Celso Ferreira Filho

Anti-hypertensive drugs have different effects on ventricular hypertrophy regression

OBJECTIVES: There is a direct relationship between the regression of left ventricular hypertrophy (LVH) and a decreased risk of mortality. This investigation aimed to describe the effects of anti-hypertensive drugs on cardiac hypertrophy through a meta-analysis of the literature. METHODS: The Medline (via PubMed), Lilacs and Scielo databases were searched using the subject keywords cardiac hypertrophy, antihypertensive and mortality. We aimed to analyze the effect of anti-hypertensive drugs on ventricle hypertrophy. RESULTS: The main drugs we described were enalapril, verapamil, nifedipine, indapamina, losartan, angiotensin-converting enzyme inhibitors and atenolol. These drugs are usually used in follow up programs, however, the studies we investigated used different protocols. Enalapril (angiotensin-converting enzyme inhibitor) and verapamil (Ca++ channel blocker) caused hypertrophy to regress in LVH rats. The effects of enalapril and nifedipine (Ca++ channel blocker) were similar. Indapamina (diuretic) had a stronger effect than enalapril, and losartan (angiotensin II receptor type 1 (AT1) receptor antagonist) produced better results than atenolol (selective β1 receptor antagonist) with respect to LVH regression. CONCLUSION: The anti-hypertensive drugs induced various degrees of hypertrophic regression.

Prevalence of burnout syndrome in clinical nurses at a hospital of excellence

Background Burnout syndrome can be defined as long-term work stress resulting from the interaction between constant emotional pressure associated with intense interpersonal involvement for long periods of time and personal characteristics. We investigated the prevalence/propensity of Burnout syndrome in clinical nurses, and the factors related to Burnout syndrome-associated such as socio-demographic characteristics, work load, social and family life, leisure activities, extra work activities, physical activities, and work-related health problems. Method We conducted a cross-sectional, quantitative, prospective epidemiological study with 188 surgical clinic nurses. We used the Maslach Burnout Inventory (MBI), which is a socio-demographic questionnaire and the most widely used instrument to assess Burnout syndrome (three basic dimensions: emotional exhaustion, despersonalization and professional underachievement). The socio-demographic profile questionnaire wascomposed of questions regarding identification, training, time at work, work characteristics and personal circumstances. Results The prevalence of Burnout syndrome was higher (10.1%) and 55, 4% of subjects had a propensity to develop this syndrome. The analysis of the socio-demographic profile of the nurse sample studied showed that most nurses were childless married women, over 35 years of age, working the day shift for 36 hours weekly on average, with 2-6 years of post-graduation experience, and without extra employments. Factors such as marital status, work load, emotion and work related stress aggravated the onset of the syndrome. Conclusion The prevalence and propensity of Burnout syndrome were high. Some factors identified can be useful for the adoption of preventive actions in order to decrease the prevalence of the clinical nurses Burnout syndrome.

Memantine prevents cardiomyocytes nuclear size reduction in the left ventricle of rats exposed to cold stress

OBJECTIVES Memantine is an N-methyl-d-aspartate (NMDA) glutamate receptor antagonist used to treat Alzheimer’s disease. Previous studies have suggested that receptor blockers act as neuroprotective agents; however, no study has specifically investigated the impact that these drugs have on the heart. We sought to evaluate the effects of memantine on nuclear size reduction in cardiac cells exposed to cold stress. METHOD We used male EPM-Wistar rats (n=40) divided into 4 groups: 1) Matched control (CON); 2) Memantine-treated rats (MEM); 3) Rats undergoing induced hypothermia (IH) and 4) Rats undergoing induced hypothermia that were also treated with memantine (IHM). Animals in the MEM and IHM groups were treated by oral gavage administration of 20 mg/kg/day memantine over an eight-day period. Animals in the IH and IHM groups were submitted to 4 hours of hypothermia in a controlled environment with a temperature of − 8°C on the last day of the study. RESULTS The MEM group had the largest cardiomyocyte nuclear size (151 ± 3.5 μm3 vs. CON: 142 ± 2.3 μm3; p<0.05), while the IH group had the smallest mean value of nuclear size. The nuclear size of the IHM group was preserved (125 ± 2.9 μm3) compared to the IH group (108 ± 1.7 μm3; p<0.05). CONCLUSION Memantine prevented the nuclear size reduction of cardiomyocytes in rats exposed to cold stress.

