Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042510 (ventricular fibrillation)
 10,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

During a 3-month period, a 33-year-old man presented to the emergency department on 4 occasions with dyspnea, palpitations, and syncope. His initial presentation was accompanied by acute myocardial injury and ventricular fibrillation. An extensive evaluation spanned the 3 months and included echocardiography, cardiac catheterization, electrophysiology study, tilt-table evaluation, pulmonary angiography, electroencephalography, and serum and urine analysis. Diagnosis eluded clinicians until a rash was recognized to be urticaria pigmentosa, and biopsy of the rash then implicated mastocytosis. Since the initiation of pharmacotherapy nearly 5 years ago, the patient has remained asymptomatic. This case demonstrates that systemic mastocytosis can present as recurrent syncope and even as cardiac arrest. Diagnosis of this rare but potentially fatal disease is made particularly challenging by its protean manifestations.
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PMID:Shortness of breath, syncope, and cardiac arrest caused by systemic mastocytosis. 1594 90

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

Bone marrow-derived stem cells may contribute to the regeneration of non-haematopoietic organs. In order to test whether an increase in circulating stem cell numbers improves impaired myocardial function we treated 16 male patients with chronic heart failure due to dilated (DCM; n = 7) or ischaemic cardiomyopathy (ICM; n = 9) with the stem cell mobilising cytokine granulocyte colony-stimulating factor (G-CSF; four 10-day treatment periods interrupted by treatment-free intervals of equal length). Safety and efficacy analyses were performed at regular intervals. Peak CD34+ cell counts remained constant from cycle to cycle. Cardiac side effects in ICM patients included occasional episodes of dyspnea or angina and one episode of fatal ventricular fibrillation. Nine (4 DCM, 5 ICM) of 12 patients receiving four full G-CSF cycles experienced an improvement by one New York Heart Association (NYHA) class and a statistically significant increase in six-minute walking distance. By contrast, none of 8 ICM historical controls had a change in NYHA class during a similar time period. Statistically significant changes in echocardiographic parameters were not recorded. Sequential administration of G-CSF is feasible and possibly effective in improving physical performance in patients with chronic heart failure. Patients with ICM may be at risk of increased angina and arrhythmias.
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PMID:Granulocyte colony-stimulating factor-induced blood stem cell mobilisation in patients with chronic heart failure--Feasibility, safety and effects on exercise tolerance and cardiac function. 1623 6

We report a case of large paradoxical embolisms through a patent foramen ovale in a patient with acquired heparin-induced thrombocytopenia type II (HIT). One large ventricular thrombus embolizing through the aortic valve was documented on videotape for the first time while performing transesophageal echocardiography. A 56-year-old man was admitted with acute respiratory failure initially believed to have an exacerbated chronic obstructive pulmonary disease. Arterial oxygen saturation was only 33%. He received antibiotic and anti-obstructive treatments and was mechanically ventilated for 7 days. Few hours after extubation, he developed recurrent severe dyspnea accompanied by acute pain and pulselessness in his left leg. Transthoracic echocardiography revealed an enlarged right ventricle and suggested the presence of free-floating thrombi both in the right and in the left-heart cavities. During transesophageal echocardiography, a large serpentine left-heart thrombus embolized through the aortic valve and disappeared. The patient developed ventricular fibrillation and underwent successful cardiopulmonary resuscitation including emergency thrombolysis with alteplase. Four hours later, the surgeon retrieved a 20-cm long thrombus from the left femoral artery.
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PMID:Large emboli on their way through the heart - first live demonstration of large paradoxical embolisms through a patent foramen ovale. 1652 95

Stress testing for detection of ischemia-induced wall-motion abnormalities has become a mainstay for noninvasive diagnosis and risk stratification of patients with suspected coronary artery disease (CAD). Recent technical developments in magnetic resonance imaging (MRI), including the adoption of balanced steady-state free precession (b-SSFP) sequences-preferentially in combination with parallel imaging techniques-have led to a significant reduction of imaging time and improved patient safety. The stress protocol includes application of high-dose dobutamine (up to 40 microg/kg/min) combined with fractionated atropine (up to a maximal dose of 1.0 mg). High-dose dobutamine stress MRI revealed good sensitivity (83-96%) and specificity (80-100%) for detection of significant CAD. Myocardial tagging methods have been shown to further increase sensitivity for CAD detection. Severe complications (sustained tachycardia, ventricular fibrillation, myocardial infarction, cardiogenic shock) are rare but may be expected in 0.1-0.3% of patients. Dobutamine stress MRI has emerged as a reliable and safe clinical alternative for noninvasive assessment of CAD. New pulse sequences, such as real-time imaging, might obviate the need for breath holding and electrocardiogram (ECG) triggering in patients with severe dyspnoea and cardiac arrhythmias, which may further improve the clinical impact and acceptance of stress MRI in the future.
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PMID:Cardiac stress MR imaging with dobutamine. 1671 37

