Cardiovascular magnetic resonance in wet beriberi

The clinical presentation of beriberi can be quite varied. In the extreme form, profound cardiovascular involvement leads to circulatory collapse and death. This case report is of a 72 year-old male who was admitted to the Neurology inpatient ward with progressive bilateral lower extremity weakness and parasthesia. He subsequently developed pulmonary edema and high output cardiac failure requiring intubation and blood pressure support. With the constellation of peripheral neuropathy, encephalopathy, ophthalmoplegia, unexplained heart failure, and lactic acidosis, thiamine deficiency was suspected. He was empirically initiated on thiamine replacement therapy and his thiamine level pre-therapy was found to be 23 nmol/L (Normal: 80-150 nmol/L), consistent with the diagnosis of beriberi. Cardiovascular magnetic resonance (CMR) showed severe left ventricular systolic dysfunction, markedly increased myocardial T2, and minimal late gadolinium enhancement (LGE). After 5 days of daily 100 mg IV thiamine and supportive care, the hypotension resolved and the patient was extubated and was released from the hospital 3 weeks later. Our case shows via CMR profound myocardial edema associated with wet beriberi

New trials and therapies for acute myocardial infarction

Acute coronary syndromes (ACSs), which include the clinical entities of unstable angina (UA), non\u96ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI), account for more than 1.5 million hospital admissions annually in the United States alone. Approximately 1 million of these admissions are classified as UA/NSTEMI and approximately 500,000 are STEMI. Because of the overwhelming number of studies on ACSs over the past several years, this article focuses on new trials and therapies for treating patients diagnosed with STEMI

New trials and therapies for acute myocardial infarction

Acute coronary syndromes (ACSs), which include the clinical entities of unstable angina (UA), non\u96ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI), account for more than 1.5 million hospital admissions annually in the United States alone. Approximately 1 million of these admissions are classified as UA/NSTEMI and approximately 500,000 are STEMI. Because of the overwhelming number of studies on ACSs over the past several years, this article focuses on new trials and therapies for treating patients diagnosed with STEMI

Extracellular nucleotide regulation and signaling in cardiac fibrosis.

Following myocardial infarction, purinergic nucleotides and nucleosides are released via non-specific and specific mechanisms in response to cellular activation, stress, or injury. These extracellular nucleotides are potent mediators of physiologic and pathologic responses, contributing to the inflammatory and fibrotic milieu within the injured myocardium. Via autocrine or paracrine signaling, cell-specific effects occur through differentially expressed purinergic receptors of the P2X, P2Y, and P1 families. Nucleotide activation of the ionotropic (ligand-gated) purine receptors (P2X) and several of the metabotropic (G-protein-coupled) purine receptors (P2Y) or adenosine activation of the P1 receptors can have profound effects on inflammatory cell function, fibroblast function, and cardiomyocyte function. Extracellular nucleotidases that hydrolyze released nucleotides regulate the magnitude and duration of purinergic signaling. While there are numerous studies on the role of the purinergic signaling pathway in cardiovascular disease, the extent to which the purinergic signaling pathway modulates cardiac fibrosis is incompletely understood. Here we provide an overview of the current understanding of how the purinergic signaling pathway modulates cardiac fibroblast function and myocardial fibrosis

Scanning electron microscopy of macerated tissue to visualize the extracellular matrix.

Fibrosis is a component of all forms of heart disease regardless of etiology, and while much progress has been made in the field of cardiac matrix biology, there are still major gaps related to how the matrix is formed, how physiological and pathological remodeling differ, and most importantly how matrix dynamics might be manipulated to promote healing and inhibit fibrosis. There is currently no treatment option for controlling, preventing, or reversing cardiac fibrosis. Part of the reason is likely the sheer complexity of cardiac scar formation, such as occurs after myocardial infarction to immediately replace dead or dying cardiomyocytes. The extracellular matrix itself participates in remodeling by activating resident cells and also by helping to guide infiltrating cells to the defunct lesion. The matrix is also a storage locker of sorts for matricellular proteins that are crucial to normal matrix turnover, as well as fibrotic signaling. The matrix has additionally been demonstrated to play an electromechanical role in cardiac tissue. Most techniques for assessing fibrosis are not qualitative in nature, but rather provide quantitative results that are useful for comparing two groups but that do not provide information related to the underlying matrix structure. Highlighted here is a technique for visualizing cardiac matrix ultrastructure. Scanning electron microscopy of decellularized heart tissue reveals striking differences in structure that might otherwise be missed using traditional quantitative research methods

Coronary Artery Bypass Grafting in Cancer Patients: Prevalence and Outcomes in the United States

Objective: To characterize the contemporary efficacy and utilization patterns of coronary artery bypass grafting (CABG) in specific cancer types. Methods: We leveraged the data from the National Inpatient Sample and plotted trends of utilization and outcomes of isolated CABG (with no other additional surgeries during the same hospitalization) procedures from January 1, 2003, through September 1, 2015. Propensity score matching was used to assess for potential differences in outcomes by type of cancer status among contemporary (2012–2015) patients. Results: Overall, the utilization of CABG decreased over time (250,677 in 2003 vs 134,534 in 2015,