Article

The Impact of Getting Patients with Both Hypertension and High Cholesterol to Target

Register or Login to View PDF Permissions
Permissions× For commercial reprint enquiries please contact Springer Healthcare: ReprintsWarehouse@springernature.com.

For permissions and non-commercial reprint enquiries, please visit Copyright.com to start a request.

For author reprints, please email rob.barclay@radcliffe-group.com.
Average (ratings)
No ratings
Your rating
Copyright Statement:

The copyright in this work belongs to Radcliffe Medical Media. Only articles clearly marked with the CC BY-NC logo are published with the Creative Commons by Attribution Licence. The CC BY-NC option was not available for Radcliffe journals before 1 January 2019. Articles marked ‘Open Access’ but not marked ‘CC BY-NC’ are made freely accessible at the time of publication but are subject to standard copyright law regarding reproduction and distribution. Permission is required for reuse of this content.

Overwhelming evidence has been available for decades that classic risk factors such as hypertension and/or dyslipidaemia lead to an increased risk of chronic disease such as heart failure, coronary heart disease, stroke, vascular dementia, chronic kidney disease and peripheral vascular disease. These cardiovascular risk factors and their related diseases are in large part the consequence of an unhealthy lifestyle, which is facilitated by the structure of modern industrialised societies. There is a ready availability of excess calories and workplace-induced inactivity with subsequent obesity, as well as tobacco and alcohol use and excessive sodium consumption.1 Individuals without these unhealthy lifestyles are largely protected from hypertension and dyslipidaemia.2 The implementation of population-based preventative strategies is a major challenge to governments and healthcare services. As individuals have been required to take responsibility for the adverse health consequences of modern society, it is not surprising that inadequate lifestyle intervention is a major barrier to improved outcomes.

The global impact on health policy and the economic burden of hypertension-related disease alone is astounding.3 Up to one billion people are hypertensive (with this figure expected to rise by at least 60% in the next 20 years) and an there is an accelerating contribution from both the ageing populations of industrialised countries and the rapid industrialisation of nations such as India and China. There are over seven million deaths per year from hypertension-related disease and many more debilitating events. Hypertension is responsible for about half of the 7.2 million fatal myocardial infarcts per year. It is the major cause of heart failure and chronic kidney disease and the primary risk factor for over 15 million strokes per year. This epidemic of vascular and renal disease threatens to overwhelm health services worldwide.3 The cost of treating hypertension and its complications in the US approaches US$60 billion per year.4

There are compelling data confirming that the treatment of these risk factors significantly reduces the incidence of related disease.5 Therapy of hypertension reduces the incidence of myocardial infarction by 20–25%, heart failure by more than 50% and stroke by 35–40%, and significantly retards the progression of chronic kidney disease to its end stage requiring dialysis or transplantation.6

Vascular and renal risk factors rarely exist in isolation. Improved outcomes require assessment of total cardiovascular risk and the targeting of these multiple risk factors, including lifestyle contributors.

All expert hypertension management guidelines since the 1999 World Health Organization (WHO) and the International Society of Hypertension (ISH) guidelines have reinforced the importance of assessing for and treating all cardiovascular risk factors, and stressed the necessity of treating to appropriate targets.7 Progressively stringent classifications and targets continue to be set, for example the controversial classification of pre-hypertension in Joint National Committee on Hypertension VII (JNCVII).8

Despite universal acceptance of this increased risk, there is remarkably poor identification and control of these readily treatable risk factors worldwide. Only 59% of American hypertensives are treated, with only 34% of these achieving blood pressure levels of less than 140/90mHg.8 In Australia, where there is universal access to free healthcare and federal government funding for all classes of antihypertensive drugs, 54% of hypertensives are treated, with 41% of these achieving levels of less than 140/90mmHg.9 The figures for dyslipidaemia are similar to those for hypertension, with some papers suggesting that more than 70% of patients do not achieve recommended targets.10

Why are so few patients, especially those with hypertension and dyslipidaemia, identified and at target when the benefits of treatment to the individual and society are so striking? This is despite education initiatives by health authorities and widely disseminated guidelines. Therapeutic agents of proven benefit are available to treat most patients with hypertension and dyslipidaemia to target, and while cost may be implicated in studies from the US, the similar figures from Australia, which has subsidised pharmacotherapy, discounts this as a probable cause. Hypertension is the most important and modifiable cardiovascular and renal risk factor and, like dyslipidaemia, should be among the easiest to treat.

Barriers to Effective Therapy and Outcomes

Hypertension management may be intrinsically problematic. There are significant issues regarding the reliable and reproducible measurement of baseline blood pressure on which to base therapeutic decisions.11 Overcoming this problem may require the use of newer technologies such as home or ambulatory blood pressure measurement, particularly with the stringent targets now required.

Apart from the multifactorial aetiology of hypertension, lifestyle factors play a significant and sometimes determining role in blood pressure control (e.g. ingesting a high-salt diet may abrogate the blood-pressure-lowering effects of angiotensin-converting enzyme [ACE] inhibitors and angiotensin receptor antagonists). There is a plethora of classes of antihypertensive agents proved to reduce blood pressure and the risk of hypertension-related disease, as well as significant differences between agents within some of these classes.

Dyslipidaemia should be readily treatable to target in most patients. Lipid profiles can be readily, reproducibly and cheaply measured. There are limited classes of lipid-lowering agents, of which only statins have unequivocal outcome data; this class is largely well-tolerated.12

Relevant lifestyle modification and therapeutic compliance is probably the most difficult factor to influence. In primary prevention the task is more difficult. Patients are generally expected to make a lifelong commitment to therapy for clinically silent disease processes and to bear the inconvenience, cost and adverse effects of therapy. These issues of adherence and persistence with therapy require patient education, simplified dosage regimens, well-tolerated therapy and surveillance programmes to ensure compliance.13 The concept of non-compliance as a cardiovascular risk factor also has merit, with one-third to half of patients not complying with treatment regimens for hypertension.14 Most studies indicate that non-compliance follows after a period of treatment and failure to achieve therapeutic goals.

