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OBJECTIVES This study was performed to evaluate an additional echocardiographic spectral Doppler marker, which would identify severe aortic stenosis (AS). BACKGROUND Echocardiography is most commonly utilized to assess AS and has been validated against invasive measurements. However, the data obtained are not always in agreement, leaving a conundrum regarding the true severity of AS and can lead to other diagnostic procedures. This highlights the importance of improved noninvasive diagnostic techniques. METHODS Forty-eight indeterminate cases of calcific AS that had been previously evaluated by both echocardiography and cardiac catheterization were included in the study, using cardiac catheterization as the gold standard for calculation of aortic valve area (AVA). The intensity of opening and closing of the aortic valve, represented by bright vertical deflections on the CW spectral waveform, was quantified using ImageJ software to generate pixel intensity histograms to create opening and closing click (OC and CC) ratios. These ratios were compared with echocardiographic variables and catheterization AVA. RESULTS Thirty-five patients were found to have severe AS and 13 patients were found to have nonsevere AS, as assessed by cardiac catheterization. CC ratio was found to be a significant predictor of severe AS with an OR 0.024 (95% CI: 0.002-0.378, P = .0079). Adding CC to a model using standard echocardiographic parameters resulted in significant improvement in the C-statistic (0.693 to 0.835, P = .0134). CONCLUSIONS An additional Doppler marker measuring the aortic valve CC ratio has been found to improve detection of severe AS.

Aortic valve calcium (AVC) is a strong predictor of aortic stenosis (AS) severity and is typically calculated by multidetector computed tomography (MDCT). We propose a novel method using pixel density quantification software to objectively quantify AVC by two-dimensional (2D) transthoracic echocardiography (TTE) and distinguish severe from non-severe AS. A total of 90 patients (mean age 76 ± 10 years, 75% male, mean AV gradient 32 ± 11 mmHg, peak AV velocity 3.6 ± 0.6 m/s, AV area (AVA) 1.0 ± 0.3 cm2, dimensionless index (DI) 0.27 ± 0.08) with suspected severe aortic stenosis undergoing 2D echocardiography were retrospectively evaluated. Parasternal short axis aortic valve views were used to calculate a gain-independent ratio between the average pixel density of the entire aortic valve in short axis at end diastole and the average pixel density of the aortic annulus in short axis (2D-AVC ratio). The 2D-AVC ratio was compared to echocardiographic hemodynamic parameters associated with AS, MDCT AVC quantification, and expert reader interpretation of AS severity based on echocardiographic AVC interpretation. The 2D-AVC ratio exhibited strong correlations with mean AV gradient (r = 0.72, p

Complex aortic atheromas are an important differential diagnosis to consider in evaluating sources of arterial embolization. Diagnosis of the embolic source is an essential first step, so treatment can then be initiated to prevent further reoccurrence. We report the case of a 36-year-old man, without significant medical history, who presented to the University of Illinois at Chicago with peripheral vascular embolism to the lower extremities. Computed tomography with contrast angiography and transthoracic echocardiography failed to reveal a source of the thromboembolism. A complex mobile atheroma was discovered in the ascending aorta during transesophageal echocardiography. The case presented is noteworthy when considering the following: the relative rarity of complex atheromas of the ascending aorta, the young age of the patient with no history of atherosclerotic disease, and the failure of computed tomography angiography to reveal the embolic source despite literature supporting high sensitivities for aortic plaque detection compared with transesophageal echocardiography.

Four clinical cases of subaortic hypertrophic muscular stenosis are discussed. All four, in addition to a loud systolic murmur, had a loud systolic click. However, the timing of the click and its relationship to the phase of the carotid pulse were different in each case varying from close to medium and to distant (or midsystolic). The comparison of the sound tracing with the carotid tracing demonstrated that, in each case, a sudden change in acceleration was taking place. In one, the click coincided with the onset of the carotid upstroke; in another, with the first peak of the carotid pulse; in the third, with the trough between first and second peak of the pulse; in the last, with a sudden drop of the pulse at mid-systole caused by sudden obstruction to flow. It is concluded that the clicks were caused by rapid changes of acceleration resulting from the abnormal aortic ejection. Thus, the study of the carotid pulse and of the sound tracing are important for a non-invasive diagnosis together with the echo study of the septum and ventricular wall.