The aim of this study was to assess in vivo whether the regional ultrasonic reflectivity, evaluated by a real-time integrated backscatter analysis, was related to the local content of connective tissue in human myocardium as estimated by quantitative histology of endomyocardial biopsies. Sixteen patients with presumptive diagnosis of cardiomyopathy were ultrasonically studied by means of an M-mode-based echocardiographic system with quantitative integrated backscatter analysis capabilities. A 2.25-MHz transducer was used. The integrated value of the rectified radiofrequency signal of the interventricular septum was taken as integrated backscatter index and expressed in percent normalized for the pericardial interface (assumed to be 100%). All patients also underwent multiple left ventricular endomyocardial biopsies, which were stained with Masson's trichrome and studied with the use of a computer-assisted image analysis system. The percent integrated backscatter index was significantly higher in the presence of connective tissue area greater than 20% (eight patients) versus less than 20% (eight patients): 51 +/- 25% versus 26 +/- 11%, p less than 0.05. A significant correlation (p less than 0.05, R = 0.55) was found between percent integrated backscatter index and percent connective tissue area. In vivo on-line quantitative ultrasound analysis is feasible in man and reliably identifies variations in the regional extent of fibrosis in human myocardium.

The ultrasonic image can offer unique information on the composition of atherosclerotic plaque, ie, the relative content of lipids, fibrous tissue, and calcific deposits. To date, however, the echographic assessment of plaque structure is based on a subjective, qualitative evaluation of the bidimensional images. We evaluated the feasibility and accuracy of assessing, in vivo, the acoustic properties of arterial carotid plaques by means of a suitably modified echographic apparatus allowing direct access to the radiofrequency signal. In 15 patients undergoing carotid thromboendarterectomy, the ultrasonic findings in 70 discrete sites (within the plaque, n = 54; normal sites, n = 11; or intraluminal thrombi, n = 5) were correlated with the histological analysis (hematoxylin-eosin and Mallory trichrome stains) independently performed on the arterial samples. The pathological examination was carried out at a similar level of the insonation; the sites analyzed within the plaque were chosen because of their uniform echoic characteristics. In each ultrasonic region of interest selected from the echographic image, the integrated amplitude of the rectified radiofrequency signal was measured as the integrated backscatter index. The intimal-medial layer of normal carotid wall (n = 11) exhibited values of -32.5 +/- 9.4 dB. The integrated backscatter index in fatty sites (n = 11, -40.3 +/- 5.4 dB) differed from that of fibrous (n = 12, -23.8 +/- 5.0 dB) and calcified (n = 26, -11.5 +/- 5.2 dB, P < .01 for all intergroup differences) sites. Intraluminal thrombotic sites (n = 5, -42 +/- 5.1 dB, P < .01) differed from fibrous and calcified subsets (P < .01) but overlapped (P = NS) with fatty sites. Histological sampling also showed two sites of intraplaque hemorrhage that exhibited very low backscatter values (-53 and -58 dB) and three fibrofatty sites showing backscatter values (-28, -28, and -32 dB) intermediate between the fibrous and the fatty subsets. Quantitative analysis of integrated backscatter of the arterial wall is feasible in humans and provides an operator-independent assessment of plaque echoic structure. In particular, integrated backscatter is effective in distinguishing lipidic, fibrotic, and calcific components in human atherosclerotic plaques.

Late potentials (LP) on the signal-averaged electrocardiogram (SAECG) are predictive of malignant ventricular arrhythmias and sudden cardiac death in patients with ischaemic and non-ischaemic cardiomyopathy. Cardiac dysfunction, both regional and global, as well as supraventricular and ventricular arrhythmias are reported in a high percentage of patients with end-stage renal failure (ESRF). The aim of the study was to assess the prevalence of LP and the effects of haemodialysis on the SAECG of ESRF patients. SAECG was recorded immediately before and within 30 min after the end of dialysis in 48 patients in sinus rhythm, free of conduction disturbances on ECG and of signs of congestive heart failure. Serum electrolytes were sampled together with the SAECG recordings. An echo-Doppler exam was performed within 2 weeks of the study. SAECGs were adequate for analysis in 45/48 patients. LP were present when at least two of the following criteria were fulfilled: QRS duration < or = 115 ms, LAS40 < or = 38 ms, RMS40 > or = 38 microV at 40 Hz high pass bidirectional filter, and noise <0.7 microV. LP were detected in 12/45 patients (25%) on the SAECG before dialysis; of these 12 patients, seven had a history of a previous myocardial infarction and two had documented coronary artery disease (CAD). A significant greater wall motion score index--calculated on a 16 segment model--was reported in patients with LP (1.20+/-0.20 vs 1.01+/-0.03, P<0.01), while left ventricular mass was comparable in the two groups of patients. At the end of dialysis, a significant prolongation of fQRS duration was found both at 25 and 40 Hz filters (from 98+/-11 to 106+/-16 ms and from 97+/-12 s to 102+/-13 ms, respectively, P<0.001). A significant inverse relationship was seen between the percentage of dialysis-induced serum potassium reduction and fQRS changes at 40 Hz (r=-0.68, P<0.001). LP were detected in a significant proportion of dialysis patients, probably related to underlying CAD with left ventricular dysfunction. Prolongation of fQRS after dialysis could be explained by the acute reduction in serum potassium levels.

Atherosclerosis is the main cause of morbidity and mortality in Western countries and carotid plaque rupture is associated to acute events and responsible of 15-20% of all ischemic strokes. Several proteomics approaches have been up to now used to elucidate the molecular mechanisms involved in plaque formation as well as to identify markers of pathology severity for early diagnosis or target of therapy. The aim of this study was to characterize the plaque secretome. The advantage of this approach is that secretome mimics the in vivo condition and implies a reduced complexity compared to the whole tissue proteomics allowing the detection of under-represented potential biomarkers.