Lifestyle INtervention for Diabetes prevention After pregnancy (LINDA-Brasil): study protocol for a multicenter randomized controlled trial.

BACKGROUND: Gestational diabetes mellitus (GDM), a hyperglycemic state detected during pregnancy, is an established risk factor for diabetes. However, treatment during pregnancy in and of itself is not able to eliminate this risk, and a considerable fraction of women with GDM will develop frank diabetes in the decade following pregnancy. Our aim is to conduct a multicenter randomized controlled trial to investigate the effectiveness of a lifestyle intervention program implemented after a pregnancy complicated by GDM in delaying or preventing the development of type 2 diabetes. METHODS: Women aged 18 or older identified as having recent GDM are recruited and followed by telephone to assess eligibility for the trial. To be eligible, women must have used insulin during pregnancy or present intermediate hyperglycemia postpartum. Women are encouraged to enter the trial as early as 10 weeks, and are permitted to do so up to 2 years after a pregnancy with GDM. An estimated 740 women will be randomized to either conventional care or to coach-based interventions focused on breastfeeding, weight loss, healthy eating, and increased physical activity, and predominantly delivered by telephone. Women are followed annually to detect new onset diabetes, the primary outcome, and additional secondary outcomes which include reversion to normoglycemia, weight loss, physical activity and fitness, and insulin resistance. DISCUSSION: Though previous studies have demonstrated that type 2 diabetes can be delayed or prevented, no study has yet demonstrated the feasibility and effectiveness of similar interventions implemented in the postpartum period for women with recent GDM. If shown to be successful, this approach could become an important means of preventing diabetes in primary care settings. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT02327286; Registered 23 December 2014.

Physical activity and cardiovascular risk factors in children: meta-analysis of randomized clinical trials.

OBJECTIVE: To assess the effects of physical activity interventions in preventing cardiovascular risk factors in childhood through a systematic review and meta-analysis of randomized clinical trials (RCTs). METHODS: A search of online databases (PubMed, EMBASE and Cochrane CENTRAL) was conducted from inception until June 2013. RCTs enrolling children 6-12years old conducted physical activity interventions longer than 6months, assessing their effect on body mass index (BMI), systolic (SBP) and diastolic blood pressure (DBP), total cholesterol (TC) and triglycerides (TG) were included. Data analysis was performed using a random-effects model. RESULTS: Of 23.091 articles retrieved, 11 RCTs (10.748 subjects) were included. Physical activity interventions were not associated with reductions of BMI [-0.03kg/m(2) (95%CI -0.16, 0.13) I(2) 0%]. However, there was an association between the interventions and reduction of SBP [-1.25mmHg (95%CI -2.47, -0.02) I(2) 0%], DBP [-1.34mmHg (95%CI -2.57, -0.11) I(2) 43%] and TG [-0.09mmol/L (95%CI -0.14, -0.04) I(2) 0%], and increase of TC [0.14mmol/L (95%CI 0.01, 0.27) I(2) 0%]. CONCLUSION: As physical activity intervention programs lasting longer than 6months are associated with reductions in blood pressure levels and triglycerides, they should be considered to be included in prevention programs for cardiovascular diseases in schoolchildren.

Capsaicin-induced metabolic and cardiovascular autonomic improvement in an animal model of the metabolic syndrome.

