[Imaging techniques in aortic dissection. Diagnosis with angiography].
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Biomedical subjects
Publications and source records attributed to F Orzan.
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Aim of this study was to assess the long-term results of PTCA in patients with a recent myocardial infarction. The study population consisted of 244 consecutive patients who underwent a PTCA < or = 30 days after myocardial infarction either because of angina (116 patients), or because of provoked ischemia (62 patients), or in the absence of both (66 patients). "Simple" balloon angioplasty, without adjunctive devices, was performed. Most of the patients were seen at 1 year intervals at the outpatient clinic; otherwise information was gathered either from the family physician or by telephone. The following events were noted during a follow-up of 6-102 months (median 39 months): death, myocardial infarction, need for re-PTCA or surgical revascularization, recurrence of angina. Survival and event-free curves were calculated according to the method of Kaplan and Meier; statistical comparisons between the curves were obtained by the log-rank test. Periprocedural deaths, infarctions and surgical revascularizations are included in the actuarial curves. Differences were examined between patients with Q and non-Q wave infarctions, single vessel versus multivessel disease, left ventricular ejection fraction > or 50% versus < 50%. A clinical success was achieved in 85% of the procedures. Sixteen patients were lost at follow-up. Overall, within the first 30 days and during follow-up, 12 (4.9%) patients died, 19 (7.7%) suffered from myocardial infarction, 34 (13.9%) required re-PTCA or surgical revascularization, and 63 (25.8%) experienced angina again.(ABSTRACT TRUNCATED AT 250 WORDS)
We have studied clinical and ECG stress features of 119 patients with left main disease and 113 matched patients with three vessels coronary disease. Clinical features and ECG stress test do not differentiate the two groups as a whole. Exercise time duration was shorter, ST criteria were more positive, and peak heart rate was lower in the subgroups of patients with left main and involvement of a right dominant coronary artery. However due to a large overlap these criteria do not seem to be clinically useful. In conclusion, in an individual patient angina and stress ECG criteria do not differentiate the patients with left main from those with three vessels coronary artery disease.
OBJECTIVES: To evaluate the diagnostic and therapeutic problems that occur in managing patients with radiation-induced constrictive pericarditis. BACKGROUND: Radiation therapy of the chest and mediastinum can damage all cardiac structures, the pericardium being the most frequently involved one. It is little appreciated, however, that radiation-induced constrictive pericarditis can be associated with significant involvement of coronary arteries, myocardium and valves. METHODS: Retrospective evaluation of clinical, hemodynamic, surgical and postoperative data in 8 patients, (7 women, 1 man, aged 26-67 years, mean 44), who had received 30-50 Gy to the chest because of Hodgkin's disease, lymphoma, or breast cancer 7-23 years before the diagnosis of constrictive pericarditis. RESULTS: Six patients had symptoms related to the pericardial disease, one had angina and syncope, one was in congestive heart failure. Hemodynamic signs of constriction were obvious in 6, and were revealed by volume load in 2. All patients had mitral regurgitation, 5 had also tricuspid insufficiency and 5 had aortic regurgitation. The degree of the valvular regurgitation was > or = 3+ in four instances. Critical coronary arterial stenoses were discovered in 3 cases. The coronary ostia were involved in 5 cases (2 critical, 3 non critical). A diagnosis of restrictive cardiomyopathy was arrived at in 4 instances, always after pericardiectomy. Seven patients were operated on: there were 6 pericardiectomies, associated with either valvular surgery or myocardial revascularization or both in 3. One patient underwent myocardial revascularization only. The remaining patient is being treated medically. One patient died at surgery, two died 16 and 72 months thereafter. The remaining 5 have mild symptoms 11-60 months (mean 29) after the discharge from the hospital. CONCLUSIONS: Radiation-induced pericardial constriction is frequently associated with coronary artery disease, mostly silent, with valvular insufficiency, and with myocardial disease. Thorough cardiac evaluation in such patients is mandatory. Surgical treatment frequently uncovers an underlying restrictive myopathy that presents a serious diagnostic and therapeutic challenge.
