Hypoalbuminemia on admission is a strong independent predictor for long-term mortality and development of advanced HF in patients with STEMI undergoing p-PCI.

Fragmentation of QRS complexes on ECG is associated with intraventricular systolic dyssynchrony and subendocardial fibrosis in NDCM patients with a narrow QRS interval and sinus rhythm.

Mitral valve aneurysms (MVAs) are rarely encountered in echocardiography laboratories. Although they are commonly associated with endocarditis of the aortic valve, various mechanisms have been suggested for the etiopathogenesis of MVAs associated with non-infectious conditions. 5,887 patients who underwent transesophageal echocardiography (TEE) between 2007 and 2012 were evaluated retrospectively for MVA. Mitral valve aneurysm is defined as a localized saccular bulging of the mitral leaflet towards the left atrium with systolic expansion and diastolic collapse. The color flow Doppler image of a perforation was described as a high-velocity turbulent jet traversing a valve leaflet in systole. We found that 12 of 5,887 patients (0.204 %) had MVA in TEE examinations. The mean age of patients with MVA was 53 years (range 21-80 years), including four females and eight males. Nine patients presented with symptoms of endocarditis. On TEE, aneurysms were located in the anterior mitral leaflet in 11 patients, and in the posterior mitral leaflet in one patient. Eight patients had severe, three had moderate, and one had trace mitral regurgitation. Of the nine patients with perforated leaflets, eight patients had severe and one patient had moderate mitral regurgitation. Aortic regurgitation was present in nine patients, being severe in three, moderate in two, mild in two, and trace in two patients. Two patients without severe mitral regurgitation were followed-up conservatively, while nine patients underwent surgery. Two patients died from septic shock, one in the postoperative period and the other one prior to surgery. Although MVAs occur during the course of aortic valve endocarditis and, in particular, due to aortic regurgitation jet, it should be borne in mind that they may develop as an isolated valvular pathology and may be misdiagnosed as chordal rupture, other cardiac masses, or vegetation. Thus, MVAs may not be so infrequent as they are thought; they may justify to be considered in the differential diagnosis of masses seen on the mitral valve on echocardiographic examination.

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Fragmentation in the resting ECG is associated with significant intraventricular dyssynchrony in patients with nonischemic cardiomyopathy, narrow QRS and sinus rhythm. Fragmentation in ECG might be useful in identifying patients who could benefit from cardiac resynchronization therapy.

In conclusion, we found that serum UA concentration and total antioxidant capacity (TAC) were significantly associated with aortic dilatation. The higher serum UA concentration may be responsible for the elevated serum antioxidant capacity that was observed among individuals with AscAA. Large-scale epidemiological studies conducted over several years are required to correlate the cross-sectional findings from this study with clinical outcome.

D-dimer is a final product of fibrin degradation and gives an indirect estimation of the thrombotic burden. We aimed to investigate the value of plasma D-dimer levels on admission in predicting no-reflow after primary percutaneous coronary intervention (p-PCI) and long-term prognosis in patients with ST segment elevation myocardial infarction (STEMI). We retrospectively involved 569 patients treated with p-PCI for acute STEMIs. We prospectively followed up the patients for a median duration of 38 months. Angiographic no-reflow was defined as postprocedural thrombolysis in myocardial infarction (TIMI) flow grade <3 or TIMI 3 with a myocardial blush grade <2. Electrocardiographic no-reflow was defined as ST-segment resolution <70%. The primary clinical end points were mortality and major adverse cardiovascular events (MACE). The incidences of angiographic and electrocardiographic no-reflow were 31 and 39% respectively. At multivariable analysis, D-dimer was found to be an independent predictor of both angiographic (p < 0.001), and electrocardiographic (p < 0.001) no-reflow. Both mortality (from Q1 to Q4, 5.7, 6.4, 11.3 and 34.1%, respectively, p < 0.001) and MACE (from Q1 to Q4, 17.9, 29.3, 36.9 and 52.2%, respectively, p < 0.001) rates at long-term follow-up were highest in patients with admission D-dimer levels in the highest quartile (Q4), compared to the rates in other quartiles. However, Cox proportional hazard model revealed that high D-dimer on admission (Q4) was not an independent predictor of mortality or MACE. In contrast, electrocardiographic no-reflow was independently predictive of both mortality [Hazard ratio (HR) 2.88, 95% confidence interval (CI) 1.04-8.58, p = 0.041] and MACE [HR 1.90, 95% CI 1.32-4.71, p = 0.042]. In conclusion, plasma D-dimer level on admission independently predicts no-reflow after p-PCI. However, D-dimer has no independent prognostic value in patients with STEMI.

Lower concentrations of Hb on admission are associated with higher rates of in-hospital mortality, heart failure and major bleeding after p-PCI.