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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Skin absorption of glyceryl trinitrate (GTN) has been recognized for a long time. The effect of GTN and a placebo ointment in prevention of chest pain has been assessed and compared by studying the exercise capacity in 17 patients with angina pectoris. The placebo cream was ineffective but the GTN ointment was found to have beneficial effect in relief of pain in 16 cases. This was established by the patients' capacity to exercise on a bicycle ergometer without chest pain. The beneficial effect was sustained for up to 3 hr in 12 patients. This preparation appears to act as a long-acting nitrate and may be valuable for patients in whom beta-blocking agents are ineffective or contra-indicated, and surgery is not feasible.
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PMID:Glyceryl trinitrate ointment in angina pectoris. 12 56

The pathogenesis of cardiac arrest in the absence of any apparent heart disease remains unclear. Based on the hypothesis that coronary spasm may be a cause of cardiac arrest in the absence of apparent heart disease, ergonovine testing and/or electrophysiologic studies (EPS) were performed to evaluate the cause of cardiac arrest. Fourteen patients resuscitated from cardiac arrest had no apparent heart disease. A spontaneous episode of angina with ST-segment elevation occurred in 4 patients while under observation. Ergonovine testing was performed in 9 patients, and coronary spasm was induced in 5. EPS were performed in 8 patients, including 3 patients with coronary spasm. No electrophysiologic abnormalities were found in the 3 patients with coronary spasm. Ventricular fibrillation was induced by programmed ventricular stimulation in 2 patients with documented ventricular fibrillation at the time of resuscitation. All but one of the patients with coronary spasm had chest pain preceding cardiac arrest or at least a history of chest pain at rest, while 4 of 5 patients without coronary spasm had no prodromal symptoms. Patients with coronary spasm had a good prognosis when treated with a Ca-antagonist and/or long-acting nitrate. In conclusion, coronary spasm is the most frequent cause of cardiac arrest in cardiac arrest survivors with no apparent heart disease. Ergonovine testing should be performed to evaluate the cause of cardiac arrest when patients have no apparent heart disease.
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PMID:High prevalence of coronary artery spasm in survivors of cardiac arrest with no apparent heart disease. 841 43

A patient is reported in whom exercise induced reversible ischemic left anterior fascicular block and far advanced right bundle branch block. Master's two step exercise test for pre-operative check-up revealed significant ST elevation in leads V1-5, negative U waves in leads V3-5 and fascicular blocks with retrosternal anginal chest pain. Long acting nitrate and nicorandil relieved the fascicular blocks.
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PMID:Intermittent anterior divisional block and far advanced right bundle branch block induced by vasospasm during exercise testing. 143 16

Treatment of patients with an esophageal source of chest pain remains a challenging problem. Although a variety of measures--including nitrates, anticholinergics, sedatives, calcium channel antagonists, esophageal dilation, and psychological reassurance--are available for the management of esophageal chest pain, none has emerged as the treatment of choice. Studies of nitrate preparations for the treatment of painful motility disorders are limited by a small number of patients and the lack of randomized, placebo-controlled investigations. The efficacy of anticholinergic drugs in hypercontractile esophageal motility disorders has not been reported. In the only prospective placebo-controlled trial using an anti-depressant, trazodone was superior to placebo in relieving symptoms in patients with a variety of esophageal motility disorders. Conflicting results have been described in placebo-controlled trials of the calcium channel antagonists nifedipine and diltiazem in patients with "nutcracker esophagus" or diffuse spasm. Information about the efficacy of verapamil and hydralazine is limited. Esophageal dilation has been useful in selected patients. For many patients, esophageal chest pain may be associated with gastroesophageal reflux. Treatment of these patients with nitrates, calcium channel antagonists, or anticholinergics may aggravate their reflux. The mechanisms of esophageal chest pain remain unknown. Recent studies have suggested that abnormal motility may not be the only factor associated with chest pain. An important number of patients have behavioral abnormalities, increased nociception, impaired coronary vasodilatory reserve, or a diffuse abnormality of smooth muscle. Research into rational therapy for chest pain patients should take into account the contribution of these other factors.
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PMID:Current medical therapy for esophageal motility disorders. 159 73

