Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiology was diagnosed by means of clinical, radiographic, electrocardiographic phonocardiographic, angiocardiographic, and pathological findings in 271 or 3,745 cats necropsied from January 1962 to April 1974. The affected cats can be divided into three groups on the basis of the gross and microscopic pathological lesions: 1)endocarditis and myocarditis in 20 young cats; 2)endomyocardial fibrosis and left ventricular hypertrophy in 182 cats; and 3)myocardial degeneration and biventricular dilatation in 69 cats. Of 271 affected cats, thromboembolus was observed in the aorta, and in the carotid, femoral, iliac, renal, pulmonary, and hepatic arteries in 104 instances. The important aspects of cardiomyopathy in cats appears to be the reduced diastolic compliance of the thick left ventricle, resulting in poor fillin. Resistance to ventricular inflow raises the diastolic pressure and causes compensatory left atrial enlargement. A pathogenesis for the onset of clinical signs at any stages as the cause of the heart disease is postulated on the basis of stress causing tachycardia and poor left ventricular filling. Acute left-sided failure with pulmonary edema may be precipitated. Approximately one-fourth of the cats have enlargement of all cardiac chambers, typical of congestive cardiomyopathy. On the basis of the close similarily to cardiomyopathy in man, the cat could serve as a suitable animal model for a conservation of time and effort in the attack against this disorder. There is a need for coordinated research programs for utilizing the multiple avenues of approach such as: epidemiological, clinical, biochemical, pathological, ultrastructural, virological, and immunological.
 ...
PMID:Feline cardiomyopathy. 12 93

In a retrospective study, 29 patients at least 20 years of age with known aortic stenosis are reported who had the peak systolic gradient (PSG) measured on at least two occasions without an intervening surgical procedure or episode of endocarditis. In these 29 patients, there were 31 intervals available for evaluation with a mean follow-up time of 43.5 months (1 week to 120 months). In 16 of the 31 intervals, the PSG increased by 50% or more and in 15, it did not. In the group where the PSG increased, the average rate of increase was 1.3 mm. Hg/month with the most rapid gradient increase at 3.8 mm. Hg/month. Progression to high gradient was correlated with the development of angina pectoris or left ventricular hypertrophy by voltage and ST-T wave changes. In this study, other symptoms were not helpful in predicting an increase in severity. It is still recommended, however, that any patient with aortic stenosis and the development of symptoms of congestive heart failure or exertional syncope should be suspected of having progressed to severe aortic stenosis and should be restudied.
 ...
PMID:Rate of progression of severity of valvular aortic stenosis in the adult. 49 18

In a 24-month period, 27 patients with idiopathic hypertrophic subaortic stenosis (IHSS), ages 65-80 years, were observed. Diagnoses were made by echocardiography (24 patients), cardiac catheterization (one patient), and both methods (two patients). The most common symptoms were angina (17 patients), dyspnea (13 patients), and syncope (11 patients). Two patients were asymptomatic, while another complained only of vague retrosternal chest discomfort with exertion. One asymptomatic patient had a completely normal physical examination, but electrocardiography (ECG) demonstrated a pattern of left ventricular hypertrophy. Another patient had an inconsistent apical holosystolic murmur. Two patients had alpha streptococcal endocarditis; neither was known to have pre-existing valvular disease. Fourteen patients had ECG criteria for left ventricular hypertrophy (LVH). Three patients were known to have associated aortic valve disease. The symptoms of IHSS may be nonspecific; asymptomatic patients with and without cardiac murmurs may be observed. Coexisting valvular disease, coronary artery disease, and bacterial endocarditis were documented. Patterns of myocardial infarction on ECG were not seen in these 27 patients.
 ...
PMID:Idiopathic hypertrophic subaortic stenosis in the elderly. 56 40

