Background Survival rates after an out-of-hospital cardiac arrest (OHCA) remain low. Extracorporeal cardiopulmonary resuscitation (eCPR) has been introduced as an attempt to increase survival in selected patients and observational studies have shown promising results. Nevertheless, inclusion criteria and timing of eCPR remain undefined. Objective The current study analyzed a load and go strategy with respect to the golden hour of eCPR as a cut-off time for survival and favorable neurological outcome. Material and methods This retrospective cohort study included 32 patients who underwent eCPR treatment due to an OHCA between January 2017 and September 2019. Routinely taken patient demographic data (age, BMI, sex) were analyzed. The main focus was set on processing times in the preclinical and clinical setting. Time intervals including OHCA until ambulance arrival, time on scene, transportation times and door to eCPR were extracted from emergency medical service (EMS) and resuscitation protocols. Low-flow times, survival and neurological outcome were analyzed. Results The use of eCPR in OHCA was associated with survival to hospital discharge in 28% and a good neurological outcome in 19% of the cases. Both groups (survivor and nonsurvivor) did not differ in patient demographics except for age. Survivors were significantly younger (47 (30-60) vs. 59 (50-68) years, p = 0.035). Processing times as well as low-flow times were not significantly different (OHCA-eCPR survivor 64 (50-87) vs. non-survivor 74 (51-85) min; p-value 0.64); however, median low-flow times were outside the golden hour of eCPR (69 (52-86)). Conclusion Despite low-flow times of more than 60 min, eCPR was associated with survival in 28% after OHCA. Hence, exceeding the golden hour of eCPR cannot act as a definitive exclusion criterion for eCPR.

Für ausgewählte Patienten mit therapierefraktärem Herz-Kreislauf-Stillstand zeigt sich die extrakorporale kardiopulmonale Reanimation (eCPR) zunehmend als vielversprechende Therapieoption. Retrospektive Kohortenstudien zeigen eine signifikante Verbesserung der Überlebensraten. In der vorliegenden Studie wurden Prozesszeiten und die Überlebensrate bei einer „Load-and-go“-Strategie im außerhospitalen Herz-Kreislauf-Stillstand (OHCA) analysiert. Insbesondere sollte geklärt werden, ob „Low-flow“-Zeiten über 60 min als Ausschlusskriterium zur eCPR dienen. In dieser retrospektiven Kohortenstudie wurden die Daten von 32 Patienten mit eCPR nach OHCA zwischen Januar 2017 und September 2019 untersucht. Standardmäßig erfasste demografische Daten sowie prähospitale und klinische Zeitintervalle wurden ermittelt und deren Einfluss auf das Überleben bis zur Krankenhausentlassung analysiert. Im untersuchten Patientenkollektiv ergaben sich eine Überlebensrate von 28 % und ein Überleben mit gutem neurologischen Behandlungsergebnis von 19 % zum Zeitpunkt der Krankenhausentlassung. Zwar zeigen die Überlebenden in der Tendenz schnellere Prozesszeiten, jedoch ohne statistische Signifikanz. Betrachtet man die Low-flow-Zeit aller Patienten, ergibt sich mit einer medianen Low-flow-Zeit von 69 (52–86) min ein Überschreiten des empfohlenen 60-min-Rahmens. Die Gruppen (Überleben vs. Verstorben) zeigten in Bezug auf die Demografie und die Prozesszeiten keinen statistisch signifikanten Unterschied, mit Ausnahme des Patientenalters (47 (30 bis 60) vs. 59 (50 bis 68) Jahre, p = 0,035). Trotz des Überschreitens einer empfohlenen Prozesszeit von 60 min bis zum Start einer eCPR konnte im OHCA ein Überleben in 28 % der Fälle erreicht werden. Überschreiten eines fiktiven „cut off“ von 60 min sollte somit kein definitives Ausschlusskriterium für eine eCPR sein.

Acute hemodynamic decompensation during catheter ablation of ventricular tachycardia is associated with increased mortality. We assessed the effectiveness of mechanical circulatory support using a micro‐axial percutaneous assist device in preventing acute hemodynamic decompensation.

