Predictors of successful cardioversion with vernakalant in patients with recent-onset atrial fibrillation.

BACKGROUND: Vernakalant is a novel atrial-selective antiarrhythmic drug able to convert recent-onset atrial fibrillation (AF) with reportedly low proarrhythmic risk. Successful cardioversion predictors are largely unknown. We sought to evaluate clinical and electrocardiographic predictors of cardioversion of recent-onset AF with vernakalant. METHODS: Consecutive patients with AF ≤48 hours admitted for cardioversion with vernakalant (n = 113, median age 62 years, 69 male) were included. Sinus rhythm (SR) within 90 minutes after infusion start was considered to be successful cardioversion. Predictive values of demographics, concomitant therapy, comorbidities, and electrocardiographic parameters were assessed. Atrial fibrillatory rate (AFR), exponential decay, and mean fibrillatory wave amplitude were measured from surface ECG using QRST cancellation and time-frequency analysis. RESULTS: Cardioversion was achieved in 66% of patients. Conversion rate was higher in women than in men (80% vs 58%, P = 0.02) while none of other clinical characteristics, including index AF episode duration, could predict SR restoration. Female gender was predictive of vernakalant's effect in logistic regression analysis (OR = 2.82 95%CI 1.18-6.76, P = 0.020). There was no difference in AFR (350 ± 60 vs 348 ± 62 fibrillations per minute [fpm], P = 0.893), mean fibrillatory wave amplitude (86 ± 33 vs 88 ± 67 µV, P = 0.852), or exponential decay (1.30 ± 0.42 vs 1.35 ± 0.42, P = 0.376) between responders and nonresponders. CONCLUSIONS: Female gender is associated with a higher rate of SR restoration using intravenous (i.v.) vernakalant for recent-onset AF. ECG-derived indices of AF organization, which previous studies associated with effect of rhythm control interventions, did not predict vernakalant's effect.

The combination of high sensitivity troponin T and copeptin facilitates early rule-out of ACS: a prospective observational study.

BACKGROUND: The combination of the new high sensitivity troponin T (hsTnT) assays and copeptin, a biomarker of endogenous stress, has been suggested to have the potential of early rule-out of acute coronary syndrome (ACS). The aim of this study was to examine the ability of this combination to rule out ACS in patients presenting with chest pain and to compare the diagnostic performance to hsTnT alone. METHOD: In this prospective observational study, patients with chest pain admitted for observation were consecutively included. Patients presenting with ST elevation were excluded. Copeptin and hsTnT were analyzed at admission and hsTnT was thereafter determined approximately every 3rd hour as long as clinically indicated. The follow-up period was 60 days. A combined primary endpoint of ACS, non-elective percutanous coronary intervention, non-elective coronary artery bypass surgery and death of all causes was used. RESULTS: 478 patients were included. 107 (22%) patients were diagnosed with ACS during hospital stay. 70 (14%) had non-ST-segment elevation myocardial infarction (NSTEMI) and 37 (8%) had unstable angina pectoris (UAP). CONCLUSIONS: In patients presenting with chest pain admitted for observation, the combination of hsTnT and copeptin analyzed at admission had a significantly higher sensitivity to diagnose ACS than hsTnT alone. We report a sensitivity of 83% and a NPV of 91% for the combination of hsTnT and copeptin and we conclude that biomarkers alone are not sufficient to rule out ACS. However, the combination of hsTnT and copeptin seems to have a significantly higher sensitivity to identify ACS than a repeated hsTnT test, and thus enables an earlier risk stratification of chest pain patients. This can be time-saving and beneficial for the individual patient by contributing to early decisions on treatment, need of further assessment and level of care.

Job strain, job demands and adrenergic beta1-receptor-polymorphism: a possible interaction affecting blood pressure in men.

BACKGROUND: Job strain and the Arg389Gly polymorphism in the adrenergic beta1-receptor gene have been linked to hypertension. We aimed to study whether there is an interaction between the Arg389Gly polymorphism and job strain and its components (job demand and decision latitude) in relation to blood pressure. METHODS: From the Malmö Diet and Cancer population cohort, 6095 individuals were randomly selected to be followed regarding cardiovascular risk factors. From this group, employed individuals with baseline data regarding work characteristics were included (1338 men and 1707 women). Determination of adrenergic beta1-receptor Arg389Gly polymorphism was possible in 1271 men and 1601 women, and these individuals formed the study group. RESULTS: Men with the combination of Arg389Arg and job strain were more often on antihypertensive medication (P = 0.04), whereas blood pressure was not significantly higher, in comparison with those without both of these two factors. The interaction term genotype x job strain was borderline significant for systolic blood pressure (P = 0.07) after adjustments for age, country of birth, and job status. The demand score showed significant interaction in men with genotype (P = 0.01 for systolic blood pressure and P = 0.009 for diastolic blood pressure) after adjustments for age, country of birth, job status, antihypertensive treatment, and BMI. Men with the Gly389 allele had lower blood pressure with increasing demand score (P = 0.001), whereas men homozygous for the Arg389 allele had lower blood pressure with increasing latitude score (P = 0.03). In women, those with job strain tended to have higher blood pressure than those without job strain, among carriers of Arg389Arg and Arg389Gly genotype. CONCLUSION: Men with job strain and the Arg389Arg polymorphism were more often on antihypertensive treatment than other men. Significant interactions between the Arg389Gly polymorphism and aspects of job stress are described, but the absolute blood pressure differences are small. Considering the commonness of the polymorphism, stress, and hypertension further studies are indicated.

