Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A retrospective study was conducted of 101 hospitalized patients who had one or more episodes of syncope. The etiology of syncope was established with relative ease in 61% of these patients. History and physical examination revealed the cause in 34%, resting ECG in 11% and 24-h ECG monitoring in 16%. Additional tests (electroencephalograms, Doppler studies of the cervical arteries, computerized tomography of the brain, ultrasonography of the heart and cardiac catheterization) either were noncontributory or did not contribute to confirmed diagnoses already established by other means. Cardiac causes were responsible for the syncope in 34% and noncardiac causes in 27%. Comparison between diagnosed and undiagnosed patients revealed no significant differences with respect to age, number of syncopal episodes or presence of hypertension or diabetes. There were, however, significantly more women, and a lower frequency of ischemic heart disease and other associated diseases in the undiagnosed group. It is concluded that all patients with syncope should undergo ambulatory ECG and 24-h ECG monitoring, and that hospitalization should be reserved for patients whose clinical condition requires admission or when further investigation is necessary.
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PMID:Syncope: a retrospective study of 101 hospitalized patients. 391 52

The clinical and electrophysiological features and the natural history of median intra-His block with a normal resting electrocardiogram were studied: 11 patients had a fixed split H1-H2 potential with a spontaneous or induced block between H1 and H2. The patients (5 men and 6 women) were aged 17 to 70 years (average 53 years). Associated pathology included 2 cases of aortic stenosis (1 severe), 1 case of ischaemic heart disease (effort angina), 1 case of mitral valve prolapse and 2 cases of hypertension. The presenting symptoms were syncope (4 cases), dizziness (2 cases), effort angina (1 case) and tiredness (3 cases); 1 patient was asymptomatic. Holter monitoring (24 hours) was performed in 8 patients and s-owed paroxysmal conduction defects in 6 cases; 4 Mobitz II 2nd degree AV block, 1 3rd degree AV block with narrow QRS complexes and 1 case of blocked atrial extrasystoles at coupling intervals longer than 480 ms and sinus cycle lengths of over 800 ms. Exercise testing by bicycle ergometry (4 patients) was normal in 1 case and revealed Mobitz II 2nd degree AV block in 3 cases. Baseline electrophysiological studies showed an A-H1 interval ranging from 60 to 100 ms (average 78 ms), a H1-H2 interval of 20 to 40 ms (average 31 ms) and a H2-V interval of 30 to 50 ms (average 32 ms). Block between H1 and H2 was observed: "spontaneously" during electrophysiological investigation in 6 cases, after IV atropine in 1 case, during overdrive atrial pacing at rates slower than 150/min in 7 cases, after atrial extrastimulus with a functional intra-His refractory period of over 420 ms in 7 cases, after ajmaline in 3 of the 4 cases in which this test was performed. A cardiac pacemaker was implanted in 10 patients in whom the initial symptoms have all regressed; the remaining patient considered to be "epileptic" had another syncopal attack under therapy and was finally paced. This series demonstrates that the diagnosis of median intra-His block depends on precise electrophysiological criteria and should be looked for even when the presenting symptoms are atypical; some of our patients complained only of tiredness. The value of Holter monitoring and careful endocavitary investigation is emphasised. Median intra-His block should be distinguished from longitudinal and functional His bundle dissociation.
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PMID:[Clinical and electrophysiological aspects of median intra-His bundle block with normal electrocardiogram at rest]. 392 29

Encainide is effective in suppressing non-life-threatening ventricular arrhythmias; however, inconsistent results have been noted in patients with more serious ventricular arrhythmias. Thirty-seven patients with drug-resistant ventricular arrhythmias were studied. Patients in group I (n = 11) has sustained ventricular tachycardia and those in group II (n = 26) had nonsustained ventricular arrhythmias. In group I, 8 patients had remote myocardial infarction, congestive heart failure and sustained ventricular tachycardia requiring repeated cardioversion (group Ia). None of these patients responded to encainide treatment, but 6 did have an antiarrhythmic response (complete in 3 and only partial in 3) to other investigational antiarrhythmic agents. Three patients in group I, all without ischemic heart disease (group Ib), had an excellent antiarrhythmic response to encainide, as did 21 of 26 patients in group II. In 4 of 5 patients in group II who did not respond, the dosage was limited due to the development of sinus pauses, atrioventricular block or bundle branch block, and in 3 of these 4 patients preexisting conduction disease was evident (PR longer than 0.2 second or QRS longer than 0.12 second). Diplopia occurred while taking the maximal oral dosage in the fifth patient. At 21.5 months of follow-up, 14 of the original 24 patients who responded to encainide continue to receive it; 3 have died (all due to natural progression of left ventricular dysfunction) and encainide was discontinued in 7: in 2 because of syncope, in 2 because of new-onset atrial fibrillation, in 1 patient because of exercise-induced polymorphic ventricular tachycardia, in 1 because of diplopia and in 1 because of skin exanthem.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Spectrum of antiarrhythmic response to encainide. 393 19