The metabolic syndrome (MetS) is associated with an increased risk of cardiac mortality, as it is characterised by the clustering of multiple cardiovascular risk factors. Studies have shown that capsaicin (red pepper) may be useful as a nutraceutical, ameliorating metabolic profile and cardiovascular function. The aim of the present study was to investigate the cardiovascular and metabolic effects of orally administered capsaicin in rats with the MetS. Neonate spontaneously hypertensive rats were injected with monosodium glutamate and subjected to one of the following three treatments by oral administration for 14 d, between 27 and 30 weeks: low-dose capsaicin (CAP05, n 18, synthetic capsaicin powder diluted in a vehicle (10 % ethyl alcohol) plus 0·5 mg/kg body weight (BW) of capsaicin); high-dose capsaicin (CAP1, n 19, synthetic capsaicin powder diluted in a vehicle (10 % ethyl alcohol) plus 1 mg/kg BW of capsaicin); control (C, n 18, vehicle). Lee's index, lipid/metabolic profile, and cardiovascular parameters with the rats being conscious, including arterial pressure (AP) and heart rate (HR) variability, as well as aortic wall thickness (haematoxylin and eosin staining) and CD68 (cluster of differentiation 68) antibody levels (monocyte/macrophage immunostaining) were evaluated. Weight, Lee's index, and lipid and metabolic parameters, as well as AP and HR and aortic wall thickness, were similar between the groups. Capsaicin determined HR variability improvement (16·0 (sem 9·0), 31·0 (sem 28·2) and 31·3 (sem 19·0) ms2 for the C, CAP05 and CAP1 groups, respectively, P= 0·003), increased vascular sympathetic drive (low-frequency component of systolic AP variability: 3·3 (sem 2·8), 8·2 (sem 7·7) and 12·1 (sem 8·8) mmHg2 for the C, CAP05 and CAP1 groups, respectively, P< 0·001) and increased α-index (spontaneous baroreflex sensitivity). The present data show that capsaicin did not improve lipid and glucose abnormalities in rats with the MetS. However, beneficial cardiovascular effects were observed with this nutraceutical.

Molecular screening for 22Q11.2 deletion syndrome in patients with congenital heart disease.

Few studies have investigated the prevalence of 22q11.2 deletion syndrome (22q11.2DS) among patients with isolated heart defects or nonconotruncal heart defects. Polymerase chain reaction (PCR) followed by length polymorphism restriction fragment analysis (RFLP) is useful for low-cost molecular diagnosis and screening. This cross-sectional study included 392 patients with congenital heart disease, described clinical features, and performed PCR-RFLP for analysis of polymorphism in three loci with a high heterozygosity rate located in the typically deleted region of 1.5 megabases. Heterozygosity excluded 22q11.2DS. Patients with homozygosity for the three markers underwent multiplex ligation-dependent probe amplification (MLPA) and fluorescence in situ hybridization (FISH) for the final diagnosis, estimating the prevalence of 22q11.2DS. The use of PCR-RFLP excluded 22q11.2DS in 81.6 % (n = 320) of 392 patients. Of the remaining 72 patients, 65 underwent MLPA, showing 22q11.2DS in five cases (prevalence, 1.27 %). Four of these five patients underwent FISH, confirming the MLPA results. All five patients with the deletion had heart diseases commonly found with 22q11.2DS (interrupted aortic arch, persistent truncus arteriosus, tetralogy of Fallot, and ventricular septal defect plus atrial septal defect). Two patients had congenital extracardiac anomaly (one with arched palate and micrognathia and one with hypertelorism). Three patients reported recurrent respiratory infections, and one patient reported hypocalcemia. All were underweight or short in stature for their age. This study contributed to showing the prevalence of 22q11.2DS in patients with any congenital heart disease, with or without other features of the syndrome. Patients with 22q11.2DS may not have all the major features of the syndrome, and those that are found may be due to the heart defect.

Diabetes increases mechanical sensitivity and causes morphological abnormalities in the sural nerve that are prevented by treadmill training.

INTRODUCTION: In this investigation we evaluated the effects of treadmill training on mechanical sensitivity and sural nerve morphology in diabetic rats. METHODS: Rats were divided into 3 groups: control (C); diabetic (D); and trained diabetic (TD). Training was performed for 8 weeks. Mechanical sensitivity was evaluated using von Frey filaments. Sural nerve analysis included fiber area, diameter, density of myelinated fibers, area occupied by connective tissue, myelin sheath thickness, and g-ratio. RESULTS: Animals in the D group had a reduced mechanical sensitivity threshold. Morphometric study showed that the D group had a smaller myelinated fiber area and diameter, higher density of fibers and area occupied by connective tissue, thinner myelin sheath, and higher g-ratio. The D group had a higher percentage of small myelinated fibers and a lower percentage of large-diameter myelinated fibers than the C and TD groups. CONCLUSION: Training prevents functional and morphological abnormalities in the sural nerve caused by diabetes.

Early choroidal changes detected by swept-source OCT in type 2 diabetes and their association with diabetic kidney disease.

