Anesthetic management of a patient with hypertrophic cardiomyopathy with atrial flutter posted for percutaneous nephrolithotomy.

Hypertrophic cardiomyopathy (HCM) is a most common genetic cardiovascular disorder, characterized by asymmetric hypertrophy of the interventricular septum that leads to intermittent obstruction of the left ventricular outflow tract (LVOT). Clinical presentation ranges from absence of symptoms to sudden death in the young and disability at any age. Although patients are asymptomatic in basal conditions, but anesthesia and surgical stress can lead to exacerbation of the LVOT obstruction and may complicate the perioperative course. Therefore, complete understanding of the pathophysiology and anesthetic implications is needed for the successful perioperative outcome. We describe the successful management of a case of HCM with atrial flutter posted for percutaneous nephrolithotomy.

Anesthetic management of Morgagni hernia repair in an elderly woman.

Adult onset congenital diaphragmatic hernia (CDH) is uncommon but not rare. Morgagni hernia is a rare variant of CDH. The defect tends to be small and patients may remain asymptomatic and diagnosed incidentally. When these patients become symptomatic, they usually present with gastrointestinal and cardiorespiratory symptoms or sometimes as an emergency due to obstruction or strangulation of herniated viscera. Chest radiograph, computed tomography scan, and magnetic resonance imaging are the imaging modalities used for diagnosis of CDH. Cardiopulmonary compromise due to mass effect of hernial contents on lungs, heart and great vessels, and obstruction or strangulation of herniated viscera poses the special challenge before anesthesiologists. Our patient was diagnosed to have Morgagni hernia, at the age of 72 years and underwent laparotomy for the same. This case highlights the key feature of the successful anesthetic management of adult onset CDH.

In Search of Aggregation Pathways of IAPP and Other Amyloidogenic Proteins: Finding Answers through NMR Spectroscopy.

The deposition of aggregates of human islet amyloid peptide (hIAPP) has been correlated with the death of insulin-producing beta (ß) cells in type II diabetes mellitus. The actual molecular mechanism of cell death remains unknown; however, it has been postulated that the process of aggregation and amyloid fibril growth from monomeric hIAPP is closely involved. Intermediate IAPP aggregates are highly toxic to islet cells, but lack of structural knowledge of these oligomers and complications in applying biophysical techniques to their study have been the main obstacles in designing structure-based therapeutics. Furthermore, the involvement of metal ions (Cu(2+) and Zn(2+)) associated with hIAPP has demonstrated an effect on the aggregation pathway. In the absence of well-defined targets, research attempting to attenuate amyloid-linked toxicity has been substantially slowed. Therefore, obtaining high-resolution structural insights on these intermediates through NMR techniques can provide information on preventing IAPP aggregation. In this Perspective, a review of avenues to obtain fundamental new insights into the aggregation pathway of IAPP and other amyloidogenic proteins through NMR and other techniques is presented.

Quartiles of peak troponin are associated with long-term risk of death in type 1 and STEMI, but not in type 2 or NSTEMI patients.

BACKGROUND: The prognostic value of peak cardiac troponin (cTn) in different types of acute myocardial infarction (AMI) under the universal clinical classification is unknown. HYPOTHESIS: We tested the hypothesis that the prognostic value of cTn varies with its peak level and type of AMI. METHODS: We studied 345 consecutive patients with AMI with mean follow-up of 30.6 months according to quartiles of peak cTn level (QPTL) and the type of AMI. The study outcomes were the major adverse cardiovascular events (MACE; composite of all causes of mortality and recurrent AMI) and the individual components of MACE. RESULTS: The study included patients with AMI Type 1 (n = 276), type 2 (n = 54), ST-segment elevation myocardial infarction (STEMI; n = 159), and non-ST-segment elevation myocardial infarction (NSTEMI; n = 186). Overall, peak cTn level was an independent predictor of MACE (hazard ratio [HR]: 1.001, 95% confidence interval [CI]: 1.000-1.003, P = 0.01) and death (HR: 1.002, 95% CI: 1.001-1.004, P = 0.003), but not of recurrent AMI. The highest risk of MACE and death was in the highest QPTL (61.6%, P = .016 and 66.3%, P = 0.021, respectively) while the highest risk of recurrent AMI was in the lowest QPTL (83.7%, P = 0.04). Quartiles of peak cTn level were significantly associated with increased risk of MACE and death in patients with Type 1 (all P = 0.01) and STEMI (P = 0.01 and P = 0.02, respectively), but no association existed in type 2 or NSTEMI patients. CONCLUSIONS: Overall, peak cTn predicts the risk of MACE and death but not the risk of AMI. While in Type 1 and STEMI patients, QPTL are associated with risk of MACE and death, no association exists in type 2 or NSTEMI patients.