CLINICAL STATEMENTS AND GUIDELINESfailed to show a significant reduction of SBP in patients with resistant hypertension. 81 Other strategies such as targeting excessive sympathetic nerve activity by carotid body denervation are awaiting clinical validation in the hypertension and HF populations. Drugs to Avoid in Patients With HFSeveral classes of drugs should be avoided in patients with HFrEF with a history of hypertension. Because of their negative inotropic properties and the increased likelihood of worsening HF symptoms, the nondihydropyridine calcium channel blockers such as diltiazem and verapamil should be avoided. 8 The dihydropyridine calcium channel blocker amlodipine appeared to be safe in patients with severe HFrEF in the PRAISE trial (Prospective Randomized Amlodipine Survival Evaluation), 82 as was felodipine. 73 In the current 2013 HF guidelines, most calcium channelblocking drugs except amlodipine are not recommended. 8Although clonidine is an effective antihypertensive agent, a similar centrally acting drug, moxonidine, was associated with increased mortality in patients with HF; thus, centrally acting norepinephrine-depleting agents may need to be avoided or used with caution in patients with HFrEF. 83In the ALLHAT trial, the α-blocker doxazosin arm of the trial was discontinued because of a 2-fold increase in the risk of developing HF compared with chlorthalidone treatment. 45 Although the ALLHAT study excluded patients with established HF and there are caveats about extrapolating these data to the management of hypertension in patients with established HF, the safety and efficacy of α-blockers in the management of patients with HF with hypertension are currently unclear. Potent direct-acting vasodilators such as minoxidil should also be avoided because of their renin-related salt and fluid-retaining effects. Nonsteroidal anti-inflammatory agents should be used with caution in these patients, given their effects on BP, volume status, and renal function. Treatment of Hypertension in Patients With HF With Preserved LVEFMost patients with HF and preserved LVEF (HFpEF), especially elderly women, have hypertension. A significant proportion of these patients also have evidence of LV hypertrophy, and some may have atrial dilatation, cardiac enlargement, and wall motion abnormalities without LV systolic dysfunction. Patients with HFpEF may respond particularly well to the treatment of hypertension with regression of hypertrophy 84 and improvement in filling pressures. 84,85 Most patients with HFpEF require treatment with cardiac medications for the comorbidities of hypertension, diabetes mellitus, coronary artery disease, and atrial fibrillation. The 2013 HF guidelines suggest that the use of β-blocking agents, ACE inhibitors, and ARBs in patients with hypertension is reasonable to control BP in patients with HFpEF. 8 The use of ARBs might also be considered to decrease hospitalizations for patients with HFpEF. recommendations Harmonized With Existing Guidelines for the recognition and Treatment of pa...
Recent epidemiological evidence suggests that some antihypertensive medications may reduce the risk for Alzheimer disease (AD). We screened 55 clinically prescribed antihypertensive medications for AD-modifying activity using primary cortico-hippocampal neuron cultures generated from the Tg2576 AD mouse model. These agents represent all drug classes used for hypertension pharmacotherapy. We identified 7 candidate antihypertensive agents that significantly reduced AD-type β-amyloid protein (Aβ) accumulation. Through in vitro studies, we found that only 1 of the candidate drugs, valsartan, was capable of attenuating oligomerization of Aβ peptides into high-molecular-weight (HMW) oligomeric peptides, known to be involved in cognitive deterioration. We found that preventive treatment of Tg2576 mice with valsartan significantly reduced AD-type neuropathology and the content of soluble HMW extracellular oligomeric Aβ peptides in the brain. Most importantly, valsartan administration also attenuated the development of Aβ-mediated cognitive deterioration, even when delivered at a dose about 2-fold lower than that used for hypertension treatment in humans. These preclinical studies suggest that certain antihypertensive drugs may have AD-modifying activity and may protect against progressive Aβ-related memory deficits in subjects with AD or in those at high risk of developing AD.
There is now sizable literature on the association between traditional cardiovascular risk factors and Alzheimer's disease (AD). Based on epidemiologic studies, both cross-sectional and longitudinal, there are statistically significant correlations between the prevalence of AD and diabetes, hypercholesterolemia, hypertension, hyperhomocysteinemia, dietary saturated fats, cholesterol, antioxidants, alcohol consumption, smoking, physical activity, the presence of atrial fibrillation, atherosclerotic disease, and the plasma concentration of some hemostatic factors. Most of the cardiovascular risk factors found to be associated with AD are age-dependent, and the prevalence of AD increases with age. Therefore, the association could simply be attributed to aging. On the other hand, the common pathogenetic mechanisms for the generation of both atherosclerotic disease and AD, such as inflammation and the generation of free radicals, suggest a causal link. If this is the case, the identification of modifiable risk factors for dementia becomes a research priority and early intervention aimed at reducing those cardiovascular risk factors a therapeutic imperative.
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