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)

Cardiac ischemia typically causes chest pain, variously radiating elsewhere. Convergence of cardiac nerve fibers on central pathways receiving somatic afferents from the head is likely to be responsible for the perception of cardiac ischemic pain as headache. A 47-year-old man was admitted to the emergency room of our hospital with a 2-hour history of occipital headache. Routine electrocardiography revealed monophasic ST-segment elevation in leads I and aVL and ST-segment depression in leads II, III, and aVF. During recording of lead VI, ventricular fibrillation occurred. Advanced life support was started immediately but failed to restore rhythm and cardiac function. Autopsy showed two-vessel disease with a ruptured plaque and total thrombotic occlusion of the proximal left anterior descending artery and 80% stenosis of the right coronary artery. In this patient, headache was the only symptom of myocardial ischemia. Anatomic convergence of cardiac nerve fibers on central pathways receiving somatic afferents from the head is likely to be responsible for the perception of cardiac ischemic pain as headache. Owing to the very rare occurrence of headache as a symptom of myocardial ischemia, diagnosis is difficult and requires a high degree of suspicion.
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PMID:Headache as a manifestation of fatal myocardial infarction. 1191 78

This report describes a case of an unusual association between vasospastic angina, coronary myocardial bridging, and Brugada syndrome. The patient complained of chest pain followed by rhythmic palpitation and syncope. Brugada syndrome ECG markers were documented with transient ST-segment elevation in lateral leads. A coronary angiogram showed a myocardial bridging in the left anterior descending artery and coronary vasospasm was reproduced after intracoronary ergonovine injection in the circumflex coronary artery. Ventricular fibrillation was induced by programmed electrical stimulation. The described association can be important because interaction between ischemia and Brugada syndrome electrophysiological substrate could modulate individual susceptibility to life-threatening ventricular tachyarrhythmias.
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PMID:Brugada syndrome: a case report of an unusual association with vasospastic angina and coronary myocardial bridging. 1199 81

In selected patients suffering from variant angina, an implantable cardioverter-defibrillator (ICD) and coronary stenting can be helpful to prevent sudden death and treat coronary artery spasm. We report a case of a 47-year-old woman suffering from variant angina, who experienced an episode of ventricular fibrillation promptly cardioverted. After coronary angiography documentation of a mild atherosclerosis, an ICD was implanted and oral nitrates and calcium antagonists were prescribed. The recurrence of chest pain and palpitations prompted us to perform a second coronary angiography that documented a focal coronary artery spasm successfully treated with stent implantation. No other episodes of angina or ventricular arrhythmia were documented during the following 6 months of follow-up.
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PMID:Coronary vasospasm and aborted sudden death treated with an implantable defibrillator and stenting. 1202 77

Malignant ventricular arrhythmias can result from isolated right ventricular infarction, and reports of this phenomenon in the literature are rare. We present a case of a 46-year-old man with acute onset of chest pain angiographically confirmed to be a result of isolated occlusion of a right ventricular branch artery. He developed ventricular fibrillation within 5 hours of symptom onset. This case highlights the point that despite its benign clinical appearance and preserved left ventricular function, necrosis of right ventricular tissue can have life-threatening consequences.
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PMID:Ventricular fibrillation resulting from acute right ventricular infarction from isolated occlusion of a right ventricular branch artery. 1265 24

We reviewed the frequency of acute coronary syndrome (ACS) in patients presenting to our emergency department (ED) with chest pain after methamphetamine (MAP) use during a 2-year interval. Thirty-three patients (25 males, 8 females; average age 40.4 +/- 8.0 years) with a total of 36 visits met study inclusion criteria: 1) non-traumatic chest pain, 2) positive MAP urine toxicology screen, 3) admission to "rule-out" myocardial infarction, 4) chest radiograph demonstrating no infiltrates. An ACS was diagnosed in 9 patients (25%). Three patients (8%) (2 ACS and 1 non-ACS) suffered cardiac complications (ventricular fibrillation, ventricular tachycardia, supraventricular tachycardia, respectively). Age, gender, cardiac risk factors, prior coronary artery disease, initial systolic blood pressure and heart rate did not differ significantly in the ACS and non-ACS groups. The initial and subsequent electrocardiograms (EKG) were normal in 1/9 (11%) patients with ACS and 16/27 (59%) without ACS (p < 0.05). Our findings suggest that: 1) ACS is common in patients hospitalized for chest pain after MAP use, and 2) the frequency of other potentially life-threatening cardiac complications is not negligible. A normal EKG lowers the likelihood of ACS, but an abnormal EKG is not helpful in distinguishing patients with or without ACS.
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PMID:Frequency of acute coronary syndrome in patients presenting to the emergency department with chest pain after methamphetamine use. 1274 36

