Mild Systemic Hypertension Research Articles

Unusual Simultaneous Occurrence of Cerebral Arterial and Venous Thromboembolism in the Setting of Antithrombin 3 (AT3) Deficiency

The subject was a 40-year-old man with a known past history of mild systemic hypertension, hyperlipidemia and ischemic heart disease. He woke up six hours prior to presentation and found that he was unable to move the left limbs. He was on Aspirin 100 mg once daily, Atorvastatin 10 mg once daily and Carvedilol 6.25 mg once daily. He had undergone coronary angioplasty fifteen years previously.

Body weight, blood pressure, and systemic changes following low-dosage prednisolone administration in dogs.

OBJECTIVE To investigate systemic changes following low-dosage prednisolone administration in dogs. ANIMALS 4 healthy purpose-bred adult male Beagles. PROCEDURES Dogs were administered prednisolone PO at a dosage of 2 mg/kg/d for 2 weeks, 1 mg/kg/d for 4 weeks, and 0.5 mg/kg/d for 3 weeks. Body weight, blood pressure, hepatic size and echogenicity, percentage of vacuolated hepatocytes, serum hepatic enzyme activities and glucose concentration, adrenal gland size, and pancreatic echogenicity were evaluated weekly for 9 weeks. RESULTS The only significant change identified was an increase in hepatic echogenicity, assessed by measuring liver-kidney contrast on ultrasonographic images. Increases in hepatic size and percentage of vacuolated hepatocytes were identified, but values did not differ from baseline values. Similarly, serum hepatic enzyme activities increased, but changes were mild and not significantly different from baseline values. Body weight, pancreatic echogenicity, and serum glucose concentration did not show noticeable changes. Mild systemic hypertension was seen, but blood pressure was not significantly different from the baseline value. Similarly, adrenal gland size steadily decreased during the first 6 weeks and increased again after the prednisolone dosage was decreased to 0.5 mg/kg/d. However, mean adrenal gland size was not significantly different from the baseline value at any time. CONCLUSIONS AND CLINICAL RELEVANCE Results suggested that in dogs, administration of prednisolone at a low dosage was associated with minimal systemic effects.

Blood pressure and renal injury in dogs with visceral leishmaniasis

Abstract: Systemic hypertension is known to be a common consequence of chronic renal disease, which is frequently diagnosed in dogs with visceral leishmaniasis. Although many veterinary investigations have looked at the renal injury caused by Leishmania spp., the role played by this complication in the development of arterial hypertension documented in some animals with visceral leishmaniasis is not completely understood. In this study, 18 adult dogs with naturally-occurring visceral leishmaniasis and varying clinical signs underwent an indirect blood pressure measurement. Also, sera and spot urine were used for laboratory tests. The median systolic blood pressure was 135.2mmHg (95% confidence interval: 128.5-147.7), median mean arterial pressure was 105.8mmHg (98.3-110.4), and median diastolic arterial pressure was 88.5mmHg (77.8-92.5). No differences existed between asymptomatic and symptomatic animals regarding arterial pressure, and no correlations were documented between blood pressure and serum creatinine, blood urea, urine protein-to-creatinine ratio, urine specific gravity, and the fractional excretion of sodium and potassium. Although an association between hypertension and the identification of inflammation on histopathology could not be demonstrated in hypertensive animals, the assessment of kidney samples from 12 dogs indicated mild inflammation with a lymphoplasmacytic infiltrate (6/12), moderate inflammation with multifocal lymphoplasmacytic and histiocytic infiltrates (3/12), and multifocal degeneration and protein casts (2/12). Anti-Leishmania spp. immunohistochemistry assays stained the renal epithelium in 2/12 of the animals. Even though mild systemic hypertension was documented in a small subset of animals, no relationship between the severity of clinical signs and hypertension could be anticipated.

Absence of the calcium-binding protein, S100A1, confers pulmonary hypertension in mice associated with endothelial dysfunction and apoptosis.