Six patients with complex partial seizures in whom the first or most prominent manifestation was cardiovascular are described. "Anginal pain," which was usually atypical, developed in five patients (mean age 34), although three were admitted to coronary care units; sinus tachycardia developed in one, sinus bradycardia leading to syncope developed in one, and a cluster of symptoms suggestive of pheochromocytoma developed in one. The causal relationship between complex partial seizures and these symptoms is based on clinical history, electrodiagnostic studies indicating epilepsy (in five of six cases) without changes of myocardial ischemia, and response to anticonvulsant but not antianginal medications. Complex partial seizures that present with cardiovascular and other visceral symptoms represent an underdiagnosed, treatable disorder.
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PMID:Cardiac manifestations of complex partial seizures. 394 34

We present a patient with a permanent ventricular pacemaker who was investigated for episodes of chest pain associated with syncope. Ambulatory electrocardiographic monitoring showed essentially paced rhythm. ST segment elevation of the paced beats was observed during spontaneous chest pain, but the significance of this finding was initially unclear in the context of the abnormal repolarization associated intrinsically with paced rhythm. At angiography, coronary spasm was demonstrated after ergonovine, and this was associated with ST segment elevation during paced rhythm and with chest pain. We conclude that ST segment elevation may indicate myocardial ischemia even when observed in the face of abnormal repolarization associated with paced rhythm.
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PMID:Electrocardiographic recognition of variant angina during permanent pacing. 618 30

A middle-aged Coloured man had a 6-year history of chest pain induced by effort and also experienced at rest. Quite dramatic episodes of associated arrhythmias, specifically 'torsade de pointes' (atypical ventricular tachycardia) and syncope were experienced by the patient, despite the use of numerous anti-arrhythmic and anti-anginal agents. Transmural anteroseptal and non-transmural anterolateral myocardial infarctions were documented in the presence of a normal left coronary artery (LCA). Severe reversible vasospasm of the right coronary artery (RCA) was provoked with the use of ergonovine (ergometrine) maleate at cardiac catheterization. It is postulated that the cause of the previous myocardial infarctions was significant vasospasm of the LCA branches, and that he was subject to multiple coronary vasospasm, as was highlighted by the visualization of spasm superimposed on atheromatous plaque within the RCA. Furthermore, it is strongly suggested that the potentially lethal ventricular arrhythmias, including 'torsade de pointes', were a direct result of coronary vasospasm, which in turn gave rise to his presyncope and syncope attacks. No evidence of sinoatrial node disease could be found. The only risk factor for ischaemic heart disease which applied in his case was heavy cigarette smoking. Control of his disabling symptoms seems to have been achieved by the use of maintenance nifedipine (a calcium-blocking agent), long-acting nitrates (isosorbide dinitrate) and quinidine gluconate, confirming the probable vasospastic aetiology of the 'torsade de pointes'. At no stage was there dangerous prolongation of the QT interval, an oft-quoted prerequisite for this arrhythmia. Some of the more important aspects of coronary vasospasm are discussed; as far as I am aware this is the first patient documented in the literature with 'torsade de pointes' associated with angiographically demonstrated coronary artery spasm.
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PMID:Multiple coronary vasospasm: a cause of repeated myocardial infarction and symptomatic 'torsade de pointes' (atypical ventricular tachycardia). A case presentation and review. 633 53