Acute aortic dissection complicated with acute myocardial infarction (AMI) is the most fatal situation. We experienced the successful treatment for acute type A aortic dissection complicated with inferior AMI following aortic valve replacement (AVR). A 60-year-old man had had AVR for aortic regurgitation. Sixteen months after the AVR, he had a sudden onset of severe chest pain with complete atrioventricular block. Immediately, temporary pacing and cardiac catheterization were conducted, showing the occlusion of the right coronary artery due to acute type A aortic dissection. On his way to our hospital, direct current shock was conducted 3 times for ventricular fibrillation. We replaced the ascending aorta combined with coronary artery bypass grafting and the postoperative course was uneventful. The key to treat acute aortic dissection complicated with AMI is early accurate diagnosis, prompt temporary pacing for bradycardia, defibrillation for lethal arrhythmia and insertion of a perfusion catheter if possible. These preoperative hemodynamic stabilization gives us the chance to save these patients.
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PMID:Acute type A aortic dissection complicated with acute inferior myocardial infarction following aortic valve replacement. 1462 Oct 23

A 55-year-old man was referred for the evaluation of frequent chest pain and syncope. While in the hospital, he experienced severe chest pain accompanied by transient ST segment elevation and a slight elevation of cardiac enzyme levels. Multiple coronary arteriograms were recorded at various times during an interval of 2 months. On one occasion, the results were normal; on another occasion, they showed total occlusion of the left anterior descending, diagonal, and circumflex coronary arteries. The occlusion was completely relieved with sublingual nitroglycerin. Because the patient's clinical condition deteriorated rapidly, double aortocoronary saphenous vein bypass was performed to the left anterior descending and circumflex coronary arteries. During the induction of anesthesia, ventricular fibrillation occurred, and the patient died from refractory recurrent fibrillation 4 hours after surgery. Postmortem examination revealed normal coronary arteries, patent vein grafts, and multiple focal areas of recent and old myocardial fibrosis. Thus, it appears that coronary spasm, in the presence of otherwise normal coronary arteries, can produce myocardial infarction with necrosis, and that medical management may provide a more successful method of treating such patients.
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PMID:Recurrent myocardial infarction in a patient with Prinzmetal's angina and normal coronary arteries. 1521 88

A 53-year-old man was admitted to Keio University Hospital because of serious dyspnea and edema of the lower extremities. Eighteen months previously, the patient had complained of chest discomfort, and was then admitted for the first time to our hospital for evaluation of chest pain. Electrocardiography showed poor R wave progression in leads Vl through V4, and diffuse nonspecific ST-segment and T wave abnormalities with low voltage. However, no definitive diagnosis could be made at this initial admission and a calcium-channel blocker was prescribed. Despite this treatment, the patient was readmitted with worsening dyspnea and lower extremity edema. The diagnosis of heart failure and nephritic syndrome was made at the second admission. In addition, immunoelectrophoresis showed a monoclonal IgD (lambda) M protein and increased plasma cells in the bone marrow, suggesting a diagnosis of multiple myeloma. The patient was thus given dexamethasone (20 mg per day for 4 days) intravenously, but his symptoms did not improve. Two weeks later, the patient deteriorated further with congestive heart failure and renal failure, and subsequently died of cardiac arrest with ventricular fibrillation. On autopsy, IgD (lambda)-positive plasma cell proliferation was found in the bone marrow, confirming the diagnosis of multiple myeloma. In addition, amyloid deposition was detected in various organs including the heart, kidneys, esophagus, duodenum, ileum, colon, tongue, and lungs. In particular, the weight of the heart was 650 g demonstrating a hypertrophic septum and amyloid deposition in the myocardium and even coronary arteries. In summary, the final diagnosis was IgD (lambda) multiple myeloma associated with systemic amyloidosis.
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PMID:IgD myeloma with systemic amyloidosis with chest discomfort as an initial symptom. 1547 32

A 65-year-old patient with history of ischemic cardiomyopathy admitted to the hospital for chest pain and subsequently experienced incessant ventricular fibrillation (VF), requiring repeated defibrillation. Coronary angiogram was unchanged, compared to a study a year before, and acute ischemia was not considered to be the etiology of the VF. A particular premature ventricular contraction morphology was noted on telemetry prior to each episode of VF. The patient subsequently underwent successful radiofrequency ablation of a focus in the left ventricular free wall. Careful examination of initiating foci of VF or polymorphic ventricular tachycardia, with radiofrequency ablation in appropriate cases, could be potentially life-saving.
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PMID:Focal origin of ventricular fibrillation in a patient with ischemic cardiomyopathy. 1548 53

A 46-year-old man complained of recurrent episodes of giddiness which was not associated with chest pain or breathlessness. There was no family history of sudden death. Clinical examination was unremarkable.12-lead electrocardiogram (ECG) showed ST segment elevation in the right precordial leads, with coved ST segment elevation at its J point followed by a negative T wave with no isoelectric separation, specifically in V2. These ECG features are characteristic of the Brugada syndrome. He underwent a flecanide challenge which produced further elevation of ST segment at its J point and spontaneous ventricular ectopy. Electrophysiological studies induced ventricular fibrillation with 3 extra stimuli. An implantable cardioverter-defibrillator was implanted for prevention of sudden cardiac death. The Brugada syndrome is discussed.
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PMID:Electrocardiographical case. Asymptomatic patient with ST-segment elevation. 1551 Mar 28


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