Anabolic steroids induce cardiac renin-angiotensin system and impair the beneficial effects of aerobic training in rats.

We evaluated the effects of swimming and anabolic steroids (AS) on ventricular function, collagen synthesis, and the local renin-angiotensin system in rats. Male Wistar rats were randomized into control (C), steroid (S; nandrolone decanoate; 5 mg/kg sc, 2x/wk), steroid + losartan (SL; 20 mg.kg(-1).day(-1)), trained (T), trained + steroid (T+S), and trained + steroid + losartan (T+SL; n = 14/group) groups. Swimming was performed 5 times/wk for 10 wk. Serum testosterone increased in S and T+S. Resting heart rate was lower in T and T+S. Percent change in left ventricular (LV) weight-to-body weight ratio increased in S, T, and T+S. LV systolic pressure declined in S and T+S. LV contractility increased in T (P < 0.05). LV relaxation increased in T (P < 0.05). It was significantly lower in T+S compared with C. Collagen volumetric fraction (CVF) and hydroxyproline were higher in S and T+S than in C and T (P < 0.05), and the CVF and LV hypertrophy were prevented by losartan treatment. LV-ANG I-converting enzyme activity increased (28%) in the S group (33%), and type III collagen synthesis increased (56%) in T+S but not in T group. A positive correlation existed between LV-ANG I-converting enzyme activity and collagen type III expression (r(2) = 0.88; P < 0.05, for all groups). The ANG II and angiotensin type 1a receptor expression increased in the S and T+S groups but not in T group. Supraphysiological doses of AS exacerbated the cardiac hypertrophy in exercise-trained rats. Exercise training associated with AS induces maladaptive remodeling and further deterioration in cardiac performance. Exercise training associated with AS causes loss of the beneficial effects in LV function induced by exercising. These results suggest that aerobic exercise plus AS increases cardiac collagen content associated with activation of the local renin-angiotensin system.

The long-term outcome of patients with hypertensive cardiomyopathy.

The prognosis of dilated cardiomyopathy due to hypertension (HT-DCM) is surprisingly unknown, particularly in the absence of coronary disease and diabetes. We aimed at investigating the long-term outcome and the predictors of mortality in patients with left ventricular systolic dysfunction exclusively due to hypertension. From October 1995 to May 2001, 90 consecutive patients with echocardiographic fractional shortening (FS) < 30% and 29 control patients with FS > or = 30% were included. Obstructive coronary disease was excluded by dipyridamole myocardial perfusion imaging in all patients and coronary angiography in 60. After a mean follow-up of 4.3+/-1.6 years, the total mortality rate of HT-DCM was twice as much higher than that of patients without left ventricular systolic dysfunction (P = 0.01). In HT-DCM, the 5-year mortality rate was 26%. Univariate analyses selected age and creatinine for being positively related to mortality, and body mass index, FS and blood pressure during follow-up for being negatively related to mortality. Neither the improvement of left ventricular FS nor the decrease in left ventricular mass index was related to survival. Multivariate analysis identified (hazard ratio; 95% confidence interval) age (1.08; 1.02-1.13), body mass index (0.86; 0.75-0.98), and baseline FS (0.88; 0.78-0.98) as independent predictors of mortality. In conclusion, poor survival in HT-DCM can be anticipated by the severity of left ventricular systolic dysfunction and advanced age. Instead of ominous signs, high blood pressure and body mass may predict a more favourable prognosis.

Left ventricular function after a new pregnancy in patients with peripartum cardiomyopathy.

