Echo Features of Posteromedial Papillary Muscle Rupture without Papillary Muscle Prolapse into the Left Atrium

A 67-year-old male presented to the hospital emergency department with a 3-day history of decreased exercise tolerance, fatigue and exertional chest tightness. These symptoms began after an initial episode of prolonged chest pain associated with diaphoresis and dyspnea.. The admission electrocardiogram (EKG) and cardiac "markers" were consistent with a recent inferolateral myocardial infarction (MI). There was no history of cardiovascular disease. Risk factors were that of a family history of heart disease, long-standing tobacco use and elevated lipids. The patient was on no medications. Bedside echocardiography (TTE) revealed left ventricular (LV) basal inferior-inferolateral aneurysmal formation with mild mitral regurgitation (MR). Significant aortic sclerosis was noted (movie clip S1). Because of continued exertional chest pain up through admission, diagnostic angiography was performed. The coronary tree was codominant, with only disease in the circumflex system noted. A large obtuse marginal (OM) branch of the circumflex artery was occluded and could not be opened percutaneously. Left ventriculography was consistent with findings by TTE, with inferobasal dyskinesis noted. The following morning, the patient developed sudden dyspnea, hypotension and pulmonary edema. Cardiac auscultation revealed only a soft systolic murmur, heard at the left sternal border and also apex. The EKG was unchanged, except that Mobitz Type I AV block developed. The patient required endotracheal intubation with mechanical ventilation, along with inotropic support. Address for correspondence and reprint requests: Edmund Kenneth Kerut, M.D., Heart Clinic of Louisiana, 1111 Medical Center Blvd, Suite N613, Marrero, LA 70072. Fax: 504-349-6621; E-mail: [email protected] A second bedside TTE was performed. Twodimensional imaging revealed new prolapse of the posterior mitral valve leaflet, "erratic" reverberations within the LV cavity, and evidence of severe MR by Doppler interrogation Based on the clinical scenario and suggestive findings by TTE, transesophageal echocardiography (TEE) was performed. Findings confirmed rupture of the posteromedial (PM) papillary muscle An intraaortic balloon pump (IABP) was placed and the patient taken to the operating room, where the PM papillary muscle was found to be ruptured In the setting of myocardial infarction, papillary muscle rupture is rather an uncommon event, occurring in 1% to 3% of patients with acute MI

TNF-alpha blockade decreases oxidative stress in the paraventricular nucleus and attenuates sympathoexcitation in heart failure rats

Oxidative stress plays an important role in the pathophysiology of cardiovascular disease. Recent evidence suggests that cytokines induce oxidative stress and contribute to cardiac dysfunction. In this study, we investigated whether increased circulating and tissue levels of tumor necrosis factor (TNF)-alpha in congestive heart failure (CHF) modulate the expression of NAD(P)H oxidase subunits, Nox2 and its isoforms, in the paraventricular nucleus (PVN) of the hypothalamus and contribute to exaggerated sympathetic drive in CHF. Heart failure was induced in Sprague-Dawly rats by coronary artery ligation and was confirmed using echocardiography. Pentoxifylline (PTX) was used to block the production of cytokines for a period of 5 wk. CHF induced a significant increase in the production of reactive oxygen species (ROS) in the left ventricle (LV) and in the PVN. The mRNA and protein expression of TNF-alpha, Nox1, Nox2, and Nox4 was significantly increased in the LV and PVN of CHF rats. CHF also decreased ejection fraction, increased Tei index, and increased circulating catecholamines (epinephrine and norepinephrine) and renal sympathetic activity (RSNA). In contrast, treatment with PTX in CHF rats completely blocked oxidative stress and decreased the production of TNF-alpha and Nox2 isoforms both in the LV and PVN. PTX treatment also decreased catecholamines and RSNA and prevented further decrease in cardiac function. In summary, TNF-alpha blockade attenuates ROS and sympathoexcitation in CHF. This study unveils new mechanisms by which cytokines play a role in the pathogenesis of CHF, thus underscoring the importance of targeting cytokines in heart failure