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Biomedical subjects

B Martini

Publications and source records attributed to B Martini.

At least 55 records · Page 3Linked to original sources
PubMed1988

The development of vitreous membranes and retinal detachment induced by intravitreal carbon microparticles.

We induced intravitreal cellular proliferation by injection of carbon microparticles (size 20-70 nm) into the vitreous of 21 eyes of 11 cynomolgus monkeys. Pathological changes were evaluated by light and electron microscopy. At 1 week, there was conspicuous cyclitis showing exudative separation of the nonpigmented and pigmented ciliary epithelium, inflammatory cells, mononuclear phagocytes, and premacular vitreous detachment. At 3 weeks, continued macrophagic response was accompanied by fibrovascular proliferation with ingrowth of vessels from the ciliary body into the vitreous. At 4-5 weeks, deposition of extracellular fibrous material and traction retinal detachment (RD) were found. At 10 weeks, all eyes had extensive RD with pre- and subretinal collagenous cellular membranes. Carbon-laden macrophages were aggregated over the optic disc and fovea with prepapillary neovascularization and cystoid macular edema. Thus, intravitreal fibrovascular proliferation, vitreous contraction, and RD were induced by inflammatory and phagocytic response to carbon particles.

Animals↗
PubMed1988

Electrovectorcardiographic study of negative T waves on precordial leads in arrhythmogenic right ventricular dysplasia: relationship with right ventricular volumes.

In 24 cases of arrhythmogenic right ventricular (RV) dysplasia, the electrovectorcardiographic (ECG-VCG) behavior of T horizontal (wave and loop) was analyzed and the data compared with RV angiographic volumes. Arrhythmogenic RV dysplasia was diagnosed on the basis of echocardiographic and angiographic data in all subjects. At ECG, T wave was negative in V1 in nine subjects (37%), in V1-V2 in six (25%), in V1-V3 in two (8%), in V1-V4 in one (4%), in V1-V5 in two (8%), and in V1-V6 in four (16%). Nine subjects (37%) presented a bifid T wave in V2-V4. At VCG, T horizontal loop showed three morphologic characteristics: (1) counterclockwise rotation with a mean axis range of +15 degrees to -10 degrees (average, +5 degrees); (2) a figure-eight pattern with a mean axis range of +10 degrees to -40 degrees (average, -17 degrees); and (3) clockwise rotation with a mean axis range of -40 degrees to -110 degrees (average, -70 degrees). T wave changes seem to be primary and independent from QRS changes. RV and diastolic volumes ranged from 100 to 320 m1/m2 (average, 169 +/- 69). The extension of T wave negativity on precordial leads has a direct relationship with RV enlargement (r = 0.89, p less than 0.01). T changes are probably caused by dislocation of the left ventricle backwards secondary to RV dilatation, asynchronous RV repolarization, or intraparietal RV conduction defects.

Adolescent↗
PubMed1988

Complex arrhythmias in a patient with predominantly right ventricular cardiomyopathy.

A 23-year-old man presented with ventricular tachycardia. The electrocardiogram revealed right bundle branch block plus right axis deviation. It also showed frequent episodes of asystole, 2: 1 sinuatrial block and couplets of left bundle branch block morphology. Electrophysiologic study demonstrated sinuatrial entrance block, with an HV interval of 65 msec. It was also possible to induce sustained ventricular tachycardia of left bundle branch block pattern with normal QRS axis. Subsequent investigations were consistent with the diagnosis of right ventricular cardiomyopathy with mild left ventricular involvement.

Adult↗
PubMed1988

Juvenile sudden death and effort ventricular tachycardias in a family with right ventricular cardiomyopathy.

