eMedicine Specialties > Cardiology > Atherosclerosis and Risk Factors

Hypertensive Heart Disease: Treatment & Medication

Author: Kamran Riaz, MD, Clinical Assistant Professor, Department of Internal Medicine, Section of Cardiology, Wright State University School of Medicine
Coauthor(s): Aqeel Ahmed, MD, Staff Physician, Department of Pathology, University of Missouri at Kansas City
Contributor Information and Disclosures

Updated: Aug 31, 2009

Treatment

Medical Care

The medical care of patients with hypertensive heart disease falls under 2 categories—treatment of the elevated BP and prevention and treatment of hypertensive heart disease. According to JNC 7, the BP goal should be less than 140/90 mm Hg in patients with uncomplicated hypertension, less than 130/85 mm Hg in those with diabetes and those with renal disease with less than 1 gram/24 hr proteinuria, and less than 125/75 in those with renal disease and more than 1 gram/24 hr proteinuria.¹² Emerging data support a target blood pressure goal of less than 150/80 mm Hg in patients more than 80 years old.¹³ Various treatment strategies include dietary modifications, regular aerobic exercise, weight loss,¹⁴ and pharmacotherapy directed toward hypertension, heart failure secondary to diastolic and systolic LV dysfunction, coronary artery disease, and arrhythmias.

• Dietary modifications
  • Studies have shown that diet and a healthy lifestyle alone or in combination with medical treatment can lower the BP and decrease the symptoms of heart failure and can also reverse LVH. Specific diet recommendations include a diet low in sodium, high in potassium (in patients with normal renal function), rich in fresh fruits and vegetables, low in cholesterol, and low in alcohol consumption.^15,16,17  In a large 2009 cohort study of women, the following 6 modifiable lifestyle and dietary factors for hypertension were identified.¹⁸
    • A body mass index (BMI) of less than 25
    • A daily mean of 30 minutes of vigorous exercise
    • A high score on the Dietary Approaches to Stop Hypertension (DASH) diet
    • Modest alcohol intake (up to 10 g/d)
    • Use of nonnarcotic analgesics less than once per week
    • Intake of 400 mcg/d or more of supplemental folic acid

• A low-sodium diet, alone or in combination with pharmacotherapy, has been shown by numerous studies to reduce BP in patients with hypertension, with a more prominent response in a subset of patients with hypertension—mainly African Americans—with low renin levels. Restriction of sodium in these patients does not lead to compensatory stimulation of the renin-angiotensin system and thus has a potent antihypertensive effect. Data also indicates that sodium reduction, previously shown to lower blood pressure, may also reduce long-term risk of cardiovascular events. The recommended daily sodium intake is 50-100 mmol, equivalent to 3-6 g of salt per day, which leads to an average 2-8 mm Hg reduction in BP.¹⁹
• In various epidemiological studies, a high-potassium diet has been associated with lowering of the BP. The mechanism of this action is not clear. Intravenous infusion of potassium has been shown to cause vasodilatation, which is believed to be mediated by nitric oxide in the vascular wall. Fresh fruits and vegetables rich in potassium, such as bananas, oranges, avocados, and tomatoes, should be recommended for patients with normal renal function.
• The DASH diet has been shown to significantly lower the BP (8-14 mm Hg) in patients with hypertension regardless of them maintaining a constant sodium content in their diet. The DASH diet is not only rich in important nutrients and fiber but also includes foods that contain far more potassium, calcium, and magnesium, than are found in the average American diet. This diet should be advised in patients with hypertension.^{20,21,22,23,24}
• A heart-healthy diet is part of the secondary prophylaxis in patients with coronary artery disease and of the primary prophylaxis in patients at high risk for this disease.
• Heavy alcohol consumption has been associated with high BP and an increase in LV mass.²⁵ Moderation in alcohol consumption is advised; no more than 1-2 drinks per day is recommended.²⁶

