26 research outputs found
Evaluation of Trastuzumab-induced early cardiac dysfunction using two-dimensional Strain Echocardiography
Abstract Aim: Trastuzumab, a chemotherapeutic agent used in the treatment of breast cancer. has been shown to induce subclinical left ventricular (LV) dysfunction during a three to six month period as evidenced by strain echocardiographic examination without any change occurring in the ejection fraction of LV. The present study evaluated the presence of subclinical LV dysfunction using strain echocardiography 1 day and 7 days after the initiation of trastuzumab therapy. Material and methods: The patients with breast cancer receiving adjuvant trastuzumab therapy underwent 2-dimensional, tissue Doppler, and strain echocardiographic examination at baseline and 1 day and 7 days after therapy. LV global longitudinal strain (GLS), global circumferential strain (GCS) values, and other echocardiographic parameters were calculated. Results: A total of 40 females, mean age 50±10 years, were evaluated. Of these patients, 97% received anthracycline and 73% received radiotherapy before the initiation of trastuzumab therapy. No change was observed in any of the echocardiographic parameters 1 day after the initiation of trastuzumab therapy (p>0.05). The LV ejection fraction, tissue Doppler parameters, and GCS values did not show any changes 7 days after the initiation of therapy, whereas significant decreases were observed in GLS value (19.2±4.0% vs. 17.2±3.4, p=0.001) and systolic annular velocity of the lateral LV wall (S' velocity) (10.5±3.2 vs. 8.6±2.2, p=0.002). Conclusion: Trastuzumab therapy is associated with subclinical LV dysfunction as early as 7 days after initiation of the therapy as evidenced by the decreases in GLS value of LV and systolic annular velocity of the lateral LV wall
A Sinus of Valsalva Aneurysm: More Complicated Than Imagined
WOS: 000288499600005PubMed ID: 21366686Sinus of Valsalva aneurysms mostly remain silent. Here, we report a case with sinus of Valsalva aneurysm which caused right ventricular outflow obstruction and ruptured into the main pulmonary artery in the setting of DeBakey type I aortic dissection (Echocardiography 2011;28:E60-E63)
Chronic Papillary Muscle Rupture: 14-Year Survival without Surgical Treatment
WOS: 000351799100013PubMed ID: 27122867Papillary muscle rupture is a life-threatening complication of myocardial infarction which is usually refractory to medical treatment. We present a very rare case of a 65-year-old woman who had a myocardial infarction and posteromedial papillary muscle rupture which was only treated with medical therapy, including her corresponding 14-year follow-up. However, surgical intervention is still strongly recommended because the prognosis of acute papillary muscle rupture associated with myocardial infarction remains poor
Left Atrial Appendage Functions in Patients With Hypertrophic Cardiomyopathy and Sinus Rhythm: Transesophageal Echocardiography and Tissue Doppler Study
82nd Scientific Session of the American-Heart-Association -- NOV 14-18, 2009 -- Orlando, FLWOS: 000271831502763Amer Heart Asso
Relationships between P wave dispersion, atrial electromechanical delay, left atrial remodeling, and NT-proBNP levels, in patients with hypertrophic cardiomyopathy
Background: We evaluated the associations among the well-known atrial fibrillation (AF) predictors including P-wave dispersion (PWD), intra- and inter-atrial electromechanical dyssynchrony (EMD), left atrial (LA) phasic functions, and plasma N-terminal prohormone of B-type natriuretic peptide (NT-proBNP) levels, in patients with hypertrophic cardiomyopathy (HCM). Methods: Seventy patients with HCM and age and sex matched 70 subjects were enrolled. PWD, LA total emptying fraction (LATEFr), active emptying fraction (LAAEFr), passive emptying fraction (LAPEFr), expansion index (LAEI) intra- and inter-atrial EMD were calculated. Levels of NT-proBNP of all subjects were determined. Results: Higher PWD (p = 0.006), significantly decreased LAEI (p < 0.001), LATEFr, and LAPEFr (both p values < 0.001) values and significantly increased inter-atrial (p < 0.001), LA (p = 0.001), and right atrial dyssynchrony (p < 0.001) were observed in the HCM group compared to controls. PWD was negatively correlated with LAEI (r = –0.236, p = 0.005) and LATEFr (r = –0.242, p = 0.04), however not with LAPEFr (p = 0.7), or LAAEFr (p = 0.3). Except for the LA lateral wall PA’ (r = 0.283, p = 0.02), PWD was not correlated with any atrial EMD parameter. Inter-atrial dyssynchrony was related to LAEI (r = –0.272, p = 0.001), LATEFr (r = –0.256, p = 0.03), and LAPEFr (r = –0.332, p = 0.006), but not, however, to LAAEFr (p = 0.4). The plasma NT-proBNP levels of patients were not correlated with either PWD (p = 0.927) or inter-atrial dyssynchrony (p = 0.102). Conclusions: PWD and inter-atrial dysynchrony seem to independently promote AF, although both are associated with LA reservoir function in HCM populations. The NT-proBNP level is not associated with these two AF predictors in patients with HCM. NT-proBNP seems to be a poor marker of atrial electrical remodeling in HCM patients
Hypereosinophilic Syndrome Presenting with Large Left Ventricular Apical Thrombus and Pulmonary Embolism
WOS: 000295971900002PubMed ID: 21854430A 45-year-old man presented with dyspnea on exertion, fatigue, and cough. Transthoracic echocardiography showed a large apical thrombus in the left ventricle. The laboratory results showed prominent eosinophilia on blood smear, elevated acute phase reactants and D-dimer serum levels. Bone marrow examination showed a Fip1-like platelet-derived growth factor receptor alfa fusion gene mutation. The case was diagnosed as myeloproliferative variant hypereosinophilic syndrome. Contrast-enhanced computed tomography demonstrated thrombi not only in left ventricle but also in multiple segmental pulmonary arteries. Cardiac magnetic resonance imaging showed left ventricular apical thrombus without subendocardial fibrosis. Cardiopulmonary manifestations of hypereosinophilic syndrome completely resolved after treatment. (Echocardiography 2011;28:E180-E182