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Biomedical subjects

G Thiene

Publications and source records attributed to G Thiene.

412 records · Page 23Linked to original sources
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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↗
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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↗
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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↗
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Global and regional left ventricular function in heart transplant patients: an angiographic follow-up study.

We studied the global and regional left ventricular function, its determinants and its modification with time, in orthotopic heart transplant recipients. We reviewed the left ventricular cineangiography performed 1 (50 patients), 2 (33 patients), 3 (18 patients), and 4 (seven patients) years after operation. Regional wall motion was quantitatively evaluated by the area method. All patients had angiographically normal coronary arteries and no evidence of acute rejection at the time of the study. One year after heart transplantation, cardiac index and left ventricular ejection fraction were mildly but significantly lower than normal. Cardiac index was more than 2.5 L/min/m2 in all but one patient, and ejection fraction was more than 50% in all patients. Only previous acute cardiac rejection necessitating therapy and arterial hypertension showed some influence on the left ventricular function. Two years after operation, the left ventricular end-diastolic volume was increased, and left ventricular mass-volume ratio decreased compared with year 1. Three years after operation, an increase of left ventricular end-diastolic pressure and of left ventricular ejection fraction was also evident. Four years after operation, the heart rate was higher, compared with previous years. Even if the changes in the parameters of left ventricular function were significant, they were small in terms of absolute value. Regional hypokinesia was detected 1 year after heart transplantation in eight patients, involving one segment in six patients and two segments in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
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Coronary artery spasm in heart transplant recipients.

Coronary artery spasm has rarely been observed in the transplanted, denervated heart. We report two patients who had coronary artery spasm after orthotopic heart transplantation that was documented by coronary angiography while ECG and Holter monitoring showed ischemic changes. Both patients were treated with calcium antagonists with no further evidence of this complication; however, one patient died suddenly at home after calcium antagonists were arbitrarily withdrawn. We believe that coronary artery spasm in heart transplant recipients may occur more frequently than expected. Careful monitoring of 24-hour ECG should be considered routinely in the follow-up of such patients, and when coronary spasm occurs it should be aggressively treated.

Adult↗
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Long-term results (from 5 to 7 years) with the Hancock S-G-P bioprosthesis.

This communication is concerned with the long-term results of the first 113 patients who underwent single or multiple heart valve replacement with the Hancock-SGP bioprosthesis at the Department of Cardiovascular Surgery, University of Padova Medical School, in a two years period (March 1970-March 1972). Hospital mortality was 18.5%; of the 92 survivors, whose follow-up is now 5 to more than 7 years, the authors report the clinical reevaluation, the complications and the causes of late death. Hemodynamic reevaluation has been performed so far in 26 patients and the prostheses have shown to function properly both in the mitral and the aortic position. The data available to date indicate that the glutaraldehyde preserved porcine valve is durable and its use is warranted in any valvular position.

Adolescent↗
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Rupture of the posterior wall of the left heart at the atrio-ventricular groove following mitral valve replacement.

The authors report 8 cases of left heart rupture at the insertion of the posterior leaflet of the mitral valve out of 693 mitral valve replacements. Special attention is paid to the anatomy of this area and to the technique of removal of annular calcifications, when present. In reviewing the literature, the authors analyze the cases reported up to now with particular reference to the age of patients, number of valves replaced, size and amount of calcifications, volume of the left ventricular cavity, type and size of the prosthesis employed, supra- or subannular insertion, time between valve application and rupture of the heart, techniques of repair with cardiopulmonary by-pass with a beating or arrested heart. The authors maintain that this dramatic iatrogenic complication can be avoided in most instances with some modifications of the surgical technique which has been adopted in the last 200 mitral valve replacements.

Adult↗
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The conduction system in corrected transposition with situs inversus.

The location and course of the conduction system were investigated by serial section in two hearts with corrected transposition of the great arteries in situs inversus. In the first case, characterized by dextrocardia, the interventricular septum was intact, while in the second case with levocardia, a high ventricular septal defect was associated with pulmonary atresia. In both hearts, a regular posterior connecting AV node was present, left-sided in one case and right-sided in the other. The bundle branches were distributed in the morphologically appropriate ventricles. Extensive hemorrhage and coagulation necrosis of the common bundle and bundle branches were observed in the first case, being consequent upon surgical replacement of the right-sided tricuspid valve. The common bundle ran below the membranous septum in this case. In the heart with ventricular septal defect it was related to the postero-inferior rim of the defect. In both cases, an accessory AV node was located anteriorly in the interatrial septum but did not connect with the ventricular musculature. The different position of the atrioventricular conducting tissue in corrected transposition, between cases in situs solitus and situs inversus, is emphasized.

Atrioventricular Node↗