Job strain, decision latitude and alpha2B-adrenergic receptor polymorphism significantly interact, and associate with higher blood pressures in men.

BACKGROUND: Job strain (high demands and low decision latitude) and the DD genotype of an I/D polymorphism in the adrenergic alpha2B-receptor have been associated with hypertension, respectively. We hypothesized that the I/D polymorphism interacts with external stress, such as job strain, in the development of hypertension. METHODS: A sample of 3045 employed men and women from the population cohort of Malmö Diet and Cancer Study, n = 28 098, with baseline data regarding work characteristics and cardiovascular risk factors, were genotyped for the adrenergic alpha2B-receptor I/D polymorphism. This was possible in 1302 men and 1662 women, and these individuals formed the study group. RESULTS: The age-adjusted systolic blood pressure (SBP) for men with the DD polymorphism and job strain (n = 26) was 147.0 +/- 3.4 mmHg, whereas for men with the DD polymorphism but without job strain (n = 184), the SBP was 138.2 +/- 1.4 mmHg (P = 0.018). Similar findings were made regarding diastolic blood pressures (DBP) in men. Job strain and the I/D polymorphism in the adrenergic alpha2B-receptor gene significantly interacted in men [P = 0.008 for SBP, P = 0.03 for DBP, adjusted for age, body mass index, occupational status and nationality (Model 1)]. Increasing latitude score was inversely correlated with SBP (beta -0.17, P = 0.03, Model 1) in DD men, but not in men with the I-allele; interaction significance for genotype x latitude score, P = 0.02 for SBP (Model 1). In women, there were no significant interactions between genotype and work characteristics (P = 0.32 for SBP, and P = 0.60 for DBP). CONCLUSION: For the first time, a significant interaction between a genetic factor and work environment, resulting in elevated blood pressures, has been described.

Job strain in men, but not in women, predicts a significant rise in blood pressure after 6.5 years of follow-up.

BACKGROUND: Job strain (high demands and low decision latitude) has been associated with hypertension and cardiovascular disease, especially in men. Most studies on job strain and hypertension have been cross-sectional, and prospective data are inconsistent. OBJECTIVE: To prospectively describe the effects of different psychosocial work characteristics on office blood pressure changes. METHODS: In total, 448 men and women, mean age 55 years, were followed for a mean of 6.5 years. At baseline, work characteristics and cardiovascular risk factors were assessed. Only employed subjects aged 63 years or younger were eligible for participation. RESULTS: Men with baseline job strain had a significantly greater increase in both systolic blood pressure (7.7 mmHg, P = 0.02), and diastolic blood pressure (5.6 mmHg, P = 0.003), compared to the group with low work demands and high decision latitude ('relaxed'). These findings were significant also after adjustments for age, follow-up time, baseline blood pressure, blood pressure treatment at baseline and follow-up, and length of education. Work demands were more strongly correlated with blood pressure increase than decision latitude. For women, no significant associations between psychosocial work characteristics and blood pressure changes were found, apart from a weak trend of association between increasing decision latitude and increasing blood pressure. CONCLUSION: Job strain significantly predicts an increase in office blood pressure in middle-aged men, but not in women. Work demands were more strongly correlated with blood pressure increase than decision latitude in men.

Early rule-out of acute coronary syndrome using undetectable levels of high sensitivity troponin T.

AIMS: To examine whether undetectable high sensitivity troponin T (hsTnT) can be used to safely rule out non-ST-elevation acute coronary syndrome (NSTE-ACS) (using the limit of detection (LOD) as the cut-off) and to compare this strategy to serial hsTnT and the use of combined hsTnT and copeptin. METHODS: In this prospective observational study, 478 patients presenting with chest pain were consecutively included. A combined primary endpoint of ACS, non-elective revascularization and/or death of all causes was used. The follow-up period was 60 days. RESULTS: NSTE-ACS was diagnosed in 107 (22%) patients during hospital stay. Undetectable hsTnT at admission ruled out NSTE-ACS with a negative predictive value of 94% (95% confidence interval (CI): 88-97) giving a sensitivity of 0.90 (95% CI: 0.80-0.95) versus 0.78 (95% CI: 0.66-0.87) for serial hsTnT testing, p=0.008. The combination of hsTnT and copeptin analysed at admission resulted in a sensitivity of 0.83 (95% CI: 0.74-0.89), p=0.07 for comparison with undetectable hsTnT. CONCLUSION: A single hsTnT test at presentation, using the LOD as the cut-off, appears to be a safe and time-saving strategy to rule out NSTE-ACS. Further, undetectable levels of hsTnT were associated with an excellent prognosis and none of the patients with undetectable hsTnT were diagnosed with NSTEMI. Together with ECG and clinical assessment this biomarker strategy might permit outpatient treatment of almost one third of the patients we currently admit for observation.

