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

Disturbances of heart rhythm, observed during 700 heart catheterizations in infants and children, are discussed. Paroxysmal supraventricular tachycardia has been observed in 25 investigations (3,6%), sinus bradycardia in 18 (2,6%), junctional rhythm in 10 (1,4%), second degree AV-block in 9 (1,3%), ventricular fibrillation in 8 (1,1%), sinus tachycardia in 7 (1%), complete block in 7 (1%), asystole and atrial flutter in 2 (0,3%) each, and ventricular tachycardia in 1 (0,15%). Supraventricular tachycardia occurred equally in all ages without preference of a special malformation. The two patients with WPW-syndrome, however, showed this disorder in each of three catheterizations. Propranolol and verapamil succeeded in terminating the attacks. Junctional rhythm and sinus tachycardia presented equal behavior and benignity. Sinus bradycardia, second and third degree AV-block, and especially ventricular fibrillation occurred mostly in neonates and infants, many of them cyanotic and suffering from complex malformations and therefore needing multiple catheter manipulations. Bradycardia was in two, asystole in one of the very sick neonates associated with subsequent death within 24 hours. Once asystole resulted in immediate death after pulmonary angiography in a child with severe pulmonary hypertension. Ventricular fibrillation could be terminated promptly by DC countershock in all patients, but three of the children died subsequently. Complete block occurred only in children with systemic right ventricular pressure, 4 of the 7 patients having pulmonary hypertension, too. In two instances the block subsided spontaneously, the rest could successfully be treated with orciprenaline (Alupent R). Life threatening arrhythmias became less frequent as a consequence of earlier investigation, if severe heart disease was suspected, and by closer control of cyanosis, acidosis and temperature before, during, and after catheterization.
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PMID:[The risks involved in the heart catheter examination. A retrospective evaluation of the complications after 700 examination. III. Irregularities of heart (author's transl)]. 53 Jul 27

The electrophysiologic effects of circulating epinephrine in humans were examined in four study groups of 10 subjects each. In 10 subjects without structural heart disease (Group 1) and in 10 patients with coronary disease or dilated cardiomyopathy (Group 2) epinephrine infusion at 25 and 50 ng/kg body weight per min for 14 min resulted in an elevation of the plasma epinephrine concentration in the physiologic range. In both groups it produced a dose-dependent decrease in the effective refractory period of the atrium, atrioventricular (AV) node and ventricle and improvement in AV node conduction. Epinephrine facilitated the induction of sustained ventricular tachycardia in 3 of the 20 subjects. In Group 3, a beta-adrenergic blocking dose of propranolol was added to the infusion of 50 ng/kg per min of epinephrine. Propranolol not only reversed the effects of epinephrine, but also lengthened these variables compared with baseline values. In Group 4, propranolol was administered first, followed by 50 ng/kg per min of epinephrine. Propranolol alone slowed AV node conduction and mildly prolonged the refractory periods. In the presence of beta-blockade, epinephrine had no effect on AV node properties but resulted in a lengthening of the atrial and ventricular effective refractory periods. In conclusion, epinephrine in physiologic doses shortens the effective refractory period of the atrium, AV node and ventricle, improves AV node conduction and may facilitate the induction of sustained ventricular tachycardia. The overall electrophysiologic effects of epinephrine result from stimulation of beta-receptors. Stimulation of alpha-receptors by epinephrine has no effect on the AV node but prolongs the effective refractory period of the atrium and ventricle, partially offsetting the shortening of refractory periods mediated by beta-receptor stimulation.
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PMID:Electrophysiologic effects of epinephrine in humans. 283 8

A 27-week fetus with severe nonimmune hydrops was found to have a reciprocating atrioventricular tachycardia with the rate of 275 beats per minute. Maternal digitalization produced improvement without conversion. Large doses of propranolol were without effect. Twelve days later quinidine was added, and conversion to sinus rhythm occurred after only two hours and persisted to term. The infant has no heart disease. Literature review confirms digoxin as the first choice for treatment of fetal reciprocating tachycardia, with excellent transplacental passage. Propranolol has not been demonstrably effective, and has poor placental passage. Verapamil also produced poor cord blood levels in two trials. Placental passage for procainamide is uncertain, but long-term use has been unsatisfactory. Quinidine is recommended as the second drug for treatment of resistant fetal tachyrhythmias.
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PMID:Hydrops from reciprocating atrioventricular tachycardia in a 27-week fetus requiring quinidine for conversion. 402 12

