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Biomedical subjects

D Corrado

Publications and source records attributed to D Corrado.

At least 37 records · Page 2Linked to original sources
PubMed1998

Screening for hypertrophic cardiomyopathy in young athletes.

BACKGROUND: For more than 20 years in Italy, young athletes have been screened before participating in competitive sports. We assessed whether this strategy results in the prevention of sudden death from hypertrophic cardiomyopathy, a common cardiovascular cause of death in young athletes. METHODS: We prospectively studied sudden deaths among athletes and nonathletes (35 years of age or less) in the Veneto region of Italy from 1979 to 1996. The causes of sudden death in both populations were compared, and the pathological findings in the athletes were related to their clinical histories and electrocardiograms. Cardiovascular reasons for disqualification from participation in sports were investigated and follow-up was performed in a consecutive series of 33,735 young athletes who underwent preparticipation screening in Padua during the same period. RESULTS: Of 269 sudden deaths in young people, 49 occurred in competitive athletes (44 male and 5 female athletes; mean age, 23+/-7 years). The most common causes of sudden death in athletes were arrhythmogenic right ventricular cardiomyopathy (22.4 percent), coronary atherosclerosis (18.4 percent), and anomalous origin of a coronary artery (12.2 percent). Hypertrophic cardiomyopathy caused only 1 sudden death among the athletes (2.0 percent) but caused 16 sudden deaths in the nonathletes (7.3 percent). Hypertrophic cardiomyopathy was detected in 22 athletes (0.07 percent) at preparticipation screening and accounted for 3.5 percent of the cardiovascular reasons for disqualification. None of the disqualified athletes with hypertrophic cardiomyopathy died during a mean follow-up period of 8.2+/-5 years. CONCLUSIONS: The results show that hypertrophic cardiomyopathy was an uncommon cause of death in these young competitive athletes and suggest that the identification and disqualification of affected athletes at screening before participation in competitive sports may have prevented sudden death.

Adolescent↗
PubMed1998

Anomalous origin of coronary arteries and risk of sudden death: a study based on an autopsy population of congenital heart disease.

Coronary arteries anomalies may be part of complex congenital malformations of the heart or be an isolated defect. In our anatomic collection of congenital heart disease, an isolated anomalous origin of coronary arteries was observed in 27 of 1,200 specimens (2.2%): left coronary artery from pulmonary trunk in five, origin from the wrong aortic sinus in 12 (both right and left coronary artery from the right sinus in four and from the left sinus in seven, left coronary artery from the posterior sinus in one), left circumflex branch from right aortic sinus or from very proximal right coronary artery in three, high takeoff of right coronary artery in three, stenosis of the coronary ostia attributable to valvelike ridge in four. In 16 (59%) patients (12 males and 4 females, age ranging from 2 months to 53 years; median, 14), the final outcome was sudden death; it occurred in all cases of left coronary artery origin from right aortic sinus, in 43% of right coronary artery origin from left aortic sinus, and in 40% of the left coronary artery from the pulmonary trunk. Sudden death was precipitated by effort in eight (50%) and was the first manifestation of the disease in eight (50%); previous symptoms consisted of recurrent syncope in four, palpitations in three, and chest pain in one. Five patients who died suddenly during effort were athletes. In conclusion, (1) more than half of our postmortem cases with anomalous origin of coronary arteries died suddenly, (2) all but two patients with sudden death had anomalous coronary artery origin from the aorta itself, (3) the fatal event was frequently precipitated by effort, (4) palpitations, syncope, and ventricular arrhythmias were the only prodromic symptoms and signs. Recognition during life of these coronary anomalies, by the use of noninvasive procedures, is mandatory to prevent the risk of sudden death and to plan surgical correction if clinically indicated.

Adolescent↗
PubMed1997

Spectrum of clinicopathologic manifestations of arrhythmogenic right ventricular cardiomyopathy/dysplasia: a multicenter study.

