Drug Antihypertensive Therapy: Factors – Concomitant Medical Conditions
Common medical conditions co-existing with hypertension may affect the choice of drug.
In non-insulin-dependent diabetes, thiazide diuretics can aggravate hyperglycemia. Angiotensin-converting enzyme inhibitors, calcium channel blockers, and central symptholytics, none of which affect blood sugar, would be preferred. The use of β-blockers in these patients is somewhat controversial (it has been suggested that they may decrease pancreatic insulin release) but is probably not contraindicated on the basis of current evidence.
In insulin-dependent diabetics, the hyperglycemic effect of thiazides is not a major concern (if the patient is already on insulin). Angiotensin-converting enzyme inhibitors may be particularly useful in patients with diabetic nephropathy to control hypertension and simultaneously slow the progression of renal insufficiency and diminish proteinuria. β-Blockers are best avoided unless the blood sugar level is well controlled and hypoglycemia is not a major problem; patients who have frequent hypoglycemic episodes may not tolerate the antigluconeogenetic effect of β-blockers.
For patients with ischemic heart disease, β-blockers and calcium channel blockers may simultaneously lower blood pressure and reduce the frequency of angina. In addition, β-blockers have been shown to prolong life in certain patients after myocardial infarction; this effect has not yet been demonstrated for calcium channel blockers.
Recent short-term studies have, however, indicated that nifedipine could help protect patients with coronary artery disease from developing new stenotic lesions. Should this be true over the long term, nifedipine would be a particularly attractive choice for treating hypertension in this patient group. The use of hydralazine to control blood pressure in a patient with ischemic heart disease who is not receiving p-blockers would be contraindicated because of baroreceptor-mediated reflex sympathetic tachycardia, increasing myocardial oxygen demand.
In the hypertensive patient with congestive heart failure, the combinations of a diuretic with an angiotensin-converting enzyme (ACE) inhibitor, or of hydralazine and nitrate, are potentially useful. β-Blockers are best avoided, because they can decrease left ventricular contractility. Calcium channel blockers (which also have some negative inotropic effects) may be considered as third-line drugs.
β-Blockers are contraindicated in asthmatic patients. Calcium channel blockers have the theoretic advantage of bronchiolar smooth muscle relaxation, although the clinical importance of this effect is uncertain. Angiotensin-converting enzyme inhibitors have the potential disadvantage of producing a confounding cough.
β-Blockers would be relatively contraindicated in patients with Raynaud’s phenomenon or severe peripheral vascular disease because β2 blockade would allow unopposed OC-mediated vasoconstriction. Calcium channel blockers, on the other hand, can produce desirable vasodilation in addition to their hypotensive effect.
Hydralazine would not be the initial choice for a hypertensive patient with a history of migraine. β-Blockers and verapamil have been associated with a decreased incidence of migraine attacks.
Thiazides are best avoided in patients with a history of gout. If they are absolutely required for control of hypertension, then concomitant therapy with allopurinol may be necessary. For patients with a history of depression, reserpine, methyldopa, and possibly β-blockers would best be avoided.
Patients with pre-existing dependent edema may balk at the increased ankle swelling sometimes produced by calcium channel blockers (especially nifedipine) or minoxidil. Diuretics, on the other hand, would be an attractive choice.
For young, anxious patients or those with a labile component to their blood pressure or a hyperkinetic circulation, β-blockers, with the ability to reduce sympathetically mediated findings, could be useful first-line agents. Hydralazine, on the other hand, would tend to augment sympathetic drive. Calcium entry blockers, with the sometimes troublesome nuisance effects of flushing and increased pulse rate, may not be well tolerated by these patients.
Controversy has arisen over whether antihypertensive drugs that adversely affect serum lipids should be avoided, as patients with abnormal lipid levels are at increased risk for cardiovascular complications. β-Blockers without ISA may worsen the lip-id profile, as may high doses of hydrochlorthiazide (100 mg daily or greater). β-Blockers with ISA and low doses of thiazides have less effect on serum lipids. Angiotensin-converting enzyme inhibitors, calcium channel blockers, and centrally acting agents have a neutral effect. Prazosin can actually improve a patient’s lipid profile. While short-term effects due to increased serum cholesterol have been observed in some studies, it remains to be established whether or not drug-induced alterations of serum lipids are clinically meaningful over the long term. The minor increase in serum cholesterol may not offset the potential benefit of blood pressure reduction.
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