Victoria Atkinson

Epicardial wave mapping in human long-lasting persistent atrial fibrillation: transient rotational circuits, complex wavefronts, and disorganized activity

OBJECTIVESnTo characterize the nature of atrial fibrillation (AF) activation in human persistent AF (PerAF) using modern tools including activation, directionality analyses, complex-fractionated electrogram, and spectral information.nnnBACKGROUNDnThe mechanism of PerAF in humans is uncertain.nnnMETHODS AND RESULTSnHigh-density epicardial mapping (128 electrodes/6.75 cm(2)) of the posterior LA wall (PLAW), LA and RA appendage (LAA, RAA), and RSPV-LA junction was performed in 18 patients with PerAF undergoing open heart surgery. Continuous 10 s recordings were analysed offline. Activation patterns were characterized into four subtypes (i) wavefronts (broad or multiple), (ii) rotational circuits (≥2 rotations of 360°), (iii) focal sources with centrifugal activation of the entire mapping area, or (iv) disorganized activity [isolated chaotic activation(s) that propagate ≤3 bipoles or activation(s) that occur as isolated beats dissociated from the activation of adjacent bipole sites]. Activation at a total of 36 regions were analysed (14 PLAW, 3 RSPV-LA, 12 LAA, and 7 RAA) creating a database of 2904 activation patterns. In the majority of maps, activation patterns were highly heterogeneous with multiple unstable activation patterns transitioning from one to another during each recording. A mean of 3.8 ± 1.6 activation subtypes was seen per map. The most common patterns seen were multiple wavefronts (56.2 ± 32%) and disorganized activity (24.2 ± 30.3%). Only 2 of 36 maps (5.5%) showed a single stable activation pattern throughout the 10-s period. These were stable planar wavefronts. Three transient rotational circuits were observed. Two of the transient circuits were located in the posterior left atrium, while the third was located on the anterior surface of the LAA. Focal activations accounted for 11.3 ± 14.2% of activations and were all short-lived (≤2 beats), with no site demonstrating sustained focal activity.nnnCONCLUSIONnHuman long-lasting PerAF is characterized by heterogeneous and unstable patterns of activation including wavefronts, transient rotational circuits, and disorganized activity.

Temporal Stability of Rotors and Atrial Activation Patterns in Persistent Human Atrial Fibrillation: A High-Density Epicardial Mapping Study of Prolonged Recordings

OBJECTIVESnThis study aimed to determine the spatiotemporal stability of rotors and other atrial activation patterns over 10 min in longstanding, persistent AF, along with the relationship of rotors to short cycle-length (CL) activity.nnnBACKGROUNDnThe prevalence, stability, and mechanistic importance of rotors in human atrial fibrillation (AF) remainxa0unclear.nnnMETHODSnEpicardial mapping was performed in 10 patients undergoing cardiac surgery, with bipolar electrograms recorded over 10 min using a triangular plaque (area: 6.75 cm2; 117 bipoles; spacing: 2.5 mm) applied to the left atrial posterior wall (nxa0= 9) and the right atrial free wall (nxa0= 4). Activations were identified throughout 6 discrete 10-s segments of AF spanning 10 min, and dynamic activation mapping was performed. The distributions of 4,557 generated activation patterns within each mapped region were compared between the 6 segments.nnnRESULTSnThe dominant activation pattern was the simultaneous presence of multiple narrow wave fronts (26%). Twelve percent of activations represented transient rotors, seen in 85% of mapped regions with a median duration of 3xa0rotations. A total of 87% were centered on an area of short CL activity (<100 ms), although such activity had a positive predictive value for rotors of only 0.12. The distribution of activation patterns and wave-front directionality were highly stable over time, with a single dominant pattern within a 10-s AF segment recurring across all 6 segments in 62% of mapped regions.nnnCONCLUSIONSnIn patients with longstanding, persistent AF, activation patterns are spatiotemporally stable over 10xa0min. Transient rotors can be demonstrated in the majority of mapped regions, are spatiotemporally associated with short CL activity, and, when recurrent, demonstrate anatomical determinism.

Implications for Cardiac Surgery in Patients With Factor XII Deficiency

Factor XII deficiency is associated with a prolonged activated partial thromboplastin time and activated clotting time used for monitoring during cardiopulmonary bypass. It does not predispose to an increased risk of bleeding. We present the strategy used for a case of coronary artery bypass grafting in a patient with factor XII deficiency, followed by a brief discussion of the important clinical considerations when patients with factor XII deficiency undergo cardiac surgery. Monitoring of heparin and the avoidance of anti-fibrinolytic agents are the main intraoperative issues. Postoperative care must include careful thromboembolic prophylaxis and vigilance against infection.

Expanding cardiac pseudotumor.

