Latest & greatest articles for Hypertension Causes

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Top results for Hypertension Causes

1. Treatment of Secondary Hypertension Due to Endocrine Causes

be performed only done after biochemical confirmation of disease. v. Definitive treatment is with surgical resection. Preoperative planning is recommended for blood pressure control and volume expansion: α-blockade should be started 10-14 days preoperatively. Typical options include oral phenoxybenzamine (a long-acting, non-selective, irreversible α-blocker), prazosin, or doxazosin. Other anti-hypertensives may be added as necessary but diuretics should be avoided if possible. Oral β-blockers may (...) Treatment of Secondary Hypertension Due to Endocrine Causes XIV. Treatment of Secondary Hypertension Due to Endocrine Causes | Hypertension Canada Guidelines Subgroup Members: Ally P.H. Prebtani, MD; Gregory Kline, MD, Ernesto L. Schiffrin, MD PhD; Andrew Don-Wauchope, MD Central Review Committee: Stella S. Daskalopoulou, MD MSc DIC PhD (Chair); Kaberi Dasgupta, MD MSc; Kelly B. Zarnke, MD MSc; Kara Nerenberg, MD, MSc; Alexander A. Leung, MD MPH; Kevin C. Harris, MD MHSc; Kerry McBrien, MD MPH

2018 Hypertension Canada

3. Subacute right heart failure revealing three simultaneous causes of post‐embolic pulmonary hypertension in metastatic dissemination of breast cancer Full Text available with Trip Pro

Subacute right heart failure revealing three simultaneous causes of post‐embolic pulmonary hypertension in metastatic dissemination of breast cancer A 72-year-old woman with history of breast cancer only treated surgically was referred to our department for pulmonary hypertension (PH) suspicion. Echocardiogram revealed elevated right ventricular systolic pressure. Computed tomography (CT) angiogram showed no pulmonary embolism (PE), but lung scan revealed two ventilation-perfusion mismatch

2016 ESC heart failure

4. A rare cause of hypertension in pregnancy: Phaeochromocytoma Full Text available with Trip Pro

A rare cause of hypertension in pregnancy: Phaeochromocytoma A 26-year-old primigravida at 35 weeks' gestation was transferred to our institution from a regional hospital for management of presumed preeclampsia. Due to the labile nature of her hypertension, further investigation was undertaken which revealed a right-sided phaeochromocytoma. Alpha blockade was commenced, and an uncomplicated elective caesarean delivery was performed at 38 weeks' gestation under spinal anaesthetic. The patient (...) underwent an elective right laparoscopic adrenalectomy six weeks post-partum. This case highlights the importance of investigating young women for secondary causes of hypertension to avoid mislabelling as essential or gestational hypertension.

2016 Obstetric medicine

5. Whom should you test for secondary causes of hypertension?

, malar rash); or laboratory analysis (elevated serum creatinine, low thyroid-stimulating hormone) (SOR: C, consensus-based guidelines). Patients with undifferentiated resistant hypertension should receive further directed evaluation for secondary causes (SOR: C, consensus-based guidelines). URI Citation Journal of Family Practice, 63(1) 2014: 41-42, 54. Rights OpenAccess. This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 License. Collections hosted by hosted by (...) Whom should you test for secondary causes of hypertension? Whom should you test for secondary causes of hypertension? Toggle navigation Shared more. Cited more. Safe forever. Toggle navigation View Item JavaScript is disabled for your browser. Some features of this site may not work without it. Search MOspace This Collection Browse Statistics Whom should you test for secondary causes of hypertension? View/ Open Date 2014-01 Format Metadata Abstract Evidence-based answer: It’s recommended

