Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two men aged 19 (patient A) and 37 (patient B) years respectively, presented with symptoms of general malaise, fever and nonspecific ECG abnormalities. After admission both patients developed shock. Cardiac ultrasound revealed severe left ventricle dysfunction. On the basis of these findings, infectious myocarditis was suspected. Patient B was placed on artificial ventilation and haemodialysis due to respiratory and renal failure. Both patients were treated with inotropic drugs and antibiotics. Neisseria meningitidis was established as the cause of the myocarditis in patient A but in patient B no cause was found despite microbiological and autoimmune investigations. PCR tests and a biopsy of the myocardium were not performed. There was a satisfactory recovery in the left ventricle function of both patients during admission. These two cases illustrate that (infectious) myocarditis should be suspected in patients presenting with symptoms of general malaise, fever and nonspecific ECG abnormalities. If (infectious) myocarditis is diagnosed, the patient should be monitored for severe heart failure.
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PMID:[Transient cardiac failure due to infectious myocarditis]. 1296 24

DEFINITION, PATHOPHYSIOLOGY, THERAPY: The hypertensive crisis is characterized by a massive, acute rise in blood pressure. Patients with underlying hypertensive disease usually have an increase in systolic blood pressure values > 220 mmHg and diastolic values > 120 mmHg. The severity of the condition, however, is not determined by the absolute blood pressure level but by the magnitude of the acute increase in blood pressure. Thus, in the presence of primarily normotensive baseline values (such as those in eclampsia), even a systolic blood pressure > 170 mmHg may lead to a life-threatening condition. The most important causes are non-compliance (reduction or interruption of therapy), inadequate therapy, endocrine disease, renal (vessel) disease, pregnancy and intoxication (drugs). The management of this condition greatly depends on whether the patient has a hypertensive crisis with organ manifestation (hypertensive emergency) or a crisis without organ manifestation (hypertensive urgency). By documenting the medical history, the medical status and by simple diagnostic procedures, the differential diagnosis can be established at the emergency site within a very short period of time. In the absence of organ manifestations (hypertensive urgency) the patient may have non-specific symptoms such as palpitations, headache, malaise and a general feeling of illness in addition to the increase in blood pressure. In a hypertensive urgency the patient's blood pressure should not be reduced within a few minutes but within a period of 24 to 48 hours. Such adjustment can be achieved on an out-patient basis, however, only if the patient can be followed up adequately for early detection of a renewed attack. In the absence of follow-up facilities, the patient's blood pressure should be reduced over a period of 4 to 6 hours, if necessary in an out-patient emergency service. While intravenous medication is given preference when a rapid effect is desired, oral medication may be used for gradual reduction on an out-patient basis, depending on the patient's medical history and on any underlying chronic disease. Organ manifestations in the course of a hypertensive emergency concern the cardiovascular system and are associated with the symptoms of acute left-ventricular heart failure, the acute coronary syndrome or acute aortic dissection. In the brain the patient may have symptoms of hypertensive encephalopathy, hemorrhage, ischemia; in the kidney he/she may develop acute failure. The patient's blood pressure should be reduced rapidly during the treatment. It should not be reduced to the normal value, but by approximately 20-30% of the baseline value. The reason for a stepwise reduction in blood pressure is the fact that patients with chronic hypertension have an altered autoregulation curve. Acute normotension would lead to hypoperfusion in these patients. Those with aortic dissection or pulmonary edema are excepted from the rule of gradual blood pressure reduction. In the presence of these diseases, blood pressure must be reduced rapidly to normal values. Patients with a hypertensive emergency should always be admitted to the hospital. Parenteral treatment is given preference, since the effect of the treatment is rapid and occurs within a calculable period of time. Thus, parenteral treatment can also be better regulated than medication administered orally or by the sublingual route. Several antihypertensives are available for this purpose. The selection of the substance greatly depends on the existing organ failure as well as the reliable effectiveness and the regulability of the applied antihypertensive.
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PMID:[Hypertensive emergency and urgence]. 1468 6

