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AimsSodium–glucose co-transporter 2 inhibition reduces the risk of hospitalization for heart failure and for death in patients with symptomatic heart failure. However, trials investigating the effects of this drug class in patients following acute myocardial infarction are lacking.Methods and resultsIn this academic, multicentre, double-blind trial, patients (n = 476) with acute myocardial infarction accompanied by a large creatine kinase elevation (>800 IU/L) were randomly assigned to empagliflozin 10 mg or matching placebo once daily within 72 h of percutaneous coronary intervention. The primary outcome was the N-terminal pro-hormone of brain natriuretic peptide (NT-proBNP) change over 26 weeks. Secondary outcomes included changes in echocardiographic parameters. Baseline median (interquartile range) NT-proBNP was 1294 (757–2246) pg/mL. NT-proBNP reduction was significantly greater in the empagliflozin group, compared with placebo, being 15% lower [95% confidence interval (CI) −4.4% to −23.6%] after adjusting for baseline NT-proBNP, sex, and diabetes status (P = 0.026). Absolute left-ventricular ejection fraction improvement was significantly greater (1.5%, 95% CI 0.2–2.9%, P = 0.029), mean E/e′ reduction was 6.8% (95% CI 1.3–11.3%, P = 0.015) greater, and left-ventricular end-systolic and end-diastolic volumes were lower by 7.5 mL (95% CI 3.4–11.5 mL, P = 0.0003) and 9.7 mL (95% CI 3.7–15.7 mL, P = 0.0015), respectively, in the empagliflozin group, compared with placebo. Seven patients were hospitalized for heart failure (three in the empagliflozin group). Other predefined serious adverse events were rare and did not differ significantly between groups.ConclusionIn patients with a recent myocardial infarction, empagliflozin was associated with a significantly greater NT-proBNP reduction over 26 weeks, accompanied by a significant improvement in echocardiographic functional and structural parameters.ClinicalTrials.gov registration NCT03087773.

In a previously healthy asymptomatic 18-year old male, Wolff-Parkinson-White syndrome (WPW) with left ventricular hypertrabeculation/noncompaction (LVHT) and systolic dysfunction was detected. Holter monitoring disclosed multiple long episodes of supraventricular tachycardia with a heart rate of about 110/min. After radiofrequency ablation of an epicardial posteroseptal accessory pathway with ante- and retrograde conduction, systolic function gradually normalized without any pharmacotherapy. After 32 months of follow-up, the patient remains asymptomatic with normal systolic function. WPW-induced tachycardiomyopathy may even occur in asymptomatic patients, who are so adapted to their arrhythmias that they do not recognize them. Learning objective: Tachycardiomyopathy in Wolff-Parkinson-White syndrome may even occur in asymptomatic patients. They seem so adapted to their tachyarrhythmia that they do not recognize them. Radiofrequency ablation of the accessory pathway may lead to complete normalization of systolic function. If left ventricular hypertrabeculation/noncompaction in the presented patient is causal or a coincidence remains unknown. Genetic testing revealed no variants. Because of left ventricular hypertrabeculation/noncompaction cardiologic follow-up is indicated.

BACKGROUND: Randomised controlled trials have shown diverse results for radial access in patients undergoing primary percutaneous coronary intervention (PPCI). Moreover, it is questionable whether radial access improves outcome in patients with cardiogenic shock undergoing PPCI. We aimed to investigate the outcome according to access site in patients with or without cardiogenic shock, in daily clinical practice. METHODS: For the present analysis we included 9,980 patients undergoing PPCI between 2012 and 2018, registered in the multi-centre, nationwide registry on PCI for myocardial infarction (MI). In-hospital mortality, major adverse cardiovascular events (MACE), and net adverse clinical events (NACE) until discharge were compared between 4,498 patients with radial (45%) and 5,482 patients with femoral (55%) access. RESULTS: Radial compared to femoral access was associated with lower in-hospital mortality (3.5% vs. 7.7%; P

