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

Though sudden cardiac death accounts for as much as 15% of all cause mortality in uremia, reports concerning advanced A-V block, requiring permanent cardiac pacing in end-stage renal disease (ESRD) hemodialysed (HD) patients are very few. This is the first long term prospective study reporting on systematic permanent pacemaker implantation, in a cohort of ESRD patients from a single HD unit. Between 01/06/1997 and 30/12/2001, 396 pacemakers were inserted for advanced, symptomatic A-V block in our institution, including 5 in ESRD, HD patients (M/F--4/1, age 47-73, M +/- SD--61 +/- 12 years) from a single dialysis center, treating 137 patients during the study period. Thus, the incidence and prevalence of A-V defects treated by permanent pacing in uremic patients was 0.81% and 3.65% respectively. Conversely, the incidence and prevalence of ESRD treated by hemodialysis, among patients with advanced A-V conduction disturbances, requiring permanent pacing were 0.28% and 1.26%. Mitral valve calcifications were present in all patients; 3 subjects also had extensive aortic valve calcifications. Left ventricular hypertrophy (echocardiographic Framingham criteria) was present in 4 patients, but the systolic function (ejection fraction and fractional shortening index) was normal in all cases, although a clinical picture of chronic heart failure was seen in 3 subjects preoperatively. A-V conduction defects were attributed to extensive metastatic calcifications, involving the cardiac squeleton, consecutive to severe hyperparathyroidism and inadvertent use of calcitriol and calcium carbonate as phosphate binders. No technical difficulties, short or long-term complications related to pacemaker implantation (4 VVI and 1 VVD devices) were encountered. Acute threshold and sensing values were similar with those of non-uremic patients. During follow-up, one patients died from a non cardiac death. If optimal hemodialysis is provided, benefits of permanent pacing are equal in uremic or non uremic patients and pacemaker implantation should be instituted as a prompt life-saving method in all dialysis patients with chronic symptomatic advanced A-V blocks.
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PMID:[Permanent cardiac pacing for chronic symptomatic atrioventricular block in uremic hemodialysed patients. A prospective study]. 1263 71

Hyperparathyroidism (HPT) is common in patients on dialysis, and parathyroidectomy (PTx) is often required. We present a retrospective, descriptive analysis of data corresponding to 148 patients on dialysis undergoing PTx due to severe refractory HPT (PTH 1401 +/- 497 pg/mL, Ca 10.6 +/- 0.8 mg/dL, P 6.9 +/- 1.7 mg/dL). Demographic data were compared with those recorded in 309 patients on dialysis not subjected to PTx who were managed at the same hospital. In the PTx group, the factors age (49.3 +/- 14 years), male gender (48.6%), and diabetes (0.7%) were significantly lower than in the non-PTx group (61.5 +/- 14.9 years, male gender 59%, diabetes 19.4%), while time on dialysis was longer (8.6 +/- 5.8 vs. 5.5 +/- 5.4 years). In 129 of the study patients (87.4%), four or more glands were identified, and total PTx plus autotransplantation (AT) in the forearm was performed. In the remaining 19 patients, two to three glands were identified, and AT was not undertaken. Four of the 19 patients were successfully operated on again for persistent HPT, seven showed PTH levels <250 pg/mL, and eight maintained severe HPT. Perioperative complications included one death due to cardiac insufficiency, two repeat operations due to bleeding, and one patient with chronic hoarseness. Hospital stay was prolonged in 20% of patients due to a hungry bone syndrome. Among those patients with PTx and AT, HPT recurred in 21 patients (16.2%) at 3.1 +/- 2.3 years. In 13 of these patients, autograft was removed at 7.5 +/- 2.9 years. Serum calcium and phosphate levels improved after PTx, and these results were maintained for 5 years (9.6 +/- 0.8 and 4.2 +/- 1.2 mg/dL, respectively). In conclusion, PTx with AT is a safe option for the treatment of severe HPT that is accompanied by low morbidity and mortality and a good outcome. Medical treatment should not be prolonged at the expense of long repeated bouts of hypercalcemia and/or hyperphosphatemia with their irreversible consequences.
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PMID:Parathyroidectomy: whom and when? 1275 76