OBJECTIVES: The aim of the present investigation was to redefine the clinicopathologic profile of arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC), with special reference to disease progression and left ventricular (LV) involvement. BACKGROUND: Long-term follow-up data from clinical studies indicate that ARVC is a progressive heart muscle disease that with time may lead to more diffuse right ventricular (RV) involvement and LV abnormalities and culminate in heart failure. METHODS: Forty-two patients (27 male, 15 female; 9 to 65 years old, mean [+/-SD] age 29.6 +/- 18) from six collaborative medical centers, with a pathologic diagnosis of ARVC at autopsy or heart transplantation, and with the whole heart available, were studied according to a specific clinicomorphologic protocol. RESULTS: Thirty-four patients died suddenly (16 during effort); 4 underwent heart transplantation; 2 died as a result of advanced heart failure; and 2 died of other causes. Sudden death was the first sign of disease in 12 patients; the other 30 had palpitations, with syncope in 11, heart failure in 8 and stroke in 3. Twenty-seven patients experienced ventricular arrhythmias (ventricular tachycardia in 17), and 5 received a pacemaker. Ten patients had isolated RV involvement (group A); the remaining 32 (76%) also had fibrofatty LV involvement that was observed histologically only in 15 (group B) and histologically and macroscopically in 17 (group C). Patients in group C were significantly older than those in groups A and B (39 +/- 15 years vs. 20 +/- 8.8 and 25 +/- 9.7 years, respectively), had significantly longer clinical follow-up (9.3 +/- 7.3 years vs. 1.2 +/- 2.1 and 3.4 +/- 2.2 years, respectively) and developed heart failure significantly more often (47% vs. 0 and 0, respectively). Patients in groups B and C had warning symptoms (80% and 87%, respectively, vs. 30%) and clinical ventricular arrhythmias (73% and 82%, respectively, vs. 20%) significantly more often than patients in group A. Hearts from patients in group C weighed significantly more than those from patients in groups A and B (500 +/- 150 g vs. 328 +/- 40 and 380 +/- 95 g, respectively), whereas hearts from both group B and C patients had severe RV thinning (87% and 71%, respectively, vs. 20%) and inflammatory infiltrates (73% and 88%, respectively, vs. 30%) significantly more often than those from group A patients. CONCLUSIONS: LV involvement was found in 76% of hearts with ARVC, was age dependent and was associated with clinical arrhythmic events, more severe cardiomegaly, inflammatory infiltrates and heart failure. ARVC can no longer be regarded as an isolated disease of the right ventricle.

Adolescent↗
PubMed1997

Sudden death in young people with apparently isolated mitral valve prolapse.

Ventricular electrical instability and sudden death in mitral valve prolapse (MVP) have been related to mitral valve regurgitation and left ventricular dysfunction, autonomic nervous system abnormalities, or underlying cardiomyopathy. The aim of the present study was to assess the frequency, nature and pathophysiologic significance of histologic myocardial abnormalities in young patients with apparently isolated MVP and sudden cardiac death. Among 163 cases of sudden cardiovascular death in young people, MVP was the only cardiac pathology found at postmortem gross examination in 17 (10%) (12 females and 5 males) aged 14 to 35 years, mean 24. In 12 cases sudden death occurred at rest (during pregnancy in 2). MVP was diagnosed during life in 8 patients, 6 of whom had experienced palpitations and/or syncope, and 3 had premature ventricular beats. In every case, postmortem gross examination revealed "floppy" mitral valve leaflets with marked myxoid degeneration, and no other cardiovascular pathology. Cardiomegaly with left chamber enlargement was observed in 5 cases (mild in 3 and moderate in 2). In 12 cases (70%), histopathologic study disclosed myocardial abnormalities which consisted of focal myocardial atrophy and fatty replacement of the right ventricular wall (mostly the outflow tract) in 9 cases, left ventricular myocardial disarray (without hypertrophy) in 2, and lymphocytic infiltrates in one. "Foetal" dispersion of specialized atrioventricular junction and fasciculoventricular Mahaim's fibers were found in 2 cases. In conclusion, apparently isolated MVP was found in nearly 10% of sudden cardiovascular fatalities in young people. Most young sudden death victims with MVP were asymptomatic females without significant mitral valve regurgitation. In more than two-thirds of the cases, histopathologic examination evidenced underlying silent but potentially arrhythmogenic myocardial substrates, mostly consisting of segmental right ventricular cardiomyopathic changes.

