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)

In a cardiological department of a non-referral hospital responsible for 80,000 inhabitants with 2500 in-hospital patients and 1500 out-hospital patients per year, the prevalence, symptoms and prognosis of arrhythmogenic right ventricular dysplasia-cardiomyopathy (ARVD/C) were examined retrospectively. From 1997 to 2002, ARVD/C was diagnosed in 35 females and 45 males (overall prevalence 1 in 1000 inhabitants) with a mean age of 45.6 years. Symptoms were chest pain (80%), palpitations (60%) and syncopes (30%), and clinical findings were repetitive ventricular premature beats (50%), supraventricular arrhythmias (30%), ventricular tachycardia (20%), aborted sudden death due to ventricular fibrillation (1%), right heart failure (4%), biventricular heart failure (1%) and high grade AV nodal block (4%). Endomyocardial biopsies were not performed. Aborted sudden death occurred in only one patient (0.3%) before the diagnosis was made, annual heart failure rate was 1%. No deaths appeared in a follow-up of 1-5 (mean 2.4) years with clinical assessment as the basis of diagnosis. The prevalence of ARVD/C is much higher and the prognosis better than expected from results of reference centers.
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PMID:Prevalence of right ventricular dysplasia-cardiomyopathy in a non-referral hospital. 1556 39

A 70-year-old man was transferred to our hospital with severe congestive heart failure and ventricular arrhythmia due to acute myocardial infarction. He had experienced chest pain 3 weeks previously and was admitted to another hospital for dyspnea, where he required assist ventilation, 1 week prior to the transfer. An echocardiogram revealed a broad anteroseptal infarction and very poor left ventricular function with an ejection fraction (EF) of 22%. He remained in a severe congestive heart failure condition despite a full administration of catecholamines. Coronary angiogram findings revealed an occlusion of the proximal left anterior descending coronary artery and 1 week later severe hypotension was suddenly presented. An echocardiogram showed pericardial effusion with signs of cardiac tamponade. A pericardiocentesis was performed and hemodynamic improvement was obtained for a short time, after which the patient underwent urgent open heart surgery. During the operation, exclusion of the anteroseptal akinetic area using an oval patch was performed under a cardiopulmonary bypass and ventricular fibrillation. Severe cardiac failure remained postoperatively and the patient could not be weaned from cardiopulmonary bypass, therefore, we implanted a percutaneous cardiopulmonary support (PCPS) and started intraaortic balloon pumping (IABP). The patient was weaned from PCPS at 26 days after surgery and from IABP at 30 days. Following hospital release, he has continued to do well without heart failure for 39 months after the operation.
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PMID:[Infarct exclusion for postinfarction left ventricular free wall rupture with severe congestive heart failure]. 1582 45

A-55-year-old man with diabetes mellitus was admitted to hospital because of chest pain. He was diagnosed as anterior acute myocardial infarction and treated with stent placement. After 7 days, ventricular fibrillation occurred because of a subacute reocclusion and balloon angioplasty was performed. Despite reperfusion therapy, intraaortic balloon pumping, antiarrhythmic drugs and beta-blocker, ventricular tachycardia or fibrillation relapsed and cardioversion was performed 29 times during 32 h. Temporary overdrive atrioventricular sequential pacing was initiated and the malignant arrhythmia finally disappeared. Even after stoppage of 25 h overdride pacing, it never recurred. Temporary overdrive pacing is an easy and feasible therapy for a drug-resistant electrical storm associated with AMI and should be performed in the early stage.
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PMID:Temporary overdriving pacing as an adjunct to antiarrhythmic drug therapy for electrical storm in acute myocardial infarction. 1584 51