Systolic and diastolic left ventricular dysfunction is common and important predictor of risk of death in end-stage renal failure. Systolic dysfunction is defined echocardiographically by a shortening fraction < 25% or an ejection fraction < 40%. Systolic dysfunction has a poor prognosis, strongly associated with myocardial ischemia and left ventricular hypertrophy (LVH). Diastolic dysfunction combines relaxation problems with compliance abnormalities and usually is associated with LVH. It is not clinically possible to distinguish systolic from diastolic LV dysfunction. This underlines the importance of echocardiographic diagnosis. In the present study we have analysed echocardiographically the left ventricular systolic and diastolic function and some possible risk factors contributing to its dysfunction development in patients with chronic renal failure (crf) treated by hemodialysis (HD). From a cohort of 85 patients with crf we selected for analysis 59 clinically stable patients. Echocardiography (ECHO), ECG, body mass index (BMI), serum creatinine, urea, total protein, albumin, hemoglobin, hematocrit, electrolytes, endothelin (ET-1) and parathyroid hormone (PTH) concentrations were evaluated in all patients after HD session. In all HD patients systolic and diastolic LV dysfunction was observed as well as LVH: concentric LVH was detected by ECHO in 46 patients and in 13 patients excentric LVH was observed. Mean serum concentrations of urea, creatinine, endothelin (ET-1), PTH and phosphate were increased while serum concentration of hemoglobin, total protein, albumin, sodium, potassium, calcium were in the normal range. Positive correlation was found between PTH serum concentration and LVM r = 0.704 (p < 0.001), between PTH serum concentration and IVS r = 0.267 (p < 0.04), between PTH serum concentration and PW r = -0.238 (p < 0.04), between ET-1 and RWT r = 0.447 (p < 0.04) and negative correlation between BMI and LVMI r = -0.451 (p < 0.05). Our observations suggests that uremic cardiomyopathy is heterogenous (systolic and diastolic dysfunction) and multifactoral. The correlations between serum PTH concentration and LVH and between BMI and LVH confirmed that both hyperparathyroidism and malnutrition are important factors influencing the development of LVH which plays an important role in the systolic and diastolic cardiac failure in HD patients.
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PMID:[Left ventricular systolic and diastolic dysfunction in patients with chronic renal failure treated with hemodialysis]. 1293 88

Development of vascular and systemic calcification is one of the more serious and often occurring complications in hemodialyzed patients. The cardiac valves calcifications are of the essential importance. They are result of the very complicated calcification process connected with hyperphosphataemia, hyperparathyroidism, calcium carbonate administering and active vitamin D3 metabolites as well as using dialysis fluids with high concentration of calcium. Elevated P and Ca x P product are both significant predictors of cardiovascular mortality in hemodialized patients. We describe two patients with cardiac failure because of cardiac valves calcification. Both patients underwent artificial valves implantation. The patients showed a marked improvement of the quality of life and haemodynamic status.
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PMID:[Calcification of heart valves in hemodialized patients and their cardiosurgical correction]. 1545 82