Adolescent↗
PubMed1996

Arrhythmogenic right ventricular cardiomyopathy. Dysplasia, dystrophy, or myocarditis?

BACKGROUND: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a frequent cause of sudden death in young individuals and athletes. Although familial occurrence has been documented and a gene defect was recently localized on chromosome 14q23-q24 the etiopathogenesis of the disease is still obscure. METHODS AND RESULTS: A pathological study was conducted in 30 hearts with ARVC (age range, 15 to 65 years; mean, 28 years). In the 27 autopsy cases, the mode of death was sudden in 24 and congestive heart failure in 3. ECG, available in 19 cases, showed inverted T waves in the right precordial leads in 15 cases (79%) and ventricular arrhythmias in 15 (79%). Right ventricular aneurysms were present in 15 hearts (50%) and located in the inferior wall in 12. Left ventricle and ventricular septum were involved in 14 (47%) and 6 (20%) cases, respectively. Scattered foci of lymphocytes with myocardial death were observed in 20 cases (67%). Electron microscopy studies, although confirming the myocardial death and lymphocyte infiltrates, did not show any specific ultrastructural substrate. Two pathological patterns, fatty (40%) and fibrofatty (60%), were identified. The fibrofatty pattern was associated with a thinner right ventricular wall (P < .0001) and a higher occurrence of focal myocarditis (P < .001). In sections of right ventricular free wall with maximal fatty infiltration, the mean percentage area of fatty tissue was 35.9 +/- 11.1% in control versus 80.4 +/- 9.6% in the ARVC, fatty variety (P < .00001). Involvement of the left ventricle and/or ventricular septum, right ventricular aneurysms, and inflammation were found almost exclusively in the fibrofatty variety. CONCLUSIONS: In the fibrofatty variety of ARVC, the myocardial atrophy appears to be the consequence of acquired injury (myocyte death) and repair (fibrofatty replacement), mediated by patchy myocarditis. Whether the inflammation is a primary event or a reaction to spontaneous cell death remains unclear.

Adolescent↗
PubMed1996

Familial cardiomyopathy underlies syndrome of right bundle branch block, ST segment elevation and sudden death.

OBJECTIVES: We sought to assess whether structural heart disease underlies the syndrome of right bundle branch block, persistent ST segment elevation and sudden death. BACKGROUND: Ventricular fibrillation and sudden death may occur in patients with a distinctive electrocardiographic (ECG) pattern of right bundle branch block and persistent ST segment elevation in the right precordial leads. METHODS: Sixteen members of a family affected by this syndrome underwent noninvasive cardiac evaluation, including electrocardiography, Holter ambulatory ECG monitoring, stress testing, echocardiography and signal-averaged electrocardiography; two patients had electrophysiologic and angiographic study. Endomyocardial biopsy was performed in one living patient, and postmortem examination, including study of the specialized conduction system, was performed in one victim of sudden death. RESULTS: Five years before a fatal cardiac arrest, the proband had been resuscitated from sudden cardiac arrest due to recorded ventricular fibrillation. Serial ECGs showed a prolonged PR interval, right bundle branch block, left-axis deviation and persistent ST segment elevation in the right precordial leads, in the absence of clinical heart disease. Postmortem investigation disclosed right ventricular dilation and myocardial atrophy with adipose replacement of the right ventricular free wall as well as sclerotic interruption of the right bundle branch. A variable degree of right bundle branch block and upsloping right precordial ST segment was observed in seven family members; four of the seven had structural right ventricular abnormalities on echocardiography and late potentials on signal-averaged electrocardiography. A sib of the proband also had a prolonged HV interval, inducible ventricular tachycardia and fibrofatty replacement on endomyocardial biopsy. CONCLUSIONS: An autosomal dominant familial cardiomyopathy, mainly involving the right ventricle and the conduction system, accounted for the ECG changes and the electrical instability of the syndrome.

Adolescent↗
PubMed1995

Congenital heart disease and sudden death in the young.

