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Although it has been over a century since RAAS was discovered by Robert Tigerstedt in 1897 (1), it took up to 1981 for the first ACE inhibitor (ACEI), Captopril, to be approved by the Food and Drug Administration (FDA) for human use in the United States. Since then numerous ACEI’s have come into the market (2). The group of physicians from Dubai Hospital have recently reviewed in this Journal the role of renin-angiotensin-aldosterone system (RAAS) inhibition in the renal continuum (3) and in the current issue, they elaborated further on RAAS in the cardiovascular continuum by examining the trial evidence and clinical practice (4). The authors have comprehensively described the benefit of different angiotensin converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), and direct renin inhibitors in cardiovascular as well as renal protection (3,4)

Asthma and chronic obstructive pulmonary disease remain a global health problem, with increasing morbidity and mortality. Despite differences in the causal agents, both diseases exhibit various degrees of inflammatory changes, structural alterations of the airways leading to airflow limitation. The existence of transient disease phenotypes which overlap both diseases and which progressively decline the lung function has complicated the search for an effective therapy. Important characteristics of chronic airway diseases include airway and vascular remodeling, of which the molecular mechanisms are complex and poorly understood. Recently, we and others have shown that airway smooth muscle (ASM) cells are not only structural and contractile components of airways, rather they bear capabilities of producing large number of pro-inflammatory and mitogenic factors. Increase in size and number of blood vessels both inside and outside the smooth muscle layer as well as hyperemia of bronchial vasculature are contributing factors in airway wall remodeling in patients with chronic airway diseases, proposing for the ongoing mechanisms like angiogenesis and vascular dilatation. We believe that vascular changes directly add to the airway narrowing and hyper-responsiveness by exudation and transudation of proinflammatory mediators, cytokines and growth factors; facilitating trafficking of inflammatory cells; causing oedema of the airway wall and promoting ASM accumulation. One of the key regulators of angiogenesis, vascular endothelial growth factor in concerted action with other endothelial mitogens play pivotal role in regulating bronchial angiogenesis. In this review article we address recent advances in pulmonary angiogenesis and remodelling that contribute in the pathogenesis of chronic airway diseases.

Cardiac inflammatory myofibroblastic tumor (IMT) is a rare entity and is associated with distinct clinical, pathological and molecular features. The clinical behavior, natural history, biological potential, management and prognosis of such tumors are unclear. We present herewith an adolescent girl who presented with similar entity involving the junction of the right atrium and the inferior vena cava (IVC) in association with thrombocytosis and IVC thrombosis leading to obstruction of blood flow. Diagnostic tools included imaging and immuno-histopathology studies. Surgical management included resection of the tumor and thrombo-embolectomy of the IVC under cardiopulmonary bypass. This case is unique due to association of complete obstruction of IVC caused by the strategic location of the tumor, thrombosis of vena cava and association of thrombocytosis. These features have not been reported yet in relation to the cardiac IMT. This report will help in better understanding and management of similar cases in terms of planning cannulation of femoral veins or application of total hypothermic circulatory arrest during cardiopulmonary bypass and prompt us to look for recurrence or metastasis during follow up using echocardiography and laboratory investigations. The possibility of IMT should be kept in the differential diagnosis of cardiac tumors especially in children and adolescents.

Three hundred and twenty (84.5%) of 379 cardiac studied in the Pediatric Cardiology Unit of King Fahd Specialist Hospital, Buraidah, between August 1988 and October 1991 had congenital heard disease. Both sexes were equally affected. Ventricular septal defects were the most common lesions (relative frequency 38.5%), followed by atrial septal defects (11.5%), pulmonary valve stenosis (9%), and patent ductus arteriosus (8%). Compared with American and European children, our patients had a paucity of obstructive aortic lesions (5% versus 109%), and an excess of atrial septal defects (11.5% versus 6.7%) and atrioventricular canal defects (5% versus 2.4%). The latter appeared to be due to the relatively high incidence of trisomy-21 in our patients, which was present in 32 (50.7%) of the 63 patients with identified etiology; that is, in 10% of the 320 patients as against a reported incidence of about 5% in other series. This comparatively high incidence was, in turn, attributable to the relatively advanced age (mean 34.0 +/- 8.3 years) of the mothers of the trisomic children. The cumulative detection rate was suboptimal: 29% at age one month, 53% at six months, and 60% at one year. There is, therefore, a need for increased awareness, especially among primary health and other front-line doctors, and earlier case detection.