BACKGROUND: A new pregnancy is usually discouraged in patients with peripartum cardiomyopathy (PPCM), particularly when there is persistent left ventricular dysfunction. This study was undertaken to evaluate left ventricular systolic function after a new pregnancy in patients with PPCM. METHODS AND RESULTS: Nine of 44 patients with PPCM became pregnant and were selected for this study. Two patients were lost to follow-up, 1 immediately after the new pregnancy diagnosis, and the other 1 after the latest delivery, and, thus, were excluded. The remaining 7 patients had regular clinical and obstetric examinations until delivery, continued follow-up, and were submitted to echocardiography 6 to 12 months thereafter. Pregnancy was relatively well tolerated in the patients, and they gave birth to 7 healthy newborns. After this latest pregnancy, 4 patients with heart failure functional class II and 2 patients with functional class III remained unchanged. A patient, initially in functional class III, improved and was then in functional class II. Although left ventricular end-diastolic diameter did not change (61 to 58 mm), left ventricular end-systolic dimension decreased (50 to 47 mm, P =.008), resulting in a significant increase in left ventricular fractional shortening (19% to 23%, P =.02). CONCLUSION: Although based only in a small number of patients, the present results suggest that cardiac function does not deteriorate during a new pregnancy in patients with PPCM.

Maximal functional capacity in patients with Chagas' cardiomyopathy without congestive heart failure.

BACKGROUND: Chagas' disease is a known dilated form of cardiomyopathy. However, a great number of patients, although showing electrocardiographic (ECG) well-recognized changes, maintain normal ventricular chamber dimensions and are asymptomatic. The aim of the present study was to objectively characterize functional capacity in asymptomatic patients with Chagas' disease and normal left ventricular function. METHODS AND RESULTS: Eighteen asymptomatic male patients with Chagas' disease, aged 33+/-6 years, were selected for the study. All showed ECG changes typical of the disease, as well as left ventricular fractional shortening (LVFS) greater than 0.30 on M-mode 2-dimensionally guided echocardiography. Twenty sedentary normal male patients, aged 29+/-6 years, served as controls. Both groups were submitted to ergoespirometry testing for assessment of exercise functional capacity. Patients with Chagas' disease, when compared with controls, showed lower (P < .001) maximal O2 consumption (VO2max, 24.3+/-4.2 v 37.0+/-5.4 mL x kg(-1) x min(-1) respectively); O2 pulse rate (PO2max, 10.5+/-1.4 v 15.1+/-2.5 mL/beat, respectively); maximal ventilation (VEmax, 50.1+/-13.5 v 113.0+/-17.6 L x min(-1), respectively); anaerobic threshold of maximal O2 consumption (VO2-AT, 15.8+/-3.6 v 24.6+/-4.7 mL x kg(-1) x min(-1), respectively); and maximal heart rate (HRmax, 154+/-21 v 186+/-7 beat x min(-1), respectively). CONCLUSIONS: Asymptomatic patients with Chagas' disease, although presenting normal left ventricular systolic function at rest, display a substantial impairment of exercise functional capacity.

Apical aneurysm and left ventricular hypertrophy.

A 59-year-old woman presented with an embolic transient ischemic attack and a history of controlled hypertension for 16 years. Both echocardiogram and MRI showed severe biventricular hypertrophy and an apical aneurysm with a thrombus. The occurrence of an apical aneurysm in the presence of cardiac hypertrophy is a rare finding and has been described in patients with hypertrophic cardiomyopathy. However, it has not been reported in patients with systemic arterial hypertension. In this patient the lack of a relationship between the severity of the hypertrophy and the levels of blood pressure, together with the presence of histologic disorganization of myocardial cardiac muscle cells by endomyocardial biopsy suggested the diagnosis of hypertrophic cardiomyopathy.

Normalization of left ventricular dysfunction in systemic hypertension.

