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Query: UMLS:C0018799 (heart disease)
34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gliosis is increased in the respiratory control area of the brainstem in victims of sudden infant death syndrome (SIDS), as it is in infants who have died of congenital heart disease. In the latter, the lesions appear to result from hypoxia or ischemia, and studies of the brainstem microvasculature of SIDS victims indicated a close relationship between the gliosis and adjacent vasculature. It is postulated that cerebral hypoperfusion may play a role in SIDS.
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PMID:Cerebral hypoperfusion in the sudden infant death syndrome? Brainstem gliosis and vasculature. 71 38

Five term and two premature newborn infants were referred for respiratory distress and congestive heart failure, and were found to have electrocardiographic Q or ST-T abnormalities suggesting ischemia. Echocardiographic and/or hemodynamic assessment excluded anatomic heart disease in six infants. In three infants, moderate or severe hemodynamic impairment within 36 hours of age was suggested by these studies. Myocardial perfusion images in all patients showed very poor myocardial uptake of thallium 201, compatible with global myocardial ischemia. Infants of similar age with myocarditis, or with congenital heart disease and congestive failure, had normal myocardial uptake. Rapid clinical improvement occurred within three to seven days. Two to five months later, all infants were well. Two had persistent electrocardiographic abnormalities but repeat thallium 201 imaging in six demonstrated almost normal myocardial uptake. These data provide further evidence that perinatal respiratory distress may be associated with myocardial dysfunction and congestive heart failure in some infants without anatomic heart disease, and suggest that myocardial dysfunction in these infants is associated with global myocardial ischemia, most of which is transient. The timing and nature of the insult causing the ischemia are unclear.
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PMID:Transient myocardial ischemia of the newborn infant demonstrated by thallium myocardial imaging. 76 22

This report consists of an analysis of 256 consecutive patients with a total of 260 arterial emboli to the upper limbs treated in the Spasokukotsky Surgical Department of the Second Moscow Pirogov Medical Institute during the 35 year period from 1939 through 1974. Cardiac diseases were the causes of embolism in 92.58 percent of these patients. Mild ischemia of the limbs was revealed only in 33.82 percent of the patients. Severe ischemia accompanied by significant restriction or full absence of active movements in the joints of affected extremities was observed in 55.94 percent of the patients. Acute ischemia with a muscular edema and partial or total contracture was observed in 9.88 percent of the patients. Forty-seven patients were treated conservatively. Arteriectomy was performed in three patients. Embolectomy was carried out on 206 patients, 101 of whom were operated on by means of the approach outside the cubital fossa and 105 by means of the antecubital approach. The best results were obtained when embolectomy was performed with the use of the Fogarty catheter by means of the antecubital approach. This method achieved full restoration of circulation in 91.59 percent of our patients. The mortality rate was approximately equal in all groups of patients. The over-all hospital mortality rate was 21.1 percent. Recurrent embolism of cerebral and mesenteric arteries was the main cause of death. Fatal postischemic complications led to the death of two patients who were operated on with a total ischemic contracture of a limb. Autopsy revealed a pulmonary microembolism in one case and a myoglobinuric nephrosis in the other.
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PMID:Artery embolism of the upper limbs. 84 43

Postmortem findings within the cardiac conduction system are described from the case of a black woman with sarcoid heart disease who died suddenly. Her clinical course had been characterized by recurring ventricular arrhythmias and bouts of syncope. Both the sinus node artery and the atrioventricular (A-V) node artery were sites of focal fibromuscular dysplasia, which thickened slightly the wall of the former but markedly narrowed the lumen of the latter. Small foci of sarcoid infiltration were present in the sinus node and the A-V node. Fatty replacement within the His bundle was attributable to the probable ischemia caused by narrowing of the A-V node artery. Sarcoid granulomata and infiltration with epithelioid cells were present throughout the ventricular myocardium, but were conspicuously less prevalent in the atria. All the large coronary arteries were normal. Many small coronary arteries in the ventricular myocardium were involved by the sarcoidosis and their lumen were narrowed. These findings and analogous ones reported by others are discussed relative to the pathogenesis of syncopal attacks and sudden death which seem to peculiarly prevalent in sarcoid heart disease.
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PMID:Clinicopathologic correlations. De subitaneis mortibus. XXV. Sarcoid heart disease. 87 28

Systemic disorders (eg, cardiac, hematologic) are commonly recognized as predisposing and sometimes actual precipitating events in cerebral ischemia. From available studies, the incidence of precipitation is not clear. To determine this, we undertook a comprehensive investigation of all patients with ischemic brain disease for a one-year period. Results reveal that brain ischemia is more commonly precipitated by systemic illness than usually supposed, particularly transient ischemic attacks of the vertebrobasilar circulation and completed infarcts in the carotid distribution. Cardiac disorders outnumber all other precipitating events. As they are more amenable to therapy than atherosclerosis, a diligent search for such precipitating events is warranted in patients with ischemic symptoms.
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PMID:Associated systemic factors in cerebrovascular ischemia. 93 99

Noninvasive myocardial imaging with potassium-43 and rubidium-81 has been used successfully to identify areas of infarction and exercise-induced ischemia as regions of decreased radioactivity. The image defects observed are believed to be due to a decreased radionuclide uptake in regions of myocardial scar or to heterogeneous myocardial accumulation of tracer as a result of regional ischemia. Of 27 patients with left bundle branch block studied with noninvasive imaging at rest and during exercise, 25 manifested at rest reduced radioactivity in the region of the interventricular septum. This pattern is similar to that seen in patients with anteroseptal myocardial infarction. Sixteen of the 27 patients underwent diagnostic coronary arteriography and left ventriculography. Only five of these patients had evidence of either previous infarction or significant obstructive coronary artery disease as assessed with clinical or angiographic criteria, or both. Although the image defect was routinely demonstrated at rest in patients with left bundle branch block, this defect was generally normalized or less distinct with exercise in patients with no anatomic heart disease. In contrast, a larger, more distinct or new image defect with exercise correctly identified the presence of significant obstructive coronary artery disease in patients with left bundle branch block. In the clinical application of noninvasive myocardial imaging, these image defects observed at rest can lead to the false pasitive radionuclide interpretation of anteroseptal myocardial infarction.
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PMID:Noninvasive myocardial imaging with potassium-43 and rubidium-81 in patients with left bundle branch block. 97 Mar 29

