Statin-Induced Myositis with Concomitant Myocarditis.

Statins are commonly prescribed medications that provide many significant cardiovascular benefits for both primary and secondary prevention in patients with and without coronary artery disease. Known adverse effects of these medications include varying degrees of muscle toxicity, including myalgia, myopathy, and rare cases of necrotizing myositis, hepatic dysfunction, and central nervous system changes. Despite known adverse effects, statins are rarely associated with myocarditis. Statins can cause skeletal muscle myopathy and myositis by upregulating HMG-CoA reductase (HMGCR) in muscle tissue, resulting in antibody-mediated inflammation. A similar proposed mechanism is likely possible within cardiac myocytes. We present a rare case of statin-induced necrotizing myositis with concomitant cardiac involvement. Severe skeletal muscle myositis was confirmed by lower extremity MRI and biopsy findings. In association, elevated and plateaued high-sensitivity troponin without evidence of cardiac ischemia warranted cardiac MRI, which further confirmed myocarditis due to inflammation within a non-vascular distribution. Given its rare presentation, the treatment for statin-induced cardiac toxicity is unclear; however, the patient in this case report was treated with pulse-dose intravenous steroids and indefinite discontinuation of statin medications.

Elevated risk of venous thromboembolism in patients undergoing therapeutic hypothermia after cardiac arrest.

INTRODUCTION: Targeted Temperature Management (TTM) reduces mortality and improves neurological outcomes after cardiac arrest. Cardiac arrest is considered a pro-thrombotic state. Endovascular cooling catheters may increase the risk of thrombosis. Targeted Temperature Management, however, increases fibrinolysis. The net outcome of these opposing effects remains largely unexplored. Moreover, the exact rate of venous thromboembolism (VTE) is uncertain in these patients. We sought to determine the incidence and potential predictors of VTE in patients undergoing TTM. METHODS: Single center retrospective analysis. Participants were age ≥18 years old, admitted with out-of-hospital or in-hospital cardiac arrest, underwent TTM between January 1, 2007 and April 30, 2019 with endovascular cooling catheter. A total of 562 patients who underwent TTM (Study group) were compared to 562 patients treated for ARDS (control group). This control group was based on presumed similarities in factors affecting VTE: intensive care setting, immobility, length of stay and likely presence of central venous catheters. RESULTS: Patients who underwent TTM had a significantly higher rate of VTE (6.6% vs 2.3%, p = 0.006) and deep vein thrombosis (DVT) (4.6% vs 1.3%, p = 0.011) when compared to control group. In multivariate analysis age, gender, race and hospital length of stay were not associated with development of VTE in the study group. CONCLUSION: Patients undergoing TTM after cardiac arrest have statistically higher incidence of VTE and DVT compared to patients with ARDS. This risk is independent of age, gender, race or length of stay.

Vasopressin therapy in cardiac surgery.

BACKGROUND: Arginine vasopressin (AVP) is a naturally occurring peptide with diverse effects mediated through selective V1 and V2 receptors. About 10% of patients undergoing cardiopulmonary bypass develop postoperative vasodilatory shock requiring high-dose catecholamines. We sought to examine the role of AVP therapy in cardiac surgery. METHODS: A search of Medline was conducted through September 2018 using key words and medical subject headings (MeSH) relating to AVP, copeptin, and cardiac surgery. A systematic review was performed on articles as they pertained to AVP for use as a vasopressor after cardiovascular surgery complicated by vasodilatory shock. RESULTS: A relative or absolute deficiency of Arginine vasopressin is associated with vasodilatory shock after cardiopulmonary bypass. Physiologic replacement with exogenous Arginine vasopressin results in significant increases in systemic vascular resistance and mean arterial pressure with decreased requirements of catecholamines. At doses of <0.1 U/min Arginine vasopressin is safe with very few adverse effects. CONCLUSION: Post-cardiopulmonary bypass vasodilatory shock is largely due to a relative deficiency of Arginine vasopressin. Exogenous administration of low-dose Arginine vasopressin alone or in combination with traditional catecholamines is a safe and effective way to manage this type of vasodilatory shock.

Impact of Sex and Contact-to-Device Time on Clinical Outcomes in Acute ST-Segment Elevation Myocardial Infarction-Findings From the National Cardiovascular Data Registry.

BACKGROUND: Emergent myocardial reperfusion via primary percutaneous coronary intervention is optimal care for patients presenting with ST-segment elevation myocardial infarction (STEMI). Delays in such interventions are associated with increases in mortality. With the shift in focus to contact-to-device (C2D) time as a new perfusion metric, this study was designed to examine how sex affects C2D time and mortality in STEMI patients. METHODS AND RESULTS: Clinical data on male and female STEMI patients were extracted and analyzed from the National Cardiovascular Data Registry from July 1, 2008 to December 31, 2014. A total of 102 515 patients were included in the final analytic cohort. The median C2D time in female patients with STEMI was delayed when compared to male patients (80 [65-97] versus 75 [61-90] minutes; P<0.001). The unadjusted mortality was higher in female patients when compared to male patients with STEMI (4.1% versus 2.0%; P<0.001). For every 5-minute increase in C2D time, the adjusted odds ratio for mortality was 1.04 (95% CI, 1.03-1.06) for female patients with STEMI and 1.07 (95% CI, 1.06-1.09) for male patients (P for sex by C2D interaction=0.003). CONCLUSIONS: To date, this is the largest analysis of STEMI patients that measures the impact of the new recommended C2D reperfusion metric on in-hospital mortality. Female STEMI patients have longer C2D times and increased mortality. The disparity can be improved and survival can increase in this high-risk patient cohort by decreasing systems issues that cause increased reperfusion times in female STEMI patients.