Unicuspid aortic valve is a rare congenital malformation that usually presents in the 3rd to 5th decade of life-and usually with severe aortic stenosis or regurgitation. It often requires surgical correction. Diagnosis can be made with 2- or 3-dimensional transthoracic or transesophageal echocardiography, cardiac computed tomography, or cardiac magnetic resonance imaging. We report the case of a 31-year-old man who presented with dyspnea on exertion due to severe aortic stenosis secondary to a unicuspid unicommissural aortic valve. After aortic valve replacement, this patient experienced complete heart block that required the placement of a permanent pacemaker.
Promoting angiogenesis is a key therapeutic target for protection from chronic ischemic cardiac injury. Endothelial-Monocyte-Activating-Polypeptide-II (EMAP II) protein, a tumor-derived cytokine having anti-angiogenic properties in cancer, is markedly elevated following myocardial ischemia. We examined whether neutralization of EMAP II induces angiogenesis and has beneficial effects on myocardial function and structure after chronic myocardial infarction (MI). EMAP II antibody (EMAP II AB), vehicle, or non-specific IgG (IgG) was injected ip at 30 min and 3, 6, and 9 days after permanent coronary artery occlusion in mice. EMAP II AB, compared with vehicle or non-specific antibody, significantly, p<0.05, improved the survival rate after MI, reduced scar size and attenuated the development of heart failure, i.e., left ventricular ejection fraction was significantly higher in EMAP II AB group, fibrosis was reduced by 24%, and importantly, more myocytes were alive in EMAP II AB group in the infarct area. In support of an angiogenic mechanism, capillary density (193/HPF vs. 172/HPF), doubling of the number of proliferating endothelial cells, and angiogenesis related biomarkers were upregulated in mice receiving EMAP II AB treatment as compared to IgG. Furthermore, EMAP II AB prevented EMAP II protein inhibition of in vitro tube formation in HUVECs. We conclude that blockade of EMAP II induces angiogenesis and improves cardiac function following chronic MI, resulting in reduced myocardial fibrosis and scar formation and increased capillary density and preserved viable myocytes in the infarct area.
Heart failure is the leading cause of hospitalization in the USA. Despite major advances in the medical and device-related therapy including chronic resynchronization therapy for management of heart failure, significant number of patients eventually require advanced cardiac therapy including mechanical circulatory support or heart transplant. Heart transplant is a gold standard for end-stage heart failure but is limited by the donor heart shortage creating a definite need for alternative effective therapies. The earliest and most common form of mechanical circulatory support is counterpulsation therapy. Annually, more than 150,000 patients worldwide receive counterpulsation therapy for various indications including cardiogenic shock or severe left ventricular dysfunction (Nanas and Moulopoulos in Cardiology, 84:156-167, 1994) and many thousands of lives are saved each year (65 % survival) (Torchiana et al. in Journal of Thoracic and Cardiovascular Surgery, 113(4):758-764, 1997). There are different types of aortic counterpulsation devices. Here, we will give an overview of different counterpulsation devices with focus on C-Pulse device. Extra-aortic balloon counterpulsation, C-Pulse (Sunshine Heart Inc., Eden Prairie, MN), is an important and novel approach in the management of patients with advanced heart failure who remain symptomatic despite optimum medical and device-based therapy. C-Pulse is designed to provide permanent, long-term, continuous partial circulatory support for New York Heart Association class III and ambulatory class IV heart failure patients. C-Pulse is a nonblood-contacting counterpulsation using an inflatable cuff around the ascending aorta, extra-aortic balloon (EAB) counterpulsation device. A pivotal, multicenter US study to assess the safety and efficacy of C- Pulse in patient with Stage C and NYHA Class III or ambulatory Class IV heart failure is in progress.
We report a case of a 59-year-old woman who presented with worsening dyspnea which rapidly progressed to severe heart failure. Coronary arteries showed no obstruction. Supportive measures stabilized the patient's hemodynamics. Initially intravenous solumedrol was given, but when the patient's condition continued to deteriorate, intravenous immunoglobulin (IVIG) was added to the treatment regimen and her condition improved. Studies show no benefit to using immunosuppressive agents in viral myocarditis, but benefits have been demonstrated in other etiologies. Patients presenting with acute fulminant myocarditis with unknown etiology that continue to deteriorate with aggressive heart failure treatment may benefit from steroids and IVIG.
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