Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the importance of usual risk factors of coronary artery disease (CAD) in patients with coronary artery spasm, 40 patients with vasospastic angina (VA), normal or nearly normal coronary arteries and without previous myocardial infarction were compared with 2 control groups of 40 patients each, matched for age and sex: 1 group with CAD and 1 without heart disease. Ninety percent of patients with VA were cigarette smokers and 70% were heavy smokers (more than 20 cigarettes daily), compared with 53% and 33% in patients with CAD (p less than 0.001) and 30% and 15% in those without heart disease (p less than 0.001). Except for cigarette smoking, the risk factor profile of patients with VA appeared more like the profile of patients without heart disease than that of patients with CAD. The results suggest that cigarette smoking may play a role in CAD independent of atherosclerosis and possibly favoring coronary artery spasm.
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PMID:Comparison of risk factors in vasospastic angina without significant fixed coronary narrowing to significant fixed coronary narrowing and no vasospastic angina. 394 8

Mitral valve prolapse is the most common form of heart disease, as it occurs in 4 to 6 per cent of the population. It has a benign course in the majority of cases, but 5 types of severe complication can occur in 15 per cent of cases. Mitral incompetence occurs in 14.8 per cent of cases. It may develop gradually or suddenly, following rupture of the chordae, which requires rapid surgical repair. Mitral valve prolapse is complicated by infectious endocarditis in 2.9 per cent of cases, hence the need for antibiotic prophylaxis prior to dental treatment or surgery in patients with a pan-systolic or end-systolic murmur. The only arrhythmias which should be considered as complications and treated as such are frequent ventricular extrasystoles of more than 30 per hour, usually associated with bigeminy, runs or polymorphism, ventricular tachycardia and ventricular fibrillation. Treatment consists, primarily, of beta-blockers. Sudden death is of course the major complication, occurring in 1.4 to 2.4 per cent of cases. The patients at risk of this complication are middle-aged women (40 years) with a past history of syncope or faintness due, in most cases, to episodes of ventricular tachycardia or ventricular fibrillation. Apart from arrhythmia, coronary artery spasm has also been found to be a cause of sudden death in these patients. Transient or definitive ocular and cerebral ischaemic episodes can also complicate mitral valve prolapse. Mitral valve prolapse is found in 20 to 30 per cent of patients with neurological accidents before the age of 45. Preventative treatment consists of anti-platelet aggregation agents and anticoagulants in recurrent cases.
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PMID:[Complications of idiopathic mitral valve prolapse. Prevention and treatment]. 614 Aug 95

Previously reported cardiac manifestations of carcinoid disease include right-sided valvular dysfunction and vasomotor disturbances. This report describes a 62-year-old white man who had electrocardiographically documented widespread elevation of the S-T segment, arrhythmias, and cardiac arrest after exercise. Noninvasive and laboratory studies confirmed the diagnosis of malignant carcinoid disease with tricuspid valve involvement. Coronary angiography revealed mild atherosclerosis. Thus, coronary artery spasm is a previously unrecognized manifestation of carcinoid heart disease and introduces what may be an important relationship of endogenous, excessive vasoactive amines to human coronary vasospasm.
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PMID:Coronary artery spasm and cardiac arrest in carcinoid heart disease. 649 52

In 100 successive patients with normal coronary arteriography performed for spontaneous precordial chest pain, a Methergine test was performed to induce coronary artery spasm, in addition to esophageal manometry, and an angiographic and echocardiographic study of the left ventricle. These tests were all normal in 39 patients, whereas the remaining 61 patients had pain due to coronary artery spasm (14 times), a non-coronary artery cardiopathy (16 times) (hypertrophic cardiomyopathy or mitral valve prolapse), or esophageal dyskinesia (35 times). The latter was an isolated finding 29 times, was associated 3 times with coronary artery spasm, and 3 times with non-coronary artery cardiopathy.
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PMID:[Normal coronary arteries and spontaneous precordial pain]. 652 28

Coronary arteries from hearts of cardiac patients contain significantly higher concentrations of histamine than do those from noncardiac patients. The coronary vessels of cardiac patients are also hyperresponsive to histamine and serotonin. These differences between groups of patients suggest an explanation for coronary artery spasm in heart disease.
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PMID:Coronary arteries of cardiac patients are hyperreactive and contain stores of amines: a mechanism for coronary spasm. 670 30

