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One female patient--with slight pure mitral stenosis, mild hypertension and ischemic cardiomyopathy and disabling pulmonary emphysema--developed at 54 years of age permanent atrial fibrillation, had a gratuitous mitral commissurotomy four months later, sustained chronic fibrillation for 13 years, then spontaneously resumed sinus node command at age 67 without any discernible reason. Sinus rhythm was being maintained at follow-up nine months later. Her cardiac status of fair compensation under modest digitoxin and diuretic therapy has neither improved nor worsened with the return of atrial systole. The duration, in this observation, of permanent auricular fibrillation before spontaneous return of sinus rhythm, is one of the longest ever published, exceeded, to the best of my knowledge, only by one case of Lewis and by another one of Reeve and associates. Such an exceptional event points out a fascinating enigma: how can major longstanding atrial dysrhythmias (fibrillation, flutter), whose causes and pathogenesis seem at least partly elucidated, spontaneously disappeer in atria so badly diseased? I think we must humbly confess that no satisfactory explanation is at present available for this disconcerting phenomenon.
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PMID:Spontaneous resumption of sinus rhythm in an elderly patient after 13 years of permanent atrial fibrillation. 47 82

Among 909 patients with acute myocardial inarction treated in an intensive care unit between 1970 and 1974, atrial flutter and (or) fibrillation occurred in 124 (13.6%). The incidence of these arrhythmias rose with increasing age and predominantly in paroxysmal form (78%). The clinic mortality of patients with arrhythmias was 42%, while in the remaining 785 it was only 26% (P less than 0.001). Patients with atrial fibrillation and (or) flutter had a higher mean age, more frequently cardiac failure (P less than 0.001) - especially in the prognostically unfavourable severe forms with pulmonary oedema (P less than 0.05) and combined right and left heart failure (P less than 0.001) - and other disorders of impulse conduction or formation and chronic arterial hypertension (P less than 0.01).
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PMID:[Atrial fibrillation and flutter as a complication of acute myocardial infarction (author's transl)]. 97

The need for prophylactic anticoagulation to prevent embolism before direct current cardioversion is performed for atrial fibrillation or atrial flutter is controversial. To examine this issue further, a retrospective review was undertaken to assess the incidence of embolic complications after cardioversion. The review involved 454 elective direct current cardioversions performed for atrial fibrillation or atrial flutter over a 7 year period. The incidence rate of embolic complications was 1.32% (six patients); the complications ranged from minor visual disturbances to a fatal cerebrovascular event. All six patients had atrial fibrillation, and none had been on anticoagulant therapy (p = 0.026). The duration of atrial fibrillation was less than 1 week in five of the six patients who had embolic complications. Baseline characteristics of patients with a postcardioversion embolic event are compared with those of patients who did not have an embolic event. There was no difference in the prevalence of hypertension, diabetes mellitus or prior stroke between the two groups, and there was no difference in the number of patients who were postoperative or had poor left ventricular function. Left atrial size was similar between the two groups. No patient in the embolic group had valvular disease. No patient with atrial flutter had an embolic event regardless of anticoagulant status; therefore, anticoagulation is not recommended for patients with atrial flutter undergoing cardioversion. Prophylactic anticoagulation is pivotal in patients undergoing elective direct current cardioversion for atrial fibrillation, even those with atrial fibrillation of less than 1 week's duration.
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PMID:Role of prophylactic anticoagulation for direct current cardioversion in patients with atrial fibrillation or atrial flutter. 154 82

The records of 598 patients undergoing a thoracic surgical procedure for lung cancer from 1975 through 1989 were reviewed for occurrence of cardiac arrhythmias and myocardial ischemic events. Atrial tachycardias occurred in 16% (94/598); atrial fibrillation was preponderant (87%), followed by supraventricular tachycardia and atrial flutter. Patients with recurrent episodes of dysrhythmias had a significantly higher mortality rate than those without episodes or with a single episode only (17% versus 2.4%; p less than 0.01). Transient ischemic electrocardiographic changes were documented in 23 patients (3.8%) and myocardial infarction in 7 (1.2%). An abnormal preoperative exercise test result and intraoperative hypotension were strongly associated with both dysrhythmia and ischemia (p less than 0.01). Pneumonectomy, ischemic changes on the electrocardiogram, and cardiac enlargement were also associated with arrhythmias (p less than 0.01). A weaker association (p less than 0.05) was found between postoperative arrhythmias and old myocardial infarction (greater than 6 months), arterial hypertension, and heart failure. Pulmonary function had no predictive value in this respect. A history of angina or old myocardial infarction was predictive of transient postoperative myocardial ischemia but not myocardial infarction. Despite improved anesthetic and monitoring techniques and more frequent use of the intensive care unit postoperatively in the last decade, the incidence of arrhythmias after thoracotomy has not decreased. More effective prevention is needed, particularly for patients with defined preoperative and perioperative risk factors.
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PMID:Cardiac arrhythmias and myocardial ischemia after thoracotomy for lung cancer. 155 74

