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Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a male patient, chromosomal complement 44 XY with Turner's phenotype, who has multiple skeletal, genitourinary and mild cardiac abnormalities, without hypogonadism. This patient developed a diffuse infiltrative pulmonary disease which result in pulmonary fibrosis, respiratory insufficiency and cardiac failure. He has also mixed cryoglobulinemia (Type III) with antigammaglobulin antibodies. The relationship among these problems and his phenotype is discussed. Apparently there is only a coincidental association.
Arch Inst Cardiol Mex
PMID:[Classical interstitial pneumonitis and mixed cryoglobulinemia in a male with Turner phenotype. Report of a case and review of the literature]. 43 55

Left heart diseases, in particular mitral stenosis, are often associated with anatomic and functional alterations of the lung. According to the pulmonary structures involved they could be named chronic secondary intersticial and vascular lung diseases. Congenital heart diseases with pre- or post-tricuspid shunts are also often associated with anatomic and functional alterations of the lung. This condition also constitutes a chronic secondary vascular lung disease (atrial septal defect) or a chronic primary vascular lung disease ( ventricular septal defect, patent ductus arteriosus). Primary lung diseases (interstitial pulmonary fibrosis, pulmonary emphysema, recurrent pulmonary embolism) are often associated with right ventricular hypertrophy with or without dilation, a condition commonly named chronic cor pulmonale. On the whole the interrelationships between heart and lung diseases are as follows: a) anatomic and functional alterations of the lung due to left heart diseases are mediated through pulmonary venous hypertension; b) anatomic and functional alterations of the lung due to congenital heart diseases are mediated through the increased pulmonary blood flow with or without transmission of the systemic blood pressure to the pulmonary vasculature, and c) anatomic and functional alterations of the right ventricle due to primary or secondary lung diseases are mediated through arterial pulmonary hypertension. In summary, the interrelationships between heart and lung diseases are mainly mediated through the pulmonary venous or pulmonary arterial hypertension.
Arch Inst Cardiol Mex
PMID:Cardiac and pulmonary diseases. A pathophysiologic interelationship. 113 Sep 7

Amiodarone was used in the treatment of 21 patients with supraventricular or ventricular arrhythmias which were refractory to conventional antiarrhythmic drugs, individually or in combination. Six of seven patients with supraventricular arrhythmias and 12 of 14 with ventricular tachycardia were controlled with amiodarone. Although side effects were common, only one patient was removed from treatment due to pulmonary fibrosis. We conclude that amiodarone is an effective antiarrhythmic drug for refractory ventricular and supraventricular arrhythmias.
Clin Cardiol 1986 Jun
PMID:Amiodarone: an effective alternative for recalcitrant supraventricular and ventricular tachycardias. 242 56

A patient affected with periarteritis nodosa and angina, presented a normal coronary angiography of the coronary trunks and an alteration of the left ventricular systolic function, improved by nicardipine, as well as a pre-capillary pulmonary hypertension with isolated, right cardiac repercussions, without pulmonary fibrosis nor thromboembolic disease. In addition, he presented three transient cerebral ischaemic accidents, with different localizations, which could not be related to a right aneurysm of the sylvian artery. Isolated precapillary pulmonary hypertension, without pulmonary fibrosis, which is not described in the course of periarteritis nodosa, seems related to an arteriolar involvement which is the known substratum of other visceral involvement in periarteritis nodosa. Improvement of the left ventricular function with nicardipine, administered acutely, suggest a partially reversible disorder of the coronary microcirculation.
Ann Cardiol Angeiol (Paris) 1989 Jun
PMID:[Angina without involvement of large coronary trunks and precapillary pulmonary hypertension in a patient with periarteritis nodosa]. 256 88

Amiodarone has remarkable efficacy, but it also has a high incidence of severe side effects. Nevertheless, it is extensively used. The findings of an amiodarone treatment follow-up period of one to 72 months (mean 19 +/- 17) in 95 patients with recurrent life threatening arrhythmias resistant to other antiarrhythmic drugs are described. The mean loading dose of 800 mg/day for one week was followed by an average dose of 600 mg/day for two weeks. The long term daily dose was 400 mg in 80 patients and 200 mg in the remaining 15 patients. Amiodarone was particularly effective in suppressing complex ventricular arrhythmias. It also decreased premature ventricular beats by 83% and atrial premature beats by 41%. Supraventricular tachycardias were completely controlled and the ventricular response to atrial fibrillation was slowed. Twelve of the 95 patients (12.6%) died while taking amiodarone, two of sudden death and 10 of heart failure. Side effects were recorded in 77 (81%) patients. They were generally dose related and subsided with a decrease in dose or discontinuation of the medication. There was a correlation between the concentration of rT3 and the significance of the side effects. Thirty-nine patients stopped taking amiodarone, however, only 14 of these stopped because of toxicity: five developed pulmonary fibrosis; three had neurological toxicity; two had bradyarrhythmias; two developed hepatic dysfunction; one had hypothyroidism; and one patient suffered an aggravation of a pre-existent heart failure. It was concluded that amiodarone is a very effective treatment for supraventricular and ventricular arrhythmias. However, it does have numerous and severe side effects.(ABSTRACT TRUNCATED AT 250 WORDS)
Can J Cardiol 1989 Mar
PMID:Long term efficacy and toxicity of amiodarone in the treatment of refractory cardiac arrhythmias. 270 79

