Jurgita Plisiene

Association of echocardiographic atrial size and atrial fibrosis in a sequential model of congestive heart failure and atrial fibrillation

BACKGROUND Cardioversion (CV) success of atrial fibrillation (AF) inversely correlates to the size of the left atrium (LA). Atrial fibrillation and its most important risk factor, congestive heart failure (CHF), both induce atrial structural enlargement and fibrosis. To investigate the effect of AF and CHF on atrial dilatation and fibrosis, and to estimate whether echocardiographically determined atrial size may be used as a marker for atrial fibrosis. METHODS In six dogs, pacemakers were implanted followed by HIS bundle ablation. After 4 weeks of rapid ventricular stimulation (185 bpm) for CHF induction, additional rapid atrial stimulation (500 bpm) was maintained for 7 weeks to induce AF. Serial determinations of echocardiographic atrial size were performed. Seven dogs with sinus rhythm served as histological controls. Postmortem tissue was obtained to determine the degree and composition of atrial fibrosis. RESULTS While the ejection fraction of the AF/CHF dogs decreased significantly from 57+/-5% to 19+/-7% (P<.01), an increased degree of atrial fibrosis was found (right atrium [RA], 4.9+/-2.0% to 19.9+/-5.4%; LA, 4.4+/-1.6% to 22.2+/-3.2%; P<.01), accompanied by a significant increase of atrial volumes (LA: 21+/-4 to 44+/-4 mm3; P<.01; RA: 10+/-3 to 18+/-6 mm3; P<.05) and LA diameters (34+/-4 to 43+/-2 mm, P<.05). Atrial fibrosis and size significantly correlated. CONCLUSIONS Atrial fibrillation/CHF leads to a significant atrial fibrosis and dilation. The increased echocardiographic size correlates to the degree of atrial fibrosis and may be used as clinical marker for atrial fibrosis. The fibrosis accompanying atrial dilatation may also explain why LA size, as determined by echocardiography, is a strong predictor of CV success.

Dilatation of the pulmonary veins in atrial fibrillation: a transesophageal echocardiographic evaluation.

Ectopic beats originating from sleeves of atrial tissue within the pulmonary veins (PVs) can induce and sustain paroxysmal atrial fibrillation (AF). Left atrial stretch and dilatation favors the development of atrial ectopy and AF. Similarly, PV dilatation, if present, might trigger PV ectopy in patients with AF. This study was designed to evaluate whether PV dilatation is present in patients with nonfocal AF and whether the PV diameter correlates to the left atrial diameter (LAD). The diameters of the right superior (RSPV) and left superior PV (LSPV) were measured at the ostium and at a depth of 1 cm in 170 patients (AF, n = 75 ; sinus rhythm [SR], n = 95) using transesophageal echocardiography. The LAD was determined by transthoracic echocardiography. The diameters of the PVs were significantly larger in patients with AF than in patients with SR (LSPVostium: AF 13.6 ± 3.5 mm vs SR 10.6 ± 2.7 mm, P < 0.001 ; LSVP1cm: AF 12.5 ± 2.9 mm vs SR 10.2 ± 2.5 mm, P < 0.001 ; RSPVostium, AF 13.9 ± 3.5 mm vs SR 11.7 ± 2.9 mm, P < 0.001 ; RSVP1cm: AF 12.8 ± 2.8 mm vs SR 10.6 ± 2.6 mm, P < 0.05). Similarly, LAD was larger in patients with AF (44.7 ± 7.7 mm) as compared to patients with SR (38.8 ± 6.8 mm, P < 0.001). Neither for the SR nor the AF group did the PV size correlate to the LAD. AF is associated with a significant enlargement of the RSPV, LSPV, and LAD. There is no correlation between LAD and PV diameters. This raises the question whether PV dilatation in patients with AF is a cause or a consequence of AF and whether it may contribute to the development and perpetuation of AF. (PACE 2003; 26:1371–1378)

Postfibrillatory enhancement of left atrial contractility after short paroxysms of atrial fibrillation.

Implantable cardioverter defibrillators and pacemakers detect an increasing number of silent episodes of AF. In a porcine model, the study evaluated the contractility of the left atrial appendage (LAA) during AF paroxysms as they may occur in patients. Peak outflow velocity of the LA and mean outflow velocity of the LAA (LAA‐Voutmean) (n = 17) were measured before, during, and after induction of self‐terminating AF. LAA‐Voutmean was also measured during incremental pacing from different atrial sites using epicardial Doppler probes (n = 6) and during continuous recordings (n = 5) of 40 minutes of pacing maintained AF. Compared to baseline sinus rhythm, LAA‐Voutmean increased during short AF episodes (41 ± 3 vs 35 ± 2 cm/s, P < 0.05). After termination of the AF episodes, LAA‐Voutmean further increased (69 ± 15 cm/s, P < 0.001 vs baseline). This “postfibrillatory enhancement” maintained after repeated induction of short AF paroxysms. During prolonged AF episodes lasting 40 minutes, an initial hypercontractility (44 ± 2 vs 38 ± cm/s, P < 0.01) was followed by a hypocontractility after 20 minutes (29 ± 12 P < 0.05 vs SR) and a postfibrillatory enhancement after cessation of AF (56 ± 12 vs 27 ± 9 cm/s at 40 minutes AF, P < 0.001). L‐type Ca channel blockade abolished the initial hypercontractility during AF and the postfibrillatory enhancement. Repetitive AF paroxysms up to 2 minutes did not decrease left atrial contractility. During maintained AF up to 40 minutes an initial hypercontractility and a consecutive hypocontractility, which is overcompensated by a postfibrillatory enhancement of atrial inotropy after cessation of AF, are present. The observed phenomenon seems to be related to an increased Ca2+ influx through the L‐type Ca2+ channel. (PACE 2004; 27:579–585)