BACKGROUND: In hypertensive heart disease, it is uncertain whether the impairment of left ventricular (LV) systolic function might be reverted by antihypertensive treatment. HYPOTHESIS: This study was undertaken to address the likelihood of recovery of LV dysfunction and to identify factors potentially related. METHODS: Twenty-six patients with primary (n = 16) and renovascular (n = 10) hypertension participated in the study and were classified into Groups A (n = 12) and B (n = 14) according to normalization or persistent left ventricular dysfunction (fractional shortening < 0.30) after 36 weeks of follow-up. All patients received standard medical therapy and appropriate procedures for renovascular disease correction. Logistic regression analysis was used to identify variables associated with recovery. RESULTS: Patients in Group A compared with those in Group B were younger (41 +/- 14 vs. 52 +/- 10 years; p < 0.05), had a greater frequency of renovascular hypertension (8 vs. 2; p < 0.05), showed shorter LV end-diastolic (54 +/- 5 vs. 61 +/- 8 mm; p < 0.05) and end-systolic dimensions (41 +/- 6 vs. 49 +/- 9 mm; p < 0.05), and lower mass index (215 +/- 64 vs. 261 +/- 47 g.m-2; p < 0.05) before treatment, whereas fractional shortening (0.24 +/- 0.4 vs. 0.20 +/- 0.5; p > 0.05) and diastolic blood pressure (116 +/- 12 vs. 122 +/- 19 mmHg; p > 0.05) were similar. On follow-up, Group A patients showed lower diastolic blood pressure (89 +/- 15 vs. 105 +/- 20 mmHg; p < 0.05) and mass index (142 +/- 34 vs. 222 +/- 40 g.m-2; p < 0.05). Logistic regression analysis identified systolic dimension and renovascular hypertension as factors associated with fractional shortening normalization. CONCLUSION: The recovery of LV dysfunction is expected to occur most likely in patients with renovascular hypertension and the shortest systolic dimensions.

Left ventricular hypertrophy predicts outcome of hypertension regardless of the type of ventricular arrhythmia present.

Left ventricular hypertrophy is associated with an increased cardiovascular mortality in hypertension. A potential role of ventricular arrhythmias is debated but not yet determined. The purpose of this study was to evaluate whether the presence of arrhythmias would ascribe any additional risk to cardiovascular mortality beyond that related to the presence of left ventricular hypertrophy. From November 1988 to February 1991, 40 mild to severe hypertensive patients (mean SBP, DBP 183/117 mm Hg) were submitted to clinical, echocardiographic and electrocardiographic evaluations complemented by 24-h Holter monitoring and then followed until November 1996. The Kaplan-Meier method supplemented by the Cox multiple regression model were performed to identify the variable(s) associated with fatal cardiovascular outcome. Twelve cardiovascular fatalities occurred as a consequence of sudden death (n = 4), stroke (n = 4), heart failure (n = 2) and myocardial infarction (n = 2). In comparison with patients who survived, those dying from cardiovascular causes had a greater percentage of electrocardiographic left ventricular hypertrophy (83 vs 36%, P = 0. 0037) and couplets of ventricular ectopic beats (58 vs 18%, P = 0. 0467). In addition, they showed larger left ventricular diastolic diameter (60 +/- 10 vs 53 +/- 8 mm), mass index (248 +/- 67 vs 154 +/- 57 g/m2) and posterior wall thickness (12 +/- 2 vs 10 +/- 2 mm), as well as shorter left ventricular fractional shortening (0.23 +/- 0.8 vs 0.32 +/- 0.9). Univariate analysis showed that electrocardiographic left ventricular hypertrophy and strain, mass index, end-systolic wall stress, fractional shortening and the presence of couplets were significantly related to cardiovascular mortality. However, only mass index was shown to be independently associated with cardiovascular death. In conclusion, left ventricular hypertrophy predicts cardiovascular outcome, regardless of the presence of other signs of cardiac damage, including ventricular arrhythmia.

Angiotensin II receptor blockade and myocardial fibrosis of the infarcted rat heart.

