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

As more effective antiretroviral therapies improve survival times, growing numbers of HIV-positive patients are at risk of developing end-organ damage or neoplasia. Heart muscle disease is the most important cardiovascular manifestation of HIV infection and seems set to become increasingly prevalent. This may take the form of either a dilated cardiomyopathy or isolated left or right ventricular dysfunction, is associated with a poor prognosis, and results in symptomatic heart failure in up to 5% of HIV patients. The precise cause of HIV-associated cardiomyopathy remains unclear but is undoubtedly complex, and most probably multifactorial. This report examines our current understanding of the immunopathogenesis of HIV-associated cardiomyopathy.
AIDS 2003 Apr
PMID:Immunopathogenesis of HIV-related heart muscle disease: current perspectives. 1287 May 27

As longevity increases in HIV-infected individuals, late effects such as cardiovascular disease and, more specifically, symptomatic heart failure are emerging as leading health issues. In the present review, we discuss possible cytokine and gene-mediated effects on HIV-associated cardiovascular illness that may play a role in diagnosis, management, and therapy of HIV-associated heart failure.
AIDS 2003 Apr
PMID:Mediators in HIV-associated cardiovascular disease: a focus on cytokines and genes. 1287 May 28

In this paper the perspective for nutritional modulation of systemic impairment in patients with chronic obstructive pulmonary disease (COPD) is discussed. Progressive weight loss is characterised by disease-specific elevated energy requirements unbalanced by dietary intake. Weight gain per se can be achieved by caloric supplementation while future studies may prove efficacy of amino acid modulation to stimulate protein synthesis and enhance muscle anabolism. Disproportionate muscle wasting resembles the cachexia syndrome as described in other chronic wasting diseases (cancer, chronic heart failure, acquired immunodeficiency syndrome (AIDS)). There is yet no adequate nutritional strategy available to treat cachexia in COPD. Muscle substrate metabolism has hardly been investigated, but the few data available point towards a decreased fat oxidative capacity that may show similarities with the "metabolic syndrome" as described in type II diabetes and obesity and could theoretically benefit from polyunsaturated fatty acid modulation. To adequately target the different therapeutic options, clearly more clinical (intervention) studies are needed in chronic obstructive pulmonary disease patients that are adequately characterised by local and systemic impairment and in which molecular and metabolic markers are linked to functional outcome.
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PMID:Nutritional and metabolic modulation in chronic obstructive pulmonary disease management. 1462 Nov 10

Cachexia is a complex syndrome. The main components of this pathological state are anorexia and metabolic abnormalities such as glucose intolerance, fat depletion, and muscle protein catabolism among others. The aim of the present article is to review the different therapeutic approaches that have been designed to fight and counteract muscle wasting in different pathological states such as cancer, AIDS and chronic heart failure.
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PMID:The pharmacological treatment of cachexia. 1505 12

To determine the extent of myocardial involvement in acquired immunodeficiency syndrome, we reviewed specimens of cardiac tissue obtained during autopsies of 54 patients with this disease. Forty-nine of the specimens showed subtle microscopic changes, the most common being lymphocytic infiltration (49 cases), unevenness of myocardial fibers (34 cases), interstitial fibrosis (28 cases), and myocardial atrophy (22 cases). Twenty-one of the specimens showed a morphologic abnormality that may be classified as a mild cardiomyopathy. Four had microscopic evidence of lymphocytic myocarditis; clinically, however, such myocarditis was diagnosed in only 1 patient, who died of cardiac failure. In a retrospective review, 7 additional hearts (among the 54) showed mild, nonspecific cardiac changes. The causative mechanism and significance of AIDS-related cardiac involvement remain uncertain; nevertheless, physicians should be aware of such involvement, to avoid overburdening the heart with medications that would further impair the myocardium.
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PMID:Pathologic findings in the hearts of patients with acquired immunodeficiency syndrome. 1522 93

Highly active antiretroviral therapy is effective in the management of AIDS. It has improved the prognosis of human immunodeficiency virus (HIV) infection. However, with increased survival, adverse effects from medications used in HIV treatment have become more apparent. Cardiac complications from HIV infection include arrhythmias, heart failure, and coronary artery disease. Heart failure in HIV disease may be related to the virus itself or to noninfectious reasons. The association of HIV medications with heart failure is controversial as patients with HIV disease often have multiple risk factors for developing heart failure. We present a case of acute onset heart failure in a patient with HIV, coronary artery disease, and hypertension who was recently started on antiretroviral therapy. There was complete resolution of heart failure after cessation of HIV medications. This case highlights the need to consider HIV medications as a cause of deterioration in cardiac function, even in the presence of other well-established risk factors for heart failure.
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PMID:Acute reversible heart failure with highly active antiretroviral therapy. 1526 27

