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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is clear that cocaine has cardiotoxic effects. Acute doses of cocaine suppress myocardial contractility, reduce coronary caliber and coronary blood flow, induce electrical abnormalities in the heart, and in conscious preparations increase heart rate and blood pressure. These effects will decrease myocardial oxygen supply and may increase demand (if heart rate and blood pressure rise). Thus, myocardial ischemia and/or infarction may occur, the latter leading to large areas of confluent necrosis. Increased platelet aggregability may contribute to ischemia and/or infarction. Young patients who present with acute myocardial infarction, especially without other risk factors, should be questioned regarding use of cocaine. As recently pointed out by Cregler, cocaine is a new and sometimes unrecognized risk factor for heart disease. Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as to acceleration of atherosclerosis. Direct toxic effects on the myocardium have been suggested, including scattered foci of myocyte necrosis (and in some but not all studies, contraction band necrosis), myocarditis, and foci of myocyte fibrosis. These abnormalities may lead to cases of cardiomyopathy. Left ventricular hypertrophy associated with chronic cocaine recently has been described. Arrhythmias and sudden death may be observed in acute or chronic use of cocaine. Miscellaneous cardiovascular abnormalities include ruptured aorta and endocarditis. Most of the cardiac toxicity with cocaine can be traced to two basic mechanisms: one is its ability to block sodium channels, leading to a local anesthetic or membrane-stabilizing effect; the second is its ability to block reuptake of catecholamines in the presynaptic neurons in the central and peripheral nervous system, resulting in increased sympathetic output and increased catecholamines. Other potential mechanisms of cocaine cardiotoxicity include a possible direct calcium effect leading to contraction of vessels and contraction bands in myocytes, hypersensitivity, and increased platelet aggregation (which may be related to increased catecholamine). The correct therapy for cocaine cardiotoxicity is not known. Calcium blockers, alpha-blockers, nitrates, and thrombolytic therapy show some promise for acute toxicity. Beta-Blockade is controversial and may worsen coronary blood flow. In patients who develop cardiomyopathy, the usual therapy for this entity is appropriate.
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PMID:The effects of acute and chronic cocaine use on the heart. 134 9

To assess the usefulness and safety of transesophageal echocardiography in critically ill patients, we analysed the transesophageal echocardiography studies in 60 of such cases (age: 58 +/- 11 and 38 males). Every patient underwent a previous transthoracic echocardiogram, that was considered inadequate for diagnostic purposes. Thirty patients (50%), were on mechanical ventilation and 17 patients (28%) showed hypotension and/or shock. Forty patients (66%) were at special care units and in 31 (52%) of them, pulmonary and systemic pressures, and continuous analysis of venous pressure of oxygen were available. Indications for study were: 17 patients with clinical suspicion of aortic dissection (confirmed in 5 cases): 9 patients infective endocarditis (4 cases showed valvular vegetations); 6 patients with mitral prosthesis dysfunction (confirmed in 4 cases); complicated acute myocardial infarction (MI) in 8 patients (2 cases with mitral insufficiency, 3 with left ventricular dysfunction, 1 with right ventricular MI, 1 with left ventricular pseudoaneurysm and other with isolated inferior MI); in 11 patients the study was performed to evaluate the result of cardiac transplantation immediately (< 4 h) and it showed 2 cases of left ventricular dysfunction; 3 patients were studied for severe cardiac dysfunction of unknown etiology (a dilated cardiomyopathy was confirmed in one and ruled out in the other, and one patient showed signs of restrictive situation); there were other causes in the rest. The procedure could be completely performed in all cases. In conclusion in critically ill patients the transesophageal echocardiography has a great usefulness and minimal complications.
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PMID:[Usefulness of transesophageal echocardiography in the critical patient]. 147 Jul 40

We performed transoesophageal echocardiography (TEE) and compared its results with transthoracic echocardiographic (TTE) studies in a consecutive series of 100 cases. TEE was performed with a 5 MHz transducer with pulsed wave, continuous wave and colour Doppler facilities. All the patients were in unsedated state; the initial 50 were, in addition, monitored noninvasively for any change in heart rate, blood pressure or arterial oxygen saturation. The procedure was well tolerated by all; one patient had transient ventricular bigeminy. Except increase in heart rate and systolic blood pressure at the time of insertion of probe, there was no change in any of the clinical parameters studied. In patients of mitral stenosis, a thrombus in left atrium (LA) or left atrial appendage (LAA) was seen in 7/52 TEE studies, as compared to 4/52 TTE studies. LAA thrombi (2 cases) were detected only on TEE. Following balloon mitral valvuloplasty, a small atrial septal defect was seen in 6/8 TEE, but only 2/8 TTE studies. In 20 cases with doubtful atrial septal defects on TTE, TEE revealed an intact septum in 6 and delineated the anatomy of the defect in the remaining 14. TEE facilitated detection and better visualisation of paravalvular regurgitation in 4 cases with mitral and 3 cases with aortic valve prosthesis. In addition, TEE helped in excluding vegetations in 3 suspected cases of infective endocarditis and in studying details of 2 intracardiac masses. We conclude, TEE can be safely performed in conscious unsedated patients and provides valuable information in addition to transthoracic echocardiography.
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PMID:Clinical utility of transoesophageal echocardiography--preliminary experience of 100 cases. 182 Sep 97

