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D Corrado

Publications and source records attributed to D Corrado.

53 records · Page 3Linked to original sources
PubMed1990

[Spontaneous dissecting coronary hematoma (aneurysm) and sudden death].

Two women, 34 and 54 years old, died suddenly from acute coronary occlusion due to spontaneous dissecting haematoma (aneurysm) involving the entire left coronary artery and the right coronary artery, respectively. In the older woman, cystic medial necrosis of the coronary tunica media was observed. The younger case was the only sudden death due to dissecting hematoma among 120 cases in the Registry of "juvenile sudden death" in the Veneto Region, Italy. From a review of the literature, following the first description in 1931, we collected 97 cases with the following characteristics: mean age in women, 39 years, in men, 48 years; only significant risk factor: peripartum (34% of women); coronary arteries involved: isolated left anterior descending (52.5%, equally distributed among women and men), right (24%, mainly men), left (13.5%, only women), multiple vessels (8%), left circumflex artery (2%). The clinical presentation was cardiac arrest with sudden death in 49.5%, acute, non-fatal myocardial infarct in 33%, and acute fatal myocardial infarct in 17.5% of the cases. The prognosis is very poor, and emergency medical or surgical myocardial revascularization is rarely feasible.

Adult↗
PubMed1989

Asystole with syncope secondary to hyperventilation in three young athletes.

We describe three athletes who had syncope after (case 1) or during (cases 2, 3) hyperventilation. During the episode, ECG showed prolonged sinus arrest. Clinical data and noninvasive investigations were normal and the phenomenon was not reproducible. Electrophysiological study after autonomic blockade allowed a prolonged intrinsic heart rate in case 1, and abnormal corrected sinus node recovery time in cases 1 and 2. During follow-up, symptomatic sinus arrest provoked by deep inspiration occurred in case 3. These cases document prolonged asystole of unknown etiology, secondary to hyperventilation, and probably caused by different vagally-mediated mechanisms.

Adolescent↗
PubMed1988

Right ventricular cardiomyopathy and sudden death in young people.

From 1979 to 1986, we conducted postmortem studies of 60 persons under 35 years of age who had died suddenly in the Veneto Region of northeastern Italy. Unexpectedly, we found that 12 subjects--7 males and 5 females ranging in age from 13 to 30 years--had morphologic features of right ventricular cardiomyopathy. This disorder had not been diagnosed or suspected before the subjects died. In five cases, sudden death was the first sign of disease; the remaining seven subjects had a history of palpitation, syncopal episodes, or both, and in five of those seven, ventricular arrhythmias had previously been recorded on electrocardiographic examination. Ten of the subjects had died during exertion. At autopsy, the subjects' heart weights were normal or moderately increased. Two main histologic patterns were identified--a lipomatous transformation or a fibrolipomatous transformation of the right ventricular free wall (6 cases each); in all cases, the left ventricle was substantially spared. Signs of myocardial degeneration and necrosis, with or without inflammatory infiltrates, were occasionally observed. These findings indicate that right ventricular cardiomyopathy, the cause of which is still unknown, may be more frequent than previously thought. At least in this area of Italy, it may represent an important cause of sudden death among young people.

Adolescent↗
PubMed1988

Sudden death as the first manifestation of coronary artery disease in young people (less than or equal to 35 years).

During 1979 to 1987, we collected 84 consecutive cases of juvenile sudden death which occurred in the Veneto Region, northeast Italy. Death was attributed to cardiovascular disease in 79 cases. Nineteen of these (24%), consisting of 17 males and two females, from 18 to 35 years of age, had 70% or greater atherosclerotic coronary stenosis, in the absence of other cardiac pathology and previous clinical evidence of angina pectoris or myocardial infarction. In 13 cases (68%), sudden death was the first manifestation of coronary artery disease; the remaining six patients had experienced atypical, non-diagnostic prodromal symptoms. At the moment of death, 16 patients were engaged in sedentary activity. Pathological examination disclosed that in 15 cases (79%), only one major vessel was stenosed, and in 12 cases it was the proximal descending coronary artery: the other four patients had three-vessel disease. Histologic study revealed uncomplicated, obstructive fibromatous plaques in 16 cases, and a preserved tunica media in all cases. Plaque fissuring with superimposed mural or occlusive thrombosis was present in only three cases. Overt myocardial infarction was not observed. Our findings indicate that coronary atherosclerosis is an important cause of sudden death in young persons. In this series, coronary disease was 'silent', and sudden death was its first clinical manifestation. The occurrence of death at rest, in the absence of an acute coronary lesion, with preservation of the coronary tunica media suggests that fatal outcome might be due to coronary vasomotor tone abnormalities culminating in ischaemia-induced cardiac arrest.

Adolescent↗
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↗
PubMed1986

Rhythm and conduction disturbances in isolated, congenitally corrected transposition of the great arteries.

