Epicardial, off-pump, beating-heart ablation with acoustic energy is safe and cures 80% of patients with permanent atrial fibrillation associated with long-standing structural heart disease.

The Perceval sutureless valve resulted in low 1-year event rates in intermediate-risk patients undergoing AVR. New York Heart Association class improved in more than three-quarters of patients and remained stable. These data support the safety and efficacy to 1 year of the Perceval sutureless valve in this intermediate-risk population.

OBJECTIVES The aim of this study was to evaluate early- and mid-term outcome and aortic remodelling in patients undergoing implantation of 2 different frozen elephant trunk prostheses, either the Thoraflex™ hybrid (Vascutek, Inchinnan, UK) and the E-vita Open (Jotec Inc., Hechingen, Germany) for acute aortic dissection. METHODS All consecutive patients [n = 88; median age 59 (49–67) years; 69% male] undergoing surgery with a frozen elephant trunk prosthesis for acute aortic dissection from August 2005 until March 2018 were included in this study. The Thoraflex™ device was implanted in 55 patients and the E-vita Open graft in 33 patients. RESULTS Preoperative characteristics did not differ significantly between groups. There was also no statistically significant difference in postoperative outcome: in-hospital mortality (11% vs 12%; P > 0.99), stroke (18% vs 6%; P = 0.12) and spinal cord injury (6% vs 6%; P > 0.99). While there was no statistically significant difference in the occurrence of distal stent graft-induced new entries (16% vs 18%; P = 0.77), there was a significantly higher rate of secondary endovascular aortic interventions in the Thoraflex™ hybrid group (22% vs 0%; P = 0.003). There was a trend towards a higher rate of false lumen thrombosis at the level of the stent graft (74% vs 95%; P = 0.085) and was comparable at the thoraco-abdominal transition (53% vs 80%; P = 0.36) 1 year after implantation of the prostheses. CONCLUSIONS In this comparison of 2 frozen elephant trunk prostheses, there is no evidence that different surgical techniques influence in-hospital outcome. At 1-year follow-up, patients who underwent implantation of the E-vita Open prosthesis showed a significantly reduced rate of secondary aortic interventions and a trend towards a higher rate of false lumen thrombosis which might be attributed to a longer coverage of the descending aorta due to a longer stent graft design and significantly more frequent implantation in zone 3.

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We have previously demonstrated that the beneficial effect of cardioselective 13-blockade on exercise-induced ischemia is due entirely to negative chronotropism. Therefore we studied the effect of a new bradycardiac agent (UL-FS 49) in 10 dogs with chronic coronary artery stenosis produced by an ameroid constrictor. Regional myocardial function (sonomicrometers, wall thickness) and blood flow (microspheres) were measured during a control treadmill exercise bout and an identical run 3 hr later after the administration of UL-FS 49 (1.0 mg/kg iv). In the control run, heart rate increased from 114 ± 20 to 230 ± 19 beats/min and systolic wall thickening (%WT) in the poststenotic myocardium decreased from 23.3 ± 5.2% at rest to 9.3 ± 5.0%, a 60% reduction. Subendocardial blood flow in the ischemic area decreased from 1.04 ± 0.30 to 0.55 0.40 ml/min/g, blood flow per beat decreased from 9.1 x 10-3 to 2.5 x 10-3 m1/g, and mean transmural flow failed to increase (1.06 + 0.30 vs 1.08 ± 0.39 ml/min/g). During exercise with UL-FS 49, heart rate increased from 89 10 to only 139 ± 10 beats/min. End-diastolic left ventricular pressure was increased compared with that during the control run (35.7 ± 3.0 vs 28.9 ± 5.5 mm Hg) but left ventricular peak systolic pressure and dP/dt were unchanged. %WT in the ischemic zone did not change significantly during exercise with UL-FS 49 (23.3 ± 7.9% at rest, 21.5 ± 8.4% during the run), and in the nonischemic zone it increased to the same extent as during the control run. Absolute subendocardial blood flow (0.75 + 0.32 mllmin/g) and flow per beat (5.3 + 2.0 x 10-3 m1/g) were significantly increased compared with those during the control run (p < .05), and transmural blood flow per beat increased to 9.8 ± 1.7 x 10-3 m1/g (p < .01). These data demonstrate that UL-FS 49 is an effective bradycardiac agent that can markedly attenuate exercise-induced ischemic dysfunction and improve regional perfusion without compromising contractile function of nonischemic areas or global left ventricular contractility. Circulation 75, No. 3, 661-669, 1987

Studies on the role of alpha-adrenergic constrictor tone in the coronary vascular bed during ischemia were performed in dogs running on a treadmill. The animals were instrumented with a left ventricular pressure transducer, and regional systolic wall thickening (%WTh) was assessed by sonomicrometry in the anterior and posterior walls of the left ventricle. An intracoronary catheter was implanted chronically in the circumflex coronary artery, and a hydraulic cuff was placed proximally around the artery. After beta-adrenergic blockade with propranolol (0.8 mg/kg i.v.), acute stenosis of the coronary artery was performed during running in five dogs to induce severe regional myocardial dysfunction in the posterior wall. Intracoronary infusion of the selective alpha 2-adrenergic blocking agent idazoxan (80 micrograms/kg) improved %WTh in the ischemic region from 5.1 +/- 1.6 to 10.8 +/- 2.8% (p less than 0.05), without any significant effect on the anterior wall. Blood flow to the subendocardium of the posterior wall (radioactive microspheres) increased from 0.17 +/- 0.05 to 0.45 +/- 0.30 (ml/min)/g (p less than 0.05). It is concluded that in exercising dogs subjected to beta-adrenergic blockade, significant postjunctional alpha 2-adrenergic receptor-mediated coronary vasoconstriction exists, even during severe ischemia. Regional alpha 2-adrenergic receptor blockade can reduce regional ischemia and improve contractile function by attenuating exercise-induced sympathetic vasoconstriction in this conscious animal model.

We examined the importance of decreased heart rate in the beneficial effect of beta-adrenergic blockade on exercise-induced regional myocardial ischemia and contractile dysfunction in conscious dogs with single vessel coronary stenosis (ameroid constrictor). Studies were performed during control treadmill exercise, which produced regional myocardial ischemia (blood flow measured with microspheres) and wall dysfunction (measured using sonomicrometers). A second run was performed after the administration of atenolol (0.3-1.0 mg/kg i.v.), and the reduced heart rate caused by atenolol during early steady-state running was then prevented by atrial pacing during the latter portion of the run. Atenolol reduced the exercise heart rate from 217 +/- 25 beats per minute (SD, n = 9) to 166 +/- 15, and ischemic zone wall thickening during systole improved from 27 +/- 22% of the resting value in the control run to 50 +/- 25% of the resting value in the atenolol run (p less than 0.01). Atrial pacing then increased heart rate to 217 +/- 23 beats per minute, and regional wall thickening deteriorated to 15 +/- 25% of the resting value. Regional subendocardial blood flow in the ischemic zone during atrial pacing with atenolol was slightly less than that observed in the control run, in both ischemic and control zones, indicating no remaining beneficial effect of atenolol when heart rate reduction was eliminated. We conclude that the only significant mechanism for the improvement in exercise-induced ischemia and wall motion produced by atenolol is a reduction in the exercise heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)