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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with rheumatic mitral stenosis often have no pulmonary oedema despite considerably increased pulmonary venous pressure. Pulmonary microvascular permeability was measured non-invasively by a previously validated method of double isotope scintigraphy with indium-113m and technetium-99m. This permits calculation of an index reflecting transferrin efflux and thus, indirectly, the microvascular permeability. Fifteen patients with severe mitral stenosis (defined as valve area less than 1.0 cm2) were compared with a control group of 11 patients with mild coronary artery disease. The permeability index was significantly lower in patients with mitral stenosis than in the control group. Furthermore, the extent of reduction of the permeability index correlated with the severity of mitral stenosis as reflected by the Gorlin valve area. This finding may account for the relative resistance of these patients to pulmonary oedema despite chronic pulmonary venous hypertension.
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PMID:Pulmonary microvascular permeability in patients with severe mitral stenosis. 186 52

To define the prevalence and role of left ventricular (LV) systolic dysfunction, LV diastolic dysfunction and mitral regurgitation (MR) in patients with acute pulmonary edema, 40 patients with coronary artery disease and acute pulmonary edema were prospectively evaluated within 36 hours of presentation. LV ejection fraction and 3 parameters of LV diastolic function were measured with radionuclide ventriculography, whereas MR was assessed with Doppler echocardiography. LV ejection fraction was normal in 11 (27%) and depressed in 29 (73%) patients. Moderate or severe MR without LV diastolic dysfunction was common and equally prevalent in patients with and without LV systolic dysfunction (33 vs 38%; difference not significant). Diastolic dysfunction without MR was less frequent but equally prevalent in patients with and without systolic dysfunction (17 vs 27%; difference not significant). Two (18%) of 11 patients without and 12 (33%) of 36 patients with LV systolic dysfunction had both MR and LV diastolic dysfunction. Furthermore, MR was clinically silent and unsuspected in two-thirds of all patients with MR, regardless of a normal or depressed systolic function. These data show that there is a high prevalence of unrecognized moderate to severe MR in patients with acute pulmonary edema, regardless of the presence or absence of LV systolic dysfunction. Furthermore, the prevalence of LV diastolic dysfunction without MR is relatively low even in patients with normal LV systolic function and pulmonary edema. Thus, unrecognized MR may be an important contributor to the syndrome of acute pulmonary edema in patients with normal or depressed LV systolic function.
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PMID:Prevalence of unsuspected mitral regurgitation and left ventricular diastolic dysfunction in patients with coronary artery disease and acute pulmonary edema associated with normal or depressed left ventricular systolic function. 198 1

An obese woman with a one-year history of episodic nocturnal chest pain was admitted because of shock and pulmonary edema. A clinical diagnosis of acute myocardial infarction and cardiogenic shock was made. She was ventilated and successfully resuscitated. Subsequent investigations showed no evidence of cardiac dysfunction or coronary disease, but sleep study confirmed the diagnosis of obstructive sleep apnea syndrome (OSAS). We suggest that the nocturnal angina and heart failure in this patient might have resulted from extreme hypoxemia produced by OSAS. This case raised the possibility that the high cardiovascular mortality rate reported in OSAS might not necessarily relate to underlying coronary artery disease. Further investigations are required to delineate the true incidence of coronary disease in patients with OSAS.
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PMID:Obstructive sleep apnea presenting with nocturnal angina, heart failure, and near-miss sudden death. 200 55

Diastolic function in coronary artery disease is modified to a variable extent. There are distinct abnormalities produced during acute ischemia, and following myocardial infarction. The pathophysiology of diastolic abnormalities in these two syndromes is reviewed. During acute ischemia filling pressures of the left ventricle are increased. Pulmonary edema may be produced. Silent ischemia causes less of an increase in filling pressures. The diastolic pressure-volume relation is shifted in an upward manner with a variable contribution from altered myocardial relaxation, increased muscle stiffness, acute pericardial restriction, ventricular interaction, and acute chamber dilatation. The impairment of myocardial relaxation plays a central role and has been quantified in multiple clinical and experimental studies. Filling of the left ventricle during ischemia is altered due to the factors which shift the pressure-volume relation. The acute increase in left atrial pressure may increase filling rates somewhat surprisingly, given the reduced left ventricular compliance. Myocardial fibrosis following infarction may elevate filling pressures, but the degree of elevation is closely tied to the intravascular volume status. Shifts in the diastolic pressure-volume relation reflect a loss of chamber compliance due to an increase in muscle stiffness. Increased amounts of extracellular matrix, specifically collagen, produce this permanent increase in muscle stiffness which is central to the diastolic abnormalities in chronic coronary artery disease.
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PMID:Diastolic function in coronary artery disease. 202 80

