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Treatment of hypertension in patients with heart failure

Treatment of hypertension in patients with heart failure
Literature review current through: Jan 2024.
This topic last updated: Dec 13, 2022.

INTRODUCTION — Hypertension is the most prevalent modifiable risk factor for the development of heart failure (HF) [1], both because hypertension increases cardiac work, which leads to the development of left ventricular hypertrophy (LVH), and because hypertension is a risk factor for the development of coronary heart disease. (See "Epidemiology of heart failure".)

The incidence of HF in hypertensive patients varies according to the population and duration of follow-up. As an example, approximately 2 percent of high-risk hypertensive patients in the Avoiding Cardiovascular Events in Combination Therapy in Patients Living with Systolic Hypertension (ACCOMPLISH) trial developed HF at three years [2]. Among the high-risk hypertensive population enrolled into the Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), 1716 out of 32,804 participants developed HF during an average follow-up of nine years (5.4 percent) [3].

In contrast to the pattern seen in the general population, in which prognosis is poorer for hypertensive compared with normotensive individuals, a higher blood pressure prior to treatment is a predictor of better survival in patients with HF [4]. It is likely that this correlation is a consequence of the fact that more severe cardiac dysfunction causes a decline in systemic blood pressure, making low blood pressure a marker for more advanced HF [4]. This observation makes it difficult to study the benefits of antihypertensive therapy in this population. Goal blood pressure in patients with HF is discussed in detail elsewhere. (See "Goal blood pressure in adults with hypertension", section on 'Patients with heart failure'.)

Treatment of hypertension in patients with HF must take into account the type of HF that is present: systolic dysfunction, in which impaired cardiac contractility is the primary abnormality; or diastolic dysfunction, in which there is a limitation to diastolic filling and therefore in forward output due to increased ventricular stiffness [5]. (See "Treatment and prognosis of heart failure with preserved ejection fraction".)

The distinction between these two, not mutually exclusive types of HF can be made by assessment of left ventricular ejection fraction using echocardiography. (See "Determining the etiology and severity of heart failure or cardiomyopathy".)

Establishing the type of HF that is present is important because it determines which antihypertensive agents should be used [5]. (See 'Treatment of hypertension in patients with heart failure with reduced ejection fraction (HFrEF)' below and 'Treatment of hypertension in patients with heart failure with preserved ejection fraction (HFpEF)' below.)

TREATMENT OF HYPERTENSION IN PATIENTS WITH HEART FAILURE WITH REDUCED EJECTION FRACTION (HFrEF) — The goals of antihypertensive therapy in the setting of reduced ejection fraction are to reduce both preload (to diminish congestive symptoms) using diuretics and afterload (to improve cardiac output) using vasodilators (in particular, antagonists of the renin-angiotensin system). Neurohormonal blockade, such as with beta blockers or antagonists of the renin-angiotensin-aldosterone system, also improves cardiac contractility and may lower blood pressure. (See "Overview of the management of heart failure with reduced ejection fraction in adults".)

Goal blood pressure in patients with heart failure (HF) with reduced ejection fraction (HFrEF) is discussed separately. (See "Goal blood pressure in adults with hypertension", section on 'Patients with heart failure'.)

Antihypertensive regimen in HFrEF — In general, patients with hypertension and HF with reduced ejection fraction (HFrEF) should be treated, if possible, with a renin angiotensin system (RAS) inhibitor (ie, an angiotensin receptor-neprilysin inhibitor, angiotensin converting enzyme [ACE] inhibitor, or an angiotensin receptor blocker [ARB]), a beta blocker, and a mineralocorticoid receptor antagonist. In addition to the mortality benefit associated with this regimen in patients with HFrEF, many patients will experience a minor to moderate improvement in their ejection fraction, with occasional patients experiencing substantial improvement. Each of these medications has an incremental benefit when added to the others.

To maximize clinical improvement, it is important, whenever possible, to try to attain the target doses of these medications that were used in the clinical trials. The use of these medications in patients with HFrEF is presented in detail in other topics. (See "Overview of the management of heart failure with reduced ejection fraction in adults" and "Primary pharmacologic therapy for heart failure with reduced ejection fraction".)

Diuretics are used to treat symptomatic hypervolemia (pulmonary and/or peripheral edema) or to further reduce blood pressure, if needed, in hypervolemic patients. (See "Use of diuretics in patients with heart failure".)

Therapy with nondihydropyridine calcium blockers is not recommended because of their lack of benefit in this population [6].