The effect of beta-adrenergic blockade (propranolol) on exercise performance was studied in 15 patients (12 men and 3 women, mean age 70 years) with complete heart block treated with a ventricular-inhibited pacemaker (VVI). In a double-blind procedure, the patients were randomly given either 0.1 mg/kg of propranolol or saline solution i.v. before a first exercise test and vice versa before a second test. The interval between the tests was 24 hours. Nine patients were in sinus rhythm, 4 patients had atrial flutter, and 2 others had atrial fibrillation. The exercise capacity was on an average 11% lower with propranolol than with placebo (p less than 0.001). The most marked reductions (20 and 33%) were found in the two patients with atrial fibrillation. The atrial rate in patients with sinus rhythm was significantly lower with propranolol than placebo both at rest (68 vs. 83 beats/min, p less than 0.001) and at maximal work load (91 vs. 141 beats/min, p less than 0.001). The present findings show that beta blockade has negative effects on exercise capacity in patients with complete heart block treated with VVI pacemakers. This finding should be considered in the selection of drug treatment in patients with fixed rate pacing and concomitant hypertension and/or ischemic heart disease.
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PMID:Exercise performance and beta-adrenergic blockade in patients with complete heart block treated with ventricular inhibited pacing. 174 9

We studied the recent alcohol consumption and other possible precipitating factors in 99 consecutive patients (53 men and 46 women) all under 65 years of age with sustained re-entry and automatic supraventricular tachyarrhythmias and compared them with those of two groups of controls. One control group was derived from the Emergency Room patients and matched for age and sex; the other group (44 men, 22 women, mean age 48.7 years) was randomly selected from the general out-of-hospital population. There were 50 patients with supraventricular tachycardia, 30 with atrial flutter, and 19 with paroxysmal atrial tachycardia. Coronary heart disease (14% of patients), hypertension (10%), and dilated cardiomyopathy (6%) were the most prevalent cardiovascular diseases associated with the arrhythmias. The self-reported alcohol consumption of patients with arrhythmias during the week preceding the arrhythmia did not differ significantly from that of hospital or population controls, although significantly more patients than controls had liver enzyme levels above normal; neither were there any significant differences between the groups regarding prevalence for alcoholism as judged by the CAGE questionnaire. The results were essentially similar when patients with supraventricular tachycardia and those with intra-atrial tachyarrhythmias (flutter and paroxysmal tachycardia) were separately compared with the controls. We conclude that alcohol consumption, although a risk factor for atrial fibrillation, is not associated with the induction of other supraventricular tachyarrhythmias in patients of working age.
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PMID:Alcohol consumption of patients with supraventricular tachyarrhythmias other than atrial fibrillation. 187 80

A 59 year-old housewife was admitted to the emergency service with a sudden onset of chest pain and nausea. Initially she was treated as an acute myocardial infarction, but conventional treatments were not effective, and she was sent to our hospital for further evaluation. Her ECG showed several abnormal findings including T-wave inversion, atrial flutter, QT-time prolongation, ST-segment depression or elevation, and frequent ventricular ectopic beats. The echocardiogram, 201thallium scintigram and coronary angiography were almost normal. Both urinary and plasma levels of catecholamines were remarkably increased, and the plasma epinephrine was extremely high during attacks. Abdominal echotomography and CT-scanning showed a large left adrenal tumor. The 131MIBG scintiscan revealed a high accumulation in this tumor. Then the patient was diagnosed as having pheochromocytoma and catecholamine-induced myocarditis. The administration of phentolamine (10 mg) normalized the inversion of T-wave and the high blood pressure. But when propranolol (2 mg) was administrated in addition to phentolamine, the ECG showed a biphasic low T-wave change. According to these phenomena, we supposed that the alpha-adrenergic receptor was involved in the development of the ST-T changes of the ECG, and the alpha-adrenergic receptor of this patient might be sensitive under excessive catecholamines, according to the inhibition of the beta-receptor by propranolol.
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PMID:[A case of pheochromocytoma with an AMI-like ECG change corrected by an alpha-blocking agent]. 196 1