•   Regular aerobic exercise
  • Regular dynamic isotonic (aerobic) exercise, such as walking, running, swimming, or cycling, has been shown to decrease BP and improve cardiovascular well-being.²⁷ It also has additional favorable cardiovascular effects, including improved endothelial function, peripheral vasodilatation, reduced resting heart rate, improved heart rate variability, and reduced plasma levels of catecholamines.
  • Regular aerobic exercise sessions of at least 30 minutes for most days of the week can produce an average reduction in BP of 4-9 mm Hg. Isometric and strenuous exercise should be avoided.
• Weight reduction
  • Obesity has been linked to hypertension and LVH in various epidemiological studies, with as many as 50% of obese patients having some degree of hypertension and as many as 60-70% of patients with hypertension being obese. Studies have shown that weight reduction is one of the most effective ways to reduce BP. A 5-20 mm Hg BP reduction occurs with each 10 kg of weight loss.²⁸
  • Abdominal adiposity, clinically measured as waist-to-hip ratio and more accurately assessed by abdominal CT scan, is a particularly sensitive risk factor for hypertension.
  • Gradual weight reduction (1 kg/wk) should be advised. Pharmacological interventions to reduce weight should be used with great caution because diet pills, especially those available over the counter, frequently contain sympathomimetics. These can raise BP, worsen angina or symptoms of heart failure, and exacerbate tendencies for cardiac arrhythmias
  • Avoid medications such as NSAIDs, sympathomimetics, or MAOIs that can elevate BP or interfere with antihypertensive therapy.
• Pharmacotherapy
• Treatment of hypertension and hypertensive heart disease can involve the following classes of antihypertensive medications: thiazide diuretics, beta-blockers and combined alpha- and beta-blockers, calcium channel blockers, ACE inhibitors, angiotensin receptor blockers, and direct vasodilators such as hydralazine.
  • Thiazide-type diuretics should be used for most patients with uncomplicated hypertension, either alone or combined with drugs from other classes, according to the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.¹²  Updated recommendations from the JNC (JNC-8) are expected in 2010.
  • Most patients require 2 or more antihypertensive drugs to achieve the BP goal, and, when the BP is more than 20/10 mm Hg above the goal, consider initiating treatment with 2 drugs, either as separate prescriptions or in fixed-dose combinations.
    • Calcium channel blockers are effective for systolic hypertension in elderly patients. In a 2008 study, an ACE inhibitor/dihydropyridine calcium channel blocker combination proved to be superior to the ACE inhibitor/thiazide diuretic combination in reducing cardiovascular events in patients with hypertension who were at high risk for such events.²⁹
    • ACE inhibitors are the first choice in patients with diabetes and/or V dysfunction.
    • Angiotensin receptor blockers are a reasonable alternative, especially for patients with adverse effects with ACE inhibitors.
    • Beta-blockers are the drugs of first choice in patients with heart failure due to systolic LV dysfunction, patients with ischemic heart disease with or without a history of myocardial infarction, and in patients with thyrotoxicosis.
    • Peripheral alpha-channel blockers should be avoided in patients with hypertension in view of recent findings of their adverse effect on cardiovascular morbidity and mortality rates.
    • Central alpha-antagonists have no evidence-based support and have more adverse effects.
  • Intravenous drugs used in patients with a hypertensive emergency include nitroprusside, labetalol, hydralazine, enalapril, and beta-blockers (avoided in patients with acutely decompensated heart failure).
  • Some evidence shows that peroxisome proliferator-activated receptor gamma (PPARγ) agonist ameliorates oxidative stress and leads to reversal of systemic hypertension-associated cardiac remodeling in chronic pressure overload myocardium and LVH.³⁰
• Treatment of LVH
  • LVH, a marker of increased risk of cardiovascular morbidity and mortality, should be treated aggressively. Whether regression in LVH leads to improvement in cardiovascular mortality and morbidity rates is not clear, although limited data support this hypothesis. Data also indicate that regression of electrocardiographic LVH is associated with less hospitalization for heart failure in hypertensive patients.³⁰
  • All the medications already listed for the treatment of hypertension have been shown to reduce LVH. Limited meta-analysis data suggest a slight advantage to ACE inhibitors.
• Treatment of LV diastolic dysfunction
  • Certain classes of antihypertensives—ACE inhibitors, beta-blockers, and nondihydropyridine calcium channel blockers—have been shown (although not consistently) to improve echocardiographic parameters in symptomatic and asymptomatic diastolic dysfunction and the symptomatology of heart failure.
  • The angiotensin receptor blocker, candesartan, has been shown to decrease hospitalization in patients with diastolic heart failure.³¹
  • Use diuretics and nitrates with caution in patients with heart failure due to diastolic dysfunction. These drugs may cause severe hypotension by inappropriately decreasing the preload, which is required for adequate LV filling pressures. If diuretics are indicated, delicate titration is necessary.
  • Hydralazine has been shown to cause severe hypotension in patients with heart failure due to diastolic dysfunction.
  • By increasing the intracellular calcium level, digoxin can worsen LV stiffness. However, a large randomized trial has not shown any increase in mortality rat.
• Treatment of LV systolic dysfunction
  • Diuretics (predominantly loop diuretics) are used in the treatment of LV systolic dysfunction.
  • ACE inhibitors are used for preload and afterload reduction and prevention of pulmonary or systemic congestion. They have been shown to decrease morbidity and mortality rates in patients with heart failure due to systolic dysfunction. The aim should be to use the target dose or the maximum tolerable doses. ACE inhibitors are also indicated in patients with asymptomatic LV dilatation and dysfunction.
  • Beta-blockers (cardioselective or mixed alpha and beta), such as carvedilol, metoprolol XL, and bisoprolol, have been shown to improve LV function and decrease rates of mortality and morbidity from heart failure. Recent trials have also shown improvement in outcomes for patients in NYHA class IV heart failure with carvedilol administration. These drugs should be started when the patient has no signs of fluid overload and is in compensated heart failure. Therapy should be initiated with low doses, increasing the dose of the beta-blocker very slowly and closely monitoring the patient for signs of worsening heart failure.
• Low-dose spironolactone has been shown to decrease the rates of morbidity and mortality in patients in NYHA class III or IV heart failure who are already taking ACE inhibitors. It is also recommended for use in post-MI patients with diabetes mellitus or a left ventricular ejection fraction <40%.³²
• Treatment of cardiac arrhythmias
  • Treatment depends upon the specific arrhythmia and the underlying LV function.
  • Anticoagulation should be considered in patients with atrial fibrillation.
  • Treatment of anxiety, stress, sleep apnea, and other contributing or precipitating factors.