Sudden death is a frequent mode of fatal outcome in cardiac disease and does not exclude young people. The aim of this investigation was to establish whether and to what extent sudden death in the young may be ascribable to the substrate of underlying congenital heart disease. Among 182 young people (< or = 35 years) who died of cardiac sudden death and underwent postmortem examination, 58 (32%) had congenital heart disease. Seven showed an intrapericardial rupture of aortic dissection, in the setting of Marfan syndrome in two, isolated bicuspid aortic valve in two, and bicuspid aortic valve and isthmic coarctation in three; all exhibited equally severe degeneration of the aortic wall. Sixteen cases had conduction system anomalies, mostly bypass tracts; 15 coronary artery anomalies (three ostial valve-like stenosis, five origin from the wrong aortic sinus, and seven deep intramyocardial course); 12 hypertrophic cardiomyopathy; five postoperative congenital heart disease including scar following ventriculotomy, conduction system injury, and defects left unrepaired; and three congenital aortic valve stenosis. One third of sudden deaths in the young was ascribable to structural defects present since birth. A large spectrum of congenital heart disease involves the risk of sudden death, but most structural defects are usually not considered to be life threatening. Some of these concealed defects are potentially detectable in life by clinical imaging techniques.

Adolescent↗
PubMed1994

The gene for arrhythmogenic right ventricular cardiomyopathy maps to chromosome 14q23-q24.

Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVD) is a dominantly inherited disorder progressively affecting the myocardium and it is one of the major causes of juvenile sudden death. The chromosomal localization of the disease gene is reported here for the first time. A maximum lod score of 6.04 was obtained at theta = 0 for linkage with the polymorphic marker D14S42 (14q23-q24) in two families, one of which has 82 subjects (19 affected) in four generations. The pre-symptomatic identification of ARVD carriers by linkage analysis in the affected families strongly increases the possibility of prevention of life-threatening complications.

Arrhythmias, Cardiac↗
PubMed1994

Sudden death in the young. Is acute coronary thrombosis the major precipitating factor?

BACKGROUND: Atherosclerotic coronary artery disease, complicated by acute thrombosis, is the usual cause of sudden death in adults. This study addresses the pathology of coronary arteries in sudden death in the young (< or = 35 years old). METHODS AND RESULTS: Among 200 consecutive cases of sudden death in youth in the Veneto region of Italy, 37 (33 men and 4 women, age 18 to 35 years; mean, 29.4 years) showed obstructive atherosclerotic coronary artery disease in the absence of other cardiac pathological conditions and causes of death. No patient had previous angina pectoris or myocardial infarction. Cardiac arrest occurred at rest in 30 subjects and was related to effort in 7. A histological study was carried out on the obstructive coronary plaques. Degree of lumen stenosis and extension of lipid core and intimal fibrocellular hyperplasia facing the lumen were calculated morphometrically. Immunohistochemistry and electron microscopy were used to further characterize the plaque cell population. Single-vessel disease was found in 33 patients and triple-vessel disease in 4, with an overall total of 45 obstructive plaques, 34 of which were located in the proximal left anterior descending coronary artery. At histological study, only 10 plaques from 10 patients showed acute thrombosis (occlusive in 5 and subocclusive in 5); the remaining 35 were uncomplicated. Thirty-one plaques were fibrous in nature, while the other 14 were atheromatous. Compared with the atheromatous lesions, the fibrous plaques were rarely complicated by thrombosis (3% versus 64%; P < .001) and distinctly exhibited a fairly well-preserved tunica media (81% versus 21%; P < .001) as well as a stratum of neointimal fibrocellular hyperplasia (68% versus 7%; P < .001), which on immunohistochemistry and electron microscopy appeared to be proliferating smooth muscle cells. CONCLUSIONS: In our study population, sudden death was precipitated by acute coronary thrombosis in only 27% of patients with obstructive coronary atherosclerotic plaque. Most of the young victims of sudden death with obstructive coronary atherosclerosis showed single-vessel disease that affected the left anterior descending coronary artery and was due to fibrous plaques with neointimal smooth muscle cell hyperplasia and a preserved tunica media in the absence of acute thrombosis.

Acute Disease↗
PubMed1993

[Juvenile sudden death from spontaneous aortic rupture].