S100A1, a 10-kDa, Ca(2+)-binding protein, is expressed in endothelial cells (ECs) and binds eNOS. Its absence is associated with impaired production of nitric oxide (NO) and mild systemic hypertension. As endothelial dysfunction contributes to clinical and experimental pulmonary hypertension (PH), we investigated the impact of deleting S100A1 in mice, on pulmonary haemodynamics, endothelial function, NO production, associated signalling pathways, and apoptosis. Compared with wild-type (WT), S100A1-knock-out mice (KO) exhibited increased right ventricular (RV) weight/body weight ratio and elevated RV pressure in the absence of altered left ventricular filling pressures, accompanied by increase in wall thickness of muscularized pulmonary arteries and a reduction in microvascular perfusion. In isolated lung preparations, KO revealed reduced basal NO, blunted dose-responsiveness to acetylcholine, and augmented basal and angiotensin (AII)-induced pulmonary vascular resistance (R₀) compared with WT. Pre-treatment of KO lungs with S100A1 attenuated the AII-induced increase in pulmonary arterial pressure and R₀. S100A1-induced phosphorylation of eNOS, Akt, and ERK1/2 is attenuated in pulmonary EC of KO compared with WT. Basal and TNF-α-induced EC apoptosis is greater in KO vs. WT, and cell survival is enhanced by S100A1 treatment. Our data demonstrate that the absence of S100A1 results in PH by disruption of its normal capacity to (i) enhance pulmonary EC function by induction of eNOS activity and NO levels via Akt/ERK1/2 pathways and (ii) promote EC survival. The ability of exogenously administered S100A1 to rescue this phenotype makes it an attractive therapeutic target in the treatment of PH.

New Diagnosis of Type A Interrupted Aortic Arch at Age 24 Years

![Figure][1] [![Graphic][3] ][3][![Graphic][4] ][4] A 24-year-old woman who had moved to the United States 5 years earlier received a routine evaluation. Mild systemic hypertension, a systolic murmur, prominent neck pulsations, and diminished lower-extremity pulses were

Acromegaly without acral changes: A rare presentation

Acromegaly is diagnosed clinically by the universal presence of acral enlargement and typical coarse facies. We report a short, elderly female developing acromegalic facies for last 10 years without acral overgrowth. She is a patient of primary hypothyroidism, well controlled for last 20 years. Acromegaly was proven by high level of serum insulin like growth factor-1 (IGF-1) and elevated and nonsuppressed level of growth hormone (GH), with other hormonal profile being undisturbed. She had mild insulin resistance and systemic hypertension in absence of any visual field defect. Magnetic resonance imaging (MRI) of brain revealed pituitary hyperplasia without any detectable adenoma. No source of ectopic secretion of GH or growth hormone releasing hormone (GHRH) could be localized. Therefore, atypical presentation of acromegaly needs high degree of suspicion even if some of the common features are lacking. Here, we have biochemically proved acromegaly with typical facies, short stature but no acral overgrowth and pituitary adenoma despite longstanding disease activity, and thus eluding diagnosis for years.

Cardiomyopathy in a patient with limb-girdle muscular dystrophy type 2D: Pathomorphological aspects

Sarcoglycanopathies are a group of autosomal recessive limb-girdle muscular dystrophies caused by mutations in the genes encoding for α-, β-, γ- and δ-sarcoglycan, which are expressed in skeletal and cardiac muscle. Cardiomyopathy has rarely been reported in patients with mutations in the α-sarcoglycan gene and descriptions of heart pathology are lacking. To our knowledge, this is the first report on characteristic pathomorphological changes in cardiac muscle detected at autopsy in a patient with a proven mutation (nucleotide substitution 229C>T (R77C) in exon 3) in the α-sarcoglycan gene. The patient had the phenotype of Duchenne-like muscular dystrophy. Due to severe weakness of the respiratory muscles, permanent nocturnal mechanical ventilation via a tracheostomy had been necessary since the age of 24 years. The patient also suffered from mild pulmonary and systemic hypertension. At the age of 36, he lost consciousness and was brought to the emergency room in asystolia and unsuccessfully reanimated for half an hour. Gross heart examination disclosed scattered unsharply demarcated grey and yellow areas, characteristically localised in the outer (subepicardial) part of the lateral and posterior left ventricular wall, while the interventricular septum was spared. Similar changes were present in the apical region of the posterior right ventricular wall. Histopathological changes in focal subepicardial myocardial lesions in the free left ventricular wall consisted of myocardial degeneration in the absence of inflammatory infiltrates, fibrosis and fatty replacement of the myocardium, strikingly similar to changes in skeletal muscle. Since autopsy did not reveal any significant coronary stenosis or valvular pathology, both chronic myocardial ischemia and valvular disease could be excluded as causes of the above-described changes, which were ascribed to α-sarcoglycanopathy. Mild myocardial hypertrophy could be attributed to pulmonary and systemic hypertension. The progression of cardiomyopathy in α-sarcoglycanopathy was considered slow, since it had not reached the stage of dilated cardiomyopathy at the time of death. Focal subepicardial myocardial lesions, most pronounced in the posterobasal segment of the left ventricle, were characteristic of cardiomyopathy in α-sarcoglycanopathy. Since focal lesions may spread further, thorough cardiac monitoring is recommended in patients with α-sarcoglycanopathy.