Acute non-ischaemic mitral regurgitation (MR) has recently generated considerable interest because of its causal relationship to ruptured chordae tendineae and infective endocarditis, advances in its diagnosis by echo Doppler studies, and its management by afterload reduction and reconstructive surgery. It is fundamentally different from chronic MR because the previously normal, unprepared left ventricle (LV) and left atrium (LA) confront a sudden dramatic increase in volume. As the normal-sized left atrium suddenly receives a marked regurgitant flow, its pressure rises and is transmitted into the pulmonary capillaries causing pulmonary congestion and oedema. At onset, the LV function is usually well preserved and the pulmonary oedema does not reflect LV failure. In acute MR, the LV empties into the left atrium, thus reducing its radius and its systolic pressure, resulting in a decline in wall tension according to Laplace's law. With a reduction in LV wall tension, there is a marked increase in contractile shortening with marked increase in total LV output. The left ventricle may fail early in acute severe MR because it is forced to dilate rapidly before hypertrophy can occur, whereas in chronic MR both the LV diastolic volume and mass increase proportionately. With chronic persistence of MR, LV dysfunction and failure occur as a manifestation of the 'cardiomyopathy of overload'. Fortunately because of the low energy cost per unit of work in shortening, as opposed to that used for tension development, there is only a slight increase in myocardial oxygen consumption in acute MR. In patients with LV failure secondary to acute MR, the ejection fraction may be only slightly decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Left ventricular function in acute non-ischaemic mitral regurgitation. 193 16

Antibiotic-induced growth inhibition and killing of a non-mucoid strain of Pseudomonas aeruginosa (PA-96) in vitro and ex vivo were studied at oxygen tensions approximating those of the right and left cardiac ventricles in vivo (pO2 = 40 VS. 80 mm Hg). This pseudomonal strain grew equally at the two oxygen tensions, yet only bacteria exposed to pO2 80 mm Hg revealed significant exopolysaccharide production as shown by PAS and ruthenium red staining. Similarly, scanning electron microscopy of pseudomonal cells within aortic (but not tricuspid) vegetations revealed surface excrescenses compatible with surrounding exopolysaccharide (glycocalyx). Amikacin at 10 x MIC caused significantly less in-vitro killing of pseudomonal cells at pO2 80 VS. 40 mm Hg. In vitro and ex vivo (within experimental aortic and tricuspid vegetations), post-antibiotic effect durations were about 50% shorter for cells exposed to amikacin at pO2 80 mm Hg than 40 mm Hg. These data demonstrate suboptimal aminoglycoside-induced growth inhibition and killing, as well as enhanced exopolysaccharide production of a non-mucoid P. aeruginosa strain at oxygen tensions reflective of the left side of the heart. These findings may in part explain the better results seen in aminoglycoside-treated right compared to left-sided pseudomonal endocarditis in man.
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PMID:Oxygen-dependent differences in exopolysaccharide production and aminoglycoside inhibitory-bactericidal interactions with Pseudomonas aeruginosa--implications for endocarditis. 250 Dec 67

Actinobacillus actinomycetemcomitans is a fastidious, facultative gram-negative rod associated with endocarditis, certain forms of periodontal disease, and other focal infections. Human neutrophils have demonstrated bactericidal activity against A. actinomycetemcomitans, and much of the oxygen-dependent killing has been attributed to the myeloperoxidase-H2O2-halide system. However, the contribution of other neutrophil components to killing activity is obscure. Lactoferrin, an iron-binding glycoprotein, is a major constituent of neutrophil-specific granules and is also found in mucosal secretions. In this report, we show that human lactoferrin is bactericidal for A. actinomycetemcomitans. Killing activity required an unsaturated (iron- and anion-free) molecule that produced a 2-log decrease in viability within 120 min at 37 degrees C at a concentration of 1.9 microM. Besides exhibiting concentration dependence, killing kinetics were affected by minor variations in temperature and pH. Magnesium, a divalent cation thought to stabilize lipopolysaccharide interactions on the surface of gram-negative organisms, enhanced lactoferrin killing of A. actinomycetemcomitans, while other cations, such as potassium and calcium, had no effect. Our data suggest that lactoferrin contributes to killing of A. actinomycetemcomitans by human neutrophils and that it may also play a significant role in innate secretory defense against this potential periodontopathogen.
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PMID:Killing of Actinobacillus actinomycetemcomitans by human lactoferrin. 341 49

