Page 860 - Cardiac Nursing
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                  836    PA R T  V / Health Promotion and Disease Prevention
                  found to increase the risk of stroke and did not affect CVD inci-  (statins), fibric acid derivatives, and the intestinal absorption
                  dence. As a result, conjugated equine estrogen is not recommended  blockers. Individual response to each of these agents is variable,
                  for prevention of chronic disease in postmenopausal women. 123  and each of the agents has potential side effects. Nursing can
                  The 2007 AHA guidelines for the primary and secondary preven-  play a major role in the management of patients by assisting the
                  tion of heart disease in women support these conclusions. 124  patient to minimize side effects while promoting adherence to
                                                                      the regimen that achieves the desired lipid profile. In this sec-
                                                                      tion, the action, indications for use, and specific adherence
                     PHARMACOLOGIC                                    strategies for each of the classes of hypolipidemic drugs are re-
                     MANAGEMENT OF                                    viewed (Table 36-10).
                     HYPERLIPIDEMIA                                   Bile Acid-Binding Resins
                                                                        Actions and Indications for Use. Bile acid-binding resins
                  The primary rationale for the treatment of hyperlipidemia is the  are insoluble in water and are not absorbed from the intestine.
                  reduction of CVD morbidity and mortality. Studies using hy-  These agents bind with bile acids in the intestine, forming an in-
                  polipidemic drug therapy to achieve LDL reductions have  soluble complex. The enterohepatic circulation of bile acids is in-
                  demonstrated lower CVD morbidity and mortality and lower  terrupted and fecal excretion of bile acids is increased. This results
                  overall mortality rates. 8,10  Angiographic studies using lipid-lower-  in increased synthesis of bile acids from hepatic cholesterol stores.
                  ing drugs have demonstrated less progression of angiographically  Reduced hepatic cholesterol stimulates LDL receptor formation
                  determined CVD with reduction of LDL. 125–128  The rate of pro-  and increases HMG-CoA reductase activity, resulting in increased
                  gression of CVD appears to be a dose-related response, with  extraction of LDL from the bloodstream and a lower plasma con-
                  slower rates of progression associated with greater LDL lowering.  centration of LDL. Hepatic production of VLDL is also en-
                     Meta-analytic techniques have been used to analyze lipid-low-  hanced, resulting in increased triglyceride levels. The expected re-
                  ering studies and suggest that the decrease in CVD mortality is  sponse to resin therapy is seen in 2 to 4 weeks and may result in a
                  offset by increased death rates from other causes, particularly can-  20% to 25% reduction in LDL. 20
                  cer deaths and non-illness-related deaths such as injury deaths and
                  suicides. 129–131 These meta-analyses did not include data from the  Strategies for Increased Efficacy and Adherence. The ma-
                  more recent very large clinical trials investigating lipid-lowering  jor side effect of the bile acid-binding resins is constipation; the
                  drugs. 7,8,10  These studies did not observe any increase in cancer or  resins can be unpalatable, which may affect compliance. Resins
                  non-illness-related deaths. Although the explanations for these  come in both powder and tablet formulations. In powder form,
                  findings remain controversial, the consensus of experts is that hy-  the resins must be mixed with water. Because they are insoluble,
                  polipidemic drug therapy should always be instituted with non-  they form a gritty solution. It is helpful to demonstrate the mix-
                  pharmacologic interventions (TLC), including a low-fat, low-  ing process and allow the patient to taste the drug as part of the
                  cholesterol  diet, regular exercise, weight control, smoking  prescription process. If constipation develops, instruct the pa-
                  cessation, control of hypertension, and control of blood glucose  tient in the use of fiber, stool softeners, and other hygienic meas-
                  (in patients with diabetes). Hypolipidemic drug therapy requires  ures, such as increased fluid intake. Bile acid-binding resins
                  careful consideration of individual risks as well as the benefits of  should be taken with meals, particularly with the largest meal of
                  such drug therapy. There is sufficient evidence that lowering LDL  the day, because intestinal bile acids are greatest during that time.
                  cholesterol, particularly with the use of HMG-CoA reductase in-  Because these drugs are binding agents, they have the potential to
                  hibitors, in persons with known CAD and with CAD equivalents  bind and interfere with the absorption of other medications.
                  provides substantial benefit to reduced morbidity and mortality.  Consequently, the patient should be instructed to take other
                                                                      medications 1 hour before or 4 hours after taking the resin. Re-
                                                                      viewing the mechanism of action with the patient promotes ad-
                  Lipid Criteria and Goals for                        herence and a better understanding of the rationale for these in-
                  Drug Therapy                                        structions.
                  Consideration of hypolipidemic drug therapy for primary preven-  Nicotinic Acid (Niacin)
                  tion (i.e., in people without existing CVD) is indicated in those
                  without CVD risk factors but with LDL levels of 190 mg/dL or  Actions and Indications for Use. Nicotinic acid, or niacin,
                  more, or in people with 0 to 1 CVD risk factors and LDL levels  is a vitamin B 3 derivative that in large doses blocks the release of
                  of 160 mg/dL or more. The target goals of treatment should be to  free fatty acids from adipose tissues, resulting in less hepatic con-
                                                                                                      132
                  achieve LDL levels of less than 160 or 130 mg/dL, respectively. In  version of free fatty acids into triglycerides.
                  secondary prevention (i.e., in patients with established CVD, with  The hepatic production of VLDL is also decreased. Because
                  CVD equivalents, and/or a CVD risk of  20% in 10 years), drug  VLDL is converted to IDL and LDL, decreased VLDL levels lead
                  therapy can be considered if LDL levels are more than 100 mg/dL  to favorable reductions in these lipoproteins as well. Contraindi-
                  and should be initiated if LDL levels are more than 130 mg/dL.  cations to use include active liver disease and peptic ulcer disease,
                  The optimal LDL goal for all adults, in particular for those with  and caution should be exercised when it is used in patients with
                               3
                  established CVD , less than 100 mg/dL (see Table 36-10).   diabetes and atrial arrhythmias.
                                                                        Strategies for Increased Efficacy and Adherence. The
                  Classes of Hypolipidemic Drugs                      most common side effect of nicotinic acid use is cutaneous
                                                                      flushing caused by a prostaglandin-mediated vasodilation effect
                  The major classes of hypolipidemic drugs include the bile acid-  on vascular smooth muscle. This effect can be minimized with
                  binding resins, nicotinic acid, HMG-CoA reductase inhibitors  the use of aspirin taken 30 minutes before the nicotinic acid
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