Cases reported "Death, Sudden, Cardiac"

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11/22. torsades de pointes as a cause of sudden death in a patient with aortic stenosis and atrial fibrillation.

    The occurrence of sudden cardiac death during Holter monitoring in patients with aortic stenosis has been reported previously. In the majority of the reported cases, the cause of death was a malignant ventricular tachyarrhythmia. The presence of a strong association between frequency and complexity of ventricular arrhythmias and sudden death in patients with aortic stenosis has been proposed. We report the case of a 77-year-old woman with aortic stenosis and atrial fibrillation who had an episode of torsades de pointes that degenerated into ventricular fibrillation during Holter monitoring. A short-long-short sequence, but not increased ventricular ectopics, precipitated torsades de pointes and sudden death in this case which is strongly indicative of triggered activity as the underlying mechanism of the lethal arrhythmia.
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12/22. swimming-triggered aborted sudden cardiac death in a patient with Andersen-Tawil syndrome.

    In this report we describe the case of a 42-year-old woman who experienced an episode of near drowning during recreational swimming. A diagnosis of Andersen-Tawil syndrome was made based on the patient's dysmorphic features, characteristic T-U-wave patterns and ventricular arrhythmias. To our knowledge, this is the first report of a swimming-triggered cardiac event in a patient with Andersen-Tawil syndrome.
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ranking = 33.04652970679
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13/22. Two cases of bi-ventricular dysplasia associated with ventricular tachycardia and familial occurrence of sudden death.

    Two strikingly similar patients with arrhythmogenic right ventricular dysplasia which severely impaired not only the right ventricle but also the left ventricle are described in association with familial occurrence of sudden death. A 49-year-old man experienced syncope which was due to ventricular tachycardia. electrocardiography revealed a first degree atrioventricular block, incomplete right bundle-branch block, T wave inversions in leads II, III, a VF and V1 to V5, and multiformal ventricular extrasystoles. echocardiography and ventricular cineangiography showed not only the right ventricular dilatation with an aneurysm in the right ventricular apex, inflow and outflow tracts, but also mild dilatation of the left ventricle with left ventricular apical and posterior aneurysms. radionuclide angiography also disclosed dysfunction of both ventricles, especially during exercise. His family history revealed that 3 members of his family died of sudden deaths. A 56-year-old woman experienced syncope secondary to ventricular tachycardia, with left bundle-branch block. electrocardiography showed complete right bundle-branch block, left axis deviation, and T wave inversions in leads V1 to V4. echocardiography and ventricular cineangiography revealed not only marked right ventricular dilatation with the "triangle of dysplasia", but also a left ventricular aneurysm in the apex and posterior portion. Her elder brother died of a sudden death, and electrocardiograms of 2 members of her family showed ventricular extrasystoles and T wave inversions. These 2 cases may well be termed "familial bi-ventricular dysplasia".
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ranking = 99.13958912037
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14/22. Sudden death in athletes.

    HCM, as well as coronary and myocardial structural abnormalities, is the most common pathology leading to SCD in young athletes. Furthermore, SCD from fatal arrhythmia seems to be the most common mechanism of death. In this population, however, data are insufficient to support either invasive or noninvasive approaches to clarify risk stratification for SCD. Because of the large population, variants of normal found within the athletic population, and the rarity of the disease, screening for individuals at risk is neither practical nor cost-effective. Not all athletes with HCM are at the same risk for SCD; a thorough history and physical examination should alert the health professional to potential risk factors. Efforts are under way to stratify athletes at risk for SCD to determine who can participate in competitive sports and who should not. However, until research can accurately define variables of hemodynamic and electrical instability that permit reliable identification of athletes with HCM who are at risk for SCD, the recommendation is to disqualify athletes with confirmed HCM from moderate- to high-intensity competitive sports. This recommendation includes athletes with or without symptoms or left ventricular outflow obstruction. Due to the decreased risk of SCD in older athletes, individual judgment of eligibility may be used. athletes thought to have had myocarditis should be withdrawn from all competitive sports for a convalescent period of approximately 6 months, with thorough cardiac assessment and testing performed before returning to training. athletes with atrial or ventricular tachyarrhythmia must be screened for structural abnormality, heart response during exercise, and the frequency and duration of the arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)
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15/22. Taxol in advanced, hormone-refractory carcinoma of the prostate. A phase II trial of the Eastern Cooperative Oncology Group.

    BACKGROUND. Recent clinical trials have documented activity for combinations of chemotherapeutic agents that target the microtubular apparatus in patients with hormone-refractory prostate cancer. Taxol has a novel antimicrotubular mechanism, acting by stabilizing polymerized tubulin. methods. Twenty-three patients with hormone-refractory prostate cancer and bidimensionally measurable disease were treated with Taxol by 24-hour continuous infusion at 135-170 mg/M2 every 21 days for a maximum of 6 cycles. RESULTS. Eighty-five courses of Taxol were administered to 23 patients. One patient (4.3%) experienced a partial response lasting 9 months, and four other patients with radiographically stable disease had minor reductions in the serum prostate-specific antigen (PSA) of 16-24%. Eleven patients (47.8%) had stable disease, and progressive disease developed in 9 patients (39.1%) during therapy. Median survival was 9 months. leukopenia was the dose-limiting toxicity with 13% of patients having Grade 3 and 61% having Grade 4 toxicity, and granulocytopenic fever developed in 26%. Three patients experienced sudden cardiovascular events while participating in the study, including one patient with a nonfatal, non-Q-wave myocardial infarction that occurred during a taxol infusion, and two patients who had sudden deaths 9 days and 30 days after receiving their last taxol dose, respectively. CONCLUSIONS. In the subset of patients with hormone-refractory prostate cancer and bidimensionally measurable disease, Taxol at this dosage has only minor activity.
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16/22. Progressive reduction of heart rate variability with eventual sudden death in two patients.