The endocardial fibroelastosis (EFE) is the most frequent cardiomyopathy. This disease is characterised by endocardial hyperplasia due to proliferation of elastic and collagenous fibres. There are primary and secondary forms. Within the primary form, the infantile form is the most frequent and of greatest importance to the pediatrician. This form is more a syndrom than a distinct disease. It is a reaction of the endocard due to several noxes. Lately a possible viral etiology is being discussed e.g. Parotitis, Coxsackie or other viruses. Clinical criteria for diagnosis are: cardiomegaly, left ventricular hypertrophy seen in 97% in the ECG, the absence of a murmur (or a soft apical mumur) absence of cyanosis and absence of systemic disease. Differential diagnosis is mainly between fibroplastic parietal endocarditis (FPE), cardiovascular collagenosis (CC) and endomyocard fibrosis (EMF). In FPE thrombosis is frequent and typically there is eosinophilia. CC is found in South Africa and is characterised by edema and fibrinoid necrosis. MEF is present mainly in Uganda, Nigeria and South India, characterised by endocardial fibrosis, valve involvement and eosinophilia. The obstructive hypertrophic cardiomyopathy is characterised by a pronounced cardiomegaly, insufficient weight gain as well as dyspnea and cyanosis. Catheterization shows a gradient across one or both of the outflow tracts due to hypertrophic subaortic or subpulmonic stenosis. Therapy of EFE consists in treating the cardiac decompensation and according to the severity of the disease, in steroids.
 ...
PMID:[Endocardial fibroelastosis (E.F.) and its differential diagnosis]. 94 82

The natural history of the cardiovascular manifestations of systemic lupus erythematosus (SLE) have been altered by corticosteroids which exert their own cardiovascular effects. This study describes clinical and necropsy observations in 36 corticosteroid-treated patients with SLE and compares them to necropsy observations in patients with SLE reported before the use of corticosteroid therapy. The 36 patients averaged 32 years of age, and 33 were women. Systemic hypertension was present in 25 (69 per cent) and left ventricular hypertrophy in 23 (64 per cent) patients. Hypertension was twice as common in the 19 patients who received this drug for more than 12 months (average 38 months) than in the 17 patients who received this drug for less than 12 months (average 6 months), and was almost five times more common among our patients than in patients with SLE in the presteroid era. Congestive cardiac failure occurred in 15 patients (43 per cent), eight times more frequent than that reported in noncorticosteroid-treated patients with SLE. Subepicardial and myocardial fat was increased in all 36 patients. Lupus carditis was similar in frequency but differed morphologically in our patients compared to those not treated with corticosteroids. Libman-Sacks-type endocardial lesions, present in 18 (50 per cent) of our patients, were smaller, fewer in number, univalvular rather than multivalvular, and mainly left-sided. Most verrucae were either partly or completely healed, and some were calcified. Pericarditis, present in 19 (53 per cent) patients, was predominantly of the fibrous type. Myocarditis was present in three patients, each of whom also had endocarditis and pericarditis. The lumen of at least one of the three major coronary arteries was narrowed more than 50 per cent by atherosclerotic plaques in 42 per cent of the 18 patients who received corticosteroids for more than 1 year, but in none of the 17 patients who received corticosteroids for less than 1 year. Four of the eight patients with narrowed coronary arteries had myocardial infarcts. Although vital to the management of SLE, corticosteroids have an over-all deleterious effect on the heart. Systemic hypertension and left ventricular hypertrophy appear or, when present, worsen; congestive cardiac failure increases; epicardial apartment of Me
 ...
PMID:The heart in systemic lupus erythematosus and the changes induced in it by corticosteroid therapy. A study of 36 necropsy patients. 111 70

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.
 ...
PMID:The effects of acute and chronic cocaine use on the heart. 134 9

A 65 year-old-man was admitted to our hospital complaining of orthopnea and precordial oppressive feeling. Chest roentgenogram revealed congestive heart failure. Electrocardiogram revealed acute myocardial infarction-like pattern. Serum enzymes (CPK, GOT, LDH) were slightly elevated, but serum antiviral antibodies were not elevated. Echocardiogram showed severe symmetrical left ventricular (LV) hypertrophy, but there was no abnormality of LV wall motion. He died of progressive heart failure and ventricular fibrillation on the second hospital day. A necropsy was performed within one hour of death. The heart was enlarged (690 g) with both left and right ventricular hypertrophy. The myocardium disclosed a diffuse infiltration predominantly of eosinophilic leucocytes. Histopathological study revealed giant cell formation and granulomatous lesions in the myocardium. There was no overt endocarditis or pericarditis. We concluded that the severe LV hypertrophy was due to myocardial inflammatory swelling. From these findings, we diagnosed this case as acute isolated (Fielder's) myocarditis.
 ...
PMID:[A case of acute isolated (Fiedler's) myocarditis diagnosed by histopathological study with rapid unfortunate course]. 158 53

