Contemporary review on spontaneous coronary artery dissection: insights into the angiographic finding and differential diagnosis.

Spontaneous coronary artery dissection (SCAD), although in the majority of cases presents as an acute coronary syndrome (ACS), has different pathophysiology from atherosclerosis that influences specific angiography findings and enables most patients to be solved by optimal medical therapy rather than percutaneous coronary intervention (PCI). Therefore, accurate diagnosis is essential for adequate treatment of each patient as management of SCAD differs from that of ACS of atherosclerotic aetiology. So far, invasive coronary angiography remains the most important diagnostic tool in suspected SCAD. However, there are ambiguous cases that can mimic SCAD. In this review, the authors summarize current knowledge about the diagnostic algorithms, particularly angiographic features of SCAD, pitfalls of angiography, and the role of intracoronary imaging in the context of SCAD diagnosis. Finally, apart from the pathognomonic angiographic features of SCAD that are thoroughly discussed in this review, the authors focus on obscure angiography findings and findings that can mimic SCAD as well. Differential diagnosis and the timely recognition of SCAD are crucial as there are differences in the acute and long-term management of SCAD and other causes of ACS.

Validation of the FEW16 questionnaire for the assessment of physical well-being in patients with heart failure with reduced ejection fraction: results from the CIBIS-ELD study.

AIMS: Patients with heart failure (HF) commonly suffer from severe impairment of quality of life (QoL). One main goal of HF treatment is improvement of QoL. Physical well-being is an essential component of QoL. To enable assessment of physical well-being in HF patients, we validated the FEW16 questionnaire in a prospective study with patients from the Cardiac Insufficiency Bisoprolol Study in ELDerly. METHODS AND RESULTS: In 127 HF patients (age 73 ± 5.5 years, 72% male, 60% New York Heart Association class II, left ventricular ejection fraction 37 ± 8.5%), we measured physical well-being (FEW16), QoL [36-Item Short-Form Health Survey (SF36)], and depressive symptoms [PRIME MD Patient Health Questionnaire German short version for depression (PHQ-D)] at baseline and two follow-up visits, and correlated FEW16 scores with QoL data and clinical parameters. FEW16 mean scores are 3.04 ± 1.04 at baseline, 3.19 ± 0.94 after 3 months, and 2.77 ± 0.94 after 2-4 years. We assessed data quality, scale assumptions, and construct validity and reliability. Cronbach's alpha for subscales resilience: 0.84; ability to enjoy: 0.80; vitality: 0.88; inner peace: 0.87; total score: 0.95. Intraclass correlation coefficient (ICC) is 0.87 (95% CI 0.84-0.89, ICC (1.4). Pearson's correlations of FEW16 with SF36 and PHQ-D were significant. Six minutes walking distance and heart rate correlated significantly with the FEW16 total score. CONCLUSIONS: The FEW16 showed good reliability, internal consistency, and intraclass correlation. FEW16 scores correlated well with psychological and physical well-being (SF36) and clinical markers of exercise tolerance (6 min walk test and heart rate). Our results indicate a strong correlation of self-reported physical well-being with psychological factors. FEW16 values at baseline predicted the development of several aspects of QoL during beta-blocker up-titration.

Impact of the ß1-adrenoceptor Arg389Gly polymorphism on heart-rate responses to bisoprolol and carvedilol in heart-failure patients.

This pharmacogenetic substudy of the prospective, double-blind, randomized CIBIS-ELD trial determined the impact of the ß1-adrenoceptor Arg189Gly polymorphism on heart-rate responses to bisoprolol or carvedilol in elderly patients with heart failure (421 with sinus rhythm, 107 with atrial fibrillation). Patients were randomized 1:1 to bisoprolol or carvedilol with a fortnightly dose-doubling scheme and guideline target doses. Patients with sinus rhythm responded essentially identically to bisoprolol and carvedilol, independent of genotype. Atrial fibrillation patients homozygous for Arg389 had a much smaller response to carvedilol than carriers of at least one Gly389 allele (mean difference 12 bpm, P < 0.00001). Carvedilol up to 2 × 12.5 mg did not reduce heart rate in Arg389Arg homozygotes at all. Interestingly, the immediate response to carvedilol did not differ between genotypes. The Arg389Gly polymorphism has a major impact on the heart-rate response to carvedilol (but not bisoprolol) in patients with heart failure plus atrial fibrillation.