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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aggravation of arrhythmia is a complication of antiarrhythmic drug therapy that is not uncommon. It may represent a worsening of an existing arrhythmia or a new arrhythmia not previously experienced by the patient. When non-invasive methods are used to evaluate drug effects, the overall incidence of aggravation is 9% while with electrophysiologic testing, it is 18%. While aggravation of arrhythmia may occur when the blood level of the drug is in the toxic range, most often this complication is observed when blood levels are in the defined therapeutic range. It is not associated with drug dose, baseline ECG intervals, changes in these intervals during therapy, the nature of the heart disease or other clinical parameters. However, it is more common in patients with a history of sustained ventricular tachycardia or ventricular fibrillation and in those with reduced left ventricular function and a history of congestive heart failure. Aggravation with one drug does not predict this complication with another agent, even if both are in the same subclass. Worsening of arrhythmia may often be precipitated by exercise testing, even when arrhythmia is suppressed on ambulatory monitoring. The frequency, unpredictability and seriousness of this side-effect demands the cautious use of antiarrhythmic drugs.
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PMID:Aggravation of arrhythmia: a complication of antiarrhythmic drug therapy. 268 May 5

The effect of thyroid hormones on vascular responses to various agents was examined in the coronary vascular bed perfused by the Langendorff's method at a fixed flow rate with Krebs-Henseleit solution in isolated rat hearts. In this study, ventricular fibrillation was induced by electrical stimulation to avoid secondary influences derived from alteration of ventricular contractility by agents. Vasodilator responses of coronary arteries to isoproterenol and methacholine were significantly enhanced in hyperthyroid preparations compared with those observed in euthyroid ones, though vasodilator responses to histamine and adenosine were not affected by hyperthyroidism. Vasoconstrictor response to 5-hydroxytryptamine (5-HT) was significantly potentiated by hyperthyroidism though that to balium chloride was not affected. So, these alterations in vascular responses by hyperthyroidism are assumed not to be nonspecific but to be mediator-specific events. As vasoconstriction in coronary arteries lowers oxygen supply to myocardium, enhanced vasoconstrictivity of coronary arteries to 5-HT by hyperthyroidism may be responsible for an exacerbation of heart disease in the case of patients having agglutinative thrombus, which should be a source of 5-HT, in their coronary arteries.
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PMID:Altered responsiveness of coronary arteries in hyperthyroid rats. 273 Feb 31

The purpose of this study was to define the natural history of 99 patients with unexplained syncope who underwent an electrophysiologic test that either was entirely normal or demonstrated nonspecific abnormalities that were nondiagnostic (inducible polymorphic ventricular tachycardia or ventricular fibrillation, a mildly prolonged sinus node recovery time of less than 2 s, a His-ventricular interval of 55 to 99 ms or supraventricular tachycardia not associated with hypotension). The mean age (+/- SD) of the patients was 56 +/- 19 years; structural heart disease was present in 47 patients and absent in 52. Complete follow-up was available in 95 patients. During 20 +/- 11 months of follow-up, 2 patients (2%) died suddenly, 19 patients (20%) had recurrent syncope and 74 patients (78%) had no further episodes of syncope. Among the 19 patients who continued to have syncope after the electrophysiologic testing, the cause of syncope was established clinically in 4 and was found to be high degree atrioventricular (AV) block (2 patients) or sinus node dysfunction (2 patients). No clinical or laboratory findings distinguished patients who had sudden death or syncope during follow-up from patients who did not. In conclusion, in patients with unexplained syncope who undergo an electrophysiologic test that is nondiagnostic 1) the incidence of sudden death is low (2%); 2) the remission rate of syncope is high (80%); 3) the electrophysiologic test may be documented to have been falsely negative in greater than or equal to 20% of patients who continue to have syncope, syncope in these patients being caused by AV block or sinus node dysfunction; and 4) patients at risk of sudden death or recurrent syncope, or both, cannot be readily identified prospectively.
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PMID:Natural history of patients with unexplained syncope and a nondiagnostic electrophysiologic study. 275 28

