Evaluation of Prothrombin Time and Activated Partial Thromboplastin Time in Hypertensive Patients Attending a Tertiary Hospital in Calabar, Nigeria

Nnenna Adaeze, Nnamani; Uchenna Emeribe, Anthony; Abdullahi Nasiru, Idris; Babayo, Adamu; Uko, Emmanuel K.

doi:https://doi.org/10.1155/2014/932039

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Volume 2014 | Article ID 932039 | https://doi.org/10.1155/2014/932039

Evaluation of Prothrombin Time and Activated Partial Thromboplastin Time in Hypertensive Patients Attending a Tertiary Hospital in Calabar, Nigeria

Nnamani Nnenna Adaeze,¹Anthony Uchenna Emeribe,²Idris Abdullahi Nasiru,³Adamu Babayo,⁴and Emmanuel K. Uko¹

Academic Editor: Bashir A. Lwaleed

Received16 Aug 2014

Revised15 Oct 2014

Accepted28 Oct 2014

Published16 Nov 2014

Abstract

Introduction. Several biomedical findings have established the effects of hypertension on haemostasis and roles of blood coagulation products in the clinical course of hypertension. Methods. This cross-sectional study aimed at determining effects of hypertension on prothrombin time (PT) and activated partial thromboplastin time (APTT) in hypertensive patients in comparison with normotensive subjects attending a tertiary hospital in Calabar. Forty-two (42) hypertensive patients and thirty-nine (39) normotensive control subjects were investigated for PT and APTT using Quick one-stage methods. Results. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) correlated positively with APTT (, ; ) in hypertensive patients. DBP, SBP, PT, and APTT were significantly higher in hypertensive patients when compared to normotensive subjects (). DBP correlated negatively with duration of illness (; ) in hypertensive patients and positively with age of normotensive subjects (; ). Conclusion. The results obtained indicated that measurements of PT and APTT may serve as indices for evaluating hemostatic abnormalities in hypertensive patients and guide for antihypertensive therapy. However, to have better understanding of hemostatic activities in hypertension, it is recommended to conduct D-dimer, platelet factors, and protein assays.

1. Introduction

Cardiovascular diseases account for about one-third of premature deaths in men and one-quarter in women and arterial hypertension is one of the most significant risk factors for cardiovascular diseases [1]. Despite current knowledge, extensive clinical and experimental research, the cause of hypertension remains unknown in about 95% of all cases [1]. Hypertension is a chronic medical condition in which the blood pressure is indisputably elevated (≥140/90 mmHg). It is one of the most common worldwide diseases afflicting humans. Globally cardiovascular disease accounts for approximately 17 million deaths a year, nearly one-third of the total. Of these, complications of hypertension account for 9.4 million deaths worldwide every year. Hypertension is responsible for at least 45% of deaths due to heart disease [2]. Due to several associated morbidity, mortality, and economic cost to society, hypertension is now a serious public health challenge to both developed and developing nations [3, 4].

According to recent epidemiologic data, the overall prevalence of 28% of the general population is suffering from hypertension in Sub-Saharan Africa, the prevalence rate in Nigeria is put at 22% with steady annual increase [5].

Hypertension is classified as either primary or secondary. It is primary when no medical cause can be found to explain the raised blood pressure. This type represents between 90 and 95% of hypertension cases [6]. Secondary hypertension represents approximately 10% of all hypertension cases. Identifiable underlying causes of secondary hypertension are kidney disease, renal hyperaldosteronism, and pheochromocytoma. Secondary hypertension has specific therapy; it is potentially curable and often distinguishable from primary one on clinical grounds [7].

Risk factors associated with hypertension include age, race, family history, obesity, sedentary lifestyle, alcohol abuse, and stress among others. Hypertension increases hardening of the arteries and predisposes individuals to heart disease, peripheral vascular disease, and strokes [7–10].

Hypertensive patients are at high risk for the development of cardiovascular diseases [11], whereas several studies have shown that treatment of hypertension diminishes the prevalence of cardiovascular diseases [12–14]. The existence of hypertension, especially in combination with other risk factors, is disadvantageous for the prognosis of cardiovascular diseases [15]. The integrity of the blood vessels is essential because damage of the intima, which may occur in hypertension, can finally cause atherosclerosis. This kind of patient is likely to develop increased platelet aggregation with heart and blood vessel problems as possible sequelae [16]. Moreover, blood vessel damage activates the coagulation system, which may also stimulate the progress of atherosclerosis.

