• Users Online: 845
  • Home
  • Print this page
  • Email this page
Home About us Editorial board Search Ahead of print Current issue Archives Submit article Instructions Subscribe Contacts Login 

 Table of Contents  
Year : 2015  |  Volume : 12  |  Issue : 2  |  Page : 158-164

Management of hypertension in Nigerians: Ad hoc or rational basis?

Department of Medicine, Division of Cardiology, University College Hospital, Ibadan, Oyo State, Nigeria

Date of Web Publication30-Jul-2015

Correspondence Address:
Ayodele O Falase
Department of Medicine, Division of Cardiology, University College Hospital, PMB 5116, Ibadan, Oyo
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0189-7969.161791

Rights and Permissions

How to cite this article:
Falase AO, Aje A, Ogah OS. Management of hypertension in Nigerians: Ad hoc or rational basis?. Nig J Cardiol 2015;12:158-64

How to cite this URL:
Falase AO, Aje A, Ogah OS. Management of hypertension in Nigerians: Ad hoc or rational basis?. Nig J Cardiol [serial online] 2015 [cited 2023 May 30];12:158-64. Available from: https://www.nigjcardiol.org/text.asp?2015/12/2/158/161791

  Introduction Top

Hypertension is an important public health problem worldwide. [1],[2],[3] It is also the commonest cardiovascular disease of black Africans. [4],[5] It is a risk factor for the development of cardiovascular diseases such as stroke, coronary artery disease, renal failure and congestive heart failure. [4],[5],[6] The heart is the most common target in hypertension among sub-Saharan Africans including Nigerians. [6],[7],[8],[9]

Studies in the last 40 years in Nigeria have not only shown a remarkable uniformity in the pattern of cardiovascular diseases among the various ethnic groups of Nigeria, but also showed that hypertension is the most common cause of cardiovascular morbidity and mortality. [8],[10] Latest surveys suggest that its prevalence is increasing, as shown in [Figure 1]. [11]
Figure 1: Causes of heart failure in Nigerians in 1969/69 and 2009/10 (Carlisle and Ogunlesi 1972, Ogah et al. 2014) (HHF - hypertensive heart failure; RHDX - rheumatic heart disease; DCM - dilated cardiomyopathy; EMF - endomyocardial fibrosis; CP - cor-pulmonale; IHDX - ischemic heart disease)

Click here to view

It is often forgotten that blood pressure (BP) is a product of cardiac output and systemic vascular resistance (SVR) and that a rise in BP may occur from one of the following:

  • Elevated cardiac output, normal SVR
  • Elevated cardiac output and raised SVR
  • Normal cardiac output and raised SVR.

Majority of the hypertensives without heart failure who attend our clinics in Nigeria usually present with normal cardiac output and raised SVR, but a few do present with high cardiac output and either normal or high SVR although their hypertension tends to be milder. Chronic elevation of the SVR in patients with hypertension is caused by the consequences of endothelial damage. It is this elevation of SVR that perpetuates chronic elevation of the BP. [12],[13]

There is a wide array of drugs available nowadays for the management of hypertension unlike in the past when only a few drugs were available and even then the drugs had so many side-effects, which made the patients more ill when they took them. Fortunately, those who manage patients with hypertension nowadays have a greater choice of safer drugs many of which have little or no side effects.

Decisions on which drug to use for treatment of primary hypertension are often taken on an ad hoc basis, and some of these are inappropriate. For example, among the drugs prescribed to a patient who presented to a clinic with hypertension and a basic heart rate of 58 beats/min was the propranolol. This dropped his heart rate to 43 beats/min. Another patient who presented with a basic heart rate of 102 beats/min and complained of palpitations and insomnia was asked to take amlodipine to control her high BP. This made her sicker. Another patient in heart failure with marked pedal swelling, ascites and a left ventricular (LV) ejection fraction of 32% on echocardiography was asked to take carvedilol. His heart failure worsened despite the high dose of frusemide he was also taking.