We studied the follow-up of 49 patients (pts), mean age 34 +/- 9 years, without coronary artery disease who had sustained (duration greater than 30 s) monomorphic ventricular tachycardia (smvt) (n = 42) or ventricular fibrillation (vf) (n = 7). There were 9/49 pts (18%) with smvt who had right ventricular dysplasia (RVD) and 32/49 pts (65%) without structural heart disease ("idiopathic" ventricular arrhythmia) (26/32 pts with smvt and 6/32 pts with vf). There were 6/49 pts (12%) with congestive (COCM) and 2/49 pts (4%) with hypertrophic (HOCM) cardiomyopathy. Mean follow-up was 49 +/- 13 months. During the follow-up 1/9 pts (11%) with RVD died postoperatively from heart failure, 1/26 pts (4%) with idiopathic smvt from cancer and 2/6 pts (33%) with COCM from heart failure. There were no deaths in pts with idiopathic vf. Recurrent smvt occurred in 5/9 pts (56%) with RVD, in 10/26 pts (39%) with idiopathic smvt, in 2/6 pts (33%) with idiopathic vf, in 3/6 pts (50%) with COCM and in 1/2 pts (50%) with HOCM. Our data show that pts with smvt or vf without coronary artery disease have a good prognosis. However, there is a high incidence of recurrent ventricular arrhythmia in these patients.
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PMID:[Prognosis and follow-up of patients with ventricular tachycardias or ventricular fibrillation without coronary heart disease]. 280 Jun 65

Findings are described in six patients with no clinical evidence of heart disease who had documented ventricular fibrillation (five patients) or ventricular flutter (one patient). The mean age of the six patients, all men, was 34 years (range 26 to 43). Cardiovascular collapse occurred in all and was followed by successful cardioversion. No patient had electrolyte or QT abnormalities. One patient had slight right ventricular enlargement on M-mode echocardiography, and another had a left ventricular pressure gradient at rest of 30 mm Hg with a normal two-dimensional echocardiogram. Holter electrocardiographic monitoring revealed incessant ventricular tachycardia in one patient and nonsustained ventricular tachycardia in three others. Exercise testing revealed nonsustained ventricular tachycardia in one patient. Ventricular fibrillation was induced at the time of programmed electrical stimulation in four of the six patients. Documented recurrence of ventricular fibrillation or ventricular flutter occurred in three patients, but in only one patient receiving antiarrhythmic drugs. Four patients were treated with amiodarone and one received an automatic implantable cardioverter-defibrillator. All patients are alive after a mean follow-up period of 78 months after the first documentation of their arrhythmia and 37 months after programmed electrical stimulation. Ventricular fibrillation can occur in the apparently structurally normal human heart. Antiarrhythmic treatment can provide effective control of this malignant arrhythmia.
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PMID:Ventricular fibrillation in six adults without overt heart disease. 292 43

Ten patients who presented with advanced heart disease and severe ventricular arrhythmia could be considered "at high risk of sudden death" caused by ventricular fibrillation. Yet they died suddenly while under Holter monitoring, and the recordings demonstrated that 4 of these deaths were due to a major disorder of conduction and 6 to ventricular fibrillation. Further analysis of these cases showed that the lethal disturbance of heart rhythm was ascribable to an anti-arrhythmic drug in 5 cases (2 with conduction disorder, 3 with ventricular fibrillation). It would appear that although patients of this kind need anti-arrhythmic drugs, these should be given with caution and in lower doses than in patients with normal left ventricular function.
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PMID:[Sudden death during Holter recording. Possible iatrogenic role of cardiovascular drugs. 10 cases]. 295 Apr 27

Left ventricular dysfunction and complex VPCs are independent risk factors for subsequent cardiac death in patients with ischemic or nonischemic heart disease. The use of antiarrhythmic drugs during acute myocardial infarction is discussed. Patients with complex VPCs associated with heart disease should be treated with antiarrhythmic drugs. Drug efficacy should be evaluated by a 24-hour ambulatory ECG recording and by a treadmill exercise stress test. Blood drug levels should be measured at appropriate times. Maintenance doses of the various antiarrhythmic drugs are listed. Electrophysiologic testing with induction of ventricular tachycardia by extrastimulation may predict the clinical efficacy of the antiarrhythmic drug or combination of drugs needed for the long-term treatment of ventricular tachyarrhythmias. Electrophysiologic testing must be used for selecting antiarrhythmic drugs in patients who have experienced sustained ventricular tachycardia or ventricular fibrillation but who are free of VPCs during ambulatory ECG monitoring and exercise stress testing. If patients have life-threatening ventricular tachycardia or fibrillation resistant to antiarrhythmic drugs, surgical intervention is indicated. Complex VPCs in asymptomatic patients without heart disease should not be treated with antiarrhythmic drugs.
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PMID:Management of ventricular arrhythmias. 304 63

