Cardiac cachexia, a syndrome characterized by systemic destruction, nutritional impairment and weight loss [1], has a prevalence ranging between 8 and 42% around the world [2]. The syndrome was first described by the father of medicine, Hippocrates, as follows: “the flesh is consumed and becomes water; shoulders, clavicles, chest and thighs melt away. The illness is fatal” [3]. Currently the most widely accepted description of primary cachexia is, in the presence of congestive heart failure, nonvoluntary loss of >6% of non-edematous body weight in less than 6 months [1,3,4]. Although the pathophysiological changes causing cardiac cachexia have not been fully clarified since the time of Hippocrates, it is suggested that nutritional impairment, gastrointestinal disorders, anabolic and catabolic imbalance, and neurohormonal and immune anomalies play a significant role in its development [1]. In addition to these major mechanisms, this perspective will focus on the possible role of irisin in the development of cardiac cachexia and heart attack.

Background: Pericardial tamponade, a life-threatening condition caused by the accumulation of fluid in the pericardial sac, can be acute or chronic. Mortality and morbidity can be minimized on prompt diagnosis and treatment with percutaneous drainage.

According to the literature data, post traumatic pseudoaneurysm is rare [1]. Most common site is common femoral artery, followed by radial and brachial artery but subclavian artery is very rare because trauma to it is rare. Incidence of complications associated with such pseudoaneurysm is estimated around 2–6% [2]. We present a case of the patient in whom pseudoaneurysm of left subclavian artery developed after five days of accidental stone chip injury and was successfully treated by surgical excision of pseudoaneurysm and removal of stone chip with direct closure of opening in subclavian artery.

Antiphospholipid syndrome (APS) is a disorder characterized by the presence of anti-phospholipid antibodies which can include Lupus anticoagulant and Anticardiolipin antibody [1]. These antibodies bind to cardiolipin and have been shown in some cases to require ß2- glycoprotein I in order to bind to cardiolipin [2]. Symptoms of this disorder include vascular thrombosis without inflammation in the vessel wall, premature birth, spontaneous abortion, and death in a morphologically normal fetus at or beyond the 10th week of gestation [1]. APS has a strong correlation to systemic lupus erythematosus (SLE) with studies showing that 30% of patients with SLE will develop APS; however, APS can still be found in patients without SLE at a low frequency [3].

In this era of percutaneous interventions and minimal invasive surgery, ministernotomy aortic valve replacement is good option to start minimal invasive cardiac surgery in any institute. Aortic valve replacement seems more feasible through ministernotomy as aorta is anterior structure and cannulation required can be done through exposed aorta and right atrium [1]. Most importantly it can be done with same intruments that are used in conventional full sternotomy aortic valve replacement. Patients with same criteria (Table 1), are selected and divided into two groups. In Group one 10 cases undergone ministernotomy AVR anvd in Group two 10 cases undergone conventional full sternotomy AVR. Observations in both groups are compared.

Transcatheter aortic valve implantation (TAVI) is an appropriate therapy to treat elderly patients with severe aortic stenosis considered high-risk surgical candidates. The safety and effectiveness of TAVI have been demonstrated in numerous observational clinical studies, national registries and also in controlled randomized trial [1,2].

The prevalence of moderate to severe calcific aortic valve stenosis in patients =75 years old is 2.8% and only 40% of patients with surgical indication undergo aortic valve replacement because of high perioperative risk, older age, lack of symptoms, and patient/family refusal [1]. In the absence of hemodynamically significant left ventricular (LV) outflow obstruction, calcific aortic valve disease (CAVD) prevalence raises up to 25% in patients aged from 65 to 74 years old [2,3] and independently predicts cardiovascular (CV) event, overall and CV mortality. As the population ages and CAVD incidence and prevalence increase, it is crucial a deeper understanding of the patho-physiology of heart valve calcification that could provide novel insight into medical therapeutic approaches to delay or modify the disease course. In the human body, several physiological processes of calcification take places and mineralized deposits are present, as bones, enamel and dentin. More than that, pathological mineralization can lead to ectopic calcification and pathologies as urinary stones, vascular calcification and calcific heart valve stenosis. Macroscopically, in aortic valve sclerosis there is an initial thickening of the valve leaflets and formation of calcium nodules, usually corresponding to the nodules of Arantio near the aortic surface, in association to angiogenesis, while end-stage calcific aortic stenosis is characterized by large, heavily calcific, nodular masses within the aortic cusps that protrude into the sinuses of Valsalva, thus interfering with valve opening along the aortic surface. While in the past heart valve calcification was seen as a passive, degenerative course of aging, evidences have shown that is an active, cell-mediated process with similarities to bone development (osseus metaplasia) [4].

The science and art of cardiac surgery has made rapid development in the past 65 years. The surgery for transposition of great arteries (TGA) symbolises the manner in which cardiac surgery has progressed. The eventually successful solution in the form of the now popular arterial switch operation (ASO) was elucidated after multiple contributions from several surgical stalwarts and geniuses over more than 35 years (Figure 1). This review traces the various milestones along this journey.

Balloon rupture in the process of percutaneous coronary intervention (PCI) leading to coronary artery dissection, subintimal hematoma and hematoma extension after stent implantation is an uncommon complication, but it has important clinical signifi cance. The reason for balloon rupture during PCI and hematoma extension after stent implantation is not clear. In this case, Balloon rupture may be due to excessive balloon dilation pressure, severe coronary artery calcifi cation, balloon dilatation with gas presence and poor quality of the balloon; hematoma extension after stent implantation may be for remaining undiscovered hematoma and dissection. We should pay attention to these risk factors and prevent the occurrence of clinical complications in the treatment of PCI.