Abstract Funding Acknowledgements Type of funding sources: None. Background Pulmonary vein (PV) isolation is the cornerstone of atrial fibrillation (AF) management. However, AF recurrence is extremely common after a single procedure. The CLOSE protocol, which is the standardisation of radiofrequency catheter ablation by delivering a point-by-point lesion set defined by ablation index (AI), has demonstrated 80% freedom of AF. Yet PV reconnection is still up to 38% in these patients (1). A small decrease in generator impedance (GI), which is not part of the AI algorithm, has been associated with recovery of PV conduction. Purpose The study aimed to identify whether lesions having a poor impedance drop (PID) after wide area circumferential ablation (WACA) are associated with PV reconnection, despite adopting to the CLOSE protocol. Methods 120 consecutive patients who had both the index (i-AFA) and redo AF ablations (r-AFA) due to AF recurrence at our centre from Jan 2018 to Jun 2021 were screened. 18 patients who had WACA around PVs using high power (40 to 50W) with a minimum AI of 400, whilst adhering the CLOSE protocol during the i-AFA, and who had evidence of PV reconnection during r-AFA, were included in the study. Ones who had left atrial (LA) substrate or cryoablation were excluded. GI was measured between the skin patch and ablation catheter. CARTO® system was used to create LA electroanatomical maps (EAMs) and register ablation lesions. Each WACA around PVs was divided into eight anatomical segments (Figure). PID was defined as an impedance change of <8Ω, based on previous studies (2). These lesions were identified and categorised to the relevant anatomical segment in the i-AFA. Locations of the discrete ablation lesions that re-isolated PVs during the r-AFA, were used as a surrogate to denote areas of PV reconnection. These were also spatially matched to the relevant anatomical segment. Each EAM was reviewed by two electrophysiologists. Results 30 out of the 36 WACAs (83%) and on average, at least 2 segments per WACA (2.6; 95% confidence interval (CI): 2.2-3.1) had reconnected. 54% of the reconnected segments had at least one lesion with PID. Having a lesion with PID in a PV segment in the i-AFA was significantly associated with evidence of PV reconnection in the same segment in the r-AFA (odds ratio: 2.1 [95% CI: 1.3-3.6; p<0.01]). Right posterior/inferior (56%) and left anterior/superior (50%) PV segments were the most common areas to reconnect and these areas were also associated with a higher incidence of PID lesions in the i-AFA (94% and 67%, respectively). Conversely, 80% of segments with all lesions having an impedance drop of ≥8Ω had no PV reconnection. Conclusion Lesions with PID in the i-AFA could impact PV reconnection, despite lesion contiguity and an adequate AI. Identifying and targeting these areas of PID, in addition to the CLOSE protocol, could potentially reduce AF recurrence. Prospective studies are needed to validate this hypothesis and its safety.

Purpose: Chronic heart failure(CHF) predominantly affects the elderly. In the UK the mean age of patients hospitalised with CHF is 78 yrs. Despite proven benefit of CRT, the mean age of UK patients undergoing CRT-P is 71 yrs. We evaluated whether CRT is feasible/safe and associated with improved symptoms in octogenarians. Methods: Consecutive patients undergoing CRT implantation at 2 UK centres(2009-11). Patients grouped according to age: < 80 & ≥80 yrs. Baseline demographics, complications and outcomes were compared between groups. Results: 439 patients were evaluated of whom 26% were aged ≥80 yrs. See table. Octogenarians more often received CRT-P. Upgrade from pacemaker was common in both groups (16% <80yrs vs 22%, p = ns). Major co-morbidities were similarly common in both groups (diabetes 25%, AF 49%, hypertension 45%). More patients age ≥80 yrs had significant chronic kidney disease(CKD, eGFR < 45 ml/min/1.73m2, 44% vs 22%, p < 0.01). Overall complication rates(any) were similar in both groups(17% ≥80 yrs vs 21%, p = ns). Both groups demonstrated significant symptomatic benefit. One year mortality rates were almost 4 fold greater in the very elderly(13.9% vs 3.7%, p < 0.01). Demographics and outcomes for patients. Conclusions: CRT appears to be safe in octogenarians despite extensive co-morbidity, and in particular frequent severe CKD. Symptomatic improvement is meaningful and similar to a younger population(mean age 14 yrs lower). Mortality at 1 year was higher in those aged ≥80 yrs. Strategies to increase the appropriate identification of elderly patients with CHF for CRT are required.