The increasing prevalence of chronic kidney disease (CKD) in the United States demands a closer evaluation of and attention to associated morbidities, and, particularly, the rising mortality related to cardiovascular disease in all age groups. Patients with CKD demonstrate an increased risk of coronary artery disease due to calcium deposition and subsequent arterial stiffening, in addition to left ventricular dysfunction with associated heart failure and arrhythmias. While clearly impacted by the traditional risk factors for development of cardiovascular disease (CVD), patients with CKD are also affected by non-traditional risk factors, including calcium overloading related to aggressive management of secondary hyperparathyroidism. Recent data have shown that a substantial number of patients with CKD are deficient in vitamin D on a nutritional basis, in addition to the known decrease in the kidney-produced active metabolite during progressive CKD. Historically, vitamin D has been described as an endocrine hormone that regulates blood calcium and parathyroid hormone levels. It has become increasingly clear, through the recognition of a vitamin D receptor in most tissues, that vitamin D possesses functions well beyond calcium homeostasis, such that a deficiency may contribute to the development of CVD. In this brief review, the role of vitamin D activation through its vitamin D receptor will serve as an introduction to the magnitude of the nutritional deficits in children, adults, and those with CKD. As therapeutic entities in the management of renal osteodystrophy, vitamin D analogues play an important role in cardiovascular health that continues to evolve. Preliminary studies indicate that vitamin D therapy for control of secondary hyperparathyroidism may confer cardioprotection and reduce mortality. Attention to care of osteodystrophy in CKD must take into account heart health as well.
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PMID:Renal osteodystrophy in children: a systemic disease associated with cardiovascular manifestations. 1662 9

An emerging body of evidence suggests secondary hyperparathyroidism (SHPT) may be an important covariant of congestive heart failure (CHF), especially in African-Americans (AA) where hypovitaminosis D is prevalent given that melanin, a natural sunscreen, mandates prolonged exposure of skin to sunlight and where a housebound lifestyle imposed by symptomatic CHF limits outdoor activities and hence sunlight exposure. In addition to the role of hypovitaminosis D in contributing to SHPT is the increased urinary and fecal losses of macronutrients Ca(2+) and Mg(2+) associated with the aldosteronism of CHF and their heightened urinary losses with furosemide treatment of CHF. Thus, a precarious Ca(2+) balance seen with reduced serum 25(OH)D is further compromised when AA develop CHF with circulating RAAS activation and are then treated with a loop diuretic. SHPT accounts for a paradoxical Ca(2+) overloading of diverse tissues and the induction of oxidative stress at these sites which spills over to the systemic circulation. In addition to SHPT, hypozincemia and hyposelenemia have been found in AA with compensated and decompensated heart failure and where an insufficiency of these micronutrients may have its origins in inadequate dietary intake, altered rates of absorption or excretion and/or tissue redistribution, and treatment with an ACE inhibitor or AT(1) receptor antagonist. Zn and Se deficiencies, which compromise the activity of several endogenous antioxidant defenses, could prove contributory to the severity of heart failure and its progressive nature. These findings call into question the need for nutriceutical treatment of heart failure and which is complementary to today's pharmaceuticals, especially in AA.
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PMID:Macro- and micronutrients in African-Americans with heart failure. 1681 77

Heart failure is thought to be more common and of greater severity in African-Americans (AAs). Potential mechanisms remain uncertain. The importance of micronutrient deficiencies in the pathophysiologic expression of congestive heart failure (CHF) in AAs remains to be explored, including hypovitaminosis D, which can promote secondary hyperparathyroidism (SHPT), together with hypozincemia and hyposelenemia, the 2 most crucial trace minerals integral to diverse biologic functions. Serum parathyroid hormone (PTH), 25-hydroxyvitamin D (25(OH)D), Zn, and Se were monitored in 30 AAs hospitalized during June through December 2005, with decompensated failure and reduced ejection fraction (EF) (<35%) of predominantly nonischemic origin treated with an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB), furosemide, and spironolactone. Based on their symptomatic status before hospitalization, 15 patients were stratified as having protracted (>or=4 weeks) CHF, whereas 15 patients had short-term (1-2 weeks) CHF. These hospitalized patients were compared with 10 AA outpatients with stable, similarly treated compensated failure and comparable EF, and 9 AA normal volunteers without cardiovascular disease. Serum PTH was elevated in all patients with protracted CHF and in 60% of patients with short-term CHF, but not in compensated patients or normal volunteers. However, serum 25(OH)D was reduced in all patients with >or=4 weeks and 80% with either 1-2 weeks CHF or compensated failure compared with volunteers. Serum Zn was below normal in 11 of 15 patients with protracted CHF, in 8 of 15 patients with shorter duration CHF, and in 5 of 10 patients with compensated failure. Serum Se was reduced in all patients with >or=4 weeks, 60% with short-term CHF, and 90% of compensated patients. Concomitant to hypovitaminosis D, hypozincemia, and hyposelenemia, SHPT is a covariant of CHF in housebound AAs.
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PMID:Micronutrients in African-Americans with decompensated and compensated heart failure. 1716 51

