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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To provide an understanding of the clinical characteristics of patients with acute myocardial infarction (MI) and bundle branch block, experience from five centers was accumulated. Patients in whom bundle branch block first appeared after the onset of cardiogenic shock were excluded. In 432 patients, the most common types of block were left (38%) and right with left anterior fascicular block (34%). In 42% of the patients, bundle branch block was new. Progression to high degree (second or third degree) atrioventricular (AV) block via a Type II pattern occurred in 22% of the patients. Hospital and first year follow-up mortality rates were 28% and 28%, respectively. Only 46% of the patients developed pulmonary edema or shock (Killip Class III or IV), and hospital mortality was related to the amount of heart failure (8%, 7%, 27%, 83% for Killip Classes I-IV, respectively). Patients with progression to second degree or third degree AV block via a Type II pattern had increased hospital mortality compared with patients without this complication (47% vs 23%, P less than 0.001). In the absence of pulmonary edema or shock, patients with Type II second degree or third degree AV block still had a higher mortality rate than patients without advanced AV block (31% vs 2%, P less than 0.005), with nearly all the deaths due to abrupt development of AV block. Thus, in many patients MI with bundle branch block is associated with severe heart failure. However, this was not true for a majority of the patients, in whom therapy aimed at preventing morbidity and mortality due to the bradyarrhythmia of advanced AV block might be beneficial.
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PMID:The clinical significance of bundle branch block complicating acute myocardial infarction. 1. Clinical characteristics, hospital mortality, and one-year follow-up. 68 79

Although both asymptomatic ventricular arrhythmias and sudden death are common in patients with chronic heart failure, there is little evidence that patients who have frequent or complex ventricular arrhythmias are at increased risk of sudden death. Two hypotheses may explain the lack of an arrhythmia-sudden death relation in this disorder. First, complex ventricular arrhythmias may be a nonspecific manifestation of a dying left ventricle rather than an indication of a specific arrhythmogenic substrate. In fact, during long-term follow-up, patients with mild heart failure who have nonsustained ventricular tachycardia are more likely to develop clinical progression of the disease rather than sudden death. Second, sudden death may be related to events other than a malignant ventricular arrhythmia. The most common myocardial ischemia, whereas the terminal event in patients with an idiopathic dilated cardiomyopathy is commonly a severe bradyarrhythmia or electromechanical dissociation. Neither outcome can be predicted by a prior history of ventricular arrhythmias on ambulatory electrocardiographic monitoring. If asymptomatic ventricular arrhythmias do not lead to sudden death, then there would appear to be little reason to expect that antiarrhythmic drugs could prevent cardiac arrest in patients with chronic heart failure. This may explain why drugs that suppress ambulatory arrhythmias do not prevent sudden death in these patients, whereas interventions may reduce the risk of unexpected circulatory collapse in this disorder without suppressing ventricular ectopic activity. To make matters more complicated, the desirable actions of antiarrhythmic drugs are attenuated and their negative inotropic and proarrhythmic actions are enhanced in patients with severe cardiac dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lack of relation between ventricular arrhythmias and sudden death in patients with chronic heart failure. 172 5

