No abstract

Full funding sources listed at the end of the paper (see Acknowledgments).

Population Health Research Institute, the Canadian Institutes of Health Research, Heart and Stroke Foundation of Ontario, Canadian Institutes of Health Research Strategy for Patient Oriented Research through the Ontario SPOR Support Unit, the Ontario Ministry of Health and Long-Term Care, pharmaceutical companies (with major contributions from AstraZeneca [Canada], Sanofi Aventis [France and Canada], Boehringer Ingelheim [Germany amd Canada], Servier, and GlaxoSmithKline), Novartis and King Pharma, and national or local organisations in participating countries.

Full funding sources listed at the end of the paper (see Acknowledgments).

Extensive data from randomised controlled trials have shown the benefit of treating hypertension. The target blood pressure (BP) for antihypertensive management is < 140/90 mmHg, and < 130/80 mmHg in patients with end-organ damage, coexisting risk factors, and co-morbidity. Benefits of management include reduced risk of death, stroke, cardiac failure, chronic kidney disease, and coronary heart disease. The correct BP measurement procedure is described, and evaluation of cardiovascular risk factors and recommendations for antihypertensive therapy, are stipulated. Lifestyle modification and patient education are cornerstones in the management of every patient. Major indications, precautions, and contraindications to each recommended antihypertensive drug are listed. Combination therapy should be considered ab initio if the BP is ≥ 20/10 mmHg above goal. First-line drug therapy for uncomplicated essential hypertension includes low-dose thiazidelike diuretics, calcium-channel blockers, angiotensin-converting enzyme inhibitors, or angiotensin-receptor blockers. The guideline was developed by the Southern African Hypertension Society. © MedpharmReprinted with permission from S Afr Fam Pract 2012;54(2)(Suppl 1):S4-S8

Extensive data from randomised controlled trials have shown the benefit of treating hypertension. The target blood pressure (BP) for antihypertensive management is < 140/90 mmHg, and < 130/80 mmHg in patients with end-organ damage, coexisting risk factors, and co-morbidity. Benefits of management include reduced risk of death, stroke, cardiac failure, chronic kidney disease, and coronary heart disease. The correct BP measurement procedure is described, and evaluation of cardiovascular risk factors and recommendations for antihypertensive therapy, are stipulated. Lifestyle modification and patient education are cornerstones in the management of every patient. Major indications, precautions, and contraindications to each recommended antihypertensive drug are listed. Combination therapy should be considered ab initio if the BP is ≥ 20/10 mmHg above goal. First-line drug therapy for uncomplicated essential hypertension includes low-dose thiazidelike diuretics, calcium-channel blockers, angiotensin-converting enzyme inhibitors, or angiotensin-receptor blockers. The guideline was developed by the Southern African Hypertension Society. © MedpharmReprinted with permission from S Afr Fam Pract 2012;54(2)(Suppl 1):S4-S8

4Angiotensin-converting enzyme (ACE) inhibitors are first-line therapy for the treatment of hypertension, congestive heart failure, and diabetic nephropathy. ACE inhibitors are associated with adverse side effects such as persistent dry cough (ACE-cough) and, rarely, life-threatening angioedema (ACE-AE). The authors investigated the influence of ACE I/D polymorphism in combination with serum ACE activity, B 2 receptor À9/+9 polymorphism, and B 2 receptor C-58T single nucleotide polymorphism (SNP) on the development of ACE-AE and ACE-cough. The frequencies of ACE I/D as well as B 2 receptor +9/À9 and C-58T polymorphisms were compared in patients with ACE-AE, ACE-cough, and ACE inhibitor-exposed controls, and serum ACE activity was measured. There were 52 cases of ACE-AE, 36 cases of ACE-cough, and 77 controls. The genotyping revealed a significant association between the B 2 À9 allele and ACE inhibitor-induced AE (62% vs 38%, P=.008), and ACE inhibitor-induced cough (61% vs 38%, P=.02) when compared with controls. There was no significant association between ACE I/D polymorphism as well as the B 2 C-58T

No abstract