Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Eleven patients with short P-R intervals and narrow QRS complexes had ventricular tachycardia due to organic heart disease: mitral valve prolapse with mitral insufficiency (2 patients); alcoholic (?) cardiomyopathy (2 patients); and coronary artery disease (7 patients). Intracardiac studies showed short A-H intervals during sinus rhythm in all cases. The onset of ventricular fibrillation (which, to our knowledge, has not been observed in patients having short P-R and A-H intervals coexisting with narrow QRS complexes) was documented in 4 cases. Only 1 patient (with quinidine syncope) had been premedicated. In the 3 other patients the episodes of ventricular fibrillation appeared during bouts of atrial fibrillation with rapid ventricular rates which could have been an exprerssion of the "enhanced A-V conduction" that had been manifested in sinus beats by short P-R and A-H intervals. In clinical settings and physiological conditions proven to be hemodynamically unstable (such as transient ischemia or acute myocardial infarction) these rapid ventricular rates could have led to ventricular fibrillation; directly because of the R-on-T phenomenon, and/or indirectly due to decreased coronary perfusion. Ventricular tachycardia and ventricular fibrillation due to organic heart disease probably occur more often than suggested by the few reported cases in the literature. Its significance, however, has to be clarified by further prospective studies.
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PMID:Ventricular tachycardia and ventricular fibrillation in patients with short P-R intervals and narrow QRS complexes. 9 18

Eight patients with transient ischemic attacks, and three with partial nonprogressive strokes associated with mitral valve prolapse, are reported. No other etiology for their ischemic events was found. Only one episode of ischemia recurred on aspirin treatment, whereas none recurred on sodium warfarin therapy.
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PMID:TIA, stroke, and mitral valve prolapse. 57 14

Patients with mitral valve prolapse (MVP) frequently experience chest pain which may, expecially in older subjects and males, be difficult to differentiate from angina pectoris. Electrocardiographic (ECG) changes, ventricular arrhythmias, metabolic abnormalities and rare reports of myocardial infarction and sudden death further suggest the presence of an ischemic process in these patients. The recognition of accompanying coronary artery disease (CAD) and exclusion of other causes of ischemia, therefore, may be important in determining the prognosis and appropriate therapy for such patients.
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PMID:Myocardial perfusion scintigraphy in patients with mitral valve prolapse: Its advantage over stress electrocardiography in diagnosing associated coronary artery disease and its implications for the etiology of chest pain. 61 88

The mechanism and temporal manifestation of functional mitral regurgitation after acute myocardial ischemia were examined in eight dogs. Regional ischemia was produced by selective microembolization of the left circumflex coronary artery. Mitral regurgitation and regional left ventricular wall motion abnormalities were evaluated with use of Doppler color flow mapping and two-dimensional echocardiography, respectively. Measurements were made at baseline (before embolization) and were repeated at 30 min and 3 weeks after embolization. Mitral regurgitation developed in all dogs 30 min after embolization and completely subsided 3 weeks later. There was no evidence of mitral valve prolapse, mitral anulus dilation or left ventricular segmental dyskinesia at any time during the study. Regional wall motion analysis showed only hypokinesia of the left ventricular segment overlying the papillary muscle at 30 min with subsequent normalization of the segment at 3 weeks. Mitral regurgitation was accompanied by an increase of the end-systolic distance between the mitral anulus plane and the point of coaptation of the mitral leaflets. This distance was 0.5 +/- 0.1 cm at baseline, increased to 0.9 +/- 0.1 cm 30 min after the embolization (p less than 0.001) and returned to near baseline (0.6 +/- 0.1 cm) 3 weeks after the embolization. These data indicate that mitral valve prolapse, mitral anulus dilation and regional left ventricular dyskinesia are not necessary conditions for the development of functional mitral regurgitation after acute myocardial ischemia. Instead, hypokinesia of the ventricular segment overlying the papillary muscle and leading to retraction of the mitral leaflets toward the apex appears to be a sufficient condition for incomplete leaflet coaptation.
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PMID:Mechanism of functional mitral regurgitation during acute myocardial ischemia. 155 1

