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At least 1,135 records · Page 63Linked to original sources
PubMed1993

Endomyocardial biopsy in right ventricular cardiomyopathy.

Right ventricular cardiomyopathy is characterized by a progressive myocyte loss and fibro-fatty substitution of the right ventricle. The aim of our study was to assess the diagnostic accuracy of right ventricular endomyocardial biopsy. Using an imaging analyser system, histomorphometric parameters of myocytes, interstitium, fibrous tissue and fatty tissue were evaluated on endomyocardial biopsy from 30 patients with arrhythmogenic right ventricular cardiomyopathy, 29 patients with dilated cardiomyopathy and 30 control patients. The percent area of myocytes decreased from 78.10 +/- 7.34 in control to 63.39 +/- 9.22 in dilated cardiomyopathy (P < 0.05) and to 47.28 +/- 15.01 in arrhythmogenic right ventricular cardiomyopathy (P < 0.01). Fibrous tissue increased from 8.10 +/- 3.89 in control to 21.80 +/- 9.29 in dilated cardiomyopathy (P < 0.05) and to 24.60 +/- 11.37 in arrhythmogenic right ventricular cardiomyopathy (P < 0.05). Fatty tissue varied from 0.33 +/- 1.44 in control and 0.07 +/- 0.31 in dilated cardiomyopathy to 13.30 +/- 17.30 in arrhythmogenic right ventricular cardiomyopathy (P < 0.05). Fatty tissue was a feature of arrhythmogenic right ventricular cardiomyopathy (67% of patients vs. 6% of control and dilated cardiomyopathy patients). Diagnostic values typifying arrhythmogenic right ventricular cardiomyopathy, obtained by excluding any overlapping between confidence intervals in the three groups, were: myocytes < 44.95%; fibrous tissue > 40.38%, and fatty tissue > 3.21%, with 67% sensitivity and 91.53% specificity for at least one parameter. In conclusion, a significant difference between arrhythmogenic right ventricular cardiomyopathy, dilated cardiomyopathy and control exists in terms of amount of myocytes, fibrous tissue and fatty tissue. Presence of fatty tissue and fibrous tissue exceeding 3.21% and 40.38%, respectively should be considered highly suspect for arrhythmogenic right ventricular cardiomyopathy in right ventricular endomyocardial biopsy.

Adipose Tissue↗
PubMed1996

Arrhythmogenic right ventricular dysplasia.

Right ventricular dysplasia is a primary disorder of the right ventricular myocardium characterised by a progressive replacement by adipose or fibrous tissue, proceeding from the epicardium towards the endocardium. Right ventricular dysplasia with the predominant clinical manifestation of an arrhythmia of right ventricular origin is defined as arrhythmogenic right ventricular dysplasia. There is, however, a wide spectrum of clinical presentation and physical findings owing to the polymorphism of the condition. The aetiology of right ventricular dysplasia remains unknown. Right ventricular angiography is currently regarded as the gold standard for the clinical diagnosis of right ventricular dysplasia Ventricular endomyocardial biopsy can be useful in confirming the diagnosis but a negative biopsy does not exclude the diagnosis of right ventricular dysplasia. There have been few electrophysiological studies and these, in general, have failed to help in risk stratification. Treatment is focused on the prevention of potentially lethal right ventricular electrical instability.

Adipose Tissue↗
PubMed1990

Pathologic changes in blood vessels following administration of an inotropic vasodilator (ICI 153,110) to the rat.

ICI 153,110 is an inotropic vasodilator compound intended for the treatment of congestive heart failure. It was administered to rats at dose levels of 5, 10, and 250 mg/kg/day for up to 6 months as part of its preclinical development program. Detailed clinical investigations were conducted during the course of the study and histopathological examination took place after 28 days and 182 days of treatment as well as 42 days following cessation of dosing. Changes were identified in blood vessels in the greater proportion of animals from the high dose group, although some of the changes were also observed at lower dose levels. Vascular tissues from a variety of sites were affected, particularly those of the mesentery, splanchnum, heart, testis, and the pampiniform plexus. Early changes characteristic of acute injury such as arterial medial necrosis and inflammation occurred, which were distinguishable from those following chronic administration of the compound where there was a pronounced arterial and venous wall thickening and accompanying plexiform vasculopathy. The essential components contributing to the thickening were a smooth muscle hypertrophy and hyperplasia of the media. At the end of the period following withdrawal of dosing, vascular thickening was still present and arteritis showed an increased incidence relative to that seen at termination of the main test. Systemic hypertension was not detected during these studies. Vasodilation occurring at or near normal blood pressure, resulting in breakdown of vascular autoregulation and excessive critical wall tension, may have been the cause of the pathological changes. Our findings indicate that medial necrosis is an early component in a sequence of adaptive, destructive, and reparative changes not only following a chemically induced perturbation of the hemodynamic status in arteries and veins but also following a shift back to the "normal state" on withdrawal of compound.