Evaluation of baroreflex function in young spontaneously hypertensive rats

FUNDAMENTO: A literatura tem descrito dados contraditorios em relacao ao inicio da diminuicao da funcao barorreflexa em ratos espontaneamente hipertensos. OBJETIVO:Este estudo foi realizado para avaliar a funcao barorreflexa em ratos jovens de 13 semanas espontaneamente hipertensos. METODOS:Foram estudados ratos machos Wistar Kyoto (WKY) (n=15) e ratos espontaneamente hipertensos (REH) de 13 semanas (n=15). Cânulas foram inseridas na arteria aorta abdominal atraves da arteria femoral direita para medir a pressao arterial media (PAM) e a frequencia cardiaca (FC). A funcao barorreflexa foi calculada como a derivada da variacao da FC em funcao da variacao da PAM (ΔFC/ΔPAM), quando submetida a teste com uma dose depressora de nitroprussiato de sodio (50µg/kg) e com uma dose pressora de fenilefrina (8µg/kg) atraves de cânula inserida na veia femoral direita em ratos espontaneamente hipertensos e WKY. Diferencas com um valor de p < 0.05 foram consideradas estatisticamente significantes. RESULTADOS:Ratos espontaneamente hipertensos: ΔPAM=43,5 mmHg±5,2, ΔFC=-59,7 ppm±17,9 e ΔFC/ΔPAM=1,3 ppm/mmHg±0,1 testados com fenilefrina; Wistar Kyoto: ΔPAM=&56mmHg±3, ΔFC=*-114,9ppm±11,3 e ΔFC /ΔPAM =#1,9ppm/mmHg±0,3 testados com fenilefrina; ratos espontaneamente hipertensos: ΔPAM=-45,6mmHg±8,1, ΔFC=40,1ppm±11,6 e ΔFC/ΔPAM=0,9ppm/mmHg±0,5 testados com nitroprussiato de sodio; Wistar Kyoto: ΔPAM=-39,8mmHg±6,2, ΔFC=51,9ppm±21,8 e ΔFC/ΔPAM=1,4ppm/mmHg±0,7 testados com nitroprussiato de sodio (*p<0,05; #p<0,01; &p<0,001). CONCLUSAO: Nossos resultados mostram que ratos espontaneamente hipertensos de 13 semanas apresentaram reducao da funcao barorreflexa quando testados com fenilefrina.BACKGROUND The literature describes contradictory data regarding the onset of the baroreflex reduction in spontaneously hypertensive rats. OBJECTIVE This investigation was undertaken to evaluate the baroreflex function in 13-week-old spontaneously hypertensive rats. METHODS Male Wistar Kyoto (n=15) and spontaneously hypertensive rats (n=15) aged 13 weeks were studied. Cannulas were inserted in the abdominal aortic artery through the right femoral artery to measure mean arterial pressure and heart rate. Baroreflex function was calculated as the derivative of the variation of HR in function of the MAP variation (Delta heart rate/Delta mean arterial pressure) tested with a depressor dose of sodium nitroprusside (50microg/kg) and with a pressor dose of phenylephrine (8microg/kg) in the right femoral venous approach through an inserted cannula in awake spontaneously hypertensive rats and Wistar-Kyoto. Differences with p values < 0.05 were considered statistically significant. RESULTS Spontaneously hypertensive rats: Delta mean arterial pressure=43.5mmHg+/-5.2, Delta heart rate=-59.7ppm+/-17.9 and Delta heart rate/Delta mean arterial pressure=1.3ppm/mmHg+/-0.1 tested with phenylephrine; Wistar Kyoto: Delta mean arterial pressure=&56mmHg+/-3, Delta heart rate=*-114.9ppm+/-11.3 and Deltaheart rate/Delta mean arterial pressure=#1.9ppm/mmHg+/-0.3 tested with phenylephrine; spontaneously hypertensive rats: Delta mean arterial pressure=-45.6mmHg+/-8.1, Delta heart rate=40.1ppm+/-11.6 and Delta heart rate/Delta mean arterial pressure=0.9ppm/mmHg+/-0.5 tested with sodium nitroprusside; Wistar Kyoto: Delta mean arterial pressure=-39.8mmHg+/-6.2, Delta heart rate=51.9ppm+/-21.8 and Delta heart rate/Delta mean arterial pressure=1.4ppm/mmHg+/-0.7 tested with sodium nitroprusside (*p<0.05; #p<0.01; &<0.001). CONCLUSION Our results showed that 13-week-old spontaneously hypertensive rats presented reduced baroreflex function when tested with phenylephrine.