2014 Clinical Inquiries

6. Do Soft Drinks Cause Hypertension?

with treatment of hyperuricemia with allopurinol ( .(3). An observational study of soft drinks intake in adolescents found increased uric acid levels [4]. Although uric acid may cause hypertension and mediate some of the pathologic consequences classically associated with longstanding high blood pressure in mice, humans are more complex. Studies have been conflicting. Antagonizing or decreasing uric acid with vitamin C was not associated with a decreased risk of hypertension in the Nurses’ Health [5-8 (...) of fructose intake and hypertension, but in a more controlled [13]. Analyzing the subjects enrolled in the PREMIER trial, the authors found that a reduction of 1 serving of sugared drink per day was significantly associated with a decrease in systolic blood pressure of 0.7 mmHg and a decrease in diastolic blood pressure of 0.4 mmHg, in the fully adjusted model. In summary There is fair to good evidence that higher intakes of fructose, either in the form of sucrose or high fructose corn syrup, seem

2011 Clinical Correlations

7. Review: atenolol may be ineffective for reducing cardiovascular morbidity or all cause mortality in hypertension Full Text available with Trip Pro

compared with placebo or with untreated controls (4 RCTs, n = 6825 ) . Mean reduction in blood pressure (BP) attributed to atenolol ranged from 4.0–18.0 mm Hg systolic and 2.9–11.0 mm Hg diastolic. The groups did not differ for MI, stroke, cardiovascular mortality, or all cause mortality (table). Atenolol compared with other antihypertensive drugs (5 RCTs, n = 17 671). Mean BP change with atenolol compared with alternatives ranged from –1.0 to 1.1 mm Hg systolic and −1.0 to 0.5 mm Hg diastolic (...) . The rates of stroke, and cardiovascular and all cause mortality were greater in the atenolol group than in the other antihypertensive drug group (table). The groups did not differ for rates of MI (table). View this table: Atenolol v placebo or no treatment or v other antihypertensive drugs in essential hypertension at mean 4.6 years* CONCLUSIONS In patients with essential hypertension, atenolol is not better than placebo or no treatment for reducing cardiovascular morbidity or all cause mortality

2006 Evidence-Based Medicine

8. ACE inhibitors reduced cardiovascular events and all cause mortality in elderly people with hypertension Full Text available with Trip Pro

. References Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA 2002 ; 288 : 2981 –97. Frohlich ED. Treating hypertension—what are we to believe? [editorial]. N Engl J Med 2003 ; 348 : 639 –41. Moser M. No surprises in blood pressure awareness study findings: we can do a better job [editorial]. Arch Intern Med 2003 ; 163 (...) cardiovascular events and all cause mortality? Design Randomised (allocation concealed ), blinded (outcome assessors), controlled trial with median follow up of 4.1 years (Second Australian National Blood Pressure Study [ANBP2]). Setting 1594 family medical practices in Australia. Patients 6083 patients who were 65–84 years of age (mean age 72 y, 51% women) without recent (previous 6 mo) cardiovascular events and had hypertension (defined as systolic blood pressure ≥160 mm Hg or diastolic blood pressure ≥90

2004 Evidence-Based Medicine

9. Inhaled nitric oxide as a cause of selective pulmonary vasodilatation in pulmonary hypertension. (Abstract)

Inhaled nitric oxide as a cause of selective pulmonary vasodilatation in pulmonary hypertension. The acute effects of inhaled nitric oxide (NO) (40 ppm in air) on pulmonary (PVR) and systemic (SVR) vascular resistance were compared with those of an intravenous infusion of prostacyclin (24 micrograms/h) in 8 patients with severe pulmonary hypertension and 10 cardiac patients with normal values of PVR. 10 healthy volunteers were studied non-invasively. In the patients with pulmonary hypertension (...) , PVR fell significantly after inhaled NO and after prostacyclin. PVR also fell significantly in the cardiac patients after inhaled NO. Although SVR fell substantially after prostacyclin in patients with pulmonary hypertension, inhaled NO had no effect on SVR in any patient or volunteer. Inhaled NO therefore seems to be both a selective and effective pulmonary vasodilator.

1991 Lancet Controlled trial quality: uncertain