ZusammenfassungNach erfolgreicher prähospitaler Reanimation ist die Prognose quo ad restitutio sehr ernst und bei Einlieferung unter laufender Reanimation gilt dies in verschärfter Form. Die Kompetenz und fallzahlabhängige Erfahrung, sowie die strukturellen und personellen Anforderungen sind essenziell für den Therapieerfolg. Konsequente Interdisziplinarität und breit konsentierte Behandlungspfade sind dabei entscheidende Faktoren. Das Klinikum Kassel hat die Cardiac-Arrest-Center-Initiative des German Resuscitation Council aufgegriffen und Ende 2017 für diese Ziele das Kassel Center for Cardiac Arrest (KCCA) gegründet.

BACKGROUND:In left atrial appendage (LAA) closure, the correct sizing of the implantable devices is crucial. Data on the time-dependent changes in the shape and positioning of LAA occlusion devices are missing. We analyzed the results of 33 consecutive patients after implantation of an Amplatzer™ Cardiac Plug (ACP) LAA closure device to get more information on the optimal device sizing during implantation.METHODS AND RESULTS:Thirty-three consecutive patients were enrolled in this observational study. ACP implantation was guided by fluoroscopy and three dimensional transesophageal echocardiography (3-D TEE). Device sizing was based on the largest measured diameter of the intended landing zone adding 2-4 mm of device oversizing. Fluoroscopies were performed at 1 day after, and after 3 months, control 3-D TEE was performed 3 months after implantation. The stability of device positioning and shape was matched with the results of 3-D TEE. Patients' mean age was 70.2 ± 8 years; mean CHA2DS2VASc score was 3.8 ± 1.1. According to the manufacture's classification, the post-implant degree of compression of the device-lobe was classified in three categories 1) undercompression "square-like shape" (1 patient); 2) optimal compression "tire-like shape" (20 patients), 3) overcompression "strawberry-like shape" (12 patients). Changes in the degree of device compression by more than one classification class occurred in 18/33 of our patients. A complete loss of device compression ("square-like shape") was observed in 9 patients. Despite the changes in device compression, a complete closure of the LAA was achieved in 32/33 patients.CONCLUSIONS:There is a temporal change in shape and positioning of the ACP within 3 months after implantation. A late decompression of the ACP lobe was observed in 61% of our patients, leading to a complete loss in device compression in 27%. This observation may be the rationale for a higher degree of ACP oversizing during implantation.

We read with interest the article of Sekine and colleagues reporting their surgical strategy in the treatment of Kommerell’s diverticulum (KD) with aberrant subclavian artery (ASA) in 9 asymptomatic patients. Both the described surgical strategy to treat the KD with ASA in those 9 asymptomatic patients and some of the concepts relating to KD with ASA raised by the authors are, in our opinion, controversial and deserve particular remarks. Interestingly, ASA, known as ‘‘arteria lusoria’’ since its first description by Hunauld in 1735 until today, still causes controversies relating either to its supposedly different course (retroesophageal, between the esophagus and trachea, or anterior to the trachea) or to its potential role in causing clinical symptoms such as ‘‘dysphagia lusoria’’ and dyspnea. An ASA originates usually from an aortic diverticular dilatation, which was extensively described in old autopsy studies such as those by Holzapfel in 1899, and later by Burckhard F. Kommerell in a living patient with aberrant right subclavian artery (ARSA). Sekine and colleagues provided two contradictory definitions of KD. The first (inaccurate one): ‘‘an aneurysmal diverticulum of the descending aorta at the origin of an [ASA], which includes both an aneurysm of the thoracic aorta and an aneurysmal orifice of the ASA, is called Kommerell’s diverticulum’’ is contradicted by the second (accurate) definition: ‘‘an embryologic remnant of the dorsal 4th aortic arch’’. In contrast, KD is neither a synonym of ‘‘aneurysm’’ nor of ‘‘aneurysm of an aberrant subclavian artery’’. From 1956 until 1991, there were only 54 reported cases of aneurysms of an ASA, 53 of these were aneurysms of an ARSA, and one was an aneurysm of an aberrant left subclavian artery (ALSA). However, aneurysmal formation, dissection, or even rupture of isolated KD are extremely rare. Sekine and colleagues refer to Austin and Wolfe to support their opinion regarding the supposedly ‘‘marked tendency to rupture or dissection in the course of aneurysms of KD’’, but they overlooked the fact that the review of Austin and Wolfe deals not with KD aneurysms but with 31 ARSA aneurysms and 1 aneurysm of an ALSA. While Sekine and colleagues ascertain that ASA occur as [a left aortic arch] associated an ARSA (0.5%–2.0% of the population), or as a [right aortic arch] with an ALSA (0.05%–0.1%)’’, they reported 7 patients with right aortic arch with an ALSA, and 2 with a left aortic arch with an ARSA, which is exactly the opposite of the normal distribution of this congenital anomaly. As all the 9 patients reported by Sekine and colleagues were completely asymptomatic, the surgical indications for the offered extensive and invasive surgical approaches through either a right or left thoracotomy, partial cardiopulmonary bypass, deep hypothermic circulatory arrest, or left heart bypass, were neither clearly explained nor even justified. While these authors refer to Ota and colleagues to support their surgical indications for KD with ASA, they overlooked the fact that Ota and colleagues recommended surgical treatment for this entity only in cases of symptomatic aneurysms of KD with diameters of 50mm or greater; only 4 of their 9 patients had KD with a diameter that exceeded 50mm, a fact that might not justify surgical treatment in the other 5 patients.

