Beyond the cardiorenal anaemia syndrome: recognizing the role of iron deficiency

Growing awareness that heart failure, renal impairment, and anaemia are frequent co‐morbidities which can exacerbate one another in a vicious circle of clinical deterioration has led to the concept of the cardiorenal anaemia syndrome (CRAS). The role of iron deficiency within this complex interplay has been less well examined. Scrutiny of data from the recent FAIR‐HF trial raises a new hypothesis: is it time for ‘CRAS’ to be supplemented with new acronyms such as CRIDS (cardiorenal–iron deficiency syndrome) or even CRAIDS (cardiorenal–anaemia–iron deficiency syndrome)? Iron deficiency occurs frequently in heart failure patients with or without anaemia. It not only impairs oxygen transport through reduced erythropoiesis, but adversely affects oxidative metabolism, cellular energetics, and immune mechanisms, and the synthesis and degradation of complex molecules such as DNA. One large observational study in patients with heart failure found iron deficiency to be an independent predictor of death or urgent heart transplantation (hazard ratio 1.58, 95% confidence interval 1.14–2.17, P = 0.005). In the FAIR‐HF trial, i.v. iron therapy was associated with significant improvements in physical functioning in iron‐deficient patients with heart failure, even in non‐anaemic patients in whom haemoglobin levels did not change following i.v. iron administration. Key questions regarding the use of i.v. iron supplementation in the setting of heart failure merit exploration and could readily be answered by appropriately designed clinical trials. It is to be hoped that these important clinical trials are conducted, to permit a more subtle characterization of the patient's pathological condition and interventional requirements.     

Computed Tomographic Findings in 50 Cases of Gall Bladder Carcinoma

Background

A retrospective assessment of contrast enhanced computed tomography (CECT) scan findings in histopathologically proven cases of carcinoma of the gallbladder (GB) was performed to review its role in diagnosis, staging and assessment of surgical resectability.

Methods

All the patients had been subjected to a standardised abdominal helical computed tomography scan. Orally administered iodinated contrast was used for opacification of bowel and dynamic intravenous injection of non-ionic iodinated contrast for studying the lesional enhancement and vascular structures.

Results

The presence of focal or diffuse mass lesions in the gallbladder fossa, infiltration of a liver and second part of duodenum were the most reliable diagnostic features in carcinoma gallbladder. Regional spread was better delineated on CT scan as compared with ultrasonography.

Conclusion

CT scan is an effective method for evaluating, characterizing and detecting the spread of GB carcinomas.Key Words: Gall Bladder, Carcinoma, Computed Tomography     

Coronary collateral circulation is less developed when ischaemic heart disease coexists with diabetes

BACKGROUND: The extent of myocardial ischaemia and the magnitude of systolic function impairment following myocardial infarction (MI) depend to a large degree on the performance of coronary collateral circulation. Endothelial function is altered in several disorders, including diabetes. An impaired development of coronary collateral circulation may be a factor responsible for post-MI complications in patients with diabetes. AIM: To compare the degree of coronary collateral circulation development between patients with advanced ischaemic heart disease (IHD), with or without diabetes. METHODS: The study group consisted of 70 consecutive patients with diabetes who underwent coronary angiography between September 1998 and December 1999 and had total occlusion of at least one of the main coronary vessels. The control group consisted of 70 age-, gender, and MI history-matched non-diabetic patients. Coronary collateral circulation was assessed using the collateral score (CS). RESULTS: Patients with diabetes had less developed coronary collateral circulation than the patients without diabetes which was reflected by a significantly lower CS value - 1.47+/-1.56 vs 2.03+/-1.81; p < 0.05. No significant relationship was found between CS and age, gender, body mass index, history of MI or the presence of IHD risk factors. There was a significant association between the number of vessels with lesions and CS: r=0.40, p=0.0006 in the control group and r=0.42, p=0.0003 in patients with diabetes. The CS values in patients with single-, two- or three-vessel disease were 1.27+/-1.34, 2.38+/-1.85 and 2.98+/-2.07 in the control group, and 0.70+/-0.90, 1.10+/-1.30 and 2.23+/-1.76 in patients with diabetes, respectively. A multivariate analysis revealed that the presence of diabetes (t=-3.04, p=0.003) and the number of affected vessels (t=5.23, p=0.0001) were independently related to the CS values. CONCLUSIONS: Patients with IHD and diabetes have less developed coronary collateral circulation than IHD patients without diabetes, regardless of the extent of coronary lesions. Patients with diabetes who undergo coronary angiography, have more advanced coronary atherosclerotic lesions than patients without diabetes.     

Impact of periodic breathing on V(O2) and V(CO2): a quantitative approach by Fourier analysis

Oscillations in oxygen uptake (V(O2)) and carbon dioxide production (V(CO2)) in patients with chronic heart failure differ in amplitude and phase from the oscillations in ventilation (periodic breathing, PB), leading some to doubt whether they result from PB. We applied Fourier transforms to a pulmonary gas exchange model to quantify the effects of fluctuations in alveolar ventilation (V(A)). We found that PB causes oscillations in V(O2) and V(CO2), but their amplitude and phase are complex, and vary with workload. At low workloads, the relative oscillations in V(O2) and V(CO2) closely mirror the relative oscillations in V(A). But at high workloads, the metabolic oscillations are attenuated (V(O2) most severely), and the V(O2) peaks precede the ventilatory peaks significantly. This study also explains why normal controls simulating PB at higher workloads fail to reproduce the V(O2) and V(CO2) oscillations seen in spontaneous PB of heart failure.     

Catabolic/Anabolic Imbalance Is Accompanied by Changes of Left Ventricular Steroid Nuclear Receptor Expression in Tachycardia-Induced Systolic Heart Failure in Male Pigs

BackgroundSteroid hormones play an important role in heart failure (HF) pathogenesis, and clinical data have revealed disordered steroidogenesis in male patients with HF. However, there is still a lack of studies on steroid hormones and their receptors during HF progression. Therefore, a porcine model of tachycardia-induced cardiomyopathy corresponding to HF was used to assess steroid hormone concentrations in serum and their nuclear receptor levels in heart tissue during the consecutive stages of HF.Methods and ResultsMale pigs underwent right ventricular pacing and developed a clinical picture of mild, moderate, or severe HF. Serum concentrations of dehydroepiandrosterone, testosterone, dihydrotestosterone, estradiol, aldosterone, and cortisol were assessed by enzyme-linked immunosorbent assay. Androgen receptor, estrogen receptor alpha, mineralocorticoid receptor, and glucocorticoid receptor messenger RNA levels in the left ventricle were determined by qPCR.The androgen level decreased in moderate and severe HF animals, while the corticosteroid level increased. The estradiol concentration remained stable. The quantitative real-time polymerase chain reaction revealed the downregulation of androgen receptor in consecutive stages of HF and increased expression of mineralocorticoid receptor messenger RNA under these conditions.ConclusionsIn the HF pig model, deteriorated catabolic/anabolic balance, manifested by upregulation of aldosterone and cortisol and downregulation of androgen signaling on the ligand level, was augmented by changes in steroid hormone receptor expression in the heart tissue.