Over the last 22 years (1965-86), the 30-day mortality rate (30-DMR) after valve replacement for primary or predominant aortic stenosis (AS, N = 690) fell from 20.0% for the first 100 consecutive patients, via 7.8% for the next 490, to 2.0% for the final 100 (P less than 0.0001). There was, however, a wide scatter in 30-DMR in the 11 consecutive 2-year periods, as well as during later years. The variation in 30-DMR was paralleled by changes in a high risk prognostic index (derived from a logistic regression model) and in a high coronary artery disease (CAD) score. In patients with a high CAD score who died within 30 days, 93% (N = 25) had CAD at autopsy compared with 37% (N = 11) of those with a low CAD score (P less than 0.0001). In 205 patients evaluated by coronary arteriography, the 30-DMR was 4.1% in 122 without CAD, 3.6% (3.8% for triple vessel/left main stem) for 55 with CAD who underwent bypass grafting, and 17.9% for 28 with CAD who did not have bypass grafting (P less than 0.0001). Left ventricular failure (LVF; episodes of pulmonary oedema and/or stasis), age, pronounced hypertrophy/strain in the ECG, and a high CAD score were independent incremental risk factors for 30-DMR. Quantitatively, LVF increased the risk 10 times more than pronounced hypertrophy/strain and a high CAD score. LVF also neutralized the influence of age. Modifying (symptom-masking) digitalis and/or diuretic treatment in functional class II patients (N = 189) increased the 30-DMR from 0.9% to 9.1% (P less than 0.01). The scatter of operative year-specific 30-DMR was related to changes in preoperative prognostic patient profiles and to unrevascularized CAD. Operative intervention in AS patients, even with discrete symptoms, and consistent revascularization of significant CAD, should be strongly advocated.
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PMID:Thirty-day mortality after valve replacement for aortic stenosis over the last 22 years. A multivariate risk stratification. 204 Mar 14

Diastolic dysfunction is being recognized increasingly as a primary cause of congestive heart failure. It may result from physiological abnormalities of myocardial relaxation, or anatomical abnormalities which increase resistance to ventricular inflow. With regard to physiological abnormalities, there is substantial evidence to indicate that myocardial ischaemia and hypertrophy are two conditions characterized by impaired inactivation and relaxation of myocardial cells. These conditions often co-exist in patients with idiopathic hypertrophic subaortic stenosis or calcific valvular aortic stenosis. Recent evidence also suggests a role for calcium overload in the diastolic dysfunction seen in some patients with advanced congestive heart failure. Diastolic dysfunction may be of fundamental importance in the pathophysiology of flash pulmonary oedema in patients with advanced ischaemic heart disease, since myocardial ischaemia in such patients may lead to a decline in relaxation rate, increased resistance to early diastolic filling and further impairment in diastolic coronary blood flow due to intramyocardial compression of capillaries and venules. During the transient ischaemia of angina pectoris, patients with multivessel coronary artery disease often show a striking upward shift in the left ventricular diastolic pressure-volume relationship, signifying a marked decrease in distensibility of the left ventricular chamber. With regard to anatomical abnormalities, diastolic dysfunction in heart failure may result from structural changes within the ventricular wall. Diastolic dysfunction of the left ventricle may result from extrinsic compression by pericardial effusion (tamponade), pericardial constriction, and right ventricular overload. Thus, a variety of physiological and anatomical abnormalities may lead to increased resistance to diastolic filling of one or both ventricles, resulting in diastolic heart failure.
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PMID:Diastolic function and heart failure: an overview. 218 38

Out of 160 prospectively followed patients with aortic regurgitation, the clinical courses of 53 patients with pure, severe, and chronic aortic regurgitation and without coronary artery disease who were selected for surgery on the basis of predefined criteria is discussed. Surgical criteria were either unequivocal symptoms or documentation of impaired left ventricular dysfunction (defined as angiographic ejection fraction of less than 50% plus and end-systolic volume index greater than 60 ml/m2). According to preoperative status, patients were divided as follows: 11 asymptomatic patients (group A), 30 patients with moderate (classes II to III) symptoms (group B), and 12 patients with dyspnea at rest and pulmonary edema when first seen (group C). Surgical mortality was one patient (from group C). Late death occurred in four patients (one from group B, three from group C). At the end of follow-up (minimum 1 year, mean 3.6 years) 41 patients were in functional class I, four patients in class II, and one patient in class III. All patients except one in functional classes II and III belonged to group C. Before surgery, patients from groups A and B had similar ventricular dimensions and ejection fractions, whereas patients from group C had larger end-systolic diameters and volumes and lower ejection fractions. End-diastolic and end-systolic diameters decreased significantly at 1 and 2 years after surgery. Patients from group C continued to have dilated hearts as did those patients from groups A and B who had preoperative end-systolic diameters greater than 55 mm.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical evaluation of a prospective protocol for the timing of surgery in chronic aortic regurgitation. 238