To the Editor We read with interest the comparative review of Al-Sabti and colleagues between the radial artery (RA) and the saphenous vein as bypass grafts for coronary artery bypass grafting (CABG) [1]. We would like to add some remarks relating to the RA as arterial conduit for CABG. In 1992, Acar and colleagues “revived” the RA after having observed that some RA grafts were, unexpectedly, still patent 14–18 years after the primary operation [2]. The earlier graft failure of the RA was attributed to spasm and intima hyperplasia [2]. Since the “revival” of the RA as coronary bypass graft, satisfying mid-term and long-term clinical results, in terms of survival rates and fewer cardiac events, have been reported [2,3]. Also, mid-term and long-term angiographical studies showed excellent patency rate of the RA bypass grafts, which are comparable with the patency rate of in situ mammary artery, and better than the patency rate of the mammary artery as free graft [2,3]. To achieve better high run-off condition, the target coronary artery receiving the RA grafts should have high grade stenosis (>70%) or be occluded, and supply viable myocardium in order to minimize the coronary resistance to graft flow and to overcome competitive flow phenomena with the native coronary arteries [2,3]. The RA, as a muscular graft, seems to lose its vascular tone and spasmogenic propensity progressively after its grafting [2]. We fully agree with Al-Sabti and colleagues that little information about both the effects of its harvesting and arm and hand circulation after the removal of the radial artery is available [1]. A justified concern about the risk of serious hand underperfusion, ischemia or neurological disabilities of the operated forearms is still present [1,2,4]. To investigate the long-term clinical consequences and outcome of removal of the RA on perfusion and functional status of the operated forearms, we conducted a clinical follow-up, which enrolled 42 patients who underwent CABG with RA between July 1997 and July 1998 [4]. These patients were submitted eight to nine years later to Doppler testing for assessment of systolic flow velocities, diameter and morphology of the ulnar artery of the operated forearms [4]. Our patient selection for CABG with RA was based on precise clinical criteria and careful preoperative assessment of adequacy of the ulnar collateral circulation [4]. Allen’s test, Doppler study and pulse oximetry were routinely used [4]. Positive (pathologic test) Allen’s test (>10 s), Raynaud’s disease, Dupuytren’s contracture, chronic renal insufficiency, vasculitis and advanced peripheral vascular disease were, in our experience, contraindications for RA harvesting [4]. Our results showed satisfying clinical functional status of the operated forearms [4]. Neither symptoms of ischemia (claudication and pain) nor functional disabilities were claimed [4]. Numbness of the thumb and slight hand tingling were reported [4]. The Doppler studies showed an increase in diameter and systolic flow velocities of the ulnar arteries of the operated forearms [4]. Neither calcifications nor significant increase in intima-media thickness index of the ulnar arteries secondary to the removal of the RA were documented [4]. Chronic compensatory mechanisms develop after the RA removal to readjust the hemodynamics and to offer an adequate blood supply to the operated forearms [4].

