BackgroundAtrial fibrillation (AF) is associated with myocardial infarction, and patients with AF and no obstructive coronary artery disease can present with symptoms and evidence of cardiac ischemia. We hypothesized that microvascular coronary dysfunction underlies these observations.Methods and ResultsMyocardial blood flow (MBF) at baseline and during adenosine stress and left ventricular and left atrial function were evaluated by magnetic resonance in 49 patients with AF (25 paroxysmal, 24 persistent) with no history of epicardial coronary artery disease or diabetes mellitus, before and 6 to 9 months after ablation. Findings were compared with those obtained in matched controls in sinus rhythm (n=25). Before ablation, patients with AF had impaired left atrial function and left ventricular ejection fraction and strain indices (all P<0.05 versus controls). MBF was impaired in patients both under baseline conditions (1.21±0.24 mL/min per g·[mm Hg·bpm/104]−1 versus 1.34±0.28 mL/min per g·[mm Hg·bpm/104]−1 in controls, P=0.044) and during adenosine stress (2.29±0.48 mL/min per g versus 2.73±0.37 mL/min per g in controls, P<0.001). Under baseline conditions, MBF correlated with left ventricular strain and left atrial function (all P≤0.001), so that cardiac function was most impaired in patients with the lowest MBF. Baseline and stress MBF remained unchanged postablation (both P=ns), and baseline MBF showed similar correlations with functional indices to those present preablation (all P≤0.001).ConclusionsBaseline and stress MBF are significantly impaired in patients with AF but no epicardial coronary artery disease. Reduction in MBF is proportional to severity of left ventricular and left atrial dysfunction, even after successful ablation. Coronary microvascular dysfunction may be a relevant pathophysiological mechanism in patients with a history of AF.

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Introduction Permanent His bundle pacing (PHBP) preserves physiological ventricular activation but technical difficulties have limited its widespread use. We report the first experience of PHBP performed with a new specific delivery sheath (Selectra 3D, Biotronik, Berlin, Germany) and an extendable‐retractable active screw, stylet‐driven pacing lead (Solia S 60, Biotronik). Methods and Results Clinical, procedural, ECG, and electrical data from consecutive patients undergoing PHBP with this system were collected at implantation, and follow‐up was performed after 1 month. Our cohort included 17 patients (71% males; mean age 76 ± 8 years) undergoing permanent pacing for sick sinus syndrome (59%) or atrioventricular block (41%). PHBP was successful in 15 (88%) procedures with mean procedure and fluoroscopy times of 63 ± 14 and 13 ± 5 min, respectively. The pacing threshold was 2.1 ± 1.1 V @1 ms and the sensed R‐wave amplitude was 5.6 ± 3.5 mV; bipolar and unipolar pacing impedances were 526 ± 115 and 369 ± 109 Ω, respectively. At discharge, neither procedure‐related complications nor lead dislodgement or pacing capture failures was reported. After 1 month, 14 (93%) patients still demonstrated His bundle stimulation and one (7%) lost His bundle capture but the lead revision was not necessary because the myocardial pacing threshold was stable. Follow‐up threshold (2 ± 1.1 vs. 2.3 ± 1.2 V@1 ms, p = .239) and sensed R‐wave amplitude (5.6 ± 3.4 vs. 6.4 ± 2.5, p = .403) was unchanged compared to the acute phase. Conclusion PHBP performed with a standard active fixation pacing lead and a new delivery sheath for His pacing is feasible, safe and demonstrates clinically acceptable electric performance both at implantation and after 1 month.

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Rupture of the interventricular septum is a rare and life-threatening complication of acute myocardial infarction. Postmyocardial infarction, ventricular septal defect is associated with very high morbidity and mortality. The therapy of this complication is the surgical closure. The Amplatzer occluder is currently used to close percutaneously atrial septal defect, patent foramen ovale, and selected congenital ventricular septal defect. Few cases are described regarding transcatheter closure of a postinfarction ventricular septal defect. Here we report a case of a large postinfarction ventricular septal defect successfully closed with Amplatzer multifenestrated atrial septal defect occluder device because of its peculiar anatomical characteristics.

Acute myocardial infarction (AMI) is caused by thrombus formation over a disrupted plaque occluding an epicardial coronary artery. Mechanical thrombectomy is effective in removing thrombus burden from native vessels and saphenous vein grafts. Here we report a case of an aneurysmatic dilatation of an infarct-related artery (IRA) referred to our Institute for rescue PCI, after failed fibrinolysis, successfully treated with only rheolytic thrombectomy (AngioJet, Possis Medical, Minneapolis, Minnesota, USA) without the need for adjunctive balloon or stent implantation.