BACKGROUND: Aim of the study is to evaluate patients compliance with therapeutic recommendations after coronary angiography. METHODS: We analyzed all patients who underwent coronary angiography in an university center during 1990. One of the following treatments were recommended: medical therapy without revascularization, percutaneous transluminal coronary angioplasty, coronary artery bypass grafting. A cohort of 392 patients was assessed one year after coronary angiography in order to evaluate clinical predictors of non compliance with the treatment recommended. RESULTS: Of the 141 patients, for whom medical treatment was recommended, 16 (11%: 95% confidence interval 6-17%) had revascularization. By stepwise discriminant regression analysis, older age, congestive heart failure and critical lesion of the left anterior descending artery were statistically significant predictors of non compliance. Of the 137 patients, for whom PTCA was recommended, 8 (6%: 2-9%) were non compliant. No variables were predictive of non compliance. Of the 114 patients, for whom CABG was recommended, 15 (13%: 7-19%) were non compliant. By stepwise regression analysis, absence of typical angina was predictive of non compliance. For 12 patients non compliance was related to personal preferences, for 10 to clinical deterioration, for 9 to a second opinion, and 3 were still in the surgical waiting list one year after coronary angiography. One year mortality was not affected by non compliance. CONCLUSIONS: Non compliance to recommended treatment after coronary angiography is uncommon and is mainly related to patients preference towards a less invasive treatment or to a change of clinical conditions over time.
AIM: To evaluate the commonly adopted ventriculographic and coronarographic criteria of hypertrophic cardiomyopathy. POPULATION: Eleven cases of obstructive cardiomyopathy, 14 non-obstructive cardiomyopathies, 15 discrete subaortic stenoses, 10 valvular aortic stenoses, and 12 cases of hypertensive heart disease. The diagnosis had been arrived at by independent clinical, electrocardiographic, echocardiographic and haemodynamic methods, as appropriate. METHODS: Retrospective "blind" examination of biplane left ventriculography (30 degrees right anterior oblique, 60 degrees left anterior oblique, with cranial tilt) and coronary arteriography. We looked for the following features: subaortic chamber, asymmetric septal hypertrophy, peculiar left ventricular shape and systolic obliteration, systolic anterior movement of the mitral leaflets, systolic narrowing or compression of epicardial coronary arteries and septal perforators. RESULTS AND CONCLUSIONS: The following left ventricular features were significantly more frequent in hypertrophic obstructive cardiomyopathy, than in other forms: subaortic chamber, "banana" configuration in systole, subaortic conus, asymmetric hypertrophy, systolic anterior movement of the anterior leaflet of the mitral valve, and mitral regurgitation. A subaortic chamber was seen both in the obstructive form and in the discrete subaortic stenosis, but the cranial left anterior oblique projection could easily discriminate between them. If non-obstructive cardiomyopathy is defined with the current criteria (provocable pressure gradient of < or = 30 mm Hg in a patient with left ventricular hypertrophy of no known cause), no distinctive angiographic features can distinguish it from other forms of secondary left ventricular hypertrophy.
We investigated the clinical, electrophysiological, haemodynamic and angiographic aspects of four patients (two men and two women, aged 31-46 years) who developed complete heart block 13-20 years after therapeutic irradiation of the chest for Hodgkin's disease. The initial cardiac symptom was syncope in three, effort intolerance in one. The electrocardiogram recorded third-degree atrioventricular block in three patients, right bundle branch block and posterior fascicular block in one. The electrophysiological study, performed in three cases, showed that the block was infranodal in two. Three patients had significant coronary arterial stenoses, that involved the ostia in two. All patients had mild-to-moderate aortic and mitral regurgitation. One patient had haemodynamic signs of constriction. Another patient had recurrent pericardial effusions. All had echocardiographic evidence of a thickened pericardium. Cardiac involvement can be extensive in patient with radiation-induced heart block. Because coronary artery disease can be particularly severe, coronary angiography appears to be warranted in such patients.