Since all anti-hypertensive drugs have different effects on the cardiovascular system, those who treat hypertension must be familiar not only with the hemodynamic changes, which occur when people have hypertension, but also with the hemodynamic changes the different drugs cause in order to make rational decisions on the appropriate drug (s) to choose for each patient. This paper suggests a basis for the use of the drugs in such a manner that makes the patients feel the benefits of such treatment, especially as hypertension requires a life-long treatment. However first of all, let us consider what hypertension does to the cardiovascular system of patients, especially the heart.

Structural/hemodynamic changes, which occur in patients with hypertension

Left ventricular structural changes

Studies have shown the following structural changes in Nigerians with hypertension without heart failure: [14],[15],[16],[17],[18],[19],[20]

  • Left ventricular wall thickness (LVWT)/LV mass: LVWT and LV mass are often normal in patients with mild hypertension. There is however progressive dilatation of the left ventricle as high BP becomes more severe as well as progressive thickening of the LV wall and increase in LV mass. This is often described as LV hypertrophy (LVH)
  • Damage to the electrical and vascular structures of the ventricle: Damage to the electrical and vascular structures of the ventricle occurs following the development of fibrosis within the myocardium. [7] This development also causes arrhythmias and bundle branch blocks including complete heart block, while disturbances to myocardial blood perfusion cause ischemia especially subendocardial ischemia often described as LV strain on the electrocardiogram (ECG). [21] Myocardial fibrosis may also lead to systolic and diastolic heart failure; the former following increased myocyte necrosis and the latter by making the ventricle stiffer [7]
  • Left atrial diameter: Progressive enlargement of the left atrium with onset of hypertension often occurs, becoming more severe in those with moderate/severe hypertension. This may ultimately cause atrial fibrillation [16],[18]
  • Cardiothoracic (CT) ratio: Significant enlargement of the heart on chest X-ray also occurs with the onset and progression of hypertension
  • Aortic unfolding: Progressive dilatation of the aortic root occurs as hypertension worsens; this is described as unfolded aorta on chest X-ray.

Left ventricular functional changes in patients with hypertension

The following functional changes also take place in the patients with hypertension without heart failure: [22],[23]

  • Heart rate: Significant increase in the heart rate is often seen in those with mild hypertension; heart rate tends to become normal as hypertension becomes more severe
  • Stroke volume: Reduction in stroke volume, an index of LV systolic function occurs as BP increases. In some of the patients with mild hypertension, stroke volume rises along with the heart rate resulting in an increase in cardiac output/index. However, stroke volume diminished significantly when compared with normal subjects in those with moderate and severe hypertension
  • Ejection fraction: Ejection fraction, another index of LV systolic function, rose in some of the patients with mild hypertension. These generally were those who presented with high pulse rate. In others, however, it was reduced. There was a marked reduction in ejection fraction as hypertension worsened [Figure 2]a
  • Cardiac output/index: These values increased in some patients with mild hypertension, becoming normal as hypertension worsened. In general, cardiac output/index was normal in those with moderate and severe hypertension despite the reduction in stroke volume and ejection fraction. This, most likely occurred because of the compensatory changes like increase in heart rate
  • SVR [Figure 2]b: This progressively increased with the onset of hypertension, rising further as hypertension became more severe [Figure 2]c.
Figure 2: (a) Left ventricular (LV) diastolic and systolic dimensions in patients with hypertension but no heart failure. Group 1 - mild hypertension; Group 2 - moderate hypertension; Group 3 - severe hypertension. (b) LV posterior wall thickness in patients with hypertension but no heart failure. Group 1 - mild hypertension; Group 2 - moderate hypertension; Group 3 - severe hypertension. (c) LV mass in patients with hypertension with hypertension but no heart failure. Group 1 - mild hypertension; Group 2 - moderate hypertension; Group 3 - severe hypertension. (d) LV ejection fraction in normal individuals, mild hypertension (HT-1), moderate (HT-2) and severe (HT-3) (e) systemic vascular resistance (SVR) in normal individuals, mild hypertension (HT-1), moderate hypertension (Group 2) and severe hypertension (Group 3)

Click here to view

In summary, these studies showed that deterioration of LV structure and function tends to occur with increased severity of hypertension. In other words, deterioration of LV structure and function occurs as the load against blood flow from the heart increases.