Using bone‐avid radiotracers, cardiac transthyretin (TTR) amyloidosis can be diagnosed by scintigraphy, thus obviating endomyocardial biopsy. Radiotracer accumulation, however, may also be due to other causes. A 68‐year‐old male with acute myocardial infarction underwent recanalization of the left anterior descending coronary artery (LAD). Postinterventionally, transthoracic echocardiography showed hypokinesia of the septum and anterior wall and a thickened myocardium with granular sparkling appearance. Cardiac amyloidosis was suspected. A 99mTc‐3,3‐diphosphono‐1,2‐propanodicarboxylic acid whole‐body scan 4 days after LAD recanalization showed Perugini 2 myocardial tracer uptake. Monoclonal gammopathy was excluded, and cardiac TTR amyloidosis was diagnosed. Three months later, 99m‐Tc‐hydroxydiphosphate scan showed no myocardial tracer uptake. Cardiac magnetic resonance imaging revealed late gadolinium enhancement within the LAD supply area. No mutation of the TTR gene was found. Suspicion of amyloidosis should consider not only echocardiography but also history and clinical findings. Myocardial oedema due to reperfusion should be acknowledged as a differential diagnosis for cardiac uptake of bone‐avid radiotracers.

Introduction: Left ventricular (LV)-thrombi occur in up to 14% of patients with acute myocardial infarction (AMI) in the era of primary percutaneous coronary intervention. For these patients, anticoagulant therapy (AC) is recommended by AMI-guidelines. When, despite AC, LV-thrombi lead to embolism, surgical thrombectomy is an option, which is not mentioned or not recommended in AMI-guidelines. Case Presentation: We report a 46-year old female patient with AMI. An 80% stenosis of the proximal left anterior descending coronary artery was treated by a drug-eluting stent. Thrombi within the akinetic LV-apex became mobile despite AC and dual antiplatelet therapy, and a cerebellar stroke occurred. By a transmitral surgical approach with endoscopic assistance the thrombi were completely removed. Postoperative course and 12-months follow-up were uneventful. Conclusions: LV-thrombi should be observed carefully regarding changes in morphology. Surgical thrombectomy of LV-thrombi is a rare treatment option to prevent imminent embolism. Benefits versus risks of surgical removal of LV-thrombi need to be carefully weighted.

Background Prasugrel and ticagrelor have similar recommendations in the setting of primary PCI by current guidelines. Data comparing both in daily clinical practice of primary PCI for ST-elevation myocardial infarction is limited. Purpose To compare the effect of prasugrel and ticagrelor on in-hospital outcomes after primary PCI. Methods and results We prospectively enrolled 5365 patients treated with prasugrel (n=2785, 51.9%) or ticagrelor (n=2580; 48.1%) in the setting of primary PCI from January 2011 to December 2018 in a nationwide registry. In-hospital outcomes were compared and multiple logistic regression analysis was performed. Prasugrel treated patients were younger, less often in cardiogenic shock, with lower rates of previous stroke and had shorter ischemic time. Both groups showed similar rates of previous MI, diabetes and current resuscitation. In the univariate analysis mortality was lower in patients with prasugrel (2.5% vs. 4.4% p After adjustment in multivariable analysis mortality (0.99 95% CI 0.57 to 1.72), MACE (OR 0.99 95% CI 0.65 to 1.52) as well as NACE (0.86 95% CI 0.61 to 1.22) did not differ in patients treated with prasugrel compared to ticagrelor. Conclusion Patients treated with prasugrel showed improved outcomes compared to ticagrelor in a large cohort of primary PCI. However, after adjustment for confounders the Advantage of prasugrel in primary PCI did not persist. Funding Acknowledgement Type of funding source: Other. Main funding source(s): Austrian Society of Cardiology

