Journal of Clinical and Diagnostic Research, 2018, Nov, Vol-12(11): BC19-BC22 19 19 DOI: 10.7860/JCDR/2018/36908.12284 Original Article Biochemistry Section Serum Creatine Kinase Activity among Hypertensive Patients and its Role as a Predictor for Failure of Antihypertensive Treatment INTRODUCTION Hypertension continues to be an important health issue worldwide. It has been associated with increased risk of coronary artery diseases and an independent risk for cardiovascular and chronic kidney diseases [1]. Global burden of diseases study has reported that in the year 2013 high systolic blood pressure led to 10.8 million deaths and 208.1 million Disability Adjusted Light Years (DALY) [2]. Worldwide cardiovascular disease accounts for approximately 17 million deaths a year of which, complications of hypertension account for 9.4 million deaths worldwide [3]. WHO data says by 2025 the global burden of hypertension will increase by 60% worldwide with higher in developing countries [4]. Developing countries specifically presents with higher incidence of undiagnosed, untreated and uncontrolled hypertension attributed to poor health system which may be because of population growth, ageing, behavioral risk factors, unhealthy food habits, lack of exercise and increase exposure to persistent stress [5]. Despite many efforts to treat hypertension JNC 7 (Joint National Committee) on prevention indicated 30% of hypertensive patients are unaware of their illness, 42% are not under treatment and 69% did not have their hypertension controlled in spite of patient’s adherence and physician’s proper treatment in accordance to required therapeutic criteria [6]. In the present scenario hypertensive treatment failure has become a major health concern in US and developing countries. In India only 25.6% of hypertensive had their BP under control with one fifth control in urban areas and even less than tenth in rural areas [7]. Substantial proportion have uncomplicated primary hypertension and not well explained why they are not able to obtain required treatment control despite therapy given in accordance to therapeutic guidelines. Adequate hypertension treatment and control is a necessity to reduce the mortality associated with it. CK is abundantly expressed in both mitochondrion and cytosol. It catalyzes the transfer of high-energy phosphate moiety between Creatine and ADP [8]. ADP+Creatine P+H + Creatine Kinase→ATP+Creatine This rate of generation of ATP by CK is much greater than that generated by oxidative phosphorylation. CK is specifically involved in skeletal muscle contraction, cardiovascular contractility, sodium retention, remodeling of the arteries where rapid generation of ATP is required. Till date CK is assayed clinically as a marker of damage of CK rich tissues [9]. Some studies have mentioned that CK is the predictor of blood pressure independent of age, sex, BMI or ethnicity [10]. High activity of these enzymes in the resistance arteries enhances pressure response leading to high blood pressure. Studies have suggested association of high creatine kinase with hypertension [11,12]. Study in animal models have shown lowering in CK with antihypertensive therapy [13]. It has been also found that high serum CK may be a genetic factor increasing hypertension risk in certain population [14]. With the above known facts in view, this study is an attempt to focus on the levels of creatine kinase in hypertensive patients under treatment and find out its probability of association with hypertensive treatment failure. MATERIALS AND METHODS The present study was done in Kalinga Institute of Medical Sciences with prior ethical clearance from institutional ethical committee from SURANKITA SUKUL 1 , JYOTIRMAYEE BAHINIPATI 2 , SAURAV PATRA 3 , KANDASAMY RAVICHANDRAN 4 Keywords: Blood pressure, Body mass index, Creatine Kinase ABSTRACT Introduction: Creatine Kinase (CK), a key enzyme of cellular energy metabolism helps the cells to function under high demands by involving in contractile processes and active trans-membrane transport by readily providing Adenosine-5’- triphosphate (ATP). Higher CK activity increases cardiovascular trophic responses and development of arterial hypertension. Hence, high CK activity may increase hypertension risk and may also be a cause behind the hypertensive treatment failure. Aim: In the present study, serum CK levels are compared between hypertensive and normotensive study subjects and association of serum CK in hypertensive treatment failure cases. Materials and Methods: A total of 75 known hypertensive patients who were under antihypertensive treatment for ≥3 months were taken as cases. Further grouping of the patients was done based upon the response to antihypertensive treatment into treatment control (n=40) and without treatment control (n=35) groups. Forty individuals age and sex matched normotensive control were taken. Serum Creatine Kinase, BMI, Systolic Blood Pressure, Diastolic Blood Pressure, was measured in the study group. Kruskal Wallis test was done to compare the parameters in all the three study groups. Correlation of serum CK with other parameters was done. Cut-Off value for serum CK was calculated in hypertensive cases. Results: CK was found to be higher in hypertensive cases with treatment control (99.55±31.34) U/L compared to normotensives (72.66±25.42) U/L. Significantly higher CK level was found in hypertensive treatment failures (313.92±133.12) U/L compared to treatment control cases. Statistically significant correlation was found between serum CK with SBP and DBP in hypertensive treatment failure cases. A cut-off value of 168.5 U/L was found out in hypertensive patients. Conclusion: Serum CK was found to be associated with severity of blood pressure and failure of antihypertensive therapy.