    In two patients with old myocardial infarction and congestive heart failure there was a progressive reduction of heart rate variability and eventual sudden death. The two patients had had three 24 h electrocardiogram recordings within two years of death. The power of two spectral bands was calculated-0.04-0.15 Hz, low frequency power, and 0.15-0.40 Hz, high frequency power. The mean low and high frequency powers over the 24 h recording progressively decreased whereas the frequency of ventricular arrhythmias showed no consistent changes in either patient. The circadian variation in hourly low and high frequency powers in the last 24 h electrocardiogram recordings was much reduced. These results suggest that sequential measurements of heart rate variability may be useful in predicting sudden death.
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17/22. New directions in cardiovascular mapping and therapy.

    Cardiovascular mapping has allowed us to fully understand the mechanisms of some of the cardiac arrhythmias and enabled us to devise new therapeutic options for them. Endocardial mapping by electrophysiological studies using three to four endocardial catheters introduced via the vein or artery to the heart allows us to directly map the electrical activity of the heart during sinus rhythm and during abnormal tachyarrhythmias. The simultaneous recording of electrical activity from the surface electrocardiogram, right ventricular apex, His bundle, high right atrium, coronary sinus, with or without a roving mapping catheter, enables us to precisely map the electrical activation sequence in the heart. This technique has been especially useful for mapping supraventricular tachycardias and the precise mapping of the accessory pathway or slow pathway potentials have now allowed us to selectively ablate them using radiofrequency energy delivered via the tip of the endocardial catheter. Intraoperative direct cardiac mapping has allowed us to reconfirm the findings of endocardial catheter mapping immediately prior to surgery. The intraoperative mapping is more precise and allows direct visualisation of the abnormal site for the surgeon to operate. Computerised mapping using multichannel recordings has facilitated mapping of the abnormal site for patients with haemodynamically unstable or nonsustained ventricular tachycardia, and thus allows the surgeon to perform surgical resection or cryoablation of the abnormal site. Cardiovascular mapping has thus enabled us not only to understand the mechanisms of cardiac arrhythmias but allows us to provide curative therapy for patients who are at risk from sudden arrhythmic death or otherwise need life long drug therapy.
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18/22. Environmental electromagnetic interference from electronic article surveillance devices: interactions with an ICD.

    A patient with an implantable cardioverter defibrillator (ICD) experienced an inappropriate firing while in close proximity to an electronic article surveillance (EAS) device. Testing revealed the ICD was able to detect high frequency "noise" when close to the EAS device. ICD patients may need counseling to avoid close contact with such devices.
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19/22. ventricular fibrillation and sudden death after radiofrequency catheter ablation of the atrioventricular junction.

    Two hundred thirty-five patients underwent RF catheter ablation of AV conduction for symptomatic drug refractory AF (84%), atrial flutter (9%), and atrial tachycardia (7%). In the first 100 patients, postablation pacing was not prospectively set at any specific rate and was always < or = 70 beats/min. In the next 135 patients, postablation pacing was prospectively set at 90 beats/min for 1-3 months. Six of the first 100 patients (6%) had VF or sudden death after the RF procedure and none (0%) of the next 135 patients did (P < 0.05). One of the six patients had recurrent VF 4 days after the ablation. Five patients were successfully resuscitated and one patient died. There were no statistically significant differences between patients with and without (aborted) sudden death or between the first 100 and the next 135 patients with respect to age, sex, underlying heart disease, EF, number of RF applications, or left-or right-sided approach of the procedure. VF mostly occurred during episodes of slow ventricular escape rhythms or during slow ventricular pacing. We conclude that malignant ventricular arrhythmias and sudden death are possible complications of RF ablation of the AV function. The mechanism of these complications could have a bradycardia dependent nature and it seems that the occurrence of malignant arrhythmias can be prevented by temporarily pacing the heart at relatively fast rates immediately after ablation.
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20/22. Bifid T waves induced by isoprenaline in a patient with brugada syndrome.

    A 41 year old man with incomplete right bundle branch block and persistent coved-type ST elevation in the right precordial leads during sinus rhythm had an episode of syncope while driving. He had never had syncope before and there was no family history of sudden cardiac death. ventricular fibrillation was induced during electrophysiological study (EPS) by double extrastimuli applied to the right ventricle. disopyramide was effective in preventing ventricular fibrillation during EPS. beta Adrenoceptor stimulation manifested bifid T waves and reduced ST segment elevation in right precordial leads. Simultaneously recorded monophasic action potential (MAP) duration at 90% repolarisation did not change in the right ventricular outflow tract, while it shortened in the left ventricular septum. These findings suggest that right precordial bifid T waves might result from relatively early repolarisation of the left ventricles. Moreover the gradient of action potential duration might explain the mechanism of ST segment abnormalities in a patient with brugada syndrome.
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