Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of atrial natriuretic peptide in the pathophysiology of heart failure is unknown. The aim of the study were changes of atrial natriuretic peptide, hemodynamic, renal and hormonal parameters during the development of cardiac failure in an animal model of congestive heart failure in the conscious dog due to rapid right ventricular pacing and in rats with chronic left ventricular failure due to a left ventricular infarction. The effects of intravenous administration of atrial natriuretic peptide were studied in patients with severe congestive heart failure, dogs with experimental cardiomyopathy and conscious rats with acute right ventricular failure due to repeated pulmonary emboli. The results suggest an important role of atrial natriuretic peptide in the early phase of heart failure as a counterregulating system concerning vasoconstrictory and volume retaining mechanisms like the renin-angiotensin-aldosterone system, the sympathetic nerve activity and vasopressin. In chronic heart failure the renal effects of atrial natriuretic peptide are attenuated. Pharmacological doses have beneficial effects on ventricular function by reducing pre- and afterload. The reduction in effectiveness of atrial natriuretic peptide in congestive heart failure may be due to a down-regulation of specific receptors, or caused by hemodynamic renal changes preventing the action of the hormone on the kidney in heart failure or may be due to an activation of counterregulating systems overridding the effects of atrial natriuretic peptide.
 ...
PMID:[Atrial natriuretic peptide in cardiac insufficiency]. 296 47

Plasma levels of atrial natriuretic peptide (ANP) were measured in patients with organic heart disease undergoing diagnostic cardiac catheterization. Independent of nature and duration of the disease (valvular heart disease, congestive cardiomyopathy) plasma ANP levels were closely related to the severity of cardiac failure. Furthermore, plasma ANP levels were found to be negatively correlated with the cardiac index and to be positively correlated with right and/or left atrial and with pulmonary artery pressures. During physical exercise (bicycle ergometer) a marked increase of plasma ANP levels was observed, which was closely related to increments in mean pulmonary artery pressure. This rise in plasma ANP levels during physical exercise was not attenuated in patients with already elevated resting plasma concentrations of ANP. In patients with congestive cardiomyopathy, afterload-reduction by ACE-inhibition resulted in changes of central hemodynamics, which were closely reflected by venous concentrations of ANP. The measurement of plasma ANP levels may serve as an indicator of the severity of cardiac failure. Plasma concentrations of ANP, however, are neither helpful in establishing the etiology of the underlying heart disease nor in differentiating left and right heart failure. However, in cases of already established organic heart disease plasma ANP levels may be used as a marker for assessing the efficacy of the therapeutic regimen.
 ...
PMID:[Does the measurement of plasma ANP have a diagnostic or prognostic value in patients with organic heart disease?]. 297 Jan 74

A naturally occurring cardiomyopathy in broiler chickens from a single Ontario farm was studied in order to define the morphologic changes. Gross and histologic features of affected birds were compared with those in age-matched control penmates. Body weight and weight and volume of individual cardiac chambers were measured. Histologic sections of 18 different tissues were examined, and lesions observed were scored subjectively. Affected birds were stunted and had marked right ventricular dilation and hypertrophy, atrial hypertrophy, ascites, pulmonary congestion and edema, and hepatic capsular fibrosis. Microscopic changes in the heart of affected birds were mild and did not suggest a specific cause of heart failure. Lungs had marked hypertrophy of parabronchial smooth muscle and collapse and apparent loss of associated air capillaries. Other histologic changes observed were thought to be the result of passive congestion of viscera caused by right heart failure and chronic debility. Although the specific etiology of this condition could not be determined, it was felt that this syndrome was unlikely to have been the result of any of the commonly recognized causes of congestive heart failure and ascites in broilers.
 ...
PMID:Lesions of right heart failure and ascites in broiler chickens. 304 56