Classification of ventricular arrhythmias into those that are benign, potentially lethal and lethal is based on their associated risk for producing sudden cardiac death. This classification system is useful in defining indications for the treatment of ventricular arrhythmias and predicting differential rates of antiarrhythmic drug efficacy and toxicity. Whether the reduction of potentially lethal ventricular arrhythmias will prevent sudden cardiac death remains to be determined. The class II antiarrhythmic agents--the beta-adrenergic blocking drugs--have been shown to reduce sudden cardiac death in postmyocardial infarction patients, but the precise mechanism of their effect has not been defined. beta blockers are efficacious in approximately 50% of patients with benign or potentially lethal ventricular arrhythmias. This response is comparable to that seen with the class IA agent disopyramide or the class IB agents tocainide and mexiletine. beta blockers have favorable side-effect profiles including a low incidence of proarrhythmia and a lack of organ toxicity such as hepatitis, pulmonary fibrosis or agranulocytosis, which are concerns with class I and class III antiarrhythmic drugs. The proper dosage of the beta blocker is critical in limiting adverse effects. In a study of 23 patients with benign or potentially lethal ventricular arrhythmias, 11 (48%) of the patients responded to nadolol with a reduction of greater than 75% in arrhythmia frequency, and several patients responded at nadolol dosages as low as 10 mg daily. Thus, it is plausible to consider beta blockers as first-choice antiarrhythmic therapy, even in patients with left ventricular dysfunction when sympathetic tone is not required to maintain cardiac compensation.
Am J Cardiol 1987 Aug 31
PMID:Antiarrhythmic effects of beta-adrenergic blocking agents in benign or potentially lethal ventricular arrhythmias. 288 97

In the adult, Amiodarone is a very effective drug in the treatment of ventricular and supraventricular arrhythmias. The presence of severe side effects such as some alterations in the thyroid function and/or pulmonary fibrosis have restricted the use in children. Nevertheless, research has shown that there is a low incidence of collateral side effects and this therapy in infancy can be very effective. For this reason we evaluated a group of 27 children with supraventricular (19 patients) and ventricular (8 patients) arrhythmias. The mean age of patients treated was 6 +/- 5 years (2 days-13 years). The follow-up period was of 13 +/- 10 months. Amiodarone has been used in 9 patients intravenously, with the loading dose of 5 mg/Kg followed by an infusion of 10 mg/Kg/day. In 18 patients we administered the drug orally with a loading dose of 10 mg/Kg/day for a period of 10 days, thereafter the maintenance was of 5-7 mg/Kg/day for 5 days every week. The patients were all checked for thyroid function and Holter monitoring quarterly; they were given an ophthalmologic examination (every 6 months) and a chest-x-ray and echocardiography annually. The efficacy of intravenous treatment was judged successful in 56% of patients, partially successful in 22% and ineffective in the remaining 22%. The oral treatment was completely effective in 77% of children, partially in 5% and ineffective in 18%. In one case we had to suspend the therapy because we found high values of T3 and T4. During the treatment, in 86% of cases, we had blood level fluctuations of T3 and T4, however these did not exceed the normal ranges. The most important side effect observed has been the photosensitivity found in 22% of children. Moreover we observed a reduction of sinusal automatism, which was more marked in patients less than year old. In 4 cases an A/V block of first degree appeared. In all patients we found changes of ventricular repolarization, while corneal deposits appeared in only one child after a year of therapy and did not cause an impairment of visual acuity. In conclusion we can assert that Amiodarone is a very effective drug in children, specially in small babies, where it can safety be used as a first choice drug.
G Ital Cardiol 1985 Aug
PMID:[Amiodarone therapy in childhood: efficacy and side effects]. 293 40

