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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with an untreated myocardial infarction may present with serious late complications. 3 patients are described. A 63-year-old woman became progressively more short of breath 4 days after an acute episode of chest pain accompanied by nausea and sweating. It proved to be a cardiogenic shock following a rupture of a papillary muscle. A man aged 65 collapsed 5 days after an episode of back pain and nausea. This was a cardiac tamponade due to rupture of the left ventricle. A woman aged 74 had transient aphasia and during investigations for this was seen to have anomalies on ECG. She had cerebral emboli and a cardiac aneurysm with associated thrombus. All 3 patients recovered following mitral-valve replacement, repair of the rupture and medicinal treatment for the clot, respectively. Around one-third of patients who have a myocardial infarction do not have chest pain but experience shortness of breath, autonomic nervous symptoms (sweating, nausea, vomiting), extreme and inexplicable tiredness and fainting. These atypical symptoms should suggest myocardial infarction. In order to avoid high morbidity and death from complications such as arrhythmias, heart failure, rupture and aneurysm formation it is important that a patient who has had a myocardial infarction should be treated as soon as possible, preferably by reperfusion therapy.
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PMID:[Complications of an unrecognized myocardial infarction]. 1635 69

Doxorubicin is a chemotherapeutic agent successfully used in the treatment of a wide range of cancers. However, with cumulative doses, doxorubicin also is known to have cardiotoxic effects, including cardiomyopathy and heart failure. Identification and quantification of myocardial cell damage has been a point of Controversy. We sought to identify these changes by measuring the levels of troponin I both 24 and 48 hr after the administration of doxorubicin as part of an antineoplastic treatment regimen. Thirty-eight patients scheduled to undergo treatment with doxorubicin were screened and approached for enrollment in the study. Thirty-one of them fulfilled all the inclusion criteria and also signed informed consent. All the patients enrolled in the study had blood drawn before the administration of doxorubicin and also 24 and 48 hr later. Electrocardiograms were performed prior to and 48 hr following the administration of chemotherapy. The dose of doxorubicin administered was calculated by the oncologist and ranged from 450 mg/m2-650 mg/m2 (mean 520 mg/m2). Only one patient was found to have en elevation of troponin levels both 24 and 48 hr (2.3 ng/mL and 2.1 ng/mL, respectively) after the administration of the drug. During that time, the patient denied any chest pain, shortness of breath or palpitations. Repeat ECG did not show any changes from the baseline. The remaining participants continued to maintain a troponin level of less than 0.3 ng/mL during the follow-up. In these patients, no electrocardiographic changes were noted in the follow-up ECG compared to the baseline; however, a slight drop in the ejection fraction without any impact on the clinical presentation was recorded. We concluded that the cTnl level does not change after the administration of doxorubicin, and thus cannot be used as a predictor of doxorubicin-induced cardiotoxicity.
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PMID:Troponin I as a marker of doxorubicin induced cardiotoxicity. 1641 82

We report a 22-year-old man who developed shortness of breath after lifting weights and then developed acute heart failure due to rupture of an aneurysm of the right sinus of Valsalva into the right ventricle. The patient developed dyspnea, and clinical findings included tachycardia, wide pulse pressure, bounding carotid and peripheral pulses, pulmonary crackles, and prominent continuous precordial murmur with thrill. Transesophageal echocardiogram with Doppler examination confirmed the diagnosis. The patient underwent surgery with cardioplegia directly infused into the coronary arteries with excision of redundant tissue and closure of the defect with a Dacron patch. He has been asymptomatic since surgery. This condition must to be included in the differential diagnosis for young patients with heart failure.
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PMID:Heart failure in rupture of a sinus of valsalva aneurysm. 1647 85

