Vascular protection with rivaroxaban in the comprehensive management of atrial fibrillation.

INTRODUCTION: In addition to an increased risk of thromboembolic complications, patients with atrial fibrillation (AF) are at risk for vascular events. Consequently, complete vascular protection is warranted in these patients. AREAS COVERED: A narrative search was conducted on PubMed (MEDLINE), using the MeSH terms [Rivaroxaban] + [Atrial fibrillation] + [Cardiovascular] + [Vascular] + [Treatment]. Original data from clinical trials, prospective and retrospective studies, useful reviews and experimental studies, were selected. EXPERT OPINION: The ROCKET-AF trial showed that rivaroxaban is effective in reducing the risk of stroke, with a lower risk of fatal and intracranial bleeding compared to warfarin. Remarkably, experimental data have provided a number of pathogenic mechanisms through which rivaroxaban could provide beneficial vascular properties beyond its antithrombotic activity. Moreover, in the AF population, additional to its ability to reduce the risk of thromboembolic complications, rivaroxaban is associated with a lower risk of myocardial infarction, major adverse cardiac and limb events, and vascular mortality in patients with diabetes, also attenuating renal impairment during follow-up. These findings suggest that rivaroxaban may provide a comprehensive vascular protection in patients with AF.

Should atrial fibrillation be considered a vascular disease? The need for a comprehensive vascular approach.

INTRODUCTION: Atrial fibrillation (AF) cannot be considered an isolated disease. Patients with AF should be managed using a comprehensive approach that is not limited to stroke prevention. AREAS COVERED: In this manuscript, the potential role of AF as a vascular disease that is managed as part of a holistic approach was reviewed. EXPERT OPINION: The residual risk of stroke in patients with AF reaches 1-2% annually, despite appropriate anticoagulation therapy. Additionally, patients with AF may develop cognitive impairment through stroke-independent pathways. Furthermore, patients with AF may have a higher risk of developing atherosclerotic vascular disease in various vascular beds and chronic kidney disease; conversely, patients with atherosclerotic disease may have an increased risk of developing AF. AF should be considered a truly systemic vascular disease, since it brings together several hemodynamic and systemic changes, including inflammation, oxidative stress, activation of the renin-angiotensin-aldosterone and sympathetic systems, as well as a prothrombotic state and endothelial dysfunction. In this regard, patients with AF should be treated based on a holistic approach that is not limited to oral anticoagulation but includes complete vascular protection.

Long-term improvement of QT dispersion is unaffected by short-term changes in blood pressure during treatment of systemic hypertension with enalapril.

BACKGROUND: We report the reduction of QT and QTc dispersion in patients treated for 7 years with enalapril for systemic hypertension with left ventricular (LV) hypertrophy. We assess the correlation between QT dispersion and LV mass during this period and at the end of an 8-week period of suspension of enalapril treatment after 5 years. METHODS: Twenty-four previously untreated patients with this condition took enalapril (20 mg twice daily) for 7 years, except during an 8-week period following 5-year follow-up. Cardiovascular parameters were determined by two-dimensional guided M-mode echocardiography, and QT interval was measured, in a pretreatment placebo phase, 8 weeks and 1, 3, 5, and 7 years after the start of the therapy, at the end of the 8-week suspension effected after 5 years, and 8 weeks after the end of the suspension. RESULTS: Therapy rapidly reduced blood pressure (BP) from 156/105 mmHg to normal values: 134/84 mmHg after 8 weeks' treatment, 130-84 mmHg at 7-year follow-up (P < 0.001 with respect to the placebo phase). LV mass index decreased progressively until at 5-year follow-up the reduction had reached 39% (P < 0.001), after which neither LV mass nor any other structural parameter underwent any further significant change. During this time, QT dispersion (DeltaQT) and the dispersion of "corrected" QT (DeltaQTc) decreased significantly: DeltaQT (from 61 +/- 21 to 37 +/- 13 ms) and DeltaQTc (from 67 +/- 27 to 41 +/- 16 ms). After suspension of treatment for 8 weeks following 5-year follow-up, DeltaQT was 40 +/- 14 ms and DeltaQTc was 44 +/- 17 ms; there were no significant changes either in DeltaQT and DeltaQTc or LV hypertrophy although BP had returned to pretreatment values (BP: 150 +/- 16; 101 +/- 10 mmHg). CONCLUSIONS: Long-term enalapril treatment of hypertensive patients with LV hypertrophy induces marked regression of LV mass and improvement of QT dispersion. These improvements occur on a longer timescale than improvement in BP, and are not affected by transient changes in BP values.