Percutaneous Closure of Patent Ductus Arteriosus in an Asymptomatic Adult

he ductus arteriosus allows deoxygenated blood from the right ventricle through the descending aorta and to the placenta in the fetal period. Functional and anatomical closure is complete by several weeks after birth. Patients with ductus-dependent physiology generally have advanced congenital malformations and require surgi-cal intervention early in life. However, some patients will present as adults with a patent ductus arteriosus (PDA). We describe a 43-year-old woman who was found to have a PDA during evaluation for a precordial murmur, and she underwent successful percutaneous closure.Case RepoRtA 43-year-old woman with mild systemic hypertension was referred after a precordial murmur was detected by her primary physician. Her only complaint was occasional pal-pitations. Her systemic blood pressure was well controlled on lisinopril 10 mg daily. A continuous murmur was pres-ent in the left first and second intercostal spaces. Echocardiogram revealed normal-sized cardiac cham-bers and normal left and right ventricular systolic function with normal valvular structure and function. Using color-flow Doppler, an atypical jet with mosaic pattern was seen in the pulmonary trunk and the descending thoracic aorta

Association between flicker‐induced vasodilatation and flow mediated vasodilatation in patients with diabetes, systemic hypertension and hypercholesterolemia

Abstract Purpose Flicker induced vasodilatation is reduced in patients with vascular related diseases. However, the reason for this diminished response is unclear, but may be related to endothelial dysfunction. Currently, the standard method to assess endothelial function in vivo is flow mediated vasodilatation (FMD). Thus, the present study was performed to investigate whether a correlation exists between flicker induced vasodilatation and FMD in patients with diabetes and patients with mild systemic hypertension and/or hypercholesteremia. Methods In the present study 20 patients with insulin dependent diabetes, 40 patients with systemic hypertension (systolic blood pressure:140‐159 mmHg; diastolic blood pressure 90‐99 mmHg) and/or serum cholesterol plasma levels > 250 mg/dl and 20 healthy control subjects were included. The flicker response was measured using the Dynamic Retinal Vessel Analyzer. FMD was determined using a high resolution ultrasound system, measuring brachial artery diameter reactivity during reperfusion after arterial occlusion. Results The flicker response of both retinal arteries and veins was significantly reduced in the two patients groups. Likewise, FMD was significantly reduced in patients as compared to healthy controls. However, only a weak correlation between flicker induced vasodilatation and FMD was observed. Conclusion The study confirms evidence that flicker responses and FMD is reduced in the selected patients groups. Whether the weak correlation between FMD and flicker is due to the different stimulation type, the different vascular beds measured or other mechanisms has yet to be investigated.

