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

High cardiac output failure/state (HCOF) is regular feature of some illnesses e.g. thiamine deficiency, hyperthyroidism, severe anemia, Paget's disease or arteriovenous fistulae. HCOF in multiple myeloma is reported quite rarely. 31-year-old man was admitted because of fatigue, dyspnea and subfebrilities. Heart rate was 116/min, sinus rythm blood pressure 110/60 mmHg. Chest film showed cardiomegaly with sings of interstitial pulmonary edema, echocardiography mild dilatation of the left ventricle with hyperkinetic wall motion and small pericardial effusion. Hemoglobin was 104 g/l, leukocyte count 13.5 x 10(9)/l with 30% of plasmatic cells. Serum protein electrophoresis demonstrated a monoclonal gammapathy, X ray studies of the skelet multiple osteolytic lesions. Diagnosis of plasmocytic leukemia-form of multiple myeloma was established and chemotherapy (vincristine + adriamycine + dexamethason) was started. Patient cardiac status deteriorated. Cardiac catheterisation demonstrated mean righ atrial pressure of 25 mmHg, mean pulmonary artery pressure of 28 mmHg and pulmonary artery wedge pressure of 24 mmHg. Co was 20.0 l/min (C.I. 11.5 l/min/m2). In continuing of chemotherapy and symptomatic therapy for heart failure patients status gradually improved and complete remission of the myeloma and normalisation of cardiac parameters was achieved. Heart failure in multiple myeloma patients has been attributed to amyloidosis of myocardium, hyperviscosity syndrome, co-existing CAD or anthracycline toxicity. HCOF should be considered in patients with clinical evidence of heart failure and normal left ventricular function.
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PMID:[Hypercirculatory heart failure in a patient with plasmacytic leukemia]. 855 97

Carotid endarterectomy (CEA) and myocardial revascularization can be performed in a single procedure, performing CEA before or during cardio-pulmonary by-pass (CPB), or using a double stage approach. Over a 4 year period, 17 patients underwent CEA and coronary artery by-pass (CAB) with a single stage procedure. Fourteen patients (82.3%) were male, 3 (17.6%) were female. The mean age was 66.3 +/- 7.07. One patient (5.8%) had a previous neurological event (stroke); 5 patients (29.4%) had a previous transient ischemic attacks (TIA). The indications for the combined operations were CAD associated to unilateral internal carotid stenosis greater than 70% or 50% when symptomatic. In all patients CEA was performed after median sternotomy and heparinization, during CPB, with moderate hypotermia (30%C), performing CEA successively. One patient (5.8%) died of acute heart failure secondary to mediastinits. Minor neurological complications were present in 2 patients (11.7%) with signs of cerebral oedema. Myocardial infarction and late neurological deficit did not occur in any patient. We conclude that it is important, in the preoperative assessment of every patients with CAD, the screening for concomitant carotid vascular diseases, in order to avoid neurological complications during CPB, treating the two different diseases with a single stage approach, if carotid stenosis is greater than 70% or greater than 50% when symptomatic.
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PMID:Carotid endarterectomy and myocardial revascularization. A single stage procedure. 871 Jan 35

Rational management of patients with CAD and poor left ventricular function relies on proper identification of the subgroup at high risk and those who have the highest potential of benefiting from a particular type of treatment. It is now well recognized that patients with CAD and left ventricular dysfunction have a high but variable mortality rate while receiving medical therapy. Many of these patients who have intractable heart failure are considered candidates for cardiac transplantation. Despite favorable survival after cardiac transplantation, this procedure cannot be performed in 90% of the heart failure patients who are potentially eligible because of the shortage of donor hearts. Cardiac transplantation is also an expensive procedure. Perfusion-FDG metabolism PET imaging has become the gold-standard noninvasive imaging method to identify the presence and extent of hibernating myocardium. Positron emission tomography accurately predicts recovery of regional and global left ventricular dysfunction after revascularization. In patients with poor left ventricular function, the PET pattern of perfusion metabolism mismatch is also predictive of improvement in heart failure symptoms and survival benefit after myocardial revascularization. These data suggest that a rational approach may be developed for cost-effective management of patients with CAD and poor left ventricular function.
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PMID:The use of positron emission tomography imaging in the management of patients with ischemic cardiomyopathy. 877 88

