Direction-dependent conduction abnormalities in the chronically stretched atria.

AIMS: There is increasing evidence of the role direction-dependent conduction plays in the arrhythmogenic interaction between ectopic triggers and abnormal atrial substrates. We thus sought to characterize direction-dependent conduction in chronically stretched atria. METHODS AND RESULTS: Twenty-four patients with chronic atrial stretch due to mitral stenosis and 24 reference patients with left-sided accessory pathways were studied. Multipolar catheters placed at the lateral right atrium, crista terminalis, and coronary sinus (CS) characterized direction-dependent conduction along linear catheters and across the crista terminalis. Bi-atrial electroanatomic maps were created in both sinus rhythm and an alternative wavefront direction by pacing from the distal CS. This allowed an assessment of conduction velocities, electrogram, and voltage characteristics during wavefronts propagating in different directions.  While differing wavefront directions caused changes in both chronic atrial stretch and reference patients (P< 0.001 for all), these direction-dependent changes were greater in chronic atrial stretch compared with reference patients, who exhibited greater slowing in conduction velocities (P= 0.09), prolongation of bi-atrial activation time (P= 0.04), increase in number (P< 0.001) and length (P< 0.001) of lines of conduction block, increase in fractionated electrograms (P< 0.001), and decrease in voltage (P= 0.08) during left-to-right compared with right-to-left atrial activation. These direction-dependent changes were associated with a greater propensity for chronically stretched atria to develop atrial fibrillation (P= 0.02). CONCLUSIONS: Atrial remodelling in chronic atrial stretch exacerbates physiological direction-dependent conduction characteristics. Our data suggest that the greater direction-dependent conduction seen in patients with chronic atrial stretch may promote arrhythmogenesis due to ectopic triggers from the left atrium.

Electrical remodelling of the left and right atria due to rheumatic mitral stenosis.

AIMS: To characterize the atrial remodelling in mitral stenosis (MS). METHODS AND RESULTS: Twenty-four patients with severe MS undergoing commissurotomy and 24 controls were studied. Electrophysiological evaluation was performed in 12 patients in each group by positioning multi-electrode catheters in both atria to determine the following: effective refractory period (ERP) at 10 sites at 600 and 450 ms; conduction time; conduction delay at the crista terminalis (CT); and vulnerability for atrial fibrillation (AF). P-wave duration (PWD) was determined on the surface ECG. In the remaining 12 patients in each group, electroanatomic maps of both atria were created to determine conduction velocity and identify regions of low voltage and electrical silence. Patients with MS had larger left atria (LA) (P < 0.0001); prolonged PWD (P = 0.0007); prolonged ERP in both LA (P < 0.0001) and right atria (RA) (P < 0.0001); reduced conduction velocity in the LA (P = 0.009) and RA (P < 0.0001); greater number (P < 0.0001) and duration (P< 0.0001) of bipoles along the CT with delayed conduction; lower atrial voltage in the LA (P < 0.0001) and RA (P < 0.0001); and more frequent electrical scar (P = 0.001) compared with controls. Five of twelve with MS and none of the controls developed AF with extra-stimulus (P = 0.02). CONCLUSION: Atrial remodelling in MS is characterized by LA enlargement, loss of myocardium, and scarring associated with widespread and site-specific conduction abnormalities and no change or an increase in ERP. These abnormalities were associated with a heightened inducibility of AF.

Exclusive carbon dioxide-guided renal artery stenting in a case of Takayasu's arteritis with a solitary functioning kidney.

We report the case of a 28-year-old female with type II Takayasu's arteritis affecting her single functioning kidney. Impaired renal function precluded the use of conventional contrast media. We used carbon dioxide-guided renal angioplasty to successfully treat the patient.

Reverse remodeling of the atria after treatment of chronic stretch in humans: implications for the atrial fibrillation substrate.

OBJECTIVES: The aim of this report was to study the effect of chronic stretch reversal on the electrophysiological characteristics of the atria in humans. BACKGROUND: Atrial stretch is an important determinant for atrial fibrillation. Whether relief of stretch reverses the substrate predisposed to atrial fibrillation is unknown. METHODS: Twenty-one patients with mitral stenosis undergoing mitral commissurotomy (MC) were studied before and after intervention. Catheters were placed at multiple sites in the right atrium (RA) and sequentially within the left atrium (LA) to determine: effective refractory period (ERP) at 10 sites (600 and 450 ms) and P-wave duration (PWD). Bi-atrial electroanatomic maps determined conduction velocity (CV) and voltage. In 14 patients, RA studies were repeated >or=6 months after MC. RESULTS: Immediately after MC, there was significant increase in mitral valve area (2.1 +/- 0.2 cm(2), p < 0.0001) with decrease in LA (23 +/- 7 mm Hg to 10 +/- 4 mm Hg, p < 0.0001) and pulmonary arterial pressures (38 +/- 16 mm Hg to 27 +/- 12 mm Hg, p < 0.0001) and LA volume (75 +/- 20 ml to 52 +/- 18 ml, p < 0.0001). This was associated with reduction in PWD (139 +/- 19 ms to 135 +/- 20 ms, p = 0.047), increase in CV (LA: 1.3 +/- 0.3 mm/ms to 1.7 +/- 0.2 mm/ms, p = 0.006; and RA: 1.0 +/- 0.1 mm/ms to 1.3 +/- 0.3 mm/ms, p = 0.002) and voltage (LA: 1.7 +/- 0.6 mV to 2.5 +/- 1.0 mV, p = 0.005; and RA: 1.8 +/- 0.6 mV to 2.2 +/- 0.7 mV, p = 0.09), and no change in ERP. Late after MC, mitral valve area remained at 2.1 +/- 0.3 cm(2) (p = 0.7) but with further decrease in PWD (113 +/- 19 ms, p = 0.04) and RA ERP (at 600 ms, p < 0.0001), with increase in CV (1.0 +/- 0.1 mm/ms to 1.3 +/- 0.2 mm/ms, p = 0.006) and voltage (1.8 +/- 0.7 mV to 2.8 +/- 0.6 mV, p = 0.002). CONCLUSIONS: The atrial electrophysiologic and electroanatomic abnormalities that result from chronic stretch due to MS reverses after MC. These observations suggest that the substrate predisposing to atrial arrhythmias might be reversed.