The causes, clinical indications and diagnosis and differential diagnosis of cardiac disorders which may lead to cerebral symptoms are illustrated on the basis of a review of the present day level of scientific research. Principally involved are cerebral ischaemias arising from cerebral embolisms or from reduction of cardiac output in cardiovalvular and myocardial disorders. The incidence of all embolisms of cardiac origin makes up 10% of all ischaemic cerebral infarcts, with auricular fibrillation, irrespective of its origin, mitral stenosis, myocardial infarct, mitral insufficiency and combined mitral valve defects, and, in younger patients, mitral valve prolapse, being, in this order of frequency, of primary clinical significance. The other cardiovalvular and myocardial disorders have, in comparison, a relatively low incidence of cerebral embolisms. Haemodynamically induced cerebral ischaemias frequently occur in the form of complications following acute cardiac arrest, in myocarditis and in case of primary cardiomyopathies resulting from cardiac insufficiency or complicating bradyarrhythmia. They are clinically apparent in the form of syncope, and other impairments of consciousness of various levels of seriousness with and without indications of cerebral origin, extending up to coma. In view of the high incidence of 25% of acute cerebral ischaemias in cases of cardiac disease, not only neurological but also detailed cardiological investigation is vital in all cases for a correct diagnosis and for the selection of a suitable course of treatment. Cerebral complications in bradyarrhythmia and endocarditis are discussed in the context of a review of the relevant literature together with consideration of their epidemiology, aetiology, pathophysiology and clinical profile. Pathological sinus-bradycardia, bradyarrhythmia absoluta, sinu-atrial and atrio-ventricular blockages, carotid-sinus and sick-sinus node syndrome, paroxysmal atrial tachycardia, AV-node tachycardias, and auricular fibrillation and flutter, taken as a whole, lead to cerebral complications affected patients in 5 to 10% of afflictions of the central nervous system occur in 50% of patients suffering from complete AV blockage and, at a not precisely definable frequency, in patients suffering from other bradyarrhythmias. In addition to transitory, uncharacteristic symptoms such as dizziness, vertigo, impairment of vision and balance, presyncope, syncope and Adams-Stokes syndrome dominate the clinical profile. Endocarditis, with an incidence of 0.01 to 0.05% in the overall population, results in central nervous system complications in 12 to 25% of cases on average.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Heart diseases as a cause of cerebral symptoms and syndromes]. 222 59

The safety and efficacy of oral sotalol, an investigational beta-adrenergic blocker with class III antiarrhythmic drug properties, were examined in a multicenter study in 236 patients with sustained ventricular tachyarrhythmias. In 104 patients, the index arrhythmia was a cardiac arrest, and all patients had undergone at least 3 previous unsuccessful antiarrhythmic trials (mean = 5 per patient). In the 106 patients assessed by programmed electrical stimulation, sotalol completely suppressed induction of ventricular tachycardia (VT) in 33 (31%) and rendered VT slower (greater than 100 ms prolongation of cycle length) or more difficult to induce in 29 (27%). Using continuous 24-hour ambulatory monitoring methods, sotalol complete- and partial-response rates were 51 and 12%, respectively. Of the 236 acute-phase patients, 151 were discharged receiving long-term sotalol therapy. The median sotalol dose was 480 mg/day. At a mean follow-up of 346 +/- 92 days, 27 patients (18%) had recurrence of sustained arrhythmia; 9, sudden death; 11, sustained VT; 5, automatic defibrillator discharge; and 2, syncope. Adverse effects forced discontinuation of therapy in 10 patients (7%): 6 secondary to symptomatic bradyarrhythmia, 2 due to refractory heart failure, 1 due to torsades de pointes, and 1 from bronchospasm. Life-table analysis of sotalol's overall long-term efficacy at 6, 12 and 18 months were 80, 76 and 72%, respectively. Although mean follow-up was short (less than 1 year), neither acute-phase programmed stimulation nor 24-hour ambulatory monitoring responses were significantly predictive of subsequent arrhythmic outcome. Proarrhythmia was documented in 18 patients (7%), 17 during the acute phase and 1 during long-term follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety and efficacy of sotalol in patients with drug-refractory sustained ventricular tachyarrhythmias. 229 89