UNLABELLED: In the time interval 1979-1991, 150 cases of juvenile sudden death (< or = 35 years) were studied. Among these, 9 were due to aortic rupture within the pericardial cavity. Two were mycotic and 7 dissecting aneurysms. The latter, all male, age ranging from 17 to 31 years (mean 24), presented the following risk factors: Marfan syndrome in 2, isthmal coarctation associated with bicuspid aortic valve (BAV) in 3, isolated and normally functioning BAV in 2. Histology of the dissected aortic wall showed an equal severity of degenerative changes consisting of elastic fragmentation, cystic medial necrosis and medionecrosis. By reviewing our anatomical collection of dissecting aneurysm we found a 12% frequency of BAV. Taking into consideration that the frequency in normal population of BAV is near 1%, the association between bicuspid aortic valve and dissecting aneurysm should not be casual (p < 0.001). IN CONCLUSION: a) natural history of BAV entails the risk of spontaneous aortic laceration and sudden death in the youth, either in the isolated form or in association with isthmal coarctation; b) the aortic tunica media in these conditions shows an intrinsic structural weakness very similar to that observed in Marfan syndrome, as to suggest a congenital, most probably genetic defect with phenotype expression not only at valve level, but also within the aortic wall; c) aortic dissection occurs nearly ten times more frequently in patients with BAV than in normal population.

Adolescent↗
PubMed1992

Enhanced A-V nodal conduction (Lown-Ganong-Levine syndrome) by congenitally hypoplastic A-V node.

The basic anatomical substrate of enhanced A-V nodal conduction, manifesting or not as Lown-Ganong-Levine syndrome, is still a controversial issue. We describe the case of a 34-year-old man who presented episodes of ventricular fibrillation. Electrophysiological studies showed that the AH interval was 55 ms, and increased by only 20 ms at paced cycle lengths of 300 ms; atrial pacing induced atrial fibrillation, with a shortest RR interval of 240 ms. Despite verapamil therapy, this patient died suddenly at home. Histological study disclosed a severe A-V node hypoplasia that was evidently congenital in nature; the rest of the conduction system was normal, and no accessory A-V pathways were present. We suggest that enhanced A-V nodal conduction in this patient was due to the developmental defect in the A-V node; this abnormality caused a loss of specific impulse-delaying function, and thus allowed rapid, unfiltered atrial impulses to reach the lower A-V junction and ventricles.

Adult↗
PubMed1992

Non-atherosclerotic coronary artery disease and sudden death in the young.

OBJECTIVE: To assess prevalence and type of non-atherosclerotic coronary artery disease in young people (< or = 35 years) who died suddenly. DESIGN: A necropsy study of 150 consecutive cases of sudden death (that is, within 6 h of the onset of symptoms). RESULTS: Death was attributed to coronary artery disease in 48 cases: in 16 (33%) of them the disease was non-atherosclerotic. Twelve subjects (eight males and four females, age range 2-35 years, mean 24.2) had congenital anomalies: a deep intramyocardial course in six, origin from the wrong sinus in three, and ostial obstructions in three. Sudden death was the first manifestation of disease in six cases. The other six had a history of palpitation or syncope or both. An electrocardiogram was available in five cases and showed ventricular arrhythmias in four; none had angina pectoris. Stress testing was available in two cases: neither showed any effort-dependent ST-T abnormalities. In six cases sudden death was related to physical exercise. Acquired non-atherosclerotic coronary artery disease was found in four cases: spontaneous coronary dissection in three previously symptom free patients and Kawasaki coronary arteritis in one child who had had acute myocardial infarction. CONCLUSION: One third of the cases of fatal coronary artery disease were non-atherosclerotic with coronary artery anomalies being the most frequent form. Coronary artery anomalies should be suspected in young patients who have symptoms of ventricular arrhythmias without any overt signs and symptoms of ischaemia.

Adolescent↗
PubMed1991

Coexistence of kent accessory pathway, enhanced AV node conduction, and various conduction disturbances in a young athlete with tricuspid valve dysplasia.

