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

There is a stage in one's career when one is mature enough to be invited to give named lectures. Usually, one has never heard of the 'named' person. This occasion is different because I know Dr Keith. (Dr John Keith died February 8, 1989, aged 80 years. Obituary in Can J Cardiol 1989;5[3]:XI). His book was my reference when I became excited by congenital heart disease and two days ago I had the pleasure of speaking to him, explaining the title which he said was "quaint and interesting." He reminded me that when he started the Canadian Cardiovascular Society with Dr Harold Segall there were only a handful of people who came together to discuss mutual problems in cardiology. Looking at the remarkable list of distinguished physicians and surgeons who have come before me to give this important lecture, I hope that I can do justice to the honour that you have given in asking me to be the John Keith Lecturer in 1988. The title of this lecture was born when I received a blue anniversary card covered with pink hearts from a once deeply cyanosed, chairbound girl with Ebstein's anomaly, 20 years after she had reparative surgery and lived a normal life, for which she thanked me. I passed the message to Donald Ross, with whom I have been privileged to work with for 25 years in the National Heart Hospital in London, United Kingdom and whose courageous innovations have created so much good life for many with complex congenital heart disease.
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PMID:Out of the blue and into the pink. Is it so rosy for the cardiologist? 239 37

Calcium antagonists have emerged as a new class of antiarrhythmic agents for the control of certain supraventricular and ventricular arrhythmias. Electrophysiologically, these agents are heterogeneous but their main action is mediated through a depressant effect on the slow calcium channel in cardiac muscle, most readily demonstrated in isolated tissue preparations. In vivo, their actions are modulated by their reflex actions and by their interaction with the autonomic nervous system due to the noncompetitive adrenergic-blocking actions that some of the compounds exhibit. The major agents exerting antiarrhythmic actions are verapamil, diltiazem, gallopamil, tiapamil and bepridil; the dihydropyridines are devoid of electrophysiologic actions in vivo. Calcium antagonists prolong intranodal conduction time, lengthen the effective and functional refractory periods in the atrioventricular node but exert little or no effect on atrial, ventricular, His-Purkinje or bypass tract conduction or refractoriness (except in the case of bepridil, which has additional electrophysiologic properties). These effects form the basis of the clinical antiarrhythmic effects of this class of agents. The most striking action is the predictable and prompt termination of the reentrant supraventricular tachycardia by intravenous verapamil and diltiazem and the slowing of the ventricular response in atrial flutter and fibrillation. These agents may also be of value in the long-term control of ventricular response in atrial flutter and fibrillation; their role in multifocal atrial tachycardia and other ectopic tachycardias is less well defined. Calcium antagonists reverse ischemic ventricular arrhythmias caused by coronary artery spasm but exert little or no action in the usual forms of sustained ventricular tachyarrhythmias associated with severe structural heart disease. They are poor suppressants of ventricular premature complexes. Recent data have established their role in exercise-induced tachycardia occurring in the context of ischemic heart disease; they are also of value in ventricular tachycardia occurring in young patients who develop tachycardia with a right bundle branch block and left axis deviation morphology, an arrhythmia thought to be due to triggered automaticity.
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PMID:Use of calcium antagonists for cardiac arrhythmias. 243 30

Thirty-five patients with bundle branch block (BBB) and unexplained syncope underwent electrophysiologic study (EPS) including programmed ventricular stimulation and ajmaline administration (1 mg/kg, IV) to induce infra-His block. A prolonged HV interval (greater than 55 ms) was present in 16 of the 35 patients. Ajmaline-induced HV block occurred in 12 patients (complete HV block in 10, and 2:1 HV block in two). Monomorphic ventricular tachycardia (VT) was inducible in nine (25.7%) and polymorphic VT in two patients (5.7%). Left ventricular ejection fraction (LVEF) was less than 40% in five patients (45.5%) with inducible VT. Two patients had an unexpected co-existence of inducible HV block and VT. The remaining 14 patients (40%) had no detectable abnormality. The incidence of inducible VT was higher (45% vs 13.3%), and the presence of negative studies was lower (30% vs 53.3%) in patients with structural heart disease (n = 20), when compared to those with no significant heart disease (n = 15) (differences not significant [NS]). During a mean follow-up period of 16.5 +/- 9.2 months, all the patients with inducible HV block have been asymptomatic after having received permanent pacemakers. Patients with inducible monomorphic VT (except one with poor left ventricular function who died suddenly) have also been asymptomatic on antiarrhythmic drugs. Of the remaining patients, seven with normal EPS, two with prolonged HV intervals but no inducible HV block (despite being given permanent pacemakers) and one patient with polymorphic VT on antiarrhythmic drugs continue to have recurrent syncope. Approximately 60% of patients with BBB and unexplained syncope have clinically significant electrophysiologic abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of patients with bundle branch block and "unexplained" syncope: a study based on comprehensive electrophysiologic testing and ajmaline stress. 245 15