Tissue angiotensin II (AngII) is increased in the infarcted rat heart, where it may have autocrine or paracrine properties that influence cellular protein synthesis and growth and therefore tissue repair. It was our hypothesis that treatment with an AT1 receptor antagonist would attenuate fibrous tissue formation after myocardial infarction (MI). To investigate a role for local AngII in the regulation of connective tissue formation during early and late wound healing that follows MI, this study was undertaken. Animals were randomized into two groups in which rats were or were not treated with the AT1 receptor antagonist losartan (10 mg x kg(-1) daily gavage). At 1 and 4 weeks after experimental MI was induced by coronary artery ligation, rat hearts were examined. Infarct size, infarct area, and collagen volume fraction at the site of infarction and in noninfarcted myocardium were determined by picrosirius red staining with videodensitometry. Quantitative in vitro autoradiography was used to detect AngII receptor binding density ((125)I-(Sar1,Ile8)AngII). Compared with an untreated MI control group, in losartan-treated rats we found (1) infarct size was comparable in both groups at weeks 1 and 4, (2) infarct area was comparable between groups at week 1 but was significantly reduced (p < 0.05) at week 4 in losartan-treated rats, (3) a detectable reduction in collagen volume fraction at the site of MI was not found at week 1 but was reduced (p < 0.05) at remote sites at week 4, (4) AngII receptor binding density was reduced (p < 0.05) by 50% at the site of MI at both weeks 1 and 4 in keeping with delivery of losartan to this site of injury. Thus AT1 receptor antagonism appears to influence late phase wound healing at and remote to the site of MI and suggests an association between AngII and the fibrogenic response that appears in the injured rat heart. Although still speculative, an attenuation in fibrosis after MI may account for less ventricular dysfunction and geometric remodeling of right and left ventricles and ventricular arrhythmias that have been observed in such rats treated with angiotensin converting enzyme inhibitor or AT1 receptor antagonist.

[Cricopharyngeal dysfunction]. / Disfunção cricofaríngea.

The idiopathic dysfunction of the cricopharyngeal muscle is a rare disease. Limited understanding of the pharyngoesophageal physiology and physiopathology make the management of this disease complex. We have studied three patients with idiopathic crycopharyngeal dysfunction submitted to cricomyotomy. One patient did not present improvement after surgery. The authors discuss the difficulties in making the diagnosis., the treatment and the selection of patients who will benefit from this surgical procedure.

Wound healing following myocardial infarction in the rat: role for bradykinin and prostaglandins.

Bradykinin and prostaglandins are established mediators of exudative and inflammatory phases of healing. Their contribution to the fibrogenic component of healing in the heart is less certain. We therefore undertook the present study in rats with acute myocardial infarction (MI) following left coronary artery ligation. Treatment with a bradykinin B2 receptor antagonist (Hoe140, 0.5 microgram/kg/min s.c.) or a cyclooxygenase inhibitor (indomethacin, 2 mg/kg p.o.), initiated 24 h after surgery, was examined for responses in MI topography (size and area), MI and nonMI tissue fibrosis (fibrillar collagen specific picrosirius red). Early (week 1) and late (week 4) phases of fibrogenesis postMI were examined. Compared to control, we found: (1) MI size at weeks 1 and 4 was comparable in untreated and treated rats: (2) infarct area, a measure of scar thickness, was reduced (P < 0.05) at week 4 by each intervention; and (3) densitometric collagen volume fraction did not reveal a reduction in collagen accumulation at the MI site, but this was evident remote to the MI (P < 0.05) at week 4 for each agent. Thus, pharmacological interference with bradykinin-receptor binding or prostaglandin synthesis following MI is associated with reduced fibrillar collagen formation. Though the mechanism responsible for observed alteration in fibrogenesis is uncertain, anti-inflammatory and anti-proliferative properties of these agents may be responsible.

[A false diagnosis of hypertrophic myocardiopathy in pheochromocytoma]. / Falso diagnóstico de miocardiopatia hipertrófica em feocromocitoma.

