from the indexed journal search by the CINHAL, SCOPUS and PUBMED database access of studies published in the period between 2006 and 2012. The Pubmed and Cinahl database search used the indicated terminology, the MeSH â Medical Subject Headings of U.S National Library of Medicine English vocabulary. The Scopus database had DeCS â Descriptors Health Science structure vocabulary. To identify the different uses of acute concept, there was a study survey with the controlled descriptors Acute Pain and Myocardial Infarction in English language and Dolor Agudo and Infarto Miocardio in Spanish language. In the three databases search descriptorÂs crossing we used the Boolean operator âANDâ. âAcute painâ and âmyocardial infarctionâ enlarge the crossing search. After applying the exclusion and inclusion criteria, 29 studies remained (from 535). There were four essential critical characteristics to understand acute pain concept. They are quality (constrictive, oppressive, pressure, tightness and weight, crushing feeling, typical ischemic, heartbreaking and grinding); location (retrosternal region, substernal, chest, the left side of the chest, sternum and through the center of the chest, right chest); time length (sudden onset, prolonged lasting 15 to 30 minutes, recurrent and intermittent); irradiation (neck, left shoulder, jaw, interscapular region, right and left arm, back, stomach, abdomen, epigastrium, left radial and brachial pulse). For the Acute Pain ND, NANDA-I presents 18 defined characteristics (DCs) identifying eight in the concept analysis adequate for Acute Pain diagnosis in AMI patients. Besides these ones, we found six more, in 15 DCs. There were elaboration of an instrument with the concept analysis definition, the constant NANDA-I and 14 DCs and their conceptual definitions and identified empiric references. Twenty-two specialists studied this instrument in nursing terminology and/or acute pain and/or acute myocardial infarction. From them (54,54%) they opted concept analysis definition. After appreciation, there were recommendation of the eight DCs identified in the NANDA-I and six new DCs for the ND Acute pain identified in the concept analysis. They were dyspnea; weakness; fatigue; nausea; Vomiting and paleness. The specialist tested in the clinical practice the 14 analyzed and validated DCs, through a transversal study done with 125 patients with AMI diagnosis. The findings showed that the acute pain, Diaphoresis, Fatigue, Paleness and Weakness are good indicators of the Acute Pain nursing diagnosis. The Elevated Blood Pressure, Sleep Disturbance, Elevated Heart Rate, Elevated Respiratory Rate, Dyspnea, Nausea, Vomiting, Anxiety and Fear DCs, were not satisfactory indicators of the study diagnosis. Therefore, five DCs were according to concept analysis, specialist validation and clinical validation, right to evaluate the Acute Pain ND in AMI patients.

Introdução: Embora estatinas sejam benéficas após o infarto agudo do miocárdio (IAM), pouco se sabe sobre seus efeitos quando usadas previamente ao evento. Objetivo: Avaliar o efeito do uso prévio de atorvastatina sobre a função cardiovascular, inflamação e GLUT4 no coração de ratos após IAM (oclusão artéria coronária). Métodos: Ratos Wistar-Kyoto, machos, foram tratados com atorvastatina (20mg/kg) ou veículo (gavagem), 14 dias antes do IAM ou cirurgia sham e avaliação ecocardiográfica 48h pós-IAM (Protocolo A) ou + 7 dias de atorvastatina após IAM e avaliação ecocardiográfica 7 dias pós-IAM (Protocolo B), divididos 16/grupo: C (sham+veículo), I (IAM+veículo), CAt (sham+atorvastatina) e IAt (IAM+atorvastatina). Foram avaliados parâmetros funcionais ecocardiográficos, marcadores inflamatórios plasmáticos e GLUT4 no coração (Western blot). Resultados: A área de infarto foi ~50% nos grupos I e IAt. No protocolo A, a fração de encurtamento foi ~60% maior no grupo IAt vs. I (C:50,9±3,9; CAt:47,9±4,0; I:20,7±3,4; IAt:33,4±3,5 %; p=0,036), o que não ocorreu no protocolo B. A fração de ejeção apresentou redução nos animais após IAM (Protocolo A: ~37%; B: ~30%) e a atorvastatina não melhorou este índice. Houve aumento de GLUT4 (miocárdio, membrana plasmática) pelo IAM 48h pós-IAM: C:35,7±6,0; CAt:32,2±10,9; I:49,8±9,8; IAt:54,1±6,3 UA/g tecido; p<0,001, sem benefício pela atorvastatina, e redução 7 dias pós-IAM: C:50,2±4,4; CAt:52,3±3,1; I:39,0±7,9; IAt:26,4±11,0 UA/g tecido; p<0,001, com prejuízo pela atorvastatina (redução de 32% na membrana plasmática). O IAM determinou aumento de marcadores inflamatórios no plasma, não revertido pelo uso de atorvastatina. Conclusão: Atorvastatina prévia ao IAM melhora a contratilidade no miocárdio precocemente independente do GLUT4 cardíaco, efeito que não foi mantido quando da avaliação mais tardia. / Background: Although statins are beneficial after acute myocardial infarction (AMI), its effects when used prior to this event remains unclear. Aim: To evaluate the effect of prior use of atorvastatin on cardiovascular function, inflammatory state and GLUT4 expression in the rat heart after myocardial infarction (coronary artery occlusion). Methods: Wistar-Kyoto male rats were treated with atorvastatin (20mg/kg) or vehicle (gavage), 14 days before the AMI or sham surgery, and echocardiographic evaluation 48 hours after AMI (protocol A) or atorvastatin + 7 days after AMI and echocardiography 7 days after AMI (Protocol B), allocated 16/grupo: C (sham + vehicle), I (AMI + vehicle), CAt (sham + atorvastatin) and IAt (AMI + atorvastatin). Functional echocardiographic parameters, plasma inflammatory markers and GLUT4 in the heart (Western blot) were measured. Results: Infarcted area was ~50% in groups I and IAt. In protocol A, left ventricular fractional shortening was ~60% higher in the IAt vs. I (C: 50.9 ± 3.9; CAt: 47.9 ± 4.0; I: 20.7 ± 3.4; IAt: 33.4 ± 3.5%, p=0.036), which not occur in protocol B. Ejection fraction was reduced in the animals after acute myocardial infarction (Protocol A: ~37%, B: ~30%) and atorvastatin did not improve this parameter. There was an increase of GLUT4 (plasma membrane) in the Protocol A (C: 35.7 ± 6.0; CAt: 32.2 ± 10.9, I: 49.8 ± 9.8; IAt: 54.1 ± 6.3 AU/g tissue, p<0.001) with no benefit by atorvastatin, and reduction in the Protocolo B (C: 50.2 ± 4.4; CAt: 52.3 ± 3.1; I: 39, 0 ± 7.9; IAt: 26.4 ± 11.0 AU/g tissue, p<0.001), damage by atorvastatin (32% reduction in the plasma membrane). The AMI resulted in an increase of inflammatory markers in plasma, not reversed by the use of atorvastatin. Conclusion: Atorvastatin prior to AMI improves myocardial contractility in early heart independent of GLUT4, an effect that was not maintained when evaluating later.