INTRODUCTION: Microvascular changes in eye and kidney shares some common factors in diabetes mellitus (DM). The purpose was to evaluate choroidal thickness (CT) and choriocapillaris (CC) density in patients with type 2 diabetes (T2D) and their association with diabetic kidney disease (DKD) using swept-source optical coherence tomography (SS-OCT). RESEARCH DESIGN AND METHODS: A cross-sectional study was conducted with patients with T2D with mild or no diabetic retinopathy (DR) and non-diabetic controls. CT was measured with SS-OCT, and CC vascular density was measured with OCT angiography. These parameters were compared with inner retinal layers thickness in patients with and without DKD and non-diabetic controls. RESULTS: Ninety-three eyes from patients with T2D and 34 eyes from controls volunteers were included. Within the T2D group, 56 eyes with DKD and 37 eyes from patients with no diabetic kidney disease were examined. A statistically significant reduction of CT was observed in patients with DKD compared with controls, with no difference in CC density. There was an association between ganglion cell layer and central choroidal thickness reduction in the DKD group. CONCLUSIONS: Patients with T2D with DKD showed a decrease in CT with no difference in CC density compared with non-diabetic controls. This thinning might be related to vascular changes of choroidal layers such as Haller's and Sattler's with preservation of CC density, which is crucial for outer retina and retinal pigment epithelium health. Longitudinal studies are warranted to determine the association of choroidal changes with the pathogenesis of diabetes, and its association with early DKD and progression to more severe DR.

Inspiratory muscle weakness is associated with autonomic cardiovascular dysfunction in patients with type 2 diabetes mellitus.

INTRODUCTION: Diabetic autonomic neuropathy is a complication of diabetes mellitus (DM) that can cause cardiovascular and respiratory abnormalities. The association between respiratory muscle weakness and autonomic cardiovascular neuropathy has not yet been studied. The aims of the present study were to assess respiratory muscle strength, pulmonary function, and heart rate (HR) variability in diabetic patients with and without diabetic autonomic neuropathy. MATERIALS AND METHODS: Twenty-four patients with type 2 DM were divided into two groups: those without diabetic autonomic neuropathy (C group, n = 12); and those with diabetic autonomic neuropathy (DAN group, n = 12). We evaluated pulmonary function, maximum static inspiratory pressure (PImax), maximum static expiratory pressure (PEmax), and HR variability. RESULTS: The results of the pulmonary function tests were similar in both the groups. PImax was lower in the DAN group (80 ± 24 vs. 102 ± 24 cmH(2)O, p = 0.03), but PEmax was similar in both the groups. RR intervals (878 ± 122 vs. 743 ± 88 ms; p < 0.01), standard deviation of RR intervals (28 ± 11 vs. 14 ± 4 ms; p < 0.01) and squared root of the sum of successive differences of squared RR intervals (15 ± 6 vs. 8 ± 5 ms; p < 0.01) were higher in the C group. In the DAN group, resting HR was higher (82 ± 10 vs. 69 ± 9 bpm; p = 0.01) than in the C group. There was a positive correlation between PImax and RR intervals (r = 0.452, p = 0.02) and a negative correlation between PImax and resting HR (r = -0.482, p = 0.01), and PImax and DM duration (r = -0.463, p = 0.02). CONCLUSION: Patients with type 2 DM and autonomic neuropathy showed reduced respiratory muscle strength and less HR variability. Respiratory muscle weakness may be associated with autonomic dysfunction in these patients.

Early neurovascular retinal changes detected by swept-source OCT in type 2 diabetes and association with diabetic kidney disease.

