Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 34-year-old woman with mitral valve prolapse, frequent ventricular dysrhythmias, and chest pain was studied. Surface electrocardiograms demonstrated short PR and prolonged Q-T intervals. A-V nodal conduction times during atrial pacing were characteristic of A-V nodal bypass tract function. The case is thus interpreted to be one of overlap between three syndromes known to predispose to cardiac dysrhythmias, i.e., mitral valve prolapse, Lown-Ganong-Levine syndrome, and prolonged Q-T interval syndrome.
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PMID:Ventricular pre-excitation and prolonged Q-T interval syndromes in a patient with mitral valve prolapse. 69 73

Two hundred consecutive patients with a history of chest pain undergoing cardiac catheterization, coronary angiography and atrial pacing have been analyzed to assess the clinical significance of Mobitz I atrioventricular (A-V) block developing with the stress of atrial pacing. Of 160 patients with coronary artery disease, 26 (16%) developed Mobitz I A-V block at rates below 140 beats/min. Eighteen of these 26 patients (69%) had electrocardiographic evidence of old inferior wall myocardial infarction, compared to only 34 of the remaining 134 patients (29%) (P = less than 0.01). During the mean follow-up of 29.5 months (range 18-50 months) none of the 26 patients has developed spontaneous second or third degree A-V block. Twenty-three of the 26 patients had an exercise test within one week of the pacing study. No A-V block was noticed during or immediately following exercise, although the mean heart rate attained during exercise was higher than the mean pacing rate at which the A-V block occurred (136 +/- 5 vs 122 +/- 3, P = less than 0.01). Eighteen of these 23 achieved heart rates equal to or higher than the pacing rate at which A-V block developed. Nineteen (83%) shortened their P-R interval during exercise and 4 (17%) did not change the P-R length. Although atrial pacing-induced Mobitz I A-V block may indicate a latent A-V nodal conduction abnormality in some cases, its demonstration does not necessarily predict the occurrence of spontaneous advanced A-V block. Exercise should not be restricted in these patients on the basis of such a finding during a pacing study.
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PMID:The clinical significance of atrial pacing-induced Mobitz I atrioventricular block in patients with coronary artery disease. 83 32

Few disorders ever provoked more interest and controversy than mitral valve prolapse (MVP). Past echocardiographic over-diagnosis led to it becoming a whipping boy for otherwise unexplained chest pain, palpitation, arrhythmias and emboli. Surgical centres reported a high incidence of endocarditis and severe regurgitation. Most investigators who have studied the prevalence of arrhythmias in MVP have concluded that they are more common in this syndrome than in the general population and that there is a causal rather than a fortuitous relationship. However, the prevalence of arrhythmias in reported studies is probably higher than in unselected MVP patients. Multiple ventricular premature beats, ventricular tachycardia and sudden death have been reported. Suggested mechanisms have included a focal cardiomyopathy with incoordinate contraction and relaxation, QRS dispersion, a long QT, traction on papillary muscles by prolapsed leaflets, interference with the blood supply of the papillary muscles, stimulation of the endocardium by the chordae and diastolic depolarisation of muscle fibres in redundant leaflets with triggered repetitive automaticity. MVP has been associated with pre-excitation giving rise to atrioventricular re-entry tachycardia. Autonomic dysfunction and a hyperadrenergic state has been claimed and this may also be responsible for supraventricular arrhythmias including atrioventricular nodal re-entry tachycardia, flutter and fibrillation. Electrophysiological studies have yielded contradictory results which may be due to the heterogeneity of the patients studied and variability of the mechanisms. Whatever the true prevalence, arrhythmias in MVP are usually benign. Syncope and sudden death are rare. Anti-arrhythmic therapy is only warranted in patients with frequent and distressing symptoms shown to be due to the arrhythmias or when arrhythmias are judged potentially life threatening.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mitral valve palpitations. 144 39

Electrophysiologic studies have shown that intravenous magnesium sulfate prolongs atrioventricular (AV) nodal conduction and refractoriness and thus could play a role in the management of patients with paroxysmal AV reentrant supraventricular tachycardia (SVT). The present study evaluates the clinical and electrophysiologic effects of intravenous magnesium sulfate in patients with SVT and compares them with those of adenosine triphosphate (ATP), one of the most potent drugs in the treatment of this arrhythmia. Patients with inducible sustained SVT were treated with ATP (10 or 20 mg) and magnesium sulfate (2 g over 15 seconds) during electrophysiologic study. If the tachycardia failed to terminate by the sixth minute, an additional 2 g dose of magnesium was given. ATP (10 or 20 mg) was significantly better than magnesium for terminating induced tachycardias (14 of 14 vs 6 of 14, p less than 0.0001). Arrhythmia termination with ATP was due to anterograde AV nodal blockade in all but 1 patient who developed retrograde block over an accessory pathway with decremental conduction. Arrhythmia termination by magnesium was due to retrograde block over an accessory pathway in 3 patients (including the patient with accessory pathway exhibiting decremental conduction), anterograde AV nodal conduction block in 2 patients and premature ventricular complexes in 1 patient. During induced tachycardias, only AH intervals were prolonged by ATP, whereas magnesium significantly prolonged AH and QRS intervals. Short-lasting side effects (chest pain, flushing, nausea) occurred after both drugs were administered but were more severe after magnesium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical and electrophysiologic effects of magnesium sulfate on paroxysmal supraventricular tachycardia and comparison with adenosine triphosphate. 152 41

