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

Since most of the toxicity associated with class 1B antiarrhythmic drugs is dose-related, this review examines adverse effects seen in both therapeutic practice and accidental or premeditated overdose. Toxicity is very common with these agents and can be life-threatening. A high percentage of patients must discontinue therapy because of adverse effects. Mexiletine and tocainide are structural analogues of lignocaine (lidocaine) and toxicity is similar with all 3 drugs. With gradual intoxication (the most common form) central nervous system effects such as lightheadedness, dizziness, drowsiness and confusion are seen first. Seizures and respiratory arrest can occur. Cardiovascular toxicity is manifested by progressive heart block, reduced cardiac contraction, hypotension and asystole. Both mexiletine and tocainide may have proarrhythmic effects. Gastrointestinal toxicity is also common. Shock, hypotension, cardiac failure and beta-blocker therapy reduce lignocaine clearance and enhance the risk of intoxication during routine therapy. Both lignocaine and mexiletine elimination is impaired in severe liver disease while tocainide clearance is reduced in renal failure. Management of toxicity is largely supportive and symptomatic. Lignocaine infusion must be discontinued and decontamination of the gut in the case of oral preparations is recommended. Serious intoxication requires intensive care unit admission. Haemodialysis or haemoperfusion may be helpful in serious lignocaine and tocainide poisoning. In institutions where extracorporeal circulatory assistance is available, massive lignocaine poisoning has been successfully treated with this intervention. In the therapeutic setting serious toxicity can be prevented by close clinical surveillance and appropriate dose reduction in patients with reduced drug clearance. Because of the large interindividual variation in lignocaine pharmacokinetic parameters, therapeutic drug monitoring is recommended if results can be reported quickly. Mexiletine and tocainide have stereoselective metabolism and assays do not distinguish the more active isomers. Therapeutic drug monitoring is less useful in this situation.
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PMID:Poisoning due to class 1B antiarrhythmic drugs. Lignocaine, mexiletine and tocainide. 251 64

Myotonia is defined as a persistent contraction of skeletal muscles after their stimulation. This contracture is not prevented or relieved by regional anaesthesia or muscle relaxants. The sensitivity to non-depolarizing muscle relaxants is usually normal. Suxamethonium, neostigmine, hypothermia, a rise in kalaemia should be avoided. There have been case reports of malignant hyperthermia in patients with myotonia congenita. Dystrophia myotonica is the second most frequent of the inherited muscle diseases, after Duchenne's dystrophy. The severity of the disease is due more to the muscular atrophy and the multiple organ involvement than to the abnormal contraction. Atrioventricular heart block and dysrhythmias are more common than heart failure. Prolonged apnoea and pneumonia are the main risks of anaesthesia. In severe cases, exists a restrictive respiratory insufficiency which is preceded by a fall in the maximum expiratory pressure. Dysphagias and inefficient coughing may occur early. An increased susceptibility to hypnotic drugs and opiates is a common feature. Spontaneous sleep apnoeas should be sought before anaesthesia, especially by using pulse oximetry. The anaesthetic implications are reemphasized.
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PMID:[Anesthesia in myotonia]. 253 24

Aortic valve replacement was performed in 31 patients with symptomatic chronic aortic regurgitation. The patients ranged in age from 13 to 66 (mean = 39) years and included 29 men and 2 women. They were followed up for a mean of 47 months. Perioperatively, 2 patients (6.5%) died, and 2 (6.5%) received a permanent pacemaker for complete heart block. Thirty patients received an M-mode echocardiographic examination both before, and 6 to 11 days after, the operation. In this early postoperative period, the end-diastolic dimension (EDD) and left ventricular end-diastolic radius/posterior wall thickness ratio (R/Th) decreased in all patients. This decrease in EDD could be predicted by preoperative ejection fraction (EF), but not by end-systolic dimension (ESD) or R/Th ratio. The ESD regressed only in patients with preoperative EF greater than 50%, or ESD less than 55mm, or R/Th less than 3.8. During the long-term follow-up, one each had mild tissue valve degeneration, stroke, infective endocarditis, and severe myocardial failure, but none died. Eighteen patients had repeated M-mode echocardiographic studies. There was no further regression of EDD and R/Th, while ESD showed significant decrease. The EF and fractional shortening (FS) did not change. Clinically, the patients who survived the operation improved or remained unchanged postoperatively in a functional status. However, those who had preoperative EF greater than 50% or ESD less than 55mm had a better postoperative functional class (1.2 +/- 0.4 vs 1.9 +/- 1.0, p less than 0.05, 1.2 +/- 0.4 vs 2.0 +/- 1.1, p less than 0.05, respectively). Thus, patients with symptomatic chronic aortic regurgitation can often benefit from valve replacement.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postoperative echocardiographic study of patients with symptomatic chronic aortic regurgitation. 253 98