PURPOSE: To evaluate retinal thickness and capillary density in patients with type 2 diabetes (T2D) and their association with diabetic kidney disease (DKD) using swept-source optical coherence tomography (SS-OCT). METHODS: A cross-sectional study was conducted with T2D patients with mild or no diabetic retinopathy (DR) and nondiabetic controls. Inner retinal layer thickness was measured with SS-OCT. Retinal capillary density and the foveal avascular zone (FAZ) were measured with SS-OCT angiography (OCTA). SS-OCT parameters were compared in patients with and without diabetic kidney disease (DKD) and nondiabetic controls. RESULTS: 131 DKD eyes showed decreased ganglion cell layer plus (GCL+) (p = 0.005 TI; p = 0.022 I), retinal nerve fiber layer (RNFL) (p = 0.003), and central retinal thickness (CRT) (p = 0.032), as well as foveal avascular zone (FAZ) enlargement (p = 0.003) and lower capillary density in the superficial vascular plexus (p = 0.016, central quadrant), compared to controls. No statistically significant changes were found between diabetic patients without significant DKD and controls. CONCLUSION: Our findings suggest early neurovascular damage in patients with T2D; these changes were more significant in patients with DKD. Larger longitudinal studies are warranted to determine the role of early neurovascular damage in the pathophysiology of severe DR.

Man vs. machine: Predicting hospital bed demand from an emergency department.

BACKGROUND: The recent literature reports promising results from using intelligent systems to support decision making in healthcare operations. Using these systems may lead to improved diagnostic and treatment protocols and to predict hospital bed demand. Predicting hospital bed demand in emergency department (ED) attendances could help resource allocation and reduce pressure on busy hospitals. However, there is still limited knowledge on whether intelligent systems can operate as fully autonomous, user-independent systems. OBJECTIVE: Compare the performance of a computer-based algorithm and humans in predicting hospital bed demand (admissions and discharges) based on the initial SOAP (Subjective, Objective, Assessment, Plan) records of the ED. METHODS: This was a retrospective cohort study that compared the performance of humans and machines in predicting hospital bed demand from an ED. It considered electronic medical records (EMR) of 9030 patients (230 used as a testing set, and hence evaluated both by humans and by an algorithm, and 8800 used as a training set exclusively by the algorithm) who visited the ED of a tertiary care and teaching public hospital located in Porto Alegre, Brazil between January and December 2014. The machine role was played by Support Vector Machine Classifier and the human prediction was performed by four ED physicians. Predictions were compared in terms of sensitivity, specificity, accuracy, and area under the receiver operating characteristic curve (AUROC). RESULTS: All graders achieved similar accuracies. The accuracy by AUROC for the testing set was 0.82 [95% confidence interval (CI) of 0.77-0.87], 0.80 (95% CI: 0.75-0.85), 0.76 (95% CI: 0.71-0.81) for novice physicians, machine, experienced physicians, respectively. Processing time per test EMR was 0.00812±0.0009 seconds. In contrast, novice physicians took on average 156.80 seconds per test EMR, while experienced physicians took on average 56.40 seconds per test EMR. CONCLUSIONS: Our data indicated that the system could predict patient admission or discharge states with 80% accuracy, which was similar the performance of novice and experienced physicians. These results suggested that the algorithm could operate as an autonomous and independent system to complete this task.

Reversal of postprandial endothelial dysfunction by cyclooxygenase inhibition in healthy volunteers.

The aim of this study was to evaluate the role of cyclooxygenase (COX) in venous vascular reactivity changes after an oral lipid overload (OLO). Venous endothelial function (dorsal hand vein technique) was evaluated in fasting, 30 minutes after COX inhibition (aspirin-fasting), 2 to 4 hours after an OLO (1000 kcal, 58% fat), and again after COX inhibition (aspirin-OLO, 600 mg/200 mL water) in 10 healthy adults (age, 28.1 +/- 1.3 years; body mass index, 22.3 +/- 0.6 kg/m). Fasting, 2- to 4-hour post-OLO, and 60-minute postaspirin plasma glucose, insulin, and lipids were also evaluated. The OLO increased triglycerides and insulin, reduced low-density lipoprotein and high-density lipoprotein, but glycemia and total cholesterol remained unchanged. There were no metabolic differences between OLO and aspirin-OLO. In fasting, aspirin reduced acetylcholine-induced venodilation (107.0% +/- 14% versus 57.3% +/- 11%; P < 0.001). Vascular reactivity was blunted after the OLO (phenylephrine dose: 0.3 +/- 0.2 fasting versus 1.9 +/- 0.8 nmol/min after OLO; P < 0.001) and was partially corrected by aspirin (0.4 +/- 0.2; P < 0.001). Similar changes were observed in maximum venodilation after acetylcholine (107.0% +/- 14% fasting versus 60.4% +/- 9% after OLO, P < 0.001; aspirin-OLO: 95.9% +/- 6%; P < 0.001). The responses to sodium nitroprusside remained unchanged during the study. We conclude that the OLO reduction in the endothelium-dependent venoconstriction and venodilation is partially the result of the action of COX.