OBJECTIVE: To define the clinical and angiographic features and the therapeutic problems in patients with coronary artery disease after therapeutic irradiation of the chest. DESIGN: An observational retrospective study. SETTING: The cardiac catheterisation laboratory, university medical school. PATIENTS: 15 subjects (8 men and 7 women, aged 25-56 years, mean 44) examined in the cardiac catheterisation laboratory, who had significant coronary artery disease years after having radiation treatment to the chest and anterior mediastinum. In the early stages of the study angiography was performed because of typical symptoms of ischaemic heart disease. Later on it was performed because of a high index of suspicion in people with signs of extensive radiation heart damage. MAIN OUTCOME MEASURES: Clinical and electrocardiographic evidence of ischaemic heart disease; echocardiographic signs of pericardial, myocardial or valvar involvement; angiographic evidence of coronary arterial stenosis, with special attention to the ostia; haemodynamic and angiographic signs of pericardial, myocardial, and valvar disease. Survival and symptomatic and functional status were ascertained after medical or surgical treatment. RESULTS: The patients were relatively young and had no risk factors. Seven patients had no signs or symptoms of ischaemic heart disease. Ten patients had ostial stenosis, which was associated with extensive involvement of other cardiac structures in nine of them. Seven required surgical treatment for coronary artery disease. Two died, one at surgery and the other one six months later. Five patients had complications associated with irradiation. CONCLUSIONS: Coronary arterial disease can be reasonably ascribed to the effects of chest irradiation when the patients are young and free from risk factors, especially if the obstructions are ostial and there is important damage to other cardiac structures. In patients with damage to other cardiac structures angina and infarction are often absent and coronary angiography seems to be mandatory. Patients often require surgical treatment and postoperative complications are common.
PURPOSE OF THE STUDY: to assess the diagnostic value of the commonly adopted haemodynamic criteria for the diagnosis of obstructive and non-obstructive hypertrophic cardiomyopathy. PATIENTS: 16 cases of hypertrophic cardiomyopathy, 7 cases of the non-obstructive form, 16 fixed subaortic stenosis, 8 valvular aortic stenosis, and 7 cases of hypertensive heart disease. METHODS: left and right heart catheterisation, with particular attention to the pressure gradient and to the aortic pulse pressure by means of simultaneous pressure recording from the left ventricle and aorta under basal conditions, after a ventricular premature beat, during the Valsalva manoeuvre, during amyl nitrite inhalation, and isoproterenol administration. RESULTS AND CONCLUSION: the Valsalva manoeuvre increases significantly (p < 0.001) the pressure gradient, and the aortic pulse pressure in the post-extrasystolic beat decreases significantly (p < 0.001) in patients with hypertrophic obstructive cardiomyopathy. This response is significantly different from that of the other 3 disease groups. If the non-obstructive form is defined by strict criteria (i.e. no gradient above 30 mmHg even after provocative manoeuvres), then it cannot be separated from other forms of secondary left ventricular hypertrophy.
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Between January 1, 1985 and June 30, 1992, 37 patients (25 women and 12 men, aged 13-65 years) who had undergone a radiation treatment to the anterior chest and mediastinum, were admitted to our Institution for cardiac evaluation, which included left and right heart catheterisation in all, but 3 patients. Seventeen had signs or symptoms of ischaemic heart disease, in 8 a pericardial disease was suspected, 5 had a complete heart block, 4 were in congestive heart failure caused by valvular dysfunction, and 3 had a dilated, hypokinetic left ventricle. Diagnostic criteria in these patients were as follows. Stenoses of the coronary ostia were always considered to be caused by radiation damage, in the absence of coronary risk factors. Obstructions of other coronary segments were taken to be of X-ray origin only when accompanied by damage to other cardiac structures. Pericardial lesions were always reckoned to be of X-ray origin in the absence of other recognisable causes. The same held true for aortic stenosis or insufficiency of any degree and for mitral insufficiency > or = 3+. Cases of complete heart block were diagnosed according to Slama's criteria. A restrictive cardiomyopathy was recognised only in patients operated on for pericardiectomy, in whom clinical or haemodynamic signs of "constriction" persisted after the operation, or