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L M Biasucci

Publications and source records attributed to L M Biasucci.

3 recordsLinked to original sources

Abnormal intraventricular flow patterns in left ventricular dysfunction determined by color Doppler study.

We examined the relation between left ventricular (LV) flow dynamics measured by color Doppler, and either global or regional LV function in 19 normal subjects (group 1), in 55 patients with old myocardial infarction (MI) (29 without [group 2] and 26 with LV aneurysm [group 3]), and in 16 with idiopathic dilated cardiomyopathy (group 4). We calculated by M-mode color Doppler a flow persistence index (FPI) (duration of flow directed in systole toward the apex/LV ejection time). Contrast echocardiography was performed as a control method in 14 patients of the four groups. In normal subjects, rapid systolic inversion of flow toward the aorta was evident (FPI: 0.11 +/- 0.16). In all but one patient in group 2, a similar LV flow pattern was observed, but FPI was greater (0.32 +/- 0.26). In groups 3 and 4, a paradoxical antegrade LV flow pattern was evident during the entire period of systole (FPI: 1.13 +/- 0.42 and 1.28 +/- 0.36, respectively). LV flow patterns were reproduced in echo-contrast studies. FPI was related to LV end-diastolic volume (r = 0.77), end-systolic volume (r = 0.82), and ejection fraction (r = -0.84). However, when data were analyzed separately in the different groups, these correlations were significant only in groups 2 and 3. Paradoxical flow pattern is not peculiar to regional LV dysfunction; it also occurs in global LV dysfunction. This LV flow abnormality may develop after MI even in the absence of severe LV dyssynergy or dilation, and is quantitatively related to the degree of LV dysfunction.

Adult

Acromegalic cardiomyopathy. Left ventricular filling and hypertrophy in active and surgically treated disease.

Myocardial hypertrophy and interstitial fibrosis are common in acromegalic hearts and may induce left ventricular (LV) dysfunction. The transmitral flow pattern was examined by pulsed-wave Doppler in 20 patients with active acromegaly and nine with acromegaly cured by pituitary microsurgery. Control groups consisted of 25 normal subjects and 13 patients with systemic hypertension. We related Doppler indices of LV filling (E and A peak velocities and E/A ratio) to the duration of acromegalic disease, the GH plasma levels and LV mass. The LV mass/BSA was significantly greater in active acromegaly (187 +/- 53 g/sq m) and systemic hypertension groups (161 +/- 48 g/sq m) than in cured acromegaly (125 +/- 35 g/sq m) and the normal control group (109 +/- 36 g/sq m) (p < 0.01 for both). No differences were found in the E peak velocity, A peak velocity, and E/A ratio in the groups with active acromegaly (E/A: 0.9 +/- 0.2), cured acromegaly (E/A: 0.9 +/- 0.3), and systemic hypertension (E/A: 0.8 +/- 0.5). An E/A ratio < 1 was found in 13 patients with active and four with cured acromegaly; (p = NS). In the active acromegaly group, the E/A ratio was related to either LV mass or the duration of disease (r:-0.45 and -0.47, respectively; p < 0.05). In the cured acromegaly group, the E/A ratio was related to the duration of disease before surgery (r:-0.70; p < 0.05) and not to LV mass (r:0.12). In conclusion, an impairment in LV filling may be present not only in the patients with active acromegaly but also in those successfully treated by surgery after a long duration of the disease, despite normal LV mass. These LV filling abnormalities may be in part determined by nonreversible myocardial changes, such as interstitial tissue fibrosis.

Acromegaly

Doppler study of precordial musical murmurs.

Using phonocardiography, continuous- and pulsed-wave Doppler, 51 patients with precordial "musical" murmurs (49 with cardiac abnormalities) and 21 patients with noisy murmurs were examined. With M-mode echocardiography, fine fluttering of the structure generating the murmur was evident in 23 patients with musical murmurs and in 5 with noisy murmurs. A continuous-wave Doppler spectral signal characterized by parallel harmonics (Doppler musical signal) was evident in all patients with musical murmurs and in none with a noisy murmur. With pulsed-wave Doppler, the musical signal had less defined spectral features because of range ambiguity. Such a signal was experimentally reproduced by activating a diapason bathed in saline solution. The source of the musical murmur was established in all 51 patients by Doppler. The musical signal was associated with a valvular regurgitation signal in 36 patients and with a ventricular septal defect in 1 patient. The musical signal always disappeared when the pulsed-wave Doppler sample volume was placed 2 cm away from the generating structure. In 11 patients with musical murmur examined by color Doppler, no abnormal bidirectional flow signal was observed in the structures generating the signal. In 6 of the patients without valvular regurgitation, no flow disturbance was found. In conclusion, Doppler is valuable in determining the source of musical murmurs, and musical murmurs are caused by a vibrating structure even in the absence of flow turbulence.

Aortic Valve Insufficiency