Complete heart block was diagnosed prenatally in 21 fetuses. Associated structural cardiac defects were present in 18 fetuses, in particular complete atrioventricular canal with atrial isomerism (5 cases), and 'corrected' transposition of the great arteries (4 cases). Maternal systemic lupus erythematosus was proved in only one case. In 11 fetuses, intra-uterine congestive heart failure with the signs of non-immune hydrops fetalis occurred. In all 11 fetuses, the hydrops was associated with a cardiac defect, in particular complete atrioventricular canal with atrial isomerism in 5 cases. A review of the literature confirms that only the association of complete heart block and cardiac malformation can cause intra-uterine congestive heart failure, whereas in the case of fetal complete heart block without cardiac malformation or with prenatally hemodynamically insignificant cardiac malformation, congestive heart failure is rare. Only 30% of newborns with complete heart block have associated cardiac malformations. In our series, however, 86% of the fetuses with complete heart block had cardiac malformations. The most important reason for this percentage discrepancy is that almost all fetuses with associated severe cardiac defects, in particular atrioventricular canal defects, develop heart failure which frequently results in prenatal death. Thus, fetal deaths are not included in pediatric statistics. Nevertheless, fetuses with isolated complete heart block generally do not develop heart failure and in almost all of the cases are born alive.
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PMID:Fetal complete heart block: antenatal diagnosis, significance and management. 265 98

Fifteen cases of congenital complete heart block were diagnosed in utero or at birth, over a nine-year period. Six cases were confirmed by fetal echocardiography between 22 and 36 weeks of gestation. Two cases were treated in utero for cardiac failure, and serial ultrasonography was used to monitor the progress. Structural heart disease was present in seven (47%) infants; in four of these infants the defect was a corrected transposition of the great arteries. Ventricular pacing was required in seven patients--four infants with anatomically-normal hearts and three infants with associated structural heart disease. Eight children did not require permanent pacing, and remained well after a mean follow-up period of 23 months (range, one to 72 months). The mortality was highest in those patients with structural heart disease, three of whom died as neonates. Only one baby died with an anatomically-normal heart. Antinuclear antibodies were present in the mothers of seven of the eight infants who were born with a structurally-normal heart. Four mothers either had pre-existing connective-tissue disease or had developed manifestations of such disease subsequent to pregnancy. Of this group, all the women were antibody-seropositive to the nuclear antigen SS-A during pregnancy. Mothers of three infants had antinuclear antibodies in low titres, were seronegative for antibody to SS-A and remained free of the manifestations of connective-tissue disease. Six of the seven most-recent cases have been diagnosed in utero, which confirms a trend towards the more-frequent prenatal diagnosis of congenital heart disease as a result of the increased use of fetal monitoring and ultrasonography.
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PMID:Fetal and neonatal congenital complete heart block. 265 84

Although, the diagnosis of myocardial sarcoidosis is difficult to establish clinically, the heart may be involved at autopsy in upto a third of cases of sarcoidosis. Cardiac sarcoidosis may remain occult, may present with arrhythmia, or may even cause sudden death. In order to avoid a diagnostic oversight, sarcoid heart disease should be considered in any patient with unexplained heart block, cardiac arrhythmia, or heart failure.
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PMID:Myocardial sarcoidosis: a review. 269 Feb 42

