Atrial cardiopathy

Introduction
Evidence suggests that left atrial thromboembolism can occur in the absence of atrial fibrillation, through changes in atrial structure and function that can precede the development of atrial fibrillation.

Atrial fibrillation itself may be an epiphenomenon, and a marker of underlying atrial cardiopathy. In the ASSERT trial, atrial fibrillation was found in 18 of 51 patients who had an ischemic stroke or systemic embolism, but in only 4 patients (8%) was atrial fibrillation detected within 30 days of the embolism and in only 1 of these 4 patients was atrial fibrillation detected at the time of the stroke. In the other 14 patients with ischemic stroke and atrial fibrillation, the most recent episode occurred at a median interval of 339 days (IQR 211-619 days). Similarly, in the TRENDS study, 40 patients had ischemic stroke or systemic embolism. Of those, 20 (50%) had atrial fibrillation detected prior to the event, but only 11 of these (28%) had atrial fibrillation detected in the 30 days prior to the event. The absence of a temporal association calls into question the causative nature of atrial fibrillation in ischemic stroke.

Characteristics

 * p-wave terminal force in V1 of >4,000 or 5,000 μV•ms
 * Severe left atrial enlargement on echocardiography
 * Elevated NT-proBNP > 250 pg/mL
 * Non-atrial fibrillation atrial arrhythmias
 * Paroxysmal supraventricular tachycardia
 * Premature atrial contractions
 * Prolonged PR interval

General
In a study of 846 patients with ischemic stroke, 158 (19%) had embolic stroke of undetermined source (ESUS). Atrial cardiopathy was noted in 26.6% of patients with ESUS, compared with 12.1% of patients with large artery atherosclerosis and 16.9% of those with small vessel disease (p=0.001).

Atrial fibrillation
Atrial fibrillation may be serve as a sign of underlying atrial cardiopathy rather than a stroke risk factor itself.

Left atrial enlargement
Several studies have suggested an association between left atrial enlargement and stroke. . In a study of 655 patients, moderate to severe left atrial enlargement (compared with normal left atrial size) was associated with a greater risk of recurrent cardioembolic stroke (aHR 2.83, 95% CI 1.03-7.81).

P-wave terminal force
P-wave terminal force in V1 is associated with recurrent ischemic stroke (aHR 1.20, 95% CI 1.03-1.39) and more specifically cardioembolic stroke or ESUS (aHR 1.31, 95% CI 1.08-1.58). In another study of 904 patients, a P-wave terminal force of >4,000 μV•ms was associated with nonlacunar stroke (HR 1.49, 95% CI 1.07-2.07). Another study showed that for every 1000 μV•ms increase, the HR for stroke was 1.04 (95% CI 1.001-1.08).

Prolonged PR interval
In a retrospective study of 644 patients with noncardioembolic stroke, a prolonged PR interval was independently associated with cryptogenic stroke (aOR 1.70, 95% CI 1.08-2.70). When excluding patients on AV nodal block agents, this relationship was more pronounced (aOR 2.64, 95% CI 1.44-4.83).

B-type natriuretic peptides
A meta-analysis has confirmed that elevated BNP and NT-proBNP are associated with cardioembolic stroke. Each doubling of NT-proBNP is associated with an increased risk of stroke (HR 1.09, 95% CI 1.03-1.16).

Should these patients be anticoagulated?
The WARSS trial randomized patients with ischemic stroke of any type (majority lacunar) to prevention with warfarin or aspirin and showed equivalent recurrent stroke rates and a slightly increased risk of hemorrhage in the warfarin group. However, in a secondary analysis, patients with NT-proBNP > 750 pg/mL, the HR for recurrent stroke was 0.30 (95% CI 0.12-0.84) significantly favoring warfarin over aspirin. Similarly, the NAVIGATE ESUS trial showed no benefit of rivaroxaban over aspirin in patients with ESUS, but a secondary analysis showed that for patients with left atrial diameter of >4.6 cm, the annual risk of ischemic stroke was lower with rivaroxaban compared with aspiriun (1.7% vs 6.5% per year, HR 0.26, 95% CI 0.07-0.94).