The present study was undertaken to clarify the natural history of primary pulmonary hypertension (PPH) from a hemodynamic point of view. The subjects consisted of 83 patients (18 men and 65 women), whose ages ranged from 14 to 69 years and averaged 33 years. They were contacted through a nationwide survey. All patients underwent right-sided cardiac catheterization; cardiac output was measured in 52 patients and pulmonary capillary wedge pressure, in 40 patients. The following results were obtained. 1. The patients who died within three months of their cardiac catheterization were in severe right ventricular failure as shown by their elevated right atrial pressures and decreased cardiac indices. 2. The patients who died suddenly within two years of their cardiac catheterization had the same degree of right ventricular failure. The only difference was severe hypoxia in the patients with cardiac failure (54 +/- 21 vs 66 +/- 4 mmHg, p less than 0.05). 3. The patients who survived more than two years had normal right ventricular function. 4. Among the hemodynamic variables used to estimate prognosis; namely, pulmonary artery diastolic pressure, pulmonary capillary wedge pressure, cardiac index, pulmonary vascular resistance and pulmonary to systemic vascular resistance ratio, the cardiac index was the best predictor of prognosis.
 ...
PMID:[Natural history of primary pulmonary hypertension elucidated by pulmonary hemodynamics]. 324 88

Using bolus-enhanced CT, we encountered an unusual constellation of findings in seven patients with clinical evidence of right heart failure. These included retrograde hepatic venous opacification on the early bolus scans and a diffusely mottled pattern of hepatic enhancement seen only during the vascular phase of contrast administration. Ancillary CT findings include cardiomegaly, pleural effusions, ascites, and intrahepatic perivascular radiolucency. We believe that these CT abnormalities are caused by passive hepatic congestion. This pattern of abnormal hepatic enhancement represents a potential pitfall in the use of dynamic bolus-enhanced CT for the detection of focal hepatic masses. Recognition of passive hepatic congestion as a possible cause of mottled hepatic enhancement on CT may help explain clinical abnormalities of liver function in patients with heart failure and prevent confusion with other disease processes that produce abnormalities of hepatic attenuation.
 ...
PMID:Passive hepatic congestion in heart failure: CT abnormalities. 326 26

Three recent cases from one institution using the total artificial heart (TAH) before transplantation are reviewed. The first patient was implanted for 12 hours with the pneumatic Phoenix total artificial heart after failure of a donor heart 1 day after transplant. Following retransplantation the patient died from severe pulmonary edema, pulmonary hypertension, right ventricular failure, and Pseudomonas septicemia. The second patient was implanted with the Jarvik-7 total artificial heart for rapidly deteriorating idiopathic cardiomyopathy. Major complications during the 9 1/2-day implant consisted of severe pulmonary edema for the first 4 days and a multifocal cerebral embolic event on the seventh day after implantation from which he fully recovered. Major problems after transplant included disseminated toxoplasmosis and two mild episodes of rejection. The patient was discharged 68 days after surgery and remains well. The third patient was a 40-year-old woman with rapidly progressing acute influenza A viral myocarditis. Despite immunosuppressive and antiviral therapy, cardiogenic shock with multiple organ failure developed. The 70 ml Jarvik-7 was implanted for 4 1/2 days. Acute humoral rejection from autoantibodies and alloantibodies led to a cardiac arrest on the second day after transplantation. A second 70 ml Jarvik-7 implant was followed by severe multisystem and infectious complications. After prolonged intensive care support, the patient recovered and is now awaiting transplantation. Nearly 100% cytotoxic antibody reactivity caused by multiple antigenic stimuli is preventing ready access to donor hearts for this patient. We view the current role of the total artificial heart as a tool to preserve life until a suitable donor heart can be found, reverse the end-organ effects of progressive heart failure and low output, and restore transplant candidacy in selected patients with temporary reversible contraindications to transplantation.
 ...
PMID:Three recent cases of the total artificial heart before transplantation. 330 69

A 69 year old male presented with clinical features of right ventricular failure. A dilated poorly contracting right ventricle was confirmed by echocardiography and radionuclide ventriculography, with subsequent improvement following thiamine replacement. Wet beriberi is a result of thiamine deficiency and is uncommon in Europe and North America except in association with chronic alcohol abuse. We report a patient with beriberi presenting unusually with severe right-sided cardiac failure, with documented impairment of right ventricular function, which improved with thiamine replacement. His dietary intake of thiamine was low because of excess intake of carbonated drinks and carbohydrates.
 ...
PMID:Carbonated drinks, thiamine deficiency and right ventricular failure. 344 82