Hormonal regulation is not possible without the cardiovascular system, and thus the heart plays a special role not only in the action and synthesis, but also in the distribution of hormones. Severe endocrine disorders with cardiac involvement are often threatening for the patient. The impact of aberrant thyroid function, the sympathetic-adrenal symptoms of which predominantly affect the heart, is well known. Diabetes mellitus and the associated metabolic syndrome are major causes of cardiovascular disease and determine its morbidity and lethality rates. Acromegaly causes a complex cardiomyopathy that may result in cardiac failure refractive to conventional treatment. The excessive production of adrenal hormones in Cushing's syndrome, hyperaldosteronism and pheochromocytoma primarily harms the heart by causing severe hypertension. The same holds true for long-standing hyperparathyroidism. Recent prospective studies did not confirm the protective effect of hormone replacement therapy on cardiovascular disease.
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PMID:[Endocrine disorders and the heart]. 1733 54

Not all patients with heart failure, defined as a reduced ejection fraction, will have an activation of the RAAS, salt and water retention, or the congestive heart failure (CHF) syndrome. Beyond this cardiorenal perspective, CHF is accompanied by a systemic illness that includes oxidative stress, a proinflammatory phenotype, and a wasting of soft tissues and bone. A dyshomeostasis of calcium, magnesium, zinc, selenium, and vitamin D contribute to the appearance of oxidative stress and to compromised endogenous defenses that combat it. A propensity for hypovitaminosis D, given that melanin is a natural sunscreen, and for secondary hyperparathyroidism in African-Americans make them more susceptible to these systemic manifestations of CHF-a situation which is further threatened by the calcium and magnesium wasting that accompanies the secondary aldosteronism of CHF and the use of loop diuretics.
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PMID:Macro- and micronutrients in patients with congestive heart failure, particularly African-Americans. 1807 25

Primary hyperparathyroidism and malignancy are responsible for greater than 90% of all cases of hypercalcemia. Compared with the hypercalcemia of malignancy, hyperparathyroidism tends to be associated with lower serum calcium levels (< 12 mg/dL) and a longer duration of hypercalcemia (more than 6 months). The hypercalcemic symptoms are usually fewer and subtle. Hyperparathyroidism tends to cause kidney calculi, hyperchloremic metabolic acidosis, and the characteristics of metabolic bone disease osteitis fibrosa cystica, but no anemia. In contrast, hypercalcemia of malignancy is typically rapid in onset, with higher serum calcium levels, and more severe symptoms. Patients so affected show marked anemia, but they never have kidney calculi or metabolic acidosis. Parathyroid hormone assay is the most useful test for differentiating hyperparathyroidism from malignancy and other causes of hypercalcemia. In hyperparathyroidism, serum parathyroid hormone levels will be elevated. In other cases, the high serum calcium concentration usually results in suppression of parathyroid hormone. Treatment of hypercalcemia should be started with hydration. Loop diuretics may be required in individuals with renal insufficiency or heart failure to prevent fluid overload. Calcitonin is administered for the immediate short-term management of severe symptomatic hypercalcemia. For long-term control of severe or symptomatic hypercalcemia, the addition of biphosphonate is typically required. Among intravenous bisphosphonates, zoledronic acid or pamidronate are the agents of choice. Glucocorticoids are effective in hypercalcemia due to lymphoma or granulomatous diseases. Dialysis is generally reserved for those with severe hypercalcemia complicated with kidney failure.
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PMID:Hypercalcemia: an evidence-based approach to clinical cases. 1939 81


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