Coagulation abnormalities in pregnant women have been reported to be more serious in women with hypertension (preeclampsia) than in those without hypertension [17]. In patients with borderline hypertension, even before the appearance of clinical manifestations of vascular damages [18], coagulation activation seems to be already present [18].

Besides platelet aggregability and coagulation activation, fibrinolysis, that is, plasma tissue-type plasminogen activator activity, appears to be a major factor related to the risk of cardiovascular disease [19–22].

Prothrombin time (PT) and activated partial thromboplastin time (APTT) have been shown to be associated with elevated systolic and diastolic blood pressures in hypertensive and normotensive patients [23]. In a study which involved the inclusion of one hundred and one patients with hypertension of mild to moderate grades, attending Al-Najaf Teaching Hospital, Iraq, significant differences were found in PT and APTT between hypertensive and normotensive patients [24]. The prothrombin time (PT) and its derived measures of prothrombin ratio (PR) and international normalized ratio (INR) are measures of the extrinsic pathway of coagulation. The APTT in contrast to the PT measures the activity of the intrinsic pathways of coagulation. Endothelial damage, platelet hyperactivity, and other changes of blood coagulation may play a role in the vascular complications of essential hypertension [25–27].

The main aim of this study is to assess possible association between prothrombin time and activated partial thromboplastin time with effects of blood pressures in hypertensive and normotensive subjects and their significant utility for screening hemostatic dysfunction in hypertensive patients.

2. Materials and Methods

2.1. Study Area

The study was conducted at the University of Calabar Teaching Hospital, Calabar, Cross River State. Calabar is the capital city of Cross River State which is divided into Calabar Municipal and Calabar South Local Governments and is located at the coastal southeastern area (4^∘57′N 8^∘19′E) of Nigeria. It has an area of 604 km² and a population of 371,022 at the 2006 census.

2.2. Study Population

A total of eighty-onesubjects were enrolled into the study. Forty-two (42) hypertensive patients aged between 30 and 80 years and thirty-nine (39) normotensive control subjects were investigated for PT and APTT using Quick one-stage methods. The selection of patients was done with the support of the physician and nursing staff of the Medical Outpatient Department (MOPD) of University of Calabar Teaching Hospital (UCTH), Calabar. The procedures employed consisted of a questionnaire interview, taking of patient’s history, and blood pressure measurement.

2.3. Inclusion Criteria for Hypertensive Patients

The inclusion criteria are as follows:(i)the presence of the history of primary hypertension;(ii)elevated blood pressure (≥140/90 mmHg);(iii)no history of administration of anticoagulant therapy;(iv)no history of chronic viral infection and/or liver diseases (HBV, HCV, HIV, and alcohol consumption);(v)having not been on long-term drug regimen;(vi)must be within normal range body mass index;(vii)being with no trace of underlying causes.

2.4. Exclusion Criteria for Hypertensive Patients

The exclusion criteria are as follows:(i)the absence of family history of primary hypertension;(ii)normal blood pressure (<140/90 mmHg);(iii)those on anticoagulant therapy;(iv)those with chronic viral infections and/or liver diseases such as HBV, HCV, HIV, and alcoholism;(v)obese individuals.

2.5. Inclusion Criteria for Normotensive Control Subjects

The inclusion criteria are as follows:(i)the absence of family history of hypertension;(ii)normal blood pressure (<140/90 mmHg);(iii)no history of administration of anticoagulant therapy;(iv)no history of chronic viral infection and/or liver diseases (HBV, HCV, HIV, and alcohol consumption);(v)having not been on long-term drug regimen;(vi)must be within normal body mass index;(vii)with no trace of underlying causes.

2.6. Exclusion Criteria for Normotensive Control Subjects

The exclusion criteria are as follows:(i)the presence of family history of hypertension;(ii)elevated blood pressure (≥140/90 mmHg);(iii)the absence of family history of primary hypertension;(iv)normal blood pressure (<140/90 mmHg);(v)those on anticoagulant therapy;(vi)those with chronic viral infections and/or liver diseases such as HBV, HCV, HIV, and alcoholism;(vii)obese individuals.

