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Lipomas, which account for approximately 10% of all neoplasms of the heart, may be detected in asymptomatic patients by chance during echocardiography, CT scan, or MRI scan. Occasionally, lipomas are complicated by arrhythmias. We describe a patient who presented with severe cardiomegaly and paroxysmal supraventricular tachycardia. An MRI scan showed a large intrapericardial lipoma with two large cavities inside communicating with each other and with the right ventricular chamber through a defect of the right ventricular wall. The mass was partially removed, and the right ventricle was patched. Surgery combined with antiarrhythmic therapy resulted in a good short-term result.

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BACKGROUND AND AIM: Studies of young patients with acute myocardial infarction (AMI) have demonstrated that conventional risk factors are usually responsible for their premature atherosclerosis. No account has yet been published of the risk profile of young Italians surviving an AMI. In this study, the conventional risk factors, lipids and apolipoproteins, and apolipoprotein E (APOE) allele distribution were evaluated in 98 consecutive AMI survivors (94 males, 4 females) aged 40.1 +/- 3.9 for at least three months after their acute event. These survivors were matched for age, sex, body mass index and presence of diabetes mellitus with 98 controls selected from subjects admitted to the same hospital for other reasons. METHODS AND RESULTS: Lipid profiles and APOE polymorphism were determined in both groups. Coronary angiography during hospitalization showed the absence of critical stenosis in 6.6% of the survivors, mono-vessel disease in 57.7%, and multi-vessel disease in 35.5%. The survivors had a higher frequency of smoking, hypertension, family history for coronary artery disease (CAD) and dyslipidemia, and a much greater frequency of 3 or more risk factors than the controls: Odd ratios (OR) 7.4, 95% confidence interval (CI) 2.5-18.6, p = 0.0000. Significant differences were found between the groups for triglycerides (p = 0.000002), total cholesterol (p = 0.003), LDL-cholesterol (p = 0.012), HDL-cholesterol (p = 0.0002), apolipoprotein AI (p = 0.00001), and Apolipoprotein B (p = 0.000001). No differences were observed in APOE allele distribution (APOE*4 0.11 vs 0.08, APOE*3 0.86 vs 0.89, APOE*2 0.03 vs 0.03), nor in lipid profile when both higher risk genotype (E3/4, E4/4, E2/4) and lower risk genotype groups (E2/2, E2/3, E3/3) were analysed. OR were calculated as measures of the association of the E4-positive genotypes with AMI. They indicated a non-significant increase in risk of AMI when the survivors were compared with the controls (OR 1.78, 95% CI 0.84-3.70, p = 0.13). CONCLUSIONS: This study provides further evidence that conventional coronary risk factors are usually present in young AMI patients. The APOE*4 allele was associated with a 1.8 non-significant increase in the risk of AMI in our group with premature CAD. Comparison with controls showed that the presence of three or more risk factors sharply increased the probability of premature CAD and that hyper-triglyceridemia is an independent risk factor. The data on APOE polymorphism are less certain and a larger study is needed.

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BACKGROUND: The aim of this study was to analyse long term results of mitral valve repair of degenerative mitral regurgitation compared to valve replacement. METHODS: A hundred-twenty-five consecutive patients with severe mitral valve insufficiency who underwent cardiac surgery from January 1987 to December 1995 were included in the study. Mean age was 55+/-16 years (77 males, 48 females). Mitral repair was performed in 62 patients and mitral valve was replaced in 63 patients. Mean follow-up was 5 years. The repair procedures were based on quadrangular resection of the posterior leaflet, chordal replacement and transposition. Annuloplasty was performed in 100% of cases. The technique of valve replacement was conventional with complete excision of the valve in the majority of cases. RESULTS: Operative mortality following valve repair was 1.6%, no death occurred in the prosthesic group. In the repair group overall survival and re-operation rate were respectively 95.2% and 6.5%, while in the replacement group were 93.7% and 7.9%. No endocarditis and thromboembolic accidents were observed following valvuloplasty, while in the prostheses 6.3% of patients had endocarditis and 1.6% had a thromboembolic event. Mild or moderate left ventricular dysfunction was present in 5 patients after valvuloplasty and in 9 patients with prostheses. CONCLUSIONS: Considering these results we conclude that, in patients with severe degenerative mitral insufficiency, mitral valve repair is warranted whenever it is possible. The advantages given by maintaining the native valve suggest that surgery should be considered in asymptomatic patients before the occurrence of the left ventricular dysfunction.

