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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of lasix (in 51 patients) and strophanthin (in 16 patients) on the dynamics of changes in the amount of fluid in the chest and leg in cardiac insufficiency was studied by impedance plethysmography. It was established that in isolated insufficiency of only the left parts of the heart, parenteral administration of 20 mg of lasix led almost in all cases to a decrease in the total amount of fluid in the chest and its organs by 14% on the average; the decrease in the volume of fluid in pulmonary edema, cardiac asthma, and insufficiency of the left parts of the heart without acute manifestations is practically the same and amounts to 17, 14, and 12% on the average, respectively. In isolated hypervolemia of the pulmonary circulation, lasix causes a decrease in the amount of fluid in the leg also, by 7% on the average, in three fourths of cases. In total cardiac insufficiency, lasix reduces the volume of fluid in the chest and leg to a similar degree (by 13 and 16% on the average) practically in all cases.
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PMID:[Dynamics of the amount of fluid in the chest cavity and lower extremities in cardiac insufficiency under the influence of strophanthin and lasix]. 34 39

Subsequent to an examination of 133 patients, made several years after transmural myocardial infarction sustained by them, features specific for the clinical course of post-infarction cardiac insufficiency are analyzed. The examination included studies of the hemodynamics, veloergometry, measurements of the end diastolic pressure in the left ventricle, ventriculography and selective coronaroangiography. A considerable proportion of patients with extensive infarction in their history were found to suffer from chronic left ventricle incompetence with recurrent attacks of cardiac asthma. In the development of congestive cardiac insufficiency along the larger circulation an important role plays a sharply diminished contractility of the left ventricle due to the presence of extensive areas of akinesia and, in individual cases, also because of mitralism of the heart.
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PMID:[Characteristics of the clinical course of post-infarct cardiac insufficiency]. 112 65

The bronchial circulation is a physiological left-to-left shunt; the venous return of the bronchial arteries vascularising the intra-pulmonary bronchi drains directly into the left heart chambers. In cardiac failure, increased left ventricular filling pressures affects the bronchial circulation and causes stasis and congestion. Congestion of the arterial and venous bronchial microcirculation leads to thickening of the bronchial mucosa and submucosa, resulting in a tendency to obstruct small and medium-sized airways. The bronchial circulation can be explored indirectly in cardiac failure by the spirometric response to adrenergic agonists and antagonists administered by inhalation: bronchial vasomotor phenomena explain the symptomatology of cardiac asthma and also seem to play a role in the genesis of the dyspnoea of effort in patients with cardiac failure.
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PMID:[Vasomotility of the bronchial circulation in cardiac failure]. 211 88

Respiratory failure accompanied by cardiac failure occurs mostly due to decreased PaO2. However, sometimes we encounter patients with cardiac failure having on increase of PaCO2, who develop CO2 narcosis in the ICU. In this study we evaluated hypoventilation respiratory failure in patients with cardiac failure. Seventy-six patients with both respiratory failure and cardiac failure caused by intrinsic heart disease, who required mechanical ventilation in the ICU were studied. The patients were divided into 2 groups; hypoxic respiratory failure group (n = 53) and hypoventilation respiratory failure group (n = 23). Blood gas analysis and cardiovascular hemodynamics including arterial blood pressure, heart rate and Swan-Ganz catheter findings were performed before, during and after mechanical ventilation in each patient. Mortality rate and its relation to hemodynamic variables were also evaluated in each group. In both groups even when it was possible to maintain oxygenation capacity by conducting mechanical ventilation against severe respiratory failure, what can be said about the prognosis is that it depended totally on the improvement of cardiac function. The mechanism by which hypoxemia is displayed due to cardiogenic pulmonary edema is already well known, but in regard to the mechanism of hypercapnia in cases with hypersensitivity of the airways it is thought that through induction of cardiogenic pulmonary edema bronchial spasms is induced, and this causes hypercapnia. However, it is also possible to consider cardiac asthma as the cause. Among respiratory failure cases due to cardiogenic pulmonary edema that occurs in association with heart failure, there is both hypoxic respiratory failure as well as hypoventilation respiratory failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Study on the respiratory failure with cardiac failure--focus on hypoventilation respiratory failure]. 221 87