Sudden cardiac death due to ventricular fibrillation is the most common cause of death in industrialized countries. Patients with an increased risk of sudden cardiac death may be found to have, in addition to high-grade ventricular arrhythmias, impaired left ventricular function. Mechanisms responsible for precipitation of ventricular fibrillation include risk factors such as increased sympathetic nervous system activity, electrolyte disturbances, coronary artery spasm and transient, thrombotic coronary artery occlusion. For detection of high-grade arrhythmias as well as for assessment of treatment, continuous 24-hour EKG monitoring and exercise EKG should be employed. The indication for antiarrhythmic therapy should be regarded as established in patients successfully resuscitated after unexpected ventricular fibrillation as well as in patients status-post myocardial infarction, with angina pectoris, cardiomyopathies, QT-prolongation, mitral valve prolapse, congenital or other markedly symptomatic heart disease and high-grade ventricular arrhythmias. The treatment initiated, after discontinuation of all antiarrhythmic drugs for at least four half lives and ambulatory EKG monitoring for 48 hours as well as maximal symptom-limited exercise testing, should be evaluated after acute drug administration and after 72 hours of maintained therapy with the aid of continuous EKG monitoring and exercise EKG. In patients with a history of malignant arrhythmias in whom no evidence of high-grade ventricular arrhythmias can be found in either the continuous EKG recording or in the exercise EKG, initiation of drug treatment should be based on the results of programmed electrical stimulation. Effective treatment can be assumed on documentation of complete suppression of arrhythmias grade IVb and V or prevention of precipitation of ventricular tachycardias, respectively, as well as 90% reduction of grade IVa and 50% reduction of premature ventricular beats. During acute testing, aggravation of arrhythmias after administration of antiarrhythmic drugs was seen in 11.1%. While the yearly mortality of successfully controlled patients ranged between 2.3 and 2.8%, the yearly mortality rate in those in whom the arrhythmias were inadequately controlled ranged from 43.6 to 56%.
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PMID:Sudden cardiac death--an approach to management of the patient at risk. 671 16

Nineteen patients survived a cardiac arrest not associated with an acute myocardial infarction, and had a normal electrophysiologic study with no inducible ventricular tachycardia despite programmed stimulation with one to three extrastimuli at two or more ventricular sites. Among 14 patients who had obstructive coronary artery disease, cardiac arrest occurred during exertion or an episode of angina pectoris in 11; 24 hour ambulatory electrocardiographic recordings demonstrated infrequent or no premature ventricular complexes in 10 and an ischemic response occurred during stage I or II (Bruce protocol) in 6 of 9 patients who underwent exercise testing. Treatment of these patients consisted of myocardial revascularization (eight patients) or antianginal medications (six patients). Only three patients were also treated with an antiarrhythmic drug. Over a follow-up period of 26 +/- 15 months (mean +/- standard deviation), only one patient died suddenly. Two patients who had coronary artery spasm were treated with coronary vasodilator medications and had no recurrence of cardiac arrest over 7 and 36 months of follow-up, respectively. Three patients who had cardiomyopathy or no identifiable structural heart disease were treated with nadolol or amiodarone and had no recurrence of cardiac arrest over 3 to 27 months of follow-up. Among patients who survive a cardiac arrest and have a normal electrophysiologic study, those with obstructive coronary artery disease or coronary artery spasm generally have an excellent prognosis with treatment directed primarily at the underlying heart disease. The clinical features of these patients suggest that cardiac arrest was related to ischemia rather than a primary arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical features and prognosis of patients with out of hospital cardiac arrest and a normal electrophysiologic study. 673 52