Purpose: Chronic heart failure (CHF) predominantly affects the elderly. In the UK the mean age of patients hospitalised with CHF is 78 yrs. Despite proven benefit of CRT, the mean age of UK patients undergoing CRT-P is 71 yrs. We evaluated whether CRT is feasible/safe and associated with improved symptoms in octogenarians.

Purpose: Chronic kidney disease (CKD) is common in patients with chronic heart failure (CHF) and associated with poor prognosis. Few data are available regarding the benefit of CRT in patients with severe CKD where it may be avoided due to concerns over implant complications. We evaluated whether CRT is safe and beneficial in patients with CKD stage 3b or worse. Methods: Analysis of patients undergoing CRT at 2 centres (2009-11). Patients grouped by estimated glomerular filtration rate (eGFR) ≥45 and <45 ml/min/1.73m2 (CKD class 3b-5). Baseline demographics, complications, change in renal function and outcomes were compared between groups Results: 429 patients were included. Of these 26% had eGFR <45 ml/min/1.73m2 (table). Use of CRT-D was similar between groups. Co-morbidities are common in both groups (overall AF 24%, diabetes 25%, hypertension 44%). Major complication rates were similar between groups; no patients experienced acute renal failure. Both groups exhibited symptomatic benefit: 65% of patients with eGFR≥45 and 71% with eGFR<45 improved by ≥1 NYHA class. The majority of patients had repeat assessment of renal function at 3 months with mean eGFR 60±15 (n=210) in those with eGFR≥45 and 36±12 (n=82) in patients in CKD3b-5. Demographics and outcomes for patients Conclusions: Significant CKD is common in patients undergoing CRT implantation. Whilst 1-yr mortality rates following CRT are greater in those in CKD class 3b-5, a similar improvement in symptom status was seen with no excess of implant related complications. Further evaluation is required to see if CRT may impact on renal function.

Infarction A 74-year-old man with no known ischaemic heart disease presented to the Cardiology Department with a history of multiple episodes of presyncope. During a head-up tilt test to investigate a neurocardiogenic cause, after glyceryl trinitrate provocation he became profoundly hypotensive and unwell. Subsequent ECGs and Troponin-T levels confirmed a Non ST-Elevation Myocardial Infarction. Angiography confirmed coronary artery disease. This case highlights a rare complication of tilt testing and emphasises that the test is not without risk. (C) 2004 The European Society of Cardiology. Published by Elsevier Ltd. All rights reserved.

