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Background: The incidence and impact of clinical stroke and silent radiographic cerebral infarction complicating open surgical aortic valve replacement (AVR) are poorly characterized., Methods and Results: We performed a prospective cohort study of subjects ≥65 years of age who were undergoing AVR for calcific aortic stenosis. Subjects were evaluated by neurologists preoperatively and postoperatively and underwent postoperative magnetic resonance imaging. Over a 4-year period, 196 subjects were enrolled at 2 sites (mean age, 75.8±6.2 years; 36% women; 6% nonwhite). Clinical strokes were detected in 17%, transient ischemic attack in 2%, and in-hospital mortality was 5%. The frequency of stroke in the Society for Thoracic Surgery database in this cohort was 7%. Most strokes were mild; the median National Institutes of Health Stroke Scale was 3 (interquartile range, 1-9). Clinical stroke was associated with increased length of stay (median, 12 versus 10 days; P=0.02). Moderate or severe stroke (National Institutes of Health Stroke Scale ≥10) occurred in 8 (4%) and was strongly associated with in-hospital mortality (38% versus 4%; P=0.005). Of the 109 stroke-free subjects with postoperative magnetic resonance imaging, silent infarct was identified in 59 (54%). Silent infarct was not associated with in-hospital mortality or increased length of stay., Conclusions: Clinical stroke after AVR was more common than reported previously, more than double for this same cohort in the Society for Thoracic Surgery database, and silent cerebral infarctions were detected in more than half of the patients undergoing AVR. Clinical stroke complicating AVR is associated with increased length of stay and mortality., (© 2014 American Heart Association, Inc.)

Background: Patients with sustained ventricular tachycardia after acute myocardial infarction frequently have characteristic abnormalities of left ventricular endocardial electrical activity, including fractionated (prolonged, multicomponent, low-amplitude), split (having discrete widely separated deflections), and late (extending after the end of the QRS complex) electrograms. The exact cause and source of these electrograms are not clear., Methods and Results: In this study, endocardial electrograms from 18 patients were recorded with a 20-electrode array from the same area immediately before and immediately after resection of subendocardial tissue at the time of surgery for ventricular tachycardia. Electrograms could be compared before and after resection from 298 of 360 (83%) of the electrodes. Before resection, split electrograms were present in 130 (44%) and late components in 81 (27%) of the recordings. Recordings made after resection showed fewer abnormalities, including complete absence of split electrograms as well as all previously recorded late components (P < .02). Mean electrogram amplitude increased from 0.5 +/- 0.8 to 1.0 +/- 1.6 mV (P < .0001) because of removal of the attenuating effect of endocardial scar; mean duration decreased from 112 +/- 38 to 65 +/- 27 ms (P < .0001) mainly because of loss of late and split components. Overall electrogram contour was very similar aside from these changes., Conclusions: These data show that (1) some of the signal recorded on the endocardial surface is derived from deeper tissue layers and (2) split and late electrogram components appear to be generated by cells in the superficial endocardial layers, since they are eradicated by removal of this tissue. These findings correspond well with previous histological studies of resection specimens that show bundles of surviving muscle cells separated by layers of dense scar that act as an insulator.

Forty-three patients with sustained ventricular tachycardia (VT) caused by prior myocardial infarction underwent intraoperative endocardial activation mapping during a total of 122 episodes of VT. Electrograms obtained during mapping were analyzed to determine the prevalence of local conduction failure during VT (defined as a portion of the local electrogram that did not repeat with every tachycardia cycle). Local conduction failure during VT was observed in 37 (86%) patients and 73 (65%) tachycardias. VT in which local conduction failure was observed were faster than VTs without local conduction failure (cycle length 315 vs 345 msec; p less than .05). Local conduction failure occurred most frequently at or near sites having the earliest recorded electrical activity during VT ("site of origin"). Twenty-three patients also had sinus rhythm endocardial mapping at the time of surgery. Areas with abnormal or fractionated electrograms in sinus rhythm were more likely to demonstrate local conduction failure in VT than areas with normal electrograms in sinus rhythm (16% vs 8%; p less than .01). Although the mechanism responsible for local conduction failure in VT is unclear, it is a common occurrence and is significant in that it can occasionally mimic "early" sites of endocardial activation, unless enough VT cycles are observed at a given site.

In the past 3 years, 86 patients had left ventricular aneurysms resected or plicated. Sixty-eight had recurrent sustained ventricular tachycardia as the indication for surgery and had preoperative and intraoperative electrophysiologic mapping. There were 14 hospital deaths (16%). Eight preoperative potential risk factors for early hospital mortality were analyzed by multivariate analysis. Only acute myocardial infarction within 30 days before surgery correlated with hospital death at the p less than 0.05 level. History of previous heart surgery and advanced New York Heart Association functional class were important risk factors at the p less than 0.1 level. Hospital mortality was 17.6% for patients who had intraoperative mapping and endocardial resection and 11.1% for the others. Patients who had aneurysm repair for ventricular tachycardia had a significantly higher incidence of low cardiac output early after surgery (p less than 0.025).

Clinical results are reviewed in 269 patients who underwent subendocardial resection for recurrent sustained ventricular tachycardia secondary to ischemic heart disease. Operative mortality is 15%. Factors increasing operative mortality rates are ejection fraction less than 20%, emergency operation, and history of previous heart operation. Use of amiodarone preoperatively does not alter operative risk. Clinical control of ventricular tachycardia is achieved in 93% of operative survivors. Two thirds of these patients do not need antiarrhythmic agents. Five-year actuarial survival is approximately 60%. Patient results with the automatic internal cardioverter defibrillator at the Hospital of the University of Pennsylvania and nationwide are also reviewed. As of June 1987, almost 1,500 patients had one or more devices implanted. Most patients had a prior documented cardiac arrest. Coronary artery disease is the cause of heart disease in over 70% of patients. Operative mortality is low (0.8-3.9%). Approximately 50% of patients have had therapeutic discharge of the device; however, asymptomatic discharge occurs in up to 45% of patients. Incidence of sudden death is 1.5% at 1 year and 5% at 5 years. Five-year actuarial survival is approximately 60%. Long-term mortality is primarily from heart failure.