Syncope, palpitations, ventricular tachycardia, and electrocardiographic changes of acute myocardial ischemia in a 19-year-old woman resulted from significant narrowing of the left main coronary artery and its ostium, producing high-grade obstruction to flow as documented by selective coronary arteriography. Because of these findings and markedly positive results of cardiovascular stress testing, surgical treatment by aortocoronary artery saphenous vein bypass grafting to the left anterior descending artery was carried out. Four years postoperatively, the patient was asymptomatic, and there are no abnormal findings on cardiovascular stress testing.
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PMID:Left main coronary artery disease in a 19-year-old woman. Treatment by saphenous vein grafting. 660 74

Coronary artery spasm may produce angina, major arrhythmias, syncope, myocardial infarction, and death in patients with normal or nearly normal coronary arteriograms. The clinical picture in patients with symptomatic coronary artery spasm is characterized by: (1) predominant angina at rest, with little or no exertional angina; (2) changes of myocardial ischemia, especially ST segment elevation, on the electrocardiogram during pain: and (3) major arrhythmias and syncope during angina. A complete electrocardiogram during pain, or at least a Holter monitor recording, is important in establishing a diagnosis. The ergonovine maleate provocative test is a reliable method of establishing the diagnosis, but it is associated with some risks. Calcium flux antagonists are more effective than nitrates or beta blockers in the treatment of coronary spasm. Coronary bypass surgery is generally ineffective in the treatment of coronary spasm unless the spasm is superimposed on a fixed severe coronary obstruction.
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PMID:Coronary artery spasm: recognition and treatment. 680 45

The concept of depressor reflexes originating in the heart was introduced by von Bezold in 1867 and was later revived by Jarisch. The Bezold-Jarisch reflex originates in cardiac sensory receptors with nonmyelinated vagal afferent pathways. The left ventricle, particularly the inferoposterior wall, is a principal location for these sensory receptors. Stimulation of these inhibitory cardiac receptors by stretch, chemical substances or drugs increases parasympathetic activity and inhibits sympathetic activity. These effects promote reflex bradycardia, vasodilation and hypotension (Bezold-Jarisch reflex) and also modulate renin release and vasopressin secretion. Conversely, decreases in the activity of these inhibitory sensory receptors reflexly increase sympathetic activity, vascular resistance, plasma renin activity and vasopressin. Long regarded as pharmacologic curiosities, it is now clear that reflexes originating in these inhibitory cardiac sensory receptors are important to the pathophysiology of many cardiovascular disorders. This paper reviews the role of inhibitory cardiac sensory receptors in several clinical states including 1) bradycardia, hypotension and gastrointestinal disorders with inferoposterior myocardial ischemia and infarction, 2) bradycardia and hypotension during coronary arteriography, 3) exertional syncope in aortic stenosis, 4) vasovagal syncope, 5) neurohumoral excitation in chronic heart failure, and 6) the therapeutic effects of digitalis.
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PMID:The Bezold-Jarisch reflex revisited: clinical implications of inhibitory reflexes originating in the heart. 682 48

We performed signal-averaged electrocardiography and 24-h ambulatory electrocardiographic monitoring in 53 patients with myotonic dystrophy to determine the incidence and clinical significance of ventricular late potentials. Patients were followed up for a mean period of 31 +/- 17 months (range 11-68 months). At entry, none of the patients had bundle branch block on 12-lead electrocardiogram and none had wall motion abnormalities on routine echocardiogram. Also, no patient had history of syncope or clinical evidence of ischemic heart disease or a documented sustained ventricular tachycardia. A group of 47 healthy subjects matched for age and sex also underwent signal-averaged electrocardiography for comparison with the patient group. Late potentials were diagnosed in the presence of at least two of the following measures: duration of the filtered QRS > 114 ms, root-mean-square voltage of the terminal 40 ms of the filtered QRS < 20 microV, and duration of the low-amplitude (< 40 microV) signals of terminal filtered QRS > 38 ms. Late potentials were more frequent in patients than in controls: 18 of the 53 patients (34%) showed late potentials compared with four of the 47 controls (8.5%) (P < 0.01). In 45 patients (85%) no ventricular ectopy (40 cases) or infrequent premature ventricular complexes (five cases) were detected on Holter monitoring. Complex ventricular arrhythmias were traced in the remaining eight patients. These were six of the 18 patients with, and two of the 45 patients without late potentials (33% vs. 6%, respectively; P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Signal-averaged electrocardiography in myotonic dystrophy. 755 65


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