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

Risk stratification is mandatory in the management of the postinfarction period. The identification of high-risk patients, on the basis of clinical data (recurrent angina, overt heart failure, etc.), is quite easy, whereas stratification of uncomplicated subjects needs an accurate noninvasive strategy. In the last 20 years, echocardiography has been gaining an increasing role, allowing increasingly precise evaluation of infarct size. This detection of the extent of infarct size has a definite prognostic value. Since 1980, we have observed that a dysfunctioning left ventricular myocardium >40% marked patients with a poor prognosis. These observations are most important in asymptomatic infarct patients, in whom clinical features may not reflect the amount of left ventricular dysfunction. Our recent results on a large series of patients with acute myocardial infarction (MI) without overt heart failure have shown that the extension of wall motion abnormalities at 2-dimensional (2D) echocardiography was highly predictive of cardiac death or new coronary events in a 3-year follow-up (univariate analysis; p <0.0005). Echocardiography also plays an important role in detecting postinfarct ischemia, as seen by its wide use during stress tests. In our experience, the response to exercise echocardiographic testing has a high prognostic value. In fact, in our series, univariate analysis (Kaplan-Meier) showed that the best predictors of coronary events were the number of markers of ischemia during exercise (p <0.00001), the work load (p <0.00001), a positive exercise echo (p <0.0005), and the echo score at rest (p <0.0005). Multivariate analysis (Cox) confirmed these data: number of markers of ischemia: odds ratio (OR) 4.45, 95% confidence interval (CI) 1.5-13.1; work load: OR 2.46, CI 1.3-4.5; positive exercise echo OR 1.88, CI 1.1-3.2. Thus, serial echocardiography together with predischarge stress echocardiography is recommended for risk stratification after acute MI. In particular, in thrombolytic-treated patients, echo examinations allow the detection of functional recovery of viable reperfused myocardium whereas stress echo may show exercise-induced worsening in the region supplied by the infarct-related vessel, a predictor of a higher rate of coronary events.
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PMID:Clinical impact of echocardiography in prognostic stratification after acute myocardial infarction. 966 22

Most patients presenting with heart failure have severe coronary artery disease. The identification of viable hibernating myocardium is of paramount clinical importance for a correct indication of revascularization. Contractile reserve may be identified when regional asynergy improves during low or moderate doses of dobutamine. Dipyridamole, given at infra-low dose, alone or preferably in association with a low dose of dobutamine, is another possible pharmacologic stress protocol. Dobutamine echocardiography has been found to be more specific than thallium scintigraphy for predicting functional recovery after revascularization. However, the absence of contractile reserve does not exclude the presence of myocardial viability: perfusion reserve may be too low because of a critical coronary artery stenosis, or profound ultrastructural changes of myocardial cells may be present, including significant loss of contractile material. Inotropic reserve can also be assessed by dobutamine stress echocardiography in patients with idiopathic cardiomyopathy. The evolution of hemodynamic variables can be measured during the stress test. Stress echocardiography, especially during exercise, could probably provide important information about heart failure associated with valvular heart disease.
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PMID:Role of stress echocardiography in heart failure. 966 40

The distinction between left ventricular (LV) dysfunction caused by fibrosis and that arising from viable (hibernating and/or stunned) myocardium has important implications for the management of patients with ischemic cardiomyopathy. In many of these patients, LV function can improve significantly, and even normalize, after revascularization. Positron emission tomography (PET) is the most accurate noninvasive imaging technique for detection of viable myocardium. Increased glucose uptake in dysfunctional segments with reduced blood flow at rest (PET mismatch) indicates the presence of viable myocardium, whereas a concordant reduction in blood flow and glucose uptake (PET match) indicates a myocardial scar. A PET mismatch pattern has a 79% average positive predictive value for predicting improved function after revascularization, whereas a PET match pattern has an 84% average negative predictive value for lack of such functional recovery. The greater the number of viable myocardial segments shown by PET, the greater the probability that revascularization will improve regional and global LV function and, consequently, improve heart failure symptoms and survival. In patients with PET mismatch, long-term survival is consistently poor with medical therapy but significantly improved by early referral to revascularization. This survival benefit is apparent in patients with and without angina. Conversely, long-term survival in patients without such PET mismatch is similar with medical therapy or revascularization, especially if minimal or no anginal symptoms are present. These observations suggest that noninvasive investigation of the amount of viable myocardium should be an important component of the diagnostic evaluation of patients with heart failure because of coronary artery disease. This approach will likely enhance the often difficult process of selecting patients with poor cardiac function in whom revascularization will likely improve both the quality and quantity of life.
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PMID:Positron Emission Tomography for Assessment of Myocardial Perfusion and Viability. 1034 52