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In our study, troponin I was not a predictor of cardiac events and a negative troponin I test did not exclude the presence of severe coronary artery disease. A positive troponin I test in patients with unstable angina identified a subgroup with probable, more active coronary disease (with higher levels of C-reactive protein).

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Patients presenting with ischemic chest pain and electrocardiographic evidence of global T-wave inversion are most frequently women with intact left ventricular function and no critical stenosis of major coronary vessels. Hence, this syndrome has a good immediate and long-term prognosis.

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New antiarrhythmic class 1C agents have been proposed in the last few years in an attempt to suppress paroxysmal atrial fibrillation at long-term, as the most commonly used class 1A agents such as quinidine gave highly variable results as regards both side-effects and efficacy. The aim of this randomized prospective study is to evaluate the efficacy and safety of oral propafenone at long term in preventing paroxysmal atrial fibrillation and to compare the results with those obtained using agents such as quinidine. Two hundred patients with recurrent episodes of symptomatic atrial fibrillation were enrolled for this study with entry criteria based upon a history of more than 3 crises in the previous 6 months, with electrocardiographic (standard electrocardiogram or dynamic registration) documentation. According to a randomized selection either propafenone at 300 mg twice daily or hydroquinidine retard 250 mg twice daily were administered to the patients; clinical check-up was carried out every 3 months or if clinical course worsened. The dosages were increased if proved to be inadequate at check-up (i.e. recurrence of atrial fibrillation) up to 300 mg 3 times daily for propafenone and 500 mg twice daily for hydroquinidine. The efficacy at the 3rd month was 71% for propafenone and 60% for hydroquinidine, at the 6th month 60% for propafenone and 56% for hydroquinidine; this trend lowered progressively as the follow-up continued, to 48% for propafenone and 42% for hydroquinidine (NS). More than 70% of the responder patients assumed 600 mg twice for propafenone or 250 twice for hydroquinidine. Propafenone had a percentage of 10% side-effects and hydroquinidine 24% (p = 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

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Between 1985 and 1990, 1242 patients with supraventricular arrhythmias were followed-up at our Institution. Six hundred and twenty patients had atrial fibrillation or flutter; 7 of them (1%) underwent modulation of atrioventricular conduction. Four hundred and twenty-eight patients had ventricular preexcitation; in 23 (5%) surgical or transcatheter ablation of an accessory pathway were performed. Atrioventricular node reentrant tachycardias were diagnosed in 111 patients; 8 patients (7%) underwent antitachycardia pacemaker implantation. Surgical and catheter ablative techniques eliminate the substrate of the tachycardia; death and complete A-V block (paraseptal pathways) are at this moment rarely reported. Antitachycardia pacemakers do not offer a definitive therapy. For their safeness and effectiveness they are still indicated in patients with A-V node reentrant tachycardias, until technological development will reduce the risks of ablative techniques.

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An intracavitary electrophysiological study was carried out on 103 patients with Wolff-Parkinson-White (WPW), 23 symptomatic patients had documented episodes of atrial fibrillation, 54 symptomatic patients had atrioventricular reentrant tachycardias, and 26 asymptomatic. Patients were examined for the relation between spontaneous atrial fibrillation and atrial vulnerability, defined as the possibility to induce sustained (greater than 1 minute) episodes of atrial fibrillation with a stimulation protocol excluding atrial bursts. Atrail fibrillation induction was attempted by single and double atrial extrastimuli during pacing at two different cycle lengths and incremental atrial pacing. Sustained atrail fibrillation was induced in 65% of the patients with spontaneous atrial fibrillation, and in 13% of the symptomatic patients with documented episodes of atrioventricular reentrant tachycardias and in 15% of the asymptomatic patients (P less than 0.0005). Atrial vulnerability was higher in patients with spontaneous atrial fibrillation than in patients without this arrhythmia. No significant difference was observed between symptomatic without atrial fibrillation and asymptomatic patients.