Clinical and experiments study with angiotensin-converting enzyme (ACE) inhibitors suggest that these agents may improve coronary artery disease by acting at multiple sites in the series of events leading to end-stage heart disease. These agents reduce blood pressure, improve prognosis and symptoms in patients with severe heart failure and in patients after acute myocardial infarction with left ventricular dysfunction. They are useful in the early, acute phase of myocardial infarction. More recently, ACE inhibitors have been shown to reduce in vitro vascular hypertrophy, to attenuate arteriosclerosis, and to maintain endothelium function. Whether these effects occur at clinical levels is still uncertain. The exciting clinical data have led to the proposal that alteration of ACE activity, particularly in tissue, is an important factor in development and progression of CAD. The ACE system is complex, with endocrine, paracrine, and autocrine effects. ACE is present in cardiac and vascular tissue. Therefore, the beneficial effects of ACE inhibitors can be classified as "cardio" and "vasculo" protective. This article summarizes a number of independent and complementary mechanisms pointing to a role of ACE and ACE inhibition in coronary artery disease.
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PMID:Cardioprotective effect of angiotensin-converting enzyme inhibitors in patients with coronary artery disease. 911 58

In a 63-year-old woman with longstanding type I diabetes mellitus, CAD and chronic heart failure, a subacute myocardial infarction developed, together with decompensation of cardiac function and diabetes and concurrent pneumonia. Acute heart failure with acute renal failure on top of diabetic nephropathy, and interstitial pulmonary edema was initially treated with hemofiltration and catechol amines together with antibiotic and perfusor-regulated insulin therapy, and systemic heparinization. Subsequent chronic treatment with digitalis, acetyl salicylic acid, insulin and a combination of an ACE inhibitor and a loop diuretic resulted in an improvement of heart failure to NYHA functional class II where PTCA of coronary multi-vessel disease could be performed with low risk.
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PMID:[Heart failure after myocardial infarct in decompensated diabetes mellitus. Acute therapy with catecholamines--long-term therapy with ACE inhibitor-loop diuretic combination]. 937 33

The objective of this study was to examine the endothelial function of internal mammary artery in patients with coronary artery disease and in heart transplant recipients. Therefore the response of this artery to increasing concentrations of acetylcholine (1, 10, 20 microg/min for 2.5 minutes each) was assessed in 6 patients in a control group, 16 patients with coronary artery disease (CAD group) matched for risk factors with 16 heart graft recipients (who underwent transplantation for nonischemic heart failure), and 12 patients with coronary artery disease and peripheral vascular disease (PVD group). Diameters of proximal and middle segments of internal mammary artery were measured by quantitative angiography. The responses to the first concentration of acetylcholine were attenuated in these three groups compared with the control group. At the highest concentration of acetylcholine the diameter increase was similar in the control and CAD groups, whereas the responses remained significantly impaired in the transplant and PVD groups. However, after selective infusion of L-arginine (30 mg/min for 11 minutes), the precursor of endothelium-derived nitric oxide, was performed, the responses to acetylcholine were restored in these two latter groups. Endothelin plasma levels were significantly enhanced in the PVD group, which exhibited the most severe impairment in acetylcholine-induced vasodilation. Thus some patients with CAD, mainly those with advanced atherosclerosis, and cardiac transplant recipients exhibit internal mammary artery endothelial dysfunction, and this abnormality seems reversible.
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PMID:Endothelial function of internal mammary artery in patients with coronary artery disease and in cardiac transplant recipients. 950 35