We read with great interest the recent report of Ay and colleagues, describing ‘‘the case of a 58-year-old man with single coronary artery anomaly, which stemmed from the left coronary sinus and caused ischemic mitral insufficiency due to left anterior descending artery (LAD) stenosis’’. We would like to make the following remarks in this regard, since whether the revealed severe mitral insufficiency, diagnosed by transthoracic echocardiography, was really caused by coronary ischemia, is in our opinion, still a matter for an open debate. On the contrary, the provided clinical history and symptomatology of this patient and the electrocardiography and echocardiography findings do not evidently support the authors’ presumption that the revealed severe mitral insufficiency was really of ischemic coronary origin. Ischemic mitral insufficiency (IMI) is a common (approximately 20%) complication after myocardial infarction, which follows more frequently an inferior infarction (38%) rather than an anteroseptal one (10%). IMI may be classified into acute and chronic types. Acute IMI occurs as a result of papillary muscle rupture and infarction, complicating acute myocardial infarction, or as a result of acute ischemic episodes involving the left circumflex or right coronary artery, resulting in cardiogenic shock. Chronic IMI should be defined as mitral regurgitation occurring more than 1 week after myocardial infarction with one or more left ventricular segmental wall motion abnormalities, significant coronary disease in the territory supplying the wall motion abnormality, and structurally normal mitral valve leaflets and chordae tendinae. Based on this information relating to either acute or chronic IMI, the clinical data and evidence provided by Ay and colleagues do not, in our opinion, support their assertion that the diagnosed severe mitral insufficiency was really caused by single coronary artery anomaly and left anterior descending artery stenosis. In this regard, Ay and colleagues stated in their report: ‘‘a telecardiogram was normal, and an electrocardiogram showed sinus rhythm with no signs of ischemia. Transthoracic echocardiography revealed severe mitral insufficiency, mild aortic and tricuspid insufficiency, an ejection fraction of 50%, a systolic pulmonary artery pressure of 45mmHg, and a borderline large left ventricle’’. Neither signs of myocardial ischemia nor history of myocardial infarction (acute or more than 1 week), which may be responsible for IMI, were claimed by the authors. Despite the presence of 80% stenosis of the left anterior descending artery, no left ventricular segmental wall motion abnormalities, which may explain the occurrence of IMI, were evidenced by the echocardiography. Furthermore, it was stated that: ‘‘the circumflex artery was normal, extending to the right coronary area after the origin of the posterior descending artery’’, which is further evidence that either acute or chronic myocardial ischemia, which may explain the severe mitral insufficiency, is highly improbable. Therefore, based on all above mentioned considerations, an another potential underlying pathology (degenerative or organic), which might explain the described severe mitral insufficiency in the case reported by Ay and colleagues cannot, in our opinion, be excluded.

We read with interest the article by Bordignon et al .1 presenting a comparative analysis of biomarker release in pulmonary vein isolation with two different cryoballoon generations. We believe, however, that the rationale of the presented data processing in this article is questionable. The authors created a biomarker index by dividing the values of …

Acute pulmonary embolism is a leading cause of death during pregnancy and delivery in the United States. We describe the case of a 25-year-old woman who presented in cardiogenic shock in week 38 of her first pregnancy After the emergent cesarean delivery of a healthy male neonate, the mother underwent immediate surgical pulmonary embolectomy. We confirmed the diagnosis of pulmonary embolism intraoperatively by means of transesophageal echocardiography and removed large clots from the patient's pulmonary arteries. Mother and child were doing well, 27 months later In addition to presenting our patient's case, we discuss the other relevant reports and the options for treating massive pulmonary embolism during pregnancy.

Introduction: Aortic valve stenosis is the most common valvular heart disease in developed countries. Transcatheter aortic valve implantation (TAVI) is a novel procedure which provides a promising treatment option for patients with high perioperative risks. TAVI is not free from complications. Strokes, paravalvular leaks, atrio-ventricular block and prosthetic endocarditis were reported.