As physicians we are probably quick to blame therapeutic failure on the limitations of drugs and patient compliance. Much of the problem of poor control relates to physician practice. It is now well recognised that regardless of the strong evidence as to the benefits of treatment and well-defined targets, doctors fail to commence and/or increase therapy despite repeated presentations with elevated readings. This phenomenon has been termed ‘clinical inertia’.15

Potential barriers to the implementation of evidence-based hypertension guidelines by primary care physicians include: lack of awareness of guidelines and their recommendations; scepticism as to the relevance of clinical trial data to patient care; higher thresholds for therapy (especially in the elderly) and ageist attitudes regarding thresholds and targets; lack of computer systems to perform systematic audits; and the low priority of hypertension as a disease state.16–18

Physician ambivalence regarding increasing therapy has also been recognised as a barrier to therapy as blood pressure readings above target, usually isolated systolic hypertension, are frequently accepted as adequate.18,19 Other studies have indicated that the absence of practice aids such as computerised prompts or treatment flow charts may also play a role,15 along with educational training that focuses on short-term care with few opportunities to participate in long-term care to achieve recognised outcomes.15

Programmes designed to address the last of these appear to have been the most successful in improving the number of patients achieving therapeutic targets.15 Success varies with the nature of the programme. Conventional lectures and dissemination of guidelines have little impact. Steps to effectively increase therapy and attain targets have proved successful. This mentoring may take various forms such as targeted feedback of individual performance that may be face-to- face or by correspondence, or the interposition of other healthcare professionals such as specialist nurses or pharmacists.20 In all cases outcome data have improved significantly. Until these educational deficiencies are addressed, the achievement of therapeutic targets for diseases such as hypertension and dyslipidaemia will remain.

References

  1. Flack JM, Peters R, Shafi T, et al., Prevention of hypertension and its complications: theoretical basis and guidelines for treatment, JASN, 2003;14(7 Suppl. 2):S92–S98.
  2. Villegas R, Kearney PM, Perry IJ, The cumulative effect of core lifestyle behaviours on the prevalence of hypertension and dyslipidemia, BMC Public Health, 2008;8:210–17.
  3. Kanavos P, Ostergren J, Weber M, High Blood Pressure and Health Policy: Where We Are and Where We Need to Go Next, New York: Ruder Finn Inc., 2007,
  4. Hodgson TA, Cai L, Medical care expenditures for hypertension, its complications and its comorbidities, Medical Care, 2001;39:599–615.
  5. Neal B, MacMahon S, Chapman N, Effects of ACE inhibitors, calcium antagonists, and other blood-pressure-lowering drugs: Results of prospectively designed overviews of randomised trials-Blood Pressure Lowering Treatment Trialists’ Collaboration, Lancet, 2000;356:1955–64.
  6. Samak MJ, Greene T, Wang X, et al., The effect of a lower target blood pressure on the progression of kidney disease- Long-term follow-up of the modification of diet in renal disease study, Ann Int Med, 2005;142:342–51.
  7. Guidelines Subcommittee, World Health Organisation- International Society of Hypertension Guidelines for the Management of Hypertension, J Hypertens, 1999;17:151.
  8. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, Hypertension, 2003;42(6):1206.
  9. The Australian Diabetes Study—Diabetes and Associated Disorders in Australia—2000, The Accelerating Epidemic. National Diabetes Strategy 2000–2004, Commonwealth Department of Health and Aged Care, Canberra 2001.
  10. Nag SS, Daniel GW, Bullano MF, Goal-attainment among patients newly diagnosed with coronary heart disease or diabetes in a commercial HMO, J Manag Care Pharm, 2007;13:652–63.
  11. Graves J, Does evidence-based medicine suggest that physicians should not be measuring blood pressure in the hypertensive patient?, Am J Hypertens, 2004;17(4):354–60.
  12. McKenney J, Improving cholesterol control in managed care populations, Am J Mang Care, 2000;6:S997–S1007.
  13. Burnier M, Medication adherence and persistence as the cornerstone of effective antihypertensive therapy, Am J Hypertens, 2006;19(11):1190–96.
  14. Munger MA, Van Tassell BW, LaFleur J, Medication nonadherence: an unrecognised cardiovascular risk factor, Med Gen Med, 2007;9(3):58.
  15.  
  16. Craney M, et al., Why do GPs not implement evidence-based guidelines? A descriptive study, Family Practice, 2001;18(4):359.
  17. Hyman DJ, Pavlik VN, Self-reported hypertension treatment practices among primary care physicians: blood pressure thresholds, drug choices and the role of guidelines and evidence-based medicine, Arch Intern Med, 2001;161(11):1458.
  18. Hyman DJ, Pavlik VN, Self-reported hypertension treatment practices among primary care physicians: blood pressure thresholds, drug choices and the role of guidelines and evidence-based medicine, Arch Intern Med, 2000;160(15): 2281–6.
  19. Oliveria SA, et al., Physician-related barriers to the effective management of uncontrolled hypertension, Arch Intern Med, 2002;162(4):413–20.
  20. Green BB, Cook AJ, Ralston JD, et al., Effectiveness of Home Blood Pressure Monitoring, Web Communication and Pharmacist Care on Hypertension Control: A Randomised Controlled Trial, JAMA, 2008;299(24):2857–67.