The reputation of mitral valve prolapse being a benign condition is based to a great extent on the fact that complications are rare in minor forms, but also because a number of studies of the condition included normal subjects, especially of the female sex. The prevalence of mitral valve prolapse in the general population is 4 to 5%. Approximately 20% of these patients have marked redundancy of valve tissue and are particularly exposed to complications. The incidence of infective endocarditis in cases with an audible murmur is 0.05% per year. The incidence of mitral regurgitation increases with age, so that the annual probability of surgical correction is 0.03%. The risk of sudden death in cases without mitral regurgitation is low (2/10,000 per year) but it is 50 to 100 times greater when mitral regurgitation is present. The frequency of arrhythmias is also higher in cases with mitral regurgitation and that of cerebro-retinian ischemia is estimated to be 0.02% per year. Therefore, a serious complication (endocarditis, sudden death, surgical mitral regurgitation, cerebral or retinian ischemia) occurs each year for every 1,000 mitral valve prolapses, or for a population of 25,000 inhabitants.
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PMID:[Mitral valve prolapse: a severe abnormality?]. 192 18

The importance of a prothrombotic state as a cause of ischemic stroke in young adults is ill defined. We examined 46 unselected patients under age 50 years with cerebral ischemia for anticardiolipin antibody (aCL) and lupus anticoagulants (LA), over a 3-year-period. Age- and sex-matched patients with other neurologic diseases served as a noncerebral ischemia comparison group to test whether (1) stroke/transient ischemic attacks (TIA) in young people is associated with aCL and/or LA, and (2) their presence is specific to cerebral ischemia. In the stroke/TIA group, 21 patients had aCL or LA and 25 had neither, whereas in the control group, 2 patients had aCL and 24 had neither. Equal numbers of stroke/TIA patients with and without antiphospholipid antibodies (aPL) had other stroke risk factors. Patients with aPL and cerebral ischemia, however, had a more frequent history of multiple events than those without them. These antibodies occur with undue frequency in young patients with stroke/TIA and are not associated with a concurrent diagnosis of systemic lupus in most cases. A coexistent aPL-associated prothrombotic state may be a key determinant of whether patients with atherosclerosis, mitral valve prolapse, or other structural lesions experience recurrent ischemia.
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PMID:Antiphospholipid antibodies and cerebral ischemia in young people. 211 4

The authors reviewed 1474 consecutive selective coronary arteriograms performed on patients with suspected coronary insufficiency for the diagnosis of obstructive coronary disease and found 281 (19.1%) cases of apparently normal coronary arteries. These patients presented mean age of 47 +/- 10 years; they were 135 (48%) males and 146 (52%) females. The objective of this study was to obtain the hemodynamic profile of these patients for the following parameters: a) aortic and left ventricular pressures; b) volumes, ejection fraction, segmentary contraction, wall thickness and mass of left ventricle; c) morphology, mobility and competence of the mitral valve. Eight groups of patients were selected: 1) without hemodynamic alterations - 18.9%; 2) with systemic arterial hypertension - 48.7%; 3) with abnormal myocardial contraction - 16.7%; 4) with idiopathic left ventricular hypertrophy - 6.4%; 5) with mitral valve prolapse - 2.5%; 7) with myocardial bridge of the left anterior descending coronary artery - 1.8%; 8) with coronary arterial microfistula of the left ventricle - 0.4%. It is desirable to determine before situations of cardiac emergencies, whether provoked ischemia, as detected by noninvasive stress testing, is present before the performing coronary arteriography in patients, specially females, with systemic arterial hypertension, left ventricular hypertrophy, disorders of ventricular contraction or mitral valve prolapse.
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PMID:[Hemodynamic profile of patients with normal coronary cineangiography]. 261 88