The incidence and types of rhythm and conduction disturbances in 11 male and 6 female patients with congenitally corrected transposition of the great arteries and no other intrinsic complicating anomalies were studied. Patient age ranged from 5 to 54 years; follow-up ranged from 5 to 37 years. Surface electrocardiograms were recorded in each patient; 15 also underwent 24-hour Holter monitoring and 10 underwent electrophysiologic study. The conduction system of a 54-year-old woman who died suddenly, with complete atrioventricular (AV) block since age 30 years, was studied by serial histologic sections. Fifteen patients were asymptomatic and 2 reported repeated episodes of palpitation since childhood. Ten patients presented with a normal PR interval and 2 with first-degree AV block (12%). Five patients had complete AV block (29%), but none had had it at birth; first- and second-degree AV block preceded complete AV block in 2 patients. The morphologic pattern and duration of QRS suggested a junctional rhythm in 4 patients and an idioventricular pacemaker in 1 patient. Electrophysiologic studies confirmed that the complete AV block site was supra-Hisian in 2 patients and proximal to the His bundle bifurcation in 1 patient. However, histologic investigation disclosed fibrosis and disruption of the proximal nonbifurcating His bundle in the patient who died suddenly. In 2 patients with recurrent supraventricular tachycardia, electrophysiologic studies suggested reentry through James fibers (or dual AV nodal pathway) in 1 and the presence of a left lateral accessory AV pathway in the other. Holter monitoring showed a high incidence of ventricular arrhythmias.

Adolescent↗
PubMed1986

Fatal paroxysmal supraventricular tachycardia in an infant.

A 37-day-old infant, without associated congenital anomalies, died following a 48-hour episode of supraventricular tachycardia. The histopathologic findings of nodoventricular and fasciculoventricular Mahaim's fibers in a setting of persistent fetal dispersion were consistent with an anatomic substrate for a reentry circuit at the specialized A-V junction.

Electrocardiography↗
PubMed1986

[Hypertrophic cardiomyopathy and juvenile sudden death. A clinical case and re-evaluation of the problem].

A 29-year-old man with non-familiar hypertrophic cardiomyopathy died suddenly. The patient experienced recurrent episodes of palpitation both at rest and during exercise. M-mode and 2-D echocardiograms showed severe asymmetric septal hypertrophy (IVS/LVPW ratio 3:1) and systolic anterior motion of anterior leaflet of the mitral valve. The ECG demonstrated deep "Q" waves from the inferior leads and inverted "T" waves in V1 to V6, but failed to register arrhythmias. Holter monitoring had been planned in order to achieve information for pharmacologic therapy, but unfortunately the patient died during the stand-by. Postmortem examination showed severe asymmetric septal hypertrophy with fibrosis and wide-spread "myocardial disarray".

Adult↗
PubMed1986

[Complete atrioventricular block and sudden death in isolated corrected transposition].

The rate of av conduction disturbances in corrected transposition of the great arteries is high, possibly as consequence of mechanical injury by ventricular output along with the mis-positioned specialized av junction. A sudden death occurred in a 54 year old female affected by a chronic "idiopathic" complete av block, who showed at autopsy a heart with av and ventricular arterial discordance in the absence of other anomalies (isolated corrected transposition). The cardiac arrest had the ecg features of ventricular fibrillation, preceded by sustained ventricular tachycardia. Histologic study of the conduction system by serial sections confirmed the anterior position of the connected av node, with a long subendocardial course of the bundle in the pulmonary outflow tract. The histologic basis of the block consisted of sclero-atrophy of the common bundle, quite similar to the substrate of acquired av block in heart with normal connections. Possible etiologies, responsible of the relation between the av block and onset of ventricular arrhythmias, are discussed.

Death, Sudden↗
PubMedDate not supplied

Cardiovascular causes of sudden death in young individuals including athletes.

From 1978 to 1993 in the Veneto region, we collected 200 cases of sudden death in the young (</=35 years). Sudden death was cerebral in 15 cases (7.5%), respiratory in 10 (5%), and cardiovascular in 163 (81.5%), whereas it remained unexplained in 12 cases (6%). Among cardiovascular sudden death, obstructive coronary atherosclerosis accounted for 23% of cases, arrhythmogenic right ventricular cardiomyopathy for 12.5%, mitral valve prolapse for 10%, conduction system abnormalities for 10%, congenital coronary artery anomalies for 8.5%, myocarditis for 7.5%, hypertrophic cardiomyopathy for 5.5%, aortic rupture for 5.5%, dilated cardiomyopathy for 5%, nonatherosclerotic-acquired coronary artery disease for 3.5%, postoperative congenital heart disease for 3%, aortic stenosis for 2%, pulmonary embolism for 2%, and other causes for 2%. Cardiac arrest remained unexplained in 6% of the cases. Specific pathology and pathogenetic mechanisms of each disease were investigated and correlated with clinical signs and symptoms in detail. A large spectrum of cardiovascular disorders, both congenital and acquired, may represent the organic substrate of sudden death in the young. The underlying abnormality is frequently concealed and discovered only at postmortem examination. Most of the diseases, although asymptomatic, are potentially detectable during life with proper imaging tests.

