Blood pressure in patients with atrial fibrillation: part 2—treatment

Hypertension and atrial fibrillation (AF) commonly coexist and hypertension is associated with a 1.8‐fold increased risk of developing new‐onset AF and a 1.5‐fold increased risk of progression to permanent AF.1, 2 Untreated or suboptimal treatment of hypertension leads to development of left ventricular hypertrophy, which is an independent risk factor for the development of AF.2 A wider pulse pressure has also been associated with an increased incidence of AF.3 Treatment of hypertension in AF needs to take into consideration specifics related to the underlying AF such as chronicity and ventricular rate. Treatment of possible underlying causes of AF that can also cause hypertension such as hyperthyroidism should also be considered. In part 1 of this series, we mentioned that detection of atrial fibrillation can be a challenge, noting that both the Omron M6 Comfort and the Micolife BP 200 home devices have been studied in this regard, and that the UK's National Institute for Health and Care Excellence recommends usage of the latter device in particular (Omron makes no claims about AF detection per se).

With regard to prevention of AF, there are no randomized studies that have consistently shown that treatment of hypertension with specific agents reduces the incidence of AF; however, there has been some evidence suggesting that treatment of hypertension with renin‐angiotensin‐aldosterone system (RAAS) blockade with either angiotensin‐converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), or mineralocorticoid antagonists (MRAs) may reduce the incidence of new or recurrent AF, particularly in patients with systolic left ventricular dysfunction or left ventricular hypertrophy.4, 5, 6, 7, 8 The hypothesis is that use of RAAS blockade prevents atrial stretch from elevated ventricular filling pressures by improving ventricular function and reducing left atrial pressures and wall stress,9 reducing atrial fibrosis10 and preventing electrical remodeling and direct antiarrhythmic effects.11 A meta‐analysis of data from 26 randomized trials showed that ACEIs and ARBs significantly reduced the risk of the development of AF to a similar degree.12 The effect was greater in preventing recurrent AF compared with new‐onset AF and the effect was greater but not significant in patients with systolic heart failure. However, due to publication bias and inclusion of post hoc analyses in many of the included studies, the evidence to support the use of RAAS blockade is weak and the greatest benefit was seen in patients with heart failure and left ventricular dysfunction in whom therapy with an ACEI or ARB is probably already indicated. Therefore, use of ACEIs or ARBs may reduce the likelihood of developing AF and is a good agent to use in patients with coexisting AF and hypertension but is NOT indicated solely for the prevention of new‐onset or recurrent AF. The American Heart Association/American College of Cardiology/Heart Rhythm Society guidelines, however, recommend use of ACEIs or ARBs for AF prevention in patients with hypertension, heart failure, and left ventricular dysfunction or HTN.13

Patients with primary hyperaldosteronism have a 12‐fold increased risk of developing AF than patients with essential hypertension. Patients with AF have also been shown to have higher aldosterone levels. There is some support for the use of MRAs for AF prevention14 and MRAs have also been shown to reduce atrial fibrosis with beneficial effects on atrial ion channels and reduced incidence of AF.15, 16, 17

β‐Blockers are not considered as initial therapy for uncomplicated hypertension; however, β‐blockers are effective agents for rate control in AF and possibly for maintaining sinus rhythm.2 Regarding prevention of AF, in a review of approximately 12 000 patients with systolic heart failure (with most patients [90%] receiving RAS blockade), the addition of a β‐blocker compared with placebo reduced the incidence of new‐onset AF by 27%.18 β‐Blockers, however, may not induce an equivalent effect as a drug class and in the Losartan Intervention For Endpoint Reduction in Hypertension study (LIFE), atenolol was shown to be inferior to losartan in the prevention of new or recurrent AF.19 β‐Blockers may be particularly useful in patients with hypertension and AF with systolic heart failure. If patients have chronic persistent AF, rate control is an important part of the treatment and agents can be used to treat both the underlying hypertension and the AF. Particularly with new‐onset AF with a rapid ventricular response, it is often useful to first start a ventricular rate–slowing drug, as rate control will usually precede any attempt to restore sinus rhythm. Rate control is usually achieved by using either β‐blockers or nondihydropyridine calcium channel blockers (CCBs) such as verapamil or diltiazem. Use of either β‐blockers or CCBs is based on physician preference and on other underlying comorbidities. β‐Blockers are preferred in patients with underlying coronary artery disease particularly after myocardial infarction. Intravenous β‐blockers are more effective than intravenous CCBs for rate control and for conversion to sinus rhythm. β‐Blockers may be effective by preventing remodeling and sympathetic hyperactivation, which could contribute to the perpetuation of AF.18, 20 Recurrence of AF is known to be high even with the use of β‐blocker prophylaxis.2

Nondihydropyridine CCBs, such as diltiazem and verapamil as mentioned above, are useful to slow the ventricular response in AF. Verapamil may also be useful in reducing recurrent AF after cardioversion21 but these agents are usually NOT used as first‐line antihypertensive agents. Dihydropyridine CCBs such as amlodipine are very effective agents for BP reduction and are often used as initial therapy for hypertension. Dihydropyridine CCBs reduce pulse pressure and therefore may have a potential role in AF reduction; however, amlodipine was shown to be inferior to valsartan in reducing new incidence of AF.22 Studies comparing RAS blockers (ACEIs or ARBS) vs CCBs, however, have shown that the prior agents are superior in preventing AF and AF‐related hospitalizations.23, 24 In a nested case‐control analysis from the UK‐based General Practice Research Database, 4661 patients with AF were compared with 18 641 matched controls with hypertension and the study showed that treatment with ACEIs, ARBs, or β‐blockers were associated with a lower risk of AF than treatment with CCBs.24

There are no formal studies evaluating the effects of diuretics on the incidence or recurrence of AF but these agents do induce electrolyte abnormalities, which may contribute to AF, and, in particular, potassium and magnesium levels should be monitored.

In our view, it makes sense to incorporate an ACEI or ARB into an antihypertensive regimen in patients with AF, adding a β‐blocker or nondihydropyridine CCB when rate control is an issue. With good renal function and normokalemia, consider an MRA, keeping in mind that good BP control together with weight and glucose management and preserved oxygenation while sleeping are likely additive in their benefits in AF, particularly after ablation therapy.25

Conflict of Interest

None.