Journal of Hypertension: Open Access

Introduction: An audit of a hypertension service in Jos, Nigeria revealed the possibility of back titration of antihypertensive therapy without untoward effect. The impact was reduction of disease economic burden. Consequently a deliberate policy of back- titration was adopted in those who have remained well controlled for >12 months. Objective: To see how low dosages could go without compromising control.

Methods: All consenting hypertensive clients in this specialist hypertension clinic who had been controlled for 12 months or longer on regular follow-up(between July and September 2011); with no heart failure, renal failure, stroke or myocardial infarction (<6 months) were enrolled. Drugs were sequentially back-titrated starting with 1 drug in those on multiple drugs. Follow up continued in the usual manner, and if controlled by the next visit a further dose lowering was advised until loss of control when dose was promptly returned to the lowest maintaining control.

Results: There were 41 patients initially. 2 did not follow up after the first back-titration visit leaving 39 as the subject of this analysis; 14 of whom were males. Their ages ranged from 40 to 91 years and they had been consistently controlled (BP <140/90 mmHg) for between 12 to 95 months. 18 remained normal at various stages of back-titration; in 5 (3F, 2M) all drugs had been completely withdrawn. In 21, control was lost in the course of backtitration and promptly recovered by returning to previous dose that controlled BP. Those who were successfully back-titrated to no drug were mostly on one drug at low doses.

Conclusion: After a minimum of 12 months of sustained BP control, it is possible to back-titrate drug dosages in about 50% of this hypertensive cohort, a quarter of whom went completely without drugs for 1 year. The exact mechanism is unknown, but the benefit is in the psychological relief of lower pill burden and reduced cost of treatment. This observation should be extended to other cohorts to prove its applicability; advisedly only under expert care.

Objectıve: It has been aimed to investigate the Galectin-3 (GAL-3) levels and clinical responses after addition of spironolactone as a mineralocorticoid receptor antagonist (MRA) to the current treatment in patients with heart failure with low ejection fraction who received no aldosterone antagonist therapy previously.

Patıents and methods: The study included 112 patients with Heart Failure (HF) who showed left ventricular Ejection Fraction (EF) of 35% or below, New York Heart Association (NYHA) Class II-IV symptoms and did not receive MRAs in their current treatment. Serum Gal-3 levels, serum BNP level, 6-minute walk test and class level of NYHA were examined before and 6 months after treatment of spironolactone in all patients.

Results: Mortality developed in 10 of 112 patients. Baseline and 6th month follow-up data obtained from 102 of 112 patients. Mean LVEF (%), BNP levels, Gal-3 levels, NYHA class of functional capacity and mean 6-minute walking test distance of the patients before treatment of spironolactone were 31.3 ± 3.2%, 451,4 ± 50.3 pg/ml, 39 ± 21 ng/ml, 2,8 ± 0.59 and 305 ± 61 m respectively whereas, the same variables were found 32.1 ± 2,8% (p=0.21), 443.6 ± 49 pg/ml (p=0.23), 33 ± 22 ng/ml (p=<0.001), 2,5 ± 0.47 (p=0.037) and 386 ± 87 m (p=<0.001) respectively at 6th follow-up after treatment of spironolactone.

Conclusıon: Spironolactone use is associated with regression of Gal-3 along with clinical improvement in HF symptoms. This may suggest that Gal-3 apart from being a biomarker of HF may also be a bio-target in HF management.

Aim: To determine the prevalence of metabolic syndrome using National Cholesterol Education Program-Adult treatment Panel III, American Heart Association-National Heart, Lung and Blood Institute and the Joint Interim Statement criteria and determine the prevalence of each of the cardiovascular risk factors in hypertensives attending a rural cardiology clinic in North central Nigeria

Methods: This cross-sectional study used the National Cholesterol Education Program-Adult treatment Panel III (NCEP-ATP III), American Heart Association-National Heart Lung and Blood institute (AHA-NHLBI) and the Joint Interim Statement (JIS) criteria to assess metabolic syndrome in 204 patients with arterial hypertension attending cardiology clinic of Federal medical centre, Bida, North central Nigeria from February 2010 to April 2013. The demographic and clinical history of the patients was taken.

Results: There were 97 men (47.5%) and 107 (52.5%) women. The mean age was 53.44 ± 11.71 years and range from 21-84years. Using the NCEP-ATP III, eighty three (40.7%) hypertensives had metabolic syndrome (33 males: 16.2%, 50 females: 24.5%) while the application of AHA-NHLBI criteria, resulted in metabolic syndrome in 96 (47.1%) of hypertensives (42 males: 20.6%, 54 females: 26.5% females) and with the JIS, 108 (52.9%) hypertensives (46 males: 22.5%, 62 females: 33.9% females). The prevalence of metabolic syndrome increases with age. In both male and female hypertensives with metabolic syndrome, low high density lipoprotein cholesterol (HDL-C) and abdominal obesity were the most common cardiovascular risk factor.

Conclusion: The prevalence of metabolic syndrome in hypertensives in rural Nigeria is high and varies considerably depending on the definition used. The need for public health promotion, screening and management of hypertension and other components of metabolic syndrome is hereby recommended

Although the plasmalemmal sodium potassium adenosine triphosphatase (Na/K-ATPase) is one of the most studied proteins in Biology or Medicine, a signaling function believed to be independent of its pumping function has only been noted in the past 20 years. This signaling function appears to require the generation of reactive oxygen species (ROS) which, in turn requires the activation of Src and the transactivation of the epithelial growth factor receptor (EGFR). Recent data suggest that the Na/K-ATPase may also serve as a receptor for some ROS and in this manner, serve to amplify oxidant signaling. The mechanisms involved and the implications for Physiology and Medicine are discussed in this review.