extensive subendocardial fibrosis was found at biopsy. According to the above-mentioned criteria, it was established that radiation therapy was the cause of the cardiac problems in 19 cases: 4 with ischaemic symptoms, 8 with pericardial disease, 4 with complete atrioventricular block, and 3 with valvular disease and congestive heart failure. Coronary ostial lesions were found in all patients with angina, and in 8 of the 14 patients without angina (in 1 the coronary arteries were not investigated), and were critical in 4. Eleven patients were operated on. A myocardial revascularisation was performed in 7 cases, a pericardiectomy in 6, a valve replacement or repair was done in 4. A combined procedure was performed in 4 instances. A pacemaker was implanted in 3 cases, 2 patients had a pericardial drainage, and 3 patients continued their medical treatment. Of the 11 operated patients, 1 died at surgery, in refractory cardiac failure, from what was suspected to be a restrictive disease (normal preoperative left ventricular volume and ejection fraction, extensive myocardial fibrosis at autopsy).(ABSTRACT TRUNCATED AT 400 WORDS)
In our department we have reviewed the use of ergonovine maleate as a provocative agent for inducing coronary spasm during coronary arteriography. From January 1978 to December 1991 the test has been performed in 116 patients. According to their symptoms, the patients were divided into 4 groups: (A) patients with exertional angina: 16 patients (13.8%), (B) patients with angina at rest: 64 patients (55.2%), (C) patients with atypical chest pain: 29 patients (25%), and (D) patients with previous myocardial infarct: 7 patients (6%). We have subdivided the patients with angina at rest, according to the electrocardiogram recorded during pain, into: (1) 16 patients with ST-segment elevation; (2) 14 patients with ST-segment depression or T wave inversion; (3) 5 patients with electrocardiogram unchanged during angina; (4) 29 patients with no electrocardiogram recorded during angina. In 67 patients (57.7%) the coronaries were normal, 17 patients (14.6%) had mild irregularities, 26 patients (22.4%) had non critical fixed obstructions (< or = 70%), and in 6 patients (3.5%) there were fixed coronary narrowings > or = 70%. The left ventricle was normal in 85 subjects (73.2%), hypo or akinetic in 31 (26.8%). After routine coronary angiography and ventriculography, ergonovine maleate, 0.05 up to 0.4 mg, was given intravenously. The ergonovine test was considered positive when a focal spasm narrowed a normal coronary artery, or one with a mild fixed obstruction (< or = 50%) to more than 70%, or when a 70% stenosis became occluded. The development of angina and/or electrocardiographic changes were not taken as a criteria of positivity. Thirteen tests (11.2%) were considered positive.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Cardiac surgery has become a possible cause of ascending aortic dissection, particularly in patients who have undergone aortic valve replacement. METHODS: From January 1979 to December 1989, 134 patients with angiographic evidence of aortic dissection, were studied in the Haemodinamic Laboratory of the University of Turin. Twelve of these patients (7 men and 5 women), mean age 51.6 years, had been previously operated for aortic valve replacement. We evaluated incidence, clinical and anatomic features of ascending aortic dissection in this group. RESULTS: A dilated ascending aorta with a mean diameter of 4.92 cm. was noted in all these patients. The interval between valve replacement and diagnosis of aortic dissection was 57 months (range 1 day to 9 years). Reoperation was performed in 11 patients. Four intraoperative deaths occurred and 2 other patients died in the early post-operative period. Survival rate at 12 months was 50%. Our incidence of ascending aortic dissection after aortic valve replacement was 0.66% (10 patients out of 1499 operated for aortic valve replacement) and it is in agreement with reports from other Authors in literature. CONCLUSIONS: Replacement of the ascending aorta must be considered if an important dilatation of aortic root is found at time of aortic valve surgery. New efforts must be undertaken to identify patients at high risk for this complication because an elevated mortality rate is observed in reoperation for aortic dissection.
Several authors have reported aortic dissection in Marfan's syndrome with familial incidence. Cases of dissecting aortic aneurysms have likewise been described in families whose members had severe systemic arterial hypertension. We report 4 cases of familial aortic aneurysm, 3 of whom had a dissection, in the absence of Marfan's phenotype but with histologic findings and genetic transmission similar to those previously described as formes frustes of Marfan's syndrome.