Animals↗
PubMed1988

Cardiac lesions in sudden infant death syndrome.

Sequential morphological changes as found in the hearts of 250 sudden infant death syndrome (SIDS) infants are described. Detailed examination of macroscopic and microscopic lesions reveal that all SIDS infants had identifiable lesions at the time of their death. The lesions can best be described as selective focal anoxic muscle fibre necrosis at chronologically different developmental stages. The extent of these lesions vary markedly from case to case, from a minimal muscle fibre eosinophilia through contraction band formation, myocytolysis, stromal condensation to scar formation. The morphological variations in the lesions amongst individual cases can be interpreted as relating to the time interval of the development of the lesions. The intramural and coronary arteries in some cases are also affected showing intimal hyperplasia. Although these sequential morphological aberrations are not specific and typical to SIDS infants only, they were present in all SIDS infants in this series.

Atrophy↗
PubMed2005

Two cases of endomyocardial disease with hypereosinophilia in Turkey.

Endomyocardial disease is characterized by fibrothrombotic thickening of apical endocardium and subvalvular regions of atrioventricular valves. The disease is uncommon in Turkey. In this report two cases of endomyocardial disease with hypereosinophilia which were medically managed are presented.

Adult↗
PubMed1996

Myocardial integrated ultrasonic backscatter in patients with old myocardial infarction: comparison with radionuclide evaluation.

The purpose of our study was to clarify whether the abnormalities in integrated backscatter may be used to assess myocardial viability in patients with old myocardial infarction by comparing these integrated backscatter parameters with conventional radionuclide and echocardiographic estimates of myocardial viability. Two myocardial integrated backscatter parameters, the magnitude of cyclic variation in integrated backscatter and the myocardial integrated backscatter calibrated with the power of Doppler signals from the blood along the same ultrasound beam (calibrated myocardial integrated backscatter), were measured in 21 normal persons and 33 patients with old anteroseptal myocardial infarction. Calibrated myocardial integrated backscatter was higher and the magnitude of cyclic variation in integrated backscatter was lower in the infarct septum compared with the septum of normal subjects. Percent thallium uptake, as assessed in scintigraphic images taken at rest or after reinjection, correlated well with the calibrated myocardial integrated backscatter (r = -0.72, p < 0.01) and more weakly but significantly with the magnitude of cyclic variation in integrated backscatter (r = 0.55, p < 0.05) in 16 of 33 patients. The measurement of calibrated myocardial integrated backscatter, in addition to the magnitude of cyclic variation of integrated backscatter, may likely be valuable in the noninvasive assessment of myocardial viability.

Adult↗
PubMed1998

Increased atrial vulnerability in arrhythmogenic right ventricular disease.

Supraventricular tachyarrhythmias (SVTA) may occur in patients with the arrhythmogenic right ventricular dysplasia (ARVD). The purpose of the study was to evaluate the incidence of SVTA in 47 patients with ARVD proved by right ventricular angiography. Thirty-three men and 14 women, aged 21 to 72 years (mean 44 +/- 18) were admitted for nonsustained or sustained ventricular tachycardia. Eight patients had a history of spontaneous SVTA several years before ventricular tachycardia occurrence. Protocol of the study consisted of programmed atrial stimulation with one and two extrastimuli delivered during sinus rhythm and two driven rhythms (600 and 400 msec), programmed ventricular stimulation with up to three extrastimuli and was performed in the control state and after infusion of isoproterenol. The results of programmed atrial stimulation were compared with those obtained in 36 asymptomatic subjects without heart disease and with a mean age of 50 +/- 18 years (control group). Sustained SVTA (> 1 minute) was induced in seven of eight patients with spontaneous SVTA, in 27 (69%) of those with ARVD, who did not have spontaneous SVTA, and in two control subjects (5.5%) (p < 0.001). SVTA was inducible in the control state, but ventricular tachycardia induction required isoproterenol in 11 of 27 patients. Two patients without SVTA history but with inducible SVTA developed later spontaneous SVTA. ARVD was associated with a significantly higher incidence of inducible SVTA than in a control population. Supraventricular tachycardias may precede ventricular tachycardias. This association argues for a diffuse myocardial disorder in ARVD.

Adolescent↗
PubMed2001

Myocardial damage and left ventricular dysfunction in patients with and without persistent negative T waves after Q-wave anterior myocardial infarction.