Do patients with electrocardiographic Brugada type 1 pattern have associated right bundle branch block? A comparative vectorcardiographic study

AIMS Previous studies have reported right bundle branch block in Brugada syndrome. Subsequent analysis of electrocardiograms (ECGs) found one-third of cases classified as right bundle branch block did not meet criteria of a wide final S wave in the left leads. We aimed to study the role of the vectorcardiogram to characterize Brugada type 1 ECG pattern. METHODS AND RESULTS Compare Frank-method vectorcardiogram in 11 patients with Brugada type 1 ECG pattern (BrS group) with vectorcardiogram of 20 healthy individuals with ECGs depicting incomplete right bundle branch block (IRBBB group) and 12 patients with complete right bundle branch block (CRBBB group). Initial 10-20 ms vector of the QRS loop in the horizontal plane (HP): BrS and IRBBB groups: Vector heading anterior and leftward. CRBBB group: Vector directed anterior and rightward. Right end conduction delay of the QRS loop: BrS group: Upper right quadrant of the frontal plane, right posterior quadrant of the HP. IRBBB group: Upper right quadrant of the frontal plane (30%) and right anterior quadrant of the HP (90%). CRBBB group: Upper right quadrant on the frontal plane (30%); all cases in the right anterior quadrant of the HP. 0 point (onset of QRS loop) and J point (end of QRS loop) relationship: BrS group: Not coincidental. IRBBB and CRBBB groups: Coincidental. T loop morphology, size, and appearance: BrS group: Circular, with symmetrical afferent and efferent limbs in 10 cases (90%). IRBBB and CRBBB groups: Elliptical or linear with slow inscription of efferent limb and rapid inscription of afferent limb. CONCLUSIONS Vectorcardiograms in patients with Brugada type 1 ECG pattern have distinctive characteristics compared with healthy individuals with incomplete and CRBBB. These differences relate to the spatial location of the end conduction delay (right superior and posterior quadrant in the BrS group) and the morphology, size, and velocity of inscription of afferent and efferent limbs of the T loop (circular, small, of symmetrical limbs) and with a 1:1 length/width ratio.

Fluoxetine effects on mitochondrial ultrastructure of right ventricle in rats exposed to cold stress

OBJECTIVE To assess fluoxetine effects on mitochondrial structure of the right ventricle in rats exposed to cold stress. METHODS The experimental study procedures were performed in 250-300g male EPM-Wistar rats. Rats (n=40) were divided into four groups: 1) Control group (CON); 2) Fluoxetine (FLU); 3) Induced hypothermia (IH) and; 4) Induced hypothermia treated with fluoxetine (IHF). Animals of FLU group were treated by the administration of gavages containing 0.75 mg/kg/day fluoxetine during 40 days. The induced hypothermia was obtained by maintaining the groups 3 and 4 in a freezer at -8 degrees C for 4 hours. The animals were sacrificed and fragments of the right ventricle (RV) were removed and processed prior to performing electron microscopic analysis. RESULTS The ultrastructural changes in cardiomyocytes were quantified through the number of mitochondrial cristae pattern (cristolysis). The CON (3.85%), FLU (4.47%) and IHF (8.4%) groups showed a normal cellular structure aspect with preserved cardiomyocytes cytoarchitecture and continuous sarcoplasmic membrane integrity. On the other hand, the IH (34.4%) group showed mitochondrial edema and lysis in cristae. CONCLUSION The ultrastructural analysis revealed that fluoxetine strongly prevents mitochondrial cristolysis in rat heart, suggesting a protector effect under cold stress condition.