Background The prognosis of patients with left ventricular hypertrabeculation/noncompaction (LVHT) is controversially assessed. LVHT is frequently associated with neuromuscular disorders (NMDs). Aim of the study was to assess cardiac and neurological findings as predictors of mortality in LVHT-patients. Methods Included were patients with LVHT diagnosed between June 1995 and December 2019 in one echocardiographic laboratory. They underwent a baseline cardiologic examination and were invited for a neurological investigation. In January 2020, their survival status was assessed. Results LVHT was diagnosed in 310 patients (93 female, aged 53±18 years) with a prevalence of 0.4%/year. A neurologic investigation was performed in 205 patients (67%). A specific NMD was found in 33 of the investigated patients (16%), NMDs of unknown etiology in 123 (60%) and the neurological investigation was normal in 49 (24%) patients. During 86 months of follow-up, 59 patients received implanted electronic devices (cardioverter/defibrillator n=21, antibradycardic pacemakers n=11, cardiac resynchronization device/defibrillator n=22, cardiac resynchronization device n=4). During follow-up 105 patients died and 6 patients underwent heart transplantation. The mortality was 4.7%/year. By multivariate analysis, the following baseline parameters were identified as predictors of mortality: increased age (p=0.0005), inpatient-status when LVHT was diagnosed (p=0.0050), presence of a specific NMD (p=0.0187) or NMD of unknown etiology (p=0.0052), atrial fibrillation (p=0.0007) and left bundle branch block (p=0.0168). Conclusions LVHT patients should be systematically investigated neurologically since neurological comorbidity has a prognostic impact. Electrocardiographic abnormalities like atrial fibrillation and left bundle branch block should be considered when planning pharmacotherapy and device-therapy. It has to be assessed by prospective studies, which measures improve the prognosis of LVHT. Funding Acknowledgement Type of funding source: None

The prognosis of patients with left ventricular hypertrabeculation/noncompaction (LVHT) is assessed controversially. LVHT is associated with other cardiac abnormalities and with neuromuscular disorders (NMD). Aim of the study was to assess cardiac and neurological findings as predictors of mortality rate in adult LVHT-patients. Included were patients with LVHT diagnosed between 1995 and 2019 in 1 echocardiographic laboratory. Patients underwent a baseline cardiologic examination and were invited for a neurological investigation. In January 2020, their survival status was assessed. End points were death or heart transplantation. LVHT was diagnosed by echocardiography in 310 patients (93 female, aged 53 ± 18 years) with a prevalence of 0.4%/year. A neurologic investigation was performed in 205 patients (67%). A specific NMD was found in 33 (16%), NMD of unknown etiology in 123 (60%) and the neurological investigation was normal in 49 (24%) patients. During follow-up of 84 ± 71 months, 59 patients received electronic devices, 105 patients died, and 6 underwent heart transplantation. The mortality was 4.7%/year, the rate of heart transplantation/death 5%/year. By multivariate analysis, the following parameters were identified to elevate the risk of mortality/heart transplantation: increased age (p = 0.005), inpatient (p = 0.001), presence of a specific NMD (p = 0.0312) or NMD of unknown etiology (p = 0.0365), atrial fibrillation (p = 0.0000), ventricular premature complexes (p = 0.0053), exertional dyspnea (p = 0.0023), left bundle branch block (p = 0.0201), and LVHT of the posterior wall (p = 0.0158). In conclusion, LVHT patients should be systematically investigated neurologically since neurological co-morbidity has a prognostic impact.

Left ventricular hypertrabeculation/noncompaction is a myocardial abnormality of unknown etiology/pathogenesis, which is frequently associated with neuromuscular disorders or chromosomal defects. LVHT in association with a MYOT mutation has not been reported. The patient is a 72-year-old male with a history of strabismus in childhood, asymptomatic creatine-kinase elevation since age 42 years, slowly progressive lower limb weakness since age 60 years, slowly progressive dysarthria and dysphagia since age 62 years, and recurrent episodes of arthralgias and myalgias since age 71 years. He also had arterial hypertension, diverticulosis, hyperlipidemia, coronary heart disease, and a hiatal hernia with reflux esophagitis. Clinical exam revealed mild quadruparesis and proximal wasting of the legs. Whole exome sequencing revealed a known variant in the MYOT gene. Muscle biopsy, previously assessed as inclusion body myopathy, was compatible with the genotype after revision. Cardiologic work-up revealed a left anterior hemiblock, mild myocardial thickening, and noncompaction. This case shows that myotilinopathy may manifest as a multisystem disease, including noncompaction.