Efficacy and Safety of Erythromycin as Sclerosing Agent in Patients With Recurrent Malignant Pleural Effusion

The aim of pleurodesis in malignant pleural effusions is to prevent reaccumulation of the fluid, symptoms, and avoid the need for repeated hospitalization for thoracentesis. The purpose of this study was to evaluate the efficacy and safety of erythromycin as a pleural sclerosing agent. Over a 2-year period, 34 patients with a symptomatic, recurrent, malignant pleural effusion who referred for chest tube drainage and pleurodesis were included. They had not received prior intrapleural therapy and had predicted survival of at least 1 month. All underwent pleural drainage and chemical pleurodesis with erythromycin. Complications and response to pleurodesis, according to clinical and radiographic criteria after 90 days, were recorded. The overall response was 88.2%. Complete response (no reaccumulation of pleural fluid after 90 days) was observed in 27 patients (79.4%). Partial response (reaccumulation of fluid but without symptoms, not requiring drainage) was observed in 3 (8.8%). No response (symptomatic reaccumulation of fluid that required drainage) was observed in 4 (11.8%). All patients experienced pleurodynia that was treated with administration of paracetamol and/or dextropropoxyphene. Sinus tachycardia and concurrent mild systemic hypertension were observed 2 and 4 hours after pleurodesis. Both of them were attributed to pleurodynia as there was remission with analgesics. This study suggests that erythromycin is effective and safe as a sclerosing agent for pleurodesis in patients with recurrent malignant pleural effusions.

Low Testosterone Levels in Patients with Mild Hypertension Recovered after Antidepressant Therapy in a Male Climacterium Clinic

Recently, middle-aged men who have begun frequently complaining of erectile dysfunction and nonspecific symptoms similar to those of postmenopausal women, visited a male climacterium clinic in Japan. Some patients, who were already taking antihypertensive medication, discontinued or reduced their dosages of antihypertensive medication after anti-depressant therapy. Forty-nine males over the age of 40 years were studied to evaluate the relationships between blood pressure, mental stress, and testosterone levels. The systemic blood pressure (sBP) of 24 patients was higher than the criteria for mild hypertension: 140/90 mmHg (HT group) at first visit. The sBP of the other 25 patients was normal (N group). The international index of erectile function (IIEF5) score (normal >21), self-rating depression scale (SDS) score (normal <40), and plasma testosterone levels were also evaluated before and after anti-depressant therapy without androgen replacement therapy. There were no significant differences between the groups in IIEF5 or SDS scores. The plasma testosterone levels in the HT group at first visit were significantly lower than those in the N group (230+/-77 vs. 343+/-92 ng/dL, p<0.001). After treatment, the IIEF5 scores were unchanged, whereas SDS scores were lower in both groups. Mean systemic blood pressure (mBP) in the HT group significantly decreased from 112+/-7 to 94+/-7 mmHg after treatment, concomitant with the disappearance of nonspecific complaints and the increase of testosterone levels. In the N group, however, neither mBP nor testosterone levels changed. Psychotherapy can ameliorate mild systemic hypertension in climacteric men with low testosterone levels. Mental stress might suppress the hypothalamic-pituitary-gonadal axis to decrease testosterone levels.

Relación entre hiperinsulinemia, disfunción diastólica e hipertrofia del ventrículo izquierdo en pacientes con hipertensión arterial sistémica

Hypertension is the main independent cardiovascular risk factor. However, there are additional factors that induce organic damage. To assess the association between hyperinsulinemia, ventricular hypertrophy and left ventricular diastolic function. Seventy-four patients aged 30 to 65 years, with mild or moderate systemic hypertension, with overweight or mild obesity and normal glucose tolerance curve (GTC), were studied. Serum insulin was measured during GTC. The maximum levels of insulin and glucose were observed 60 minutes after the oral glucose load and they were expressed as rG/1. Patients were stratified in three groups according to their glucose and insulin fasting levels (I0) and post-glucose challenge levels (rG/I): Group 1 (normoinsulinemic patients) I0 <17 mU/mL and rG/I >2 (2.45+0.4). Group 2 (post-prandial hyperinsulinemic patients) I0 <17 mU/mL and rG/I <2> 1 (1.34+0.3). Group 3 (persistently hyperinsulinemic patients) I0 >17 mU/mL and <1 (0.7+0.3). Left ventricular mass and its diastolic function were measured by Doppler echocardiography. No differences in blood pressure or age were observed between groups. There was a negative correlation between ventricular mass and rG/1 (r =-0.282, p =0.015). Left ventricular diastolic dysfunction was significantly more deteriorated in group 3, as compared with group 1 (p <0.001 ANOVA). There was a significant correlation between g/GI and diastolic dysfunction (r =0.232 p =0.047). Fasting, post challenge hyperinsulinemia and a rG/I <1 are associated with higher ventricular mass and left ventricular diastolic dysfunction, independent of blood pressure and age.

