For decades, conventional wisdom has held that coffee and caffeine act as triggers for heart rhythm disorders, particularly atrial fibrillation (AF). Patients with arrhythmias are routinely advised to avoid caffeinated beverages to reduce the risk of palpitations and AF episodes. This belief stems mainly from the known stimulant effects of caffeine and anecdotal patient reports. However, scientific evidence supporting this theory has been inconsistent. While caffeine can acutely raise heart rate, several large observational studies have actually suggested a neutral or even protective association between regular coffee consumption and the development of AF. Until recently, randomized clinical trial data to definitively settle this debate has been lacking.

The DECAF (Does Eliminating Coffee Avoid Fibrillation?) randomized clinical trial, published in JAMA in 2025, sought to address this gap. The study enrolled 200 adults who were regular coffee drinkers and had a history of persistent AF or atrial flutter. Following successful electrical cardioversion to restore normal sinus rhythm, participants were randomly assigned to either continue drinking caffeinated coffee (at least one cup daily) or to completely abstain from all coffee and caffeine products for six months. The primary outcome was the clinically detected recurrence of AF or atrial flutter. Surprisingly, the group randomized to coffee consumption experienced significantly fewer arrhythmia recurrences. Specifically, AF or atrial flutter recurred in 47% of the coffee consumption group compared to 64% of the abstinence group. This difference translated to a 39% lower hazard of recurrence for those who continued drinking coffee (Hazard Ratio 0.61; 95% CI, 0.42-0.89; P=.01). Adherence to the study protocols was good, with the coffee group consuming a median of 7 cups per week and the abstinence group reducing intake to near zero.

These findings directly contradict the long-standing assumption that coffee worsens AF. The authors suggest several potential mechanisms for this protective effect, including caffeine's blockade of adenosine receptors (adenosine can promote AF), coffee's anti-inflammatory properties, and potential diuretic effects. While the study had some limitations, such as its open-label design and modest sample size, it provides the strongest evidence to date that moderate caffeinated coffee consumption is safe and potentially beneficial for patients with atrial fibrillation. For patients who enjoy their daily cup, these results offer reassurance that coffee does not need to be on the restricted list.

• Caffeinated Coffee Consumption or Abstinence to Reduce Atrial Fibrillation: The DECAF Randomized Clinical Trial, JAMA (2025)
• Atrial fibrillation review
• Article on webpage

Lynkuet (elinzanetant), a nonhormonal treatment for vasomotor symptoms (VMS) due to menopause, was recently approved by the FDA. It is the second drug approved in the neurokinin (NK) receptor antagonists class, following Veozah (fezolinetant), approved in 2023. The drugs differ slightly in their NK receptor binding; Veozah selectively binds NK3 receptors while Lynkuet binds NK1 and NK3 receptors. During menopause, estrogen withdrawal increases neurokinin activity in the brain's thermoregulatory center, and NK receptor antagonists suppress neurokinin secretion.

In their respective phase 3 trials, both agents demonstrated a statistically significant reduction in VMS frequency and severity (≥ hot flashes over 24 hours) compared to placebo. In two 12-week trials, the placebo-subtracted reduction in VMS episodes (baseline ∼ 11 episodes/day) with Veozah was about 2.5 per 24 hours. Similarly, the placebo-subtracted reduction in VMS episodes (baseline ∼ 14 episodes/day) with Lynkuet was about 3.2 per 24 hours in 12-week trials. Notably, across all trials, the placebo group experienced reductions of 4 to 6 episodes per day, suggesting a significant psychological component in VMS improvement. Common side effects for both agents include gastrointestinal issues like abdominal pain and diarrhea, as well as nervous system effects such as insomnia, back pain, and headache. Lynkuet's label notes a central nervous system (CNS) depressant effect, with somnolence and dizziness occurring in ≥ 5% of patients. Veozah has a Boxed Warning for hepatotoxicity, with transaminase elevations >3X ULN reported in 2.3% of women in pooled clinical trials. In Linkuet trials, transaminase elevations ≥ 3X ULN occurred in 0.6% of Lynkuet-treated women and 0.4% of placebo-treated women. Both manufacturers recommend monitoring liver function tests during therapy. A major difference in drug-drug interactions stems from different metabolic profiles: Veozah is a CYP1A2 substrate and is contraindicated with CYP1A2 inhibitors, while Lynkuet is primarily metabolized by CYP3A4 and requires dosage modification or avoidance when used with CYP3A4 inhibitors or inducers.

Women suffering from menopause-related VMS now have two nonhormonal options; however, both medications are significantly more expensive than hormone replacement therapy (HRT) and often require prior authorization along with stepped therapy for insurance coverage. A study comparing Veozah or Lynkuet to HRT would be informative.

• Lynkuet (elinzanetant) review
• Veozah (fezolinetant) review
• HRT guidelines
• Article on webpage

The historical paradigm of recommending beta-blockers for all post-myocardial infarction (MI) patients arose from trials predating modern acute coronary syndrome (ACS) management. With widespread adoption of early revascularization (PCI or CABG) and intensive secondary prevention pharmacotherapy, the incidence of heart failure (HF) and severely reduced left ventricular ejection fraction (LVEF) following MI has significantly decreased. This improvement in acute care has raised questions about the necessity of long-term beta-blocker therapy for patients with coronary artery disease (CAD) who maintain a preserved or mildly reduced LVEF (≥ 40%) and no other primary indication.