A 42-year-old woman with a past medical history of i.v. drug abuse and endocarditis presented in our emergency department with severe and persisting chest pain. Cardiac markers were elevated (hsTrop T 1.210 µg/L; CK 800 U/L; CK-MB 100 U/L) and ECG revealed descending ST-segment depression in lead I and aVL with negative T waves and horizontal ST-segment depression in lead V4–V6. Inflammatory parameters were negative. Three months before, the patient was referred to our institution because of antibiotic-resistant fever, chills, elevated inflammatory parameters, and splenomegaly. Following microbiological analysis, Staphylococcus aureus was verified and transoesophageal echocardiography (TEE) demonstrated aorto-ventricular disconnection caused by a circumferential partly thrombosed aortic annulus abscess ( Panel A ). Surgery was performed, replacing …

Randomized controlled trials have shown conflicting results regarding the outcome of bivalirudin in primary percutaneous coronary intervention (PPCI). The aim of this study was to evaluate the in-hospital outcomes of patients receiving heparin or bivalirudin in a real-world setting of PPCI: 7,023 consecutive patients enrolled in the Austrian Acute PCI Registry were included between January 2010 and December 2014. Patients were classified according to the peri-interventional anticoagulation regimen receiving heparin (n = 6430) or bivalirudin (n = 593) with or without GpIIb/IIIa inhibitors (GPIs). In-hospital mortality (odds ratio [OR] 1.13, 95% confidence interval [CI] 0.57 to 2.25, p = 0.72), major adverse cardiovascular events (OR 1.18, 95% CI 0.65 to 2.14, p = 0.59), net adverse clinical events (OR 1.01, 95% CI 0.57 to 1.77, p = 0.99), and TIMI non–coronary artery bypass graft-related major bleeding (OR 0.41, 95% CI 0.09 to 1.86, p = 0.25) were not significantly different between the groups. However, we detected potential effect modifications of anticoagulants on mortality by GPIs (OR 0.12, 95% CI 0.01 to 1.07, p = 0.06) and access site (OR 0.25, 95% CI 0.06 to 1.03, p = 0.06) favoring bivalirudin in femoral access. In conclusion, this large real-world cohort of PPCI, heparin-based anticoagulation showed similar results of short-term mortality compared with bivalirudin. We observed a potential effect modification by additional GPI use and access favoring bivalirudin over heparin in femoral, but not radial, access.

Background Reversible left ventricular dysfunction, also termed Takotsubo cardiomyopathy, is rarely reported in Addison’s disease after initiation of hormone replacement therapy. The pathogenesis of this cardiomyopathy is unknown. Case presentation A 41-year-old white woman with a history of autoimmune Hashimoto thyroiditis diagnosed 3 years earlier and acute adrenal insufficiency diagnosed 3 weeks earlier presented with new onset of heart failure New York Heart Association class IV, which had started shortly after initiation of hormone replacement therapy with hydrocortisone 20 mg/day and fludrocortisone 0.3 mg/day. Nine days before admission she had collapsed because of dizziness and had a cerebral concussion and open fracture of her nasal bone, however, no further investigations were carried out at that time. A physical examination revealed leg edema, tachycardia, tachypnea, bilateral basal crepitations, and blood pressure 110/70 mmHg. An electrocardiogram showed sinus tachycardia, low voltage, negative T-waves in V5 and V6 and a corrected QT interval of 590 ms. Echocardiography revealed a reduced left ventricular systolic function with an ejection fraction of 30 %, and septal, apical, and anterior wall akinesia. Cardiac magnetic resonance imaging showed relative enhancement of gadolinium, indicating hyperemia and capillary leakage, and no myocardial scars. Because of the improvement in her cardiac function, lack of cardiovascular risk factors, and lack of signs for ischemia on magnetic resonance imaging, no coronary angiography was carried out. The results of sellar and renal magnetic resonance imaging were normal. Her troponin T was slightly elevated. Bisoprolol and ramipril were started. Her fludrocortisone dose was reduced to 0.05 mg/day. Her electrocardiogram and systolic function, documented by echocardiography and magnetic resonance imaging, normalized within 6 months. Conclusions Although we could not exclude coronary artery disease by coronary angiography, her clinical course and instrumental findings suggest Takotsubo cardiomyopathy of the apical type. Fludrocortisone overdosage and increased myocardial vulnerability due to cortisol deficiency might be pathogenetic factors, whereas myocarditis is unlikely. When hormone replacement in patients with Addison’s disease is initiated, cardiac function should be monitored by electrocardiogram and echocardiography.