There is increasing evidence that the availability of different metabolic substrates can influence post-ischemic functional recovery of the heart and the damage incurred during episodes of myocardial ischemia. Here we present the rationale for metabolic interventions, describe their mechanisms of action and suggest potential clinical applications. In cardiac surgery, basic research, studies of human myocardial metabolism after cardiac operations, and available experience with metabolic interventions provide a rationale for metabolic support with glutamate and/or high-dose glucose-insulin-potassium (GIK) in postoperative cardiac failure. In the treatment of acute myocardial infarction GIK deserves serious evaluation as recent randomized studies in diabetics with myocardial infarction and in patients undergoing reperfusion strategies demonstrate significant reductions in mortality. However, before large scale prospective randomized studies are undertaken, further studies of myocardial metabolism in acute myocardial infarction and the impact of different GIK regimes may be advisable in order to determine appropriate doses. A brief overview of metabolic modulation with pharmacological measures is given as it eventually may prove that we have to await the introduction of pharmacological agents which enhance full glucose oxidation at the expense of free fatty acids to create the commercial interest necessary to achieve widespread use of metabolic therapies.
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PMID:Metabolic intervention for the ischemic and post-ischemic heart. 1044 3

1. In order to investigate the changes of reduced urinary free dopamine excretion (uDA) in heart failure, 15 patients with symptomatic mitral stenosis were investigated on their uDA, endogenous creatinine (Cr) clearance, urinary excretion of sodium (UNaV), fractional excretion of sodium (FENa), plasma noradrenaline (pNA) and plasma L-dopa concentration before and early after percutaneous transvenous mitral commissurotomy (PTMC) by the clearance study. The delivery of L-dopa to renal proximal tubules (plasma L-dopa x Cr clearance), and the conversion ratio of plasma L-dopa to urinary dopamine in the kidney [uDA/(plasma L-dopa x Cr clearance)] were also estimated. 2. After successful PTMC, uDA, UNaV and FENa showed a significant but incomplete improvement and the changes of uDA were correlated positively with those of cardiac index (CI) (r = 0.665, P < 0.01), not with changes of pulmonary wedge pressure. While plasma L-dopa and plasma L-dopa x Cr clearance improved, uDA/(plasma L-dopa x Cr clearance) was not significantly changed early after PTMC. 3. From these results, it was suggested that reduced uDA tended to increase incompletely in relation with functional recovery of heart, and that increased plasma L-dopa and a delivery of L-dopa to renal proximal tubules have some positive role on urinary dopamine excretion, at least, early after PTMC.
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PMID:Changes of urinary dopamine excretion early after balloon mitral commissurotomy in mitral stenosis. 1047 79

