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

We compared 41 patients with angiographic proof of pulmonary embolism and clinical signs of pulmonary infarction (as evidenced by an infiltrate on x-ray study and pleuritic pain in the area of the embolus) with 24 patients with pulmonary embolism but without infarction. Only 18 of the 41 patients with pulmonary infarction had associated heart disease. Pulmonary infarction was uncommon when emboli obstructed central arteries but frequent when distal arteries were occluded. Follow-up x-ray examination showed that the infiltrates resolved in the patients with pulmonary infarction without heart disease, but persisted when heart disease was present. We suggest that obstruction of distal arteries results in pulmonary hemorrhage owing to an influx of bronchial arterial blood at systemic pressure. Hemorrhage causes symptoms and x-ray changes usually attributed to pulmonary infarction. However, hemorrhage resolves without infarction in patients without, but progresses to infarction in those with, heart disease.
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PMID:Pulmonary embolism, pulmonary hemorrhage and pulmonary infarction. 86 13

Endovascular infections that involve the right side of the heart present their own unique etiologies, pathophysiologies, clinical manifestations, and therapeutic issues. The pathology of the vegetations of right-sided endocarditis is identical to that of left-sided endocarditis. These vegetations are irregular, friable masses of varying size the contain platelets, fibrin, RBCs, and microorganisms. These lesions serve as a nidus for deep-seated infection and produce sustained bacteremia. Right-sided endocarditis occurs in 5% to 10% of all cases of endocarditis. The most common predisposing factors are IV drug abuse and congenital heart disease. S. aureus is the most common pathogen. The clinical manifestations include fever, chills, rigor, dyspnea, pleuritic pain, productive cough, and hemoptysis. The cardiac manifestations can be notably absent early in the course of the disease, with only 20% of patients initially showing a significant murmur on physical examination. Peripheral embolic lesions can be seen. Echocardiography is helpful in identifying vegetations on the tricuspid valve in a significant proportion of patients. The chest radiograph is characteristic, showing features typical of multiple septic pulmonary emboli. The radiograph shows multiple, small, fuzzy, patchy, peripherally located densities that can change rapidly on serial films. Complications of right-sided endocarditis include pulmonary infarction, pulmonary abscess, progressive right-sided heart failure, and renal abnormalities. The treatment of right-sided endocarditis includes prolonged therapy, with high doses of IV bactericidal antibiotics. Four weeks of antibiotic therapy is generally required, but newer regimens using combination antibiotic therapy can be successful in sensitive strains of viridans group streptococci and S. aureus. Surgical resection of the tricuspid valve is recommended for organisms that do not respond to initial antibiotic therapy, fungal endocarditis, resistant relapsing organisms, or coexistent infection with S. aureus and P. aeruginosa. The prognosis of right-sided endocarditis is generally favorable when compared with left-sided endocarditis. The prognosis is especially favorable in IV drug abusers infected with S. aureus. Patients infected with fungal organisms, Pseudomonas or Serratia, have a worse prognosis. The presence of significant right-sided heart failure also imparts a worse prognosis.
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PMID:Endovascular infections arising from right-sided heart structures. 173 55

We report our experience with five children with pulmonary embolism and infarction. Two with congenital heart disease, one with rheumatic cardiopathy and two with a previously healthy cardiopulmonary system. The risk factors, clinical behavior and ECG were similar to those in adults. In chest roentgenogram we found pulmonary infarction with cavitations in three patients because of a delayed diagnosis. All patients had hypoxemia and hypocapnia, and diagnosis was made on the basis of segmentary or larger defects in perfusion gammagraphy. In just one case we obtained V/Q gammagraphy and pulmonary angiography. In one case we confirmed the clinical diagnosis by autopsy. We conclude that it is very important to keep this diagnosis in mind in all children with respiratory failure.
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PMID:[Pulmonary thromboembolism in children]. 177 17

Acute pulmonary embolism with infarction can delay urgently needed heart transplantation and increase the postoperative pulmonary complications. Few data are available concerning pulmonary embolization in the pediatric patient with end-stage congestive heart failure. Sixty-two consecutive pediatric patients awaiting heart transplantation were monitored for evidence of acute pulmonary embolism. Acute pulmonary infarction was documented by ventilation-perfusion scan, pulmonary angiography or pathologic examination in six patients. The prevalence differed by diagnosis; 5 of 36 patients with dilated cardiomyopathy and 1 of 20 patients with congenital heart disease developed acute pulmonary embolism with infarction. No significant difference in age at the time of transplantation evaluation, duration of congestive heart failure, presence of cardiac arrhythmias or degree of cardiac dysfunction was seen between patients with and without pulmonary embolism. Two-dimensional echocardiography failed to detect the presence of an intracardiac thrombus in four of the six patients. Two patients who developed acute pulmonary infarction are alive after successful heart transplantation. The remaining four patients died within 6 weeks of initiation of anticoagulant therapy before transplantation could safely be performed. In summary, pediatric patients with end-stage congestive heart failure are at risk for acute pulmonary embolism. No specific clinical factor identified those patients who developed acute pulmonary infarction. Anticoagulant therapy is strongly recommended in the pediatric patient with poor ventricular function awaiting heart transplantation.
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PMID:Acute pulmonary embolism in pediatric patients awaiting heart transplantation. 179