Renin-angiotensin antagonists — RAS inhibitors, given to patients with mild to advanced HF (many of whom are not hypertensive), increase cardiac output, diminish congestive symptoms, reduce the rate of progressive cardiac dysfunction, and decrease cardiovascular mortality at one to four years (figure 1) [7]. The drugs also benefit patients with asymptomatic left ventricular dysfunction (figure 2) [8]. (See "Management and prognosis of asymptomatic left ventricular systolic dysfunction" and "Overview of the management of heart failure with reduced ejection fraction in adults", section on 'Pharmacologic therapy'.)

Despite these beneficial cardiovascular effects, RAS inhibitors generally do not improve kidney function in patients with HF. To the contrary, there is a rise (usually modest) in the plasma creatinine concentration in approximately 30 percent of cases [9]. This complication is most likely to occur in patients in whom maintenance of the glomerular filtration rate is dependent upon angiotensin II, such as those on high-dose diuretic therapy. These patients are also at greater risk of first-dose hypotension. The RAS inhibitor does not generally need to be discontinued unless there is an increase in plasma creatinine that exceeds 30 to 35 percent from baseline or the plasma creatinine continues to rise and does not stabilize. Care must be taken not to attribute laboratory abnormalities that may be due to excessive diuresis to the effect of the RAS inhibitor. (See "Renal effects of ACE inhibitors in heart failure".)

Simultaneous treatment with two RAS inhibitors (eg, combination therapy with an ACE inhibitor and ARB) should be avoided [10]. (See "Major side effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers", section on 'Combination of ACE inhibitors and ARBs'.)

Race — Although Black patients have a lesser antihypertensive response than White patients to RAS inhibitors [11], the bulk of evidence supports similar cardiovascular protection in patients with HF [11]. As a result, it is generally recommended that Black patients be treated the same as White patients.

Dosing — Dosing and titration of RAS inhibitors in patients with HFrEF is presented elsewhere in detail. (See "Primary pharmacologic therapy for heart failure with reduced ejection fraction", section on 'Dosing'.)

Nonsteroidal antiinflammatory drugs (NSAIDs) can reduce the hemodynamic improvement associated with RAS inhibitors in advanced HF and should therefore be avoided. The vasoconstriction induced by angiotensin II in HF is partially ameliorated by the release of vasodilator prostaglandins; blocking this response with NSAIDs may minimize the degree to which the vascular resistance falls after the administration of an RAS inhibitor. Alternate analgesics should be considered whenever possible; if NSAIDs must be used, the dose and duration of therapy should be minimized [12]. (See "NSAIDs: Adverse cardiovascular effects", section on 'NSAIDs and heart failure'.)

Combination angiotensin receptor-neprilysin inhibitors — In patients who have symptomatic HF and reduced ejection fraction, drugs that combine an ARB with a neprilysin inhibitor are generally preferred in place of an ACE inhibitor or ARB. The use of these drugs is discussed in detail elsewhere. (See "Primary pharmacologic therapy for heart failure with reduced ejection fraction", section on 'General cautions'.)

Beta blockers — Certain beta blockers, including carvedilol, metoprolol succinate, and bisoprolol, have been shown to improve overall and event-free survival in patients with mild to advanced HF (figure 3). The improvement in survival appears to be additive to that induced by ACE inhibitors. Beta-blocker therapy should be considered, independent of hypertension, in patients with New York Heart Association (NYHA) class II, III, or IV HF who have been stabilized on an ACE inhibitor and diuretics. Carvedilol may be particularly useful for blood pressure lowering in patients with HF. (See "Primary pharmacologic therapy for heart failure with reduced ejection fraction", section on 'Beta blocker'.)

Beta blockers can also provide anginal relief in patients with ischemic heart disease and provide rate control in patients with atrial fibrillation. (See "Beta blockers in the management of chronic coronary syndrome" and "Control of ventricular rate in patients with atrial fibrillation who do not have heart failure: Pharmacologic therapy".)

Dosing — Beta blockers in patients with systolic HF are usually begun with very low doses; these issues are discussed in detail elsewhere [13]. (See "Primary pharmacologic therapy for heart failure with reduced ejection fraction", section on 'Beta blocker'.)

Mineralocorticoid receptor antagonists — In addition to fluid removal with loop diuretics, mineralocorticoid receptor antagonists (spironolactone [25 mg] or eplerenone at a dose of 50 mg/day) have been shown to improve survival in patients with advanced HF (figure 4) [14] or in patients with a recent myocardial infarction and left ventricular dysfunction [15]. There is evidence for at least two mechanisms of benefit: an elevation in the serum potassium concentration, and prevention of the toxic effect of hyperaldosteronism on the heart. These issues are discussed elsewhere. (See "Primary pharmacologic therapy for heart failure with reduced ejection fraction" and "Primary pharmacologic therapy for heart failure with reduced ejection fraction", section on 'Mineralocorticoid receptor antagonist'.)

