Analysis of the population attended through a tele-electrocardiography in mobile emergency medical service

The study presented now had as objective to analyze the population attended by tele-electrocardiography in a public service that is a reference for mobile emergency medical service in the city of Porto Alegre, RS, Brazil. It is a retrospective cross-sectional study. We analyzed all electrocardiograms performed by Samu Porto Alegre, from September 2013 to August 2014, and their medical reports produced remotely by the Hospital do Coração (HCor), SP, Brazil. The study was based on the STROBE (Strengthening Reporting Observational Studies Epidemiology) guidelines. From tele-electrocardiograms, 115 (8.6%) patients were diagnosed having a ST-segment elevation. This electrocardiographic alteration was more prevalent in men (p = 0.012) who were 60 years old or over (p = 0.014). Among the symptoms expressed by patients, 314 (54.3%) men and 726 (56.3%) women felt typical retrosternal chest pain. Syncope was reported by 94 (16.3%) men and 107 (14.2%) women. Dyspnea was a symptom reported by 47 (8.1) men and 84 (11.1) women. The results of the study revealed that electrocardiographic alterations suggesting ACS (Acute Coronary Syndrome) are more prevalent in elderly men. Although women request more frequently the mobile emergency medical service, the ST-segment elevation was more prevalent in men. The chest pain was the most symptom mentioned, a result in agreement with the current literature. The knowledge of our reality can help the organization of service protocols

Sildenafil Preserves Diastolic Relaxation After Reduction By L-name And Increases Phosphodiesterase-5 In The Intercalated Discs Of Cardiac Myocytes And Arterioles.

We investigated the influence of sildenafil on cardiac contractility and diastolic relaxation and examined the distribution of phosphodiesterase-5 in the hearts of hypertensive rats that were treated with by NG-nitro-L-arginine methyl ester (L-NAME). Male Wistar rats were treated with L-NAME and/or sildenafil for eight weeks. The Langendorff method was used to examine the effects of sildenafil on cardiac contractility and diastolic relaxation. The presence and location of phosphodiesterase-5 and phosphodiesterase-3 were assessed by immunohistochemistry, and cGMP plasma levels were measured by ELISA. In isolated hearts, sildenafil prevented the reduction of diastolic relaxation (dP/dt) that was induced by L-NAME. In addition, phosphodiesterase-5 immunoreactivity was localized in the intercalated discs between the myocardial cells. The staining intensity was reduced by L-NAME, and sildenafil treatment abolished this reduction. Consistent with these results, the plasma levels of cGMP were decreased in the L-NAME-treated rats but not in rats that were treated with L-NAME + sildenafil. The sildenafil-induced attenuation of the deleterious hemodynamic and cardiac morphological effects of L-NAME in cardiac myocytes is mediated (at least in part) by the inhibition of phosphodiesterase-5.661253-

Sildenafil preserves diastolic relaxation after reduction by L-NAME and increases phosphodiesterase-5 in the intercalated discs of cardiac myocytes and arterioles

OBJECTIVES: We investigated the influence of sildenafil on cardiac contractility and diastolic relaxation and examined the distribution of phosphodiesterase-5 in the hearts of hypertensive rats that were treated with by NG-nitro-L-arginine methyl ester (L-NAME). METHODS: Male Wistar rats were treated with L-NAME and/or sildenafil for eight weeks. The Langendorff method was used to examine the effects of sildenafil on cardiac contractility and diastolic relaxation. The presence and location of phosphodiesterase-5 and phosphodiesterase-3 were assessed by immunohistochemistry, and cGMP plasma levels were measured by ELISA. RESULTS: In isolated hearts, sildenafil prevented the reduction of diastolic relaxation (dP/dt) that was induced by L-NAME. In addition, phosphodiesterase-5 immunoreactivity was localized in the intercalated discs between the myocardial cells. The staining intensity was reduced by L-NAME, and sildenafil treatment abolished this reduction. Consistent with these results, the plasma levels of cGMP were decreased in the L-NAME-treated rats but not in rats that were treated with L-NAME + sildenafil. CONCLUSION: The sildenafil-induced attenuation of the deleterious hemodynamic and cardiac morphological effects of L-NAME in cardiac myocytes is mediated (at least in part) by the inhibition of phosphodiesterase-5