Correlation between cine-coronary arteriographic findings and various cardiac arrhythmias or conduction defects were studied in 40 patients with arteriosclerotic heart disease. These cases were divided into 3 groups according to the type of arrhythmias or conduction defects. The following conclusions were drawn. 1. In the group I of 25 patients whose arrhythmias were atrial origin, there were sinus bradycardia in 9, suins tachycardia in 5, atrial premature beats in 2 and atrial fibrillation in 9. Cine-angiographically, the degree of luminal stenosis of the main coronary arterial branches were mild to moderate in severity compared to that of the other two groups. However, it was remarkable that the sinus node artery was not visualized in 9 of 25 cases (36%). 2. The group II of 5 patients who have shown premature ventricular contractions exhibited moderate to severe degree of stenosis of coronary artery trees, especially much more often in left anterior descending coronary arteries. 3. In the group III of 10 patients who had various type of intraventricular conduction defects, the degree of stenosis of the main coronary artery branches were usually severe and also, the number of the coronary artery involved in stenosis was increased. Interestingly, atrioventricular node arteries were not opacified in 5 of 10 cases. There were 2 cases of complete A-V block where the atrioventricular node artery was not visualized at all both either from right or left coronary artery opacification. It seemed to be hard to draw a clear cut correlation between cine coronary angiographic pictures and a certain type of cardiac arrhythmias or conduction defects in such a small scale of study. However, cind coronary angiography may contribute to rule out local ischemia of the conduction tissue as a primary cause of the development of arrhythmias or conduction defects in patients with arterisclerotic heart disease.
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PMID:["Coronary arteriographic findings in the patients of arteriosclerotic heart disease combined with cardiac arrhythmias or conduction defects" (author's transl)]. 103 96

Fifteen postoperative surgical patients, in whom noncardiac pulmonary edema developed were studied. A presumptive diagnosis of left ventricle failure would have been based on historical evidence of heart disease (80%), electrocardiographic changes of ischemia or arrythmia (87%), or cardiogenic shock (20%). (see article) Fig. 6. PAEDP-PCW gradient. Note that arterial oxygen tension had an inverse relationship to this pressure differential. Roentgenographic findings included pulmonary edema (73%), pulmonary vascular congestion (60%), cardiomegaly or congestive heart failure (40%). Mean increase in A-aDO2 was 290 torr. Further cardiovascular investigation seemed to exclude left ventricular failure. Mean cardiac index was 4.1 plus or minus 1.3 L/min/m2; pulmonary capillary wedge pressure 4 plus or minus 2.7 torr, and stroke work was 87 plus or minus 8.7 gm-meters. Possible etiologic agents included elevated pulmonary artery pressure (67%), allergic reactions (27%), peritonitis or multiple system trauma (54%), or multiple transfusions (33%). Forty-seven per cent of the entire group survived. Therapy was directed toward the underlying noncardiogenic suspected etiology. Direct cardiovascular measurements were necessary to correct the erroneous though seemingly well founded suspected diagnosis of left ventricular failure in these patients.
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PMID:"Pseudocardiogenic" pulmonary edema. 111 52

The known risk factors for atherosclerosis do not possess the same significance in young people as in the elderly. Hypercholesterolemia, diabetes and cigarette smoking appear to have a greater bearing below the age of 50 than later, particularly in myocardial infarction but also in apoplexy. On the other hand, hypertension is an important factor in the young and, especially in the case of apoplexy, even more so in advanced age. There is marked difference with regard to preexisting heart disease, which scarcely plays a role in myocardial infarction of the younger patient but is a factor in some 50% of hemiplegia cases. Only one fifth of elderly patients with this disease have no preexisting carcdiopathy. The similarity of the risk factors in elderly patients either with or without apoplexy is due to the fact that arteriosclerosis is already established in both groups and the risk factors which give rise to ischemia, thrombosis or embolism assume prominence. The therapeutic implications are briefly discussed.
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PMID:[Risk factors and age]. 113 58

Over the span of two or three days in August, 1972, in two separate communities in eastern Massachusetts two men, one aged 39, the other 66, each without previous overt heart disease, were stung by wasps. Each went into shock rapidly after an interval of over a half-hour developed chest pain and, later, sequential electrocardiographic changes diagnostic of acute myocardial infarction. Each survived; each had normal electrocardiograms before the sting. Though preexistent coronary artery disease can be excluded in neither, the view is favored that acute myocardial infarction in each was caused by deficient coronary perfusion secondary to anaphylactic shock induced by the wasp stings. An intriguing case was just recently reported58 of a 62-year-old man with previous angina who developed pulmonary edema but no chest pain following wasp sting and went on to show rapidly reversed electrocardiographic changes attributable to subendocardial ischemia or infarction. In a sense, this sequence fills the gap as an intermediate phase between the normal and the two individuals described here who developed pain after anaphylactic shock, then proceeded, perhaps through this phase, to develop transmural infarction.
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PMID:Acute myocardial infarction following wasp sting. Report of two cases and critical survey of the literature. 125 36


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