Dobutamine and enoximone stimulate independently inotropic reserve by increasing intracellular cyclic adenosine monophosphate. The potential of enoximone (0.75 mg/kg body weight over 10 minutes) followed by very low dose (2.5 microg/kg/min) dobutamine echocardiography to predict recovery of ventricular function in akinetic and dyskinetic postinfarcted areas was studied. We enrolled 22 patients with previous Q-wave myocardial infarction and regional wall motion abnormalities related to left anterior descending arterial disease, left ventricular ejection fraction <40%, and all scheduled for myocardial revascularization. A 10 microg/kg/min dobutamine test was performed 48 hours before the study protocol. Test images obtained at peak of pharmacodynamic effects were compared with those obtained at 4 months after myocardial revascularization. We used a 16-segment ventricular model and a 5-grade scoring system. Resting regional myocardial dysfunction graded > or =2 was present in 267 of 352 segments evaluated. Contractile reserve (decrease in resting wall motion score > or =2 grades) at peak effect of enoximone infusion was present in 34 of 112 severely hypokinetic, 42 of 117 akinetic, and 14 of 38 dyskinetic segments. The inotropic reserve evaluated after very low dose dobutamine was observed in 34 of 112 severely hypokinetic, 49 of 117 akinetic, and 20 of 38 dyskinetic segments. After revascularization, recovery of function was observed in 31 of 112 severely hypokinetic, 49 of 117 akinetic, and 21 of 38 dyskinetic segments. Overall, there was a significant correlation between absolute score changes of segments which were abnormal at baseline (n = 267) to enoximone peak effects (r = 0.49, p <0.001) to predict absolute changes after revascularization; after dobutamine there was progress toward identity (r = 0.62, p <0.001) and the difference was significant among correlation slopes of dobutamine alone, enoximone alone, and enoximone plus very low dose dobutamine echocardiograophy (0.45+/-0.04, 0.51+/-0.04, and 0.63+/-0.04, respectively, F = 5.25, p = 0.005). Therefore, enoximone followed by very low dose dobutamine may assess myocardial viability of postinfarcted akinetic and dyskinetic areas. This test may be useful when evaluating patients with more severe cardiac failure and/or life-threatening arrhythmias.
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PMID:Enoximone coupled to very low dose dobutamine echocardiography detects myocardial viability in akinetic and dyskinetic post-myocardial infarcted areas. 1049 33

To evaluate the functional recovery after coronary bypass surgery in patients with severe left ventricular (LV) dysfunction (ejection fraction (EF) < or = 35%), 100 consecutive patients with viable myocardium in the territory supplied by the left anterior descending artery (LAD) underwent coronary bypass grafting. In addition, cardiac catheterization and single-photon emission computed tomography (SPECT) perfusion imaging with thallium-201 were repeated 1-year postoperatively. Although 12 patients with severe LV dysfunction were preoperatively in a worse New York Heart Association functional class (3.1+/-0.7 vs 2.4+/-0.8; p<0.01), had a higher incidence of heart failure (10/12 vs 14/88; p<0.001) and had a worse LVEF (29+/-5 vs 61+/-14%; p<0.001) compared with 88 patients without severe LV dysfunction, the operative mortality was similar in the 2 groups (1/12 vs 2/88; p=NS). The postoperative NYHA functional class in the patients with severe LV dysfunction was similar to that in the patients without such dysfunction (1.6+/-0.7 vs 1.3+/-0.6; p=NS). In addition, the 1-year postoperative study revealed a significant improvement in the thallium defect score in both the LAD territory (1.7+/-1.2 to 0.7+/-1.0, p=0.01) and all the territories (5.2+/-2.2 to 3.2+/-1.9, p=0.002) in patients with severe LV dysfunction, whereas no improvement in defect score was found in either of these territories in those without severe LV dysfunction (LAD: 0.6+/-1.4 to 0.4+/-1.2, p=NS; All: 1.9+/-2.2 to 1.8+/-2.0, p=NS). Furthermore, a marked 1-year postoperative improvement (15-24%; 95% confidence interval) in LVEF (29+/-5 to 48+/-10%, p<0.001) was demonstrated in patients with severe LV dysfunction, but not in those without such dysfunction (60+/-13 to 61+/-11%, p=NS). These results indicate that myocardial viability in the LAD territory, as demonstrated by thallium-201 SPECT perfusion imaging, predicts a significant improvement in functional class and LVEF of at least 10% or more after coronary artery bypass grafting in patients with severe LV dysfunction.
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PMID:Functional recovery after coronary artery bypass grafting in patients with severe left ventricular dysfunction and preserved myocardial viability in the left anterior descending arterial territory as assessed by thallium-201 myocardial perfusion imaging. 1055 16