Cold stress effects on cardiomyocytes nuclear size in rats: light microscopic evaluation

INTRODUCTION Total body induced hypothermia and myocardial cooling are effective methods regarding myocardial protection during heart surgery and ischemia. It is described in previous studies that extreme low temperature exposure causes mitochondrial cristae and myofilament disarrangement in cardiomyocytes, however, no investigation has analyzed the effects of cold stress on nuclear size of cardiomyocytes. OBJECTIVES To evaluate the effects of acute cold stress exposure on the nuclear size of cardiomyocytes in rats. METHODS The experimental study procedures were performed on 300-310 g adult male Wistar rats. Rats (n=20) were divided into two groups: 1) Control (CON) and; 2) Induced hypothermic (IH) group. Animals of IH group were exposed during 4 hours once at a controlled temperature of - 8 degrees C. It was performed histological analysis of liver and adrenal gland to examine the stress condition of animals. Cardiomyocytes nucleus size were examined by three independent investigators with the same and standardized criteria and analyzed by Bartkos intra-class correlation coefficient (R>0.75 = positive concordance). Students t test was applied. The significance level was set at P<0.05. RESULTS The induced hypothermic group presented higher lipid depletion in adrenal gland cells (P<0.05) and higher glycogen depletion in liver glycogen (P<0.05). The experimental group showed lower cardiomyocytes nuclear volume (108 + 1.7 microm(3); P<0.05), it decreased in 76% compared to the control group (142 + 2.3 microm(3)). Bartkos correlation: CON=0.44; IH=0.96, variation analysis between groups means differences was significant. CONCLUSION These data suggest that acute cold stress exposure induces cardiomyocytes nucleus size reduction in rats.

Kearns-Sayre syndrome: electro-vectorcardiographic evolution for left septal fascicular block of the his bundle

The Kearns-Sayre syndrome is a neuromyopathic disorder associated with mitochondrial abnormalities and characterized by the triad of chronic external ophthalmoplegia, atypical pigmentary retinopathy, and progressive conduction system disorders. Ragged red muscle fibers that seem to contain an excess of altered mitochondria are observed. The disease affects both sexes alike, during the first or the second decade of life. The following manifestations are observed: central bilateral sensorineural deafness, pyramidal signs, ataxia, asymmetrical ptosis, external ophthalmoplegia, and progressive muscular weakness secondary to myopathy associated with a significant increase of proteins of cephalorachidian liquid. A variety of endocrinopathies may occur.

Wellens syndrome associated with prominent anterior QRS forces: an expression of left septal fascicular block?

Wellens syndrome is a clinical-electrocardiographic entity also referred to as left anterior descending (LAD) coronary T-wave syndrome or acute coronary T-wave syndrome. It is a complex of symptoms and signals indicating the existence of an undesirable condition secondary to critical high-grade proximal stenosis of the LAD coronary artery characterized by the association of prior history of acute coronary syndrome with little or no elevation of markers of myocardial damage (unstable angina) and characteristic electrocardiographic changes consistent with subepicardial anterior ischemic pattern (persistently symmetrical, deep negative and broad-based T waves) or plus-minus T waves with inversion of the terminal portion in the LAD coronary artery territory (V1 through V5 or V6). We present a case of a variant of Wellens syndrome that reveals association and, transitorily, the criteria described in literature for left septal fascicular block.

Myocardium tissue changes caused by electrical transthoracic discharges in rats

Background Cardiomyocytes cytoarchitecture changes caused by transthoracic countershocks have been focused recently. We aimed to evaluate the effects of electrical discharge application in the mitochondria structure in atrial myocardium of rats. Methods An electrical cardioverter was adapted to small rodent animals for our research. Electrical discharges were applied to the precordial region of 30 albino rats: (1) control group - animals that remained on resting period and were afterwards sacrificed; (2) electrical discharge group - animals that remained on resting period, followed by ten electrical discharges of 300 mV and sacrificed, and; (3) electrical post-discharge group - animals that remained on a resting period and received ten electrical discharges like the electrical discharge group, but were sacrificed seven days subsequently. We examined liver, adrenal and left atrium tissue fragments of the three groups. Results It was observed in control and post-discharge groups a normal cellular structure aspect with preserved architecture of cardiomyocytes and continuous sarcoplasmic membrane integrity. On the other hand, cardiac muscle fibers with mitochondrial edema and lysis occurred in the discharge group. Glycogen and adrenal lipids were not depleted in all groups. Conclusion These data suggest that transthoracic electrical discharges induce mitochondrial injuries in atrial cardiac cells of rats.