Characterization of Myocardial Injury With High-Sensitivity Troponin.

BACKGROUND: High-sensitivity troponin I, cardiac form (hs-cTnI) accelerates the assessment of acute coronary syndrome. Little has been documented about its performance, how it relates to different types of myocardial injury, and its impact on morbidity and mortality. This study sought to expand understanding of hs-cTnI by characterizing types of myocardial injury, the impact of comorbidities, and 30-day outcomes. METHODS: The study retrospectively evaluated 1,975 patients with hs-cTnI levels obtained in the emergency department or inpatient setting from June to September 2020. Troponin was considered elevated if it was higher than the 99th percentile for either sex. Charts were reviewed to determine the presence of myocardial injury. Troponin elevation was adjusted for demographics, comorbidities, and kidney dysfunction. Thirty-day mortality and readmission rates were calculated. RESULTS: Of 1,975 patients, 468 (24%) had elevated hs-cTnI, and 330 (17%) had at least 1 type of myocardial injury, type 2 myocardial infarction being the most frequent. Sensitivity and specificity using the 99th percentile as a cutoff were 99% and 92%, respectively. The average maximum hs-cTnI level was significantly higher for type 1 myocardial infarction (P < .001). Being male, Black, non-Hispanic, and a hospital inpatient were all associated with higher initial and peak hs-cTnI levels (P < .001). Elevated hs-cTnI level, age, heart disease, kidney dysfunction, and inpatient status were predictive of 30-day mortality on multivariate analysis. CONCLUSION: Elevated hs-cTnI levels in emergency department and inpatient settings occurs most commonly because of type 2 myocardial infarction. Maximum hs-cTnI level is associated with the patient's particular type of myocardial injury, certain demographics, and cardiovascular comorbidities, and it may be a predictor of 30-day outcomes.

An Evidence-Based Review of Galcanezumab for the Treatment of Migraine.

PURPOSE OF REVIEW: This is a comprehensive review of the current literature on the usage of galcanezumab for migraine treatment. It reviews the biology, pathophysiology, epidemiology, diagnosis, and conventional treatment of migraines, then compares the literature available for galcanezumab with historical treatment options. RECENT FINDINGS: Migraine is a common headache disorder and constitutes a significant source of distress from both a personal and societal perspective. Conventional treatment includes abortive and preventive treatment. Treatment options are limited and may be only partially or minimally effective in some of the population. Recent evidence points to metabolic changes in the brain as possible causes of migraine, via reduced available energy or a spiking need for it, resulting in a relative insufficiency. This leads to trigeminocervical complex (TCC) activation and a headache episode, modulated by calcitonin gene-related peptide (CGRP). Galcanezumab (Emgality) is a monoclonal antibody targeting CGRP that is given in a monthly injection for the prevention of migraines. Its safety was previously shown in phase 1 and 2 trials, and recent phase 3 trials showed efficacy, with up to 50% reduction in monthly migraine days and improved functional capacity in migraineurs. Studies show that the drug is well tolerated and safe. Migraine headache is a common neurological syndrome that causes great pain and suffering. Treatment options today are limited. Galcanezumab does not prevent migraines, but it is effective in decreasing their frequency and length. It is also much better tolerated than the currently existing therapies. While it is unlikely to provide monotherapy for migraines, it is a novel therapy that may be added for cases of severe or frequent migraines.

A Review of Patisiran (ONPATTRO®) for the Treatment of Polyneuropathy in People with Hereditary Transthyretin Amyloidosis.

Hereditary variant transthyretin amyloidosis (ATTRv) is a rare genetic defect that affects about 5000-10,000 people worldwide, causing amyloidosis secondary to misfolding of mutant transthyretin (TTR) protein fibrils. TTR mutations can cause protein deposits in many extracellular regions of organs, but those deposits in cardiac and axonal cells are the primary cause of this clinical syndrome. Treatment options are limited, but new drugs are being developed. Patisiran, a novel drug, is a liposomal siRNA against TTR that specifically targets this protein, reducing the accumulation of TTR in tissues, with subsequent improvement in both neuropathy and cardiac function. Patisiran is likely to serve as a prototype for the development of further intelligent drug solutions for use in targeted therapy. In this review we summarize the evidence currently available on the treatment of polyneuropathy in people with ATTRv with patisiran. We review the evidence on its efficacy, safety, and indications of use, citing novel and seminal papers on these subjects.