A 62-year-old man with a history of coronary artery disease and coronary artery bypass graft, chronic heart failure, and peripheral vascular disease required percutaneous coronary intervention (PCI) after progression of shortness of breath and fatigue over 2 years. Four hours after the procedure, the patient developed hematemesis and was found to be thrombocytopenic. The thrombocytopenia was presumed to be due to the abciximab infusion the patient received during and shortly after the PCI. Further review of the patient's medical history revealed that a similar episode had occurred 11 years earlier. At that time, he was enrolled in a clinical trial comparing tirofiban and heparin in patients with unstable angina; he developed profound thrombocytopenia within 24 hours of randomization. After the study unblinding, investigators discovered that the patient received tirofiban, which was thought to be the cause of his thrombocytopenia. Both abciximab and tirofiban are glycoprotein IIb-IIIa inhibitors, and thrombocytopenia induced by this class of drugs is a serious and potentially life-threatening adverse reaction. The mechanism is not well understood but has been described as immune mediated with both ligand-mimetic agents (tirofiban and eptifibatide) and abciximab. Our patient's situation was unusual in that he developed thrombocytopenia from a ligand-mimetic agent and subsequently had a similar reaction to abciximab. To our knowledge, this case report is the first documentation of thrombocytopenia associated with both tirofiban and abciximab in a single patient, and suggests that care should be given in administering glycoprotein IIb-IIIa inhibitors of either type to patients with a history of thrombocytopenia due to one of these agents.
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PMID:Abciximab-associated thrombocytopenia after previous tirofiban-related thrombocytopenia. 1650 24

Absent pulmonary valve syndrome (APVS) is an uncommon variant of tetralogy of Fallot (TOF), which manifests morphologically as vestigial pulmonary valve cusps at the right ventricle-pulmonary trunk junction. The aneurysmally dilated pulmonary arteries may compress the tracheobronchial tree and cause severe respiratory distress in the neonatal or infant stage. Early surgical correction in these patients is necessary despite the high operative mortality rate. A 1-day-old male neonate suffered from progressive shortness of breath after birth. Echocardiography confirmed the diagnosis of TOF with APVS. The marked dilatation of pulmonary arteries resulted in airway compression in addition to heart failure. Total surgical correction was performed at 40 days of age, using a homemade bicuspid equine pericardial tube for right ventricular outflow reconstruction. The short-term follow-up echocardiogram demonstrated good motility of the pericardial leaflet. However, patients receiving this type of valved conduit require meticulous long-term follow-up.
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PMID:Correction of tetralogy of fallot with absent pulmonary valve syndrome in a young infant using a bicuspid equine pericardial tube. 1661 13

Help for physicians in zeroing in on the cause of high BP. Impedance cardiography (ICG) has been used to guide treatment decisions for heart failure and shortness of breath for many years. However, now there is new evidence that the approach can help physicians target the underlying cause of high BP, and technology is available to facilitate non-invasive ICG testing in primary care settings. It's a new tool that could potentially make a big difference in tackling one of the major risk factors for heart disease and strokes.
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PMID:Impedence cardiography: a new tool in the treatment of hypertension. 1668 Oct 75

