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F Loperfido

Publications and source records attributed to F Loperfido.

At least 19 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

Catecholamine-induced cardiomyopathy in multiple endocrine neoplasia. A histologic, ultrastructural, and biochemical study.

A catecholamine-induced dilated cardiomyopathy is reported in a patient with multiple endocrine neoplasia, type 3. A histologic and ultrastructural study has been undertaken in cardiac biopsy samples, together with determination of myocardial Ca++ and cellular membrane fatty acids. Contraction band necrosis of cardiocytes with supercontraction of sarcomeres progressing to myofibrolysis and increased levels of myocardial Ca++ have been found as morphologic and biochemical abnormalities, respectively. No lipoperoxidation of cellular membranes or an alpha-adrenergic mediated reduction of coronary supply could be recognized in the study. We indicate a receptor-mediated intracellular Ca++ overload as the main abnormality responsible for myocardial impairment.

Adrenal Gland Neoplasms

[Forme fruste of Gorlin's syndrome with a left ventricular neoplasm].

We report on a 25-year-old man, referred for atypical chest pain and negative T waves in leads V5-V6. A cardiac tumor, localized in the posterolateral left ventricular wall was diagnosed in this patient by nuclear techniques and bidimensional echocardiography. A complex form of pluridistrectual dysmorphic disorder (hypertelorism, prognathism, frontal bossing, multiple cysts of the mandible, calcification in falx cerebri, etc) was also present, suggesting a limited form of Gorlin's syndrome (nevoid basal cell carcinoma syndrome).

Adult

[Diagnosis of recent posterolateral myocardial infarction: an electrocardiographic, echocardiographic and scintigraphic study].

ECG and 2D echocardiography were studied in 64 patients with previous myocardial infarction and evidence of posterolateral fixed defect at 201 TI scintigraphy. The defect was isolated posterolateral in 47 patients (group 1), and posterolateral + inferoapical in 17 (group 2). Thirty subjects with no history of myocardial infarction and no 201 TI defects constituted the control group. We calculated sensitivity, specificity and predictive value of ECG and 2D echocardiography (pertinent wall motion abnormality) in the recognition of posterolateral infarction. ECG data were also analyzed using multivariate analysis. Among the ECG criteria, a positive T wave in V1 proved to be 100% sensitive and 76% specific both in group 1 and in group 2. At multivariate analysis, a 2-variable model (positive T wave inV1 + R/S ratio greater than or equal to 1 in V1-V2) had a sensitivity of 95 and 100% in group 1 and 2, respectively; the specificity was 80%. A 3-variable model (+ R wave duration in V1-V2 greater than or equal to 0.04 sec) proved to be less sensitive (70 and 88% in group 1 and 2, respectively), with a specificity of 97%. A pertinent dyssynergy at 2D echocardiography was 70% sensitive for posterolateral myocardial infarction in group 1, but only 29% in group 2, with a specificity of 100%. These results indicate: 1) standard ECG is more sensitive but less specific than 2D echocardiography in the recognition of previous postolateral myocardial infarction; 2) the recognition of posterolateral involvement can be frequently missed by 2D echocardiography in patients with associated inferior myocardial infarction.

Adult

[Increase of plasma levels of beta-endorphin during maximum bicycle ergometry effort in sedentary and trained subjects].

Plasmatic levels of beta-endorphin during maximal graded bicycle stress test were measured by RIA on extracted plasma in 10 well-trained (A group) and in 8 untrained subjects (C group). Blood samples were obtained at rest, at peak work load and at the third, 10th and 90th min of recovery. For every stress test the following were evaluated: exercise time, maximum work load, total work load, maximum double product and mean K (an index of velocity of heart rate recovery during the first three minutes after the exercise). Both groups A and C showed a significant rise in beta-endorphin activity at the third minute of recovery; the increase was significantly greater in trained rather than in sedentary subjects (p less than 0.01). Beta-endorphin release was closely related to mean K; no relationship was found between exercise time, maximum work load, total work load, maximum double product and beta-endorphin rise. Our data shows that a release of beta-endorphin occurs during the initial phase of recovery after a maximal stress test; beta-endorphin rise is greater in trained subjects and correlates with the speed of heart rate recovery, but has no relationship with the duration and the grade of the effort. Whether beta-endorphin increase plays a role in the rapid decrease of adrenergic tone which occurs after exercise or represents a secondary phenomenon remains to be determined.