The fitness of patients with Wolff-Parkinson-White syndrome to indulge in sporting activities is a practical cardiology problem. The major risk is sudden death due to atrial fibrillation deteriorating to ventricular fibrillation. This risk is small or even theoretical, but signing a fitness certificate engages the clinician's responsibility. Non invasive complementary examinations are useful. Echocardiography may detect a heart disease that would preclude any sport. Exercise tests explore the behaviour of the accessory pathway and rarely trigger off arrhythmias. Holter recordings mainly investigate disorders of the atrial rhythm. The decision concerning fitness may be based on clinical symptoms. Exercise-induced tachycardia is a classical contra-indication to competitive sports. In patients whose tachycardia is unrelated to exercise, fitness may be discussed according to the results of exercise tests and of the electrophysiological study. A refractory period which would be considered as rather prolonged at rest does not protect against fast ventricular rate during passage to atrial fibrillation. If pre-excitation disappears during the exercise test in an asymptomatic patient, then competitive sports can be authorized without limitations. If not, only surgical excision or fulguration would provide full protection against a potentially dangerous fibrillation. It is concluded that Wolff-Parkinson-White syndrome contra-indicates competitive sports in most cases. Games played outside competitions remain possible in the absence of symptoms or when arrhythmias are well controlled by medical treatment.
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PMID:[Fitness for sports of patients with Wolff-Parkinson-White syndrome]. 311 45

This study assessed the relation between acute antiarrhythmic drug efficacy and left ventricular (LV) function in patients with sustained ventricular tachyarrhythmias, that is, sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). Electrophysiologic studies (n = 560) were performed in 201 patients, separated for analysis into less than 30 and greater than or equal to 30% ejection fraction groups. Coronary artery disease was present in all patients. The 8 acute antiarrhythmic regimens were procainamide, quinidine, mexiletine, mexiletine + type 1A agent, flecainide or indecainide, amiodarone, amiodarone + type 1A and "miscellaneous" agents. At least 1 successful acute antiarrhythmic regimen was found in 47% of patients and in a significantly greater proportion of patients with ejection fraction greater than or equal to 30% (52 of 81 = 64%) than in those with ejection fraction less than 30% (43 of 120 = 36%, p less than 0.001). Drug trials were successful (initiation of less than 15 repetitive ventricular responses) in 32% of patients with ejection fraction greater than or equal to 30% versus 19% of those with ejection fraction less than 30% (p less than 0.001). There were no statistically significant differences between the 2 ejection fraction groups in type of heart disease, acute antiarrhythmic dosages or mean serum drug levels. A logistic regression analysis incorporating multiple clinically relevant factors found that ejection fraction was the only factor that correlated significantly with drug success or failure (p less than 0.002). Acute antiarrhythmic drug efficacy relates to LV function per se or to other pathophysiologic mechanisms of which ejection fraction may be a marker.
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PMID:Relation of acute antiarrhythmic drug efficacy to left ventricular function in coronary artery disease. 328 19

The risk factors for sudden coronary heart disease (CHD) death have been well described. Sudden CHD deaths should be classified as those occurring in individuals with and those in individuals without a prior history of clinical heart disease. The extent of coronary artery disease, left ventricular dysfunction, and cardiac arrhythmias are the primary pathophysiologic determinants of ventricular fibrillation and sudden death. Psychosocial factors influence the threshold of response to the numerous physical and social environmental stimuli that can precipitate sudden death. The degree of pathology is probably inversely related to the intensity of the stimuli necessary to precipitate sudden CHD death. In the presence of extensive disease the precipitants of sudden deaths are probably ubiquitous in the environment and unlikely to be prevented. Thus, prevention of the basic cardiac disease is of higher priority.
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PMID:Environmental and psychosocial determinants of sudden death. 329 2


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