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Biomedical subjects

A Frustaci

Publications and source records attributed to A Frustaci.

At least 55 records · Page 3Linked to original sources
PubMed1992

Prevalence of left ventricular hypertrophy and cardiac arrhythmias in borderline hypertension.

Seventy-eight men with borderline hypertension according to the World Health Organization criteria underwent echocardiographic examination, followed by simultaneous ambulatory blood pressure and electrocardiographic monitorings for 24 h. The prevalence of echocardiographic left ventricular hypertrophy was 16.6% (13/78). Borderline hypertensives with left ventricular hypertrophy had more supraventricular (P less than .001) and ventricular ectopic beats (P less than .001) than normotensive controls and borderline hypertensives without cardiac involvement. Furthermore, ventricular ectopic activity was significantly related to left ventricular mass (r = 0.58, P less than .05) in borderline hypertensives showing echocardiographic evidence of left ventricular hypertrophy. Our findings suggest that noninvasive assessment of target organ status, including echocardiography, should be employed to optimize risk stratification in borderline hypertension.

Adult↗
PubMed1992

[An unusual chronic microvasculitis: Goodpasture's syndrome with late myocardial involvement].

We describe a disease, started in a female young adult patient as an apparent pulmonary siderosis, followed nine years later by an extracapillary proliferative nephritis, which developed to uremia in a few months. Later an intra-myocardial vasculitis, responsible of heart failure, appeared. Immune-histochemistry and serological tests exclude a disease mediated by anti-GMB antibodies, and pathologic features suggest a vasculitis mainly affecting lungs and kidneys.

Adult↗
PubMed1991

Cardiac biopsy in patients with "primary" atrial fibrillation. Histologic evidence of occult myocardial diseases.

Fourteen patients (ten men and four women; mean age, 37 years) with lone atrial fibrillation (AF) (1 to 18 months' duration) were evaluated by thyroid function tests, two-dimensional echocardiography, hemodynamics, coronary angiography, and left ventricular endomyocardial biopsy, because of unresponsiveness to the usual antiarrhythmic therapy. The results of the T3, T4, TSH, and TRH tests were normal in all patients; cardiac valves and ventricular and atrial sizes (left atrium less than 40 mm) were within the normal limits; also normal were LVEDP (less than or equal to 10 mm Hg) and EF (greater than 0.50). Histologic findings were abnormal in all cases, with three patients showing cardiomyopathic changes, three other patients showing active myocarditis (lymphocytic in two and eosinophilic in one), and eight patients with nonspecific necrosis or fibrosis or both. Steroids (prednisone; 50 mg/m2 of body surface area daily) used in addition to antiarrhythmic therapy in patients with eosinophilic and lymphocytic active myocarditis were able to cause reversion to sinus rhythm, while the other patients continued to have AF. This study documents that occult myocardial diseases (myocarditis, cardiomyopathy, and nonspecific necrosis or fibrosis) can underlie "primary" AF. The addition of steroids to antiarrhythmic therapy in patients with refractory AF and histologic evidence of active myocarditis seems to be useful in controlling the arrhythmia.

Adult↗
PubMed1991

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↗
PubMed1990

Echocardiography and pathology of left ventricular "false tendons".

The anatomic incidence of left ventricular false tendons has been determined in 100 hearts obtained from consecutive autopsies on patients who had a wide variety of cardiac conditions. In this series, an anomalous band was found in 34 cases. A retrospective two-dimensional (2D) echocardiographic study was able to identify false tendons in only 18 percent of cases with anatomic evidence of them, indicating 2 mm as the limit of resolution of 2D echocardiography even with appropriate projections. Finally, the histologic examination has shown false tendons to contain conduction tissue and thus it is assumed to be intracavitary radiations of the bundle of His. This last consideration introduces new physical and electrophysiologic implications.

Adolescent↗
PubMed1990

Assessment of neuron in congenital heart disease with heart failure.

Pathological studies in five hearts from patients with congenital heart diseases have demonstrated that the number of neurons is similar to that found in normal controls. The number of neurons has been counted in a strip of right atrial wall between the venae cavae. The hearts were selected from a wide spectrum of the population, the youngest being 5-months old and the oldest 35 years old (mean age: 12 years); all were in failure. The neuronal counts are comparable to those found in a normal population of mean age 40 years.

Adult↗
PubMed1990

Fatal measles myocarditis.