Traditionally when considering the pharmacologic basis of therapy in angina pectoris, attention is focussed on alterations of coronary blood flow. Yet the diseased coronary arteries in these patients often do not appear to be capable of responding to vasodilatory drugs. Since the pain of myocardial ischemia is relieved by a number of interventions without an increase in coronary blood flow, the concept herein considered is that angina pector is best viewed as an unfavorable relation between myocardial oxygen requirements and availability. Thus, the clinical value of the major antianginal agents is thought to be based importantly upon their actions to reduce myocardial oxygen consumption rather than to increase coronary blood flow. Sublingual nitroglycerin possesses a powerful dilator effect on veins which reduces venous return and thereby the size of the heart and intra-myocardial tension; thus myocardial oxygen requirements are diminished. The beta-adrenergic receptor blocking drug, propranolol (Inderal(R)), inhibits sympathetic stimulation of the heart at rest and during exercise. Thus, myocardial oxygen requirements are diminished by the reduction in heart rate and diminished contractility. As a result of this latter action, cardiac output is reduced and thereby arterial pressure and intramyocardial tension is lowered. In patients with advanced heart disease and borderline cardiac compensation, propranolol is hazardous because it removes the availability of one of the important reserve mechanisms for maintaining cardiac compensation-the sympathetic support of the failing heart. The introduction of electrical stimulation of the carotid sinus nerves as a means of therapy in patients with angina pectoris has provided a powerful tool for the treatment of patients with refractory ischemic pain.
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PMID:New trends in the treatment of angina pectoris. 498 Aug 81

The Beta-Blocker Heart Attack Trial was a multicenter, randomized, double-blind, placebo-controlled trial of propranolol therapy in 3837 men and women with acute myocardial infarction. The patients began their treatment 5-21 days after hospital admission (mean 13.8 days). During an average follow-up of 25 months, there were statistically significant reductions in total mortality (26%), cardiovascular mortality (26%), arteriosclerotic heart disease (27%), sudden death (28%) and coronary incidence (definite nonfatal reinfarction plus coronary heart disease mortality) (23%). There was no group difference in incidence of congestive heart failure. Of the many potential side effects that were monitored, broncho-spasm, cold hands and feet, and fatigue occurred more frequently in the propranolol group. Propranolol not only reduced coronary mortality and morbidity, but also was administered with a great degree of safety. Based on these results, its use is recommended for at least 3 years in patients with no contraindications to beta blockade who have had a recent myocardial infarction.
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PMID:Propranolol therapy in patients with acute myocardial infarction: the Beta-Blocker Heart Attack Trial. 634 40

This study was undertaken to establish the nature (intrinsic or extrinsic) of sinus node dysfunction in patients presenting with syncope and abnormal response (sinus pause greater than 3'') to vagal manoeuvres (carotid sinus massage and/or eye-ball compression). To this purpose 29 patients (20 males, 9 females, aged 18-79 yrs, mean = 60) underwent an electrophysiologic study. In all we measured before and after autonomic blockade with Propranolol (0.2 mg/kg) and Atropine sulfate (0.04 mg/kg) the following parameters: sinus rate, corrected sinus node recovery time and sino-atrial conduction time. According to the presence or absence of electrocardiographic signs of sinus node dysfunction the patients were divided into three groups: Group A: 11 patients without electrocardiographic signs of sinus node dysfunction; Group B: 13 patients with borderline electrocardiographic signs of sinus node dysfunction (sinus bradycardia between 40 and 60 beats/min); Group C: 5 patients with definite electrocardiographic signs of sinus node dysfunction (sinus bradycardia less than or equal to 39 beats/min and/or sinoatrial block and/or sinus arrest). Fifteen patients (52%) had signs of organic heart disease. The main results obtained were: At least one electrophysiological test (sinus rate, corrected sinus node recovery time or sino-atrial conduction time) was abnormal in 10 patients (34,5%) before autonomic blockade and in 8 patients (27%) after autonomic blockade. Two of these 8 patients belonged to Group A (18%), 1 to Group B (8%) and 5 to Group C (100%). Six of these 8 patients were suffering from an organic heart disease and 2 were not.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intrinsic function of the sinus node in patients with syncope and positive vagal maneuvers]. 647 23