A family with occurrence of juvenile sudden death and effort polymorphous ventricular tachycardias is reported. Nineteen members aged 9 to 63 years were investigated. Four of them died suddenly in their youth. Postmortem investigation performed in 2 deceased subjects disclosed an apparently normal heart at macroscopy but fibro-fatty substitution of the right ventricular free wall was noted at histologic examination. The 14 living members underwent physical examination, resting electrocardiography, chest X-radiography, Holter monitoring, exercise stress testing, and M-mode and cross-sectional echocardiography. Four patients underwent hemodynamic and electrophysiologic studies. All 14 subjects had normal physical examination as well as normal electrocardiographic and cardiothoracic indices. Localized right ventricular structural and dynamic abnormalities were noted at cross-sectional echocardiographic and angiographic investigation of 9 of the patients. The right ventricular volumes in these subjects were normal or slightly increased. In 7 of them, polymorphous ventricular tachycardias were induced by exercise stress testing. The arrhythmias which were responsive to beta-blockade, do not seem to depend on reentry. Enhanced automaticity appeared to be the more likely mechanism of their production. These data demonstrate that right ventricular cardiomyopathy may occur in an occult form with life-threatening electrical instability.

Adolescent↗
PubMed1988

Familial occurrence of right ventricular dysplasia: a study involving nine families.

Right ventricular pathologic involvement, with autopsy evidence of fibrous and fatty infiltration of the right ventricle, was investigated in members of families in which cases of juvenile sudden death had occurred. Seventy-two subjects from nine families were studied. Sixteen died at a young age and 56 are living. Postmortem investigation in 11 cases (mean age at death 24 years) revealed massive replacement of the right ventricular free wall by fat or fibrous tissue. In the 56 living patients clinical examination included an electrocardiogram (ECG) at rest, ambulatory ECG recording, posteroanterior and lateral chest roentgenograms, M-mode and two-dimensional echocardiograms and exercise stress tests. In 14 patients, hemodynamic, angiographic and electrophysiologic studies were also carried out; right ventricular endomyocardial biopsy was performed in four. Structural and dynamic right ventricular impairment was detected in 30 living patients (mean age 25 years), and concomitant mild left ventricular abnormalities were present in 4. In eight of the nine families studied at least two members were affected. Ventricular arrhythmias (Lown grade greater than or equal to 4a) were recorded in more than half of the cases. The data reveal that right ventricular dysplasia shows a familial clustering and causes electrical instability that may place affected subjects at risk of sudden death. The mean age of these subjects suggests that the disease is manifested at a young age with a polymorphic clinical and arrhythmic profile. Finally, because this disease is a primary disorder of the ventricular myocardium, it should be included among the cardiomyopathies.

Adolescent↗
PubMed1988

Accelerated idioventricular rhythm of infundibular origin in patients with a concealed form of arrhythmogenic right ventricular dysplasia.

Five apparently healthy people (aged 16-47) presented with recurrent episodes of accelerated idioventricular rhythm characterised by left bundle branch block and right axis deviation. Clinical history, physical findings, basic electrocardiogram, chest x ray, and blood tests were within normal limits in all. Holter monitoring, exercise stress test, and electrophysiological study (in three patients) showed that accelerated idioventricular rhythm was mainly bradycardia dependent, easily suppressed by effort and overdrive pacing, and originated from the outflow tract of the right ventricle. The mechanism could be enhanced automaticity. Data from cross sectional echocardiography (in all patients) and from haemodynamic evaluation (in three) identified structural or wall motion abnormalities of the right ventricle or both without appreciable dilatation of the ventricle. Biopsy specimens of the right ventricular endomyocardium showed fibrosis in one patient, fibrosis and fatty infiltration in the second, and pronounced fatty infiltration in the third. These results show that some patients with accelerated idioventricular rhythm have right ventricular abnormalities that are typical of the localised and concealed forms of arrhythmogenic right ventricular dysplasia.

Adolescent↗
PubMed1988

Two simultaneous right ventricular tachycardias in a case of arrhythmogenic right ventricular dysplasia.

A 51 year old woman with arrhythmogenic right ventricular dysplasia had two types of ventricular tachycardia--(a) a regular and sustained tachycardia and with normal frontal plane axis on electrocardiography and (b) an irregular non-sustained tachycardia with a leftward frontal plane axis. Changes in the QRS complex were sometimes seen during the sustained ventricular tachycardia. The clinical, electrocardiographic, and electrophysiological data were consistent with the diagnosis of two different and sometimes simultaneous tachycardias originating in the right ventricle. This case suggests a possible new mechanism for the multiform appearances of the ventricular tachycardia.

Cardiomyopathies↗
PubMed1988

Bidirectional tachycardia. A sustained form, not related to digitalis intoxication, in an adult without apparent cardiac disease.