New modes of circulatory support for right ventricular dysfunction have recently been described. The present study compared the effectiveness of pulmonary artery balloon counterpulsation with a right ventricular assist device for support of surgically induced right ventricular dysfunction. Right ventricular hypertrophy was created in 16 neonatal lambs by pulmonary artery banding. Right ventricular dysfunction was produced in all animals by performing a right ventriculotomy and maintaining the pulmonary artery band. Four unassisted animals developed severe acute right heart failure and died. Six sheep had pulmonary artery balloon counterpulsation with a Dacron graft anastomosed to the proximal pulmonary artery as a reservoir for a 40 ml intra-aortic balloon after the onset of heart failure. The remaining six sheep had a pneumatically activated ventricular assist device inserted between the proximal pulmonary artery and the right ventricular apex. Periods of circulatory support with the balloon pump and the assist device on and off were compared. Decreases in right atrial pressure were observed with both balloon counterpulsation and right ventricular assistance: 14 +/- 1 to 11 +/- 1 mm Hg, p less than 0.0001, versus 19 +/- 2 to 12 +/- 2 mm Hg, p less than 0.0002, respectively. Cardiac output increased with both balloon counterpulsation and ventricular assistance: 1.45 +/- 0.16 to 2.03 +/- 0.13 L/min, p less than 0.001, versus 0.72 +/- 0.15 to 2.24 +/- 0.23 L/min, p less than 0.0002, respectively. Aortic systolic pressure increased in both support groups: 78 +/- 7 to 99 +/- 6 mm Hg, p less than 0.0004, versus 53 +/- 9 to 85 +/- 9 mm Hg, p less than 0.0001, respectively. Ventricular assistance produced greater changes in the right atrial pressure (39% +/- 6% versus 17% +/- 3%, p less than 0.01), cardiac output (153% +/- 39% versus 54% +/- 11%, p less than 0.05), and aortic systolic pressure (85% +/- 13% versus 39% +/- 9%, p less than 0.01). The insertion of a right ventricular assist device caused a significant increment in right ventricular dysfunction. These data, obtained with the devices in place but not operating, showed significantly increased right atrial and right ventricular end-diastolic pressures and approximately 50% less cardiac output than with the pulmonary artery balloon counterpulsation system. The results demonstrate that both modes of circulatory support were effective in reversing surgically induced right ventricular failure.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Circulatory support for right ventricular dysfunction. 360 14

Studies are reported of four patients (all lifetime non-smokers) who presented with right heart failure as a consequence of unrelieved asthmatic airways obstruction. These patients demonstrated severe airways obstruction with crackles on auscultation and hypercapnia. As shown here, such a presentation, without the usual pattern of dyspnoea and wheeze, tends to obscure the diagnosis and delays effective treatment. In three of the patients, treatment to relieve airways obstruction improved gas exchange, and the heart failure resolved. In the remaining patient, improvement was limited, and death ensued from respiratory failure. In patients who present with right heart failure, a relationship with airways obstruction and respiratory failure should be considered and assessed by objective tests. Delays in the effective treatment of these patients may result in the progression of their disease to a stage at which airways obstruction no longer responds to medical therapy.
 ...
PMID:Malignant asthma presenting as right heart failure. 360 Apr 57

Arrhythmias in patients with heart failure may result from altered electrophysiological properties of the myocardium. To examine changes in ventricular excitability during cardiac failure and to relate these changes to ventricular structural and neurochemical abnormalities, right ventricular failure was produced in dogs by pulmonary artery banding and by creating tricuspid regurgitation. Right and left ventricular excitability thresholds were tested biweekly in heart failure (HF) and sham-operated conscious dogs by means of strength-duration curves (1-40 ms) at basic cycle lengths (BCL) of 300-500 ms until time of death (21-188 days). Marked increases in the excitability threshold of the right ventricle occurred in HF (mean maximum % increase, 205 +/- 42 at BCL 500 ms). Smaller, though significant increases in the left ventricular excitability threshold in HF were also seen (mean maximum % increase 103 +/- 36 at BCL 500 ms). Increases in the excitability threshold of the left as well as the right ventricles occurred, even though ventricular dilation (2-D Echo) was confined to the right ventricle. The time course of changes in the excitability threshold was variable (maximum occurrence at 21 +/- 3 days right ventricle, 23 +/- 11 days left ventricle). Tyrosine hydroxylase activity and norepinephrine content of the right ventricle were markedly depleted at death, when the excitability threshold was high. Similar though nonsignificant trends in reductions of these sympathetic neurochemicals were seen in the left ventricle. Levels of choline acetyltransferase and QNB binding in both ventricles were unaffected.
 ...
PMID:Alterations in ventricular excitability in conscious dogs during development of chronic heart failure. 371 56


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>