Adult

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

[Echo-Doppler study of musical heart murmurs].

The origin of systolic or diastolic musical murmurs was investigated by means of echo-doppler examination in 51 patients with various cardiac diseases. In all cases a typical doppler spectrum was identified, showing bi-directional clusters of frequencies which were concentric in systole and parallel in diastole. The doppler audio signal was musical. A similar echo-doppler signal was obtained by a diapason vibrating in isotonic solution. These data allowed us to identify the site of the vibrating cardiac structure causing the typical echo-doppler spectrum and characteristic audio signal.

Echocardiography

[Release of beta-endorphin and beta-lipotropin during submaximal exertion in sedentary and active subjects. Endogenous opiate peptides during exertion in sedentary and active subjects].

Some recent studies suggest that changes in the endogenous opioid peptides (POE) secretion during stress may be involved in various hemodynamic, respiratory and hormonal responses to exercise. To evaluate the relationship between fitness and POE release, 10 mixed-type exercise trained athletes (A) and 10 sedentary normal controls (C) were examined by bicycle stress testing; maximum oxygen uptake (VO2max) and peak work load (PWL) were greater in A than C (VO2max = 61.8 +/- 5.2 vs 40.2 +/- 6.1 ml/kg; PWL = 1525 +/- 229 vs 915 +/- 305 kgm.both p less than 0.01). After 24 hours A and C underwent rectangular bicycle stress testing (two 20' steps at 60% and 80% VO2max). Total plasmatic beta-endorphin (BEP) and its precursor beta-lipotropin (BLPH) were dosed by radioimmunoassay at rest, at 60% VO2max, at 80% VO2max and after complete recovery. Physical exercise caused a transient rise of BEP + BLPH plasma levels in both A and C. In A the increase was greater and occurred earlier than in C. The POE release under submaximal exercise showed a close correlation with oxygen uptake and therefore with fitness. This relation appeared in A at both low and high effort levels, whereas in C it was more strict at higher effort level. There results suggest that POE system play an important role in the adaptive mechanisms in sport practice.

Adult

Assessment of left ventricular hypertrophy by ECG and VCG in patients with inferior and posterior myocardial infarction. A comparison with echocardiographic data.

Electrocardiographic (ECG) and vectorcardiographic (VCG) QRS voltage criteria have been analyzed in 26 patients with inferior and 17 with posterior myocardial infarction (MI) in comparison with left ventricular (LV) mass and global and regional wall motion as assessed by M-mode and two-dimensional (2D) echocardiography. Transverse plane QRS maximal vector correlated significantly with LV mass in patients with both inferior and posterior MI (r = 0.65 and 0.87, respectively, p less than 0.01). A transverse plane QRS maximal vector greater than 1.5 mV correctly recognized 12 of 15 (80%) and 9 of 12 (75%) patients with respectively inferior and posterior MI and LV mass greater than 221 gm. Of the ECG measurements, S V1-2 + R V5-6 correlated moderately with LV mass in patients with inferior MI (r = 0.47), and R V1-2 + R V5-6 correlated moderately with LV mass in those with posterior MI (r = 0.67). ECG and VCG QRS voltage data did not correlate with global and regional LV function as assessed by M-mode and 2D echocardiography. We conclude that: ECG and VCG QRS voltage parameters can be utilized for assessing non-invasively LV enlargement in patients with postero-inferior MI; ECG and VCG QRS voltage parameters should be utilized with caution for analyzing LV function or MI size in postero-inferior MI.

Adult