FIGURE 1. Computed tomography scans. Long-axis images show dense calcification attached to the left ventricular endocardium and mitral annulus. LA, Left atrium; LV, left ventricle; A, Anterior; P, posterior; X, calcific mass. CLINICAL SUMMARY A 75-year-old woman presented with episodic presyncope associated with palpitations. She was diabetic and hypertensive with a history of rheumatic fever with associated valvular dysfunction. Physical examination revealed an irregular pulse rate of 82 beats/min and no signs of left heart failure. On auscultation, a soft diastolic murmur was heard. Biochemical investigation results were all within normal limits, including serum calcium, parathormone levels, and proteins C and S. Electrocardiography confirmed atrial fibrillation and showed periods of sinus rhythm and firstdegree heart block. In-hospital telemetry demonstrated episodes of complete heart block rate that required permanent pacemaker. Transthoracic and transesophageal echocardiography showed the presence of a large echogenic mass at the basal inferior wall and inferoposterior mitral annulus extending into both the interventricular and interatrial septae. The mass appeared encapsulated, intramyocardial, and extensive (5.4 3 4.2 cm). The posterior mitral valve leaflet was clearly compressed by the mass, causing mild mitral stenosis and mild mitral regurgitation. Left ventricular function was preserved. Transthoracic echocardiography, performed 3 years previously to investigate a diastolic murmur, revealed a 2.5 3 1.8-cm calcific mass behind the posterior mitral valve leaflet. The patient was lost to follow-up. Computed tomography (Figure 1) of the chest and cardiac magnetic resonance imaging confirmed the presence

Cutaneous Microangiopathic Thrombosis Complicated by Pyoderma Gangrenosum in Post-Cardiac Surgery Heparin-Induced Thrombocytopaenia

Thrombotic cutaneous gangrene is a rare complication of heparin-induced thrombocytopaenia after cardiac surgery. We report a case and discuss management issues with cardiopulmonary bypass for cardiac surgery in this condition.

Acute Atrial Stretch Results in Conduction Slowing and Complex Signals at the Pulmonary Vein to Left Atrial JunctionCLINICAL PERSPECTIVE

Background—The pulmonary vein–left atrial (PV–LA) junction is key in pathogenesis of AF, and acute stretch is an important stimulus to AF. We aimed to characterize the response of the junction to acute stretch, hypothesizing that stretch would result in electrophysiological changes predisposing to re-entry. Methods and Results—Fifteen participants undergoing cardiac surgery underwent evaluation of the right superior PV–LA junction using an epicardial mapping plaque. In 10, this was performed before and after atrial stretch imposed by rapid volume expansion, and in 5, it was performed with an intervening observation period. Activation was characterized by conduction slowing and electrogram fractionation transversely across the PV–LA junction, with lines of block also demonstrated perpendicular to the junction. Conduction was decremental (plaque activation time 135.8±46.8 ms with programmed extra stimuli at 10 ms above effective refractory period versus 66.1±22.9 ms with pacing at 400 ms; P<0.001) and percentage fractionation was greater with programmed extra stimuli at 10 ms above (33.5%±15.3% versus 20.7%±14.0%, P=0.001). Right atrial pressure increased by 2.5±1.8 mm Hg (P=0.002) with volume expansion. Stretch resulted in conduction slowing across the PV–LA junction (increase in activation time 10.9±14.6 ms in acute stretch group versus −0.1±4.5 ms in control group; P=0.002). Conduction slowing was more marked with programmed extra stimuli at 10 ms above effective refractory period than with stable pacing (13.4±16.5 ms versus 1.7±5.4 ms; P=0.003). Stretch resulted in a significant increase in fractionated electrograms (7.9%±7.0% versus −0.4±3.3; P=0.004). Conclusions—Acute stretch results in conduction slowing across the PV–LA junction, with a greater degree of signal complexity. This substrate may be important in AF initiation and maintenance by promoting re-entry.

Acute Atrial Stretch Results in Conduction Slowing and Complex Signals at the Pulmonary Vein to Left Atrial JunctionCLINICAL PERSPECTIVE: Insights Into the Mechanism of Pulmonary Vein Arrhythmogenesis

Background—The pulmonary vein–left atrial (PV–LA) junction is key in pathogenesis of AF, and acute stretch is an important stimulus to AF. We aimed to characterize the response of the junction to acute stretch, hypothesizing that stretch would result in electrophysiological changes predisposing to re-entry. Methods and Results—Fifteen participants undergoing cardiac surgery underwent evaluation of the right superior PV–LA junction using an epicardial mapping plaque. In 10, this was performed before and after atrial stretch imposed by rapid volume expansion, and in 5, it was performed with an intervening observation period. Activation was characterized by conduction slowing and electrogram fractionation transversely across the PV–LA junction, with lines of block also demonstrated perpendicular to the junction. Conduction was decremental (plaque activation time 135.8±46.8 ms with programmed extra stimuli at 10 ms above effective refractory period versus 66.1±22.9 ms with pacing at 400 ms; P<0.001) and percentage fractionation was greater with programmed extra stimuli at 10 ms above (33.5%±15.3% versus 20.7%±14.0%, P=0.001). Right atrial pressure increased by 2.5±1.8 mm Hg (P=0.002) with volume expansion. Stretch resulted in conduction slowing across the PV–LA junction (increase in activation time 10.9±14.6 ms in acute stretch group versus −0.1±4.5 ms in control group; P=0.002). Conduction slowing was more marked with programmed extra stimuli at 10 ms above effective refractory period than with stable pacing (13.4±16.5 ms versus 1.7±5.4 ms; P=0.003). Stretch resulted in a significant increase in fractionated electrograms (7.9%±7.0% versus −0.4±3.3; P=0.004). Conclusions—Acute stretch results in conduction slowing across the PV–LA junction, with a greater degree of signal complexity. This substrate may be important in AF initiation and maintenance by promoting re-entry.