An asymptomatic 19-year-old top-level athlete had electrocardiographic evidence of intermittent cardiac preexcitation and intermittent left bundle branch block. The electrophysiologic study demonstrated the presence of a direct accessory pathway and enhanced atrioventricular node conduction that resulted in infrahisian and intraventricular conduction disturbances. The echocardiogram disclosed tricuspid valve dysplasia.

Adult↗
PubMed1991

[The anatomicofunctional picture of the atherosclerotic lesion].

The natural history of atherosclerotic disease is characterized by a first asymptomatic phase, when the lesion develops and a second one, the more dramatic symptomatic phase, when the mature plaques, which represent the progression of the early lesions, and their complications produce a wide range of clinical phenomena. After 1 year of age all children show changes in coronary arterial wall, consisting of cell proliferations, which may be considered as precursors of atherosclerosis. These cells migrate from the tunica media of the coronary artery, proliferate, may synthetize connective tissue and lose the ability to degrade plasma lipoproteins. As a consequence, they may be laden of cholesterol, which accounts for fatty streaks. Later on, near 25% of 15-20 year old children are found to be affected by silent non-obstructive coronary atherosclerotic plaques, which consist of raised lesions, the fibrous plaque, made up of frequently lipid laden cells and fibrous tissue. The lesion-prone area is chiefly the proximal anterior descending coronary artery at the site where the worst precursors of atherosclerosis are usually detected. The medial coat of the vessel retain at this stage a good thickness, which accounts for the vasoreactivity of the coronary artery in youths and young-adults. The trigger in the cascade of dynamic events which lead to the advanced lesions remains a mystery. The plaque is not a static immutable structure, but is subjected to growth with consequent stenosis of the lumen and continuing modification and remodelling which involve all the 3 coats of the arterial wall.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1990

Sudden death in young competitive athletes: clinicopathologic correlations in 22 cases.

PURPOSE: To investigate the pathologic substrates of sudden death in young competitive athletes. PATIENTS AND METHODS: Twenty-two cases of sudden death in young competitive athletes occurring in the Veneto region (northern Italy) in the period January 1979 to December 1989 were studied by postmortem examination. The athletes included 19 males and three females, ranging in age from 11 to 35 years (mean, 23 years). RESULTS: In 18 cases, sudden death occurred during (16 cases) or immediately after (two cases) a competitive sport activity. In 10 subjects, sudden death was apparently the first sign of disease. Postmortem examination disclosed that this fatality was due to arrhythmic cardiac arrest in 17 cases; among these, right ventricular cardiomyopathy, also known as "right ventricular dysplasia," was the most frequently encountered cardiovascular disease (six cases), followed by atherosclerotic coronary artery disease (four cases), conduction system pathology (three cases), anomalous origin of right coronary artery from the wrong aortic sinus (two cases), and mitral valve prolapse (two cases). In two athletes, the abrupt lethal complication was "mechanical" and consisted of pulmonary embolism and rupture of the aorta; in three athletes, death was due to a cerebral cause. All athletes with right ventricular cardiomyopathy died during effort, and most had a history of palpitations and/or syncope. Whenever available, electrocardiographic (ECG) tracings showed inverted T waves in precordial leads and/or left bundle branch block ventricular arrhythmias. CONCLUSIONS: Clinicopathologic correlations indicate that in the Veneto region of Italy, right ventricular cardiomyopathy is not so rare among the cardiovascular diseases associated with the risk of arrhythmic cardiac arrest, and seems to account for the majority of cases of sudden death in young athletes; this disorder can be suspected during life on the basis of prodromal symptoms and ECG signs.

Adolescent↗
PubMed1990

The relationship between growth of atherosclerotic plaques, variant angina and sudden death.

Clinico-pathological findings are described in two patients with typical variant angina who died suddenly during an ischemic attack. In both cases, detailed pathologic examination of the coronary arteries disclosed severe focal atherosclerosis of the anterior descending coronary artery. The only distinctive histological finding was new intimal proliferation of smooth muscle cells enmeshed within mucoid substance, superimposed on the old fibrous cap of the plaque. These findings agree with experimental and clinical data which suggest that coronary vasospasm may be related to growth of atherosclerotic plaques. This study provides histological evidence that progression of an atherosclerotic plaque may underlie variant angina and sudden death.

Angina Pectoris, Variant↗