Persistent T-wave inversions during the chronic stage of Q-wave myocardial infarction (MI) indicate the presence of a transmural infarction with a fibrotic layer pathologically. The aim of the present study was to examine the relation between left ventricular (LV) damage and changes in polarity of the T waves from the acute to chronic phase in patients with Q-wave anterior wall MI. We studied 140 patients with persistent T-wave inversions in leads with Q waves (negative T-wave group) and 158 patients with positive T waves (positive T-wave group) at 12 months after anterior MI. In the positive T-wave group, the precordial T waves reverted from a negative to a positive morphology < 3 months after MI in 21 patients (3 M-positive T-wave subgroup), 3 to 6 months in 52 patients (6 M-positive T-wave subgroup), and 6 to 12 months in 75 patients (12 M-positive T-wave subgroup). Ten patients had persistent positive T waves without initial T-wave inversion (persistent positive T-wave group). Wall motion index and LV dimension were higher and the wall thickness for the infarct area and LV ejection fraction were lower in the negative T-wave than in the positive T-wave groups, except the persistent positive T-wave group in the chronic stage (p < 0.0001). Wall motion in the infarcted area improved over the course of 1 year in the 3 M-, 6 M-, and 12 M-positive T-wave subgroups (p < 0.0001), but not in the persistent positive T-wave group. Among the patients with T-wave inversions after admission, those who had persistent negative T waves after 12 months had worse LV function. In patients with initial T-wave inversion, earlier normalization of the precordial T waves was associated with greater improvement in LV function. Patients with persistent positive T waves without initial negative T waves had poorer recovery of LV function than patients with persistent negative T waves. We conclude that the presence of inverted T waves in leads with abnormal Q waves 12 months after MI and the time required for T-wave normalization can be used to assess the degree of LV dysfunction.

Aged↗
PubMed2001

Infant partial left ventriculectomy for failure to wean from cardiopulmonary bypass.

Following aortic reimplantation of anomalous left coronary artery from the pulmonary artery in a 6-month-old infant, the heart failed to wean after prolonged supportive cardiopulmonary bypass and maximal inotropic support. We performed partial left ventriculectomy (Batista procedure) that halved left atrial pressure and enabled discontinuation of bypass. Postoperative recovery was then uneventful.

Cardiopulmonary Bypass↗
PubMed1985

Laser photoablation of pathological endocardium: in vitro findings suggesting a new approach to the surgical treatment of refractory arrhythmias and restrictive cardiomyopathy.

In selected patients, malignant ventricular tachyarrhythmias have been successfully abolished by excision of subendocardial arrhythmogenic foci. Likewise, in certain patients in whom restrictive cardiomyopathy is due to endocardial thickening, endocardial resection has resulted in hemodynamic improvement. The present study was designed to explore the utility, in vitro, of laser photoablation of pathologically thickened endocardium. Endocardial photoablation was easily accomplished regardless of etiological or anatomical variations using either the focused beam of a carbon dioxide laser or argon laser light delivered through a 200-microns optical fiber. Photoablation of areas as large as 3.9 X 1.3 cm was performed within 40 seconds. The extent or depth of endocardial photoablation could be limited to 2 mm2 in area or 1 mm in depth using either form of laser therapy. These in vitro results suggest that either carbon dioxide or argon laser phototherapy can be successfully applied to the surgical treatment of refractory arrhythmias and restrictive cardiomyopathy. Advantages of laser photoablation include speed and precision. Furthermore, laser photoablation obviates the difficulty associated with conventional techniques in establishing tissue planes.

Argon↗
PubMed1998

The surgical anatomy of the left ventricular outflow tract in hearts with ventricular septal defect and aortic arch obstruction.

BACKGROUND: Profound understanding of the left ventricular outflow tract (LVOT) anatomy is crucial to improve surgical results in patients with aortic arch obstruction, ventricular septal defect, and subaortic stenosis. METHODS: We studied the morphology of the LVOT in 32 postmortem hearts with aortic arch obstruction and a ventricular septal defect. In case of subaortic obstruction, the length of the subaortic muscular component was measured anteriorly and posteriorly within the left ventricle. RESULTS: Seven of the 32 hearts had no subaortic stenosis. Nine had aortic override, which caused LVOT narrowing. Sixteen hearts contained a subaortic shelf, downstream to the ventricular septal defect, which deviated into the left ventricle in 15. In 10 of these the shelf was muscular; in 6 it was a fibrous ridge. In cases with a muscular shelf, the posterior part was significantly shorter than the anterior part (p < 0.004). In 9 hearts the LVOT was further narrowed because of the abnormal relationship between the mitral valve and the subaortic shelf. CONCLUSIONS: The present study confirms the complexity of LVOT stenosis in aortic arch obstruction and ventricular septal defect and provides a better understanding of the options to achieve surgical relief.

Aorta, Thoracic↗