Adolescent↗
PubMedDate not supplied

What is the Brugada syndrome?

In 1992, Brugada and Brugada reported a distinct subgroup of patients with episodes of "idiopathic"polymorphic ventricular tachycardia or ventricular fibrillation characterized by a unique electrocardiographic (ECG) pattern, which consisted of right bundle branch block and ST-segment elevation from V1 to V2-V3. As in patients with long QT syndrome, the ECG changes and the ventricular electrical instability could not be explained by structural heart disease, myocardial ischemia, or electrolyte disturbances. The syndrome can be inherited and predominantly affects males. Clinical presentation includes cardiac arrest or syncope caused by rapid ventricular tachycardia or fibrillation characteristically occurring at rest or during sleep. The clinical outcome of affected patients is poor unless they receive an implantable cardioverter defibrillator. The ECG pattern and the electrical ventricular instability have been explained by the dispersion of repolarization between the right ventricular epicardium and endocardium, which predisposes to local reexcitation of myocytes with different action potential durations. A disease-causing missense mutation in the cardiac sodium channel gene SCN5A has been recently reported in patients with Brugada syndrome. It is mandatory for the clinician to carefully rule out any organic heart disease before suggesting a diagnosis of Brugada syndrome, because the typical ECG pattern with the risk of sudden arrhythmic death is also observed in patients with structural heart diseases in the setting of arrhythmogenic right ventricular cardiomyopathy.

Adult↗
PubMedDate not supplied

Arrhythmogenic right ventricular cardiomyopathy: current diagnostic and management strategies.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a heart muscle disease of unknown etiology characterized by the peculiar right ventricular (RV) involvement. Distinctive pathologic features are myocardial atrophy and fibro-fatty replacement of the RV free wall, and clinical presentation is usually related to ventricular tachycardias with a left bundle branch block pattern or ventricular fibrillation leading to cardiac arrest, mostly in young people and athletes. Later in the disease evolution, progression and extension of RV muscle disease and left ventricular involvement may result in right or biventricular heart failure. The diagnosis of ARVC may be difficult because of several problems with specificity of ECG abnormalities, different potential etiologies of ventricular arrhythmias with a left bundle branch morphology, assessment of RV structure and function, and interpretation of endomyocardial biopsy findings. Therefore, standardized diagnostic criteria have been proposed by the Study Group on ARVC of the European Society of Cardiology. According to these guidelines, the diagnosis of ARVC is based on the presence of major and minor criteria encompassing electrocardiographic, arrhythmic, morphofunctional, histopathologic, and genetic factors. Since the assessment of sudden death risk in patients with ARVC is still not well established, there are no precise guidelines to determine which patients need to be treated and what is the best management approach. The therapeutic options include beta-blockers, antiarrhythmic drugs, catheter ablation, and implantable cardioverter defibrillator (ICD). The ICD is the most effective safeguard against arrhythmic sudden death. However, its precise role in changing the natural history of ARVC by preventing sudden and nonsudden death needs to be evaluated by a prospective study of a large series of patients. In patients in whom ARVC has progressed to severe RV or biventricular systolic dysfunction with risk of thromboembolic complications, treatment consists of current therapy for heart failure including anticoagulant therapy. In cases of refractory congestive heart failure, patients may become candidates for heart transplantation.

Anti-Arrhythmia Agents↗
PubMedDate not supplied

Congenital coronary artery anomalies as an important cause of sudden death in the young.

Unlike sudden cardiac death in adults and elderly people, sudden cardiac death in young people (< or =35 years) is often triggered by nonatherosclerotic coronary artery disease, either acquired (arteritis, spontaneous dissection) or congenital in origin. In particular, congenital coronary artery malformations were reported as the cause of 5%-35% of sudden death in the young, and a wide range of abnormalities including anomalous origin, course, or both were described.

Adolescent↗
PubMedDate not supplied

[Superior axial deviation in the young adult. An electro-vectorcardiographic study].

We analyzed the VCGs of 100 young subjects without apparent cardiac disease showing an ECG superior Axis Deviation, i.e. AQRS greater than - 30 degrees, and a rS aspect in V1. Our findings demonstrated that, in these subjects, the superior axis deviation is due to a distal right bundle branch block with posterior displacement of the terminal forces in 78% of the cases. The other cases being left anterior hemiblocks, either isolated (12%) or associated with a block of the anterior subdivision of the right bundle branch (10%). The differential diagnosis, easy on VCG, is sometimes very difficult on ECG. The most reliable ECG criteria to discriminate this kind of right bundle branch block from left anterior hemiblock are: intrinsic deflection in a VL-V6 greater than or equal to 0.015" (sensitivity 100%; specificity 57%), RV6/Ra VL ratio greater than 1 (sensibility 100%; specificity 50%) and the presence of a notched R wave in L2, L3 and a VF (sensitivity 90%; specificity 100%).

Adolescent↗