[1] Nissen SE, Yock P. Intravascular ultrasound. Novel Pathophysiological insights and current clinical applications. Circulation 2001; 103: 604–16. [2] Pasterkamp G, Falk E, Woutman H, Borst C. Techniques characterizing the coronary atherosclerotic plaque: influence on clinical decision making? J Am Coll Cardiol 2000; 36: 13–21. [3] Kern M J. Coronary physiology revisited. practical insights from the cardiac catheterization laboratory. Circulation 2000; 101: 1344–51. [4] Pijls NHJ, de Bruyne B. Fractional flow reserve and clinical outcome. In Pijls N, de Bruyne B ed. Coronary Pressure. Dordrecht/Boston/London: Kluwer Academic Publishers; 2000: 307–26. [5] Sutsch G, Buchi M, Zeiher AM et al. Effects of calcium antagonism and HMG-coenzyme reductase inhibition on endothelial function and atherosclerosis: rationale and outline of the ENCORE trials. Eur Heart J Supplements 1999; 1(Suppl M): M27–M32. [6] Serruys PW, di Mario C, Piek J et al. Prognostic value of intracoronary flow velocity and diameter stenosis in assessing the shortand long-term outcomes of coronary balloon angioplasty. The DEBATE Study (Doppler Endpoints Balloon Angioplasty Trial in Europe). Circulation 1997; 96: 3369–77. [7] Piek JJ, Boersma E, Voskuil M et al. The immediate and long-term effect of optimal balloon angioplasty on the absolute coronary blood flow velocity reserve: a subanalysis of the DEBATE-study. Eur Heart J 2001; 22: 1725–32. [8] van Liebergen RAM, Piek JJ, Koch KT et al. Immediate and long-term effect of balloon angioplasty or stent implantation on the absolute and relative coronary blood flow velocity reserve. Circulation 1998; 98: 2133–40. [9] Ward MR, Pasterkamp G, Yeung AC, Borst C. Arterial remodeling. mechanisms and clinical implications. Circulation 2000; 102: 1186–91. [10] Serruys PW, de Bruyne B, Carlier S et al. Randomized comparison of primary stenting and provisional balloon angioplasty guided by flow velocity measurement. Circulation 2000; 102: 2930–7. [11] Di Mario C, Moses JW, Anderson TJ et al. randomized comparison of elective Stent implantation and coronary balloon angioplasty guided by online quantitative angiography and intracoronary Doppler. Circulation 2000; 102: 2938–44. [12] Lafont A, Dubois-Randé JL, Steg PG et al. The French Randomized Optimal Stenting Trial: a prospective evaluation of provisional stenting guided by coronary velocity reserve and quantitative coronary angiography. J Am Coll Cardiol 2000; 36: 404–9. [13] Weaver WD, Reisman MA, Griffin JJ et al. Optimum Percutaneous Transluminal Coronary Angioplasty Compared with Routine Stent Strategy Trial (OPUS-1): a randomized trial. Lancet 2000; 355: 2199–203. [14] Meuwissen M, Chamuleau SAJ, Siebes M et al. Role of variability in microvascular resistance on fractional flow reserve and coronary blood flow velocity reserve in intermediate coronary lesions. Circulation 2001; 103: 184–7.

Objective: To assess the value and safety of tracheal extubation in the operating room at the end of liver transplantation.Design: Retrospective chart review.Setting: University Medical Center.Participants: Eighteen adult patients extubated in the operating room at the end of liver transplantation (study patients) compared with 17 patients who were not extubated and had less than or equal to 3 U of blood transfused during liver transplantation (control patients).Interventions: Data collected include severity of preoperative liver disease, anesthetic technique, use of venovenous bypass, surgical time, intraoperative blood replacement, core temperature and arterial blood gases on admission to the intensive care unit (ICU), times to discharge from ICU and the hospital.Measurements and Main Results: Except for age (43.9 +/- 2.7 in study patients v52.4 +/- 2.5 years; p = 0.03), patients were similar with regard to preoperative Child's-Pugh class and liver function tests. Study patients received more crystalloid in the OR (5,306 +/- 561 v3,771 +/- 454 mL; p = 0.04), were warmer (36.6 degrees C +/- 0.2 degrees C v35.6 degrees C +/- 0.3 degrees C; p = 0.01), had a lower arterial pH (7.29 +/- 0.01 v7.36 +/- 0.02; p = 0.003) and higher arterial carbon dioxide tension (45 +/- 1 v35 +/- 2 mmHg; p < 0.001) on admission to ICU than controls. There were no significant differences between groups with regard to discharge times from the ICU (50.6 +/- 2.7 hours in the study group v61.2 +/- 4.7 in control group; p = 0.06), or discharge from the hospital (14.8 +/- 1.6 in the study group v21.3 +/- 3 days in control group; p = 0.06).Conclusions: Tracheal extubation of selected patients at the end of liver transplant surgery in the operating room is safe but did not result in decreased ICU or hospital stay. Copyright (C) 1997 by W.B. Saunders Company.