The clinoco-hemodynamic and angiocardiographic indices were analysed in 122 patients to determine the risk factors of postoperative development of acute cardiac insufficiency after surgery for chronic postinfarction aneurysm of the heart. The risk of the development of the complication was high in patients with the ejection fraction of the contracting part less than 38%, the stoke index below 38 ml/m2, and affection of the trunk of the left coronary artery. Other prognostically unfavourable indices are a clinical picture of cardiac asthma, a history of more than two infarctions, poor blood supply to the lateral wall of the left ventricle, total ejection fraction of less than 25%, cardiac index below 2.5 l/min/m2, and end diastolic pressure of more than 24 mm Hg. Appraisal of the risk index in marks made it possible to determine quantitatively the significance of each prognostic index, classify the patients according to the degree of the initial severity, and prognosticate the development of acute cardiac insufficiency objectively.
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PMID:[Predicting postoperative acute heart failure after surgical treatment of patients with post-infarction heart aneurysm]. 239 89

Disorders of the heart frequently cause pulmonary dysfunction because of the close structural and functional association of the heart and lungs. The pulmonary vasculature is very commonly affected by cardiac pathology. The pulmonary vasculature is normally a low-pressure, low-resistance circuit with high compliance and tremendous vascular reserve. Although resting vascular tone is low, there are many identified mediators of pulmonary arterial tone that may help mediate pulmonary blood flow. Alveolar hypoxia is clearly a stimulus for increasing pulmonary vascular resistance although factors that mediate the response to hypoxia are not fully understood. Patients with left-to-right shunting due to congenital heart disease because of elevations in pulmonary artery flow and pressure tend to develop progressive anatomic changes in the pulmonary vasculature. This leads to an increase in pulmonary vascular resistance, irreversible pulmonary hypertension, right heart failure, reversal of shunt flow, and Eisenmenger's syndrome. The degree of anatomic vascular damage due to left-to-right shunting can be graded histologically. Lesser grades of damage are reversible with corrective surgery, whereas more severe grades show no improvement or progression with operation. Chronic left-sided congestive heart failure seen in rheumatic mitral stenosis can cause secondary changes in the pulmonary vasculature. Pulmonary hypertension and increased pulmonary vascular resistance can increase reflexly and form a "second stenosis" that further limits cardiac output. Unlike congenital heart disease, severe grades of pulmonary arterial damage are not seen in left heart failure from mitral stenosis or other causes, and consequently with surgical correction pulmonary hypertension reverses. Pulmonary function testing is adversely affected by congestive heart failure. Both restrictive (stiff lungs) and obstructive (cardiac asthma) defects are observed in congestive heart failure. DLCO is abnormally decreased. With treatment of heart failure these defects reverse. Both elevated systemic and pulmonary venous pressures affect fluid filtration in the pleural space and cause pleural fluid accumulation. The fluid is transudative with low protein, low lactate dehydrogenase, and low cell counts. Transudative effusions from heart failure resolve with treatment. With large effusions and cardiomegaly, pulmonary dysfunction results because of atelectasis from compression and space-occupying effects of the heart and pleural fluid. Following myocardial infarction, cardiac surgery, or other cardiac trauma, the postcardiac injury syndrome can result. The syndrome is characterized by exudative pleural and pericardial effusions along with pulmonary infiltrates, fever, chest pain, leukocytosis, and an elevated ESR. The syndrome must be diagnosed by exclusion of bacterial pneumonia, pulmonary emboli, and congestive heart failure. Treatment is with nonsteroidal anti-inflammatory agents or systemic co
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PMID:Pulmonary and pleural complications of cardiac disease. 268 66