2.7. Ethical Clearance and Informed Consent

The ethical clearance was obtained from the Ethical Committee of UCTH, Calabar, Cross River State, Nigeria. Informed consent was obtained from all participating subjects. This was done via an informed consent form duly completed by all the subjects.

2.8. Questionnaire

Semistructured administered questionnaires were used to obtain data such as age, marital status, clinical signs and symptoms, and provisional diagnosis.

2.9. Sample Collection

Four and a half-millilitres (4.5 mL) of blood sample was drawn from hypertensive and normotensive subjects and discharged into a 0.5 mL of 3.13% trisodium citrate sample bottle. The anticoagulated samples were centrifuged at 4000 rpm for 10 minutes and platelet poor plasma stored in a deep freezer at −20°C until assayed. Standard method of Quick one-stage analysis by [28] was used for PT and APTT.

2.10. Statistical Method

The generated data was systematically analysed as appropriate for means, standard deviation, Student’s -test, Pearson’s correlation analysis, and analysis of variance on Microsoft Excel and SPSS software version 18 (California Inc.). Results were presented as the mean ± standard deviation. A two-sided was considered statistically significant for -test (used to determine the differences between the groups) and Pearson’s correlation analysis was used to determine the intervariable associations of the various groups.

3. Results

Table 1 shows the mean and standard deviation for the systolic pressure, diastolic pressure, prothrombin time test, and activated partial thromboplastin time test of hypertensives and normotensives including the duration of hypertensive subjects enrolled in the study. The mean and standard deviation for systolic blood pressure, diastolic blood pressure, prothrombin time test, activated partial thromboplastin time test, and duration of hypertensives were mmHg, mmHg, seconds, seconds, and years, respectively, while the mean and standard deviation for the systolic pressure, diastolic pressure, prothrombin time test, and activated partial thromboplastin time test of normotensives studied were mmHg, mmHg, seconds, and seconds, respectively.

Diastolic blood pressures, systolic blood pressures, Prothrombin Time Test and Activated Partial Thromboplastin Time Test were significantly higher in hypertensive patients when compared to normotensives ().

Based on the duration of hypertension, the hypertensive patients were grouped into three different groups (≤3 years, 4–7 years, and ≥8 years); their prothrombin time was , , and seconds, respectively, while their activated partial thromboplastin time was , , and seconds, respectively, as shown in Table 2.

Systolic blood pressure correlated positively with PTTK (; ) (Figure 4) and with diastolic blood pressure (; ) (Figure 2) in hypertensive patients, respectively. Diastolic blood pressure correlated negatively with duration of illness (; ) in hypertensive patients (Figure 1) and positively with age (; ) in normotensive subjects (Figure 5). A positive correlation was observed between PTT and PTTK both in hypertensive patients (; ) (Figure 3) and in normotensive subjects (; ) (Figure 6). More so positive correlation of systolic and diastolic blood pressure of normotensive subjects was observed across gender distribution (Figure 8) but negative correlation between systolic blood pressure and male hypertensive subjects (Figure 7). There was a statistical relationship between PT and APTT and age of hypertensive patients () (Table 3). However there was no statistical relationship between PTT and APTT across ages of normotensive patients (Table 4).

4. Discussion

Haemostatic system is directly involved in the atherosclerotic process. Hypertension is an atherosclerotic risk factor causing endothelial dysfunction; therefore, endothelial damage, platelets hyperactivation, and drugs are involved in the coagulation and fibrinolytic system [29, 30]. Prothrombin time and activated partial thromboplastin time are important clinical parameters for assessing extrinsic and intrinsic factors/pathways of the coagulation system [30].

The findings of this study show significant increases in the prothrombin time and activated partial thromboplastin time of hypertensive patients when compared to those of the normotensives (control). This increase could be due to endothelial damage as a result of atherosclerosis caused by hypertension on these patients () [31].

The prothrombin time and activated partial thromboplastin time of hypertensive patients increase with increase in duration of hypertension which may be due to prolonged endothelial wall effect as this will lead to sustained release of vasoactive substances that interfere coagulation cascades, and these indices eventually decrease as the antihypertensive therapy continues, even lower than before they started treatment; this finding is in consonance with Lee’s work and that of Mirsaiedi et al. [32, 33].

There was a positive correlation between systolic pressure and activated partial thromboplastin time in hypertensive patients which could be due to the risk factors associated with hypertension, for example, atherosclerosis, endothelial dysfunction and antihypertensive drugs [34, 35].

