Clinical Inertia as a Clinical Safeguard

Inertia is the resistance of a physical object to a change in its state of motion or rest. Phillips et al¹ have described clinical inertia as “failure of health care providers to initiate or intensify therapy when indicated.” Although clinical inertia may apply to all medical fields, given the lag time between advances in clinical understanding and incorporation into clinical guidelines, as well as the other time needed for the translation of clinical guidelines into clinical practice, Phillips et al¹ intended to limit the discussion of inertia to disorders in which abnormal values may be the only manifestation of the disease, such as diabetes, hypertension, and dyslipidemia. Quiz Ref IDMain causes of clinical inertia include overestimation of care provided, use of “soft” reasons to avoid intensification of therapy (incorrect perception of clinical improvement, dietary nonadherence, and concerns about translation of clinical trials results to individual patients), and lack of understanding about achieving therapeutic goals. While physicians may cite patient refusal or nonadherence as the reason for clinical inertia, it seems likely that in many instances, physician inertia is the reason for the problem.

Why physicians—who may have knowledge of and may be familiar with standard-of-care guidelines—seem to be subject to clinical inertia is still an open question. However, there may be an alternative interpretation for the phenomenon: clinical inertia may be a clinical safeguard for the drug-intensive style of medicine fueled by the current medical literature.

In the United States, the use of antidiabetic drugs by adults 45 years and older increased from 7% in 1988-1994 to 11% in 2003-2006; in 2003-2006, adults 65 years and older were significantly more likely to take antidiabetic drugs (15% for men, 15.6% for women) than adults aged 45 through 64 years (7.9% for men, 8.7% for women), reflecting differences in diabetes rates by age.² Despite the increasing use of these drugs, fewer than half of US adults with type 2 diabetes reach a glycated hemoglobin (HbA_1c) level of less than 7%, recommended by the American Diabetes Association, American Heart Association, and American College of Cardiology for most patients to minimize the risk of vascular complications.³ Clinical inertia has been implicated because the time required for intensification of diabetes therapy may range from 2 to 3 years.

To date, it has not been unequivocally demonstrated that macrovascular disease would respond to tight glycemic control in type 2 diabetes. Combined analysis of recent intervention trials exploring the role of aggressive lowering of blood glucose levels in reducing the incidence of cardiovascular disease found relatively minor benefits for an approximately 1-percentage-point reduction of HbA_1c level for preventing coronary events and no benefits for preventing stroke, cardiovascular mortality, total mortality, blindness, or renal failure.⁴ Quiz Ref IDIn the ACCORD (Action to Control Cardiovascular Risk in Diabetes) trial,⁵ the all-cause death rate was 22% higher in the intensive-therapy group (target HbA_1c level <6%) compared with the standard-therapy group (target HbA_1c level between 7% and 7.9%), and hypoglycemia requiring assistance and weight gain were more frequent in the intensive-therapy group.

Recent data from NHANES (National Health and Nutrition Examination Survey)⁶ showed that hypertension control improved from 27.3% in 1988-1994 to 50.1% in 2007-2008. The progress in blood pressure control reflected increases in awareness, treatment, and proportion of patients with hypertension treated and controlled. For almost 20 years, guidelines have recommended lower blood pressure goals in patients with diabetes. The observational subgroup analysis of 6400 of the 22 576 participants in INVEST (International Verapamil Trandolapril Study) showed that decreasing systolic blood pressure to lower than 130 mm Hg in patients with diabetes and coronary heart disease was associated with a 15% to 20% increase in risk of all-cause mortality, compared with patients with systolic blood pressure lower than 140 mm Hg.⁷

Quiz Ref IDIn the ACCORD trial,⁸ targeting a systolic blood pressure of less than 120 mm Hg, as compared with less than 140 mm Hg, did not reduce the rate of a composite outcome of fatal and nonfatal major cardiovascular events in patients with type 2 diabetes at high risk for cardiovascular events. Serious adverse events attributed to antihypertensive treatment occurred in 3.3% of participants in the intensive-therapy group and 1.3% of participants in the standard-therapy group.

Because of their demonstrated efficacy and safety, statins have become the drug class of choice used to lower cholesterol levels. From 1988-1994 to 2003-2006, the use of statin drugs by adults 45 years and older increased almost 10-fold, from 2% to 22%.² There was a concurrent decline in the percentage of Americans with high cholesterol levels over this period. Regardless of age category, men and women 45 years and older had increases in statin drug use and decreases in high cholesterol levels.²

However, more treatment is not necessarily better. Statin medications for persons without coronary heart disease may be an example of the widespread use of medications despite the absence of data supporting patient benefit for these indications. Quiz Ref IDIn a meta-analysis of 11 clinical trials involving 65 229 participants among high-risk individuals without prior cardiovascular disease, Ray et al⁹ reported that statin therapy was associated with reductions in average levels of low-density lipoprotein cholesterol from 139 to 98 mg/dL over an average treatment period of 3.7 years but did not result in reduction in all-cause mortality. Today, many patients are prescribed statins for primary prevention, although the short-term benefits, if any, are very small for primary prevention.

The widespread application of the lower-is-better philosophy has been disputed, at least for HbA_1c, blood pressure, and low-density lipoprotein cholesterol levels; treatment of diabetes, hypertension, and dyslipidemia is commonly influenced by clinical inertia. Cost of therapy does not appear to contribute much to clinical inertia, either for patients or for physicians. In addition, even though newer medications or multiple-drug regimens in primary prevention may promise to reduce the burden of future cardiovascular disease morbidity and mortality, some physicians may have examined the evidence behind these recommendations with a critical view, even before studies challenging the lower-is-better school of thought appeared. Given the uncertainty in medicine, clinical inertia may be a clinical safeguard through which physicians acknowledge the uncertainty in some current practice guidelines. An alternative explanation is that some physicians have true inertia, and thereby have unintentionally benefited patients by not prescribing new therapies or adopting more aggressive approaches for treatment of these conditions.

Quiz Ref IDClinical inertia also may apply to the failure of physicians to stop or reduce therapy no longer needed. Ironically, this neglected side of clinical inertia does not seem to generate as much concern among physicians or scientific associations; in fact, one study found that 58% of medications could be discontinued in elderly patients and that quality of life improved with drug discontinuation.¹⁰ The drugs discontinued included, among others, antihypertensive drugs, statins, and antidiabetic agents.

Clinical inertia is usually considered a barrier to appropriate clinician responses to asymptomatic patients. Because clinical guidelines are seldom the definitive answer and are subject to change as new evidence emerges, it seems unlikely that clinical inertia may disappear from clinical decision-making. Whether this will translate to benefits or harms for patients is still an open question.