Annexins are a unique family of membrane-associated, Ca2+ and phospholipid-binding proteins found in various tissues. Among the 12 isoforms, Annexin II, V and VI exist in heart tissue in the highest amounts. Annexin VI has been shown to affect intracellular Ca2+ cycling and contractility in isolated cardiomyocytes. Annexin V is present in both cardiomyocytes and non-myocyte cell types in the heart and may play a role in the regulation of cellular ion fluxes, organization and secretion, while the cardiac effects of annexin II are unclear. To identify changes in annexin II, V and VI isoforms that might occur in human heart failure, we measured mRNA and protein levels of these three annexins in transplanted left ventricular tissue of 12 patients with end-stage congestive heart failure due to coronary artery disease (CAD, n=6) or idiopathic dilated cardiomyopathy (DCM, n=6) who underwent cardiac transplantation. Normal heart tissue (C, n=6) was used as a control. Northern blot analyses showed a significant decrease (61%) in annexin VI mRNA levels in heart failure patients compared with controls (1.08+/-0.16 v 2.79+/-0.20 A.U.C. unit, determined by laser densitometry, mean+/-s.e.). In contrast, we found a 67% increase (2. 32+/-0.27 v 3.88+/-0.29) in annexin II mRNA levels and a two-fold increase (1.00+/-0.24 v 2.21+/-0.29) in annexin V mRNA levels in cardiomyopathic hearts as compared to normal hearts. Western blot analyses demonstrated a corresponding decrease (46.1%) in annexin VI protein levels in the heart failure group as compared to controls (2. 63+/-0.22 v 4.88+/-0.52), while annexin II protein levels showed a significant 40.7% increase in patients with heart failure compared to those in normal hearts (5.08+/-0.67 v 3.61+/-0.32). Annexin V protein levels were also significantly increased (45%) in heart failure patients compared with normal (2.14+/-0.19 v 1.48+/-0.11). No difference in either annexins II, V or VI mRNA and protein levels were found between CAD and DCM patients. We conclude that human end-stage heart failure is associated with a down regulation of annexin VI and up regulation of annexin II and V proteins. Coordinate changes were observed in steady-state mRNA levels. These results suggest that these annexin isoforms may contribute to the regulation of intracellular Ca2+ homeostasis in the cardiomyopathic heart.
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PMID:Altered cardiac annexin mRNA and protein levels in the left ventricle of patients with end-stage heart failure. 951 22

Preventing the progression of established heart failure can be difficult, as multiple factors contribute to the continual decline of cardiac function. Blunting the activated neurohormonal response to a decreased systolic function is a proven means of slowing progression of CHF. Preventing further CAD and cardiac ischemia may also prove to be an effective mechanism. Two trials with HMGCoA reductase inhibitors lend support to this hypothesis. Studies using ACE inhibitors may also support this notion. Since a major portion of heart failure in the USA is caused by CAD, preventing CHF progression may be related to the prevention of CAD. Using ACE inhibitors and lipid-lowering agents, in addition to standard measures of CAD risk factor modification, may prove useful in future trials to retard the progression of heart failure. Further research and clinical trials involving this method of CHF prevention are warranted.
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PMID:Role of secondary prevention in congestive heart failure due to coronary artery disease. 989 17

Initial pharmacologic therapy for hypertension is low-dose thiazide diuretics, beta-blockers, and ACE inhibitors. Increasing data have confirmed that ACE inhibitors have specific benefit in patients with diabetes, atherosclerosis, left ventricular dysfunction, and renal insufficiency. CCBs are alternative agents for ISH in the elderly and appear to decrease stroke with perhaps less protection against progression of renal insufficiency and proteinuria, CAD mortality and new onset heart failure versus other initial agents, especially ACE inhibitors. ARBs are well tolerated and effective blood pressure lowering agents but have not been confirmed as effective as ACE inhibitors for reducing renal progression, clinical events, or mortality from heart failure. Effective pharmacologic antihypertensive therapy may avoid disabling and undetected cerebrovascular disease, cognitive dysfunction, and disturbing symptoms of elevated blood pressure. Vasopeptidase inhibitor, such as omapatrilat, and endothelin-1 antagonist, such as bosentan, may become future agents approved for the reduction of morbidity and mortality with hypertension. The ALLHAT trial continues to examine the potential benefits and harms of amlodipine versus chlorthalidone and lisinopril in a diverse high-risk population. Based on ALLHAT data, however, doxazosin is no longer an acceptable initial pharmacological agent. Intensive pharmacologic treatment with blood pressure lowering to less than 130/85 mm Hg is recommended with diabetes, renal insufficiency, and heart failure with additional goal of less than 125/75 mm Hg with renal failure and proteinuria greater than 1 g/24 h, based on multiple outcome studies.
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PMID:Update in pharmacologic treatment of hypertension. 1140 10