FUNCTIONAL CAPACITY IN CHILDREN AND ADOLESCENTS WITH CONGENITAL HEART DISEASE.

OBJECTIVE: To evaluate the physical activity level and functional capacity of children and adolescents with congenital heart disease and to describe correlations between functionality, surgical and echocardiographic findings, metabolic and inflammatory profile and differences between acyanotic and cyanotic heart defects. METHODS: A cross-sectional study including children and adolescents with congenital heart disease between six and 18 years old that were evaluated with the 6-minute walk test (6MWT) to assess functional capacity. The short version form of the International Physical Activity Questionnaire (IPAQ) was performed to evaluate physical activity levels. Also, echocardiography and blood collection, to evaluate the metabolic (blood glucose, lipids, insulin) and inflammatory markers (C-reactive protein), were assessed. RESULTS: Twenty-five individuals were evaluated. Of them, 14 had acyanotic heart defects and 11 cyanotic heart defects. Mean age was 12.0±3.7 years, and 20 (80%) were male. IPAQ showed that six (24%) individuals were very active, eight (32%) were active, nine (36%) had irregular physical activity, and two (8%) were sedentary. The mean distance walked in the 6MWT, considering all studied individuals, was 464.7±100.4 m, which was 181.4±42.0 m less than the predicted (p=0.005). There was a positive correlation between Z score 6MWT and the number of surgical procedures (r=-0.455; p=0.022). CONCLUSIONS: Children and adolescents with congenital heart disease have low functional capacity, but they are not completely sedentary.

In situ delivery of bone marrow cells and mesenchymal stem cells improves cardiovascular function in hypertensive rats submitted to myocardial infarction.

This work aimed to evaluate cardiac morphology/function and histological changes induced by bone marrow cells (BMCs) and cultured mesenchymal stem cells (MSCs) injected at the myocardium of spontaneously hypertensive rats (SHR) submitted to surgical coronary occlusion. Female syngeneic adult SHR, submitted (MI) or not (C) to coronary occlusion, were treated 24 h later with in situ injections of normal medium (NM), or with MSCs (MSC) or BMCs (BM) from male rats. The animals were evaluated after 1 and 30 days by echocardiography, histology of heart sections and PCR for the Y chromosome. Improved ejection fraction and reduced left ventricle infarcted area were observed in MSC rats as compared to the other experimental groups. Treated groups had significantly reduced lesion tissue score, increased capillary density and normal (not-atrophied) myocytes, as compared to NM and C groups. The survival rate was higher in C, NM and MSC groups as compared to MI and BM groups. In situ injection of both MSCs and BMCs resulted in improved cardiac morphology, in a more physiological model of myocardial infarction represented by surgical coronary occlusion of spontaneously hypertensive rats. Only treatment with MSCs, however, ameliorated left ventricle dysfunction, suggesting a positive role of these cells in heart remodeling in infarcted hypertensive subjects.

Systemic delivery of adult stem cells improves cardiac function in spontaneously hypertensive rats.

1. Heart regeneration after myocardial infarction (MI) can occur after cell therapy, but the mechanisms, cell types and delivery methods responsible for this improvement are still under investigation. In the present study, we evaluated the impact of systemic delivery of bone marrow cells (BMC) and cultivated mesenchymal stem cells (MSC) on cardiac morphology, function and mortality in spontaneously hypertensive rats (SHR) submitted to coronary occlusion. 2. Female syngeneic adult SHR, submitted or not (control group; C) to MI, were treated with intravenous injection of MSC (MI + MSC) or BMC (MI + BM) from male rats and evaluated after 1, 15 and 30 days by echocardiography. Systolic blood pressure (SBP), functional capacity, histology, mortality rate and polymerase chain reaction for the Y chromosome were also analysed. 3. Myocardial infarction induced a decrease in SBP and BMC, but not MSC, prevented this decrease. An improvement in functional capacity and ejection fraction (38 +/- 4, 39 +/- 3 and 58 +/- 2% for MI, MI + MSC and MI + BM, respectively; P < 0.05), as well as a reduction of the left ventricle infarcted area, were observed in rats from the MI + BM group compared with the other three groups. Treated animals had a significantly reduced lesion tissue score. The mortality rate in the C, MI + BM, MI + MSC and MI groups was 0, 0, 16.7 and 44.4%, respectively (P < 0.05 for the MI + MSC and MI groups compared with the C and MI + BM groups). 4. The results of the present study suggest that systemic administration of BMC can improve left ventricular function, functional capacity and, consequently, reduce mortality in an animal model of MI associated with hypertension. We speculate that the cells transiently home to the myocardium, releasing paracrine factors that recruit host cells to repair the lesion.