A 24 year-old man was admitted with hypertensive crises and diagnosis hypothesis of neurofibromathosis and pheochromocytoma with blood pressure of 150 x 110mmHg and in use of anti-hypertensive drugs. The electrocardiogram (EKG) showed left ventricle hypertrophy. An echocardiogram showed interventricular septum (IVS) thickness of 16mm, posterior wall (PW) thickness of 11mm (ratio IVS/PW was 1.4). Diastolic ventricular diameter was 39mm with gradient of 52mmHg and mild mitral-valve murmur by pulsate Doppler. Increased vanillylmandelic acid and metanephrines in a 24-hour sample of urine has confirmed diagnosis of pheochromocytoma within was localized by 131I metaiodobenzyl-guanidine scan and computerized axial tomography. The patient was submitted to right adrenalectomy. Blood pressure was normalized. Evaluation an year later revealed a healthy man with normal laboratory exams, EKG and echocardiogram. It seems that the hypertrophy was consequence of the hypertension and pheochromocytoma, was not hypertrophic cardiomyopathy.

[The role of hypertrophy and left ventricular function on the occurrence of ventricular arrhythmias in arterial hypertension]. / Papel da hipertrofia e da função ventricular esquerda sobre a ocorrência de arritmias ventriculares na hipertensão arterial.

PURPOSE: To evaluate the role of left ventricular hypertrophy (LVH), left ventricular systolic function an other clinical parameters on prevalence and complexity of ventricular arrhythmias in hypertension. METHODS: Ventricular arrhythmias were studied in 39 hypertensives by 24 hours ambulatory electrocardiographic monitoring. Frequency and complexity of ventricular arrhythmias were compared among 3 groups: A and B, respectively without and with LVH, both with normal left ventricular function; and C with LVH and systolic dysfunction. LVH and systolic dysfunction were established echocardiographically. Linear regression analysis was performed in order to identify an independent correlation between clinical parameters and presence of arrhythmias. RESULTS: Group C patients were older and had significantly higher systolic and diastolic blood pressures, greater mass index, diastolic posterior wall thickness and end-systolic stress and increased prevalence of electrocardiographic strain. Left ventricular diastolic diameter in C group patients was increased only when compared to A group. Frequencies of cases with more than 10 ectopic ventricular beats/hour, pairs and nonsustained ventricular tachycardia episodes were all significantly increased in C when compared to B and to A. However, only left ventricular mass index or diastolic posterior wall thickness identified independently patients with ventricular arrhythmias. CONCLUSION: Left ventricular hypertrophy is the main predictor of potential high risk rhythm disturbances in hypertension.

[Role of blood pressure in rest and exercise conditions and importance of clinical factors in left ventricular hypertrophy in arterial hypertension]. / Papel da pressão arterial casual e do exercício e a influência de fatores clínicos sobre a hipertrofia ventricular esquerda na hipertensão arterial.

PURPOSE: To evaluate the role of casual and exercise blood pressure as well as the importance of clinical factors on the presence and degree of left ventricular hypertrophy in hypertension. METHODS: Fifteen normotensives (control group) and 30 hypertensives, 14 of them with and 16 without left ventricular hypertrophy (groups with LVH and without LVH, respectively) were studied. LVH diagnosis was established when mass index was higher than 2 standard-deviations of the mean values calculated for each sex in control group. Resting, casual determined, and bicycle exercise systolic and diastolic blood pressures along with age, body surface area, sex and race distribution were compared between groups. In addiction, their relation with mass index as independent variables were also tested. RESULTS: Hypertensives in group with LVH had higher diastolic septal, posterior wall, and relative wall thicknesses. No significant statistical difference was observed neither in sex and race distribution, nor in age and body surface area between groups. Otherwise, there were significant differences in both resting and exercise blood pressure. In the entire population studied, left ventricular mass index significantly correlated with age (r=0,33, p=0,03) as well as with both casual (systolic - r=0,72, p=0,0001; diastolic - r=0,69, p=0,0001) and exercise (systolic - r=0,62, p=0,0001; diastolic - r=0,66, p=0,0001) blood pressures. However, linear regression analysis demonstrated that only resting systolic (p=0,0001) and exercise diastolic (p=0,0303) blood pressures were significant and independent determinants of mass index. CONCLUSION: Resting and exercising blood pressures are the main determinants of left ventricular hypertrophy in hypertension.

