A 60-year-old man experienced catastrophic haemodynamic decompensation 3 days following coronary artery bypass grafting (CABG). Aspiration thrombectomy to remove a left main coronary artery saddle embolus resulted in immediate haemodynamic improvement with no requirement for angioplasty or repeat bypass grafting. Coronary thromboembolism should be considered in the differential diagnosis of haemodynamic collapse post CABG. Urgent coronary angiography and aspiration thrombectomy may result in significant improvement for this condition.

Background: Measuring health status is becoming increasingly important in both clinical practice and research for patients with chronic heart failure (CHF). The Heart Failure Needs Assessment Questionnaire (HFNAQ) is a new, validated, self-administered, 30-item questionnaire that quantifies physical, psychological, social and spiritual domains. Objectives: To assess the prevalence of needs in patients with CHF recently discharged from hospital. Methods: The HFNAQ was administered to patients (n = 132; mean age 72.3 (SD 9.69) years; 37% female) consenting to participate in a heart failure cardiac rehabilitation program. Results: In this sample, the overall mean HFNAQ Score was 67.3 (95% CI = 65.03-69.75), indicating an average level of need around the mid-range of the scale used. In this vulnerable post-discharge phase there was evidence of predominance of psychosocial and existential issues over physical needs. None of the variables that were examined for associations with the measures of needs, reached statistical significance. Conclusions: The findings of high levels of unmet needs in the psychosocial and existential domains identify this as an important focus for health care interventions. Failure to identify physical, social or demographic predictors of needs in this sample underscores the importance of assessing the individual's unique perspective of the CHF illness experience. These findings emphasize the importance of the individualized care planning for individuals with CHF following discharge from hospital.

Apolipoprotein A-I (apoA-I) overexpression inhibits atherogenesis in mice, and apolipoprotein E (apoE) secreted by foam cell macrophages may exert antiatherogenic effects within the arterial wall. We hypothesized that interaction between apoA-I and apoE contributed to the antiatherogenic properties of apoA-I, and therefore investigated whether apoA-I stimulated secretion of apoE by foam cell macrophages. Cholesterol enrichment of primary murine and human macrophages increased spontaneous apoE secretion 2-fold, as quantified by Western blot and chemiluminescence detection. Human apoA-I caused a further marked increase of apoE secretion from both murine (3.8-fold,p < 0.01) and human (3.2-fold, p = 0.01) foam cells in a time- and concentration- dependent manner, and this increase was confirmed by immunoprecipitation of [35S]methionine-labeled macrophage apoE. The protein synthesis inhibitor cycloheximide, but not the transcription inhibitor actinomycin D, markedly inhibited apoE secretion to apoA-I (73.1 ± 9.8% inhibition at 4 h) and completely suppressed apoE secretion beyond 4 h. Pretreatment of macrophages with Pronase inhibited initial apoA-I-mediated apoE secretion by 70.5 ± 6.5% at 2 h, but by 8 h apoA-I-induced apoE secretion was the same in Pronase-pretreated and non-pretreated cells. Non-apolipoprotein-mediated cholesterol efflux induced by trimethyl-β cyclodextrin did not enhance apoE secretion, whereas phospholipid vesicles inducing the same degree of cholesterol efflux substantially enhanced apoE secretion, and apoA-I and phospholipid vesicles in combination demonstrated additive induction of apoE secretion. We conclude that apoA-I concurrently stimulates apoE secretion and cholesterol efflux from foam cell macrophages and that lipoprotein-derived apoA-I may enhance local secretion and accumulation of apoE in atherosclerotic lesions.