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Biomedical subjects

A Saponaro

Publications and source records attributed to A Saponaro.

At least 19 recordsLinked to original sources
PubMed1993

[Cutaneous microcirculation in systemic sclerosis. Morpho-functional research using capillaroscopy and laser-Doppler].

Our previous researches proved that, in patients affected by Raynaud disease, microcirculatory alterations were greater in those cases in which the small vessels showed evocative appearances of a sclerodermatous connectivopathy. In this study we evaluated cutaneous microvasculature in 18 patients suffering from clear systemic sclerosis, compared with a group of 16 subjects affected by primitive Raynaud disease and a group of healthy subjects. We used videocapillaroscopy and laser-Doppler fluxmetry for morphological and functional study respectively. In patients affected by systemic sclerosis the rest flow was clearly reduced and morphological pattern of cutaneous small vessels deranged. The response to ischemic test allowed us to subdivide the skin-bounds in two subgroups: "no responders" 8 subjects (44%), in which reactive hyperaemia was completely absent, "responders" 10 patients (56%) in which the hyperaemia was completely overlapped with that of the two other groups, but with longer reaction times. In skinbounds the capillaroscopic pattern was clearly severe in comparison with other two groups (18.8 +/- 5.7 vs 5.7 +/- 2.3 and 3.6 +/- 1). Thus, in advanced stage of the pathology, is microangiopathy (in its tromboischemic and inflammatory aspects) that plays a very important role in the development of organ damage. Therefore, all those clinical and instrumental tests which may allow a differential early diagnosis between a primitive and a secondary Raynaud phenomenon be done, for its prognostic value in connection with the appearance of systemic sclerosis.

Adult↗
PubMed1993

Effects of sympathetic stimulation on microcirculatory dynamics in patients with essential acrocyanosis. A study using mental stress.

With the aim of examining possible alterations of the neurogenic regulation of microvascular hemodynamics, the cutaneous microcirculation in 21 patients with essential acrocyanosis was studied using a laser-Doppler method both in basal conditions and during mental stress using an arithmetic test. The analysis of results showed a significant reduction in basal flow (p < 0.02) in patients with acrocyanosis in comparison to control subjects. In 15 out the 21 patients studied it was found that there was an increase in the flowmetric curve during mental stress, whereas the test caused a diminished flow in normal subjects. The altered response to sympathetic stimulus might be the result of microcirculatory stasis which would provoke an alteration in the neurogenic regulation mechanisms of microvascular dynamics.

Adolescent↗
PubMed1993

[Cutaneous microcirculation and diabetic disease. A functional and flowmetry study in subjects with diabetes mellitus type 2].

Laser-Doppler single fingertip skin blood flow has been evaluated in 41 euglycemic type II diabetic patients under basal conditions and after dynamic testing (both ischemia and thermal stress). The same subjects have also undergone tests for the assessment of the degree of autonomic nervous system (ANS) dysfunction. The results have been compared to those obtained in 38 age-matched healthy subjects. In diabetic patients: baseline flow levels were much higher; the post-ischemic flow increase was less evident; a shorter hyperemic phase followed ischemia; a longer latency period was noticed, during thermal stress, together with a lower and slower hyperemic peak level. According to the results of ANS dynamic tests, diabetic subjects were divided into 3 groups: Group 1 (subjects with negative results); Group 2 (subjects with only one positive result); Group 3 (subjects with more than one positive test). Microcirculation disturbances were more often found in Group 3. These results show that a correlation exists between diabetic microangiopathy and ANS dysfunction. They also support the hypothesis, already pointed out by other research groups, of a similar mechanism causing diabetic neurologic and vascular complications.

Adult↗
PubMed1992

[Microcirculatory changes in mitral prolapse as an expression of a systemic change in the connective tissue].