In two men, aged 19 and 64, with chronic renal insufficiency and subacute symptoms of malaise and weakness of the leg muscles, broad QRS complexes were seen in the ECG. The younger patient developed an asystole and resuscitation was unsuccessful. His blood potassium level was found to be 8.3 mmol/l. The older patient recovered after administration of calcium gluconate. His blood potassium level was found to be 8.5 mmol/l. An 80-year-old woman who was taking various drugs because of heart failure also complained of muscle weakness. Her blood potassium level was 7.2 mmol/l and her ECG showed narrow complexes. She recovered without calcium gluconate after a change in medication. Hyperkalemia is a potentially life-threatening electrolyte disorder that may require immediate treatment. The changes in the ECG, especially widening of the QRS complexes, are the most important clues to the severity of the hyperkalemia. A treatment protocol based on ECG changes may reduce the mortality in these patients.
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PMID:[Life threatening hyperkalemia: the value of the electrocardiogram]. 1518 20

We present a case of myeloperoxidase antineutrophil cytoplasmic antibody (MPO-ANCA)-associated vasculitis that demonstrated a systemic granulomatous lesion at autopsy. The patient initially showed anorexia, general malaise and anemia. Colon fiber was examined to detect the bleeding site, which revealed ischemic mucosal damage associated with venous fibrin thrombus. Because a high titer of MPO-ANCA was found, ANCA-associated vasculitis was suspected and the patient was started on steroid pulse therapy. However, anemia, renal failure and respiratory failure worsened and the patient died of sudden cardiac failure 2 days after the start of the therapy. An autopsy revealed systemic arteritis in multiple organs including the kidneys, liver, spleen, gastrointestinal system and genital organs that indicated fibrinoid necrosis accompanied by granulomatous reaction with multinucleated giant cells; the granulomatous reaction further extended along the splenic capsule. Glomerulonephritis and diffuse pulmonary damage, which are common in MPO-ANCA-associated vasculitis, were almost absent but parapleural fibrosis was present. The direct cause of death was presumed to be hemorrhagic shock due to rupture of an aneurysm in the gastric subserosa. As far as we know, this is the first case of a systemic granulomatous reaction in MPO-ANCA-positive vasculitis, although the cause of the granulomatous lesion is unknown.
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PMID:Systemic granulomatous necrotizing vasculitis in a MPO-ANCA-positive patient. 1526 Aug 56

It is well established now that beta-blockers are an important treatment of heart failure due to left ventricular systolic dysfunction. It has been shown that this drugs counteract the negative effects of sympathetic stimulation on the myocardium (myocardial hypertrophy, fibrosis and ischemia arythmogenic effect, increase of cardiac loading, apoptosis). Many big trials as CIBIS-II, MERIT-HF and CAPRICORN show that Bisoprolol, Metropolol and Carvedilol decrease the hospitalization rate due to heart failure, improve the functional status and increase the survival rate of patients in class II, Ill and IV. However, beta-blockers are not always safe and there use must be guided by some rules: respect of contra-indications (asthma, severe bradycardia, second or third atrio-ventricular block, arterial hypotension), initiation after 2 or 4 weeks of clinical stability, low initial doses with an increase every 2 or 4 weeks.
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PMID:[Beta blockers in the treatment of heart failure due to left ventricular systolic dysfunction]. 1577 41

A 84 year-old woman presenting with evolving breast cancer was admitted in the intensive care unit for malaise. Profound hyponatremia in the context of symptomatic heart failure was documented. Intravenous infusion of NaCl 0.9% was unsuccessful. Treatment with oral urea was begun and sodium level returned to nearly normal values 5 days later.
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PMID:Correction of hyponatremia by urea in a patient with heart failure. 1639 21

