Pallavi Solanki

Blockade of EMAP II Protects Cardiac Function after Chronic Myocardial Infarction by Inducing Angiogenesis

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.

Unicuspid unicommissural aortic valve: an extremely rare congenital anomaly.

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.

Hypertension in African Americans with Heart Failure: Progression from Hypertrophy to Dilatation; Perhaps Not

AimConcentric hypertrophy is thought to transition to left ventricular (LV) dilatation and systolic failure in the presence of long standing hypertension (HTN). Whether or not this transition routinely occurs in humans is unknown.MethodsWe consecutively enrolled African American patients hospitalized for acute decompensated volume overload heart failure (HF) in this retrospective study. All patients had a history of HTN and absence of obstructive coronary disease. Patients were divided into those with normal left ventricular ejection fraction (LVEF) and reduced LVEF. LV dimensions were measured according to standard ASE recommendations. LV mass was calculated using the ASE formula with Devereux correction.ResultsPatients with normal LVEF HF were significantly older, female and had a longer duration of HTN with higher systolic blood pressure on admission. LV wall thickness was similarly elevated in both groups. LV mass was elevated in both groups however was significantly greater in the reduced LVEF HF group compared to the normal LVEF HF group. Furthermore, gender was an independent predictor for LV wall thickness in normal LVEF HF group.ConclusionIn African American patients with HF our study questions the paradigm that concentric hypertrophy transitions to LV dilatation and systolic failure in the presence of HTN. Genetics and gender likely play a role in an individual’s response to long standing hypertension.

Anteriorly displaced right coronary artery in acute myocardial infarction: what should every cardiologist know

Anteriorly displaced right coronary artery (RCA) and anomalous origin RCAs occur in ≈ 1% and 0.1% of adult patients, respectively, and are the leading cause of incomplete coronary angiography and prolonged procedure times. We present a case in which anteriorly displaced RCA occlusion resulted in an acute inferior-posterior-right ventricular myocardial infarction complicated by complete atrioventricular block and hypotension. Failure to image the RCA resulted in considerable delay in reperfusion time with fibrinolysis. The authors discuss the most frequent anatomic locations of ectopic RCAs and suggest an algorithm to be employed when an ectopic RCA cannot be imaged with conventional diagnostic catheters. Contrary to popular belief, the search for an ectopic RCA has <90° boundaries limited to the anterior third of the right sinus and anterior half of the left sinus.

TRENDS IN UTILIZATION OF INPATIENT PALLIATIVE CARE SERVICES AND RACIAL DISPARITY OF DISPOSITION TO HOSPICE CARE AMONG PATIENTS WITH HEART FAILURE IN THE UNITED STATES BETWEEN 2003 AND 2012

Background: The latest American Heart Association guidelines have recommended palliative/hospice care in selected patients with end-stage heart failure (HF). However, limited information exists regarding the trends in utilization of hospice care in this patient population. Methods: Data from the

Encasement of the Left Internal Mammary Arterial Graft to the Left Coronary Artery by Adenosquamous Carcinoma, an Unusual Tumor

We report a case of a patient with a previous coronary artery bypass graft who presented with chest pain and was found to have adenosquamous carcinoma encasing the left internal mammary graft to left anterior descending artery - the only viable vessel to his coronary circulation. Adenosquamous carcinoma, a rare lung cancer with a poor prognosis, causing obstruction of a bypass graft has not been previously reported.