This study delineates the clinical spectrum of 15 patients with polymorphic ventricular tachycardia and normal QT intervals in the absence of apparent structural heart disease, adverse drug effects, or electrolyte disturbances. Patients presented with either palpitations (n = 2), presyncope (n = 5), syncope (n = 4), no symptoms (n = 1), or aborted sudden death (n = 3). Mean age was 41 years (range 20 to 64), and mean follow-up 38 months (range 4 to 109). Left ventricular function was normal as determined by either echocardiogram (n = 9) or left ventriculography (n = 9). Episodes of polymorphic ventricular tachycardia (VT) were analyzed in terms of the preceding interval, and the relation of the initiating coupling interval to the QT interval (coupling interval/QT interval = polymorphic VT index). The mean QT for the group as a whole was 0.41 +/- 0.02 second. Patients could be separated into 3 distinct groups. Four patients had polymorphic VT reproducibly induced by exercise and initiated by late-coupled beats (mean polymorphic VT index 1.27 +/- 0.21). Isoproterenol induced polymorphic VT in 3 of 4 patients, and all 4 responded to chronic beta blockade. Two patients had polymorphic VT during episodes of coronary artery spasm, and both responded to calcium channel blockade. Polymorphic VT unrelated to exertion or coronary vasospasm occurred in 9 patients. Tachycardia onset was initiated by closely coupled beats (mean polymorphic VT index 0.95 +/- 0.16), and was preceded by a pause in 4 patients, and no pause in 5 patients. Sudden death occurred in 5 of 9 patients with the shortest polymorphic VT indexes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sudden cardiac death and polymorphous ventricular tachycardia in patients with normal QT intervals and normal systolic cardiac function. 790 Jun 61

We present three patients without significant coronary or other structural heart disease who were resuscitated after ventricular fibrillation attributed to coronary spasm. Angina pectoris was present in two of the cases and silent myocardial ischemia in the third. All patients were given calcium antagonists at discharge. A defibrillator was also implanted in the patient with silent myocardial ischemia because further episodes of ischemia would probably have occurred without premonitory symptoms. Coronary spasm might be a mechanism of ventricular fibrillation in patients without significant structural heart disease. Diagnostic tests should therefore be performed to confirm or exclude coronary spasm in such cases. The implantation of an automatic defibrillator seems justified in selected patients with documented coronary spasm, silent myocardial ischemia, and associated sustained ventricular tachyarrhythmia, although prospective studies are not yet available.
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PMID:Ventricular fibrillation related to coronary spasm in patients without significant coronary or other structural heart disease. 804 79

Toxic manifestations of digitalis are one of the most prevalent adverse drug reactions encountered in clinical practice. The estimated incidence is about 20% in hospitalized patients in the USA. The authors describe a rare case of myocardial "catecholamine necrosis" (anteroseptal myocardial infarction) during accidental digitalis intoxication. A male patient, 75 years old, suffering from cirrhosis and ascites, take on by mistake a tablet of digoxin 0.25 mg. four times at day for eleven days. He hadn't heart disease in the past. At the eleventh day the patient showed a deep tiredness and so he was submitted to a clinical examination and electrocardiogram. The ECG demonstrated an anteroseptal myocardial infarction in the second-third electrical stage. The patient was hospitalized. The successive examination revealed: very high plasma digitalis concentrations; an increase of the serum levels of CPK and LDH; a significant increase of plasmatic and urinary catecholamine levels which return to normal values after fifteen days; apical akinesia at the echocardiographic examination; no signs of residual myocardial ischemia to the echo-dypiridamole stress test; normal coronary artery to the coronary arteriography and absence of coronary artery spasm to the ergonovine test. Furthermore the abdominal echography and the abdominal computerized tomography didn't reveal surrenal disease but showed an important liver disease. The patient was free from other cardiac events in the follow-up. Generally, during the digitalis intoxication we observe various rhythm and conduction disturbances. Instead in this case no serious arrhythmias were registered and the main expression of the drug toxicity was an anteroseptal myocardial infarction with undamaged coronary artery. Also the usual extracardiac symptoms and signs of the digitalis intoxication were absent in this case. All these observations can be explained with the pathological increase of the cathecholamine levels, indirectly induced by digitalis; with the direct toxic effect of the drug at the myocardic level; with the contemporary absence of ionic disturbances; with the concomitant liver disease. The direct toxic effect of the digitalis produced an increase in calcium ions availability for the electromechanical coupling and an increase of the intramyocardial pressure; the increase of the adrenergic activity determined contemporary an increase in the oxygen consumption of the myocardial cells, a rise of vascular tone and coronary artery tone and a reduction of the duration of the diastole. All these factors provoked a "primary and secondary" ischemia which evolved toward a real "cathecholamine necrosis" and produced a myocardial infarction. This hypothesis explains the myocardial infarction in absence of injury at the coronary arteriography and without coronary spasm at the ergonovine test; moreover it explains the transient increase in cathecholamine plasma levels observed in the acute phases an normalized after fifteen days. The "cathecholamine necrosis" is an anatomical definition, nevertheless in our opinion it gives account of the rare clinical situation observed.
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PMID:[An unusual case of "catecholamine necrosis" caused by accidental digitalis poisoning]. 855 67


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