The data indicate that L-arginine prevents xanthoma formation and reduces atherosclerosis in LDL receptor knockout mice fed a high-cholesterol diet. The abrogation of the beneficial effects of L-arginine by L-NA suggests that the antiatherosclerotic actions of L-arginine are mediated by NOS. The data suggest that L-arginine may be beneficial in familial hypercholesterolemia.

Apoptosis of myocardial cells occurs during cardiac allograft rejection. Apoptosis during rejection parallels the expression of iNOS, which suggests that apoptosis may be triggered by NO and peroxynitrite.

Excessive nitric oxide (NO) production within the heart is implicated in the pathogenesis of myocyte death, but the mechanism whereby NO kills cardiac myocytes is not known. To determine whether NO may trigger programmed cell death (apoptosis) of adult rat ventricular myocytes in culture, the NO donor S-nitroso- N-acetylpenicillamine (SNAP) was shown to kill purified cardiac myocytes in a dose-dependent fashion. In situ analysis of ventricular myocytes plated on chamber slides using nick-end labeling of DNA demonstrated that SNAP induces cardiac myocyte apoptosis, which was confirmed by the identification of oligonucleosomal DNA fragmentation on agarose gel electrophoresis. Similarly, treatment of cardiac myocytes with cytokines that induce inducible NO synthase was shown to cause an NO-dependent induction of apoptosis. Addition of reduced hemoglobin to scavenge NO liberated by SNAP extinguished both the increase in percentage of apoptotic cells and the appearance of DNA ladders. Treatment with SNAP (but not with N-acetylpenicillamine or SNAP + hemoglobin) not only induced apoptosis but resulted in a marked increase in p53 expression in cardiac myocytes detected by Western blotting and immunohistochemistry. These data indicate that NO has the capacity to kill cardiac myocytes by triggering apoptosis and suggest the involvement of p53 in this process.

Background Takotsubo cardiomyopathy (TCM) is a non-ischemic syndrome characterized by transient acute left ventricular dysfunction as evident on transthoracic echocardiography. It can often mimic myocardial ischemia and is characterized by the absence of angiographic evidence of obstructive coronary artery disease. Reports of Takotsubo syndrome in elderly with asthma exacerbations have been noted. Case presentation We describe a case of TCM in a 68-year-old female who presented with acute shortness of breath secondary to status asthmaticus. Her electrocardiogram showed ST segment elevations in multiple coronary artery distributions and mildly elevated troponin levels. Coronary angiography showed no significant stenosis of the coronary arteries with left ventriculography that showed systolic apical ballooning with a 10% ejection fraction, consistent with TCM. Conclusions Takotsubo syndrome should be considered in the differential diagnosis of patients presenting with status asthmaticus and elevated troponin levels on admission. Patients should be asked about the use of beta agonist prior to admission. A thorough literature review including a summary of 11 previously published case reports of TCM with acute asthma exacerbations has been presented.

Atrial fibrillation remains one of the most common conditions that clinical physicians encounter on a daily basis in the inpatient setting. This arrhythmia brings with it numerous complications if not treated properly and leads to intensive analysis of its primary etiology which is unique to every patient. In this case, we present a previously asymptomatic individual who presented to the hospital with respiratory complaints and was found to have a large lung mass, consistent with neuroendocrine lung cancer with direct compression of the left atrium leading to new-onset atrial fibrillation.