(Sopher, Braunfeld, Sangwan) Associate Professor, Department of Anesthesiology, University of California Los Angeles.(Shackleton) Associate Professor, Department of Surgery, University of California Los Angeles.(Busittil) Professor, Department of Surgery, University of California Los Angeles.(Csete) Associate Professor, Department of Anesthesiology, University of California Irvine.Received from the University of California Los Angeles School of Medicine, Los Angeles, California. Submitted for publication October 11, 1996. Accepted for publication March 24, 1997.Address reprint requests to Dr. Csete: Caltech Biology, Mail Code 156–29, Pasadena, California 91125. Address electronic mail to: csetem@starbase1.caltech.edu.Fatal pulmonary embolism is a very rare intraoperative complication of orthotopic liver transplantation (OLT), despite the use of antifibrinolytic agents in cirrhotic patients prone to hyperfibrinolysis in the setting of clotting activation and thrombin generation. [1] We report two such fatal complications to which aprotinin may have contributed.The patient was a 38-yr-old man with Laennec's cirrhosis and hepatitis C. Eight months before transplantation he presented with esophageal variceal bleeding and spontaneous bacterial peritonitis. He became progressively encephalopathic and short of breath and was admitted to the hospital. Laboratory studies included hematocrit, 21%; leukocyte count, 18.5 x 103/mm3; platelet count, 103,000/mm sup 3; and prothrombin time (PT) 16.3 s (INR, 1.6). The patient was hyponatremic, hyperkalemic, and oliguric, with creatinine level of 4.6 mg/dl, and required hemodialysis. Thoracentesis and paracentesis revealed negative bacterial cultures. He was treated with ciprofloxacin, and his leukocyte count fell to 9.4 x 103/mm3.The patient underwent an uncomplicated rapid sequence induction of anesthesia, after which a radial arterial catheter and two 9-French introducers were placed in the right internal jugular vein. Anesthesia was maintained with isoflurane and fentanyl, and dopamine was infused at 3 micro gram [center dot] kg sup -1 [center dot] min sup -1. The first hemodynamics recorded (before incision) were pulmonary artery (PA) pressure of 23/10 mmHg; CVP, 10 mmHg; and cardiac output (CO), 9.8 l/min. On FIO2of 0.6, first arterial blood gas (ABG) analysis revealed pH, 7.34; PaCO2, 35 mmHg; PaO2, 109 mmHg; base deficit, -5.7. Hct was 25%; PT, 19.1 s; and fibrinogen, 135 mg/dl. TEG is not used in our center. Before incision, 1 g/h infusion of epsilon-aminocaproic acid (EACA) was started after a 5-g bolus. Thirty minutes after incision, the patient experienced acute hypotension (systolic blood pressure, 65 mmHg) associated with rapid blood loss, which responded quickly to transfusion with 2 U packed red cells, 4 U fresh frozen plasma (FFP), 250 cc 5% albumin, and administration of CaCl sub 2 (500 mg) and phenylephrine (400 micro gram). After this episode, blood pressure was 130/75 mmHg, and PA was 41/23 mmHg; CVP, 14 mmHg; and CO, 12.7 l/min. The patient was hemodynamically stable through the rest of the dissection phase. Venovenous bypass with a heat exchanger and nonheparinized tubing was instituted without problems (flows, 2.1–2.5 l/min). Thirty minutes later, after hepatectomy, the surgeons noted extremely poor hemostasis and requested that aprotinin be given. The EACA infusion was discontinued, and after a test dose of aprotinin (10,000 KIU), the patient received a loading dose of 2 million KIU, followed by infusion of 200,000 KIU/h. Blood gas level a few minutes later (FIO20.45) was pH, 7.4; PaCO2, 28 mmHg; PaO2, 218 mmHg, Hct, 25%; platelets, 37,000/mm3; PT, 16 s, and fibrinogen 154 mg/dl. Venous anastomoses were completed, and portal bypass was discontinued. Approximately 20 min after aprotinin was first given, the patient's blood pressure dropped acutely to 45/20 mmHg. Dopamine was increased to 10 micro gram [center dot] kg sup -1 [center dot] min sup -1, and boluses of epinephrine, neosynephrine, CaCl2, sodium bicarbonate, and intravenous fluids were given with only transient improvement in blood pressure. PA pressures were also noted to