LV systolic function and dilation after Ml have been extensively studied and have been related to heart failure and cardiac mortality. In recent years, it has been increasingly apparent that LV diastolic dysfunction contributes to signs and symptoms of heart failure and LV diastolic dysfunction is associated with increased mortality rates in patients chronic heart failure independent of systolic function. LV diastolic dysfunction is difficult to assess on basis of clinical examination including chest radiography and electrocardiography. LV diastolic filling has traditionally been evaluated by cardiac catherization with direct measurement of filling pressures and relaxation. However, the invasive approach describing LV compliance and relaxation as the major determinants of LV diastolic function, is not feasible and suitable for routine investigations of diastolic function. Two-dimensional and Doppler echocardiography has become a well accented practical and safe non-invasive method for diagnosis of LV diastolic dysfunction. Combined invasive and echocardiographic studies have shown that analysis of mitral and pulmonary venous flow velocities relate to invasively measured filling pressures and relaxation rate in cardiac diseases. Based on Doppler analysis of mitral and pulmonary venous flow three abnormal LV filling patterns are identified: impaired relaxation, "pseudonormalization" and restrictive. These LV filling patterns have been related to symptoms, relaxation rate, filling pressure and prognosis in patients with restrictive and dilated cardiomyopathy. The Doppler flow profiles are influenced by several factors including age, heart rate, load conditions and valve heart diseases which must be taken into consideration during evaluation. During the last decade information about LV diastolic function assessed non-invasively by Doppler echocardiography has gained in patients with CAD. Myocardial ischemia induced by brief coronary artery occlusion or pacing leads to abnormal myocardial relaxation which can be reversed to normal by restoring normal myocardial blood flow. The diastolic abnormality is present within seconds and a characteristic impaired relaxation filling pattern are identified by mitral and pulmonary venous flow analysis. Diastolic dysfunction has been recognized during the early as well during the post-MI phase with or without LV systolic dysfunction. In the acute phase both an abnormal relaxation pattern and restrictive LV filling pattern are present which has been related to in-hospital heart failure. The identification of a pseudonormal or restrictive LV filling pattern are associated with later readmission to hospital with heart failure and cardiac death. Abnormal relaxation filling is the most pronounced filling pattern after one year which might be related to the remodeling process including compensatory hypertrophy, scarring of the infarct zone leading to a non-uniform relaxation of the LV. Remodeling of the LV following a MI is subject to several factors which might involve diastolic function. This is supported by the presence of an impaired relaxation and restrictive filling pattern are associated with progressive LV dilatation following Ml. Furthermore, the LV remodeling process following the very early phase includes the scarring process with collagen deposition in the infarcted and non-infarcted myocardium. The extent and quality of the repair process involving collagen deposition are believed to influence the remodeling process. Increased collagen deposition in the subacute phase of Ml indicated by elevated values of the collagen marker PIIINP is found to be related to LV dilation, depressed systolic function and restrictive LV filling. Development of a restrictive filling in patients with increased collagen deposition might be due to increasing LV volume but also to increased myocardial stiffness. Regarding prognosis diastolic dysfunction seems to be an important marker of outcome as abnormal diastolic properties are related to progressive LV dilatation, development of heart failure and cardiac death following MI. The beneficial effects of BB on morbidity and mortality in post-MI patients are well established. Recently, it has been demonstrated that BB has beneficial effects on progressive CHF and cardiac mortality in patients with chronic heart failure and moderate to severe systolic dysfunction. The mechanisms behind these effects are not fully understood. However, improvement of both systolic and diastolic function during BB therapy are demonstrated in patients with CHF. A few studies in patients with MI indicates that long-term BB therapy improves LV diastolic function which seems to be followed by improvement in systolic function. BB has the potential to lengthening diastole, improving subendocardial myocardial perfusion and affecting symptomatic amd neurohumoral activation following MI which might affect LV systolic and diastolic function and thereby improving outcome. Functional capacity following Ml is a well known predictor for outcome in MI patients. LV diastolic function a closely related to exercise capacity in contrast to measures of systolic function. BB therapy in patients with mild to moderate systolic dysfunction seems to improve exercise capacity which is related to improvement in LV diastolic function. Thus, BB improves exercise capacity and diastolic function by increasing LV compliance which might have prognostic implications. Even though LV systolic and diastolic dysfunction coexist, few two-dimensional and Doppler echocardiographic variables combine measurements of both phases of the cardiac cycle. Recently, the MPI has been suggested as a measure of combined systolic and diastolic myocardial performance which is based on Doppler time intervals of the systolic and diastolic phases. The MPI is easily obtained, reproducible, non-geometric and seems less dependent on heart rate and load conditions compared to traditional Doppler measurements. In patients with MI is has shown to reflect disease severity and contain prognostic information. The assessment of MPI seems therefore to be a relevant attractive alternative to established measurements of LV function following MI.
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PMID:Clinical aspects of left ventricular diastolic function assessed by Doppler echocardiography following acute myocardial infarction. 1176 25


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