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)

Emergency triage and therapeutic decisions using the recently developed whole blood rapid troponin T test were evaluated and compared with conventional electrocardiographic (ECG) diagnosis in a total of 155 patients with chest pain who visited 16 emergency outpatient clinics in the Tokyo metropolitan area. Thirty-seven patients (23.9%) had a final diagnosis of acute myocardial infarction or high-risk unstable angina requiring emergency coronary intervention and these events were defined as acute coronary syndrome. Diagnostic values using the second-generation rapid troponin T test were evaluated according to 3 time-windows in 85 patients. The sensitivity of the test was 10% for patients assessed within 3 h after the onset, 62.5% for 3-6 h after, and 75% for more than 6h, whereas conventional ECG diagnosis had 100% sensitivity at any time-window. In contrast, the specificity of the rapid troponin T test was 100%, 100%, and 97.4%, whereas that of conventional ECG diagnosis was 25%, 57.1%, and 42.2%, respectively for the 3 time-windows. The positive predictive value of ECG diagnosis was inferior to the rapid troponin T test, which reflected the prudent attitude of physicians taking ECG decisions as positive when myocardial ischemia was suspected. The diagnostic efficacy of the rapid troponin T test was remarkable in patients with the non-ST elevation type of acute coronary syndrome. A questionnaire survey on therapeutic decisions revealed that only 10% of Tokyo outpatient institutes performed prehospital thrombolytic therapy, 30-33% administered aspirin or nitrate, and 16.7% gave heparin. The rapid troponin T test is extremely useful for cardiac emergency triage and therapeutic decision making. There is a requirement for practical guidelines for the primary therapeutic decisions for patients with suspicious acute coronary syndrome.
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PMID:Cardiac emergency triage and therapeutic decisions using whole blood rapid troponin T test for patients with suspicious acute coronary syndrome. 1134 47

The authors report on the case of a 61 year-old female patient who was repeatedly taken to hospital because of chest pain and temporary loss of consciousness. During her hospitalization there was no ST elevation on the ECG, sinus bradycardia, other times atrial fibrillation was detected. The diagnosis was made by Holter monitoring three years after the onset of complaints. At this time chest pain set in after midnight, which was followed by loss of consciousness. Significant ST elevation and IIIrd degree AV block were detected. The coronarography showed non-significant coronary stenosis. According to the vasospastic patomechanism nitrate, calcium antagonist and acetylsalicylic acid therapy was administered and because of the complete AV block leading to syncope a VVI, M pacemaker was implanted. During the two years passed since the implantation of the pacemaker the patient had chest pain only once and it was not accompanied by syncope.
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PMID:[Prinzmetal angina pectoris associated with 3rd degree atrioventricular block]. 1157 52

Nicorandil, a hybrid nitrate and ATP-sensitive potassium channel opener, has had a preconditioning effect in some coronary angioplasty studies. The present study investigated whether the cardioprotective effects of nicorandil involve coronary collateral function. Thirty-two patients with stable angina pectoris were randomized to receive a 1-min intravenous infusion of nicorandil (100 microg/kg) or normal saline. Five minutes later they underwent three 2-min balloon inflations 5-min apart. The maximum ST-segment elevation (deltaSTmax), the sum of ST-segment elevations in all leads (sigmaST), and the chest pain score were determined at the end of each balloon inflation. The collateral flow index (CFI) was derived from simultaneous measurement of the mean aortic pressure and the coronary wedge pressure obtained from a pressure guidewire during balloon inflation. The deltaSTmax, sigmaST, and chest pain score decreased progressively during the 3 sequential balloon inflations in both groups, and the deltaSTmax and sigmaST were less in the nicorandil group than in the control group during each inflation. The CFI did not change during the 3 inflations in either group and was similar in the 2 groups during each inflation. In conclusion, pretreatment with intravenous nicorandil enhances myocardial tolerance to ischemia without progressive collateral recruitment during coronary angioplasty.
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PMID:Nicorandil enhances myocardial tolerance to ischemia without progressive collateral recruitment during coronary angioplasty. 1195 43

Cardiotoxicity is an uncommon adverse effect of 5-fluorouracil (5-FU). Coronary artery spasm has been postulated to be involved in the mechanism of this incident Patients may present with angina, myocardial infarction, arrhythmias and/or even sudden death. When the drug is readministered, there is a high risk of relapse. The underlying mechanisms of cardiotoxicity are not yet fully understood, although coronary vasospasm may be responsible. We report one woman receiving 5-fluorouracil therapy with typical chest pain and electrocardiographic changes consistent with acute coronary syndrome. A resolving pain and normalisation of ECG changes with nitrate therapy and normal coronary arteries indicate that this incident was about a coronary spasm caused by 5-FU.
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PMID:A case of coronary spasm induced by 5-fluorouracil. 1240 79

On October 12, 1998, the Nobel Assembly awarded the Nobel Prize in Medicine and Physiology to scientists Robert Furchgott, Louis Ignarro, and Ferid Murad for their discoveries concerning nitric oxide as a signalling molecule in the cardiovascular system. In contrast with the short research history of the enzymatic synthesis of NO, the introduction of nitrate-containing compounds for medicinal purposes marked its 150th anniversary in 1997. Glyceryl trinitrate (nitroglycerin; GTN) is the first compound of this category. Alfred Nobel (the founder of Nobel Prize) himself had suffered from angina pectoris and was prescribed nitroglycerin for his chest pain. Almost a century later, research in the NO field has dramatically extended and the role of NO in physiology and pathology has been extensively studied. The steady-state concentration and the biological effects of NO are critically determined not only by its rate of formation, but also by its rate of decomposition. Biotransformation of NO and its related N-oxides occurs via different metabolic routes within the body and presents another attractive field for our research as well as for the venture of drug discovery.
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PMID:Nitric oxide (NO)--biogeneration, regulation, and relevance to human diseases. 1245 75