Diuretics — Diuretic therapy for signs of fluid overload (pulmonary and/or peripheral edema) is usually initiated with a loop diuretic (eg, furosemide). The fall in intracardiac filling pressure that results from diuretic-induced fluid removal may lower blood pressure, particularly when the renin-angiotensin system is inhibited. In hypervolemic individuals, cardiac output is usually not affected, although excessive diuresis may reduce cardiac output. (See "Use of diuretics in patients with heart failure".)

Other antihypertensive drugs

Hydralazine/nitrates — The combination of hydralazine and isosorbide dinitrate may be beneficial in patients with HF who were already being treated with standard therapies [16]. However, it requires multiple daily doses and may produce more side effects than an ACE inhibitor.

Calcium channel blockers — Studies show a deleterious decrease in cardiac function of many calcium channel blockers in patients with HF. Amlodipine and felodipine, however, do not decrease cardiac function or increase mortality [17,18]. Thus, while there is no direct role for these drugs in the management of HF, amlodipine and felodipine appear to be safe and well tolerated and can be used for the treatment of coexisting hypertension. (See "Calcium channel blockers in heart failure with reduced ejection fraction".)

TREATMENT OF HYPERTENSION IN PATIENTS WITH HEART FAILURE WITH PRESERVED EJECTION FRACTION (HFPEF) — The optimal therapy of hypertension in patients with HFpEF (ie, diastolic dysfunction) is uncertain. Therapy in such patients, which usually consists of diuretics and, if tolerated, mineralocorticoid receptor antagonists [19], is discussed in detail elsewhere. (See "Treatment and prognosis of heart failure with preserved ejection fraction", section on 'Pharmacotherapy'.)

Diuretics and venodilators (such as nitrates) must be used cautiously because patients with a small, stiff left ventricular chamber are particularly susceptible to excessive preload reduction, which can lead to underfilling of the left ventricle, a fall in cardiac output, and hypotension [20]. However, they are often needed for symptomatic relief of dyspnea that is secondary to fluid overload.

Goal blood pressure in patients with HFpEF is presented elsewhere. (See "Goal blood pressure in adults with hypertension", section on 'Patients with heart failure'.)

Regression of left ventricular hypertrophy (LVH) — LVH is frequently present in patients with diastolic dysfunction. Regression of LVH is an important therapeutic goal since diastolic function may be improved [21]. A meta-analysis published in 2003 evaluated the relative efficacy of different antihypertensive drugs for their ability to reverse LVH in patients with hypertension [22]. Eighty trials that included 146 and 17 active treatment and placebo arms, respectively, were evaluated. After statistical adjustments for length of therapy and degree of blood pressure lowering, the relative reductions in left ventricular mass index were (figure 5):

ARBs – 13 percent

Calcium channel blockers – 11 percent

ACE inhibitors – 10 percent

Diuretics – 8 percent

Beta blockers – 6 percent

The clinical significance of these differences is unknown because the effect of LVH regression on long-term clinical outcomes is not clear.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Heart failure in adults".)

SUMMARY AND RECOMMENDATIONS

Hypertension is the most prevalent modifiable risk factor for the development of heart failure (HF), both because hypertension increases cardiac work, which leads to the development of left ventricular hypertrophy (LVH), and because hypertension is a risk factor for the development of coronary heart disease. (See 'Introduction' above.)

Treatment of hypertension in patients with HF must take into account the type of HF that is present: systolic dysfunction, in which impaired cardiac contractility is the primary abnormality; or diastolic dysfunction, in which there is a limitation to diastolic filling and therefore in forward output due to increased ventricular stiffness. (See 'Introduction' above.)

In general, patients with hypertension and HF with reduced ejection fraction (HFrEF) should be treated, if possible, with a renin angiotensin system (RAS) inhibitor (ie, an angiotensin receptor-neprilysin inhibitor, angiotensin converting enzyme [ACE] inhibitor, or an angiotensin receptor blocker [ARB]), a beta blocker, and a mineralocorticoid receptor antagonist. In addition to the mortality benefit associated with this regimen in patients with HFrEF, many patients will experience improvement in their ejection fraction. (See 'Renin-angiotensin antagonists' above and 'Beta blockers' above and 'Mineralocorticoid receptor antagonists' above.)

Diuretics are used to treat symptomatic hypervolemia (pulmonary and/or peripheral edema) or to further reduce blood pressure, if needed, in hypervolemic patients. (See 'Diuretics' above.)

The optimal therapy of hypertension in patients with HF and preserved ejection fraction (ie, diastolic dysfunction) is uncertain; most antihypertensive agents can reduce left ventricular mass. (See 'Treatment of hypertension in patients with heart failure with preserved ejection fraction (HFpEF)' above.)

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Topic 3838 Version 21.0

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