Insulin Therapy does not Interfere with Venous Endothelial Function Evaluation in Patients with Type 2 Diabetes Mellitus

INTRODUCTION: Endothelium-dependent dilation is improved in insulin-treated diabetic patients, but this effect is probably due to improved glycemic control. The objective of the present study was to compare endotheliumdependent dilation in patients with well-controlled type 2 diabetes who are or are not using insulin as part of their therapy. METHODS: We studied 27 patients with type 2 diabetes (11 women, 60.3 years ¡ 6 years, with HbA1c , 7% and no nephropathy), including 16 patients treated with anti-diabetic agents (No-Ins, 8 women) and 11 patients treated with insulin alone or in combination with anti-diabetic agents (Ins, 3 women). Endothelial function was evaluated by the dorsal hand vein technique, which measures changes in vein diameter in response to phenylephrine, acetylcholine (endothelium-dependent vasodilation) and sodium nitroprusside (endothelium-independent vasodilation). RESULTS: Age, systolic blood pressure (No-Ins: 129.4 mmHg ¡ 11.8 mmHg, Ins: 134.8 mmHg ¡ 12.0 mmHg; P = 0.257), HbA1c, lipids and urinary albumin excretion rate [No-Ins: 9 mg/24 h (0-14.1 mg/24 h) vs. Ins: 10.6 mg/24 h (7.5- 14.4 mg/24 h), P = 0.398] were similar between groups. There was no difference between endothelium-dependent vasodilation of the No-Ins group (59.3% ¡ 26.5%) vs. the Ins group (54.0% ¡ 16.3%; P = 0.526). Endotheliumindependent vasodilation was also similar between the No-Ins (113.7% ¡ 35.3%) and Ins groups (111.9% ¡ 28.5%; P = 0.888). CONCLUSIONS: Subcutaneous insulin therapy does not interfere with venous endothelial function in type 2 diabetes when glycemic and blood pressure control are stable

Hyperglycemia can delay left ventricular dysfunction but not autonomic damage after myocardial infarction in rodents

<p>Abstract</p> <p>Background</p> <p>Although clinical diabetes mellitus is obviously a high risk factor for myocardial infarction (MI), in experimental studies disagreement exists about the sensitivity to ischemic injury of an infarcted myocardium. Recently, our group demonstrated that diabetic animals presented better cardiac function recovery and cellular resistance to ischemic injury than nondiabetics. In the present study, we evaluated the chronic effects of MI on left ventricular (LV) and autonomic functions in streptozotocin (STZ) diabetic rats.</p> <p>Methods</p> <p>Male Wistar rats were divided into 4 groups: control (C, n = 15), diabetes (D, n = 16), MI (I, n = 21), and diabetes + MI (DI, n = 30). MI was induced 15 days after diabetes (STZ) induction. Ninety days after MI, LV and autonomic functions were evaluated (8 animals each group). Left ventricular homogenates were analyzed by Western blotting to evaluate the expression of calcium handling proteins.</p> <p>Results</p> <p>MI area was similar in infarcted groups (~43%). Ejection fraction and +dP/dt were reduced in I compared with DI. End-diastolic pressure was additionally increased in I compared with DI. Compared with DI, I had increased Na⁺-Ca²⁺exchange and phospholamban expression (164%) and decreased phosphorylated phospholamban at serine¹⁶(65%) and threonine¹⁷(70%) expression. Nevertheless, diabetic groups had greater autonomic dysfunction, observed by baroreflex sensitivity and pulse interval variability reductions. Consequently, the mortality rate was increased in DI compared with I, D, and C groups.</p> <p>Conclusions</p> <p>LV dysfunction in diabetic animals was attenuated after 90 days of myocardial infarction and was associated with a better profile of calcium handling proteins. However, this positive adaptation was not able to reduce the mortality rate of DI animals, suggesting that autonomic dysfunction is associated with increased mortality in this group. Therefore, it is possible that the better cardiac function has been transitory, and the autonomic dysfunction, more prominent in diabetic group, may lead, in the future, to the cardiovascular damage.</p

Short-term diabetes attenuates left ventricular dysfunction and mortality rates after myocardial infarction in rodents