Transient pathologic Q waves in a case of apical ballooning

A 73-year-old woman with known mild systemic hypertension was admitted to our hospital because of a 2hour history of chest pain. As a remarkable fact, her husband had died that day. Physical examination showed a normal blood pressure (130/60 mm Hg) and a heart rate of 100 beats per minute. Hematologic values and serum creatinine levels were normal. Sodium and potassium serum levels were also within normal limits. Initial serum creatine kinase (CK) level was slightly increased (220 U/L; reference range, 24-170 U/L), with a troponin I level of 11.8 lg/mL (normal values up to 0.4 lg/mL). Chest x-ray was unremarkable. The first electrocardiogram (EKG) was performed when the patient still had chest pain and showed Q waves and ST elevation in all the precordial leads and leads I, II, and aVL (Fig. 1). Simultaneously, 2-dimensional echocardiography was carried out showing apical akinesis and mild ventricular dysfunction accompanied by ventricular dilatation. With the diagnosis of extensive acute anterior myocardial infarction (AMI), an urgent coronarography was undertaken to perform a primary angioplasty, but the coronary angiogram revealed a normal coronary tree. Left ventriculogram demonstrated extensive apical akinesis with hypercontractility of the basal segments (Fig. 2). An ejection fraction of 0.35 was calculated. Peak CK and troponin I serum levels were 2005 U/L and 31 lg/mL, respectively. An EKG performed 5 days later showed deep negative T waves in precordial leads, but Q waves could not be observed (Fig. 3). Three weeks after admission, a 2dimensional echocardiography showed normal ventricular function with no regional motion abnormalities. An almostnormal EKG was obtained with absence of Q waves and ST-T abnormalities (Fig. 4).

Usefulness of Ventricular Premature Complexes to Predict Coronary Heart Disease Events and Mortality (from the Atherosclerosis Risk In Communities Cohort)

The clinical relevance of ventricular premature complexes (VPCs) in apparently healthy patients is not clear and is typically not considered when evaluating risk. We conducted a prospective longitudinal study of the population-based Atherosclerosis Risk In Communities (ARIC) study of 15,070 Caucasians and African-Americans, 45 to 64 years of age, to assess the risks of coronary heart disease (CHD) events and mortality associated with VPCs among participants with and without prevalent CHD at baseline. VPCs on a single 2-minute electrocardiogram were identified in 940 participants (6.2%). After a follow-up of >10 years, 1,762 participants died, with 366 deaths related to CHD, and 1,736 had cardiac events. The percentage of participants with CHD mortality was >3 times greater for those with VPCs compared with those without VPCs. After controlling for cardiovascular risk factors and therapy with proportional hazards regression, participants with VPCs were >2 times as likely to die due to CHD than were those without VPCs. Increased risk was found for participants with and without baseline CHD. In conclusion, a clinical finding of VPCs on electrocardiography of even apparently healthy patients may warrant a heightened awareness of and attention to cardiovascular risk assessment and management.

Vasculopathy of the large arteries in children infected by the human immune deficiency virus

We report on two children with advanced acquired immune deficiency syndrome presenting with vasculopathy involving the large vessels. Both patients had extensive involvement of the aorta and its branches. One patient presented with heart failure, and mild systemic hypertension secondary to renal arterial stenosis, while the other patient manifested with gangrene of both arms.

Association between exercise capacity and left ventricular geometry in overweight patients with mild systemic hypertension

The purpose of this study was to determine the relation between left ventricular (LV) geometry and exercise capacity in unmedicated, hypertensive patients. Analysis of the data revealed peak oxygen consumption (ml kg(-1) min(-1)) for concentric hypertrophy (corrected mean +/- SE 23.5 +/- 1.2) was significantly less (F = 3.68, p <0.02) than the concentric remodeling (28.1 +/- 1.2) and normal (27.3 +/- 0.6) geometries. The LV geometric pattern was found to be associated with exercise capacity in unmedicated, hypertensive patients, such that patients with concentric hypertrophy showed reduced capacity.

