Congenital anomalies of the coronary arteries are relatively uncommon conditions with an incidence of approximately 2% in the adult population. Although less common than acquired coronary artery disease, these anomalies may be associated with myocardial ischemia and its consequences; angina, arrhythmia, infarction, and sudden death. A 21-year-old female patient with no significant prior medical history was found dead at home. Postmortem examination revealed high take-off of the right coronary artery with acute downward angulation of the proximal right coronary artery and acute downward angulation of the left main coronary artery. Microscopic examination revealed global myocardial ischemia consistent with a terminal ventricular dysrhythmia. There was no evidence of any other disease processes. Detailed toxicological investigation was negative. The Regional Forensic Pathology Unit experience with sudden death due to congenital coronary artery anomalies is presented along with a review of the current literature.

Fig 1 CT scan showing pulmonary fibrosis and organizing empyema. (A) At the level of aortic arch; (B) at the level of carina; (C) at the level of left ventricle, and showing extensive fibrotic changes and honeycombing effect in both lower lobes. Pig-tailed drain also shown.

Objective The main objective of this article is to study the usefulness of coronary sinus filling time (CSFT) as a predictor of coronary microvascular obstruction (CMVO) and future cardiovascular (CV) events after percutaneous coronary intervention (PCI) for left anterior descending (LAD) in stable coronary artery disease patients. Materials and Methods We analyzed 50 patients with stable angina who underwent elective PCI for single LAD significant stenosis. After stent deployment, coronary sinus was visualized in left anterior oblique 40 degree cranial 30 degree views, CSFT, and corrected thrombolysis in myocardial infarction frame count (cTFC) calculated from frame count. Post-procedure electrocardiographic changes noted and cardiac biomarker creatine phosphokinase and creatine phosphokinase-myocardial band levels estimated, and follow-up was done for 6 months. Patients classified into two groups: Group 1 with major adverse cardiac events (MACE) and Group 2 (without MACE). CSFT and cTFC measurements were compared among the two groups. Results Out of 50 patients who were recruited in the study, Group 1 comprises 20 patients, and Group 2 comprises 30 patients. Among the Group 1, 40% were females, while in Group 2, they were 16%. Group 1 showed high CSFT values compared to Group 2, and such are post-procedure ST, T changes (90% in Group 1, 20% in Group 2), cardiac biomarkers elevation (80% in Group 1, 23.3% in Group 2). At 6 months follow-up ejection fraction was lower in Group 1 (31.8 ± 6.4%) compared with Group 2 (58.8 ± 5.8%) at p < 0.0001, and angina (85%) versus (20%). Mean CSFT was significantly more in Group 1 (5.77 ±0.75s) compared with Group 2 (4.61 ± 0.55s) at p < 0.0001. With respect to cTFC, no significant differences were seen between the two groups (p < 0.5628). Receiver operating characteristic curve analysis showed CSFT of > 5.2s was the best cutoff value to differentiate the two groups. Conclusion CSFT significantly prolonged in patients with adverse cardiac events, and it may be used as a simple and quantitative predictor of CMVO and future CV events after elective PCI.

No abstract

BACKGROUNDSleep is a highly organized, complex behaviour characterized by a relative disengagement from the outer world and variable, but specific brain activity. It is an endogenously generated, homeostatically regulated and reversible. During sleep, there are profound physiological changes. This is particularly true of breathing and in number of conditions this had important implications. Breathing alters according to the state of consciousness. In healthy subjects, ventilation falls with the onset of sleep and is reduced during all phases of sleep compared with waking levels, alterations in the pattern of breathing occur including periodic breathing, apnoea, hypopnoea with gradual progression from stage I, II (18% decreased) to REM sleep (35% of decrease ventilation to awake stage). REM sleep related alterations in ventilation is more severe in respiratory disordered patients who had already some Hypoxemia, COPD is of best example.