A case of pulmonary infarction secondary to subacute bacterial endocarditis of pulmonary valve which is associated with subpulmonary VSD is presented. The jet stream of blood through the subpulmonary VSD made damage to the pulmonary valve, which may be one of the reasons why subacute bacterial endocarditis was associated with the subpulmonary VSD. Echocardiography of the right-sided valves will be very useful in order to detect the pulmonary valve endocarditis in congenital heart disease presenting with fever.
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PMID:[A case of pulmonary infarction secondary to subacute bacterial endocarditis with subpulmonary VSD]. 273 96

Although recent advances have been made in understanding its epidemiology, diagnosis and treatment, pulmonary embolism (PE) is still largely undetected and untreated, and the mortality rate has not appreciably changed in the last decades. The aim of this study was to: compare the postmortem frequency of massive and sub-massive PE during two different time periods in the same general hospital; ascertain whether the percentage of correct clinical diagnosis of PE has changed; identify factors which might contribute to the inaccuracy of the clinical diagnosis of PE. Altogether, 288 patients with autopsy-proven PE and adequate clinical data were collected in the first period; 182 subjects with the same characteristics were found in the second period. Cases observed from 1989 through 1994 were evaluated in terms of frequency of false negatives and false positives, predictive value of the clinical diagnosis of PE, and correlations between clinical and post-mortem diagnosis of PE on one side and several independent variables such as age, gender, associated diseases, recent surgery on the other. In our hospital the frequency of massive and submassive PE at autopsy was 8.6% from 1966 through 1974, 12.6% from 1989 through 1994 (p < 0.01). The percentage of correct clinical diagnosis of PE was 19.6% in the former period, 21.6% in the latter (NS) with 78.57% of false negatives and only 1.73% of false positives. Altogether the true positives were 21.42%, most of them being patients with massive PE. Clinical findings showed the coexistence of heart disease in 51.6% of the cases, congestive heart failure in 20.15%, metabolic disease in 7%, stroke in 12.5%, recent surgery in 12.5%. Autopsy revealed the presence of pulmonary infarction in 22% of cases, malignancy in 24.0%, pneumonia in 17.05%, acute myocardial infarction in 14.8%. Seventy percent of the cases in whom the point of origin of thromboemboli could be demonstrated had one or more thrombus in the district of inferior vena cava, more frequently at the level of the femoral and iliac veins. The positive predictive value of the clinical diagnosis of PE was 0.60, the negative predictive value 0.84. Multivariate logistic regression analysis showed that the clinical diagnosis of PE was hindered by the presence of pneumonia, facilitated by admission to the Cardiological Department. Age, duration of hospitalization, presence of pulmonary infarction, cancer, obesity, stroke, heart failure and recent surgery did not influence the clinical diagnosis of PE in this series. A positive correlation (p < 0.05) was found between autopsy rate and the percentage of correct clinical diagnosis of PE in the various hospital departments. This relationship needs further investigation, all the more so as in most countries the autopsy rate has been dramatically declining in recent times, especially in late life. In conclusion, at least in some institutions, the autopsy frequency of PE has increased during the last decades, and this increase has not been paralleled by a significant improvement in clinical diagnosis.
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PMID:"False negatives" and "false positives" in acute pulmonary embolism: a clinical-postmortem comparison. 909 Jan 62

The autopsy protocols of 560 patients were studied in order to detect the incidence of pulmonary embolism, 83 cases were found (15%). The clinical data was analyzed to establish the existence of differentiating points between subjects with pulmonary infarcts and those with embolism but without infarction. The necropsy findings were further scrutinized to determine the effect of the anatomic localization of the embolus upon the production of infarction. Pulmonary infarctions were present in 60% of the cases with pulmonary embolus. The presence of cardiac failure, valvular heart disease and left ventricular hypertrophy was significantly more frequent in patients with pulmonary infarcts. In subjects with or without infarction the age, sex and the presence of medical debilitating diseases, recent trauma, surgical interventions or postpartum, cardiac diseases, arteriosclerotic heart disease, clinical evidence of thrombophlebitis, prolonged bed rest and atrial fibriliation preceding the pulmonary embolism, did not evidenciate any significant difference. In the cases with infarction the pulmonary embolus was significantly more frequently located in the small and sublobar pulmonary artery branches, while when pulmonary infarction was not found the embolic process was more frequently located in the main, right or left pulmonary arteries; occlusion of the lobar arteries had approximately the same incidence in the two groups. The most common clinical signs of pulmonary thromboembolism were dyspnea, tachycardia, cough and shock. The presence of hyperthermia, cough, jaundice, bloody sputum, pleuritic pain, pleural friction rub and pleural effusion was significantly more frequent in those cases with pulmonary infarction; the last five features were present only in the presence of infarction. The electrocardiogram was strongly suggestive of pulmonary embolism in the 6% of all cases, while the chest X-ray in 30% of those with pulmonary infarct. The diagnosis was established antemortem in 40% of the cases with infarction and in 20% of the cases with embolus but without pulmonary infarction. In 23% adequate anticoagulant therapy was established.
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PMID:[Anatomoclinical study of pulmonary embolism in patients with or without pulmonary infarction]. 1515 31