There was a negative correlation between diastolic pressure and duration of illness and a probable explanation to this could be that reduced exposure of the vascular walls to pressure in those with lower duration will give a higher pressure than those who have higher exposure to this tension because their blood vessels might be weaker and cannot exert resistance or pressure against blood flow when compared to those with lower duration [35–38].

Positive correlation of systolic and diastolic blood pressure of normotensive subjects was observed across gender distribution, but negative correlation between systolic blood pressure in male hypertensive subjects; these findings are in conformity with previous studies [38–41]. There was a statistical relationship between PT and APTT and age distribution of hypertensive patients (); this supports the findings of Akputuzor et al. and Mirsaiedi et al. [33, 42]. Prolonged PT and APTT were common with elderly hypertensive subjects; one could speculate that this phenomenon is due to diminished prostacyclin synthesis and/or release by the endothelial cells during old age.

Due to the fact that there was significant increase in prothrombin time and activated partial thromboplastin time of hypertensive patients when compared with normotensive (control) subjects, assessment of these parameters may serve as prognostic indices for evaluating hypertensive patients in whom there was clinical evidence of hemostatic abnormality and guide for antihypertensive therapy. However, to have complete understanding of hemostatic activities in hypertension, it is recommended to conduct D-dimer, platelet factors, and protein assays.

Conflict of Interests

The authors declare that there is no conflict of interests regarding the publication of this paper.

Acknowledgments

The authors would like to acknowledge the staff of Medical Laboratory Department, University of Calabar Teaching Hospital, Nigeria, for their technical support and Pharmacist Ibrahim Abdulkadir for typesetting the final paper.

