European Heart Journal: Acute Cardiovascular Care

Cardiac arrest (CA) is still associated with high mortality and morbidity. Data on the changes in management and outcomes over a long period of time are limited. Using data from a single emergency department (ED), we assessed changes over two decades.

In this single-center observational study, we prospectively included 4133 patients receiving cardiopulmonary resuscitation and being admitted to the ED of a tertiary care hospital between January 1992 and December 2012.

There was a significant improvement in both 6-month survival rates (+10.8%; p < 0.001) and favorable neurological outcome (+4.7%; p < 0.001). While the number of witnessed CA cases decreased (-4.7%; p < 0.001) the proportion of patients receiving bystander basic life support increased (+8.3%; p < 0.001). The proportion of patients with initially shockable ECG rhythms remained unchanged, but cardiovascular causes of CA decreased (-9.6%; p < 0.001). Interestingly, the time from CA until ED admission increased (+0.1 hours; p = 0.024). The use of percutaneous coronary intervention and therapeutic hypothermia were significantly associated with survival.

Outcomes of patients with CA treated at a specialized ED have improved significantly within the last 20 years. Improvements in every link in the chain of survival were noted.

Extracorporeal life support (ECLS) has shown encouraging survival rates in patients with in-hospital cardiac arrest; however, its routine use is still controversial. We compared the survival of patients with in-hospital cardiac arrest receiving conventional cardiopulmonary resuscitation (CCPR) to that of patients with ECLS as an adjunct to cardiopulmonary resuscitation (ECPR).

A total of 353 patients with in-hospital cardiac arrest (272 CCPR and 52 ECPR) were included in this retrospective, propensity score-adjusted (1:1 matched), single-centre study. Primary endpoints were survival at 30 days, long-term survival and neurological outcome defined by the cerebral performance categories score.

In the unmatched groups patients undergoing ECPR initially had significantly higher APACHE II scores (P=0.03), increased norepinephrine dosages (P=0.03) and elevated levels of creatine kinase (P<0.0001), creatinine (P=0.04) and lactate (P=0.02) before cardiopulmonary resuscitation compared with those undergoing CCPR. After equalising these parameters significant differences were observed in short and long-term survival, favouring ECPR over CCPR (27% vs. 17%; P=0.01 (short-term) and 23.1% vs. 11.5%; P=0.008 (long-term); median follow-up duration after discharge 1136 days (interquartile range 823–1416)). There was no significant difference in the incidence of a cerebral performance categories score of 1 or 2 between the matched groups (CCPR 66.7% vs. ECPR 83.3%; P=0.77). ECLS implantation was the only significant and independent predictor of mortality in multivariate Cox regression analysis (hazard ratio 0.57, 95% confidence interval 0.35–0.90; P=0.02).

In our cohort of cardiovascular patients ECPR was associated with better short- and long-term survival over CCPR, with a good neurological outcome in the majority of the patients with refractory in-hospital cardiac arrest.

In previous guidelines, intra-aortic balloon pump (IABP) use was strongly recommended in the treatment of cardiogenic shock in the context of acute myocardial infarction. The recent IABP-SHOCK II trial demonstrated no benefit in short- and medium-term mortality with the use of IABP. It was our objective to evaluate in a real life nationwide population of patients with acute myocardial infarction the impact of IABP in short- and medium-term mortality.

We included patients admitted with acute myocardial infarction in Killip class IV in the first 24 hours, all submitted to urgent coronary angiography. Our study objective was the occurrence of hospital and six-month all-cause mortality.

From the 33,300 patients included in the registry, 4.2% presented with Killip class IV in the first 24 hours and 646 (43.6%) were submitted to urgent coronary angiography. IABP was implanted in 19.8% of these patients. The IABP group was younger, had higher admission heart rate, more multivessel disease and more left main disease. There were 260 hospital deaths (40.2%), similar between groups (46.1% vs. 38.8%, p=0.132). IABP use was associated with a deleterious effect in patients with previous MI and beneficial effect in patients with mechanical complications. IABP use had a neutral effect on mortality (hazard ratio 1.14, 95% confidence interval 0.84–1.56). This was further confirmed in a propensity score matching analysis.

In a real life population of patients with acute myocardial infarction, the use of IABP for the treatment of cardiogenic shock was associated with a neutral effect.

Ethnicity, although known to influence cardiovascular outcome in assorted clinical settings, has not been investigated previously as a risk factor in patients presenting to the emergency department with suspected acute myocardial infarction.