It is well known that radiation therapy to the anterior mediastinum may induce lesions of all cardiac structures. The pericardium is most frequently involved, but atrioventricular conduction disorders, cardiomyopathy, coronary stenosis may also be produced. Aortic, mitral and tricuspid lesions have been described. However, clinical evidence of pulmonic valve involvement has not been reported. Only at necropsy has fibrotic thickening of the pulmonic cusps occasionally been found. We report a case of infective endocarditis of the pulmonic valve in a 53-year-old patient who had undergone thoracic radiation therapy for Hodgkin's disease 31 years previously. Four years prior to the endocarditis he had also been submitted to myocardial revascularisation for critical lesions of the left main and right coronary ostia, and to aortic valve replacement because of stenosis and insufficiency. At that time, the pulmonic valve was fibrotic on echo examination. It is noteworthy that, of all the cardiac valves, the infective process involved only the pulmonic one, which is seldom the target of an infection. To our knowledge this is the first case of bacterial endocarditis of a heart valve that had been previously damaged by radiation therapy.
Results of our prospective, randomised pilot trial to evaluate the clinical effects and the angiographic correlates of early thrombolysis in patients with unstable angina are reported. Sixty-seven patients had coronary angiography 10 +/- 8 (median 7) hours after an episode of transient chest pain at rest with reversible ischaemic changes on the electrocardiogram. Patients with left main disease (4), or diffuse coronary disease and unidentified ischemia-producing lesions (13) were excluded, as were those without severe (greater than or equal to 70%) stenosis (10). Intracoronary thrombus was identified at angiography in 7 patients (17%) and complex coronary lesions in 5 (12%) of the remaining 40 patients who were randomised to either intracoronary streptokinase 250,000 IU followed by intravenous heparin along with conventional treatment (20 patients), or to conventional treatment alone (20 patients). All patients received Aspirin. No differences between the streptokinase and the conventional treatment groups were observed with respect to demographic and clinical characteristics at admission to the study. During observation in the intensive care unit for 3 +/- 1 days, 8 patients (40%) with streptokinase and 10 (50%) with conventional treatment were free from angina and infarction (p = 0.75; 95% confidence interval for the difference in response rates = -20 to 40%). There were no bleeding complications and no patient died. Patients enrolled in our study had fewer coronary thrombi at angiography than currently reported. Our data did not show that adjunct treatment with streptokinase and heparin is superior to conventional treatment alone in these patients.
In 8 patients aged 41-66 years, a second left heart catheterisation done 27-98 months after the first study, demonstrated a pressure gradient across the aortic valve, that had not previously existed, or had been trivial. No significant change of the cardiac output had occurred. All but 1 patient were hypertensive. The etiology was rheumatic in 4, degenerative in 4. Electrocardiographic, radiographic, and echocardiographic evolution could not separate the patients with a gradient greater than or equal to 70 mmHg from those whose gradient was less than or equal to 40 mmHg. The intensity of the aortic component of the second heart sound, however, decreased in all former patients, and in only 1 of the latter. Aortic valvular stenosis can arise and rapidly develop in adult patients. Concomitant rheumatic mitral valve disease, coronary artery disease and hypertension can mask and/or modify symptoms, signs and laboratory findings. Changes of the aortic component of the second sound may suggest its occurrence.
In the experimental model of porcine carotid artery angioplasty, whenever a deep lesion--involving the media--is produced, thrombus deposition invariably follows. It has been shown that the thrombus formation can be prevented by heparin administration, albeit at higher doses than usually employed in the clinical setting. In patients with unstable angina and acute myocardial infarction there appears to be a hitherto ill-defined thrombogenic state and, in fact, percutaneous transluminal coronary angioplasty is still plagued by a higher incidence of acute reocclusion in such conditions. It appears reasonable to infer that during percutaneous transluminal coronary angioplasty higher dose of heparin should be infused, under close monitoring, particularly in such patients. However, at the moment this remains an unproven hypothesis that needs careful clinical testing.