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

Levosimendan increases the sensitivity of the cardiac fibrils to calcium, favorably affects hemodynamics in patients with heart failure. It is a positive inotrope and a peripheral vasodilator. The elimination half-life of the compound is about 1 hour. The drug decreases pulmonary capillary wedge pressure, increases cardiac output with the improvement in left ventricular ejection fraction leading to symptomatic improvement which includes decreased dyspnea and fatigue. Levosimendan can be used safely with diuretics, nitrates, beta-blockers, digoxin, and angiotensin-converting enzyme inhibitors. The most common adverse effects of levosimendan are headache and hypotension. Prolongation of the QTc interval does not appear to increase the incidence of arrhythmias, including ventricular tachycardia, ventricular fibrillation, and torsades de pointes. Levosimendan is a novel agent in the treatment of decompensated heart failure, representing a newer class of medications aimed at increasing calcium sensitivity. Its properties holds promise for the treatment of heart failure but further large-scale studies will be needed to determine its precise efficacy, safety, as well as the compound's long-term impact on mortality.
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PMID:Levosimendan and calcium sensitization of the contractile proteins in cardiac muscle: impact on heart failure. 1908 50

We present the case of a 72-year-old woman referred for dyspnea and vertigo when admitted to the hospital with a diagnosis of aortic stenosis. She had hypertension with previous deep venous thrombosis with no known hypercoagulable diathesis. She underwent aortic valve replacement with a Carpentier-Magna bioprosthesis without intraoperative complications; selective cardioplegia before aortic wall suture confirmed that coronary ostia were free. After extracorporeal circulation weaning, an episode of ventricular fibrillation occurred; sinus rhythm was restored using 20 J shock. Considering new episodes of ventricular fibrillation, the increasing number of polymorph ectopic ventricular systoles and the worsening of patient condition despite the use of high doses of inotropes, an intra-aortic balloon pump 1: 1 was inserted via the right femoral artery. Echocardiography (ECG) did not show alteration of the bioprosthesis in the presence of severe left ventricular impairment (ejection fraction <30%) with ipokinesia of the anterior-lateral wall and moderate-severe mitral regurgitation. Considering the rapid decline of the patient's condition despite the use of high doses of inotropes and an intra-aortic balloon pump, the aortic wall was reopened to control bioprosthesis. The intraoperative finding was unexpected; a thrombus of length 3-4 cm was found, attached to the prosthetic annulus and protruding into the left main trunk. The thrombus was immediately sucked up to avoid coronary embolization and, after that, the prosthesis was replaced with a Mitroflow 19 (Sorin Group Inc, Mitroflow Division, Vancouver, Canada) bioprosthesis. Probably, an association between factors could induce thrombosis-like aortic sinuses: annulus dimensions, endothelium damage caused during decalcification, tears in the bioprosthetic sewing ring, unknown coagulation diathesis and the structure of the Carpentier-Magna support may have induced this very unusual complication. However, we do not have enough information to establish with certainty the causes of this complication, but discussion of this topic may be useful.
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PMID:Acute bioprosthetic thrombosis immediately after aortic valve replacement. 1919 76

On a rare occasion, pulmonary artery dilatation can be complicated by an extrinsic compression of the left main coronary artery (LMCA) whose effects are immediately evident, whereas a delayed presentation is unusual. We report the uncommon case of a delayed acute coronary syndrome caused by the extrinsic compression of the LMCA due to pulmonary artery enlargement and the potential problems related to its management. An 82-year-old woman with a history of severe chronic obstructive pulmonary disease, a previous episode of deep venous thrombosis and a computed tomography-documented pulmonary artery dilatation was referred to the emergency room for worsening dyspnoea and chest pain. Five days after admission to the coronary care unit, the patient developed a cardiogenic shock with consecutive episodes of ventricular fibrillation. Urgent coronary angiography showed severe LMCA stenosis caused by extrinsic compression from the pulmonary artery with no other lesions in the coronary arteries; coronary angioplasty was successfully performed with a direct drug-eluting stent implantation that led to a significant improvement of the haemodynamic conditions in the following days. Planned control angiography performed 10 days later showed the recurrence of the LMCA stenosis together with a forward displacement of the previously implanted drug-eluting stent, which was managed with a further direct implantation of a bare metal stent. The immediate good results of this second procedure were confirmed by follow-up angiography performed 2 months later and by the 6-month follow-up clinical examination.
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PMID:Life-threatening left main stenosis induced by compression from a dilated pulmonary artery. 1937 83


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