We have used a combination of a beta-blocker and verapamil to treat 42 consecutive patients with angina resistant to either agent alone. Patients with heart failure, heart block or uncontrolled hypertension were excluded. The mean duration of follow-up was 6.5 months. Thirty-six patients (81%) reported an improvement and the number of angina attacks was reduced from 17/week to 5/week. Side effects necessitated withdrawal of one or both drugs in 6 patients, 2 of whom developed bradyarrhythmias not solely related to drug treatment. The most common complication was mild left ventricular failure (6) treated by reducing or stopping the beta-blocker. The data suggest that the combination of verapamil and a beta-blocker may be used in a relatively unselected group of patients with difficult angina. However, as dosage adjustment and close observation may be necessary to minimise side effects, the use of this combination should be limited to hospital practice.
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PMID:Tolerability of combined treatment with verapamil and beta-blockers in angina resistant to monotherapy. 285 47

At present nitrates remain the initial treatment for relief or prevention of angina in patients with coronary artery disease. In cases where nitrates and beta blockers have been used and are ineffective for managing effort angina, calcium antagonists may be substituted or added to the beta-blocking treatment. When the predominant symptom is rest angina, and there is evidence suggesting coronary artery spasm, nitrates and a calcium antagonist can be effective therapy. In patients with heart block, bradyarrhythmias, heart failure, or hypertension nifedipine may be the drug of choice. In contrast verapamil merits choice when supraventricular tachycardia is present. Diltiazem appears intermediate between nifedipine and verapamil and may be particularly useful when hypotension or other side effects must be avoided.
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PMID:Calcium antagonists. 286 40

Adverse effects of beta-adrenergic receptor blocking drugs can be divided into two categories: 1) those that result from known pharmacological consequences of beta-adrenergic receptor blockade; and 2) other reactions that do not appear to result from beta-adrenergic receptor blockade. Adverse effects of the first type include bronchospasm, heart failure, prolonged hypoglycemia, bradycardia, heart block, intermittent claudication, and Raynaud's phenomenon. Neurological reactions include depression, fatigue, and nightmares. It is not yet proven whether the beta 1-selective adrenergic blockers or those with partial agonist activity reduce the overall frequency of adverse reactions seen with propranolol. Patient age does not appear, in itself, to be associated with more beta-blocker side effects. Side effects of the second category are rare. They include an unusual oculomucocutaneous reaction and the possibility of oncogenesis. There are also many drugs that interact with beta-blockers, which may increase toxicity. Finally, there are specific patient characteristics where one beta-blocker may be more effective and safer than another.
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PMID:Beta-adrenergic receptor blockers. Adverse effects and drug interactions. 289 72

PN 200-110 (isradipine) is a new dihydropyridine calcium antagonist with selective actions on the heart as well as the peripheral circulation. It selectively inhibits the sinus node but not atrioventricular conduction and its negative inotropic action is minimal, about 20 times weaker than its negative chronotropic effect. This in vitro pattern also expresses itself in vivo: partial suppression of the reflex tachycardia induced by its peripheral vasodilatation and no effect on the P-Q interval on the electrocardiogram even at large doses. The presence of first- or second-degree heart block should therefore not limit its use, whereas the sick sinus syndrome might. PN 200-110 does not decrease myocardial contractile force even in vagotomized animals with full beta blockade. PN 200-110 nevertheless lowers myocardial oxygen consumption mainly by its action on afterload. It should therefore be useful in angina pectoris. PN 200-110 is a powerful peripheral vasodilator. It preferentially dilates coronary, cerebral and skeletal muscle vasculature. Its long lasting (24 to 48 hours) antihypertensive action is not accompanied by tachycardia in spontaneously hypertensive rats and it enhances sodium and water excretion in normotensive rats. It should be useful in the treatment of hypertension, and, considering its pattern of cardiac actions, perhaps also as an after-load-reducing agent for the treatment of heart failure. Antiarteriosclerotic effects in conscious rabbits were found at reasonably small doses, suggesting that such effects might occur in man at therapeutic doses.
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PMID:Selective effects of PN 200-110 (isradipine) on the peripheral circulation and the heart. 294 86


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