  Left ventricular structural and functional changes in patients with hypertension after heart failure has developed Top

As hypertension progresses through absence of heart failure to presence of heart failure, all the cardiac parameters discussed above deteriorate. [22] What makes the disease require urgent intervention is the continued deterioration of the cardiac indices in the presence of high SVR. In other words, a damaged myocardium is working against a high load.

Classes of anti-hypertensive drugs

The classes of drugs currently available for treatment of hypertension are as follows:

  • Thiazide diuretics
  • Thiazide-related diuretics - indapamide, chlorthalidone
  • Beta-blockers especially atenolol, propranolol, carvedilol, metoprolol
  • Calcium-channel antagonists
  • Dihydropyridines-nifedipine, amlodipine, isradipine, felodipine
  • Nondihydropyridines-verapamil, diltiazem
  • Centrally acting drugs, e.g., alpha-methyl-dopa and clonidine
  • Other peripheral vasodilators, e.g., hydralazine, minoxidil
  • Alpha-adrenoceptor blocking drugs, e.g., prazosin, terazosin, doxazosin
  • Angiotensin converting enzyme (ACE) inhibitors especially lisinopril, ramipril
  • Angiotensin-II receptor blockers (ARBs) - losartan, candesartan, telmisartan, valsartan
  • Renin inhibitors, e.g., aliskiren.

All these drugs reduce the BP through several mechanisms mostly through reduction of SVR, but sometimes through reduction of cardiac output/index or both.

Management of hypertension

Hypertension caused by predominantly high cardiac output

Reduction of high BP can be achieved by using drugs, which reduce cardiac output, SVR or both.

[Figure 3]a is the ECG of a 24-year-old man who complained of high BP when he measured it electronically, variability of his BP, palpitations, especially at night, insomnia and general feeling of unease. Clinical examination was normal except for high pulse rate and pressure and a BP of 170/95 mmHg. The ECG was normal, but for sinus tachycardia. Thyroid function tests and other investigations were normal. It was concluded that his hypertension was being driven by a high cardiac output. He improved when he was given Atenolol 25 mg twice daily.
Figure 3: (a) The electrocardiogram (ECG) of a 24-year-old patient with mild hypertension. (b) ECG of a 59-year-old patient with mild hypertension

Click here to view

[Figure 3]b is the ECG a 59-year-old man who presented with similar symptoms as the patient described above - insomnia, restlessness, palpitations and general feeling of unease. Clinical examination was again normal but for a BP of 180/100 mmHg and a high pulse rate. Investigations, which included thyroid function tests were normal except for his ECG, which showed sinus tachycardia, left atrial enlargement and LVH. It was concluded that he had both elevation of cardiac output and SVR. He improved with a combination of atenolol 50 mg daily and hydrochlorothiazide 12.5 mg daily (tenoretic 50/12.5 mg one tablet daily).

One of the beta-adrenoceptor blocking agents was used to treat these two patients because of sinus tachycardia and diagnosis of high BP predominantly driven by high cardiac output. The nondihydropyridine calcium-channel blockers (verapamil, diltiazem) are good alternatives in patients in whom the use of beta-adrenoceptor blockers are contraindicated, for example in asthmatics. Verapamil and diltiazem slow conduction at the atrioventricular nodes hence they reduce heart rate but since they can depress myocardial contractility they should as much as possible be avoided in those with cardiac failure because they may further worsen the failure. On the other hand, the use of dihydropyridine calcium-channel blockers (nifedipine, amlodipine, felodipine, etc.) in these patients may further worsen their tachycardia and provoke more distressful symptoms.

Hypertension caused by high systemic vascular resistance

As earlier stated, majority of the patients who present with hypertension at the clinics in Nigeria usually have normal cardiac output/index and elevated SVR. In treating this cohort of patients, therefore attention should be focused on reduction of SVR. All the drugs used in treating hypertension reduce the SVR albeit through different mechanisms. Majority of them however reduce the SVR through vasodilatation. These include the calcium-channel blockers, the most widely used antihypertensive (particularly nifedipine and amlodipine), ACE inhibitors (especially lisinopril and ramipril), ARBs (losartan, telmisartan, and valsartan), direct renin inhibitors (aliskiren), alpha-adrenoceptor blocking drugs (prazosin, doxazosin), and other peripheral vasodilators like hydralazine and minoxidil.