Ventricular fibrillation (VF), a cause of sudden cardiac death (SCD) in the setting of acute myocardial infarction (MI), remains a major therapeutic challenge. In humans, VF may occur within minutes or hours after the onset of chest pain, so its precise timing in relation to the onset of ischaemia is variable. Moreover, because VF usually occurs unobserved, out of hospital, and is usually lethal in the absence of intervention, its precise timing of onset is actually unknown in most patients. In animal models, the timing of susceptibility to VF is much better characterised. It occurs in two distinct phases. Early VF (defined as phase 1 VF, with possible subphases 1a and 1b in some animal species) occurs during the first 30 min of ischaemia when most myocardial injury is still reversible. Late VF, defined as phase 2 VF, occurs when myocardial necrosis is becoming established (after more than 90 min of ischaemia). Although much is known about the mechanisms and pharmacology of phase 1 VF, little is known about phase 2 VF. By reviewing a range of different types of data we have outlined the likely mechanisms and clinical relevance of phase 2 VF, and have evaluated possible future directions to help evolve a strategy for its suppression by drugs. The possibility that a proarrhythmic effect on phase 2 VF contributes to the adverse cardiac effects of certain cardiac and noncardiac drugs is also discussed in relation to the emerging field of safety pharmacology. It is concluded that suppression of phase 2 as well as phase 1 VF will almost certainly be necessary if drugs of the future are to achieve what drugs of the past and present have failed to achieve: full protection against SCD. Likewise, safety will require avoidance of exacerbation of phase 2 as well as phase 1 VF.
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PMID:Phase 2 ventricular arrhythmias in acute myocardial infarction: a neglected target for therapeutic antiarrhythmic drug development and for safety pharmacology evaluation. 1585 34

Tako-tsubo-like left ventricular dysfunction phenomenon (TTP) has primarily been described in Japan and is characterized by transient left ventricular apical ballooning in the absence of coronary artery disease, associated with chest symptoms, electrocardiographic changes and minimal cardiac enzymes release. Aim of the present review is to summarize the current knowledge about TTP. TTP has been described predominantly in females. TTP occurs also outside Japan. Clinical symptoms comprise anginal chest pain, dyspnea and syncope. TTP occurs frequently after acute emotional or physical stress. Electrocardiographic ST- elevations may be present only for several hours. Then, normalization of the ST-segment occurs, followed by negative T waves, which persist for months. Arterial hypertension in TTP is found in up to 76%, hyperlipidaemia in up to 57%, diabetes mellitus in up to 12% and smoking in up to 18% of the patients. Several pathomechanisms have been proposed: myocardial stunning due to increased catecholamine levels, coronary vasospasm, atherosclerotic plaques rupture, myocarditis, catecholamine-induced hyperkinesis of the basal left ventricular segments and genetic. Patients with TTP should be monitored like patients with myocardial infarction. Care should be taken in the application of catecholamines and nitrates. Betablockers should be given in the acute and chronic phase, and possibly indefinitely to prevent recurrences. The prognosis of TTP is assumed to be good, but in the acute phase there are deaths due to multisystem organ failure, cardiogenic shock, ventricular fibrillation and ventricular rupture. The long term prognosis of TTP patients is largely unknown.
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PMID:Tako-tsubo-like left ventricular dysfunction: clinical presentation, instrumental findings, additional cardiac and non-cardiac diseases and potential pathomechanisms. 1598 8

Vasospastic angina (VSA) and Brugada syndrome (BS) are classified into different categories of cardiac disease, but both can be causes of sudden cardiac death from ventricular fibrillation (VF). The coexistence of VSA and BS in the same patient is possible, and this raises several questions: (1) what is the incidence of the coexistence of BS and VSA in the same patient? (2) is susceptibility to VF enhanced by the coexistence of the 2 diseases? and (3) is there any possibility of Ca-antagonists being used for the treatment of VSA-aggravated BS? In our institution, VSA coexisted in 5 of the 38 patients with BS (13.1%). Anginal episodes were confirmed clinically in 4 of the 5 patients, and syncope attack occurred after the symptom of chest pain in 2 patients. However, VF did not develop during the coronary vasospasm in any of the patients. Treatment with Ca-antagonist was effective for VSA, and neither aggravation of Brugada-type electrocardiographic abnormality nor an increase in the incidence of syncope attack was observed. Although the coexistence of BS and VSA in the same patient is not rare, neither enhanced susceptibility to VF nor the proarrhythmic effect of Ca-antagonist has been confirmed in our experience. However, careful attention is required in such patients because the influence of myocardial ischemia and/or the effect of Ca-antagonist may be different in each patient with BS.
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PMID:Similarities between Brugada syndrome and ischemia-induced ST-segment elevation. Clinical correlation and synergy. 1622 69