In this study, the effect of bradykinin on coronary flow in the isolated rat heart was significantly potentiated when cysteine or the sulfhydryl-containing converting enzyme inhibitors captopril and zofenoprilat were administered simultaneously. In contrast, the effect of concomitant administration of enalaprilat only slightly increased the effect of bradykinin on coronary flow. In nitrate-tolerant hearts of rats pretreated with isosorbide dinitrate (15 mg daily), the increase in coronary flow by nitroglycerin and bradykinin was significantly less when compared to control hearts. The effect of captopril was not affected by pretreatment. The involvement of endothelium-derived relaxing factor (EDRF) in the effect of captopril was apparent from experiments with L-arginine, the precursor of EDRF, and L-NMMA, the "false" precursor of EDRF. L-Arginine increased the effect of captopril, whereas L-NMMA showed a competitive antagonism for the effect of captopril on coronary flow in the isolated rat heart. Clinically, the effect of captopril was studied in 10 patients with stable, exercise-induced angina pectoris that had been treated for 3 weeks with slow-release isosorbide dinitrate (20 mg four times daily). At day 7, a baseline exercise test was obtained. Subsequently, patients with chest pain and at least 1-mm ST-segment depression on the ECG during exercise were included. They received on day 14 and 21 either captopril (25 mg) or placebo 1 h before exercise testing in a randomized, double-blind, crossover design. Captopril significantly improved the combined score of maximal ST-segment depression, maximal workload, and time to angina when compared to placebo. No differences in the pressure-rate index at rest and during exercise were seen. These results indicate that the sulfhydryl group of certain angiotensin converting enzyme inhibitors can potentiate their effect on the endogenous nitrovasodilator EDRF. In the clinical situation, this may lead to an improved exercise performance in patients with stable angina pectoris during chronic nitrate treatment, independent of its systemic vascular effects.
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PMID:Converting enzyme inhibitors and the role of the sulfhydryl group in the potentiation of exo- and endogenous nitrovasodilators. 172 Aug 43

We prospectively studied 69 consecutive patients hospitalized with a primary diagnosis of acute left ventricular failure so as to assess the impact of vasodilators on incidence and morbidity of acute symptomatic left ventricular failure. The determinants of duration of hospitalization, in-hospital mortality and symptomatic status 2 months after discharge were examined. There were 9 in-hospital deaths (13%), and survival at 60 days was 77%. Median duration of hospitalization was 9 days, and 33% of the surviving patients remained in New York Heart Association functional class III-IV 60 days subsequent to discharge. Of the patients, 49 (76%) had previously received treatment for left ventricular failure: 30 (61%) of these had received vasodilators, most commonly angiotensin converting enzyme inhibitors and nitrates. Ischaemic chest pain was present in 34 (49%) of the patients. Acute utilization of vasodilators (45% of patients) was largely limited to nitrate therapy associated with ischaemic chest pain (P less than 0.01). Multiple logistic regression revealed previous left ventricular failure, advanced age and hypokalaemia as significant correlates of prolonged hospitalization (greater than 9 days). Previous left ventricular failure was also predictive of persistent severe disability two months subsequent to discharge. No factor was a significant predictor of in-hospital death. Although preceding treatment with digoxin and incremental angiotensin converting enzyme inhibitor therapy tended to predict brief hospitalization, the parameter of acute ischaemia, other biochemical anomalies and modes of acute or chronic therapy were not significant correlates of any end point. We conclude that preceding disability, rather than mode of treatment, predicts an adverse outcome in acute left ventricular failure.
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PMID:Acute heart failure: determinants of outcome. 179 Oct 90