In this paper we report the first adult case of an "idiopathic" ventricular bidirectional tachycardia (BT), in a 57 year old woman. The tachycardia, at the time of our observation, was incessant in type and had a slightly irregular frequency of about 140 bpm. BT initiated and terminated abruptly, without any temporal relationship to the preceding RR interval, or the QRS morphology. The interval between the two alternating QRS patterns often varied over a wide range of values. The BT could be interrupted only by overdrive atrial and ventricular stimulation, but promptly reappeared as pacing was discontinued. Therapy with quinidine associated with propranolol was effective on a long term trial. The vectorcardiographic analysis and the electrophysiologic investigation demonstrated a ventricular origin of the BT, localizing its site of origin to common myocardial tissue, probably near the two left hemifascicles. Our data could not elucidate the electrogenetic mechanism of this ventricular arrhythmia, because of its chaotic behavior.

Digitalis↗
PubMed1988

[Termination of idiopathic ventricular tachycardia with QRS morphology of right bundle branch block and anterior fascicular hemiblock (fascicular tachycardia) by vagal maneuvers. Presentation of 4 cases].

We present 4 patients aged 51, 19, 22 and 16 years respectively, with no overt heart disease. They complained of recurrent episodes of paroxysmal sustained tachycardia with QRS morphology of right bundle branch block and left fascicular hemiblock. The analysis of the electrocardiogram during the tachycardia and, in two cases, the electrophysiologic study showed a complete a-v dissociation and capture beats confirming the ventricular origin of the arrhythmia. In all the patients the interruption of the tachycardia was obtained by the vagal maneuvers; in two of them the tachycardia was also sensitive to verapamil iv. These cases demonstrate the efficacy of the vagal maneuvers in the termination of fascicular tachycardia and support the hypothesis of slow-response nodal-like fibers, distally displaced, as the anatomical substrate of this arrhythmia.

Adolescent↗
PubMed1988

[Arrhythmogenic right ventricular dysplasia. Study of a selected population].

268 patients (pts) aged between 4 and 63 (average block 33.6) years were examined in an effort to detect structural and/or wall motion abnormalities of the right ventricle, consistent with a diagnosis of Arrhythmogenic Right Ventricular Dysplasia (ARVD). The patients included in this study had some of these features: 1) sudden juvenile death (age less than 35 years) due to heart disease; 2) relatives of pts died suddenly of pathologically proven ARVD; 3) pts with ventricular arrhythmias grade Lown greater than 3, and with QRS morphology mainly of left bundle branch block; 4) pts between the ages of 18 and 40, with negative T waves beyond V2; 5) pts with ventricular arrhythmias of left bundle branch block morphology, and grade Lown greater than 1, and negative T waves beyond V1. ARVD was recognized in 108 living and 18 deceased pts. Our data confirm that ARVD is a wide spectrum disease, going from the classical form described by Marcus and Fontaine to concealed forms characterized mainly by premature ventricular complexes.

Adolescent↗
PubMed1987

[Atrial desynchronization induced by Valsalva's maneuver in a patient with reciprocating supraventricular tachycardia and Wolff-Parkinson-White syndrome].

A 22 years old man with ventricular preexcitation syndrome due to a left accessory pathway, was admitted because of orthodromic reciprocating tachycardia, 205 bpm in frequency. The patient was invited to perform a Valsalva Maneuvre, and at its ending, the tachycardia degenerated into atrial fibrillation (AF) associated with high ventricular rate, reverted to sinus rhythm by D.C. shock. The electrophysiologic study documented a left lateral by pass tract, with an anterograde refractory period of 230 msec. AF was inducible and had a minimal RR interval of 220 msec. Vagal stimulation, induced at the end of Valsalva maneuvre, probably caused dispersion of atrial refractorines and intraatrial reentry, converting the orthodromic tachycardia into atrial fibrillation.

Adult↗
PubMed1986

Experimental intravitreal proliferation and neovascularization in the cynomolgus monkey.