The pathogenesis of preeclampsia stems from aberrant changes at the placental interface. The trophoblastic endovascular invasion of tonic spiral arteries that converts them to passive conduits falters. Uteroplacental insufficiency and fetoplacental hypoxemia result. Secondary maternal oxidative stress and an excessive inflammatory response to pregnancy generate the clinical syndrome of preeclampsia. Current treatment focuses on preventing seizures, controlling hypertension, preserving renal function and delivering the baby. We propose that the pathophysiological changes induced by preeclampsia in the placenta parallel those caused by persistent hypoxemia in the lungs at high altitude or with chronic obstructive pulmonary disease. Unrelenting pulmonary hypoxic vasoconstriction induces pulmonary hypertension and cor pulmonale. Inhalation of nitric oxide and phosphodiesterase-5 inhibitors opposes pulmonary hypoxic vasoconstriction, alleviates pulmonary hypertension and improves systemic oxygenation. Notably nitric oxide donor therapy also counters hypoxemic fetoplacental vasoconstriction, a biological response analogous to pulmonary hypoxic vasoconstriction. Fetal oxygenation and nutrition improve. Placental upstream resistance to umbilical arterial blood flow decreases. Fetal right ventricular impedance falls. Heart failure (cor placentale) is avoided. Emergency preterm delivery can be postponed. Other than low dose aspirin and antioxidants vitamins C and E no available therapy specifically targets the underlying disease profile. We hypothesize that, like nitric oxide donation, pharmacological inhibition of placental phosphodiesterase-5 will also protect the fetus but for a longer time. Biological availability of guanosine 3'5'-cyclic monophosphate is boosted due to slowed hydrolysis. Adenosine 3'5'-cyclic monphosphate levels increase in parallel. Cyclic nucleotide accumulation dilates intact tonic spiral arteries and counters hypoxemic fetoplacental vasoconstriction. Intervillous and intravillous perfusion pick up. Maternal to fetal placental circulatory matching improves. Enhanced placental oxygen uptake alleviates hypoxemic fetal stress. Appropriate fetal nutrition resumes. Cor placentale and severe intrauterine growth restriction are averted. Increased maternal cyclic nucleotide concentrations promote systemic vasodilatation so that blood pressures fall. Preemption of oxidative stress initiated by "consumptive" oxidation of nitric oxide stabilizes the vascular endothelium and corrects coagulopathy. Anti-inflammatory and immunosuppressant adenosine 3'5'-cyclic monphosphate offsets the extreme gestational inflammatory response. Cellular injury and multi-organ damage are prevented. One tablet a day of the new long acting phosphodiesterase-5 inhibitor, tadalafil (half life of 17.5 h) theoretically should allow a preterm pregnancy affected by preeclampsia to continue safely. Selective monitoring of vital organ functions guards against life-threatening maternal complications. Regular biophysical profiling warns the obstetrician of impending fetal compromise. Fetal growth and vital organ maturation can continue. As a result workloads imposed upon neonatal intensivists will lighten. Parental anxiety and concern will be allayed. The cost of treating preeclamptic mothers and their extremely low birth weight infants will decrease. Money saved by midwifery services in poorer states can be used to pay for better prenatal care. Severe preeclampsia/eclampsia will be less common. Maternal and perinatal morbidity and mortality will be reduced. Because the human immunodeficiency virus often infects individuals at a workforce eligible age, the global acquired immunodeficiency syndrome pandemic has already brought many nations to the brink of economic ruin. Potentially productive lives saved for the future will help restore them fiscally.
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PMID:Hypothesis: selective phosphodiesterase-5 inhibition improves outcome in preeclampsia. 1550 76

In maintenance hemodialysis (MHD) patients, associations between demographic, clinical and laboratory values and mortality, including cardiovascular death, are significantly different and, in some cases, in the opposite direction of those derived from the general population. This phenomenon, termed 'reverse epidemiology', is not limited to MHD patients but is also observed in populations that encompass an estimated 20 million Americans including those with an advanced age, heart failure, malignancies, and AIDS. A significant portion of this reversal may be due to the overwhelming effect of the malnutrition-inflammation complex syndrome (MICS). Since two thirds of MHD patients die within 5 years of initiation of dialysis treatment, traditional cardiovascular risk factors such as obesity, hypercholesterolemia and hypertension cannot exert a long-term deleterious impact, and instead, their short-term beneficial effects on MICS provides a survival advantage. In order to improve survival and quality of life in MHD patients, extrapolated ideal norms derived from the general population should be substituted with novel norms obtained from outcome-oriented epidemiologic analyses while accounting for the differential effect of MICS in different case-mix subgroups.
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PMID:Reverse epidemiology: a spurious hypothesis or a hardcore reality? 1562 38

We report on two children with advanced acquired immune deficiency syndrome presenting with vasculopathy involving the large vessels. Both patients had extensive involvement of the aorta and its branches. One patient presented with heart failure, and mild systemic hypertension secondary to renal arterial stenosis, while the other patient manifested with gangrene of both arms.
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PMID:Vasculopathy of the large arteries in children infected by the human immune deficiency virus. 1568 5

In the general population, a high body mass index (BMI; in kg/m(2)) is associated with increased cardiovascular disease and all-cause mortality. However, the effect of overweight (BMI: 25-30) or obesity (BMI: >30) in patients with chronic kidney disease (CKD) undergoing maintenance hemodialysis (MHD) is paradoxically in the opposite direction; ie, a high BMI is associated with improved survival. Although this "reverse epidemiology" of obesity or dialysis-risk-paradox is relatively consistent in MHD patients, studies in CKD patients undergoing peritoneal dialysis have yielded mixed results. Growing confusion has developed among physicians, some of whom are no longer confident about whether to treat obesity in CKD patients. A similar reverse epidemiology of obesity has been described in geriatric populations and in patients with chronic heart failure (CHF). Possible causes of the reverse epidemiology of obesity include a more stable hemodynamic status, alterations in circulating cytokines, unique neurohormonal constellations, endotoxin-lipoprotein interaction, reverse causation, survival bias, time discrepancies among competitive risk factors, and malnutrition-inflammation complex syndrome. Reverse epidemiology may have significant clinical implications in the management of dialysis, CHF, and geriatric patients, ie, populations with extraordinarily high mortality. Exploring the causes and consequences of the reverse epidemiology of obesity in dialysis patients can enhance our insights into similar paradoxes observed for other conventional risk factors, such as blood pressure and serum cholesterol and homocysteine concentrations, and in other populations such as those with CHF, advanced age, cancer, or AIDS. Weight-gaining interventional studies in dialysis patients are urgently needed to ascertain whether they can improve survival and quality of life.
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PMID:Survival advantages of obesity in dialysis patients. 1621 Jul 24


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