High-sensitivity troponin T as a diagnostic tool for acute coronary syndrome in the real world: an observational study.

BACKGROUND: The 2011 European Society of Cardiology guidelines state that acute coronary syndrome (ACS) may be excluded with a rapid 3 h high-sensitivity troponin T (HsTnT) sampling protocol. We aimed to evaluate the diagnostic and prognostic performance of HsTnT in patients with chest pain admitted with possible ACS in routine care. METHODS: A total of 773 consecutive patients admitted for in-hospital care for chest pain suspicious of ACS were included retrospectively. HsTnT values at admission and at 3-4 and 6-7 h were analysed for diagnostic performance. In addition, prognostic performance towards a combined 60-day endpoint of ACS, nonelective revascularization or death of all causes was studied. RESULTS: Twenty-three per cent of the patients had ACS during the hospital stay and 1.6% had an endpoint after discharge but within 60 days. The sensitivity of HsTnT for ACS at admission, 3-4 and 6-7 h was only 68, 79 and 81%, respectively. Sensitivity and negative predictive value for acute myocardial infarction alone were 80 and 93% on admission and 97 and 99% at 3-4 h. Among patients aged 75 years and older, 63% had a positive HsTnT on admission, but only 39% of these had an ACS during hospital stay. CONCLUSION: Our data confirm that prolonged testing with HsTnT after 3-4 h does not improve diagnostic performance for ACS. However, although sensitivity for acute myocardial infarction was very good, sensitivity for ACS was insufficient to rule out ACS even at 6-7 h. Less than half of all recorded positive HsTnT were true positives. On the basis of these results, we find it unlikely that HsTnT has improved the diagnosis of ACS in the emergency care setting.

Epidemiology and characteristics of hyponatremia in the emergency department.

BACKGROUND: Hyponatremia is the most common electrolyte abnormality and it is associated with increased morbidity and mortality. The aim of the study was to investigate the underlying causes and management of hyponatremia in an unselected population presenting with hyponatremia to the emergency department. METHODS: A descriptive, retrospective hospital record study was performed. A database search was conducted for all patients presenting to the emergency departments in Lund and Malmo and patients with a P-Na-value<135mmol/L were identified. Patients were divided into four groups based on the severity of hyponatremia (Group 1: P-Na<120mM, Group 2: Na 120-124mM, Group 3: Na 125-129mM, Group 4: Na 130-134mM) and 100 patients from each group were included. Groups 2-4 were matched to Group 1 for age, gender and month for ER visit. RESULTS: The prevalence of hyponatremia (P-Na<135mmol/L) was 3% in the entire emergency population. A single underlying cause was identified in 45% of patients in Group 1. The leading aetiologies were thiazide diuretics (17%), SIADH (17%) and other diuretics (14%). The likelihood of being on thiazide diuretics increased with hyponatremia severity (p<0.0001) and patients in Group 1 were 3.6 times (CI95%:1.9-6.8) more likely to be on thiazide diuretics compared to Group 4. The in-hospital mortality ranged between 2 and 7% between the groups (NS). One patient developed osmotic demyelinisation syndrome but survived. Only 31% of patients in Group 1 were evaluated with a basic laboratory investigation. CONCLUSIONS: Thiazide diuretics and SIADH were dominating underlying causes of hyponatremia, however, the frequency of adequate diagnostic testing was low. The majority of patients were treated with sodium chloride infusion.

Acute right ventricular failure caused by concomitant coronary and pulmonary embolism: successful treatment with endovascular coronary and pulmonary thrombectomy.

Patent foramen ovale (PFO) is present in approximately 25% of the general population. PFO is characterized by intermittent shunting of blood from the right to the left atrium, especially in the context of increased right-sided filling pressures, with risk of paradoxical embolism. We describe a 69-year-old woman presenting with acute chest pain, severe dyspnoea, and acute inferolateral ST-segment elevation on the electrocardiogram. The patient was diagnosed with myocardial infarction and failure of the right cardiac ventricle, which was considered to be secondary to extensive pulmonary embolism leading to increased filling pressures and paradoxical coronary embolism. The patient underwent emergent percutaneous interventions with coronary thrombus extraction and pulmonary thrombus fragmentation and local thrombolysis. The patient was free of symptoms at follow up 6 months later and echocardiography showed substantially improved right ventricular function. We discuss issues related to the diagnosis, treatment, and secondary prevention for patients with concomitant pulmonary and coronary arterial thrombosis.