All vasodilators, however, have the side-effect of triggering an increase in heart rate when they are used. This often causes the patient to complain of palpitations, insomnia and general unease whenever they take the drugs. Such effects should either be blunted with beta-blockers, or the drugs should be withdrawn. A few of the patients may develop ankle edema, which may be severe and troubling enough to require the addition of a small dose of diuretics. Some of those taking ACE inhibitors may develop troublesome cough, which can only be ameliorated by discontinuing the drug.


When monotherapy is contemplated the only drugs, which have been proven to be efficacious in low doses among Nigerians and indeed among the black people of the world are thiazide diuretics and calcium-channel antagonists (10). No one knows why this is so, but the use of all other classes of antihypertensive drugs as monotherapy often require very high doses for effective BP control unless the hypertension is mild. Side-effects are commoner when such high doses are used.


Drug combinations are much more commonly used for the treatment of hypertension, and they include:

  • Diuretic and beta-blocker
  • Diuretic and ACE inhibitor (or angiotensin-II receptor antagonists/blockers (ARBs))
  • Calcium antagonist (dihydropyridine, e.g. nifedipine or amlodipine) and beta-blocker
  • Calcium antagonist and ACE inhibitor (or angiotensin II antagonists)
  • Calcium antagonist and a diuretic
  • Alpha-blocker and beta-blocker.

Other vasodilators, like hydralazine (apresoline), are equally effective when used as monotherapy.

General comments on the use of drugs to treat hypertension

The following should be kept in mind when patients are treated for hypertension:

  • An adequate blood level of the drug (s) being used must be achieved for a good control of high BP to occur
  • A stepwise increase of the drugs is always advisable
  • Avoid the use of the same class of drugs in a patient, e.g., combination of amlodipine and nifedipine
  • Once a good control of high BP is achieved, the drug (s) must be continued for life. On no account must the drugs be discontinued simply because the BP has normalized
  • Those who present with sinus tachycardia, atrial ectopics, should preferentially be treated with beta-blockers or verapamil or diltiazem if beta-blockers are contraindicated
  • Calcium-channel blockers can cause reflex tachycardia and edema of the legs as stated earlier. If this class of drugs suddenly become ineffective, make sure the patient is not taking calcium simultaneously. Furthermore, remember that these drugs can affect the teeth. If this occurs, the patient must be jointly managed by the physician and the dental surgeon
  • Thiazide diuretics can cause hypokalemia, increase serum uric acid and cholesterol. It also impairs glucose tolerance in some patients. They are however not contraindicated in diabetics if they are absolutely necessary, for example in patients with heart failure. It is however advisable to use them in smaller doses in elderly patients
  • When an ACE inhibitor causes cough, the drug should be discontinued and substituted with an ARB
  • Arrhythmias are fairly common in hypertensives, especially those who have progressed to the stage of heart failure. These should be identified and treated along the usual lines
  • The cost of treatment to the patient must always be borne in mind otherwise the patients may discontinue the drugs or at best cherry-pick them. In poor people, the cheapest, most effective drugs available should be used even when such drugs are no longer in fashion
  • Sexual difficulties in the male patient must be taken seriously as it may cause the patient to abandon the drugs. A change in medication in such a situation is advisable
  • Factors, which contribute to the development of myocardial failure in hypertensives should be identified and treated. The most common ones are anemia and excessive alcohol intake. Myocarditis is another factor, which should be borne in mind. It can damage the hypertensive heart through myocyte necrosis, but the only problem is that it is often difficult to diagnose and treat. To prevent myocarditis, patients should be advised on the basic rules of hygiene, which include regular hand washing and good toilet habit. Anyone who has cold symptoms must desist from heavy exercise during the period.