In this multi-ethnic cohort study conducted in Singapore and The Netherlands, 2784 patients presenting to the emergency department with chest pain were enrolled (788 Caucasians, 1281 Chinese, 404 Indians and 311 Malays) and were followed up for 1 year.

Although Caucasian patients on average were older and had incurred more cardiovascular adverse events, the Asian ethnic groups carried a greater burden of cardiovascular risk factors. Caucasian and Malay patients were most frequently diagnosed with acute myocardial infarction (Caucasians 11.2%, Chinese and Indians 6.4%, Malays 10.6%, P<0.001), also after correction for baseline differences. Chinese and Indian patients, however, more often had unstable angina. Asian patients had strikingly more extensive coronary artery disease than Caucasian patients (triple-vessel disease: Caucasians 6.5%, Chinese 22.8%, Indians 32.4%, Malays 32.8%, P<0.001) and Chinese patients with myocardial infarction more frequently underwent coronary revascularisation compared with Caucasian patients (Caucasians 41.4%, Chinese 67.5%, Indians 62.5%, Malay 46.7%, P=0.005). Ethnicity was not an independent predictor of major adverse cardiovascular events during 1-year follow-up in all chest pain patients.

The prevalence of myocardial infarction and unstable angina, revascularisation rate and extent of coronary artery disease differ significantly among chest pain patients of different ethnic groups. These findings have important clinical implications and support consideration of ethnicity in risk stratification and determination of the patient management strategy in patients with symptoms suggestive of myocardial infarction.

Aspirin hypersensitivity is not a rare condition among patients with acute coronary syndrome. However, despite the publication of several successful desensitization protocols, the procedure is not as widespread as expected. We present a cohort of patients with acute coronary syndrome undergoing aspirin desensitization to evaluate its short- and long-term efficacy and safety and to reinforce data from previous studies.

Of 1306 patients admitted to our Coronary Care Unit between February 2011 and February 2013, 24 (1.8%) had a history of aspirin hypersensitivity. All 24 patients underwent an eight-dose aspirin desensitization protocol (0.1, 0.3, 1, 3, 10, 25, 50 and 100 mg of aspirin given by mouth every 15 minutes) after premedication with antihistamines and corticosteroids or antileucotrienes. Previously prescribed β blockers and angiotensin-converting enzyme inhibitors were not discontinued. All patients were desensitized within 72 hours of admission. Those requiring urgent catheterization (five patients with ST segment elevation myocardial infarction) were desensitized within 12 hours of catheterization and the remainder before catheterization.

All patients were successfully desensitized and only one presented with an urticarial reaction. The five patients with ST segment elevation myocardial infarction were treated with abciximab until desensitization was complete. All but one patient underwent catheterization and 20 underwent percutaneous coronary intervention, most (66%) with the implantation of a bare metal stent. At follow-up (a minimum of 6–24 months), only two patients had discontinued aspirin, both due to gastrointestinal bleeding, and no hypersensitivy reaction had occurred.

Aspirin desensitization is effective and safe in unstable patients with acute coronary syndrome in both the short and long term.

Despite troponin assay being a part of the diagnostic work up in many conditions with acute chest pain, little is known about its frequency and clinical implications in acute aortic syndromes (AASs). In our study we assessed frequency, impact on diagnostic delay, inappropriate treatments, and prognosis of troponin elevation in AAS.

Data were collected from a prospective metropolitan AAS registry (398 patients diagnosed between 2000 and 2013). Cardiac troponin test, using either standard or high sensitivity assay, was performed according to standard protocol used in chest pain units. Troponin T values were available in 248 patients (60%) of the registry population; the overall frequency of troponin positivity was 28% (ranging from 16% to 54%, using standard or high sensitivity assay respectively, p = 0.001). Troponin positivity was frequently associated with acute coronary syndromes (ACS)-like electrocardiogram findings, and with a twofold increased risk of long in-hospital diagnostic time (odds ratio (OR) 1.92, 95% confidence interval (CI) 1.05–3.52, p = 0.03). The combination of positive troponin and ACS-like electrocardiogram abnormalities resulted in a significantly increased risk of in-hospital delay/coronary angiography/antithrombotic therapy due to a misdiagnosis of ACS (OR 2.48, 95% CI 1.12–5.54, p = 0.02). However, troponin positivity was not associated with in-hospital mortality (OR 1.63, 95% CI 0.86–3.10, p = 0.131).

Troponin positivity was a frequent finding in AAS patients, particularly when a high sensitivity assay was employed. Abnormal troponin values were strongly associated with ACS-like electrocardiogram findings and with in-hospital diagnostic delay but apparently they did not influence in-hospital mortality.