A case of fulminant measles myocarditis is reported. Diagnosis has been obtained at autopsy, due to absence of skin rash, by identification of measles giant cells in the myocardium and by positive reaction of myocardial tissue to measles-specific immunoperoxidase. Unusual outcome is interpreted as due to defective cell-bound immunity and extentive involvement of myocardial microcirculation.

Acute Disease↗
PubMed1990

Congenital lymphangiectasia of interventricular septum.

A case of congenital lymphangiectasia of ventricular septum obstructing outflow tract is reported. It mimicks hypertrophic cardiomyopathy or a primary tumor of the heart. Surgical operation has been successful and the expected prognosis is good.

Heart Septal Defects, Ventricular↗
PubMed1990

Coenzyme Q10 in dilated cardiomyopathy.

The authors have tried to study the therapeutic efficacy of coenzyme Q10 (CoQ10) in patients with dilated cardiomyopathy (DCM). In fact, CoQ10 has been shown to be deficient in myocardial tissue biopsies taken from DCM hearts, compared to normal hearts. Thirty patients with histological diagnosis of DCM were orally treated with CoQ10 (100 mg/die) for 2 months. Before and after treatment a clinical examination with determination of NYHA class and an echocardiographic examination with determination of ejection fraction (EF) and of telediastolic (TDV) and telesystolic (TSV) volumes were performed, and blood was drawn for plasma CoQ10 determination. In seven patients the pretreatment endomyocardial level of CoQ10 was also assayed. Seven patients left the study because of poor therapeutic compliance. In 47% of patients the clinical symptomatology regressed, with improvement of NYHA class. The EF improved from 0.31 +/- 0.09 to 0.37 +/- 0.11 (p less than 0.001). The TDV passed from 262.2 +/- 85 ml to 203.3 +/- 83 ml (p less than 0.05), and the TSV from 166.13 +/- 75 ml to 126.9 +/- 56 ml (ns). The CoQ10 plasmatic levels improved in 95% of the patients: from 0.74 +/- 0.37 micrograms/ml to 2.27 +/- 0.99 micrograms/ml (p +/- 0.0001). The CoQ10 myocardial levels did not show univocal values, but the patients with lower myocardial levels seemed to have a better therapeutic response. These data suggest that the CoQ10 deficiency in DCM may be reversible and that the therapeutic effects depend on the basal plasmatic and myocardial levels. Therapy with coenzyme Q10 may be considered to be an efficacious aid in the traditional treatment of chronic cardiac failure.

Cardiomyopathy, Dilated↗
PubMed1989

Right ventricular dysplasia vs idiopathic dilated cardiomyopathy.

Dilated cardiomyopathy and right ventricular dysplasia, although their aetiologies are unknown, are separate entities which can be recognized by endomyocardial biopsy (EMB) and differentiated from other heart muscle diseases. Biventricular EMB is the most appropriate approach for the diagnosis. Histological definition is relevant to establish prognosis and treatment and for research purposes.

Adipose Tissue↗
PubMed1989

Persisting hypereosinophilia and myocardial activity in the fibrotic stage of endomyocardial disease.

An unusual case of endomyocardial fibrosis is reported complicating an idiopathic hypereosinophilic syndrome. Persisting hypereosinophilia, degranulated eosinophils in the blood, and myocardial activity have been found accompanying the fibrotic phase of endomyocardial disease. This occurrence supports the unitarian theory on tropical and temperate endomyocardial disease and suggests in such a condition the use of steroids or cytotoxic drugs in addition to surgery.

Endocardium↗
PubMed1989

Hypertrophic cardiomyopathy mimicking athlete heart: risk of progression and opportunity for a bioptical approach.

A case of hypertrophic cardiomiopathy (HCM) mimicking athlete heart, is reported. Performing competitive activity was followed by progression of HCM to cardiac dilation and hypokinesis so that transplant was needed at young age. The Authors suggest a more aggressive approach possibly inclusive of cardiac biopsy when doubtful cases of athlete heart require permission for competitive sports.

Adult↗
PubMed1989

Low atrial tachycardia as primary cause of the heart failure complicating congestive cardiomyopathy.

A 50-years-old man with severe heart failure was diagnosed to have congestive cardiomyopathy and low atrial tachycardia at a fixed rate of 103 bpm. Conventional therapy for heart failure exerted a beneficial effect but complete clinical improvement was achieved only by reducing the rate of low atrial tachycardia with amiodarone. This suggests that in this situation tachycardia itself played a main role in the genesis of hemodynamic derangement.

Amiodarone↗