OBJECTIVES: To investigate the effects of hyperglycemia on left ventricular dysfunction, morphometry, myocardial infarction area, hemodynamic parameters, oxidative stress profile, and mortality rate in rats that had undergone seven days of myocardial infarction. INTRODUCTION: Previous research has demonstrated that hyperglycemia may protect the heart against ischemic injury. METHODS: Male Wistar rats were divided into four groups: control-sham, diabetes-sham, myocardial infarction, and diabetes + myocardial infarction. Myocardial infarction was induced 14 days after diabetes induction. Ventricular function and morphometry, as well as oxidative stress and hemodynamic parameters, were evaluated after seven days of myocardial infarction. RESULTS: The myocardial infarction area, which was similar in the infarcted groups at the initial evaluation, was reduced in the diabetes + myocardial infarction animals (23 ± 3%) when compared with the myocardial infarction (42 ± 7%, p<0.001) animals at the final evaluation. The ejection fraction (22%, p = 0.003), velocity of circumferential fiber shortening (30%, p = 0.001), and left ventricular isovolumetric relaxation time (26%, p = 0.002) were increased in the diabetes + myocardial infarction group compared with the myocardial infarction group. The diabetes-sham and diabetes + myocardial infarction groups displayed increased catalase concentrations compared to the control-sham and myocardial infarction groups (diabetes-sham: 32± 3; diabetes + myocardial infarction: 35± 0.7; control-sham: 12 ± 2; myocardial infarction: 16 ± 0.1 pmol min-1 mg-1 protein). The levels of thiobarbituric acid-reactive substances were reduced in the diabetes-sham rats compared to the control-sham rats. These positive adaptations were reflected in a reduced mortality rate in the diabetes + myocardial infarction animals (18.5%) compared with the myocardial infarction animals (40.7%, p = 0.001). CONCLUSIONS: These data suggest that short-term hyperglycemia initiates compensatory mechanisms, as demonstrated by increased catalase levels, which culminate in improvements in the ventricular response, infarcted area, and mortality rate in diabetic rats exposed to ischemic injury

Dynamic Aerobic Exercise Induces Baroreflex Improvement in Diabetic Rats

The objective of the present study was to investigate the effects of an acute aerobic exercise on arterial pressure (AP), heart rate (HR), and baroreflex sensitivity (BRS) in STZ-induced diabetic rats. Male Wistar rats were divided into control (n = 8) and diabetic (n = 8) groups. AP, HR, and BRS, which were measured by tachycardic and bradycardic (BR) responses to AP changes, were evaluated at rest (R) and postexercise session (PE) on a treadmill. At rest, STZ diabetes induced AP and HR reductions, associated with BR impairment. Attenuation in resting diabetes-induced AP (R: 103 ± 2 versus PE: 111 ± 3 mmHg) and HR (R: 290 ± 7 versus PE: 328 ± 10 bpm) reductions and BR dysfunction (R: −0.70 ± 0.06 versus PE: −1.21 ± 0.09 bpm/mmHg) was observed in the postexercise period. In conclusion, the hemodynamic and arterial baro-mediated control of circulation improvement in the postexercise period reinforces the role of exercise in the management of cardiovascular risk in diabetes

Simvastatin-induced cardiac autonomic control improvement in fructose-fed female rats

OBJECTIVE: Because autonomic dysfunction has been found to lead to cardiometabolic disorders and because studies have reported that simvastatin treatment has neuroprotective effects, the objective of the present study was to investigate the effects of simvastatin treatment on cardiovascular and autonomic changes in fructose-fed female rats. METHODS: Female Wistar rats were divided into three groups: controls (n=8), fructose (n=8), and fructose+ simvastatin (n=8). Fructose overload was induced by supplementing the drinking water with fructose (100 mg/L, 18 wks). Simvastatin treatment (5 mg/kg/day for 2 wks) was performed by gavage. The arterial pressure was recorded using a data acquisition system. Autonomic control was evaluated by pharmacological blockade. RESULTS: Fructose overload induced an increase in the fasting blood glucose and triglyceride levels and insulin resistance. The constant rate of glucose disappearance during the insulin intolerance test was reduced in the fructose group (3.4+ 0.32%/min) relative to that in the control group (4.4+ 0.29%/min). Fructose+simvastatin rats exhibited increased insulin sensitivity (5.4+0.66%/min). The fructose and fructose+simvastatin groups demonstrated an increase in the mean arterial pressure compared with controls rats (fructose: 124+2 mmHg and fructose+simvastatin: 126 + 3 mmHg vs. controls: 112 + 2 mmHg). The sympathetic effect was enhanced in the fructose group (73 + 7 bpm) compared with that in the control (48 + 7 bpm) and fructose+simvastatin groups (31+8 bpm). The vagal effect was increased in fructose+simvastatin animals (84 + 7 bpm) compared with that in control (49 + 9 bpm) and fructose animals (46+5 bpm). CONCLUSION: Simvastatin treatment improved insulin sensitivity and cardiac autonomic control in an experimental model of metabolic syndrome in female rats. These effects were independent of the improvements in the classical plasma lipid profile and of reductions in arterial pressure. These results support the hypothesis that statins reduce the cardiometabolic risk in females with metabolic syndrome