Glycemia and inflammatory markers in acute coronary syndrome: association with late post-hospital outcomes.

BACKGROUND: Glycemia and inflammatory markers were associated with clinical outcomes in patients with acute coronary syndrome (ACS). OBJECTIVES: To evaluate the role of glycemia and inflammatory markers as predictors of late cardiovascular outcomes after ACS. METHODS: One hundred and ninety-nine ACS patients of a Coronary Care Unit were included, from March to November 2002. They were reassessed clinically after approximately 3 years. Clinical variables, glycemia, CRP and fibrinogen were evaluated as event and mortality predictors. Statistical analyses included Cox multivariate analysis and survival curves (Kaplan-Meier). RESULTS: At admission, 16.7% had normal glycemia. After 3 years, this proportion increased to 55.2%; the 40.6% who belonged to the borderline category decreased to 27.1%; the 42.7% with elevated glycemia decreased to 17.7%. Glycemia was not associated with the development of major cardiovascular events (MACE) and mortality at follow-up ( approximately 3 years). Considering MACE, CRP (p<0.001), but not fibrinogen, was predictive in bivariate analysis. Regarding mortality, both fibrinogen (p=0.020) and CRP (p=0.008) were predictive in bivariate analysis. CONCLUSION: Glycemia was not associated with late mortality after ACS, but inflammatory markers were, suggesting that these are more sensitive markers to predict events in long-term. Moreover, glucose intolerance prevalence is lower in the follow-up after the ACS episode.

Autonomic modulation of arterial pressure and heart rate variability in hypertensive diabetic rats.

OBJECTIVE: The aim of the present study was to evaluate the autonomic modulation of the cardiovascular system in streptozotocin (STZ)-induced diabetic spontaneously hypertensive rats (SHR), evaluating baroreflex sensitivity and arterial pressure and heart rate variability. METHODS: Male SHR were divided in control (SHR) and diabetic (SHR+DM, 5 days after STZ) groups. Arterial pressure (AP) and baroreflex sensitivity (evaluated by tachycardic and bradycardic responses to changes in AP) were monitored. Autoregressive spectral estimation was performed for systolic AP (SAP) and pulse interval (PI) with oscillatory components quantified as low (LF:0.2-0.6Hz) and high (HF:0.6-3.0Hz) frequency ranges. RESULTS: Mean AP and heart rate in SHR+DM (131+/-3 mmHg and 276+/-6 bpm) were lower than in SHR (160+/-7 mmHg and 330+/-8 bpm). Baroreflex bradycardia was lower in SHR+DM as compared to SHR (0.55+/-0.1 vs. 0.97+/-0.1 bpm/mmHg). Overall SAP variability in the time domain (standard deviation of beat-by-beat time series of SAP) was lower in SHR+DM (3.1+/-0.2 mmHg) than in SHR (5.7+/-0.6 mmHg). The standard deviation of the PI was similar between groups. Diabetes reduced the LF of SAP (3.3+/-0.8 vs. 28.7+/-7.6 mmHg2 in SHR), while HF of SAP were unchanged. The power of oscillatory components of PI did not differ between groups. CONCLUSIONS: These results show that the association of hypertension and diabetes causes an impairment of the peripheral cardiovascular sympathetic modulation that could be, at least in part, responsible for the reduction in AP levels. Moreover, this study demonstrates that diabetes might actually impair the reduced buffer function of the baroreceptors while reducing blood pressure.

