Peter Ammann

B-type natriuretic peptide in patients with sepsis and preserved left ventricular ejection fraction

B-type natriuretic peptide (BNP) as a marker of left ventricular end-diastolic pressure [1] has proven to be a useful diagnostic tool to differentiate dyspnea caused by congestive heart failure (CHF) from non-cardiac dyspnea in patients presenting at the emergency room [2,3]. It has been demonstrated that a normal BNP level (<80 to 100 pg/mL) has a high negative predictive value to exclude CHF [2,3], whereas a markedly elevated BNP has a high positive predictive value for CHF [4]. Therefore, BNP testing seems to be very useful not only for emergency room settings, but also for the intensive care unit (ICU), where a rapid assessment of the cause of a patient’s worsening oxygenation is required. However, while introducing BNP testing in our ICU we have observed surprisingly high BNP levels in critically ill patients with echocardiographically preserved left ventricular ejection fraction (LVEF).

Clinical Characteristics, Sex Hormones, and Long-Term Follow-Up in Swiss Postmenopausal Women Presenting With Takotsubo Cardiomyopathy

The overwhelming majority of patients with stress cardiomyopathy (SC) are postmenopausal women, suggesting an important pathophysiologic role of the female sex hormones. Preliminary data suggest that myocardial stunning might be provoked by estrogen deficiency.

Bland-White-Garland syndrome in a 39-year-old mother

We report the case of a 39-year-old mother of 3 children presenting with exertion fatigue. Coronary angiography revealed an anomalous left coronary artery arising from the pulmonary artery. The patient underwent an operation with the direct implantation of the left coronary artery into the ascending aorta. This less symptomatic course stands in contrast to the high risk for sudden death in untreated adults.

Design of the Swiss Atrial Fibrillation Cohort Study (Swiss-AF): structural brain damage and cognitive decline among patients with atrial fibrillation

BACKGROUNDnSeveral studies found that patients with atrial fibrillation (AF) have an increased risk of cognitive decline and dementia over time. However, the magnitude of the problem, associated risk factors and underlying mechanisms remain unclear.nnnMETHODSnThis article describes the design and methodology of the Swiss Atrial Fibrillation (Swiss-AF) Cohort Study, a prospective multicentre national cohort study of 2400 patients across 13 sites in Switzerland. Eligible patients must have documented AF. Main exclusion criteria are the inability to provide informed consent and the presence of exclusively short episodes of reversible forms of AF. All patients undergo extensive phenotyping and genotyping, including repeated assessment of cognitive functions, quality of life, disability, electrocardiography and cerebral magnetic resonance imaging. We also collect information on health related costs, and we assemble a large biobank. Key clinical outcomes in Swiss-AF are death, stroke, systemic embolism, bleeding, hospitalisation for heart failure and myocardial infarction. Information on outcomes and updates on other characteristics are being collected during yearly follow-up visits.nnnRESULTSnUp to 7 April 2017, we have enrolled 2133 patients into Swiss-AF. With the current recruitment rate of 15 to 20 patients per week, we expect that the target sample size of 2400 patients will be reached by summer 2017.nnnCONCLUSIONnSwiss-AF is a large national prospective cohort of patients with AF in Switzerland. This study will provide important new information on structural and functional brain damage in patients with AF and on other AF related complications, using a large variety of genetic, phenotypic and health economic parameters.

Cardiomyocyte apoptosis and elevation in cardiac troponin I

vated cTnI levels are present in a relatively high proportion of hemodynamically stable patients with sepsis or systemic inflammatory response syndrome [5]. We showed that an increase in cTnI is sometimes present without a permanent myocardial injury. We therefore postulate reversible, cytokine-mediated myocardial cell injury leading to myocardial “cell membrane gaps” with leakage of troponins into the extracellular fluid. Reversible myocardial ischemia induced by an activated clotting system in sepsis or systemic inflammatory response syndrome may be another explanation for troponin elevation in these conditions. We therefore agree with Beranek that troponin elevation and the frequently observed reversible myocardial dysfunction in the hemodynamically stable septic patients are possibly due to an incomplete apoptotic process. There is growing evidence that increased troponin levels are associated with adverse clinical outcome in patients after stroke and in patients on hemodialysis [6, 7]. If these findings are confirmed in further studies, it is of great interest to understand the underlying pathophysiological mechanism to develop therapeutic strategies for patients at high risk.