Management of heart failure in hypertension in Africans

When hypertension has progressed to the stage of heart failure, the following changes have taken place in the myocardium: [24]

  • Within the LV myocardium: Structural remodeling of the heart starting with concentric (CH)/asymmetric septal hypertrophy (ASH) and small/normal cavity [Figure 4]a progressing if untreated to CH/ASH with cavity enlargement [Figure 4]b. This is often referred to as LVH. LVH is an adaptive response of the myocardium to increased cardiac workload. Its development normalizes wall tension and is thought to preserve systolic ventricular function. The amount of fibrosis within the myocardium begins to increase during this period and contributes to the increased stiffness of the ventricle and diastolic dysfunction often encountered at this stage. Although most of the patients have systolic heart failure, the heart failure of some of them may solely be caused by diastolic dysfunction. An echocardiogram is required to detect this
  • The vascular and the electrical structures are often affected by the presence of fibrosis within the myocardium, and this may cause fascicular and bundle branch blocks together with regional ischemia described earlier
  • Progression of myocardial damage continues if hypertension is left untreated. There is continued remodeling of the ventricle in form of further dilatation of the left ventricle, myocardial cell necrosis and increased myocardial fibrosis until the stage of eccentric hypertrophy is reached. This is characterized by the return of wall thickness to normal or near normal although LV mass remains high unless the myocyte necrosis is massive. Eccentric hypertrophy is seen in those with systolic dysfunction and LV chamber enlargement [Figure 4]c
  • Damage to the electrical and vascular structures is almost invariably present at this stage. In fact, the presence of left bundle branch block in some of the patients may be indicative of diffuse LV myocardial damage
  • BP is manifestly high in such patients until terminally when systolic pressure drops to very low levels because of myocardial failure while the diastolic BP hovers around 90 mmHg indicating that SVR is still high despite myocardial systolic failure. Pulse pressure becomes abysmally low and at this stage such patients are virtually in cardiogenic shock requiring intensive care treatment. Treatment is difficult if the patient has reached this stage because of the low BP. Such patients had been classified as dilated cardiomyopathy with refractory heart failure in the past. [9],[24]
Figure 4: (a) Concentric hypertrophy of the left ventricle in a patient who died of hypertension. Note the reduced ventricular cavity. (b) Concentric hypertrophy of the left ventricle in a patient who died of hypertension. (c) Another patient who died of hypertensive heart failure. Note that the heart has started to dilate

Click here to view

All these hemodynamic changes must be reversed if the doctor hopes to salvage the patient. The key to success is to focus on reducing the SVR to normal. This means that the diastolic BP must be gradually lowered to a level below 90 mmHg. Many of such patients improve without the need for inotropic support when this is successfully done and of course if the myocardial reserve is still relatively good.

Inotropic support is however indicated if, despite successful reduction of SVR, recovery is poor or slow or when there is no appreciable improvement. For those who do not improve despite these measures, cardiac transplantation is the only option left if the patient can afford it and if facilities permit such a procedure.

For ease of management, we have divided the clinical presentation of the patients into four stages although some patients may straddle two of the stages. [24] Generally speaking inotropic support is not required for patients in Stages 1 and 2 but are definitely necessary if the patient has progressed to Stages 3b and 4. Reduction of SVR, that is, reduction of the diastolic BP below 90 mmHg is often enough in those in Stages 1 and 2.

For those in Stage 4, the myocardial function had become too poor to sustain an adequate BP and the priority during treatment of such patients is inotropic support. Less consideration should be put on the reduction of SVR at this stage since this may compromise the perfusion of vital organs of the body.

The clinical stages are as follows

Stage 1

This is the stage of asymptomatic systolic dysfunction. It can only be detected by echocardiography. Cardiac output is maintained by an increase in heart rate, but SVR is high. Improvement is dependent on control of BP, preferably with the initial use of ACEI/ARBs and thiazide diuretics. A combination of hydralazine, nitrates and thiazide diuretics has also been found to be effective. A calcium-channel blocker may be added to either of these combinations if BP remains uncontrolled.

Stage 2

Is characterized by a further decrease in the degree of LV systolic function progressing into the stage of symptomatic systolic dysfunction. Cardiac output may drop or still be maintained by tachycardia, but there is a further rise in SVR. High SVR increases the work of the already compromised heart, and this creates a vicious cycle for the heart of the patient. Consequently, LV failure progressively increases and S3 or S4, or S3 and S4 become audible on cardiac auscultation. BP is still recognizably high, usually about 160/100 mmHg and above. Treatment is similar to Stage 1. Loop diuretics are required during the initial management of heart failure.