Pleural effusion may complicate acute Stanford type B aortic dissection (ABAD).

To identify the relationships between the quantity and side of the pleural effusion, biomarkers and outcomes in patients with ABAD.

We undertook a retrospective review of 105 patients with ABAD. Their demographics, the data on admission and during hospital stay, the volume of pleural effusion calculated from the area on computed tomography images and clinical outcomes were analysed.

The median estimated peak volume (median 6.7 days after onset) was 129 ml (63–192, range 26–514 ml) on the left and 11 ml (6–43, range 2–300 ml) on the right. On univariate analysis, the volume of bilateral effusions was associated with anaemia, hypoalbuminaemia and inflammatory markers, whereas the volume of left-sided effusions was associated with older age, low diastolic blood pressure and maximum aortic diameter. Multivariate analysis revealed that hypoalbuminaemia was independently associated with bilateral effusion volume (P<0.001), while maximum aortic diameter was associated with left-sided effusion volume (P=0.019). A greater volume of bilateral plural effusion was associated with longer intensive care unit stay.

Larger bilateral pleural effusions in patients with ABAD were associated with hypoalbuminaemia and potentially with anaemia and inflammation, and may increase the length of intensive care unit stay. Left-sided effusion volume appears to be influenced by the nature of the aortic dilatation. Multiple mechanisms may underpin the development of pleural effusion in ABAD, and are likely to influence clinical outcomes.

Acute decompensated heart failure is the most common acute heart failure phenotype. Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) can provide bridging support for patients with acute decompensated heart failure to transplantation. We studied the association between baseline (<6 months), pre-ECMO (<24 h) parameters and outcome of VA-ECMO support in patients with severe acute decompensated heart failure.

We included 26 consecutive patients with acute decompensated heart failure (acute myocarditis, myocardial infarction or post-cardiotomy shock were excluded) who were bridged with peripheral VA-ECMO to transplantation. Data within six months (baseline) and immediately pre-ECMO were collected. Model for end-stage liver disease (MELD) with sodium (MELD-Na) and without international normalized ratio (MELD-XI) scores were calculated. Outcome was defined as death at 30 days following VA-ECMO support.

Thirteen of the 26 patients died within 30 days of VA-ECMO support. Univariate associations with 30-day mortality were baseline MELD-XI, baseline sodium, creatinine, bilirubin, pre-ECMO alanine aminotransferase and lactate. However, only baseline MELD-XI score (hazard ratio 2.678 (95% CI 1.085–6.607), p=0.033) was associated 30-day survival on logistic regression analysis. Survivors demonstrated greater reduction in inotropic and vasoactive drug support and improvement in alanine aminotransferase and lactate levels. Using a threshold based on the median MELD-XI of 14.1, 30-day survival in patients with a baseline MELD-XI ⩽ 14.1 was 69% compared with 31% in patients with baseline MELD-XI > 14.1 (p=0.046).

Baseline MELD-XI score, but not pre-ECMO parameters, is independently associated with outcomes from VA-ECMO support in patients with acute decompensated heart failure.

The aim of this study was to evaluate the association of anemia and renal dysfunction with in-hospital outcomes in acute heart failure syndromes patients with preserved or reduced ejection fraction.

Of the 4842 patients enrolled in the Acute Decompensated Heart Failure Syndromes (ATTEND) registry, 4693 patients were evaluated to investigate the association among anemia, renal dysfunction, a preserved or reduced ejection fraction and in-hospital mortality. They were divided into four groups based on hemoglobin and estimated glomerular filtration rate at admission. The in-hospital mortality rate was 5.9% and 6.9% of the preserved and reduced ejection fraction groups, respectively. After adjustment for multiple comorbidities, there was no association of either anemia or renal dysfunction alone with in-hospital mortality in preserved ejection fraction patients, but the combination of anemia and renal dysfunction was associated with a somewhat higher risk of in-hospital mortality than that without either condition (odds ratio (OR), 2.75; 95% confidence interval (CI), 0.72–10.41; p=0.137). In reduced ejection fraction patients, adjusted analysis showed that a significantly higher risk of in-hospital mortality was associated with anemia alone (OR, 2.56; 95% CI, 1.10-5.94; p=0.029) and with anemia plus renal dysfunction (OR, 2.34; 95% CI, 1.09–5.03; p=0.029) relative to the risk without either condition.

Our findings demonstrate that anemia combined with renal dysfunction is not a risk factor for in-hospital mortality in patients with a preserved ejection fraction, whereas anemia is an independent predictor of in-hospital mortality risk in reduced ejection fraction patients regardless of renal dysfunction.