be elevated to 50/29 mmHg, CVP to 29 mmHg, and CO could not be measured. End-tidal CO2dropped, and ABG on FIO21.0 was pH, 7.49; Pa sub CO2, 27 mmHg; PaO2, 47 mmHg, base deficit, -1.7. Venovenous bypass was discontinued, and the aprotinin infusion stopped. Large doses of pressors were administered without improvement.A transesophageal echocardiographic (TEE) probe was placed and revealed a large right atrium and ventricle, with a large thrombus in the right atrium, through the tricuspid valve, and into the right ventricle. The right ventricle was severely hypocontractile, and the left ventricle appeared empty but normally contractile. Despite pharmacologic interventions, blood pressure continued to fall, and chest compression was begun, followed by direct myocardial compression for several minutes. One hour into the resuscitation, ABG on FIO21.0 was pH, 7.12; PaCO2, 33 mmHg; PaO2, 75 mmHg; base deficit, -16.5. Systolic blood pressure never increased above 45 mmHg. The new liver was grafted and reperfused without any improvement in the patient's blood pressure. Cardiac surgeons were called and removed a large thrombus from the right atrium and pulmonary artery, without bypass. Nonetheless, the patient died 2 h after the onset of hypotension.A 37-yr-old man with subacute hepatic failure of unknown cause presented 1 month before transplantation with fever, weakness, nausea, and vomiting. Hematocrit was 32%, platelets, 289,000/mm3; glucose, 57 mg/dl; creatinine, 1.4 mg/dl; albumin, 2.0 g/dl; and total bilirubin, 27.7 mg/dl. PT was 19.2 s; aspartate aminotransferase, 556 U/l; and alanine aminotransferase, 321 U/l-all significantly higher than 1 month previous. The patient's hospital course was significant for septic arthritis of the knee and bacteremia, managed with multiple antibiotics, and for spontaneous bacterial peritonitis. The patient's renal function deteriorated, and he was transferred to University of California, Los Angeles. He required hemodialysis, which was complicated by hypotension. Dopamine was administered for 8 days in dosages ranging from 3.5 to 7.5 micro gram [center dot] kg sup -1 [center dot] min sup -1. Dobutamine stress echo showed an ejection fraction of 55–60%.The patient underwent an uncomplicated liver transplantation, during which 10 U packed cells, 17 U FFP, 20 U platelets, and 10 U of cryoprecipitate were given. He received aprotinin (2 million KIU bolus, 500,000 KIU/h) from the dissection phase through the end of surgery. The postoperative course was complicated by renal failure requiring dialysis and poor graft function. Two days later, the patient underwent a second liver transplantation for primary nonfunction.After induction of anesthesia, aprotinin was administered in the same dose as for the first transplantation. Dissection and institution of venovenous bypass were uncomplicated. After hepatectomy, the patient developed acute systemic hypotension, and PA pressures rose suddenly to 40/30 mmHg. The surgeons noted a poorly contracting right ventricle (compared with normal hyperdynamic contractions), and PA pressures remained increased. The hypotension was unresponsive to dopamine, 8 micro gram [center dot] kg sup -1 [center dot] min sup -1, atropine given when the heart rate fell to 45 beats/min, and boluses of epinephrine. For these reasons, TEE was placed. A large thrombus was seen in the inferior vena cava and right atrium. Cardiac surgery consultants elected to remove the thrombus, and the patient was placed on cardiopulmonary bypass with heparin anticoagulation. Cardiotomy was performed, and large clots (some appearing fibrinous and likely to be days old, some appearing newly formed or gelatinous) were removed from the inferior vena cava, right atrium and ventricle, and pulmonary artery. After cardiopulmonary bypass, the patient required large doses of epinephrine, and then norepinephrine, to maintain blood pressure. The liver graft was placed without improvement in the pressor requirement. Hemostasis in the neohepatic phase was poor despite administration of cryoprecipitate, FFP, and 100 mg of protamine. New thrombus was noted on TEE in the RA and RV and