Four recent randomized controlled trials have explored this issue, yielding conflicting results. The BETAMI-DANBLOCK study (N=5574, duration 3.5 years) reported a modest, yet statistically significant, benefit for beta-blockers, finding a lower risk of death or major adverse cardiovascular events (14.2% vs. 16.3%; HR 0.85; p=0.03). Conversely, the large REBOOT-CNIC (N=8505, median duration 3.7 years) and REDUCE-AMI (N=5020, median duration 3.5 years) studies found no significant benefit of long-term beta-blocker therapy on their respective composite endpoints. Lastly, the ABYSS study (N=3698, median duration 3 years), which enrolled stable patients already on therapy, found that beta-blocker interruption was not noninferior to continuation (HR 1.16; p=0.44 for noninferiority).

Collectively, the results from these trials do not make a strong case either for or against the continued, routine use of beta-blockers in post-MI patients with preserved LVEF and no other compelling indications (e.g., angina, atrial fibrillation, uncontrolled hypertension). While the BETAMI-DANBLOCK suggests a small benefit and ABYSS cautions against stopping therapy in stable patients, the overall lack of robust, consistent benefit in the major trials does not support the uniform use of beta-blockers in this patient population. Current guidance reflects this evolving evidence, leaning toward reassessing the long-term need for beta-blockers after the first year post-MI in the absence of reduced LVEF or other indications.

• Beta-blockers in CAD Without Heart Failure
• Article on webpage

Catheter ablation has become a common treatment for atrial fibrillation (AF), and many patients undergo the procedure in hopes of stopping anticoagulation. Catheter ablation success, defined as no atrial arrhythmias, depends on the type of AF and the length of follow-up. One-year success rates for paroxysmal AF are 70% to 85%, while persistent AF has a success rate of 50% to 70%. Over longer follow-up periods, success rates decline. Since catheter ablation is not 100% curative, and AF can come and go without symptoms, stopping anticoagulation after the procedure may increase stroke risk. Conversely, continuing anticoagulation increases bleeding risk. To examine the issue, researchers performed the ALONE-AF trial, where 840 patients (median CHA2DS2-VASc score of 2) with AF who had undergone catheter ablation and had no documented AF recurrence for at least one year were randomized to continuing anticoagulation (with apixaban or rivaroxaban) or stopping it. No atrial arrhythmia recurrence was documented with ECGs and at least two sessions of 24- to 72-hour Holter monitoring, with at least one performed within two months of enrollment. After two years, the primary outcome, a composite of stroke, systemic embolism, and major bleeding, was observed in 0.3% of the discontinue group and 2.2% of the continue group (P=0.02). Stroke was seen in 0.3% and 1.4%, respectively, and major bleeding in 0% and 1.4% (P=0.03).

Prior to this study, providers had limited data on the risks and benefits of stopping anticoagulation after ablation. The criteria used in the study for documenting no AF recurrence (at least two sessions of 24- to 72-hour Holter monitoring without atrial arrhythmia) serve as a starting point for selecting patients for anticoagulant discontinuation. Most patients in the study had paroxysmal AF (68%), which is more responsive to ablation. Although the study did not find differences in outcomes for patients with persistent AF, this subgroup was underrepresented.

• ALONE-AF Study: Discontinue vs Continue anticoagulation after ablation, JAMA (2025)
• Article on webpage

Primary aldosteronism (PA), excess aldosterone secretion by the adrenal glands, raises blood pressure and is prevalent in up to 14% of patients with hypertension. Despite this, it is rarely diagnosed. The Endocrine Society recently published guidelines on primary aldosteronism that cover screening, diagnosis, and treatment. Important points from the recommendations include the following:

• Screening: Screen all patients with hypertension for primary aldosteronism by measuring serum/plasma aldosterone concentration and plasma renin (concentration or activity) to determine the aldosterone to renin ratio (ARR)
• Diagnosis: If screening is positive, determine the probability of lateralizing disease, which is excess aldosterone from one adrenal gland. Findings consistent with lateralizing disease include hypokalemia, age less than 35 years, a unilateral adrenal mass, and/or very low renin with high aldosterone. If probability is high, proceed directly to adrenal CT scan and adrenal venous sampling. If probability is intermediate, consider an empiric trial of a mineralocorticoid receptor antagonist (MRA) versus proceeding to aldosterone suppression testing. If probability is low, consider a trial of an MRA.
• Treatment: If disease is lateralizing, offer surgery. Otherwise, treat with an MRA.

There are no controlled trials supporting the cost-effectiveness or benefits of screening all patients with hypertension for primary aldosteronism. Given that 120 million U.S. adults have hypertension, it's unlikely many providers are going to spend their time chasing this diagnosis in every patient. Other issues with screening include: (1) many common medications interfere with testing (e.g., beta blockers, NSAIDs, diuretics, ARBs, ACE inhibitors, SGLT2 inhibitors) and need to be withdrawn before screening, making the process onerous, (2) studies evaluating the accuracy of the ARR for diagnosing primary aldosteronism have found that it performs poorly.

These guidelines are helpful when assessing patients for primary aldosteronism. However, the recommendation to screen all individuals with hypertension is impractical and unlikely to be cost-effective. The American Heart Association recommends a more targeted approach when selecting patients for secondary hypertension screening (see who to evaluate for secondary hypertension).

• Primary aldosteronism recommendations
• Aldosterone in potassium regulation
• Article on webpage