To the Editor: We read with interest the story from Dr. Medins1 about his volunteer medical work during the 1970s in Africa. He described his emergent removal of shrapnel from the bifurcation of a patient's pulmonary artery (PA) “via the old-fashioned Trendelenburg procedure…. The aorta was clamped, the pulmonary artery incised at its bifurcation, the shrapnel removed, and the pulmonary artery closed—all in 5 minutes. The patient survived.”1 This accomplishment by Dr. Medins—without benefit of hypothermia or a heart-lung machine—is laudable indeed. However, in the original account by Trendelenburg,2 he did not report clamping the aorta when removing thromboembolic clots from his patients with massive pulmonary embolism. Instead of cross-clamping the main PA, he looped a rubber tube behind the aorta and the main PA through the transverse sinus, compressing the pulmonary conus from behind to reveal the clots and optimize their removal.2 From what we could determine, neither the aorta nor the main PA was clamped during any old-fashioned Trendelenburg procedure (TP) reported from 1908 through 1957.2–6 The description by Dr. Medins might influence some to believe that the original TP was a valuable or practicable operation. In actuality, when the TP was used to treat pulmonary embolism, the outcomes were usually fatal.2–6 Trendelenburg's own patients did not survive the procedure.2,6 Thereafter, 20 more unsuccessful attempts were reported.6 In March 1924, Kirschner (Trendelenburg's pupil) reported the first successful outcome.7 During the next decade, only 3 more successes were documented, all in Europe.6 In 1934, Edward Churchill noted the dampened enthusiasm for the TP at his hospital after 10 consecutive failures.3 Through 1957, approximately 300 total procedures yielded a dozen survivors at most.4–6 Despite Trendelenburg's intent, the procedure was hazardous, technically difficult, and perhaps performed too late—the patients were often in advanced cardiogenic shock or dying states. The challenge was to balance their precarious clinical course with the timing of the operation.3 Churchill endorsed postponing the TP until the patient was nearing death but cautioned that unnecessary delay would decrease the chance of success: “At times … the procedure could perhaps be more properly termed an immediate postmortem examination than a surgical operation.”3 In this regard, the TP cannot compare with modern open surgical pulmonary embolectomy. Giovanni Saeed, MD Department of Cardiovascular Surgery Rainer Gradaus, MD, PhD Jorg Neuzner, MD, PhD Department of Internal Medicine II and Cardiology, Klinikum Kassel GmbH, Kassel, Germany

To the Editor: We read with interest the story from Dr. Medins1 about his volunteer medical work during the 1970s in Africa. He described his emergent removal of shrapnel from the bifurcation of a patient's pulmonary artery (PA) “via the old-fashioned Trendelenburg procedure…. The aorta was clamped, the pulmonary artery incised at its bifurcation, the shrapnel removed, and the pulmonary artery closed—all in 5 minutes. The patient survived.”1 This accomplishment by Dr. Medins—without benefit of hypothermia or a heart-lung machine—is laudable indeed. However, in the original account by Trendelenburg,2 he did not report clamping the aorta when removing thromboembolic clots from his patients with massive pulmonary embolism. Instead of cross-clamping the main PA, he looped a rubber tube behind the aorta and the main PA through the transverse sinus, compressing the pulmonary conus from behind to reveal the clots and optimize their removal.2 From what we could determine, neither the aorta nor the main PA was clamped during any old-fashioned Trendelenburg procedure (TP) reported from 1908 through 1957.2–6 The description by Dr. Medins might influence some to believe that the original TP was a valuable or practicable operation. In actuality, when the TP was used to treat pulmonary embolism, the outcomes were usually fatal.2–6 Trendelenburg's own patients did not survive the procedure.2,6 Thereafter, 20 more unsuccessful attempts were reported.6 In March 1924, Kirschner (Trendelenburg's pupil) reported the first successful outcome.7 During the next decade, only 3 more successes were documented, all in Europe.6 In 1934, Edward Churchill noted the dampened enthusiasm for the TP at his hospital after 10 consecutive failures.3 Through 1957, approximately 300 total procedures yielded a dozen survivors at most.4–6 Despite Trendelenburg's intent, the procedure was hazardous, technically difficult, and perhaps performed too late—the patients were often in advanced cardiogenic shock or dying states. The challenge was to balance their precarious clinical course with the timing of the operation.3 Churchill endorsed postponing the TP until the patient was nearing death but cautioned that unnecessary delay would decrease the chance of success: “At times … the procedure could perhaps be more properly termed an immediate postmortem examination than a surgical operation.”3 In this regard, the TP cannot compare with modern open surgical pulmonary embolectomy. Giovanni Saeed, MD Department of Cardiovascular Surgery Rainer Gradaus, MD, PhD Jorg Neuzner, MD, PhD Department of Internal Medicine II and Cardiology, Klinikum Kassel GmbH, Kassel, Germany

