From the Guidelines
Treatment of atrial fibrillation with rapid ventricular response (AFib RVR) should prioritize rate control using beta blockers, such as metoprolol, unless contraindicated, due to their favorable effect on morbidity and mortality in patients with systolic heart failure 1. When managing AFib RVR, it is crucial to consider the patient's symptoms, hemodynamic stability, and underlying cardiac conditions. The primary goal is to prevent thromboembolism and control symptoms.
- Rate control is essential to prevent worsening heart failure (HF) and to improve symptoms.
- Beta blockers, such as metoprolol, are the preferred agents for achieving rate control due to their beneficial effects on morbidity and mortality in patients with systolic HF 1.
- Digoxin may be used as an adjunct to beta blockers for rate control.
- Nondihydropyridine calcium antagonists, like diltiazem, should be used with caution in patients with depressed EF due to their negative inotropic effect.
- For patients with HF and preserved EF, nondihydropyridine calcium antagonists can be effective for achieving rate control, especially when used in combination with digoxin.
- If a rhythm-control strategy is chosen, amiodarone can be initiated, and cardioversion can be arranged a month later, as it has the advantage of being both an effective rate-control medication and the most effective antiarrhythmic medication with a low risk of proarrhythmia 1.
- Anticoagulation therapy is essential for stroke prevention in most patients with AFib, and the choice of treatment depends on the patient's individual risk factors and underlying conditions.
From the Research
Treatment of Right Ventricular Fibrosis (RVF)
The treatment of RVF is a complex issue, and various studies have investigated different approaches. Some of the key points to consider are:
- The underlying cause of RVF should be identified and addressed, as treatment should be directed at the underlying cause 2.
- Therapeutic options range from pharmacological treatment to mechanical RV support and heart transplantation 2.
- Novel pharmacological interventions targeting metabolism, calcium homeostasis, oxidative stress, extracellular matrix remodeling, endothelial function, and inflammation are needed to address RVF effectively 3.
- There are no therapies directly targeting the failing RV, but development of RV-targeted therapies may improve quality of life and enhance survival for patients with pulmonary arterial hypertension (PAH) 4.
Role of Fibrosis in RVF
Fibrosis plays a crucial role in the development of RV failure, and alterations of the collagen network of the extracellular matrix may help prevent ventricular dilatation in the pressure-overloaded RV 5. However, fibrosis also impairs cardiac function, and a growing body of experimental data suggests that fibrosis is a key factor in the development of RV failure. The correlation between fibrosis and RV function is complex, and RV fibrosis has a dual role in patients with pressure-overloaded RVs: as part of an adaptive response to prevent cardiomyocyte overstretch and to maintain RV shape for optimal function, and as part of a maladaptive response that increases diastolic stiffness, perturbs cardiomyocyte excitation-contraction coupling, and disrupts the coordination of myocardial contraction 5.
Potential Therapeutic Strategies
Potential novel therapeutic strategies for RVF include:
- Targeting metabolism, calcium homeostasis, oxidative stress, extracellular matrix remodeling, endothelial function, and inflammation 3.
- Developing RV-targeted therapies to improve quality of life and enhance survival for patients with PAH 4.
- Quantifying RV fibrosis using more sensitive techniques to clarify the causal relation between RV fibrosis and RV function in future research 5.