[Percutaneous angioplasty and surgical revascularization in renovascular hypertension: experience in treatment and long-term follow up in 124 patients]. / Angioplastia percutânea e revascularização cirúrgica em hipertensão renovascular. Experiência no tratamento e seguimento de longo prazo em 124 pacientes.

PURPOSE: To report the experience in the treatment and long-term follow-up of patients with renovascular hypertension submitted to angioplasty and/or surgical revascularization, and to compare blood pressure and renal function responses to both treatment. METHODS: One hundred and twenty-four patients diagnosed with renovascular hypertension, divided, according to the etiology, as atherosclerosis (76 patients), fibromuscular dysplasia (32) and arteritis (16), were submitted to isolated or associated treatment of renal revascularization by percutaneous transluminal angioplasty (71 patients) or surgery (84). The patients were followed-up during 2.5 +/- 1.5 years and we evaluate blood pressure response and renal function preservation. In relation to blood pressure control, the patients were considered as cured when normotensives without antihypertensives, improved when normotensives with fewer drugs than previously, and unchanged, when out of these criteria. RESULTS: From 124 patients, 20% were considered cured, 54% improved and 26% unchanged, after a mean follow-up of 2.5 +/- 1.5 years. Patients with atherosclerosis and fibromuscular dysplasia presented a higher rate of care and improvement after surgery. The blood pressure and the number of antihypertensive drugs decreased significantly during the follow-up among patients that cured or improved arterial hypertension, either after angioplasty (190 +/- 26/115 +/- 14 mmHg vs 130 +/- 34/85 +/- 7 mmHg. 2.70 vs 1.60 drugs) or after surgery (194 +/- 17/115 +/- 16 mmHg vs 143 +/- 18 mmHg vs 88 +/- 8 mmHg, 1.88 vs 1.51 drugs). It was also observed a significant decrease of serum creatinine among these patients. CONCLUSION: Renal revascularization in patients with renovascular hypertension, either by angioplasty or surgery, is beneficial to control blood pressure and to preserve renal function in the majority of patients.

[Hypertension and complex ventricular arrhythmias. Evolution following a long-term blood pressure treatment]. / Hipertensão arterial e arritmias ventriculares complexas. Evolução após tratamento de longo prazo da pressão arterial.

PURPOSE: To evaluate the effects of long-term antihypertensive treatment in the frequency as well as in the complexity of ventricular arrhythmias in arterial hypertension. METHODS: Twenty three patients, 14 males and 11 whites, with mean age of 46 years, were submitted to 24 hours ambulatory electrocardiographic monitoring and echocardiographic studies before and 9 months after antihypertensive treatment. RESULTS: There was no significant serum potassium level alteration, but significant reductions of both systolic (from 192 +/- 29mmHg to 161 +/- 25mmHg) and diastolic (from 122 +/- 17mmHg to 99 +/- 16mmHg) blood pressure. Left ventricular percent of fiber shortening significantly increased, even though only from 26 +/- 9% to 30 +/- 9%, and end-systolic wall stress did not change at all (before 258 +/- 94 10(3) dyn/cm2, after 255 +/- 101 10(3) dyn/cm2). Left ventricular mass index showed significant but also a discrete reduction from 211 +/- 75g/m2 to 196 +/- 70g/m2. Ambulatory electrocardiographic monitoring did not show any significant decrease in neither ventricular ectopic beats nor in couplets. Non-sustained ventricular tachycardia episodes remained unchanged too. Four out of 8 patients with more than 30 ventricular ectopic beats per hour reduced it by more than 70%. On the other hand, the number of patients with couplets was reduced from 10 to 8 whilst those with non-sustained ventricular tachycardia increased from 5 to 7. Furthermore, in 7 patients reevaluated 24 months thereafter results were not expressively dissimilar. CONCLUSION: In hypertensive patients with either severe degree of left ventricular hypertrophy or myocardial dysfunction, long-term blood pressure treatment that produce no impressive changes in these abnormalities also do not modify complex ventricular arrhythmias, in spite of a great reduction in the increase blood pressure.