After implantation of a permanent pacemaker, patients may experience severe symptoms of dyspnea, palpitations, malaise, and syncope resulting from pacemaker syndrome. Although pacemaker syndrome is most often ascribed to the loss of atrioventricular (A-V) synchrony, more recent data may also implicate left ventricular dysynchrony caused by right ventricular pacing. Previous studies have not shown reductions in mortality or stroke with rate-modulated dual-chamber (DDDR) pacing as compared to ventricular-based (VVI) pacing. The benefits in A-V sequential pacing with the DDDR mode are likely mitigated by the interventricular (V-V) dysynchrony imposed by the high percentage of ventricular pacing commonly seen in the DDDR mode. Programming DDDR pacemakers to encourage intrinsic A-V conduction and reduce right ventricular pacing will likely decrease heart failure and pacemaker syndrome. Studies are currently ongoing to address these questions.
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PMID:New concepts in pacemaker syndrome. 1694 33

We present the fatal case of a patient with a 3-month history of malaise, fatigue, low-grade fever and increasing signs of heart failure. Because of a sudden loss of sight and elevated sedimentation rate, arteritis temporalis was mistakenly suspected and treatment with high dose prednisolone was initiated. Five weeks later the patient presented with worsening of symptoms and septicemia with coagulase negative staphylococcus (CoNS). Transesophageal echocardiography revealed a left atrial mass and stenosis of a severely calcified aortic valve, but no definite vegetations. The diagnose of infectious endocarditis was established during surgery, with the discovery of an abscess cavity at the non-coronary cusp of the aortic valve and by the growth of the same CoNS from tissue samples from the abscess in the atrial wall, as had been found in blood cultures. A systolic murmur was heard initially, but echocardiography was not performed until 5 weeks later and illustrates the pivotal role of echocardiography in the early diagnosis and treatment of infectious endocarditis.
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PMID:Substantial myocardial abscess in an immunocompromised patient: fatal outcome after coagulase-negative Staphylococcal native valve infection. 1733 63

The EVADEF registry enrolled 2296 patients implanted with a defibrillator between june 2001 and june 2003 and followed up 24 months. Their main characteristics were the following: their mean age was 60+/-15S years, they were male in 86 %. Their left ventricular ejection fraction was 38.9 +/- 15.9 %. They were in NYHA class I or II for 83.8% of them, in class Ill for 14.7% and in class IV for only 1.5%. Secondary prevention indications concerned 82.1%, primary prevention 18.3%. Underlying cardiopathies were coronary artery disease in 61.3%, dilated cardiomyopathies in 15.9%. In a group of 7.1% there was no underlying heart disease. The implanted devices were VVI in 48.3%, DDD in 42.9%, biventricular pacemaker with defibrillator in 8.3% and dual defibrillator in 0.5%. Periprocedure complications concerned 13.8%. The most frequently reported was the presence of an haematoma. Periprocedure mortality concerned 8 patients, i.e. 0.3% of the total cohort. Mortality was 7.2% at 1 year and 11.3% at 2 years. Among the 274 deaths, a majority was due to heart failure (42%), arrhythmic storms represented only 6.2% of deaths. Hopefully it is likely that in the future association of cardiac resynchronization therapy to defibrillator will be able to decrease this death rate due to heart failure.
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PMID:[EVADEF registry, main data]. 1747 83

Acute hypoxia is experienced by a variety of individuals (neonates to the elderly) and in an assortment of conditions and diseases (terrorist bomb attack to decompensated heart failure). Increasingly, elaboration of inflammatory cytokines appears key to the brain-based response to hypoxia, as evidenced by the biobehaviors of malaise, fatigue, lethargy, and loss of interest in the physical and social environment. These sickness symptoms implicate hypoxia-dependent activation of the neuroimmune system as a key component of acute hypoxia. Type 2 diabetes (T2D) is associated with increased incidence, severity, and delayed recovery from hypoxic events. Why T2D negatively affects acute hypoxia is not well understood. Recent work, however, reveals that anti-inflammatory pathways tied to the interleukin (IL)-1beta arm of the neuroimmune system may be critical. In this review, the authors examine the link between acute hypoxia, T2D, and neuroimmunity.
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PMID:Acute hypoxia, diabetes, and neuroimmune dysregulation: converging mechanisms in the brain. 1800 66


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