In view of the paucity of reports describing symptoms of increased degree, and deterioration of left ventricular systolic function in patients with apical hypertrophic cardiomyopathy (apical HCM), two cases with congestive heart failure and progressive thinning of previously hypertrophied apical portions of the left ventricle are reported. These were among 13 patients observed from eight to 10 years. Case 1: A 56-year-old man was diagnosed as having apical HCM at the age of 49 years. Severe left ventricular hypertrophy and prominent ST-T changes were observed on ECG during his first admission. His left ventricular end-diastolic pressure (LVEDP) was 24 mmHg and a left ventriculo-gram revealed a decrease in the left ventricular cavity in the apex and marked hypertrophy of the apical wall. Moderate interstitial fibrosis without hypertrophy or disarray of myocytes was observed in a left ventricular endomyocardial biopsy specimen. In two episodes of cardiac arrest he was successfully resuscitated at the age of 50 years. At the age of 55 years, two-dimensional echocardiography revealed thinning and abnormal motion in the apical wall, and a defect in 201T1 accumulation was observed in the same region by perfusion scintigraphy. This patient was readmitted with a diagnosis of cerebral embolism at the age of 56 years. Cardiac catheterization revealed normal LVEDP (8 mmHg), and a left ventriculogram revealed an aneurysm in the left ventricular apex with normal major epicardial coronary arteries. He has been under treatment with antiarrhythmic medications, calcium antagonists and anticoagulants, and has become relatively asymptomatic. Case 2: A 69-year-old-man was diagnosed as having apical HCM after a complete evaluation, including cardiac catheterization, at the age of 59 years. His LVEDP was elevated (17 mmHg), and a left ventricular angiogram revealed marked hypertrophy localized to the apex. Ejection fraction was 64%. A left ventricular endomyocardial biopsy revealed interstitial fibrosis without hypertrophy of myocytes. Thereafter, he has been followed as a New York Heart Association functional class III to IV with occasional elevation of cardiac enzymes but without chest pain or acute changes in his ECGs. However, atrial fibrillation with complete right bundle branch block developed at the age of 60 years. Apical wall thinning and dyskinesis were diagnosed by 2D echocardiography and a defect in the 201T1 accumulation was observed at about 65 years of age. He was readmitted in severe cardiac failure at the age of 69 years, and he was diagnosed as having cardiac asthma with pulmonary capillary wedge pressure of 35 mmHg.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Advanced sequelae of apical hypertrophic cardiomyopathy: report of two cases with wall motion abnormalities]. 322 16

The improved cardiac function in patients with congestive heart failure treated with coenzyme Q10 supports the hypothesis that this condition is characterized by mitochondrial dysfunction and energy starvation, so that it may be ameliorated by coenzyme Q10 supplementation. However, the main clinical problems in patients with congestive heart failure are the frequent need of hospitalization and the high incidence of life-threatening arrhythmias, pulmonary edema, and other serious complications. Thus, we studied the influence of coenzyme Q10 long-term treatment on these events in patients with chronic congestive heart failure (New York Heart Association functional class III and IV) receiving conventional treatment for heart failure. They were randomly assigned to receive either placebo (n = 322, mean age 67 years, range 30-88 years) or coenzyme Q10 (n = 319, mean age 67 years, range 26-89 years) at the dosage of 2 mg/kg per day in a 1-year double-blind trial. The number of patients who required hospitalization for worsening heart failure was smaller in the coenzyme Q10 treated group (n = 73) than in the control group (n = 118, P < 0.001). Similarly, the episodes of pulmonary edema or cardiac asthma were reduced in the control group (20 versus 51 and 97 versus 198, respectively; both P < 0.001) as compared to the placebo group. Our results demonstrate that the addition of coenzyme Q10 to conventional therapy significantly reduces hospitalization for worsening of heart failure and the incidence of serious complications in patients with chronic congestive heart failure.
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PMID:Effect of coenzyme Q10 therapy in patients with congestive heart failure: a long-term multicenter randomized study. 824 97

We investigated the effect of amrinone, a phosphodiesterase III inhibitor, on rat airway smooth muscle, and thereafter, compared its activity with aminophylline and diltiazem. Amrinone produced relaxation of the acetylcholine-induced airway contraction in a dose-related manner. This bronchodilatory activity of amrinone was similar to that of aminophylline, but smaller than that of diltiazem. The 50% relaxant effect (ED50) of amrinone, aminophylline and diltiazem were 3.6 x 10(-4) M, 1.4 x 10(-4) M and 1.4 x 10(-5) M, respectively. Diltiazem was the most potent airway relaxant, and amrinone was less potent in these experiments. Taken together in its positive inotropic and chronotropic effects and anti-inflammatory activity, however, amrinone could be beneficial for treatment of patients suffering from asthma or heart failure with cardiac asthma.
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PMID:Comparative effect of amrinone, aminophylline and diltiazem on rat airway smooth muscle. 1090 23

A 55-year-old woman with a blank cardiac history was admitted in a regional hospital because of acute left sided heart failure. Initial evaluation showed a subacute inferior wall myocardial infarction with preserved left ventricular function and moderately severe mitral regurgitation. Before referral, coronary angiography was performed. Ventriculography revealed a posterior pseudoaneurysm that was missed initially. Fortunately she survived two almost fatal episodes of cardiac asthma in that hospital. After the diagnosis was made, she was sent to our tertiary care hospital, where she was urgently and successfully operated. A short review, with emphasis on diagnosing left ventricular pseudoaneurysm is presented.
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PMID:Ventricular pseudoaneurysm after subacute myocardial infarction. 1672 36


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