Many authors hypothesize that mitral valve prolapse (MVP) can be, in most cases, only a clinical sign of a primitive and systemic disorder of the connective tissue, like in Marfan Syndrome (MS). In our previous works we supported the presence of morphological and functional alterations of the microcirculation in patients affected by MS. In order to characterize a possible common denominator between these pathologies we have studied the cutaneous microcirculation in a group of patients affected by MVP, divided into 2 groups: anatomic MVP (MVP) and MVP syndrome (MVPS). The morphologic parameters have been investigated by nailfold capillaroscopy while digital laser-Doppler was used to study skin flowmetry. The results have been compared with a control group. Capillaroscopic remarkers showed an architecturally disorganized microvasculature with aspects related to a reduced compactness of the microvasculature unit with a significatively higher score compared with controls (7.3 +/- 2.9 vs 3.6 +/- 1 p less than 0.0005). Laser-Doppler flowmetry showed a significatively reduced rest flow; ischemic test showed: spike time 48.9 +/- 36.9 vs 15.3 +/- 7.7 s (p less than 0.0005), hyperemic acme 6.6 +/- 2.7 vs 12.5 +/- 8.4 UP (p less than 0.002); % increase 32.1 +/- 20.2 vs 51.5 +/- 15.4 (p less than 0.002). Thermic test showed a significatively higher thermic acme 8.7 +/- 4.2 vs 12.6 +/- 9.11 UP (p less than 0.05). These results appeared to be correlated with stage pathology as it was observed a severe microvasculature disorders in MVPS. Therefore we suppose that a phenotypic continuum may exist between MS and MVP.

Adult↗
PubMed1983

[Idiopathic mitral valve prolapse].

Current knowledge concerning idiopathic prolapse of the mitral valve is illustrated. The histopathological cause is myxoid degeneration of the mitral cusps, which sometimes extends to the tendinous cords, the valve implant ring, and the apex of the papillary muscles. Primary damage to these structures, whose intactness is essential for correct closure of the ostium, causes protrusion of the ventricular cusps into the left atrium during ventricular systole (i.e. prolapse). The reason for this degeneration is not known. The high familial incidence of prolapse lends credit to the most widely held suggestion, namely a hereditary defect. The clinical progress is benign in the great majority of cases ("crystallized" form) and is often asymptomatic. Complications are possible, however, and must always be borne in mind. They include progressive and acute mitral insufficiency, infective endocarditis, arrhythmias, motor or sensitive neurological complications, and sudden death. Particular attention must be paid to the path to be followed to arrive at the correct diagnosis. Careful evaluation of some of the clinical signs arousing suspicion in the previous history and/or objective examination enable a diagnosis to be formed with relatively simple, non-invasive instrumental techniques, such as echocardiography and polycardiography, provided other forms of prolapse secondary to ischaemic heart disease, mitral endocarditis, etc. are excluded. "Therapy is obviously necessary in the presence of complications; however, even in "crystallized" form, in the presence of subjective symptoms, tranquillizers and possibly beta-blockers may be necessary".

Adrenergic beta-Antagonists↗
PubMed1983

[Marfan's syndrome].

Marfan's disease is a hereditary condition (usually dominant) characterised by variously significant skeletal muscle, ocular, cardiac and above all respiratory alterations attributable to congenital disorder of the fibrous support proteins (particularly of collagen and elastin). Sporadic forms whose interpretation is uncertain, however may, also be observed. The exact nature of the biochemical error responsible for the syndrome, however, is not known. In the absence of fully indicative laboratory tests, diagnosis is based on recognition of he typical lesions and their systemic nature. Careful symptomatological examination of suspected subjects may lead to the detection of less common sites such as the respiratory system. Personal experience shows that it can also reveal clinically obsolete lesions, such as heart impairment discovered in some cases solely through elevation of the polycardiographic telediastolic index (in inverse relation to the pattern of the echocardiographic telediastolic volume), which is an expression of reduced ventricular compliance, and the presence of areas with a low thallium uptake, offering scintigraphic evidence of fibrosis replacing destroyed muscle fibres. Prognosis depends on the clinical expressiveness of the disease, i.e. the apparatuses involved and the extent of their damage. Heart alterations and their extent are undoubtedly an aggravating factor quoad vitam. The current position with regard to both drug management and possible surgical treatment is also discussed.

Adolescent↗