Two brothers had familial hypertrophic cardiomyopathy and vasospastic angina pectoris concurrently. Their family history showed that one of their sisters had hypertrophic cardiomyopathy and another brother died suddenly at age 52. The clinical diagnosis of hypertrophic cardiomyopathy was confirmed by an echocardiogram and left ventriculography. They had typical chest pain at rest, and a significant vasospasm of coronary arteries with chest pain and obvious ST-T changes in the electrocardiograms was provoked by intracoronary injection of acetylcholine in both patients. The administration of a calcium antagonist and nitrate was effective for ameliorating chest pain with no cardiovascular events during the follow up period of more than 3 years. Although underlying pathophysiologic abnormalities of familial hypertrophic cardiomyopathy and vasospastic angina pectoris are considered to be transmitted genetically, the genetic backgrounds of these cases remain to be clarified.
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PMID:Coexistence of familial hypertrophic cardiomyopathy and vasospastic angina pectoris in two brothers. 1458 59

Erectile dysfunction (ED) is often a marker for serious underlying cardiovascular disease (CVD), and cardiologists are increasingly involved in the care of men with ED. It is important to ask specifically about ED when evaluating men with CVD, since they may be embarrassed to volunteer this information. During the clinical workup, it is also important to check for contributing factors to ED such as diabetes, depression, stress, alcohol abuse, and cardiovascular risk factors. Patients should be advised that many treatment options are available for ED, including the phosphodiesterase type 5 (PDE5) inhibitors. The PDE5 inhibitors are safe and effective in most patients with CVD, including those taking multiple antihypertensive drugs. Furthermore, they have no deleterious effect on exercise capacity, heart rate, or extent of exercise-induced ischemia. In the future, the PDE5 inhibitors may have a role in reducing pulmonary hypertension in persons with primary pulmonary arterial hypertension (PAH) or congestive heart failure. The one major precaution for men taking PDE5 inhibitors is to avoid concomitant administration of therapeutic and recreational nitrate preparations. Patients with chest pain suggestive of a heart attack need to inform emergency room (ER) personnel if they are taking a PDE5 inhibitor. Similarly, before giving nitrates, ER personnel need to ask patients if they have used PDE5 inhibitors. Nitrates should not be given for at least 24 h after a patient uses sildenafil or vardenafil and at least 48 h after a patient uses tadalafil.
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PMID:Role of the cardiologist: clinical aspects of managing erectile dysfunction. 1511 89

An 86-year-old woman was admitted with unstable angina pectoris. Plain old balloon angioplasty (POBA) was performed for 90% stenosis at segment 7 of the left coronary artery with concomitant treatment with nitrate, calcium antagonists, and nicorandil. Five days after POBA, she again suffered chest pain at rest with ST depression by electrocardiography, despite increased doses of calcium-antagonist and nicorandil. Coronary arteriography showed no evidence of restenosis (50%) at the POBA site. The involvement of coronary artery spasm was considered and intravenous treatment with a Rho-kinase inhibitor, fasudil, was started, which resulted in disappearance of the anginal attacks. She refused to continue the fasudil treatment on day 5, which resulted in reappearance of anginal attacks. Third coronary angiography showed a 90% restenosis at POBA site and percutaneous coronary intervention was again performed. This case suggests that a Rho-kinase inhibitor is potentially effective to prevent anginal attacks in spastic angina.
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PMID:[Inhibition of Rho-kinase by fasudil preventing anginal attacks associated with spastic angina: a case report]. 1553 47

Chest pain is a common complaint in adolescents. It is mostly from musculoskeletal origin. Variant angina is a rare cause of chest pain in adolescents. Here we report a 17-year-old male with severe chest pain accompanied by transient ST-segment elevation in leads II, III, avF of the electrocardiogram showing/revealing variant angina associated with acute myocardial ischaemia. Data obtained from laboratory tests, including serial cardiac markers, were normal and subsequent cardiac catheterization revealed a normal coronary anatomy. The patient has been asymptomatic since discharge, and treatment with calcium channel antagonists with nitrate seems to assure a good prognosis.
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PMID:Variant angina in a 17-year-old male. 1577 57

We report on the case of a 64 year old male who received chemotherapy for a metastatic squamous cell carcinoma of the oropharynx. The chemotherapeutic regimen consisted of 5-fluorouracil (5-FU) and cisplatin. Six hours after completion of the first 24 h continuous infusion of 5-FU, the patient developed severe chest pain accompanied by vegetative symptoms and a pronounced ST-elevation of the precordial leads. Under the suspicion of an acute anterior myocardial infarction an immediate coronary angiogram was performed, demonstrating a total occlusion of the left anterior descending (LAD) coronary artery close to the left main stem. The other coronary arteries appeared smooth. After the intracoronary administration of nitroglycerine, the LAD reopened spontaneously without any residual stenosis, paralleled by complete relief of all symptoms. Therefore, 5-FU induced coronary spasm was diagnosed. After initial therapy with intravenous nitrate followed by oral calcium channel blocker, the patient remained free of symptoms and no rise in cardiac enzymes were noted. The chemotherapeutic regimen was changed to cisplatin plus docetaxel. No new attacks of chest pain occurred and the antivasospastic therapy could be stopped without further events.
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PMID:[Angina pectoris and ST-elevation after chemotherapy with 5-fluorouracil]. 1717 34


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