Surgical Care

Surgical treatment may be necessary for definitive treatment in selected cases of secondary causes for hypertension, such as aortic coarctation or pheochromocytoma.

Consultations

• Preventive cardiologist
• Hypertension specialist
• Heart failure specialist
• Heart failure nurse
• Electrophysiologist for treatment of complex arrhythmias
• Sleep specialist (if sleep apnea is suspected)

Diet

Specific diet recommendations include a diet low in sodium, high in potassium, rich in fresh fruits and vegetables, low in cholesterol, and low in alcohol intake. See Dietary modifications for more information.

Sinha et al concluded that high intakes of red or processed meat were associated with modest increases in total mortality, cancer mortality, and cardiovascular disease mortality. The baseline population was a cohort of half a million people aged 50-71 years from the National Institutes of Health-AARP (formerly known as the American Association of Retired Persons) Diet and Health Study.³³

Activity

Regular 30-minute sessions of aerobic exercise 3-4 times a week should be advised. Isometric and strenuous exercise should be avoided. See Regular aerobic exercise for more information.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Diuretic, Thiazide

Studies have shown that these agents reduce LVH. However, there is increasing evidence that chlorthalidone may be superior to hydrochlorothiazide in both efficacy and outcomes in patients with hypertension.^34,35

Chlorthalidone (Thalitone, Hygroton)

Inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water as well as potassium and hydrogen ions.

Hydrochlorothiazide (Microzide, Esidrix, HydroDIURIL)

Inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water as well as potassium and hydrogen ions.

Alpha/beta-adrenergic Blocking Agents

Beta-adrenergic blockers inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation. At low doses, alpha-adrenergic receptor blockers may be used as monotherapy in the treatment of hypertension. At higher doses, they may cause sodium and fluid to accumulate. As a result, concurrent diuretic therapy may be required to maintain the hypotensive effects of alpha-receptor blockers.

Carvedilol (Coreg)

Nonselective beta- and alpha-adrenergic blocker. Does not appear to have intrinsic sympathomimetic activity. May reduce cardiac output and decrease peripheral vascular resistance.

Beta-adrenergic blocking agents

Cardioselective and noncardioselective agents are used to treat hypertension. In addition, they can be used in treatment of arrhythmias (eg, ventricular ectopy) and for rate control in atrial fibrillation. They are also an important part of therapy for heart failure due to systolic or diastolic LV dysfunction. Whether they have any special influence in treatment of heart failure due to hypertension is not clear.³⁶

Bisoprolol (Zebeta)

Selectively blocks beta1 receptors, with little or no effect on beta2 types.