The heart of the elderly is characterized by increased occurrence of characteristic calcifications on mitral and aortic valves. These valves have been found calcified in persons older than 70 years at about equal frequency, in nearly 50% of these individuals simultaneously. A calcified mitral ring was more common in females of all age classes, aortic calcifications showed a less marked difference for gender. Only the most severe calcifications of the mitral ring have hemodynamic consequences. The clinical significance of these calcifications lie in their propensity for bacterial colonisation. The risk for infective endocarditis rises tenfold. Aortic valves, calcified by degenerative processes, lead to more pronounced alterations of hemodynamics. In nearly one half of the patients this type of calcification results in stenosis with corresponding left ventricular hypertrophy. Since coronary arteriosclerosis has a similar age distribution the risk for ischemic heart disease is increased. Early and particularly frequent calcifications of the aortic valve develop in patients with bicuspid valves. Risk for infective endocarditis is also raised by a factor of ten in patients with calcified aortic valve.
 ...
PMID:[Degenerative calcification of mitral and aortic valves]. 158 79

Thrombus formation in the left atrium and left ventricle is primarily due to stasis of blood which causes activation of the coagulation system. Migration of thrombotic material into the circulation depends on the dynamic forces of the circulation. Atrial fibrillation is the commonest underlying cardiac disorder predisposing to thromboembolism. Rheumatic mitral stenosis, left atrial enlargement, prior myocardial infarction, hypertension, and echocardiographic left ventricular hypertrophy are risk factors for thromboembolic stroke in elderly patients with chronic atrial fibrillation. Non-valvular atrial fibrillation accounts for 45% of cardiac sources of thromboembolic stroke and includes patients with ischemic heart disease, hypertension, thyrotoxic heart disease, hypertrophic cardiomyopathy, chronic sinoatrial disorder, and idiopathic atrial fibrillation. 15% of cardiac sources of thromboembolic stroke are associated with acute myocardial infarction, 10% with left ventricular aneurysm and mural thrombi remote from an acute myocardial infarction, 10% with rheumatic valvular heart disease, and 10% with prosthetic cardiac valves. Mitral valve prolapse, mitral annular calcium, nonischemic cardiomyopathies, infective endocarditis, nonbacterial thrombotic endocarditis, left atrial myxoma, paradoxical embolism associated with congenital heart disease, calcific aortic stenosis, and complex atherosclerotic plaque within the proximal aorta also contribute to thromboembolism.
 ...
PMID:Etiology and pathogenesis of thromboembolism. 176 43

The authors have studied the immediate and long term outcome of surgical treatment of acute phase infective endocarditis in a group of 33 high risk patients with valvular heart disease. The age varied from 2 to 68 years, 18 patients were male and 22 were of the white race. The aortic valve was the most frequently involved (18/54.5%), followed by mitral valve (13/39.3%), and tricuspid valve (2/6.0%). Twenty-four patients (72.7%) were in functional class III and seven (21.0%) in functional class IV. The noninvasive studies in those patients revealed 13 cases (39.4%) with normal cardiac size. The EKG was abnormal in 27 cases (81.8%) mostly with left atrial and ventricular hypertrophy. The echocardiogram revealed the presence of vegetations in 27 patients (81.8%) and the blood cultures were positive in 24 cases (72.7%). All patients were treated with antibiotics. The pathologic analysis revealed the presence of vegetations in 94% and structural alterations in 16.5%. Twenty-one patients had heart valve replacement with mechanical prosthesis (63.6%), 11 (33.3%) had bioprosthesis and one had tricuspid excision without replacement (3.0%). The hospital mortality was 12% and the late mortality 3%. Three deaths occurred in patients who had prolonged clinical treatment (more than 35 days) and one patient died of severe fungal endocarditis. The follow-up of the remaining 26 patients varied from 1 to 596 weeks (mean 183) demonstrating important clinical improvement and a normally functioning valve prosthesis. All patients remained in functional class I or II. The analysis of our data indicates that surgical treatment is the best option for high risk endocarditis and should be undertaken earlier in all patients in this group.
 ...
PMID:[Surgical treatment of high-risk valvar endocarditis]. 262 78


1 2 3 4 Next >>