with the provided high quality images, describ-ing the case of a 39-year-old man who was, as stated bythe authors, ‘‘referred with a diagnosis of double aorticarch’’ (DAA). The title of the report: ‘‘Right-sidedaortic arch with Kommerell’s diverticulum causing tra-cheal stenosis’’ is, in our opinion, somewhat misleadingbecause the report and the provided images describe thecase of a patient not with a ‘‘right-sided aortic arch withKommerell’s diverticulum’’, but rather a patient withdouble aortic arch (DAA).

We thank Dr. Girerd and his coauthors for their interesting contribution on this important topic. As pointed out by many recent studies, the coexistence of chronic kidney disease and chronic heart failure (HF) is associated with increased morbidity and mortality [ 1 Khan N.A. Ma I. Thompson C.R. et al. Kidney function and mortality among patients with left ventricular systolic dysfunction. J Am Soc Nephrol. 2006; 17: 244-253 Crossref PubMed Scopus (114) Google Scholar , 2 McAlister F.A. Ezekowitz J. Tonelli M. Armstrong P.W. Renal insufficiency and heart failure: prognostic and therapeutic implications from a prospective cohort study. Circulation. 2004; 109: 1004-1009 Crossref PubMed Scopus (614) Google Scholar ]. In such patients, different potentially interrelated factors may contribute to an adverse outcome, including neurohumoral activation, inflammation, dysbalance between nitric oxide and reactive oxygen species or activation of the renin angiotensin system [ [3] Bongartz L.G. Cramer M.J. Doevendans P.A. Joles J.A. Braam B. The severe cardiorenal syndrome: ʻGuyton revisited'. Eur Heart J. 2005; 26: 11-17 Crossref PubMed Scopus (376) Google Scholar ]. However, not only the increased mortality rate, but also the mode of death is of particular interest in subjects with the so-called “cardiorenal syndrome”. In patients with moderate to severe chronic HF, there is accumulating evidence, that around 50% of patients die suddenly, whereas the other 50% die due to worsening HF. Interestingly, patients with cardiorenal syndrome show an increased rate of sudden cardiac death [ [4] McCullough P.A. Sandberg K.R. Chronic kidney disease and sudden death: strategies for prevention. Blood Purif. 2004; 22: 136-142 Crossref PubMed Scopus (43) Google Scholar ] as well as a higher prevalence of structural abnormalities such as left ventricular (LV) hypertrophy, concentric remodelling and diastolic dysfunction [ 5 Stewart G.A. Gansevoort R.T. Mark P.B. et al. Electrocardiographic abnormalities and uremic cardiomyopathy. Kidney Int. 2005; 67: 217-226 Abstract Full Text Full Text PDF PubMed Scopus (168) Google Scholar , 6 Bruch C. Rothenburger M. Gotzmann M. et al. Chronic kidney disease in patients with chronic heart failure-impact on intracardiac conduction, diastolic function and prognosis. Int J Cardiol. 2007; 118: 375-380 Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar ], all of which may precipitate deterioration of HF. Unfortunately, only few studies have addressed the potential link between structural abnormalities and sudden cardiac death [ [4] McCullough P.A. Sandberg K.R. Chronic kidney disease and sudden death: strategies for prevention. Blood Purif. 2004; 22: 136-142 Crossref PubMed Scopus (43) Google Scholar ]. In addition, little is known about a potential “triggering” effect of other comorbidities observed in patients with combined cardiac and renal dysfunction.