attached to the PA catheter, and so, further protamine and antifibrinolytics were not given (despite partial thromboplastin time [PTT] > 180 s). Cardiac surgeons did not believe a second procedure was indicated. The patient received 36 U each of packed cells and FFP. The patient was transported to the intensive care unit on a norepinephrine infusion (2 micro gram [center dot] kg sup -1 [center dot] min sup -1). He never regained consciousness and was declared brain dead on the second postoperative day.The two cases presented here occurred within 1 month of each other, at a time just after the introduction of aprotinin into clinical use during OLT; 15 patients before these received aprotinin during OLT. Before this time, the standard antifibrinolytic regimen during OLT at our center was EACA, given to more than 600 patients without evidence of abnormal clot formation. The proximity of these cases in our center is striking and should motivate reevaluation of antifibrinolytic therapy during liver transplantation.Liver transplantation centers vary in their practice of administration of procoagulant drugs. EACA is probably the most commonly administered antifibrinolytic drug in the United States for patients undergoing OLT. A combination of release of tissue plasminogen activator (t-PA) from graft endothelium and decreased hepatic clearance of t-PA generally is accepted as one contributor to enhanced fibrinolysis during liver transplantation. [2] Thus, EACA is used during liver transplantation for its effect of interfering with plasmin(ogen) binding to fibrin. Almost a decade ago, the drug was reported to reverse thromboelastographic evidence of fibrinolysis without causing thrombotic complications during liver transplantation. [3] Although EACA was not rigorously, prospectively studied, such reports influenced clinical practice tremendously. A prospective study on EACA was reported at a national meeting [4] and greatly influenced our local practice. In this blinded study, transfusion requirements were significantly decreased when EACA was given to patients undergoing liver transplantation (5-g bolus, then 1- g/h infusion). This study caused our center to standardize the administration and dose of EACA.Several reports from outside the United States suggested that the antifibrinolytic drug, aprotinin, was effective in reducing transfusion requirements during OLT. A 50% reduction in transfusion requirements was reported when aprotinin (2 million KIU bolus, then 500,000 KIU/h infusion) was given during liver transplantation. [5] However, this study was small and used retrospective control subjects. Similar problems plague other reports, [6–9] and further, drug dose is not standardized from report to report. [10,11] Recent studies have helped elucidate some of the mechanisms of aprotinin action during liver transplantation, such as its antikallikrein effect, [12] but the number of patients prospectively studied against either placebo or EACA has not been large. Nonetheless, aprotinin is used routinely in many European liver transplantation centers, and some authors report that they will not study the drug with a control arm because withholding aprotinin would be unethical. [13] Not all studies support a role for aprotinin in reducing transfusion requirements during OLT. [14]One case report increased concern that aprotinin contributed to a fatal pulmonary embolism during OLT. [15] This patient (after receiving a bolus of aprotinin 1.6 million KIU and an infusion at 0.5 million KIU/h) developed a large thrombus attached to the pulmonary artery catheter, spanning the superior vena cava into the pulmonary artery. The authors suggested that the complication may have been a result of very low antithrombin III levels and of two introducers in the internal jugular vein leading to endothelial activation. Further, in a report of six perioperative liver transplantation deaths attributed to pulmonary platelet aggregates, three of the six patients received aprotinin, and two of these died during surgery. [16]Rare cases of pulmonary embolism during OLT have been reported before the use of aprotinin. [17–19] Another