Diltiazem is a calcium antagonist effective in the treatment of stable, variant and unstable angina pectoris and mild to moderate systemic hypertension, with a generally favourable adverse effect profile. It is also effective in terminating supraventricular tachycardia and in controlling the ventricular response to atrial fibrillation/flutter. Atrioventricular block, the risk of which may be exacerbated by concomitant beta-adrenoceptor antagonist therapy, occurs rarely as an adverse effect of diltiazem treatment. Diltiazem appears to exert complex cardioprotective effects which have been of benefit after intracoronary administration to patients undergoing coronary angiography and bypass procedures. In addition, long term diltiazem treatment has produced a significant reduction in subsequent cardiac events in patients with non-Q wave myocardial infarction. Thus, diltiazem is an effective and well-tolerated first-line or alternative treatment of patients with ischaemic heart disease, systemic hypertension, and supraventricular arrhythmias, with possible potential in limiting ischaemia-induced myocardial damage.
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PMID:Diltiazem. A reappraisal of its pharmacological properties and therapeutic use. 219 51

Long-term follow-up data on young patients receiving amiodarone is lacking, especially in relation to growth and late side effects. The records of 95 young patients (mean age 12.4 years; range 3 weeks to 31.5 years) who received amiodarone were reviewed. Minimal follow-up time for those continuing to take amiodarone was 1.5 years; the mean duration of therapy was 2.3 years (maximal 6.5). The mean maintenance dosage was 7.7 (1.5 to 25) mg/kg body weight per day. Initial success (based on symptoms and 24 h electrocardiogram) was achieved in 23 of 34 patients with ventricular tachycardia, in 32 of 33 with atrial flutter and in 21 of 28 patients with supraventricular tachycardia. However, in 7 of 33 patients with atrial flutter, the arrhythmia returned after 6 months. Patient growth continued in the same percentiles achieved before amiodarone in all but eight patients, improving in six and worsening in two with severe underlying disease. Proarrhythmia occurred in three patients: one had torsade de pointes that disappeared when amiodarone administration was stopped; two with severe anatomic heart disease died suddenly during the loading period (one with atrial flutter and one with ventricular tachycardia). Side effects occurred in 28 (29%) of the 95 patients: keratopathy (in 11), abnormal thyroid function test (in 6), chemical hepatitis (in 3), rash (in 3), peripheral neuropathy (in 2), hypertension (in 1) and vomiting (in 1). All side effects disappeared when amiodarone was discontinued or the dose was reduced.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term follow-up of amiodarone therapy in the young: continued efficacy, unimpaired growth, moderate side effects. 231 68

251 untreated patients with mild to moderate hypertension were included in a multicenter study aimed 1) to detect arrhythmias (24-H Holter recording) and 2) to assess the efficacy of sotalol on blood pressure and possible arrhythmias. Patients with coronary heart disease or previously documented arrhythmias were excluded. Atrial arrhythmias such as premature beats, fibrillation, flutter and paroxysmal atrial tachycardia were detected in 16% of patients. Monomorphic ventricular premature contractions (VPCs) (Lown I and II) were detected in 41% of patients and polymorphic VPCs or duplets/triplets (Lown III and IV) in 14%. A correlation seems to exist between the level of hypertensive cardiopathy, judged on electrocardiographic data (Tarazi classification), age of patients and severity of arrhythmias. Sotalol was administered during 2 months at a mean dose of 160 mg per day. The treatment was effective on blood pressure and arrhythmias (82% improvement of severe VPCs) and the drug was well tolerated. It was difficult to conclude if these good results are due to the betablocking properties or specific class II antiarrhythmic effects of sotalol or to the combined activity.
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PMID:[Cardiac arrhythmia in moderate arterial hypertension. Epidemiologic survey of 251 cases. Effect of sotalol]. 264 67


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