[Pheochromocytoma. Its diagnostic and therapeutic characteristics]. / Feocromocitoma. Peculiaridades diagnósticas e terapêuticas.

Pheochromocytoma is a cause of hypertension that frequently can be cured by surgery. The aim of this paper, based on 5 cases of pheochromocytoma, is to relate our experience in diagnosis and treatment in this pathology. In four of 5 patients with pheochromocytoma we observed unusual characteristics of the disease. Association with neurofibromatosis in one case, with rheumatic mitral regurgitation in another; and in a third case the tumor was malignant. One patient had catecholamine-mediated electrocardiographic changes which disappeared with treatment. Since symptoms of adrenergic hyperactivity were present in all cases, the rise in the levels of vanilmandelic acid and urinary metanephrines were useful in confirming the diagnosis. Computed tomography and I-131 meta-benzylguanidine for radioisotopic imaging, displayed not only all tumoral masses but also bone metastases in the malignant case. During the follow-up period, from the sixth month to the fourth year after surgery, four patients were asymptomatic, and have normal urinary catecholamine metabolite levels. The patient with a malignant form of pheochromocytoma continued to show elevated catecholamines release and remained hypertensive in spite of adrenal mass resection.

Ventricular function by radionuclide ventriculography in malignant hypertension.

Malignant hypertension is a unique and natural model for the study of abnormalities of left ventricular function due to arterial hypertension, because the development and regression of these abnormalities can be observed in a short period. Studies of ventricular function by radionuclide ventriculography, either before or after therapy, have not been previously reported in malignant hypertensive patients. We used this methodology to study left ventricular function in 17 malignant/accelerated hypertensive patients at the time of admission to the hospital and 3, 6, and 9 months after discharge. Seventy percent of patients (12 of 17) had symptoms of congestive heart failure at admission. We compared these data with those obtained in 12 normotensive subjects and 13 mild-to-moderate untreated hypertensive patients. Blood pressure of malignant hypertensive patients was 213 +/- 26/140 +/- 17 mm Hg at admission and 165 +/- 23/101 +/- 15 after 9 months of therapy. Radionuclide ventriculography at admission showed that peak filling rates of malignant hypertensive patients (2.13 +/- 0.21 end-diastolic volume [counts] [EDV]/sec) were significantly lower than those in normotensive subjects (2.40 +/- 0.41) and in mild-to-moderate hypertensive patients (2.46 +/- 0.21). In contrast, peak ejection rates were significantly higher in malignant hypertensive patients (3.44 +/- 0.38 EDV/sec) than in the two control groups (3.01 +/- 0.32 and 3.10 +/- 0.43, respectively). Ejection fractions were similar in the three groups of patients. After 9 months of therapy, peak filling rates of malignant hypertensive patients increased to 2.38 +/- 0.35 EDV/sec, whereas peak ejection rates decreased to 2.89 +/- 0.43 EDV/sec, both not significantly different from data in controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Lesao de via biliar principal corrigida no ato cirurgico ou no pos-operatorio imediato. / Main bile duct injury corrected in the surgical act or in immediate postoperative period

As lesoes acidentais das vias biliares extra-hepaticas nas colecistectomias constituem complicacoes serias e que nem sempre sao identificadas no ato cirurgico inicial O reconhecimento imediato da lesao da ao cirurgiao a possibilidade de uma reconstrucao adequada. Neste trabalho sao analisados nove doentes com lesoes da via biliar principal em colecistectomias, sete com diagnostico e correcao imediata e dois com reconstrucao no pos-operatorio. Como complicacao ocorreram duas fistulas pos-operatorias com resolucao espontanea e uma estenose cicatricial. Nao houve mortalidade e no seguimento todos os doentes se apresentam, bem