Stage 3

Occurs with unrelenting hypertension and at this stage full blown congestive cardiac failure develops. Cardiac output drops further still because although there is tachycardia, this cannot compensate for the drop in stroke volume. SVR on the other hand remains high and there is therefore a rapid decline in cardiac function. On auscultation, S3 with or without mitral regurgitation are audible. In later stages, functional tricuspid regurgitation due to right ventricle/right atrial dilatation develops. Measured BP is above 160/90 mmHg (Stage 3a) but later on systolic BP drops to about 100 mmHg systolic or less while diastolic BP hovers between 90 and 95 mmHg (Stage 3b). This causes an abnormally low pulse pressure. The patient at this stage requires treatment with ACEI/ARBs (or hydralazine with nitrates) together with diuretics starting with intravenous frusemide to remove gut edema and permit adequate drug absorption. This is followed by the use of thiazide diuretics, which are effective in controlling the BP of the patients and at the same time excess fluid. Inotropic support, in the form of digitalization, is often required.

It should be noted that the BP may sometimes, depending on the myocardial reserve, rise to greater levels following recovery from heart failure. At this stage, the patient may require other antihypertensive drugs for control of high BP.

Stage 4

At this stage, BP drops to hypotensive levels. Cardiac output has dropped further while SVR remained the same or might have risen further. Such patients are in cardiogenic shock, which requires powerful inotropic drugs like dopamine or dobutamine infusion for the treatment. ACEI/ARBs/hydralazine/nitrates are contraindicated at this stage because of the low BP. Frusemide is the preferred diuretic. [24]

Areas of controversies requiring further research

Use of beta-blockers in patients with hypertensive heart failure

Beta-blockers are now widely used in the routine treatment of heart failure. Indiscriminate use of beta-blockers has however tilted some of the patients to left heart failure. There is a need for more research to guide those who wish to use beta-blockers in treatment of patients with hypertensive heart failure when it is safe to use. Beta-blockers are however safe in those with normal systolic function and diastolic heart failure.


The trend in the management of hypertension is to restrict salt intake. However, studies from Nigeria have shown a tendency for hypertensives to leak more salt in their urine compared with normotensives although the extent of leakage between the two groups has never reached significant levels. [25] More studies are needed to clarify whether restriction of salt is really beneficial in Nigerian hypertensives including those who have progressed to the stage of heart failure.

Systolic hypertension

How to handle those with abnormally high systolic BP deserves further studies. Systolic BP tends to be high when there is leakage from the circulation, for example in patients with aortic regurgitation, and in conditions, which cause arterial vasodilatation. It is also elevated when the arterial system is stiff, either because of ageing or due to atherosclerosis. Moreover, several studies have shown that the BP tends to rise with age. Elderly people are therefore expected to have higher systolic BPs and the risk of a stroke should be borne in mind when the BP of such patients is forcibly brought too low. High systolic BPs are notoriously difficult to treat, and studies are needed to determine whether treatment of such high BPs is beneficial.

Resistant hypertension

When a patient's BP has become difficult to reduce, efforts must be made to ensure that the patient is first of all taking the drugs. Too often, the patients are not, especially when the treatment is making them sicker or interfering with their sexual activities. In addition, the patient may be taking other forms of medication which may be interfering with the anti-hypertensive drugs prescribed for them, for example "cold" medications. In the absence of these, more advanced investigations must be conducted to rule out secondary forms of hypertension, particularly renal/endocrine-induced secondary hypertension [Figure 5]. Studies are still needed on how much endocrine-induced hypertension contributes to the prevalence of resistant hypertension in this community.
Figure 5: A patient referred because of resistant hypertension. The presence of these striae led to the diagnosis of Cushing's syndrome, which was confirmed on magnetic resonance imaging

Click here to view


Several population studies have linked obesity with hypertension, and the community has rightly been advised to reduce weight as part of control of hypertension. [26] What is however not clear is how obesity causes hypertension and why some obviously obese people do not have high BP nor suffer from the complications of hypertension.