Comparative effects of candesartan cilexetil and amlodipine in patients with mild systemic hypertension

The comparative antihypertensive efficacy and tolerability of the angiotensin II receptor blocker candesartan cilexetil and the calcium channel blocker amlodipine were evaluated in an 8-week, multicenter, double-blind, randomized, parallel-group, forced-titration study in 251 adult patients (45% women, 16% black) with mild hypertension (stage 1). Following a 4- to 5-week placebo run-in period, patients with sitting diastolic blood pressure (BP) of 90 to 99 mm Hg received candesartan cilexetil 16 mg (n = 123) or amlodipine 5 mg (n = 128) once daily. After 4 weeks of double-blind treatment, patients were uptitrated to candesartan cilexetil 32 mg or amlodipine 10 mg once daily. There were no significant differences between the candesartan cilexetil and amlodipine regimens for reducing BP; mean systolic BP/diastolic BP reductions were −15.2/−10.2 mm Hg versus −15.4/−11.3 mm Hg, respectively (p = 0.88/0.25). Overall, 79% of patients on candesartan cilexetil and 87% of those on amlodipine were controlled (diastolic BP <90 mm Hg). A total of 3.3% of patients on candesartan cilexetil discontinued treatment, compared with 9.4% of patients on amlodipine, including 2.4% versus 4.7% for adverse events and 0% versus 1.6% for peripheral edema, respectively. Peripheral edema, the prespecified primary tolerability end point, occurred with significantly greater frequency in patients on amlodipine (22.1%; mild 8.7%, moderate 11.8%, severe 1.6%) versus patients on candesartan cilexetil (8.9%; mild 8.1%, moderate 0.8%) (p = 0.005). Candesartan cilexetil and amlodipine are both highly effective in controlling BP in patients with mild hypertension. Candesartan cilexetil offers a significant tolerability advantage with respect to less risk of developing peripheral edema.

Asymptomatic Atrial Fibrillation: Problems of Management

78-year-old man presented to his personal physician for a yearly examination. He was totally asymptomatic. Findings of a physical examination performed 1 year previously were normal, and an ECG displayed normal sinus rhythm (NSR) and minor nonspecific T-wave changes. Five years previously, he was found to have mild systemic hypertension and was administered combined hydochlorothiazide (25 mg) and triamterene (37.5 mg) daily with satisfactory control of the BP throughout this time period. Physical examination disclosed a BP of 140/80 mm Hg and an irregular cardiac rhythm, at the average rate of 115 beats/min. The cardiac findings were otherwise normal, and the remainder of the general examination was also normal. ECG disclosed atrial fibrillation (AF) with a moderate ventricular response rate of 100 to 120 beats/min. Minor T-wave abnormality was again found but did not differ significantly from previous patterns. An echocardiogram was performed and demonstrated a normalsized left ventricle with a normal contraction pattern (estimated ejection fraction, 56%). This chamber demonstrated mild hypertrophy (wall thickness, 1.3 cm). Mild left atrial dilatation was observed (diameter, 4.2 cm), and the remainder of the examination was normal, including the absence of flow abnormalities by intracardiac Doppler echocardiographic interrogation. Additional test results included a normal chest radiograph and a normal blood profile (CBC count, general chemistry values, electrolytes, and lipid profile).