An experimental model for intravitreal cellular proliferation was produced by injection of carbon microparticles into the vitreous of nine cynomolgus monkeys. Eighteen eyes were studied following enucleations 10 weeks after the injections. Histological examinations showed retinal folds or detachments in 16 eyes, while 6 of those had total detachments. Eight eyes contained transvitreal fibrovascular strands, passing from the optic disk to a "cyclitic" retrolental membrane. The strands and membranes were composed mainly of infiltrates of macrophages, inflammatory cells, fibroblasts, newly formed vessels and van Gieson-staining collagen. Epiretinal proliferation of glial cells also occurred. These experiments indicate that a primarily phagocytic cellular invasion into the vitreous is capable of stimulating further cellular migration and growth and for inducing fibrovascular proliferations.

Animals↗
PubMed1986

[Vectorcardiographic analysis of late potentials].

We analyzed by high amplification vectorcardiography the morphology of the QRS ending loop and the ST segment of patients with previously recorded Lown 4A, 4B ventricular arrhythmias and the healthy subject. Eight patients were affected by ischemic heart disease and 7 by arrhythmogenic right ventricular dysplasia. All had some irregularities at the end of the QRS or in the ST segment, on the standard ECG. The VCG showed one or more of these three morphologies: complete or incomplete ring, rapidly inscripted isodi-triphasic potentials, sinusoidal irregularities. In the 20 healthy subjects, the loop corresponding to the last 30 msec of the QRS, till the end of the afferent portion of T, was regular, without any particular morphology. We think that these aspects could be related to delayed fragmentation of the ventricular depolarization.

Arrhythmias, Cardiac↗
PubMed1986

[Tachycardia and ventricular fibrillation in the arrhythmogenic right ventricle (arrhythmogenic dysplasia of the right ventricle). Clinical and electrocardiographic spectrum].

In this paper we report the arrhythmias recorded on basal ECG, on Holter monitoring or on exercise test, in 32 pts affected by arrhythmogenic right ventricle (ARV). A sustained ventricular tachycardia (VT) was present in 11 pts a non sustained VT in 15 pts, a slow VT in 2 pts, a ventricular fibrillation (VF) in 3 pts and both sustained VT and VF in 1 pt. All but 1 case of sustained VT showed a LBBB like pattern. The heart rate during VT ranged between 170 and 280 beats/min. The frontal axis of the VT showed a wide range of deviation. Among non sustained VT, 9 cases had LBBB like pattern and 6 cases had polymorphic configuration. The 2 cases of slow VT showed LBBB like pattern with right axis deviation. A comparison between ventricular arrhythmias and RV impairment was made. The data obtained suggest that the effort plays an important role in the induction of VT in pts with localized RV impairment. In conclusion a wide spectrum of ventricular tachyarrhythmias is present in the ARV. Probably the RV "arrhythmogenic" zones and the electrophysiological mechanism causing the arrhythmias are various.

Adolescent↗
PubMed1985

Sequelae of intravitreal phagocytic activity in response to microparticles.

Cynomolgus monkeys were injected intravitreally with a colloidal suspension of carbon microparticles (size 20-70 nm) under aseptic surgical conditions. An intravitreal cellular proliferation occurred, inducing retinal detachment and neovascularization that started from the optic nerve head, ciliary body and ora serrata. Transmission electron microscopy revealed the features of the intravitreal cellular response to be inflammatory cells, mononuclear phagocytes (the predominant cell type), and fibroblasts. Newly-formed collagen fibrils (banding 70 nm) were found in the vitreous. The newly-formed vasculature generally showed continuous endothelial lining, but some intravitreal cellular proliferation is primarily a macrophagic response. We suggest that mononuclear phagocytes play a major role by triggering the collagen formation and neovascularization in the vitreous.

Animals↗
PubMed1983

[Supraventricular tachycardia in children].

Supraventricular tachycardia is one of the most frequent arrhythmias in childhood. It may accompany congenital heart disease. W.P. W. syndrome, or a normal state of health. A re-entry circuit is the most commonly observed electrophysiological mechanism. Persistence is followed by decompensation. Drug management is based on digitalis, ATP, amiodarone, and verapamil. Atrial and ventricular pacing and surgery are alternatives when other means fail. Persistent tachycardia (i.e. its presence over long periods) is much less frequent that the paroxysmal form, and its aetiology is generally unknown. Even here, the clinical picture is substantially related to decompensation. Digitalis + amiodarone is the best treatment, though the arrhythmia may resolve spontaneously.

Adenosine Triphosphate↗