References

I. Bernatova, “Endothelial dysfunction in experimental models of arterial hypertension: cause or consequence?” BioMed Research International, vol. 2014, Article ID 598271, 14 pages, 2014.
View at: Publisher Site | Google Scholar
A. V. Chobanian, G. L. Bakris, H. R. Black et al., “Seventh report of the joint national committee on prevention, detection, evaluation, and treatment of high blood pressure,” Hypertension, vol. 42, no. 6, pp. 1206–1252, 2003.
View at: Publisher Site | Google Scholar
P. M. Kearney, M. Whelton, K. Reynolds, P. Muntner, P. K. Whelton, and J. He, “Global burden of hypertension: analysis of worldwide data,” The Lancet, vol. 365, no. 9455, pp. 217–223, 2005.
View at: Publisher Site | Google Scholar
I. Hajjar and T. A. Kotchen, “Trends in prevalence, awareness, treatment, and control of hypertension in the United States, 1988–2000,” Journal of the American Medical Association, vol. 290, no. 2, pp. 199–206, 2003.
View at: Publisher Site | Google Scholar
World Health Organisation, Global Health Observatory Data Repository, World Health Organisation, Geneva, Switzerland, 2013, http://apps.who.int/gho/data/view.main.
O. A. Carretero and S. Oparil, “Essential hypertension. Part I: definition and etiology,” Circulation, vol. 101, no. 3, pp. 329–335, 2000.
View at: Publisher Site | Google Scholar
M. Mayo, Foundation for Medical Education and Research on Secondary Hypertension, McGraw-Hill, London, UK, 2008.
E. Agabiti-Rosei, “From macro- to microcirculation: benefits in hypertension and diabetes,” Journal of Hypertension, vol. 26, no. 3, pp. 15–19, 2008.
View at: Google Scholar
D. R. J. Singer and A. Kite, “Management of hypertension in peripheral arterial disease: does the choice of drugs matter?” European Journal of Vascular and Endovascular Surgery, vol. 35, no. 6, pp. 701–708, 2008.
View at: Publisher Site | Google Scholar
W. B. White, “Defining the problem of treating the patient with hypertension and arthritis pain,” The American Journal of Medicine, vol. 122, no. 5, supplement, pp. S3–S9, 2009.
View at: Publisher Site | Google Scholar
G. M. Patrassi, F. Fallo, A. Santarossa, M. T. Sartori, A. Casonato, and A. Girolami, “Clotting changes in borderline hypertension,” Journal of Human Hypertension, vol. 1, no. 2, pp. 101–103, 1987.
View at: Google Scholar
M. A. DeWood, J. Spores, R. Notske et al., “Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction,” The New England Journal of Medicine, vol. 303, no. 16, pp. 897–902, 1980.
View at: Publisher Site | Google Scholar
J. Gram and J. Jespersen, “A selective depression of tissue plasminogen activator (t-PA) activity in euglobulins characterises a risk group among survivors of acute myocardial infarction,” Thrombosis and Haemostasis, vol. 57, no. 2, pp. 137–139, 1987.
View at: Google Scholar
J. Franzen, B. Nilsson, B. W. Johansson, and I. M. Nilsson, “Fibrinolytic activity in men with acute myocardial infarction before 60 years of age,” Acta Medica Scandinavica, vol. 214, no. 5, pp. 339–344, 1983.
View at: Google Scholar
A. Hamsten, M. Blomback, B. Wiman et al., “Haemostatic function in myocardial infarction,” British Heart Journal, vol. 55, no. 1, pp. 58–66, 1986.
View at: Publisher Site | Google Scholar
T. K. Nilsson and O. Johnson, “The extrinsic fibrinolytic system in survivors of myocardial infarction,” Thrombosis Research, vol. 48, no. 6, pp. 621–630, 1987.
View at: Publisher Site | Google Scholar
M. C. Stone and J. M. Thorp, “Plasma fibrinogen—a major coronary risk factor,” The Journal of the Royal College of General Practitioners, vol. 35, no. 281, pp. 565–569, 1985.
View at: Google Scholar
L. Wilhelmsen, K. Svärsudd, L. Korsan-Bengtsenj, B. Larsson, L. Welin, and G. Tibblin, “Fibrinogen as a risk factor for stroke and myocardial infarction,” Northern England Journal of Medicine, vol. 377, pp. 501–505, 1984.
View at: Google Scholar
K. S. Sakariassen, P. A. Bolhuis, and J. J. Sixma, “Human blood platelet adhesion to artery subendothelium is mediated by factor VIII-Von Willebrand factor bo und to the subendothelium,” Nature, vol. 279, no. 5714, pp. 636–638, 1979.
View at: Publisher Site | Google Scholar
T. Jensen, “Increased plasma concentration of von Willebrand factor in insulin dependent diabetics with incipient nephropathy,” British Medical Journal, vol. 298, no. 6665, pp. 27–28, 1989.
View at: Google Scholar
J. A. Panza, A. A. Quyyumi, J. E. Brush Jr., and S. E. Epstein, “Abnormal endothelium-dependent vascular relaxation in patients with essential hypertension,” The New England Journal of Medicine, vol. 323, no. 1, pp. 22–27, 1990.
View at: Publisher Site | Google Scholar
J. R. Vane, E. E. Anggard, and R. M. Botting, “Regulatory functions of the vascular endothelium,” The New England Journal of Medicine, vol. 323, no. 1, pp. 27–36, 1990.
View at: Publisher Site | Google Scholar
N. Uren and D. Rutherford, High blood pressure (hypertension), Net Doctor, 2004, http://www.netdoctor.co.uk/diseases/facts/hypertension.htm.