  Conclusion Top

Hypertension is highly prevalent in Nigeria, and heart failure is its commonest complication. Untreated or inadequately treated hypertension progressively leads to heart failure, initially from LV diastolic dysfunction, but later and more commonly from different degrees of systolic dysfunction. Hypertension is however a treatable disease, and there is a need for a basic understanding of the pathological and hemodynamic changes, which have taken place in every patient before an appropriate treatment can be prescribed. Not only that, we must continue to educate patients about drug compliance with the aim of preventing the devastating consequences of cardiac and other complications of hypertension within the populace.

  References Top

Kearney PM, Whelton M, Reynolds K, Muntner P, Whelton PK, He J. Global burden of hypertension: Analysis of worldwide data. Lancet 2005;365:217-23.  Back to cited text no. 1
Mancia G, Fagard R, Narkiewicz K, Redón J, Zanchetti A, Böhm M, et al. 2013 ESH/ESC Guidelines for the management of arterial hypertension: The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens 2013;31:1281-357.  Back to cited text no. 2
Lim SS, Vos T, Flaxman AD, Danaei G, Shibuya K, Adair-Rohani H, et al. A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990-2010: A systematic analysis for the Global Burden of Disease Study 2010. Lancet 2012;380:2224-60.  Back to cited text no. 3
Damasceno A, Cotter G, Dzudie A, Sliwa K, Mayosi BM. Heart failure in sub-saharan Africa: Time for action. J Am Coll Cardiol 2007;50:1688-93.  Back to cited text no. 4
Damasceno A, Mayosi BM, Sani M, Ogah OS, Mondo C, Ojji D, et al. The causes, treatment, and outcome of acute heart failure in 1006 Africans from 9 countries. Arch Intern Med 2012;172:1386-94.  Back to cited text no. 5
Ogah OS, Okpechi I, Chukwuonye II, Akinyemi JO, Onwubere BJ, Falase AO, et al. Blood pressure, prevalence of hypertension and hypertension related complications in Nigerian Africans: A review. World J Cardiol 2012;4:327-40.  Back to cited text no. 6
Aje A, Adebiyi AA, Falase AO. Hypertensive disease in Africa. S Afr Heart 2009;6:42-51.  Back to cited text no. 7
Mensah GA, Barkey NL, Cooper RS. Spectrum of hypertensive target organ damage in Africa: A review of published studies. J Hum Hypertens 1994;8:799-808.  Back to cited text no. 8
Falase AO, Ogah OS. Cardiomyopathies and myocardial disorders in Africa: Present status and the way forward. Cardiovasc J Afr 2012;23:552-62.  Back to cited text no. 9
Carlisle R, Ogunlesi TO. Prospective study of adult cases presenting at the Cardiac Unit, University College Hospital, Ibadan 1968 and 1969. Afr J Med Sci 1972;3:13-25.  Back to cited text no. 10
Ogah OS, Stewart S, Falase AO, Akinyemi JO, Adegbite GD, Alabi AA, et al. Contemporary profile of acute heart failure in Southern Nigeria: Data from the Abeokuta Heart Failure Clinical Registry. JACC Heart Fail 2014;2:250-9.  Back to cited text no. 11
Attah EB, Falase AO. Large flabby hearts in hypertension. Am Heart J 1977;94:189-95.  Back to cited text no. 12
Falase AO, Ayeni O, Sekoni GA, Odia OJ. Heart failure in Nigerian hypertensives. Afr J Med Med Sci 1983;12:7-15.  Back to cited text no. 13
Aje A, Adebiyi AA, Oladapo OO, Dada A, Ogah OS, Ojji DB, et al. Left ventricular geometric patterns in newly presenting Nigerian hypertensives: An echocardiographic study. BMC Cardiovasc Disord 2006;6:4.  Back to cited text no. 14
Adebiyi AA, Ogah OS, Aje A, Ojji DB, Adebayo AK, Oladapo OO, et al. Echocardiographic partition values and prevalence of left ventricular hypertrophy in hypertensive Nigerians. BMC Med Imaging 2006;6:10.  Back to cited text no. 15
Adebiyi AA, Aje A, Ogah OS, Ojji DB, Dada A, Oladapo OO, et al. Correlates of left atrial size in Nigerian hypertensives. Cardiovasc J S Afr 2005;16:158-61.  Back to cited text no. 16
Adebiyi AA, Aje A, Ogah OS, Ojji DB, Oladapo OO, Falase AO. Left ventricular diastolic function parameters in hypertensives. J Natl Med Assoc 2005;97:41-5.  Back to cited text no. 17
Adebayo AK, Oladapo OO, Adebiyi AA, Ogunleye OO, Ogah OS, Ojji DB, et al. Changes in left atrial dimension and function and left ventricular geometry in newly diagnosed untreated hypertensive subjects. J Cardiovasc Med (Hagerstown) 2008;9:561-9.  Back to cited text no. 18
Adebayo AK, Oladapo OO, Adebiyi AA, Ogunleye OO, Ogah OS, Ojji DB, et al. Characterisation of left ventricular function by tissue Doppler imaging technique in newly diagnosed, untreated hypertensive subjects. Cardiovasc J Afr 2008;19:259-63.  Back to cited text no. 19
Ogah OS, Akinyemi RO, Adegbite GD, Udofia OI, Udoh SB, Adesina JO, et al. Prevalence of asymptomatic left ventricular systolic dysfunction in hypertensive Nigerians: Echocardiographic study of 832 subjects. Cardiovasc J Afr 2011;22:297-302.  Back to cited text no. 20
Ogah OS, Adebiyi AA, Oladapo OO, Aje A, Ojji DB, Adebayo AK, et al. Association between electrocardiographic left ventricular hypertrophy with strain pattern and left ventricular structure and function. Cardiology 2006;106:14-21.  Back to cited text no. 21
Lawal SO, Osotimehin BO, Falase AO. Mild hypertension in patients with suspected dilated cardiomyopathy: Cause or consequence? Afr J Med Med Sci 1988;17:101-12.  Back to cited text no. 22
Lawal SO, Falase AO. The effect of hypertension on the heart of adult Nigerians. Trop Cardiol 1988;14:153-9.  Back to cited text no. 23
Aje A, Adebiyi AA, Falase AO. Hypertensive heart disease in Africa: Hypertensive heart disease. SA Heart 2009;6:42-51.  Back to cited text no. 24
Adebiyi AA, Akinosun OM, Nwafor CE, Falase AO. Plasma catecholamines in Nigerians with primary hypertension. Ethn Dis 2011;21:158-62.  Back to cited text no. 25
Oladapo OO, Salako L, Sodiq O, Shoyinka K, Adedapo K, Falase AO. A prevalence of cardiometabolic risk factors among a rural Yoruba south-western Nigerian population: A population-based survey. Cardiovasc J Afr 2010;21:26-31.  Back to cited text no. 26