Dilated cardiomyopathy (DCM) is defined as a syndrome of dilated ventricles with gross impairment of ventricular systolic function. However, few reports on perioperative management of DCM were obtainable. This paper describes perioperative management of two patients with DCM. A 72-year-old man, whose DCM had been treated with medication, was planned for gastrectomy. His cardiac signs indicated NYHA class II. Cardiac function, evaluated prior to the surgery with echocardiography to determine an operative indication, turned out to be well compensated. Minimal cardiac derangements were anticipated perioperatively. The procedure was carried out under general anesthesia with neuroleptanalgesia utilizing butorphanol and vasoactive agents. No circulatory complications were observed throughout the surgery. A 66-year-old man, who had long-standing heart disease, hemiplegia and hydronephrosis due to ureteral stone, was planned for percutaneous nephrolithotomy. However, the planned surgery was withdrawn because he had DCM with minimal compensatory function and perioperative cardiac derangements were anticipated according to the categorized data classified with echocardiography. We conclude that preoperative assessment of cardiac function is essential to minimize perioperative cardiac derangements in patients with DCM.
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PMID:[Perioperative management of patients with dilated cardiomyopathy]. 273 70

The clinical, ECG and electrophysiological data of 37 patients (28 males and 9 females) with spontaneous intra-hisian block are reported. Of these patients, 11 had hypertensive heart disease and 5 had ischemic heart disease with previous myocardial infarction; in 21 patients, clinical signs of heart disease were not evident. In 18 patients, a single or recurrent episode of syncope had occurred. One patient had junctional rhythm and 36 sinus rhythm; among these, 12 patients presented PR greater than 200 msec (7 with a narrow and 5 with a wide QRS); 12 patients had a single or bilateral bundle branch block; 12 had a normal ECG. The electrophysiological study showed a split H-H1 in 22 patients, a wide His deflection (H greater than 25 msec) in 4 and HV greater than 65 msec with narrow QRS in 11. In 17 patients a more or less marked sinoatrial node and/or atrioventricular node dysfunction was present. Atrial pacing, performed in all, induced 2nd degree Mobitz 2 intra-hisian block in 9 patients. Ajmaline was used in 16 patients but induced a complete intra-hisian block in only one. In 28 patients a preventive pacemaker was implanted after electrophysiological study. During the follow-up (mean 25 months/pt.), 38% of the patients developed complete atrioventricular block. No recurrence of syncope occurred in the paced patients. Comparison of patients who developed atrioventricular block and those who maintained normal atrioventricular conduction did not show differences as far as heart disease, previous syncope, ECG pattern and results were concerned.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Spontaneous grade I bundle of His block. Clinical, electrocardiographic and electrophysiological studies in 37 patients]. 274 10

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

Eppinger and Rothberger in 1909 and 1910 first acknowledged the importance of the conduction system, yet a confusion of the pattern of left bundle branch block with right bundle branch block resulted which persisted for 25 years. In left bundle branch block, right ventricular endocardial activation begins before, and is often completed before, initiation of left ventricular endocardial activation. Most likely, right to left septal activation then follows, resulting in left ventricular endocardial activation. Although it is hazardous to make definitive diagnoses of infarction in the presence of left bundle branch block, clues do exist. Benign left bundle branch block is rare; usually disease becomes manifest. Electrocardiographic criteria of hypertrophy are not as helpful in older patients with chronic left bundle branch block (mainly because of the very high incidence of left ventricular hypertrophy) as in younger patients with block of nonatherosclerotic origin. Left bundle branch block is often associated with other abnormalities of the conduction system. Fascicular blocks may mask or mimic myocardial infarction. Left posterior fascicular block is most often an indicator of left ventricular myocardial deficit if right ventricular enlargement is eliminated. Mortality is higher in patients with associated left axis deviation than in those with a normal axis, although the incidence of progression of atrioventricular (AV) block is low. In symptomatic patients with prolonged His to ventricular intervals, the incidence of progression of AV block is higher (12%). Preexisting left bundle branch block in the absence of clinical evidence of heart disease is rare, yet carries with it a slightly increased mortality. Newly acquired left bundle branch block carries a 10-fold increase in mortality; the incidence of sudden death as the first manifestation of heart disease is increased 10-fold.
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PMID:Left bundle branch block: a continuously evolving concept. 295 Jan 57