Forty-seven patients with spontaneous and inducible nonsustained ventricular tachycardia (VT) underwent serial electrophysiologic studies to evaluate the effects of antiarrhythmic agents on inducible arrhythmias, the role of electrophysiologic testing in the evaluation of pharmacologic therapy for these arrhythmias, and potential mechanisms underlying these arrhythmias. Type I antiarrhythmic agents prevented induction of VT by programmed stimulation in 18 of 37 patients and by isoproterenol in 9 of 11 patients. Verapamil and propranolol did not prevent or alter the mode of induction of VT by programmed stimulation, nor did they slow the induced tachycardias. Propranolol prevented induction of VT by isoproterenol in all 14 patients tested. Type I antiarrhythmic agents converted nonsustained into sustained VT in 2 of 37 patients. Inducible VT was prevented in 88% of patients without underlying heart disease, in contrast to only 38% of patients with associated cardiac disease (p less than 0.02). This study demonstrates that electrophysiologic studies may be used to identify antiarrhythmic agents with both beneficial and potentially harmful effects in patients with nonsustained VT. The responses of inducible tachycardias to antiarrhythmic agents in this group of patients with spontaneous nonsustained VT are similar to those previously observed in patients with sustained VT. Finally, the results suggest that VT induced by isoproterenol may frequently respond to type I antiarrhythmic agents in addition to beta blockers.
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PMID:Electropharmacology of nonsustained ventricular tachycardia: effects of class I antiarrhythmic agents, verapamil and propranolol. 670 22

The effects of chagasic sera, containing an antibody (EVI antibody) which reacts with the plasma membrane of working myocardial cells, on "toxic" and "non-toxic" actions of ouabain upon isolated self beating or paced rat atria suspended in different media, were explored. Although ouabain produced a dose-dependent positive inotropic influence on atria suspended in Krebs-Ringer-bicarbonate (KRB) and in KRB plus normal human serum (KRB + NHS) it did not elicit any significant positive inotropic effect on atria beating in KRB plus EVI positive human chagasic serum (EVI(+)S). Additionally, EVI(+)S dose-response curves of classical signs of digitalis cardiac toxicity shifted to the left. The threshold concentration of ouabain required to elicit the onset of "toxic" effects was higher in control preparations (kept in KRB or KRB + NHS) than in EVI(+)S exposed preparations. (-)-Propranolol attenuated the overall toxic action of ouabain in EVI(+)S and facilitated its positive inotropic influence. In control media, the beta-adrenoceptor blocker failed to modify either the "non-toxic" or the "toxic" effect of ouabain. On the other hand, with control atria, subthreshold exogenous norepinephrine inhibited the positive inotropism of ouabain. The data suggest that an adrenergic mechanism is involved in the action of ouabain on cardiac tissue immersed in an EVI(+)S-containing solution. The foregoing results may explain the severe "toxic" effects observed with cardioactive glycosides when they are used in patients with Chagas' heart disease, even at low doses.
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PMID:Chagasic sera alter the effects of ouabain on isolated rat atria. Participation of adrenergic mechanisms. 720 7

We report the case of a 42-year-old male who suffered from ventricular fibrillation (VF) without obvious QT prolongation. His electrocardiogram showed incomplete right bundle branch block (IRBBB) and persistent ST segment elevation in the right precordial leads during sinus rhythm. Cardiac catheterization revealed no overt heart disease except moderate endocardial and subendocardial fibrosis in the left ventricle. Mental stress seemed to trigger VF, and ST elevation became prominent just before VF. Propranolol and mexiletine have been effective in preventing VF for over 3 years.
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PMID:A case of idiopathic ventricular fibrillation with incomplete right bundle branch block and persistent ST segment elevation. 830 52

Congestive heart failure is a relatively uncommon manifestation of thyrotoxic heart disease, and different mechanisms have been proposed. The authors present a possible explanation of congestive heart failure in some cases of thyrotoxicosis. A 39 year-old woman with Graves' disease was hypermetabolic, in atrial fibrillation, and had signs of congestive heart failure. She had a loud murmur of mitral regurgitation, clinical cardiomegaly, accentuated pulmonic sound, and peripheral edema. Propranolol reduced the heart rate to 60 beats per minute, but the loud mitral regurgitation murmur persisted. Echocardiographic and angiographic data were consistent with moderate to severe mitral regurgitation, serious enough to consider mitral valve replacement. As the patient's hyperthyroid state came under control, weight increased and the cardiac murmur resolved. After radioactive iodine treatment and the return to a eumetabolic state, an echocardiogram revealed only trace mitral regurgitation, with near normal left ventricular function and pulmonary arterial systolic pressures. These findings were confirmed by subsequent cardiac catheterization. The authors believe that mitral regurgitation, perhaps secondary to intrinsic papillary muscle dysfunction from hyperthyroidism, was the major cause of reversible congestive heart failure in this case. Valvular disease may play a more substantive role in thyrotoxic heart disease than previously recognized.
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PMID:Case report: reversible mitral regurgitation and congestive heart failure complicating thyrotoxicosis. 861 90


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