Authors present the case of the sudden death of a 30-year-old man, 3 h since his hospitalization by the onset of aspecific chest pain. ECG findings revealed the presence of localized ST segment elevation in precordial leads (V1-V4) and DII-DII, and aVF mimicking acute antero-inferior myocardial infarction. A diagnosis of acute antero-inferior myocardial infarction was advanced and the patient introduced to thrombolytic therapy. Suddenly, on ECG monitor, conduction abnormalities were early recorded (ventricular extrasystole) followed by ventricular tachycardia degenerating in fatal ventricular fibrillation. An alleged medical malpractice was sued against the cardiologist. A complete immunohistochemical study was performed. Histologically, the heart presented massive interstitial lymphocytic infiltrate and focal myocytes necrosis. The diagnosis of acute lymphocytic myocarditis was established as the cause of death.
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PMID:Acute myocarditis mimicking acute myocardial infarction: a clinical nightmare with forensic implications. 1631 Feb 66

Coronary angiography was performed in a 43-year-old man admitted to hospital for chest pain. The first frames after the injection of contrast medium showed plaque in the left main coronary artery and subtotal stenosis of the mid-left anterior descending coronary artery. Dissection of the left main coronary artery appeared, with intimal flaps at the proximal segment of the main trunk and the origin of the left anterior descending artery. Dissection rapidly progressed into the circumflex artery and left anterior descending coronary artery. Although two stents were deployed in the left main coronary artery, the patient died of ventricular fibrillation.
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PMID:Onset and progression of fatal coronary dissection during angiography. 1645 23

Tako-tsubo-like left ventricular dysfunction phenomenon (TTP) is characterized by transient left ventricular apical ballooning associated with symptoms, electrocardiographic changes and minimal cardiac enzyme release in the absence of coronary artery disease. Initially described in Japan, TTP occurs worldwide, predominantly in women and frequently after emotional or physical stress. Symptoms include anginal chest pain, dyspnea and syncope. Electrocardiographic ST elevations may be present only for several hours, and are followed by negative T waves that persist for months. Arterial hypertension is found in up to 76% of TTP patients, hyperlipidemia in up to 57% and diabetes mellitus in up to 12%. Potential pathophysiological mechanisms for TTP include catecholamine-induced myocardial stunning or hyperkinesis of the basal left ventricular segments, coronary vasospasm, plaque rupture, myocarditis and genetic factors. TTP patients should be monitored similarly to myocardial infarction patients because organ failure, cardiogenic shock, ventricular fibrillation or rupture may occur. Beta-blockers are indicated, whereas catecholamines and nitrates should be avoided. The long-term prognosis is unknown.
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PMID:Transient left ventricular dysfunction (tako-tsubo phenomenon): Findings and potential pathophysiological mechanisms. 1703 1

A 70-year-old male with a prior coronary artery bypass operation presented with increasing episodes of chest pain. Coronary angiography revealed severe disease of the left anterior descending artery (LAD), CX, and RCA. A left internal mammary artery to LAD was patent. A jump venous graft, with four distal anastomoses, had two significant stenoses. Percutaneous coronary intervention with distal protection, and direct stenting with a drug-eluting stent, was planned. A 3.00 x 16 mm TaxusExpress (Boston Scientific) was used. At an inflation pressure of 10 atm the stent balloon seemed to extend 20 mm proximally with a diameter of 4.5 mm, and the balloon ruptured. Angiography showed rupture of the vessel proximal to the implanted stent, and the patient developed severe hypotension. The rupture was treated with a covered stent and pericardiocentesis was performed with evacuation of 600 mL blood. However, it was not possible to resuscitate the patient, who died due to severe pump failure and incessant ventricular fibrillation.
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PMID:Unusual balloon rupture during direct stenting with a TaxusExpress stent in a venous graft complicated by vessel rupture: a device-related fatal event. 1730 Mar 93


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