Atenolol (Tenormin)

Selectively blocks beta1 receptors, with little or no effect on beta2 types.

Metoprolol (Lopressor, Toprol XL)

Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor BP, heart rate, and ECG.

Alpha-adrenergic Blocking Agent, Oral

Labetalol

Blocks beta1-, alpha-, and beta2-adrenergic receptor sites decreasing blood pressure.

Angiotensin-converting enzyme inhibitors

Have been shown to decrease morbidity and mortality rates in patients with heart failure. ACE inhibitors lower elevated BP and decrease afterload with a favorable influence on remodeling; they also have been shown to reduce LVH at doses not known to decrease BP. Studies have shown improved outcomes in patients with diabetes, proteinuria, and/or renal failure, especially when compared with dihydropyridine calcium channel blockers.^37,38

Benazepril (Lotensin)

Prevents conversion of angiotensin I to angiotensin II, which is a potent vasoconstrictor. Also causes lower aldosterone secretion, thus reducing systemic and glomerular capillary pressure.
Comparative studies show ACE inhibitors are more effective than other antihypertensives (ie, beta-blockers, calcium channel blockers) in reducing blood pressure and proteinuria, protecting renal function, and delaying onset of end-stage renal disease.

Should be used once a day. Should be started at the lowest possible dose and titrated upwards as tolerated.

Fosinopril (Monopril)

Competitive inhibitors of ACE. Reduce angiotensin II levels, decreasing aldosterone secretion.

Ramipril (Altace)

Prevent conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

Captopril (Capoten)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

Rapidly absorbed, but bioavailability is significantly reduced with food intake. It achieves a peak concentration in an hour and has a short half-life. The drug is cleared by the kidney.

Impaired renal function requires reduction of dosage. Absorbed well PO. Give at least 1 h before meals. If added to water, use within 15 min.

Can be started at low dose and titrated upward as needed and as patient tolerates.

Enalapril (Vasotec)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Helps control blood pressure and proteinuria. Decreases pulmonary-to-systemic flow ratio in the catheterization laboratory and increases systemic blood flow in patients with relatively low pulmonary vascular resistance. Has favorable clinical effect when administered over a long period. Helps prevent potassium loss in distal tubules. Body conserves potassium; thus, less oral potassium supplementation needed.

Patients who develop a cough, angioedema, bronchospasm, or other hypersensitivity reactions after starting ACE inhibitors should receive an angiotensin-receptor blocker.

Lisinopril (Prinivil, Zestril)

Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

Quinapril (Accupril)

Competitive inhibitor of ACE. Reduce angiotensin II levels, decreasing aldosterone secretion.

Trandolapril (Mavik)

Prevent conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

Angiotensin II receptor antagonists

Can be used in patients intolerant of ACE inhibitors. Have been shown effective in hypertension and heart failure. Early data suggest they also reverse LVH, and recent trial data support their renal protective effect. Angiotensin II receptor antagonists include losartan (Cozaar), valsartan (Diovan), candesartan (Atacand), irbesartan (Avapro), eprosartan (Teveten), and olmesartan (Benicar).³⁹

Valsartan (Diovan)

Prodrug that produces direct antagonism of angiotensin II receptors. Displaces angiotensin II from AT1 receptor and may lower blood pressure by antagonizing AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. For use in patients unable to tolerate ACE inhibitors.

Irbesartan (Avapro)

Blocks vasoconstrictor and aldosterone-secreting effects of angiotensin II at tissue receptor site. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors and do not affect response to bradykinin (less likely to be associated with cough and angioedema).

Losartan (Cozaar)

Nonpeptide angiotensin II receptor antagonists that block vasoconstrictor and aldosterone-secreting effects of angiotensin II at tissue receptor site. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors and do not affect response to bradykinin (less likely to be associated with cough and angioedema).

Candesartan (Atacand)

Blocks vasoconstriction and aldosterone-secreting effects of angiotensin II. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. Use in patients unable to tolerate ACE inhibitors.

Angiotensin II receptor blockers reduce blood pressure and proteinuria, protecting renal function, and delaying onset of end-stage renal disease.

Eprosartan mesylate (Teveten)

Nonpeptide angiotensin II receptor antagonist that blocks vasoconstrictor and aldosterone-secreting effects of angiotensin II. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors and do not affect response to bradykinin and are less likely to be associated with cough and angioedema.