report increased concern that EACA may contribute to rare pulmonary embolism. [20] Two of 12 patients who had received EACA experienced massive thromboembolism during transplantation. Of note, both patients were critically ill and intubated before surgery.In the two cases reported here, several factors may have contributed to abnormal clot formation. The first patient received EACA followed by aprotinin, and it is possible that the drugs had a synergistic action on clot formation. The second patient was septic in the weeks before transplantation. If he had ongoing infection, disseminated intravascular coagulation (DIC) may have contributed to clot formation. In addition, patients with acute liver disease may be more prone to DIC than those with chronic disease. [21] Drug dosage may be a factor. A recent prospective study of aprotinin suggests that much lower dosages (0.2 million KIU/h infusion without a bolus) than originally reported may be sufficient to decrease fibrinolytic activity during liver transplantation, [22] increasing concern that high- dose aprotinin may be an unnecessary risk. The timing of the second transplantation may have placed the second patient at risk for clotting complications because there may be a relative abundance of procoagulants (such as plasminogen activator inhibitor) and slow recovery of protein C and S several days after OLT. [23]In summary, the complicated coagulopathy in liver disease combined with an equally complex superimposed coagulopathy during surgery are inherently difficult to study. For example, there often is insufficient clinical information to clearly distinguish between primary and secondary fibrinolysis in these patients. Large prospective trials to determine optimal antifibrinolytic therapy are needed to determine minimal effective doses and to carefully document the balance between thrombogenic factors and antifibrinolytic parameters after drug administration. In experienced transplantation centers, aggressive transfusion therapy of coagulopathy combined with potent procoagulant drugs may lead to increased thrombotic complications. These cases highlight the need for a reevaluation of procoagulant therapy during liver transplantation.The authors thank Dr. Hillel Laks for his contributions.

Low energy biatrial shock is an effective means of restoring sinus rhythm in patients with atril fibrillation (AF). Ventricular proarrhythmia is avoided provided that shocks are well synchronized to R waves that are not at closely coupled intervals or preceded by long‐short cycles. Based on these principles, an implantable atrial defibrillator has been developed and was implanted in three patients with drug refractory paroxysmal AF. The device detects AF via an actively fixed right atrial and a self‐retaining coronary sinus defibrillating leads, and delivers 3/3 ms biphasic shocks up to 300 V synchronized to the R wave. The mean implant threshold (ED50) was 195V (1.8 J), and minimum voltage at conversion during follow‐up assessments at 1, 3, and 6 months were 260 V, 2.5 J, 250 V, 2.3 J, and 300 V, 3.0 J respectively. Detection of AF was 100% specific and shocks were 100% synchronized, although only a proportion of synchronized R waves were considered suitable for shock delivery primarily because of closely coupled cycles. Three patients had 9 spontaneous AF episodes. 8/9 (89%) successfully defibrillated by shocks of 260–300 V. Sedation was not used in 4 out of 9 (45%) episodes. Backup ventricular pacing was initiated by the device in 6 out of(67%) episodes. One patient had more frequent AF after lead placement, which subsided after a change of medication. There was no ventricular proarrhythmia. It is concluded that an implantable atrial defibrillator is a viable therapy for selected patients with paroxysmal AF. The device is capable of accurate AF detection, R wave synchronization and ventricular support pacing after successful defibrillation of AF.

An incarcerated hernia containing peritoneal secondaries from carcinoma of the prostate is presented. Abdominal carcinomatosis may be due to a prostatic primary and will benefit from hormonal treatment.