Using 123I-omega-heptadecanoic acid (HDA) and 201Tl, respectively, myocardial fatty acid metabolism and perfusion were studied in 51 symptomatic patients with mitral valve prolapse (MVP) as diagnosed by ventriculography, and no evidence of coronary artery disease. Twelve subjects with normal coronary arteries and normal ventriculogram served as a control group for the evaluation of elimination kinetics of HDA. In the control group, the mean elimination half-life was 26.1 +/- 3.6 min, whereas the patients with MVP had a mean value of 25.0 +/- 6.4 min. In patients with MVP, a high incidence concerning abnormalities of accumulation and/or elimination of HDA occurred, namely accumulation defects in 31% and both prolonged and shortened elimination half-lives in 16% and 29%, respectively. Myocardial perfusion scintigraphy using 201Tl showed abnormalities in 76%. Correlations were found between decreased uptake of HDA and prolonged elimination half-life as well as defects by 201Tl, presumably due to ischemia based on small-vessel disease or abnormalities of cellular metabolism.
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PMID:Fatty acid metabolism in symptomatic patients with mitral valve prolapse but without coronary artery disease--comparison with 201Tl myocardial perfusion scintigraphy. 367 Oct 99

Eighty-eight consecutive patients referred to a neurosurgical Department (63 men and 25 women) aged from 14 to 68 years, with cerebral ischemia in the carotid territory were subjected to M-mode and two-dimensional echocardiography, carotid angiography and assessment of risk factors. There were 27 patients (average age 54 years) in whom carotid angiography demonstrated a probable source for the ischemia. Carotid angiography was normal in 51 of the remaining 61 (average age 39 years) while 10 revealed distant emboli. Although the incidence of "abnormal echocardiograms" was similar in the two groups (56% and 54% respectively) the spectrum of abnormalities were different. Only 5 (18%) of the 27 patients with abnormal angiograms had a potential cardiac source of emboli while 24 (39%) out of the remaining 61 patients had a potential cardiac source demonstrated at echocardiography. There was a high incidence of mitral valve prolapse (34%) in this latter group of patients. Mitral valve prolapse was not seen in the present series in patients with a probable carotid source on angiography.
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PMID:Frequency of echocardiographic abnormalities in patients with ischemia of the carotid territory--a preliminary report. 396 55

Therapeutic modalities for ventricular tachycardia include antiarrhythmic drugs, direct current cardioversion, electrical pacing and surgical intervention. Lidocaine, procainamide and bretylium are all capable of controlling recurrent ventricular tachycardia; bretylium has the advantage of also being antifibrillatory and of raising the threshold for ventricular fibrillation. Lidocaine and bretylium are available only in i.v. form. Procainamide is available in i.v. as well as oral form. Other oral antiarrhythmic agents include quinidine, disopyramide, beta-blockers such as propranolol and verapamil. The latter may be useful in ventricular arrhythmias induced by ischemia; of these, only beta-blockers appear to significantly raise the threshold for ventricular fibrillation. Control of ventricular ectopy does not always preclude ventricular tachycardia and ventricular fibrillation. In treating ventricular tachycardia, bretylium tosylate is generally given 5 to 10 mg/kg i.v. over 10 to 20 minutes. Given too rapidly, it may cause nausea and vomiting. Orthostatic hypotension, a common side effect, generally abates with continued use and may be ameliorated with tricyclic antidepressants such as protriptyline. Significant supine hypotension may be encountered in patients with acute myocardial infarction and may be managed with pressor agents or fluids, or both. The antiarrhythmic efficacy of bretylium was analyzed in 40 patients. Five etiologic groups were defined by cardiac catheterization: 19 patients had atherosclerotic heart disease, 6 had primary myocardial disease, 4 had mitral valve prolapse, 4 had rheumatic heart disease and 7 had miscellaneous or no heart disease. All patients had recurrent ventricular tachycardia (VT); 23 had ventricular fibrillation (VF) as well. Other antiarrhythmic agents had failed in 38 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Therapy of ventricular tachycardia. 646 97


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