The delayed recovery of function after brief episodes of ischemia is known as stunning. Myocardial stunning and heart failure would, at first glance, appear to have little in common other than the obvious contractile dysfunction in both settings. Here I describe studies which shed new light on the underlying mechanisms of these two forms of contractile dysfunction, revealing unexpected fundamental similarities.
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PMID:[Heart failure: the electrophysiological connection. Myocardial stunning and heart failure: mechanisms in common?]. 1100 64

Ageing is often associated with a decrease in the quality of sleep. In older subjects, sleep-related breathing disorders (SRBD) are increasingly recognized as being responsible for alterations in the quality of sleep. The prevalence of obstructive sleep apnea (OSA) increases with ageing; despite sometimes major disturbances in sleep structure, clinical symptoms are often subtle in this age group. Central apnea and periodic breathing, also more frequent in older subjects, most often occur in patients suffering either from neurological problems (such as tumors, brain infarcts, sequelae of infection, diffuse encephalopathies) or moderate to severe heart failure. In fact, patients suffering from cerebro-vascular diseases (such as brain infarcts or transient ischemic attacks) have a higher prevalence of SRBD than a control age-matched population. In these patients, SRBD are associated with a poorer prognosis in terms of functional recovery and survival. The clinical impact of SRBD on cognitive function appears to be modest in patients without dementia, albeit for a slight increase in daytime somnolence. However, in patients suffering from Alzheimer's disease, SRBD occur more frequently than in non-demented subjects, and indexes of severity of SRBD have been correlated with the importance of cognitive impairment. The hypothesis of a causal relationship between SRBD and the degree neuropsychological impairment in either Alzheimer's disease or multi-infarct dementia remains a matter of controversy. SRBD should be considered as a possible cause of "reversible dementia" and sought for in the presence of daytime somnolence, delirium, or unexplained right-sided heart failure in older patients.
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PMID:[Respiratory sleep disorders in the elderly]. 1114 Mar 5

Diabetes increases both the incidence of cardiovascular disease and complications of myocardial infarction and heart failure. Studies using diabetic animals have shown that changes in myocardial sodium transporters result in alterations in intracellular sodium (Na(i)) homeostasis. Because the changes in sodium homeostasis can be due to increased entry of Na+ via the electroneutral Na+-K+-2Cl- cotransporter (NKCC), we conducted experiments in acute diabetic hearts to determine if 1) net inward cation flux via NKCC is increased, 2) this cotransporter contributes to a greater increase in Na(i) during ischemia, and 3) inhibition of NKCC limits injury and improves function after ischemia-reperfusion. These issues were investigated in perfused type I diabetic and nondiabetic rat hearts subjected to ischemia and 60 min of reperfusion. A group of diabetic and nondiabetic hearts was perfused with 5 microM of bumetanide, an inhibitor of NKCC. Flux via NKCC, Na(i), and ATP was measured in each group with the use of radiotracer 86Rb, 23Na, and 31P nuclear magnetic resonance spectroscopy, respectively, whereas ischemic injury was assessed by measuring creatine kinase release on reperfusion. Cation flux via NKCC, as measured by 86Rb uptake, was significantly increased in diabetic hearts. Inhibition of NKCC significantly reduced ischemic injury in diabetic hearts, improved functional recovery on reperfusion, attenuated the ischemic rise in Na(i), and conserved ATP during ischemia-reperfusion. Parallel studies in nondiabetic hearts showed that NKCC inhibition was not cardioprotective. These findings demonstrate that flux via NKCC is increased in type I diabetic hearts and that inhibition with bumetanide attenuates changes in Na(i) and ATP during ischemia and protects against ischemic injury. The data suggest a therapeutic role for pharmacological agents that inhibit flux via NKCC in diabetic patients with myocardial ischemia.
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PMID:Protection of ischemic myocardium in diabetics by inhibition of electroneutral Na+-K+-2Cl- cotransporter. 1145 52


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