[The role of post-prandial lipids in atherogenesis: particularities of diabetes mellitus]. / O papel da lipemia pós-prandial na gênese da aterosclerose: particularidades do diabetes mellitus.

Atherosclerosis is a complex and multifactorial disease, which determines clinical events that cause significant morbidity-mortality, represented by acute myocardial infarction, angina and sudden death. It is associated with lipid disturbances, platelet activation, thrombosis, endothelial dysfunction, inflammation, oxidative stress, altered matrix metabolism, among other disturbances. All these abnormalities are usual and more pronounced in diabetic patients, as well as in the post-prandial state. Among the coronary artery disease risk factors that are not usually employed in clinical practice in the whole population, postprandial hyperlipemia plays a major role, being a possible early marker of metabolic abnormalities and vascular dysfunction not yet seen in the fasting state. Recent results showed that post-oral lipid overload changes are negatively associated with endothelial dysfunction, and vascular reactivity abnormalities are strongly related to atherosclerosis progression and cardiovascular events. These abnormalities could disclose a lipid intolerance state that can be detected in apparently healthy subjects even before fasting abnormalities are seen. This review will deal with the pathophysiology changes involved in post-prandial hyperlipemia and its relationship with atherogenesis, with particular emphasis to diabetes mellitus.

[Percutaneous coronary intervention in diabetes mellitus: an updated analysis of medical practice]. / Intervenção coronária percutânea no diabetes mellitus: análise da prática médica atual.

Patients with diabetes and coronary artery disease are frequently considered for myocardial revascularization procedures, aiming at cardiovascular events risk reduction and a better quality of life. In clinical practice, decisions concerning surgery or percutaneous coronary intervention are frequently difficult, because of cases' severity, disease extension and co-morbidities association. Beyond that, the bulk of literature information was generated by subgroup analysis of randomized clinical trials, which were designed for the general population, not for diabetics. The aim of this study was to review literature on coronary percutaneous intervention in diabetic patients, and also to show recent data from the experience in this procedure at the Catheterization Laboratory of the Cardiology Institute of RS.

[Molecular bases of diabetic nephropathy]. / Bases moleculares da glomerulopatia diabética.

The determinant of the diabetic nephropathy is hyperglycemia, but hypertension and other genetic factors are also involved. Glomerulus is the focus of the injury, where mesangial cell proliferation and extracellular matrix occur because of the increase of the intra- and extracellular glucose concentration and overexpression of GLUT1. Sequentially, there are increases in the flow by the poliol pathway, oxidative stress, increased intracellular production of advanced glycation end products (AGEs), activation of the PKC pathway, increase of the activity of the hexosamine pathway, and activation of TGF-beta1. High glucose concentrations also increase angiotensin II (AII) levels. Therefore, glucose and AII exert similar effects in inducing extracellular matrix formation in the mesangial cells, using similar transductional signal, which increases TGF-beta1 levels. In this review we focus in the effect of glucose and AII in the mesangial cells in causing the events related to the genesis of diabetic nephropathy. The alterations in the signal pathways discussed in this review give support to the observational studies and clinical assays, where metabolic and antihypertensive controls obtained with angiotensin-converting inhibitors have shown important and additive effect in the prevention of the beginning and progression of diabetic nephropathy. New therapeutic strategies directed to the described intracellular events may give future additional benefits.

Cardiac surgery unmasks latent hypoparathyroidism in a child with the 22q11.2 deletion syndrome.

The 22q11.2 deletion syndrome is a developmental field defect of the third and fourth pharyngeal pouches characterized by a spectrum of thymic and parathyroid gland abnormalities and conotruncal cardiac defects. Latent hypoparathyroidism, defined as normocalcaemia at rest but reduced ability to secrete parathyroid hormone (PTH) in response to pharmacologically evoked hypocalcaemia, is found in 30-50% of people with this syndrome. Its natural history is unknown. We describe a 1.5 year-old girl with tetralogy of Fallot, normal calcium metabolism and few facial dysmorphic features who developed transient hypoparathyroidism in the postoperative period, which lasted months and waxed and waned during this observation period. The clinical picture led us to the diagnosis of 22q11.2 deletion syndrome.