Subject(s)
Chest Pain/etiology , Dyspnea/etiology , Histiocytoma, Benign Fibrous/complications , Lung Neoplasms/complications , Neoplastic Cells, Circulating , Constriction, Pathologic/pathology , Histiocytoma, Benign Fibrous/pathology , Humans , Lung Neoplasms/pathology , Male , Middle Aged , Pulmonary Artery/pathologyABSTRACT
This is a report of a 25-year-old patient with known aortic valve stenosis since early youth and hemophilia A, showing recurrent joint bleeding. Acute Streptococcus endocarditis induced aortic valve insufficiency resulting in cardiac failure. Aortic valve replacement was performed after substitution of factor VIII, during which intra- and postoperative bleeding was prolonged by pericardial adhesions. Heparin was administered during cardiopulmonary-bypass as usual, but usual postoperative cumarin therapy was not initiated due to prolonged PTT time. One year postoperatively, the patient was in an excellent condition and fully rehabilitated.
Subject(s)
Aortic Valve Insufficiency/surgery , Aortic Valve Stenosis/surgery , Endocarditis, Bacterial/surgery , Heart Valve Prosthesis , Hemophilia A/blood , Streptococcal Infections/surgery , Adult , Aortic Valve Insufficiency/blood , Aortic Valve Stenosis/blood , Blood Vessel Prosthesis , Endocarditis, Bacterial/blood , Factor VIII/administration & dosage , Humans , Male , Partial Thromboplastin Time , Streptococcal Infections/bloodSubject(s)
Furosemide/administration & dosage , Hydrochlorothiazide/administration & dosage , Hypertension/drug therapy , Minoxidil/administration & dosage , Propranolol/administration & dosage , Pyrimidines/administration & dosage , Blood Pressure/drug effects , Cardiac Output/drug effects , Clinical Trials as Topic , Drug Evaluation , Drug Therapy, Combination , Electrocardiography , HumansSubject(s)
Hemodynamics/drug effects , Hypertension/drug therapy , Minoxidil/therapeutic use , Pyrimidines/therapeutic use , Blood Pressure/drug effects , Cardiac Output/drug effects , Clinical Trials as Topic , Humans , Hypertension/physiopathology , Minoxidil/pharmacology , Pulmonary Circulation/drug effects , Vascular Resistance/drug effectsABSTRACT
1. The chronic administration of minoxidil, 0-024-0-212 mmol (5-40 mg) daily, to fifty-two severely hypertensive patients resulted in an average reduction of mean arterial pressure from 170 to 111 mmHg. 2. Haemodynamic studies in twelve of these patients indicated that the rise in pulmonary arterial pressure in patients without heart failure appears to be a direct result of a disproportionately large increase in cardiac output with respect to a relatively small decrease in pulmonary vascular resistance. Anti-hypertensive treatment of patients with congestive heart failure resulted in a decrease in mean pulmonary arterial pressure.
Subject(s)
Hypertension/drug therapy , Minoxidil/therapeutic use , Pulmonary Circulation , Pyrimidines/therapeutic use , Adult , Aged , Cardiac Output/drug effects , Female , Humans , Male , Middle Aged , Pulmonary Artery , Vascular Resistance/drug effectsABSTRACT
Regional myocardial blood flow was measured by means of a computerized gamma-camera system in 30 patients with coronary artery disease (CAD) and in 14 healthy control subjects. Ventricular wall motion was quantitatively analyzed in 65 CAD-patients. Global and semiregional blood flow measurements yielded only limited information. In contrast, measurements of regional blood flow permitted detection of hypoperfused myocardium and the effects of pharmacologic intervention. The administration of 15 mg isosorbide dinitrate (ISDN) resulted in an increase in blood flow in post-stenotic hypoperfused myocardial regions of 20p.c. and a decrease in flow through normal myocardium of 14 p.c. These observations represent the adaption of flow to a newly-established level of metabolic demand. This increase in blood flow coupled with a reduction in afterload leads to improved ventricular wall motion in 65-75 p.c. of areas of hypokinetic myocardium and, to a markedly lesser degree, in only 20-25 p.c. of akinetic regions. Dyskinetic regions show no improvement. As compared with the 13ml/loog/min increase in blood flow seen after intracoronary administration of 0.45 mg ISDN in normal coronary vessels, the compromised dilatory capacity of diseased coronary vessels results in a relatively small increase in flow of 6 ml/100 g/min. The reduction of the extravascular component of coronary resistance, thus, appears to be the mechanism primarily responsible for the therapeutic effect of nitrates.