Atrial natriuretic peptide (ANP) which is secreted from atrial muscle has been shown to produce relaxation of vascular smooth muscle, anti-hypertensive effects, and natriuresis, and to implicate renin-angiotensin-aldosterone network. In human, ANP (hANP) exists as three subtypes: alpha-, beta-, gamma-hANP which have molecular weight of 3,000, 6,000 and 13,000, respectively. In human tissue hANP has been shown to be present not only in heart atria, but also submandibular gland. In addition, it has been reported that in some conditions of heart disease hANP can be found in the ventricles. However, the exact distribution outside of the atrial system has not been definitely established. In our studies, we attempted by using immunohistochemical methods on human and dog hearts to answer this question. In addition, by using nucleic acid probes we have investigated possible areas where hANP may be synthesized. In the initial studies specific antibody to hANP was prepared in rabbits by immunization with synthetic alpha-hANP coupled to porcein thyroglobulin. The specificity of this antibody was confirmed by Western Immunoblotting. Immunoperoxidase staining demonstrated hANP in His-bundle and major branching bundles as well as atrial wall and AV-node of both human and dog hearts. Ventricular muscle cells outside of the conduction system did not contain hANP. The possibility of non-specific staining by antibody to thyroglobulin was muled out as antibody to thyroglobulin alone never showed positive staining. However, staining of the atrial muscles was always granular in the perinuclear areas, while that of the conduction system was usually diffuse.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Localization of atrial natriuretic peptide in the heart. Immunohistochemical and northern blot analyses]. 297 21

In recent years calcium channel blockers have emerged as a new class of antiarrhythmic agents for the control of certain supraventricular and ventricular arrhythmias. Electrophysiologically, they are heterogeneous but their main action is mediated through a depressant effect on the slow calcium channel in cardiac muscle. In isolated muscle, their actions are modulated by their reflex actions and by their interaction with the autonomic nervous system due to the nonocompetitive adrenergic blocking actions that some of the compounds exhibit. The major agents exerting antiarrhythmic actions are verapamil, diltiazem, gallopamil, tiapamil, and bepridil; the dihydropyridines are devoid of significant electrophysiologic actions in vivo. Calcium antagonists prolong intranodal conduction time, lengthen the effective and functional refractory periods in the AV node, but exert little or no effect on atrial, ventricular, His-Purkinje, or bypass tract conduction or refractoriness (except in the case of bepridil, which has additional electrophysiologic properties). These effects form the basis of the clinical antiarrhythmic effects of this class of agents. The most striking action is the predictable and prompt termination of reentrant supraventricular tachycardia by intravenous verapamil and diltiazem and the slowing of the ventricular response in atrial flutter and fibrillation. These agents may also be of value in the chronic control of ventricular response in atrial flutter and fibrillation; their role in multifocal atrial tachycardia and other ectopic tachycardias is less well defined. Calcium antagonists reverse ischemic ventricular arrhythmias due to coronary artery spasm but exert little or no action in the usual forms of sustained ventricular tachyarrhythmias associated with severe structural heart disease. They are poor suppressants of premature ventricular contractions. Recent data have established their role in exercise-induced tachycardia occurring in the context of ischemic heart disease; they are also of value in ventricular tachycardia occurring in young subjects developing tachycardia with a right bundle branch block with left axis deviation morphology, an arrhythmia thought to be due to triggered automaticity. The role of calcium antagonists in reducing the incidence of sudden death in the survivors of acute myocardial infarction remains uncertain.
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PMID:Control of cardiac arrhythmias by calcium antagonism. 328 60

Disopyramide is an oral antiarrhythmic drug which reduces conduction velocity, prolongs duration of action potential and the effective refractory period, and exerts vagolytic properties. The drug is usually well absorbed orally. The principal use of the drug is to suppress ventricular extrasystoles with usual oral dosage of 100 to 200 mg every 6 h, until blood levels of 2 to 4 micrograms/mL are attained. The use of the drug for suicide is uncommon as it is a prescription drug. Two cases of fatal disopyramide intoxication seen at the Los Angeles County Medical Examiner's Office will be discussed followed by a review of the literature of fatal suicidal disopyramide overdose. Case 1 was a 31-year-old male pharmacist with known history of depression and no history of heart disease. His decomposed remains were found with a suicide note and with several disopyramide tablets. At autopsy the blood level for disopyramide was 146 micrograms/mL. Case 2 is a 40-year-old male with history of alcoholism and prior suicidal attempts who regularly took disopyramide to control ventricular arrhythmias. He apparently ingested 36 100-mg tablets of disopyramide before his final collapse. At autopsy his blood level of disopyramide was 63 micrograms/mL.
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PMID:Fatal disopyramide intoxication from suicidal/accidental overdose. 332 13


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