Objective The interplay between oxidative stress and inflammation is crucial in the pathogenesis of atherosclerosis. The adaptor protein p66Shc is implicated in atherogenesis and oxidative stress related responses in animal models of diseases. However, its role in humans remains to be defined. In this study, we hypothesized that expression of p66Shc increases in peripheral blood monocytes of patients affected by acute coronary syndromes (ACS). Methods Male subjects aged 59 ± 4 (mean ± SD) years admitted for cardiac catheterization were subdivided in three groups: (a) no local stenosis for the control group, (b) at least one stenosis ≥75% in either left, circumflex or right coronary artery for the coronary artery disease (CAD) group or (c) ST-elevation/non-ST-elevation myocardial infarction for the ACS group. Monocytes were isolated from whole blood and p66Shc RNA levels were determined by quantitative real time PCR. Results p66Shc RNA levels were increased in ACS patients as compared to CAD (p = 0.007) and controls (p = 0.0249). Furthermore, malondialdehyde (MDA) and C-reactive protein (CRP) were increased in plasma of ACS patients. Levels of MDA correlated positively to p66Shc (r = 0.376, p = 0.01). Our data demonstrate increased p66Shc levels in monocytes of ACS but not CAD patients. Conclusion This study suggests an involvement of p66Shc in the transition of a stable CAD to an ACS patient. p66Shc was associated with states of increased oxidative stress. Further work is needed to understand whether p66Shc may represent a possible pharmacological target or whether it represents an interesting novel biomarker.

Congestive heart failure developing after acute myocardial infarction (AMI) is a major cause of morbidity and mortality. Clinical trials of cell-based therapy after AMI evidenced only a moderate benefit. We could show previously that suspensions of apoptotic peripheral blood mononuclear cells (PBMC) are able to reduce myocardial damage in a rat model of AMI. Here we experimentally examined the biochemical mechanisms involved in preventing ventricular remodelling and preserving cardiac function after AMI. Cell suspensions of apoptotic cells were injected intravenously or intramyocardially after experimental AMI induced by coronary artery ligation in rats. Administration of cell culture medium or viable PBMC served as controls. Immunohistological analysis was performed to analyse the cellular infiltrate in the ischaemic myocardium. Cardiac function was quantified by echocardiography. Planimetry of the infarcted hearts showed a significant reduction of infarction size and an improvement of post AMI remodelling in rats treated with suspensions of apoptotic PBMC (injected either intravenously or intramoycardially). Moreover, these hearts evidenced enhanced homing of macrophages and cells staining positive for c-kit, FLK-1, IGF-I and FGF-2 as compared to controls. A major finding in this study further was that the ratio of elastic and collagenous fibres within the scar tissue was altered in a favourable fashion in rats injected with apoptotic cells. Intravenous or intramyocardial injection of apoptotic cell suspensions results in attenuation of myocardial remodelling after experimental AMI, preserves left ventricular function, increases homing of regenerative cells and alters the composition of cardiac scar tissue. The higher expression of elastic fibres provides passive energy to the cardiac scar tissue and results in prevention of ventricular remodelling. Electronic supplementary material The online version of this article (doi:10.1007/s00395-011-0173-0) contains supplementary material, which is available to authorized users.