G. Giacchetti, F. Turchi, M. Boscaro, and V. Ronconi, “Management of primary aldosteronism: its complications and their outcomes after treatment,” Current Vascular Pharmacology, vol. 7, no. 2, pp. 244–249, 2009.
View at: Publisher Site | Google Scholar
J. Schrader, “Stroke and hypertension,” Der Internist, vol. 50, no. 4, pp. 423–432, 2009.
View at: Publisher Site | Google Scholar
J. A. Blumenthal, M. A. Babyak, A. Hinderliter et al., “Effects of the DASH diet alone and in combination with exercise and weight loss on blood pressure and cardiovascular biomarkers in men and women with high blood pressure: the ENCORE study,” Archives of Internal Medicine, vol. 170, no. 2, pp. 126–135, 2010.
View at: Publisher Site | Google Scholar
O. M. Alhamami, J. Y. AL-Mayah, N. R. AL-Mousawi, and H. I. AL-Mousawi, “Pleiotropic effects of antihypertensive drugs,” The Islamic University Journal (Series of National Studies and Engineering), vol. 15, no. 1, pp. 1–12, 2007.
View at: Google Scholar
M. Laffan and R. Manning, “Investigation of haemostasis,” in Practical Haematology, S. M. Lewis, B. J. Bain, and I. Bates, Eds., pp. 380–463, Elsevier, Philadelphia, Pa, USA, 10th edition, 2006.
View at: Google Scholar
R. Junker, J. Heinrich, H. Schulte, M. Erren, and G. Assmann, “Hemostasis in normotensive and hypertensive men: results of the PROCAM study,” Journal of Hypertension, vol. 16, no. 7, pp. 917–923, 1998.
View at: Google Scholar
J. E. Deanfield, J. P. Halcox, and T. J. Rabelink, “Endothelial function and dysfunction: testing and clinical relevance,” Circulation, vol. 115, no. 10, pp. 1285–1295, 2007.
View at: Publisher Site | Google Scholar
A. H. Kamal, A. Tefferi, and R. K. Pruthi, “How to interpret and pursue an abnormal prothrombin time, activated partial thromboplastin time, and bleeding time in adults,” Mayo Clinic Proceedings, vol. 82, no. 7, pp. 864–873, 2007.
View at: Publisher Site | Google Scholar
A. J. Lee, “The role of rheological and haemostatic factors in hypertension,” Journal of Human Hypertension, vol. 11, no. 12, pp. 767–776, 1997.
View at: Publisher Site | Google Scholar
M. Mirsaiedi, Z. Fallah, P. Farzanegi, and M. B. Khameslu, “Comparing the fibrinogen, prothrombin time, Partial thromboplastin time and Platelets number and d-dimerin aerobic, control and resistance groups in Sari elderly sedentary men,” Annals of Biological Research, vol. 3, no. 5, pp. 2087–2090, 2087.
View at: Google Scholar
P. M. Vanhoutte, M. Feletou, and S. Taddei, “Endothelium-dependent contractions in hypertension,” British Journal of Pharmacology, vol. 144, no. 4, pp. 449–458, 2005.
View at: Publisher Site | Google Scholar
G. S. Berenson, S. R. Srinivasan, S. Hunter MacD et al., “Risk factors in early life as predictors of adult heart disease: the Bogalusa Heart Study,” The American Journal of the Medical Sciences, vol. 298, no. 3, pp. 141–151, 1989.
View at: Publisher Site | Google Scholar
A. W. Zieske, G. T. Malcom, and J. P. Strong, “Natural history and risk factors of atherosclerosis in children and youth: the PDAY study,” Pediatric Pathology and Molecular Medicine, vol. 21, no. 2, pp. 213–237, 2002.
View at: Publisher Site | Google Scholar
S. Mendis, P. Nordet, J. E. Fernandez-Britto, and N. Sternby, “Atherosclerosis in children and young adults: an overview of the World Health Organization and International Society and Federation of Cardiology study on Pathobiological Determinants of Atherosclerosis in Youth study (1985–1995),” Prevention and Control, vol. 1, no. 1, pp. 3–15, 2005.
View at: Publisher Site | Google Scholar
S. S. Lim, T. Vos, A. D. Flaxman 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,” The Lancet, vol. 380, pp. 2224–2260, 2010.
View at: Publisher Site | Google Scholar
E. Jervase, D. Barnabas, A. Emeka, and N. Osondu, “Sex differences and relationship between blood pressure and age among the Ibos of Nigeria,” The Internet Journal of Biological Anthropology, no. 2, pp. 37–43, 2012.
View at: Google Scholar
Y. S. Kusuma, B. V. Babu, and J. M. Naidu, “Blood pressure levels among cross-cultural populations of Visakhapatnam district, Andhra Pradesh, India,” Annals of Human Biology, vol. 29, no. 5, pp. 502–512, 2002.
View at: Publisher Site | Google Scholar
T. S. Bowman, H. D. Sesso, and J. M. Gaziano, “Effect of age on blood pressure parameters and risk of cardiovascular death in men,” American Journal of Hypertension, vol. 19, no. 1, pp. 47–52, 2006.
View at: Publisher Site | Google Scholar
J. O. Akputuzor, E. C. Akwiwu, and I. A. Udoh, “Prothrombin time and relative plasma viscosity of hypertensive patients attending university of Calabar teaching hospital, Calabar, Nigeria,” International Journal of Natural and Applied Sciences, vol. 7, no. 2, 2011.
View at: Google Scholar

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Copyright © 2014 Nnamani Nnenna Adaeze et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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