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Cases of familial arrhythmogenic right ventricular dysplasia (ARVD) have been reported by many authors, and a genetic mechanism of transmission has been hypothesized. Both autosomal dominant and autosomal recessive mechanism of inheritance were suggest. We present a father and a daughter affected by arrhythmogenic right ventricular dysplasia, belonging to a family with many cases of sudden death. Both of them presented with an episode of ventricular tachycardia with left bundle branch block. The clinical diagnosis was made according to electrocardiographic, echocardiographic, angionuclear and hemodynamic criteria of ARVD. The familia analysis suggest an autosomal dominant mechanism of transmission.

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It is well known that in patients with Wolff-Parkinson-White (W.P.W.) adrenergic activity stimulation induced by exercise or isoproterenol I.V. infusion shortens the anterograde effective refractory period (E.R.P.) of the accessory pathway. Our purpose was to evaluate whether the upright position produces similar changes on the electrophysiologic properties of the accessory pathway and influences reciprocating tachycardias induction. In 18 patients, with W.P.W. syndrome, who underwent electrophysiologic study, we determined the anterograde E.R.P. of the accessory pathway and attempted to induce a reciprocating tachycardia in the supine and in the upright position. In 13 patients (72%) the anterograde E.R.P. of the accessory pathway shortened in the upright position (303 +/- 104 msec vs 331 +/- 123 msec; p less than 0.001); in 4 patients (22%) it was unchanged; in 1 patient was not defined, being inferior to the atrium E.R.P. We were able to induce a reciprocating tachycardia in 3 patients in the supine position, in 6 patients in the upright position. Electrophysiologic testing in the upright position improves the evaluation of the accessory pathway electrophysiologic properties.

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The effectiveness of short- (15 days) and long- (12 months) term propafenone treatment was assessed in 53 patients presenting with more than 30 premature ventricular complexes per hour as detected by 24-hour ambulatory Holter monitoring. Thirty-nine patients had no apparent concomitant heart disease while 14 had chronic coronary artery disease. The effects of propafenone were analysed by ambulatory Holter monitoring after 15 days and at 3, 6 and 12 months. The initial dose was 150 mg four times daily and was increased up to 300 mg four times daily when necessary. Favourable short-term effects were obtained in 39 patients (73.6%). After 12 months, 17 patients (32.1%) were still on propafenone treatment with good results. Treatment was discontinued on account of low compliance in 28.3%. This was because treatment was ineffective even at high doses in 15.2%, because of severe side effects in 13.2%, because of proarrhythmic effects in 5.6% and for other causes in 5.6%.

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To demonstrate the effect of elastic and myogenic properties of the vessel wall on the mean coronary vascular resistance during ventricular diastole (m.d.c.r.), this resistance was assessed in twenty dogs anaesthetized with sodium pentobarbitone during a 10 s period of arterial haemorrhage and 20 s of recovery from this haemorrhage. In a first stage of the study ten dogs were investigated following sectioning of the vagal nerves in the neck, beta-blockade, and ligation of the carotid arteries. During haemorrhage and reduction in aortic blood pressure (A.B.P.) in these dogs, there was an initial rise (at 2 s after the start of the haemorrhage) in m.d.c.r. which quickly decreased to a value similar to that obtained during the control period. After the abrupt cessation of haemorrhage, and a rise in A.B.P., there was an initial decrease in m.d.c.r. which eventually increased to the control levels. In the second stage of study identical patterns of changes were obtained in a group of five dogs in which the cervical vagi were not sectioned and beta-blocking agents not given. In another group of five dogs, during infusion of dipyridamole to force maximal coronary vasodilation, the increase in m.d.c.r. was maintained throughout the period of haemorrhage and reduction in A.B.P., and m.d.c.r. did not decrease below the control values following the abrupt cessation of haemorrhage and a rise in A.B.P. The findings in the dogs without dipyridamole infusion suggested that the pattern of changes in m.d.c.r. was due to changes in the perfusion pressure and their effect on the elasticity and myogenic properties of the coronary vascular wall. This suggestion was supported in the second stage of the study, when the reductions in m.d.c.r. were abolished by forcing coronary vasodilation using the infusion of dipyridamole.