Treinamento físico melhora a disfunção quimiorreflexa em ratos diabéticos por estreptozotocina

The aim of the present study was to investigate the effects of exercise training on arterial pressure, heart rate and chemoreflex sensitivity in STZ-induced diabetic rats. The animals were divided into three groups: control (SC, n = 6), sedentary diabetic (SD, n = 6) and trained diabetic (TD, n = 6). After 1 week of diabetes induction (Streptozotocin, 50 mg/kg, iv), male Wistar rats were submitted to exercise training for 10 weeks on a treadmill. Arterial pressure signals were obtained and processed with a data acquisition system (CODAS, 1 KHz). Potassium cyanide (KCN, 100ug/kg) was used to evaluated bradycardic response evoked by chemoreflex activation. Diabetes bradycardia and hypotension (SD: 274 ± 6 bpm and 94 ± 2 mmHg vs SC: 332 ± 5bpm and 108 ± 2 mmHg) were attenuated by training (TD: 299 ± 5 bpm and 107 ± 2 mmHg). Bradycardic response was decreased in SD rats (33 ± 5 bpm) when compared to SC rats (182 ± 3 bpm) and TD rats (89 ± 10 bpm). In conclusion, exercise training reversed hypotension and bradycardia and improved chemreflex sensitivity in STZ-diabetic rats. Considering that diabetics with abnormal cardiovascular reflexes show higher mortality than diabetics with normal autonomic reflex function, the results obtained suggest that exercise training may contribute to the reduction in cardiovascular risk in this population and must be considered in the management of diabetic patientsO objetivo do presente estudo foi avaliar os efeitos do treinamento físico na pressão arterial, na freq üência cardíaca e na sensibilidade quimiorreflexa em ratos diabéticos por estreptozotocina. Os animais foram divididos em grupos controle (CS, n = 6), diabético sedentário (DS, n = 6) e diabético treinado (DT, n = 6). Uma semana após a indução do diabetes (Estreptozotocina, 50 mg/kg), ratos machos Wistar foram submetidos a um protocolo de treinamento físico em esteira ergométrica por 10 semanas. Os sinais de pressão arterial foram gravados e processados em um sistema de aquisição de dados (CODAS,1KHz). Cianeto de potássio (KCN,100 ug/kg) foi utilizado para avaliar a resposta bradicárdica desencadeada pela estimulação dos quimiorreceptores. A bradicardia e a hipotensão do diabetes (DS:274 ± 6 bpm e 94 ± 2 mmHg vs CS:332 ± 5 bpm e 108 ± 2 mmHg) foram atenuadas pelo treinamento físico (DT:299 ± 5 bpm e 107 ± 2 mmHg). A resposta bradicárdica foi menor nos ratos DS (33 ± 5 bpm) quando comparado aos ratos CS (182 ± 3 bpm) e DT (89 ± 10 bpm). Concluindo, o treinamento físico reverteu a hipotensão e a bradicardia e melhorou a sensibilidade quimioreflexa em ratos STZ. Considerando que diabéticos com reflexos cardiovasculares anormais apresentam maior mortalidade que diabéticos com função reflexa autonômica normal, os resultados obtidos sugerem que o treinamento físico pode contribuir para a redução do risco cardiovascular nesta população devendo ser considerado no manejo do paciente diabétic