For patients unable to tolerate ACE inhibitors.

Angiotensin II receptor blockers reduce blood pressure and proteinuria, protecting renal function, and delaying onset of end-stage renal disease.

Olmesartan (Benicar)

Blocks vasoconstrictor and aldosterone-secreting effects of angiotensin II at tissue receptor site. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors and do not affect response to bradykinin (less likely to be associated with cough and angioedema).

Calcium channel blockers, nondihydropyridines

Used for lowering BP, treating angina, and controlling ventricular rate in atrial fibrillation. Potentially can have favorable effect in patients with heart failure due to diastolic dysfunction, although randomized controlled trials currently are lacking. Have significant negative inotropic effects and, thus, should be used with caution in patients with CHF due to systolic LV dysfunction.

Verapamil (Calan, Covera, Verelan)

During depolarization, inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.

Diltiazem (Dilacor, Cardizem, Tiazac)

During depolarization, inhibit calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.

Calcium channel blockers, dihydropyridines

Long-acting dihydropyridine calcium channel blockers can be used to treat hypertension, although usually are not drugs of choice. Have good antihypertensive effects, have been shown to decrease LVH, and recently have been used safely in patients with CHF. Short-acting dihydropyridine calcium channel blockers should be avoided because of fluctuation in 24-hour BPs with potential detrimental cardiovascular and cerebrovascular effects due to unpredictable hypotension. Have been shown to be inferior to ACE inhibitors in patients with renal insufficiency.

Nicardipine

Relaxes coronary smooth muscle and produces coronary vasodilation, which in turn improves myocardial oxygen delivery and reduces myocardial oxygen consumption.

Amlodipine (Norvasc)

Relax coronary smooth muscle and produce coronary vasodilation, which, in turn, improves myocardial oxygen delivery. Benefits nonpregnant patients with systolic dysfunction, hypertension, or arrhythmias. Can be used during pregnancy if indicated clinically.

Nifedipine (Adalat CC, Procardia XL)

Relaxes coronary smooth muscle and produces coronary vasodilation, which in turn improves myocardial oxygen delivery. Benefits nonpregnant patients with systolic dysfunction, hypertension, or arrhythmias. Can be used during pregnancy if indicated clinically.

Felodipine (Plendil)

Relaxes coronary smooth muscle and produces coronary vasodilation, which in turn improves myocardial oxygen delivery.

Benefits nonpregnant patients with systolic dysfunction, hypertension, or arrhythmias. Can be used during pregnancy if indicated clinically.

Calcium channel blockers potentiate ACE inhibitor effects. Renal protection is not proven, but these agents reduce morbidity and mortality rates in congestive heart failure. Calcium channel blockers are indicated in patients with diastolic dysfunction. Effective as monotherapy in black patients and elderly patients.

Vasodilators, peripheral

Hydralazine can be used in combination with nitrates to lower BP in patients with heart failure due to systolic LV dysfunction if other medications are contraindicated, especially when renal failure is present. Has not been shown to promote regression of LVH.

Nitroprusside

Nearly immediate onset of action and short half-life. Acts by causing relaxation of vascular smooth muscle, resulting in vasodilation and inotropy. Blood pressure can be titrated to the desired level.

Administration requires an IV infusion pump and an arterial line for continuous measurement of blood pressure.

Hydralazine (Apresoline)

Decreases systemic resistance through direct vasodilation of arterioles.

Aldosterone antagonists

Used for hypertension due to primary hyperaldosteronism and in patients with NYHA class III or IV heart failure. Beneficial effects of spironolactone are probably due to antifibrotic properties of the drug in interstitium.⁴⁰

Spironolactone (Aldactone)

Used for management of hypertension. May block effects of aldosterone on arteriolar smooth muscles.

Renin inhibitor

Newest class of antihypertensive drugs. Acts by disrupting the renin-angiotensin-aldosterone system feedback loop.

Aliskiren (Tekturna)

Direct renin inhibitor. Decreases plasma renin activity and inhibits conversion of angiotensinogen to angiotensin I (as a result, also decreasing angiotensin II) and, thereby, disrupts the renin-angiotensin-aldosterone system (RAAS) feedback loop. Indicated for hypertension as monotherapy or in combination with other antihypertensive drugs.

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