An analysis has been made of long-term ECG recordings in 11 patients, 9 men and 2 women, mean age 69 +/- 7 years, who were carrying ECG recording equipment at the time of sudden death. Nine patients had coronary heart disease, one patient a dilatative cardiomyopathy and another one a combined aortic valve defect. Seven patients had a history of syncope. All patients had signs of cardiac insufficiency (NYHA index 3.0 +/- 0.6, heart-thorax quotient 0.55 +/- 0.05). Sudden death occurred predominantly whilst resting. In one patient it was due to bradyarrhythmia, in 10 to tachyarrhythmia, mostly ventricular tachycardia (initial heart rate 198 +/- 43/min; n = 8) which degenerated into ventricular fibrillation. Atrial fibrillation was present in 8 patients at the time of sudden death. Premonitory warning arrhythmias were not consistently detectable: comparison of arrhythmias in the first and last hour showed significant increases only in single ventricular extrasystoles (135 vs. 278 VES/h, P less than 0.05), not however in repetitive arrhythmias. An R-on-T phenomenon, as trigger mechanism of ventricular tachycardia, occurred in 5 cases. A synopsis of the published reports on approximately 110 patients with sudden death during long-term electrocardiographic monitoring confirmed that acute death is caused by bradyarrhythmias in approximately 15% (17 patients), and by tachyarrhythmias in 85% (94 patients). An increase in ventricular arrhythmias in the hour prior to death was observed in about 50% of patients and the R-on-T phenomenon, as the initiating mechanism for ventricular tachycardia, in 42%.
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PMID:[Sudden cardiac death in long-term electrocardiography]. 241 Feb 15

The purpose of this study is to evaluate the directions, reliability and long-term results of ventricular programmable pacemakers (PPM's). One hundred and ten PPM's, types Cordis and Medtronic, were implanted in 60 patients (pts) with intermittent or paroxysmal 2 degrees, 3 degrees a-v block and in 50 pts with S.S.S., mostly symptomatics, with a follow-up of 45 months. We did not observe either spontaneous or wrong reprogrammations nor circuit failure. In 92% of pts with Omni-Stanicor Cordis PM's, the stimulation was effective at the "lower" current amplitude, hence a longer life of the generator. Eighteen pts (16.3%) needed to raise ventricular rate (average 65 bpm): 6 pts for dizziness, syncopes or cardiac failure; 2 pts to control ventricular arrhythmias; 10 pts for a stable bradycardia lower than 50 bpm. In 11 pts with bradyarrhythmia due to S.S.S., cardiac output (CO) was measured both with thermodilution and echocardiography ("mitral valve echogram", being "r" of the two methods = 0.92), in spontaneous rhythm (63.3 +/- 3.13 bpm) and increasing artificially heart rate to 74.8 +/- 3.0 bpm; CO decreased from 4.65 +/- 0.13 l/min to 3.58 +/- 0.09 l/min, likely for the loss of atrial pumping. Similar results were obtained in other pts evaluated only with echocardiographic method after PM implantation: some of these underwent a further echocardiographic haemodynamic evaluation after 15 days of constant ventricular pacing at a mean rate of 75 bpm, with a different behaviour among them. This emphasizes the utility of PPM's in preserving spontaneous rhythm until bradycardia reaches dangerous levels and also the usefulness of echocardiography to evaluate, haemodinamically, the paced patient's ventricular performance.
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PMID:[The permanent electrostimulation with ventricular programmable pacemaker (author's transl)]. 723 7

Twenty patients (complete AV block n = 13, sick sinus syndrome n = 4 (replacement of a VVI system), bradyarrhythmia n = 3) with rate-adaptive pacemakers (respiration volume guided n = 10, QT-driven n = 1, dual sensor (QT/activity) system n = 9) were randomly assessed by ergospirometry after 4 weeks of VVI- (70 bpm), VVIR1-(70-110 bpm, low upper rate) and VVIR2-pacing (70-130 bpm, high upper rate). Oxygen uptake (VO2), work load (W), and heart rate were determined at peak exercise (max) and at the anaerobic threshold (AT). In the whole population, rate adaptation led to a significantly higher VO2-max than VVI-pacing for both VVIR1- (15.5 +/- 5.1/12.6 +/- 4.1 ml/kg/min, 28 +/- 37%, p < 0.01) and VVIR2-pacing (14.8 +/- 4.4/12.6 +/- 4.1 ml/kg/min, 20 +/- 23%, p < 0.01). At the AT, however, VO2 was significantly improved only by the VVIR1 mode (low upper rate, 9.8 +/- 2.5/8.0 +/- 2.1 ml/kg/min, 28 +/- 36%, p < 0.01). Regarding only patients with moderately limited exercise capacities (Weber class C, n = 11), rate adaptive VVIR1 and VVIR2 pacing could not produce a significant increase of VO2-max and VO2-AT. In contrast, patients with severely reduced exercise capacities (Weber class D, n = 9) significantly profited from the rate adaptation, but only in the VVIR1 mode (VO2-max 48 +/- 45%, VO2-AT 51 +/- 38%, p < 0.01). Thus, in the whole population an increase of oxygen uptake and of exercise workload at the anaerobic threshold could only be achieved by pacing with the low upper rate of 110 bpm. By this, particularly patients with heart failure and a severely limited exercise tolerance (Weber D) had a significant benefit. Therefore, the upper rate should be programmed in a lower range in patients with heart failure, at least for rate-adaptive ventricular pacemaker systems.
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PMID:[Chronic frequency-adaptive pacemaker therapy in patients with heart failure]. 750 71