Multivessel coronary artery disease (MVCAD) is common in patients with ST-elevation myocardial infarction (STEMI), thereby negatively affecting mortality and outcome. Currently there is increasing evidence that complete revascularisation should be considered in haemodynamically stable patients. There are few larger randomised controlled trials available showing a lower risk of major adverse cardiac events after complete revascularisation, mainly driven by a reduction of repeat revascularisation. However, these trials are not adequately powered to show a mortality benefit or reduced risk of myocardial infarction. As there are several possible strategies, the presence of MVCAD often poses a therapeutic dilemma for interventional cardiologists and there is still ongoing debate on when and how to perform complete revascularisation. Pending further trials that may clarify which strategy is best, an individualised approach should be adopted.

Atrial fibrillation (AF) is by far the most frequent heart rhythm disorder and is associated with a significantly increased risk of stroke, heart failure and death. Despite improvements in prevention and treatment, the prognosis has not changed significantly. To use new and promising pharmacological and interventional concepts for thromboembolic prophylaxis and treatment of AF, as well as prevention of recurrence, patient compliance has to be improved, physicians have to be trained and experience hast to be gained. A consistently carried 'anticoagulation pass' might be a promising piece of the puzzle.

Background This study aimed at understanding whether investigators from less wealthy countries were at a disadvantage in disseminating their research, after accounting for potential differences in research quality and infrastructure. Methods and Results In this bibliometric analysis a representative random selection of 10% (n=1002 studies) of all abstracts submitted to the European Society of Cardiology (ESC) congress 2006 was followed for publication and citation from September 2006 to December 2011. The main variable of interest was the per-capita gross domestic product (GDP) of the country of the principal investigator. Using multivariable models that adjusted for socioeconomic indicators and previously identified markers of research quality, we examined the relationship between per-capita GDP and three study endpoints: Acceptance at the ESC congress, full-text publication, and number of two-year citations. Among 1002 abstracts from 63 countries, per-capita GDP was positively correlated with all three study endpoints. After adjusting for markers of research quality and infrastructure, per-capita GDP remained a strong predictor for acceptance at the ESC congress (adjusted OR for every 10,000 USD increase in per-capita GDP, 1.44; 95% CI, 1.15 to 1.80), full-text publication within 5years (adjusted OR, 1.49; 95% CI, 1.17 to 1.90), and high citation frequency (adjusted OR, 2.30; 95% CI, 1.31 to 4.04). These findings were largely consistent in a subgroup of abstracts of high-quality, prospective clinical trials. Conclusion Investigators in less wealthy countries face challenges to disseminate their research, even after accounting for potential differences in the quality of their work and research infrastructure.

Background Inflammation plays a key role in atherosclerosis. Sirt1 regulates transcription factors involved in inflammatory processes and blunts atherosclerosis in mice. However, its role in humans remains to be defined. This study was therefore designed to investigate the role of Sirt1 in the development of atherosclerosis. Methods and Results 48 male subjects admitted for cardiac catheterization were subdivided into healthy subjects, patients with stable coronary artery disease (CAD), and with acute coronary syndromes (ACS). Monocytes were isolated and Sirt1 mRNA levels were determined. Sirt1 gene expression was higher in healthy subjects as compared to patients with CAD or ACS (P

