Background/Objectives
Insufficient blood supply to the heart results in ischemic injury manifested clinically as myocardial infarction (MI). Following ischemia, inflammation is provoked and related to the clinical outcomes. A recent basic science study indicates that complement factor MASP-2 plays an important role in animal models of ischemia/reperfusion injury. We investigated the role of MASP-2 in human acute myocardial ischemia in two clinical settings: (1) Acute MI, and (2) Open heart surgery.
Methods
A total of 187 human subjects were enrolled in this study, including 50 healthy individuals, 27 patients who were diagnosed of coronary artery disease (CAD) but without acute MI, 29 patients with acute MI referred for coronary angiography, and 81 cardiac surgery patients with surgically-induced global heart ischemia. Circulating MASP-2 levels were measured by ELISA.
Results
MASP-2 levels in the peripheral circulation were significantly reduced in MI patients compared with those of healthy individuals or of CAD patients without acute MI. The hypothesis that MASP-2 was activated during acute myocardial ischemia was evaluated in cardiac patients undergoing surgically-induced global heart ischemia. MASP-2 was found to be significantly reduced in the coronary circulation of such patients, and the reduction of MASP-2 levels correlated independently with the increase of the myocardial necrosis marker, cardiac troponin I.
Conclusions
These results indicate an involvement of MASP-2 in ischemia-related necrotic myocardial injury in humans.
Olmesartan is an angiotensin II receptor blocker (ARB) drug approved in 2002 for the treatment of hypertension. Since 2012, there have been reports of a rare adverse effect suspected to be related to its use. The author presents a case of a 63-year-old female with refractory gastrointestinal (GI) symptoms including diarrhea with associated weight loss and severe electrolyte abnormalities necessitating hospitalization. An extensive inpatient evaluation ensued and was initially unremarkable. Esophagogastroduodenoscopy (EGD) discovered an endoscopically normal duodenum that was biopsied and notably revealed villous atrophy and intraepithelial lymphocytosis. Colonoscopy was normal appearing though biopsy findings were significant for nonspecific colitis. The endoscopy findings in the setting of the clinical presentation confirmed the diagnosis of olmesartan-associated enteropathy (OAE). Clinical improvement was noted after cessation of olmesartan and histological resolution was confirmed with repeat EGD post-discharge.
Several studies have reported influenza A (H1N1) virus as a cause of fulminant myocarditis. We report the first fatal case of fulminant myocarditis presenting as an acute ST-segment elevation myocardial infarction and ventricular tachyarrhythmia associated with influenza A (H1N1) in a previously healthy pregnant woman. A 38-year-old Asian woman, gravida 3, para 1-0-1-1, presented with flu-like symptoms. Initially, she developed wide-complex tachycardia requiring several defibrillations and was later intubated. Electrocardiogram showed ST-segment elevation. Coronary angiogram was negative and a pulmonary angiogram ruled out pulmonary embolism. Fetal compromise was noted on the monitor, and the patient underwent an emergent cesarean section. She subsequently expired. Autopsy confirmed severe myocarditis. Further testing confirmed influenza A (H1N1) virus. This case of a rare, yet lethal, complication of H1N1 infection underscores the importance of increased awareness among health care professionals to provide pregnant women with vaccination and prompt treatment.
BackgroundCongestive heart failure (CHF) is one of the leading causes of hospital readmissions within 30 days of discharge. Due to the substantial costs associated with these readmissions, several interventions to reduce CHF readmissions have been developed and implemented.MethodsTo reduce CHF readmissions at our community teaching hospital, the Smooth Transitions Equal Less Readmission (STELR) program was developed. Utilizing the Plan-Do-Check-Act cycle for quality improvement, resident physicians tracked patients enrolled in the STELR program. The resident contribution to the program was substantial in that they were able to quantify the improvement in both physician practices and patient readmissions. This provided insight into program areas requiring further modification, which the hospital would not have obtained without resident participation.ResultsThe readmission rate for patients diagnosed with heart failure decreased from 32% prior to program implementation, to 24% hospital wide (including patients who were not tracked in the STELR program), and 21% among patients tracked by the residents.ConclusionThis effective CHF readmission reduction program requires less financial resources compared to government funded programs. The resident involvement in the STELR program helped to assess and improve the program and also allowed the residents to gain an awareness of the resources available to their patients to facilitate their transition home. The program exposed the residents to systems-based practice, a fundamental element of their residency training and, more generally, community care.
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