We studied one hundred consecutive patients with rheumatoid arthritis from the cardiological point of view through non invasive methods to detect the frequency of cardiovascular complications. Seventy three (73%) were females and twenty seven (27%) males. Mean age, 48.6 years. Mean age of presentation of the disease, 34.2 years. Mean age of duration of the illness, 21.8 years. Fifty seven per cent had some type of cardiopulmonary complication. Clinically 52 per cent referred some type of cardiopulmonary symptoms. The physical examination was abnormal in 27 per cent. Rheumatoid factor (Waaler-Rose) was positive in 82 per cent. The cardiac X ray series was abnormal in 33 per cent, the resting electrocardiogram in 48 per cent and the M mode echocardiogram in 52 per cent of the cases. The complications detected were: pericardial effusion (21%); pleural effusion (9%); pulmonary fibrosis (6%) which represents a higher incidence of previously reported in the literature; congestive heart failure (10%); valvular lesion (9%) among those are included six patients with valvular heart disease of non detectable etiology; ischemic heart disease (8%); myocarditis (6%); rythm disturbances (22%) and conduction defects (20%) including a 46 year old female patient who developed a complete AV block during an exacerbation of her illness, requiring the insertion of definitive pacemaker. Our results showed that some of the detected lesions are in part more frequent and severe than those reported in the literature, probably due to, that on one hand their search was intentional and on the other, our group was constituted by with severe and long standing rheumatoid arthritis.
Arch Inst Cardiol Mex
PMID:[The heart and rheumatoid arthritis. Prospective study of 100 cases]. 295 63

The radiologic appearance of atypical cardiogenic pulmonary edema (ACPE) is presented in 10 cases admitted from 1983 to 1985, with age ranges from 74 to 89, and with diagnosis of ischemic heart disease, with myocardial infarction in 50% of them. Clinically they had asthenia, adynamia and anorexia in 80%, cough and weight loss in 50%. All of them had tachycardia, pulmonary rales and 50% pericardial rub. ECG showed in 80% anterior subepicardial ischemia, 60% posteroinferior subepicardial ischemia, 60% bifascicular block, and 50% left anterior fascicular block. Chest films were interpreted at first as pulmonary fibrosis in 90% of the cases with superior lobe involvement in 50%. Heart enlargement was present in 50%. A chronic lung disease was disclosed on clinical and pulmonary physiological grounds. It is concluded that asthenia, adynamia and anorexia were atypical manifestations of heart failure in the elderly. Silent myocardial infarction was observed in half of our patients and it was complicated with pericardial involvement in 50%. Irregular distribution of fluids in pulmonary edema was attributed to anatomic changes in elder lung. These atypical behaviour of pulmonary edema, has been misinterpreted on radiologic basis with pulmonary infection, tumours, metastasis or fibrosis. Those radiologic changes disappeared or improved in 72 hrs. with treatment of left ventricular failure.
Arch Inst Cardiol Mex
PMID:[Radiologic characteristics of cardiogenic pulmonary edema in the elderly]. 296 66

We evaluated the hemodynamic effects of the calcium antagonist nifedipine in 13 consecutive patients admitted to the intensive care unit with secondary pulmonary hypertension. Etiology of secondary pulmonary hypertension was: chronic obstructive pulmonary disease (n = 9), pulmonary emboli (n = 2), pulmonary fibrosis (n = 2). We obtained the resting hemodynamic parameters before, and 60, 120, 180 minutes after the sublingual administration of nifedipine 20 mg. All patients had normal pulmonary artery wedge pressure before nifedipine. After 60 minutes, systolic pulmonary artery pressure fell from 72.3 +/- 7 to 57.3 +/- 5.4 mm Hg (p less than 0.005) and mean pulmonary artery pressure from 44.6 +/- 4.0 to 33.6 +/- 3.2 mm Hg (p less than 0.001). Cardiac output rose from 6.36 +/- 0.56 to 7.65 +/- 0.64 l/min (p less than 0.005). The pulmonary vascular resistance fell from 431 +/- 58 to 238 +/- 36 dynes. sec. cm-5 (p less than 0.001). Heart rate, mean systemic arterial pressure, pulmonary artery wedge pressure, total systemic vascular resistance and arterial partial pressure of O2 (PaO2) remained unchanged. In this heterogenous population we were unable to reproduce the results of other authors, showing a correlation between PaO2 and fall of pulmonary vascular resistance. These findings confirm the pulmonary vasodilating effect of nifedipine in patients with secondary pulmonary hypertension.
Acta Cardiol 1985
PMID:Hemodynamic effects of nifedipine on secondary pulmonary hypertension in man. 387 56


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