The purpose of our article is to describe a patient with severe hypertension and moderate renal insufficiency, unstable angina, and a 6 cm abdominal aortic aneurysm. A previous aortogram had demonstrated severe bilateral renal artery stenoses. Cardiac catheterization demonstrated severe coronary disease. After cardiac catheterization acute renal failure and pulmonary edema requiring dialysis developed in the patient. In addition, evidence of impending myocardial necrosis developed. Because of the critical nature of the myocardial and renal ischemia it was necessary to perform combined myocardial and renal revascularization rather than staged procedures. At the time of coronary artery bypass grafting, a vein graft was anastomosed to the right coronary artery vein graft and tunneled through the diaphragm into the abdomen to revascularize both renal arteries. After surgery renal function gradually improved, and no further dialysis was required. The abdominal aortic aneurysm was repaired at a subsequent operation. At 2-year follow-up all grafts remained patent. The serum creatinine is 1.2 mg/dl. Although most patients with combined coronary artery disease and renal artery disease can be treated with staged operations, our procedure may be of value in patients in whom staged procedure are not feasible and in whom the infrarenal aorta is severely diseased or aneurysmal.
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PMID:Combined coronary artery bypass grafting and bilateral renal revascularization for unstable angina and impeding renal failure. 199 71

Hypertension is a well known risk factor of coronary artery disease. The aim of the study was to evaluate a clinical course and prognosis in hypertensive patients with acute myocardial infarction (MI). 100 consecutive patients with acute MI underwent the study. In 38 of them (28 males and 10 females) a history of hypertension and intermittent rises of arterial blood pressure in a course of MI were stated. All patients underwent 2-DE examination and 24 hours Holter ecg monitoring. Clinical characteristics consisted of the heart failure and arrhythmias occurrence as well as the in-hospital mortality. Significantly higher rate of MI in the past and/or angina pectoris as well as a diabetes mellitus was stated in hypertensive patients. In these patients inferior, transmural MI was more often observed, while there was no difference in life-threatening arrhythmias, pulmonary edema and cardiogenic shock between normotensive and hypertensive patients.
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PMID:[Myocardial infarction in patients with hypertension]. 281 Oct 21

Thirty-nine patients with symptomatic ectopic atrial tachycardia (9 paroxysmal, of which 5 were incessant) and atrial fibrillation (AF) (25 paroxysmal, 5 chronic) were treated with oral flecainide acetate (100 to 400 mg/day). Thirty-two patients had organic heart disease (16 coronary artery disease, 6 valvular, 10 cardiomyopathy, 7 primary electrical abnormality). Previous antiarrhythmic trials consisted of 0 to 5 drugs (mean 2.2). Of 39 patients with atrial tachycardia or AF, a complete response (no recurrent symptomatic atrial arrhythmia) was achieved in 22 (56%), a partial response (more than 95% reduction in arrhythmia occurrence) in 3 (8%) and no response in 14 (36%). Left atrial size, ejection fraction, underlying heart disease, duration of symptoms before treatment and drug levels were not useful for predicting clinical response. Therefore, during the follow-up period of 5.4 +/- 6.7 months (range 4 weeks to 2.5 years), flecainide had a complete or partial effect in 25 patients (64%). Complete or partial responses were noted in 8 of 9 patients (90%) with ectopic atrial tachycardia and 17 of 30 (57%) with AF. In 14 patients with concurrent ventricular arrhythmias, a significant reduction in episodes of nonsustained ventricular tachycardia was also achieved. Treatment was discontinued in 8 patients (20%) because of cardiac adverse reactions, including pulmonary edema and ventricular or atrial proarrhythmic response. Thus, oral flecainide acetate is effective therapy for some patients with ectopic atrial tachycardia or AF.
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PMID:Efficacy and safety of flecainide acetate for atrial tachycardia or fibrillation. 310 29


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