Breast cancer is the most common malignancy in women around the world. About one in 12 women in the West develop breast cancer at some point in life. It is estimated that 5%-10% of all breast cancer cases in women are linked to hereditary susceptibility due to mutations in autosomal dominant genes. The two key players associated with high breast cancer risk are mutations in BRCA 1 and BRCA 2. Another highly important mutation can occur in TP53 resulting in a triple negative breast cancer. However, the great majority of breast cancer cases are not related to a mutated gene of high penetrance, but to genes of low penetrance such as CHEK2, CDH1, NBS1, RAD50, BRIP1 and PALB2, which are frequently mutated in the general population. In this review, we discuss the entire spectrum of mutations which are associated with breast cancer.

Aim-To determine whether elective direct current (dc) cardioversion of atrial fibrillation/flutter causes myocardial damage. Methods and results-Cardiac troponin T and creatine kinase were estimated 20-28 hours after dc cardioversion in 51 patients who received dc shocks for elective cardioversion of chronic atrial fibrillation/ flutter. Although creatine kinase was raised in 44 patients, cardiac troponin T was undetectable in all patients. Conclusion-Cardiac damage does not occur as a result of cardioversion. (Heart 1998;80:229-230) Keywords: cardioversion; troponin T; creatine kinase; atrial fibrillation Direct current (dc) cardioversion 1 revolutionised the management of cardiac arrhythmias. However, before the standardisation of outputs from external defibrillators there was controversy about the most appropriate strength of current to be used.2 Animal experiments have suggested that repeated high energy dc shocks result in myocardial damage.3 4 In humans, dc cardioversion causes a rise in the concentration of creatine kinase and its MB subfraction. [5][6][7] This observation, along with the electrocardiogram (ECG) changes (repolarisation abnormalities) sometimes seen after dc cardioversion, led to the suggestion that dc cardioversion causes myocardial damage. Most of the creatine kinase released after cardioversion comes from the chest wall skeletal muscles, 8 which also liberate the MB subfraction. Therefore, the extent that emergency dc cardioversion contributes to raised creatine kinase or its MB isoenzyme is unclear. The belief that myocardial damage might result from higher strengths of current may also have influenced recommendations about the choice of current strength. It remains uncertain whether dc cardioversion does actually cause myocardial damage.Cardiac troponin T is a cardiac specific protein component of the troponin/tropomyosin complex. 9 A rise in serum troponin T concentrations is specific for cardiac damage. It remains raised for up to 48 hours after myocardial injury, thus providing a wide time window. 9Currently available data suggest that the kinetics of cardiac troponin T release from acutely damaged myocardium are identical whatever the cause of damage. 10Our study was undertaken to determine whether there was any evidence of myocardial damage after elective dc cardioversion of atrial fibrillation/flutter by measuring concentrations of cardiac troponin T in patients undergoing dc cardioversion. MethodsFifty one consecutive patients undergoing elective dc cardioversion for atrial fibrillation/ flutter were entered into the study. None had chronic renal failure, acute myocardial infarction, or skeletal muscle disease. As described previously, 11 dc shocks were administered in increasing strengths of 100 J, 200 J, 300 J, and 360 J (only one shock of each strength), until either sinus rhythm was restored or 360 J was applied.A blood sample was taken 20-28 hours after dc cardioversion. Samples were centrifuged and analysed or frozen at −70°C until analysis (all analyses were p...

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Objective: The aim of the present study was to evaluate the time to syncope in Nitroglycerine potentiated short Head-up tilt test.Study Design, Settings & Duration: This was a descriptive cross sectional study conducted in Armed Forces Institute of cardiology from May2006 to May, 2007. Patients and methods: A total number of 90 patients with orthostatic intolerance both male and female were studied.Head-up tilt test protocol consisted of a Stabilization phase which lasted for five minutes Passive tilt phase: Patients were tilted at 70̊ fororthostatic stress for 15 minutes. In case of no symptoms the test continued with the drug provocation phase which lasted for 15 minutes. Thepatients were administered 400μg of nitroglycerine sublingually in aerosol preparation. Development of symptoms were noted at 5, 10 and 15minutes. Results: A total number of 90 patients were examined during the study period. The tilt table test was classified as positive in 58.9 % ofpatients and was negative in 41.1%. The test was positive in five patients without the drug provocation (9.4%). The responses were classifiedas positive vasodepressor in 35.8%, 15.09% as mixed and cardioinhibitory 15.09% in patients of neurally mediated syncope. The total time todisplay of symptoms to positivity in HUTT was 17.89± 6.99. The mean time to syncope after the administration of nitroglycerine was 5.61± 4.17minutes. Conclusions: Our study concludes that the drug administered phase can be reduced to 12±3 minutes.

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