Hypertrophic cardiomyopathy (HCM) is the most common cause of sudden cardiac death (SCD) in the young, particularly among athletes. Identifying high risk individuals is very important for SCD prevention. The purpose of this review is to stress that noninvasive diagnostic testing is important for risk assessment. Extreme left ventricular hypertrophy and documented ventricular tachycardia and fibrillation increase the risk of SCD. Fragmented QRS and T wave inversion in multiple leads are more common in high risk patients. Cardiac magnetic resonance imaging provides complete visualization of the left ventricular chamber, allowing precise localization of the distribution of hypertrophy and measurement of wall thickness and cardiac mass. Moreover, with late gadolinium enhancement, patchy myocardial fibrosis within the area of hypertrophy can be detected, which is also helpful in risk stratification. Genetic testing is encouraged in all cases, especially in those with a family history of HCM and SCD.

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The following case involves a 62-year-old female patient suffering from heart failure with reduced ejection fraction (HFrEF) secondary to non-ischemic cardiomyopathy and Graves disease, who developed ventricular fibrillation (VF) after discontinuation of methimazole in preparation for radioiodine ablation. Electrocardiogram (ECG) showed a severely prolonged QTc in the setting of thyrotoxicosis, which significantly improved with high dose methimazole. VF secondary to thyrotoxicosis has rarely been reported and the literature review shows scarce data on its mechanism. Our case demonstrates not only a possible mechanism for the arrhythmia, but also highlights a potential risk factor for it. The report details how discontinuing antithyroid medication leads to VF in our patient and reviews the current literature on antithyroid withdrawal prior to radioiodine ablation therapy. Caution should be taken when discontinuing antithyroid medications in patients with advanced heart failure as potentially lethal ventricular arrhythmias can ensue.

The survival rate of pancreatic cancer is approximately four months. Most pancreatic carcinomas overexpress MUC1. MUC1 is a glycoprotein that serves as a barrier to infection in normal cells. However, MUC1 protects cancer cells from immune responses and cell death. Therefore, reducing MUC1 protein expression is expected to increase the sensitivity of tumor cells to killing by cells of the immune system. PPARs are transcription factors of the nuclear receptor family. PPARγ heterodimerizes with retinoid X receptor and binds to PPAR response elements. Recent studies in our laboratory have shown that rosiglitazone reduces cytokine‐stimulated MUC1 expression in various cancer cell lines. Therefore, we hypothesized that rosiglitazone will reduce MUC1 protein expression in pancreatic cancer cells. Pancreatic cancer cell lines were cultured and serum starved for several days. The cell lines were treated with and without rosiglitazone. Western blotting and autoradiography were used to separate and detect the MUC1 proteins synthesized by the cells. Our results indicate that rosiglitazone significantly reduces MUC1 protein expression in Capan2 and HPAF2 cell lines. PPARγ agonists in combination with tumoricidal agents offer a promising avenue to increase pancreatic tumor cell sensitivity to killing by decreasing MUC1 levels. Funding provided by the HHMI Science Education Grant and the McNair Scholars Program.