The most important symptoms in bradycardia are vertigo, dizziness and syncopy due to diminished cerebral blood sypply. Cardial symptoms are cardiac insufficiency and angina pectoris. By means of ECG, especially Holter-ECG, carotid sinus massage, atropin test and invasive methods (atrial stimulation, His-bundle ECG) sinu-nodal dysfunction, carotid sinus syndrome, bradyarrhythmia absoluta and AV-block can be diagnosed. Pharmacological treatment is only useful in acute situations. For symptomatic bradyarrhythmias the implantation of a Pacemaker is the therapy of choice. Individual treatment of the various types of bradyarrhythmia and the patients special needs is possible through the evolution of pacemaker technology.
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PMID:[Differential diagnosis and therapy of bradycardic arrhythmias]. 782 27

Cardiac amyloidosis, an uncommon disease, has been reported to manifest as congestive heart failure (CHF) and/or various arrhythmias. Herein, we report a case of CHF and sick sinus syndrome. The patient, a 66-year-old man, was admitted to the National Taiwan University Hospital because of dizzy spells and recurrent syncope. Electrocardiogram showed a sinoatrial block, first degree atrioventricular block, right bundle branch block and low-voltage Q wave, R wave and S wave (QRS) complex. Prolonged corrected sinus node recovery time was documented by an atrial pacing study. A permanent pacemaker was implanted for the patient's bradyarrhythmia, but he developed progressive heart failure. Echocardiography revealed a normal-sized ventricular chamber, concentric left ventricular hypertrophy with a "granular sparkling" appearance of the myocardium, and impaired diastolic and systolic function of the left ventricle. Despite aggressive treatment, the patient expired due to intractable heart failure. Postmortem needle aspiration revealed amyloidosis involving the heart, lung and skin. We conclude that cardiac amyloidosis should be considered in elderly patients with conduction disturbance and unexplained congestive heart failure.
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PMID:Cardiac amyloidosis presenting as sick sinus syndrome and intractable heart failure: report of a case. 810 85

Adenosine versus Verapamil and other Antiarrhythmic Drugs: Paroxysmal supraventricular tachycardia is the most common sustained arrhythmia during pregnancy. Verapamil has been the most commonly used agent for the treatment of PSVT with a narrow QRS complex. Potential side effects of verapamil including systemic hypotension, acute heart failure, bradyarrhythmia and heart block may occur in pregnant women; after placental transfer bradycardia, heart block, depression of contractility and hypotension may be induced in the fetus. We report on the case of a 22-year old pregnant woman with hypotension and tachycardia, who was admitted for suspected haemorhagic shock. Indeed, she suffered from paroxysmal supraventricular tachycardia, which was successfully terminated by intravenous adenosine. Because of its known rapid onset, high effectivity, low incidence and brevity of side effects in the mother and comparative safety in the fetus, adenosine seems to be the drug of choice for treating PSVT during pregnancy.
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PMID:[Paroxysmal supraventricular tachycardia in pregnancy. Value of adenosine and other anti-arrhythmia agents]. 876 89


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