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]

This article has been cited by
1 Community Pharmacists and Promotion of Lifestyle Modification in Adults with Hypertension
Olanike Kehinde, Kimberly Dixon-Lawson, Aaron Mendelsohn
International Healthcare Review (online). 2023;
[Pubmed] | [DOI]
2 Reported adherence to antihypertensive treatment and outcome at postmortem in Southwestern Nigerians
UchennaSimon Ezenkwa,SebastianAnebuokhae Omenai,JohnOlufemi Ogunbiyi
Nigerian Medical Journal. 2020; 61(1): 22
[Pubmed] | [DOI]
3 Evaluating the quality of antihypertensive drugs in Lagos State, Nigeria
Elizabeth Thithi Ndichu,Kelechi Ohiri,Oluwafemi Sekoni,Olasunmbo Makinde,Kevin Schulman,Geofrey Musinguzi
PLOS ONE. 2019; 14(2): e0211567
[Pubmed] | [DOI]
4 Blood pressure control in treated hypertensive Nigerians in South-South Nigeria: Experience from Benin City
Odigie Ojeh-Oziegbe,IgboinJoseph Ikhidero
CHRISMED Journal of Health and Research. 2019; 6(4): 229
[Pubmed] | [DOI]


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
Left ventricular...
Article Figures

 Article Access Statistics
    PDF Downloaded685    
    Comments [Add]    
    Cited by others 4    

Recommend this journal