Pleuropulmonary and cardiovascular consequences of thoracoscopy performed in healthy standing horses

Six healthy, awake, and pharmacologically restrained mature horses were studied in order to define the changes in cardiopulmonary function during and after exploratory thoracoscopy and to determine the presence of postoperative complications occurring 48 hours after thoracoscopy. In a randomised 3 x 3 latin square design with 2 replications, 18 procedures were performed: 6 right (RTH) and 6 left thoracoscopies (LTH) and 6 sham procedures (STH). Prior to each procedure a physical examination and a bronchoalveolar lavage fluid analysis were performed. During thoracoscopy and sham protocols, horses were sedated with a continual drip of detomidine HCl and data were collected at 6 time intervals: T1 (baseline), T2 (10 min detomidine administration), T3 (first 15 min pneumothorax), T4 (5 min recovery from pneumothorax), T5 (second 15 min pneumothorax), and T6 (10 min recovery from the second pneumothorax and detomidine). An endoscopic thoracic examination was conducted during the 2 pneumothorax periods. An identical protocol was followed for sham procedures without surgery or pneumothorax. Data were analysed by ANOVA with time and surgical procedure as main factors. Physical examinations, thoracic radiography and ultrasound, CBC and bronchoalveolar lavage fluid analysis were performed 48 h after thoracoscopy. Heart rate, respiratory rate, and cardiac output decreased following detomidine administration. There was a trend for cardiac output to be lower during thoracoscopy. Mild systemic hypertension was associated with thoracoscopy although there was no effect on pulmonary arterial pressure. Total and pulmonary vascular resistances were increased following detomidine administration. Thoracoscopy caused a further increase in systemic and pulmonary vascular resistances especially during the second pneumothorax. Arterial O2 tension decreased following detomidine administration and was further decreased during the second pneumothorax period. PaO2 values were lower when thoracoscopy was performed on the left rather than the right hemithorax. No significant complications were found during the 48 h follow-up evaluation. A subclinical postoperative pneumothorax occurred in 2 horses, one of which had sustained a lung laceration by the trocar. Thoracoscopy performed in healthy, awake, and pharmacologically restrained horses did not have detrimental cardiopulmonary effects and did not cause postoperative complications within the first 48 h period.

Comparison of the efficacy and tolerability of candesartan cilexetil and amlodipine in patients with mild systemic hypertension (CASTLE study)

The antihypertensive efficacy and tolerability of candesartan cilexetil (CAND), a potent, selective angiotensin II (AT1) receptor blocker, vs amlodipine (AML), a potent, dihydropyridine calcium channel blocker, were evaluated in patients with mild (JNC VI, Stage 1) hypertension. In this 8-week, multicenter, double-blind, randomized, parallel-group, forced-titration study, a total of 251 adult patients (45% female, 16% black) with sitting diastolic blood pressures (DBP) of 90 to 99 mmHg, inclusive, during a 4- to 5-week placebo run-in period were randomly assigned to treatment with CAND 16 mg or AML 5 mg, once daily. After 4 weeks of double-blind treatment, patients were uptitrated to CAND 32 mg or AML 10 mg, once daily. The primary efficacy endpoint was the reduction in trough (24 ± 3 hours after dose) DBP at Week 8. The primary pre-specified tolerability endpoint was peripheral edema, defined as pitting edema that was evident in the morning or afternoon after applying gentle pressure for 5 seconds to the pedal, ankle, and/or pre-tibial regions. There were no significant differences between the CAND (16 ⇒ 32 mg) and AML (5 ⇒ 10 mg) regimens for reducing BP; changes in mean trough sitting systolic/DBP were −15.2/−10.2 mmHg vs −15.4/−11.3 mmHg, respectively (p = 0.88/0.25). Overall, 79% of patients on CAND were controlled (DBP <90 mmHg) compared with 87% on AML. Ratios of trough to peak (6 ± 2.5 hours after dose) effect on DBP were 1.0 for CAND vs 0.95 for AML, indicating persistence of BP reduction for a full 24 hours for each drug with once daily dosing. A total of 3.3% of patients on CAND discontinued treatment prematurely, compared with 9.4% of patients on AML, including 2.4% vs 4.7% for adverse events, respectively. Peripheral edema occurred with significantly (p = 0.005) greater frequency in patients on AML (22.1%: mild 8.7%, moderate 11.8%, severe 1.6%) vs patients on CAND (8.9%: mild 8.1%, moderate 0.8%). Candesartan cilexetil and amlodipine are both highly effective in controlling blood pressure in patients with mild hypertension. Candesartan cilexetil offers efficacy similar to amlodipine with significantly less peripheral edema.