In our study we have examined 198 patients admitted to hospital for shortness of breath at rest due to left ventricle failure. We have divided the patients into two groups according to the presence of diabetes mellitus. We have excluded the patients with noncardiac cause of pulmonary congestion, with valvular or congenital heart disease and with acute coronary syndromes. We have evaluated the presence of hypertension, value of blood sugar on admission, systolic and diastolic blood pressure, heart rate and medication given for heart insufficiency. We have also compared two dimensional transthoracal echocardiogaphic examination in diabetics to nondiabetics. Finally we compared hospital mortality in both groups. Diabetes mellitus (all the patients were type 2 diabetics) was present in 94 patients (47,5 %), in the group of diabetics there were 50 women, in nondiabetics 52 women (n.s.). The average age of diabetics was 75,5 +/- 8 years and 76,6 +/- 10,1 years in nondiabetics (n.s.). History of hypertension had 45 nondiabetics (43 %) and 69 diabetics (73,5 %), p < 0.05. Systolic blood pressure was significantly higher in diabetics 151 +/- 20,8 mm Hg to 140,5 +/- 18,4 mm Hg in nondiabetics, p < 0.05. The values of diastolic pressure and heart rate were comparable in both groups. We have not noticed any significant difference in the application of ACE inhibitors, beta blockers and diuretics for heart failure in both groups. Echocardiographic examination revealed the significantly higher ejection fraction of left ventricle in diabetics as well as the thicker septum and posterior wall of left ventricle. These findings support the role of the diastolic dysfunction in pathogenesis of left ventricle failure. In hospital mortality rate was 8,5 % in diabetics and 7,6 % in nondiabetics (n.s.). Our results confirmed that in pathogenesis of left ventricle failure hypertension and elevated systolic blood pressure play the important part. Apart from the complex secondary prevention of ischemic heart disease the correct treatment of hypertension represents the very important part of the prevention of left ventricle failure. The role of the proper compensation of diabetes mellitus in the prevention of left ventricle failure is also discussed.
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PMID:[The comparison of clinical and echocardiographic changes in diabetics 2nd type and nondiabetics in patients with shortness of breath due to left ventricular failure]. 1673 36

Intracavitary tumors such as angiosarcomas are prone to embolize, and occlude valves and vessels. Intramyocardial tumors cause cardiac failure and arrhythmias. Pericardial tumors cause effusions which result in tamponade. It is very rare that an intracavitary tumor presents itself with a cardiac tamponade. A 32-year old woman presented to the emergency room with palpitation and shortness of breath. Her physical examination revealed pulsus paradoxus and jugular venous distention. The transthoracic echocardiography showed normal left ventricular function, and an intracavitary right atrial mass. As the patients clinical status deteriorated an emergency operation was performed. The hemorrhagic pericardial fluid was cytologically positive for malignant cells. Histopathological findings were indicative of an angiosarcoma.
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PMID:Right atrial mass presenting as cardiac tamponade. 1688 95

Sirolimus-induced interstitial pneumonitis (SIP) has been reported mainly in renal transplant recipients. However, it has recently been reported with increasing frequency in heart transplantation (HT) patients switched from calcineurin inhibitors (CNIs) to sirolimus. We reviewed the medical records of 30 patients who were treated with sirolimus. Twenty-seven patients were switched from a CNI, 2 patients were initially treated with sirolimus and in 1 patient sirolimus was used to treat a persistent cellular acute rejection. Three patients developed SIP. Symptoms included dry cough, shortness of breath and hypoxemia. High-resolution computed tomography (HRCT) scans showed patchy pulmonary consolidation in a peribronchial distribution or diffuse interstitial pulmonary infiltrates. Before onset of SIP, 2 patients had previous heart failure. Sirolimus discontinuation resulted in a complete resolution of symptoms. SIP is a common and severe adverse event (10%) in HT recipients treated with sirolimus. Drug discontinuation can dramatically improve clinical status. Previous lung injury may play a role in SIP pathogenesis.
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PMID:Sirolimus-associated interstitial pneumonitis in 3 heart transplant recipients. 1696 83

An 87-year-old man had been treated under a diagnosis of idiopathic dilated cardiomyopathy and sick sinus syndrome since 1996. His heart failure was worsened by atrial fibrillation in August 2004. He received amiodarone from October 2004. He was admitted to our hospital with shortness of breath in February 2005. Chest radiography revealed a diffuse reticular shadow in the right lung field and pleural effusion. The diagnosis was interstitial pneumonitis induced by amiodarone. However, 10 days after the discontinuation of amiodarone, the serum sodium concentration fell to 114mEq/l. The blood and urine chemical data were consistent with syndrome of inappropriate antidiuretic hormone secretion (SIADH). The serum sodium concentration improved with fluid restriction. Clinicians should be aware that SIADH may occur during amiodarone therapy.
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PMID:[Interstitial pneumonitis followed by syndrome of inappropriate antidiuretic hormone secretion induced by amiodarone therapy for dilated cardiomyopathy: a case report]. 1706 25


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