Adenosine (adenine riboside), administered either as the free base or as the 5'-triphosphate (ATP) by rapid intravenous bolus, depresses atrioventricular (AV) nodal conduction, resulting in transient AV block. Adenosine is the active agent and ATP is rapidly converted to adenosine after exogenous administration. By blocking the anterograde AV nodal limb of a re-entrant circuit, adenosine 6 to 12 mg (or ATP 10 to 20 mg) converts almost all episodes of paroxysmal supraventricular tachycardia (PSVT) involving the AV node within 30 seconds of administration. This is at least equivalent in efficacy to verapamil in adults, and superior to lanatoside C in children, with a considerably more rapid onset of action. Furthermore, if a dose of adenosine is ineffective, the exceptionally short plasma half-life of the adenyl nucleosides (less than 10 sec) allows rapid upward dosage titration until PSVT is terminated. Because the induced conduction block primarily affects the AV node, adenosine is a useful diagnostic tool in patients with broad or narrow QRS complex tachycardia; it terminates arrhythmias dependent on the AV node, unmasks other supraventricular mechanisms during transient AV block, but almost always has no effect on ventricular tachycardia. Noncardiac adverse effects, i.e. flushing, dyspnoea and chest pain, may occur during acute arrhythmia termination or diagnosis with adenosine, and arrhythmias may develop; however, these effects are usually transient (lasting less than 1 minute). Adenosine has also been used to induce coronary vasodilation in patients undergoing thallium-201 single photon emission computed tomography (201Tl SPECT), 2-dimensional echocardiography or positron emission tomography to evaluate suspected coronary artery disease. Intravenous infusion of adenosine 140 micrograms/kg/min for 6 minutes was generally associated with only mild adverse effects. These usually resolved within 1 to 2 minutes of discontinuing adenosine, although occasionally patients required aminophylline and/or nitroglycerin (glyceryl trinitrate). Diagnoses based on the results of scintigraphy were of a sensitivity, specificity and predictive accuracy comparable to those achieved with exercise- or dipyridamole-201Tl SPECT. Adenosine is therefore particularly suitable for the diagnosis of tachycardias and the acute management of PSVT involving the AV node in all age groups, without the risks of cardiac arrest and hypotension associated with verapamil. Furthermore, intravenous adenosine infusion may be used to induce coronary vasodilation in patients unable to perform exercise stress tests for 201Tl scintigraphy, and is well tolerated.
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PMID:Adenosine. An evaluation of its use in cardiac diagnostic procedures, and in the treatment of paroxysmal supraventricular tachycardia. 171 62

The Authors describe a case of a patient showing, during an episode of chest pain, an ecg-pattern of wide and tall "Q" wave simulating inferior myocardial infarction. In fact, a further ecg recorded during sinus rhythm denotes that the "Q" wave was a retrograde P wave generated by a nodal rhythm. The other known causes of "pseudonecrosis" are discussed.
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PMID:[Pseudonecrosis waves: simulation of myocardial necrosis by retrograde P wave]. 180 40

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of adenosine in the treatment of episodes of paroxysmal supraventricular trachycardia (PSVT) are reviewed. Adenosine is an endogenous adenine nucleoside that markedly decreases heart rate and prolongs atrioventricular (AV)-nodal conduction. Adenosine is rapidly cleared from plasma by the cellular elements of the blood and by vascular endothelial cells and subjected to enzymatic metabolism. The drug has a half-life of 0.6 to 10 seconds. In noncomparative clinical trials, adenosine terminated 85% to 100% of induced or spontaneous episodes of PSVT involving the AV node in the reentrant circuit. In patients with arrhythmias that do not involve the AV node in the reentrant circuit, adenosine produces AV block and does not restore sinus rhythm. Prospective, randomized trials comparing adenosine with verapamil in adults have not yet been performed. The adverse effects of adenosine include flushing, dyspnea, headache, cough, chest pain, sinus bradycardia, atrial fibrillation, ventricular arrhythmias, and various degrees of AV block. Because of the short half-life of adenosine, these effects are transient and well tolerated. The initial dose of adenosine in treating acute PSVT is 6 mg given by rapid i.v. bolus injection, followed in one to two minutes by up to two additional 12-mg boluses if necessary. Adenosine has been found to be effective in terminating PSVT and thus offers an alternative to verapamil. Prospective, randomized trials comparing adenosine with verapamil are needed to definitively establish adenosine's role in the therapy of PSVT.
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PMID:Adenosine in the episodic treatment of paroxysmal supraventricular tachycardia. 218 71

