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interval assessed as a continuous variable remained a significant independent predictor of cardiovascular risk in both univariate and multivariate cox proportional hazard models, with 34% increase of cardiovascular mortality for each 17ms increase in QTcd. In multivariate analysis QTcd > 58ms (the upper 95th percentile in a separate population of normal subjects) was associated with a 3.2 fold increase of cardiovascular mortality (95%CI 1.8 – 5.7)88.
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Data from within black and African populations show striking BP gradients (rural < urban)
that predictably track directly with Western lifestyles97. Cooper et al98http://hyper.ahajournals.org/content/56/5/780.full - ref-52 studied populations in rural Cameroon, urban Cameroon, and Chicago in 1995 and showed that the hypertension rates in these locations were 15%, 19% and 33% respectively.
It has been documented as a threat to the health of the people in Sub Saharan Africa and a major contributor to the morbidity and mortality in this region99. According to Kearney et al, by 2025, about 75% of the hypertensive populations will be in developing countries100. Emerging data from hospital’s studies shows that hypertension or its complication is the commonest non communicable disease in Nigeria101.
The crude prevalence of hypertension in Nigeria has been documented as 11.2%102 (based on BP threshold of 160/95mmHg) with an age adjusted ratio of 9.3. However, according to the current definition of hypertension from the JNC VII guidelines, many more Nigerians (20-25%) would be classified as hypertensive7. A recent systematic review puts the prevalence of hypertension in Nigeria between 8-46.4%.103
QT interval is a predictor of cardiovascular events and increase QT duration is associated with risk of sudden death in the hypertensive population. In subjects with uncomplicated hypertension, a prolonged QTc carries a two fold increase in the risk of coronary artery events and cardiovascular death after adjusting for the effects of age, sex, diabetes mellitus, serum cholesterol, serum creatinine, smoking, left ventricular hypertrophy, and 24 hour blood pressure104. In hypertensive patients, the QT interval is viewed as a non-specific marker of cardiac pathology. Various studies have confirmed presence of QT prolongation in the setting of hypertension and/or hypertensive heart disease 105,106. Prevalence of prolonged QTc among hypertensive patients in a study by Familoni et al107 was 48% and this is comparable to that of Akintunde et al108 who found a prevalence of 52.14%.
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A large proportion of hypertensive patients have left ventricular hypertrophy (LVH) which significantly increases their morbidity and mortality and in particular, their risk of sudden death. Hypertensive individuals especially those with LVH and prolonged QT have been noted to have an increase in ventricular arrhythmias109.
At microscopic level, LVH is characterised by both myocyte hypertrophy and an increase in collagen interstitial matrix. Myocyte hypertrophy may cause a lengthening of action potential duration, and increase in interstitial fibrosis may be associated with a reduced action amplitude and membrane potential, shortened action potential duration or electrical quiescence110. Either of these features could result in an increase QTd if the changes in different part of the ventricle are non-homogenous and it is apparent how such changes may result in re-entry circuits and ventricular arrhythmias.
The presence of LVH suggests poor prognosis, and is predictive of adverse outcome. In hypertensive patients, both echocardiographic and electrocardiographic LVH increased the risk of sudden death, possibly in part based on the LVH induced pro-arrhythmic repolarization changes.
QTd is a useful non-invasive parameter for detection of LVH in hypertensive patients and may play an important role to improve the identification of LVH by 12 lead ECG compared with other ECG criteria111.
Attempts have also been made to assess the effect of anti-hypertensive agents on QTd .The potential for antihypertensive drugs to alter the QT interval and dispersion must be considered within the context of the effect of blood pressure, reduction in left ventricular mass as well as the effects of specific drugs on the autonomic nervous system which in turn affect the duration of the QT interval and exerts additional effects on the heart. Losartan and its metabolites may directly affect the membrane currents controlling the action potential duration and hence shortens the QT interval as well as cause a reduction in QTd112. Nebivolol
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is a selective β1-blocker with vasodilatory properties due to modulation of nitric oxide release, which decreases peripheral vascular resistance. In addition, it has been demonstrated that in patients with hypertension, nebivolol reduces QT dispersion and corrected QT interval (QTc) and corrected QT dispersion (QTcd), which are indicators of the heterogeneity of myocardial repolarisation and electrical instability113.
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CHAPTER THREE METHODOLOGY 3.1 Study Design
This is an experimental study involving two groups of participants; the hypertensives and apparently normal or healthy controls. The study tested the effects of electromagnetic energy emitted from mobile phone on the heart in these two groups. It also compared the possible effects of this EM field exposure from mobile phone placed at different positions on the body (chest compared with hip position). Only participants who gave informed consent were enrolled in this experimental study. They all had detailed history taken from them including drug history as well as full physical examination including checking for features that may suggest hypothyroidism or hyperthyroidism. Also, all participants had some screening tests done which included serum electrolytes and urea, haematocrit level as well echocardiography. All information obtained was entered into the questionnaire (Appendix III). All participants did not use medications such as antimalarial, antiarrhythmic, antipsychotic, or antibiotics for at least a week prior. Only participants who were in sinus rhythm were considered in the final analysis.
Each participants had ECG done while in supine position and after a stabilizing period of fifteen minutes. Five ECGs were done by each participant using the Schiller AT-1 ECG machine in the cardiac laboratory.
The first ECG was done without any mobile phone present and this was considered as the baseline ECG. Then, the phone was placed on the left side of the chest (without contact with any of the electrodes) in an ON mode but not ringing and the second ECG was done. This phone was then called by another cellphone held by the research assistant few metres away while allowing the praecordial phone to ring twice for a total duration of 40seconds with 3rd ECG simultaneously recorded. These 2nd and 3rd ECGs were considered as ECGs at the
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praecordial level (praecordial- ON and praecordial- Ringing respectively). After 5minutes, the mobile phone was placed at the belt level in an ON mode but not ringing and then called by the assistant few metres away while allowing it to ring for 40seconds with 4th and 5th ECGs done at both modes respectively. These fourth and fifth ECGs were taken as ECGs at the hip level (Hip –ON and Hip- Ringing).
The same phone was used throughout the study and this standardized phone was a NOKIA 202 mobile phone with IMEI- 35471059471542. This device was designed not to exceed the limits for exposure of radio waves to humans with its Specific Absorption Rate (SAR) being
<2.0 Watts/kg according to the Independent Scientific Organization guidelines22. NOKIA phone was used because it was one of the commonest brands of mobile phones in the Nigerian market as at the time of this study. The mobile phone technology that was considered in this study was based on the GSM standard. This standard defines that the RF communication signal is transmitted in two bands; the first is around 900MHz and the second is located around 1800MHz.