Aims Through a 4-year follow-up of the abstracts submitted to the European Society of Cardiology Congress in 2006, we aimed at identifying factors predicting high-quality research, appraising the quality of the peer review and editorial processes, and thereby revealing potential ways to improve future research, peer review, and editorial work. Methods and results All abstracts submitted in 2006 were assessed for acceptance, presentation format, and average reviewer rating. Accepted and rejected studies were followed for 4 years. Multivariate regression analyses of a representative selection of 10% of all abstracts ( n = 1002) were performed to identify factors predicting acceptance, subsequent publication, and citation. A total of 10 020 abstracts were submitted, 3104 (31%) were accepted for poster, and 701 (7%) for oral presentation. At Congress level, basic research, a patient number ≥ 100, and prospective study design were identified as independent predictors of acceptance. These factors differed from those predicting full-text publication, which included academic affiliation. The single parameter predicting frequent citation was study design with randomized controlled trials reaching the highest citation rates. The publication rate of accepted studies was 38%, whereas only 24% of rejected studies were published. Among published studies, those accepted at the Congress received higher citation rates than rejected ones. Conclusions Research of high quality was determined by study design and largely identified at Congress level through blinded peer review. The scientometric follow-up revealed a marked disparity between predictors of full-text publication and those predicting citation or acceptance at the Congress.

Cardiovascular disease (CVD) accounts for more than 4.3 million deaths in Europe representing 48% of all deaths (British Heart Foundation. European Cardiovascular Disease Statistics 2008) and is predicted to be the number one killer by 2020 in our ageing societies facing major societal and economic changes around the globe [1]. The clinical manifestations of CVD are diverse and comprise myocardial infarction, stroke, aortic aneurysms, renal artery stenosis and gangrene (Fig. 3.1). In Europe, the single most common cause of death is coronary artery disease (CAD; 21% of men and 21% of women) followed by stroke (11% of men and 17% of women) and the remaining manifestations of CVD (11% of men and 15% of women) (British Heart Foundation. European Cardiovascular Disease Statistics 2008). Despite major reductions in mortality obtained in the setting of acute myocardial infarction [2], morbidity due to CVD remains of eminent importance across the world as quantified with the Disability Adjusted Life Years (DALY) as an aggregate of years of life lost to due to premature death and years of healthy life lost to disability (British Heart Foundation. European Cardiovascular Disease Statistics 2008). Currently, 70% of clinical events cannot be prevented with available drug therapy including statins [3] and at least 10% of coronary events occur in apparently healthy individuals in the absence of major traditional risk factors [4].

[Figure][1] A 52-year-old woman was admitted to our hospital with a 2-day history of nausea and dizziness and a subsequent pre-syncope. Because of a known bipolar disorder, an emergency psychiatric evaluation was performed and an attempted suicide as suggested by relatives was considered

Objectives We wanted to test whether there is a difference between the total number and duration of malfunctions and a correlation between the oxygen saturation and pulse rate values of two new generation pulse oximeters (Masimo 'Radical 7' and Nellcor 'N 600') during emergency ambulance transportation. Methods Patients were monitored with two pulse oximeters ('Radical 7' and 'N 600') on different randomly selected fingers of the same hand during transportation. Data of both devices were recorded continuously by a laptop computer. Results Fifty-two patients with signs of peripheral vasoconstriction (including 22 patients with a blood pressure ≤100/60) were included. There were 0.21 ± 0.72 (0-4) malfunctions per patient lasting for a mean 113.55 ± 272.55 s in the 'Radical 7' and 0.13 ± 0.49 (0-3) malfunctions per patient with a mean duration of 301.0 ± 426.58 s in the 'N 600'. Oxygen saturation and pulse rate values correlated significantly [r² = 0.9608 (SpO₂), r² = 0.9608 (pulse rate)] between the devices and showed a bias of -0.177770 (SpO₂) and 0.310883 (pulse rate) with a standard deviation of 1.68367 (SpO₂) and 4.46532 (pulse rate) in a Bland-Altman test. Conclusion Although number and duration of malfunctions did not differ significantly between the devices, they showed a very low number of malfunctions even in hypotensive patients with peripheral vasoconstriction. Oxygen saturation correlated significantly in the two devices investigated at 49.409 time points. In addition, pulse rate also correlated significantly.