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Myopotential inhibition was produced by a combination of different provocative maneuvers in 423 (77%) out of 550 consecutive unipolar pacemaker patients. The most useful maneuvers were the hand-to-shoulder press (90% positivity) and the hand-to-hand press (60% positivity). Three groups of 20 patients were then submitted to 24 hours of Holter monitoring. Group A during the provocative maneuvers had shown myopotential inhibition and symptoms of cerebral ischemia. In group B symptomless myopotential inhibition had been induced. Group C had no myopotential inhibition nor symptoms during the tests. Abnormal pacemaker pauses related to myopotential inhibition were recorded during Holter monitoring in 90% of group A and in 80% of group B patients, but only group A patients showed symptoms. Thus in patients who are able to practice provocative isometric maneuvers and who can be selected according to their response, Holter monitoring seems to offer few advantages in discovering myopotential inhibition and related symptoms.

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Spontaneous variability of premature ventricular complexes was evaluated by 72 hour continuous ambulatory electrocardiographic monitoring in 38 patients. Nineteen patients had coronary artery disease and 19 subjects had no documented signs of cardiac disease. Using multifactorial analysis of variance we determined the minimal percent reduction of premature ventricular complexes frequency that could not be ascribed to spontaneous variability alone in both single subject and in groups of 10 and 19 individuals and analyzed the difference between the two groups of ischemic and healthy patients. Our results show that in each subject with or without coronary artery disease the minimal reduction of premature ventricular complexes is similar: 71% and 72% respectively. On the other hand when the two groups were compared the percentage of reduction was 49% in healthy subjects and 40% in patients with coronary artery disease. Spontaneous variability of premature ventricular complexes decreases as the period of monitoring lengthens; however the improvement obtained with longer electrocardiographic monitoring doesn't justify the prolongation of the examination beyond 24 hours.

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Electrophysiological evidence of dual intrahisian pathways has been shown in a patient with diseased His bundle. The main electrocardiographic features, in this case were: 1). 1:1 A-V conduction with alternating short and long PR intervals; 2). unexpected A-V Wenckebach sequences; and 3). unexpected interruption of Wenckebach sequences by early captures of the ventricles with short and fixed PR intervals. These features were due to the following causes: 1). different E.P. properties of the two pathways producing a shift of conduction from a fast conducting pathway (FCP) to a slow conducting pathway (SCP); 2). a concealed reentry from the SCP into the FCP; and 3). a phase of "unexpected conduction" in the FCP.

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The efficacy of amiodarone in the prevention of atrial tachycardia is well recognised. However, there remains some controversy over its use in patients with a basal sinus bradycardia because of the risk of further depression of sinus node function. We studied the effects of acute and chronic amiodarone therapy in 13 patients with paroxysmal supraventricular tachycardia and intercritical sinus bradycardias of between 40 and 50/min. All patients underwent electrophysiological investigation under basal conditions and after 5 mg/kg IV amiodarone. Five patients were excluded from chronic oral amiodarone therapy after IV amiodarone for the following reasons : sinus bradycardia of less than 30/min; sinus node recovery times greater than 2 s; 2nd or 3rd degree sino-atrial block. The other 8 patients were administered oral amiodarone on a long term basis. They were followed up clinically with dynamic ECGs every three months over a period of 1 to 3 years. All symptoms regressed in 6 patients. In one patient, the daily attacks of palpitations decreased to one a week. One patient did not improve. No cases of sino-atrial standstill were observed, although the sinus rate remained unchanged. The results of our study show that amiodarone may be administered for long periods in patients with sinus bradycardia and attacks of paroxysmal supraventricular tachycardia if the dynamic ECG during the waking hours shows a heart rate of no less than 40/min, and if electrophysiological investigations do not show significant depression of sinus node function after acute intravenous administration of the drug.

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One hundred and twenty asymptomatic patients underwent a submaximal treadmill exercise 2-3 weeks after an acute myocardial infarction. These patients were subsequently followed from 15 to 54 months (average 2 years). Coronary events (cardiac death or angina) occurred in 14% of the patients with normal response, in 55% of those with ischemic response and in 12% of those with abnormal but non-ischemic response. The incidence of coronary events in patients with ischemic response is significantly higher than in the other two groups. However, among the patients who had a normal response, one out of seven suffered from a coronary event during the follow-up period. More than 25% of our patients with an ischemic response to the early exercise testing showed a non-ischemic response during a second one. On the other hand, more than 25% of our patients with normal early exercise test had an ischemic response when the test was performed at the end the follow-up period. Submaximal exercise testing of asymptomatic patients early after an acute myocardial infarction does not seem to be predictive of future coronary events and its long-term reproducibility is poor.

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