Myocardial abscess caused by anaerobic infection is rare and usually occurs in cases of myocardial infarction, in which it may be related to areas of low oxygen tension. Bacteroides CDC group F-1 infective endocarditis complicated by an aortic valve ring abscess with resultant complete heart block developed in a patient with steroid dependent systemic lupus erythematosus. The genitourinary system was the presumed source of the infection. Endocarditis developed after an elective abortion, despite antibiotic prophylaxis according to American Heart Association recommendations. This case shows that an anaerobic abscess of the aortic valve ring can affect contiguous vital structures of the conducting system. Immunosuppression may increase the risk of anaerobic infection after genitourinary procedures, and in this situation the recommended antibiotic prophylaxis may be inadequate.
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PMID:Myocardial abscess with complete heart block complicating anaerobic infective endocarditis. 373 Feb 2

Chloramphenicol was introduced into medical practice in 1949. At therapeutic concentrations of 10 to 20 micrograms drug per ml, the drug inhibits bacterial ribosomal and, to a lesser extent, mammalian mitochondrial protein synthesis but concentrations above 60 micrograms drug per ml induce progressive reduction of oxygen-dependent cellular metabolism. Some adverse reactions (e.g. bone marrow suppression and the "gray baby syndrome") reflect these effects. The pathogenesis of chloramphenicol-induced aplastic anemia remains unclear. Chloramphenicol is most bioavailable after oral administration and has a remarkable ability to diffuse into body fluids and tissues. However, there are wide interindividual variations in its metabolism and elimination, particularly in newborns. Chloramphenicol is indicated for invasive ampicillin-resistant H. influenzae infections; for patients allergic to penicillin with pneumococcal, meningococcal or H. influenzae meningitis; in patients under 8 years of age with Rocky Mountain spotted fever; and for the treatment of brain abscess and other severe anaerobic infections (excluding endocarditis) due to B. fragilis. Other indications include selected patients with Salmonella meningitis or carditis, rickettsioses and intraocular infections. Unravelling the pathogenesis of chloramphenicol-induced aplastic anemia is critical to more widespread application of this remarkable antimicrobial.
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PMID:Chloramphenicol: properties and clinical use. 717 17

Patients with infective endocarditis are at risk for the development of a fistulous communication between chambers or great vessels of the heart. The presence of a continuous murmur may suggest the diagnosis. The first case of aortic valve endocarditis complicated by the development of a fistulous communication between the left ventricular outflow tract and the pulmonary artery is reported. Transesophageal Doppler echocardiography did not detect the defect preoperatively. However, pulmonary artery catheterization revealed very high mixed venous oxygen saturation which supported the presence of a left-to-right shunt.
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PMID:Left ventricular outflow tract pulmonary artery fistula in endocarditis. 748 13

In a series of 416 women with congenital heart disease seen in the Royal Brompton National Heart and Lung Hospital, London, and the Hospital Giovanni Bosco, Torino, Italy, there were 822 pregnancies. The outcomes of 96 pregnancies in 44 patients with cyanotic congenital heart disease were studied. Patients with the Eisenmenger reaction were excluded. Patients were divided arbitrarily into groups according to the type of maternal congenital cardiac anomaly, and factors influencing maternal and fetal outcome were evaluated. The incidence of maternal cardiovascular complications was high (32%), with one death from endocarditis 2 months after delivery. Forty-one (43%) of 96 pregnancies resulted in a live birth; 15 (37%) were premature. Mean weight of full-term infants was 2575 g. Univariate analysis suggested that maternal disease, Ability Index, hemoglobin, and arterial oxygen saturation before the pregnancy were factors that discriminated between successful and unsuccessful fetal outcome, with hemoglobin and arterial oxygen saturation being the most important predictors. Women with cyanotic congenital heart disease can go through pregnancy with a low risk to themselves, with frequent treatable complications, but there is a high incidence of miscarriage, premature births, and low birth weights. An incidence of congenital heart disease in the fetus of 4.9% (2 of 41 live births) is higher than that found in the normal population.
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PMID:Pregnancy in cyanotic congenital heart disease. Outcome of mother and fetus. 820 80


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