The diagnostic and therapeutic potential of intravenous adenosine was studied in 64 patients during 92 episodes of regular sustained tachycardia. In 40 patients who had narrow complex tachycardias (QRS less than 0.12 s) adenosine (2.5-25 mg) restored sinus rhythm in 25 with junctional tachycardias (46 of 48 episodes) and produced atrioventricular block to reveal atrial or sinus tachycardia in 15. In 24 patients with broad complex tachycardias (QRS greater than or equal to 0.12 s) adenosine terminated the tachycardias in six patients and revealed atrial or sinus arrhythmias in four. The tachycardias persisted in 14 patients despite doses up to 20 mg, but adenosine allowed the diagnosis of ventricular tachycardia with retrograde atrial activation in two patients by producing transient ventriculoatrial dissociation. Diagnosis based on adenosine induced atrioventricular nodal block was correct in all patients with narrow complex tachycardias and in 92% of those with broad complex tachycardias, compared with correct electrocardiographic diagnoses in 90% and 75% respectively. Adenosine gave diagnostic information additional to the electrocardiogram in 25%. The response to adenosine in broad complex tachycardias identified those of supraventricular origin with 90% sensitivity, 93% specificity, and 92% predictive accuracy. Adenosine restored sinus rhythm in all patients with junctional reentrant tachycardias, but in 10 (35%) the arrhythmias recurred within two minutes. Symptomatic side effects (dyspnoea, chest pain, flushing, headache) were reported by 40 (63%) patients and, although transient, were severe in 23 (36%). There were ventricular pauses of over 2 s in 16% of patients, the longest pause being 6.1 s. Adenosine is of value in the diagnosis and treatment of narrow and broad complex tachycardias, but its use is limited by symptomatic side effects, a tenfold range in minimal effective dosage, occasional action at sites other than the atrioventricular node, and early recurrence or arrhythmia.
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PMID:Value and limitations of adenosine in the diagnosis and treatment of narrow and broad complex tachycardias. 278 11

Seven of 214 patients (3%) with acute myocardial infarction (120 inferior and 94 anterior) developed atrial fibrillation within 3 hr of the onset of chest pain. All seven patients had an inferior infarction and in all seven the left circumflex artery was occluded proximal to the origin of its left atrial circumflex branch. In five patients this occlusion was acute and was the cause of inferior infarction and in the remaining two patients the occlusion was old and the inferior infarction was due to an acute occlusion of the right coronary artery that also supplied extensive collaterals to the previously occluded left circumflex artery. All seven patients also had impaired perfusion to the atrioventricular nodal artery, as evidenced by total occlusion proximal to its origin or by stenosis proximal to its origin associated with second- or third-degree atrioventricular block. In contrast, early atrial fibrillation did not occur in any of the 18 patients with inferior myocardial infarction due to acute occlusion of the distal left circumflex artery or in any of the five patients with inferior infarction due to acute occlusion of the proximal left circumflex artery if perfusion to the atrioventricular nodal artery was not impaired. Early atrial fibrillation did not occur in any of the 90 patients with inferior infarction due to acute occlusion of the right coronary artery, including 12 patients with occlusion proximal to the sinus nodal artery, but without coexistent occlusion of the left circumflex artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early atrial fibrillation during evolving myocardial infarction: a consequence of impaired left atrial perfusion. 379

In 67 consecutive patients with inferior wall acute myocardial infarction (AMI), 99m-technetium pyrophosphate scintigraphy was performed 36 to 72 hours after the onset of chest pain to detect right ventricular (RV) involvement. All patients were continuously monitored during at least 3 days to detect rhythm and conduction disturbances. In 29 patients RV involvement was diagnosed by scintigraphy. None of these 29 patients showed clinical signs of right-sided heart failure. Fourteen of the 19 patients showing atrioventricular (AV) nodal condution disturbances in the setting of inferior AMI also had RV involvement. Therefore, the incidence of high-degree AV nodal block in patients with RV involvement (14 of 29 patients) was 48% compared to only 13% (5 of 38) in patients with inferior AMI without RV involvement.
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PMID:Right ventricular involvement with acute inferior wall myocardial infarction identifies high risk of developing atrioventricular nodal conduction disturbances. 632 59


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