The patient was a 47 year-old man, who has been known to have effort angina since September 1989. His exercise stress ECG has revealed ST elevation in V2-V4 with maximum exercise. He experienced severe chest pain lasting for an hour on the way to his office in the early morning on November 16, 1989, and was admitted to our hospital. His ECG and laboratory findings indicated typical acute anteroseptal myocardial infarction, but the coronary arteriography (CAG) which was performed 7 hours after the onset showed no significant stenotic lesion. After administrating nitrate and calcium antagonist, he has had no attack of angina pectoris and his exercise stress test has revealed no ST-T changes on his ECG. 1 month later, while antianginal drugs were discontinued in order to perform an ergonovine stress test, the patient frequently complained of left anterior chest pain with remarkable ST elevation in precordial leads on his ECG. The CAG at chronic stage revealed that there was a 99% stenosis at Segment 6 of the left anterior descending artery (LAD) which was supplied with good collateral flow from the right coronary artery. The LAD was completely occluded at Segment 6 after intracoronary administration of ergonovine maleate 0.005 mg to the left coronary artery. After the intracoronary infusion of isosorbide dinitrate, there was no significant stenosis seen in the LAD except the minimum wall irregularity at Segment 6. These findings suggested that coronary spasm might play a major role of the occurrence of acute myocardial infarction in this case.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of acute myocardial infarction due to coronary spasm]. 191 Feb 3

Questionnaires were sent to 61 Norwegian hospitals treating acute coronary syndromes, and 90% replied. Thrombolytic drug treatment is now the routine when the history of chest pain is short and ischemia appears in ECG. Use of glyceryl trinitrate and beta blocking drugs varies considerably, as does the use of oral anticoagulants and platelet inhibitors. Practice also varies in unstable angina. However, a combination of aspirin, intravenous nitrate, and betablockers is common. Several treatment regimens have an uncertain scientific foundation. The varying practice reflects international scientific debate.
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PMID:[Drug therapy of acute myocardial infarction and unstable coronary syndrome]. 197 6

Variant angina is frequently accompanied by serious arrhythmias. The aim of our study was to verify the role of early nitrate administration in prevention of these arrhythmias. We compared arrhythmias occurrence in the course of 104 episodes of chest pain with ST elevation during which short acting nitrate was not administered (group I) and 114 episodes with administration of 2.5 mg isosorbit dinitrate (ISDN) spray (group II). Serious arrhythmias occurred in spontaneous episodes in 41 cases (39%) and in episodes with early ISDN administration in 15 cases (13%). Particular types of arrhythmias were as follows: ventricular premature beats in group I 32 and in group II only 12, supraventricular premature beats 4, resp. 3, A-V block IInd or IIIrd degree 5, resp. 1, ventricular tachycardia 5, resp. 0, junctional bradycardia 0, resp. 1. In conclusion, early administration of nitrates at the very beginning of stenocardia during coronary spasm can prevent or reduce the occurrence of serious arrhythmias.
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PMID:[Decreasing the occurrence of arrhythmia during coronary spasm by the early administration of nitrates]. 226 24

In differentiating the various etiologies of acute chest pain syndromes, the clinician is faced with identifying life-threatening situations. This article has presented a diagnostic approach for establishing the cardiovascular and noncardiovascular etiologies of acute chest pain syndromes. Cardiovascular etiologies must be identified early upon presentation in order to minimize morbidity and mortality. Myocardial ischemia and particularly necrosis is time dependent: early intervention preserves myocardium, particularly when initiating thrombolytic therapy. Aortic valvular disease, particularly critical aortic stenosis, if unrecognized, can precipitate rapid patient deterioration if inappropriately treated with nitrate therapy for presumed ischemic disease. Aortic dissection, if not properly diagnosed, can progress to stroke, MI, paralysis, and death. Noncardiovascular etiologies are similarly complex but often have less potential for life-threatening consequences. In identifying gastrointestinal bleeding, a careful rectal exam may be safely performed even in the setting of MI. A tension pneumothorax can suddenly compromise vascular return and progress to sudden death if unrecognized. Finally, chest wall symptoms, though seldom life-threatening, can be debilitating to the patient and often respond to anti-inflammatory therapy. In conclusion, the goals of this article were to present a step-wise approach to the diagnosis and management of an often complex presentation. By systematically approaching these patients with a thorough understanding of etiologies, diagnostic options, and therapeutic considerations, both physician anxiety as well as patient complications will be greatly diminished.
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PMID:Management of acute chest pain syndrome. 267 88


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