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F Loperfido

Publications and source records attributed to F Loperfido.

At least 37 records · Page 2Linked to original sources

[Plasma levels of basal beta-endorphin and after effort in patients with severe left ventricular dysfunction and heart failure].

BACKGROUNDS: Purpose of the study was to evaluate beta-endorphin plasma levels at rest and after exercise, and the beta-endorphin release, in relation to exercise capacity, in patients with severe left ventricular dysfunction and heart failure. METHODS: Beta-endorphin plasma levels were assayed by radio-immunoassay before and after cardiopulmonary exercise testing in 28 heart failure patients with radionuclide ejection fraction < 35%, left ventricular end-dyastolic dimension > 60 mm and heart failure, and in 9 age-matched normal subjects. According to Weber's classification, 10 patients were in class A, 9 in class B, and 9 in class C. RESULTS: Beta-endorphin plasma levels at rest were respectively 3.52 +/- 2.31 pmol/L in patients, and 1.77 +/- 0.84 pmol/L (p < 0.05) in normals. In patients, baseline beta-endorphin correlated to VO2max (r = -0.76), peak rate-pressure product (r = -0.60) and exercise time (r = -0.56), then progressively increasing from class A to C. After exercise, beta-endorphin plasma levels increased respectively to 6.42 +/- 3.44 pmol/L (p < 0.001 vs baseline) in patients, and to 5.46 +/- 2.14 pmol/L (p < 0.001 vs baseline and NS vs patients) in normals. In patients, the release during exercise of beta-endorphin (exercise - baseline/baseline x 100) correlated to VO2max (r = 0.82), peak rate-pressure product (r = 0.64) and exercise time (r = 0.55), then progressively decreasing from class A to C. At multivariate analysis beta-endorphin release showed the greater correlation to exercise capacity parameters. CONCLUSIONS: In heart failure patients, beta-endorphin plasma levels are elevated at rest and its release during exercise is reduced in relation to functional impairment.

Adult↗

Left atrial thrombus and spontaneous echo-contrast in nonanticoagulated mitral stenosis. A transesophageal echocardiographic study.

OBJECTIVE: The aim of the study was to investigate if evidence at transthoracic echocardiography (TTE) of left atrial (LA) thrombus and LA spontaneous echo-contrast (LA SEC), which are potential precursors of embolization, can be predicted by clinical and TTE variables in nonanticoagulated mitral valve stenosis (MS). DESIGN: Clinical (age, NYHA class, rhythm, previous embolization) and TTE variables were related to transesophageal echocardiography (TEE) evidence of LA thrombus and/or LA SEC. SETTING: Nonanticoagulated MS was the setting. PATIENTS: Fifty-nine patients had MS, and they were not receiving anticoagulant or antiplatelet therapy (24 in sinus rhythm and 35 in atrial fibrillation). Previous arterial embolization had occurred in 12 patients (20.3 percent). MEASUREMENTS: The following TTE variables were analyzed: mitral orifice area (pressure half-time method), mitral gradient (Bernouilli's equation), LA end-systolic area, and mitral regurgitation (color Doppler grading). LA thrombus and LA SEC were analyzed by monoplane TEE. RESULTS: LA thrombus was found by TEE in 12 patients (20.3 percent). Of these 12, 11 (91.6 percent) were in atrial fibrillation. LA SEC was found by TTE in 2 patients (3.5 percent) and by TEE in 40 (67.8 percent) (p < 0.001). Previous embolization had occurred only in patients with LA SEC, of whom 5 had and 7 did not have LA thrombus. Patients with LA SEC, compared with those without LA SEC, were characterized by more frequent advanced NYHA class, atrial fibrillation, smaller mitral valve area, and larger LA size. By multivariate regression analysis, atrial fibrillation and LA end-systolic area were factors related to both LA thrombus and LA SEC, whereas mitral area was related only to LA SEC. However, whereas LA SEC was accurately predicted by the presence of atrial fibrillation (sensitivity: 87.5 percent; specificity: 100 percent) and a LA area > or = 30 cm2 (sensitivity: 72.5 percent; specificity: 89.5 percent), among patients with LA SEC no clinical or TTE variable accurately identified those with actual LA thrombus. CONCLUSIONS: TEE is not necessary in many patients with MS in order to recognize LA SEC. However, when actual LA thrombus detection is necessary for clinical decision making, TEE should be performed.

Adult↗

Doppler analysis of portal vein flow in tricuspid regurgitation.

Portal and hepatic vein flow-velocity profiles were examined by pulsed Doppler in 66 patients with tricuspid regurgitation (color Doppler grading: severe: 37, moderate: 18; mild: 11) and 20 normal subjects to determine if portal vein flow analysis is useful in the evaluation of tricuspid regurgitation. Portal vein flow was defined as one of the following categories: subcontinuous (dependent on respiration), pulsatile systolic (not inverted), inverted after systole, and continuous (not dependent on respiration). An index of portal vein flow pulsatility was also calculated. Standard classification of hepatic vein flow pattern was performed. Portal vein flow was pulsatile in 20% of normals subjects, and in 27.3% 44.5% and 51.3% of patients with respectively mild, moderate and severe tricuspid regurgitation; portal vein flow was inverted after systole in further 32.4% of patients with severe tricuspid regurgitation. Portal vein pulsatility index correlated with color Doppler grading of tricuspid regurgitation (r:0.63; p < 0.001) and right ventricle-atrium pressure gradient (r:0.39; p < 0.01). However, when compared with hepatic vein flow, both sensitivity and specificity of quantitative portal vein flow analysis was less reliable in diagnosing and grading tricuspid regurgitation. In particular, in patients with severe tricuspid regurgitation, the portal vein flow pattern was quite variable (pulsatile in 19 patients, inverted after systole in 12, and continuous in six). Liver biopsy was performed in nine patients, four of them with severe tricuspid regurgitation and continuous portal vein flow. Histology showed severe liver fibrosis in all four.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

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↗

[Not Available].

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Cataract↗

[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↗