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

Our objective was to evaluate if peritoneal dialysis (PD) could improve survival of patients with progressive severe congestive heart failure resistant to drug therapy. The patients were selected by the cardiologist in cooperation with a nephrologist, including patients not responding to conventional medication with an expected fatal outcome within the next months. The study included 16 consecutive patients with a chronic progressive severe refractory heart failure (sHF) of NYHA class III (n = 6) or IV (n = 10) who did not respond to diuretics and angiotension converting enzyme (ACE) inhibitors. They had a mean age of 60 years (+/- 14, range 30-75, median 62 years). Nine of the patients had sHF as the only reason for initiating PD (all NYHA IV), while 7 also needed dialysis due to uremia. Five of 7 had been on hemodialysis but switched to PD due to a progressive congestive sHF. In 2 patients, PD was decided already at start of dialysis therapy due to the severity of their heart failure. The reason for sHF was: valvular dysfunction (n = 5) with defect prosthesis (n = 3); in the course of a myocardial infarction (n = 4); and cardiomyopathy (n = 4). Tenckhoff catheters were inserted under local anesthesia and ultrafiltration was started and maintained until discharge. The survival time and change in heart size by x-ray was used for analyses. All patients improved their stage of congestive heart failure by NYHA classification already during the first month. Six patients died during the follow-up period due to cardiac reasons (sudden death, relapse of sHF) after a mean of 10.7 months (+/- 3.7, range 1-24 months). Ten were alive after a median observation period of 10 months (+/- 12.5, range 1-36 months). Heart size was reduced in 15 of the patients. Three of the patients with sHF but without uremia could stop the PD. The results showed that ultrafiltration by PD was easy to perform despite low initial blood pressure. The sHF was reduced and life span was prolonged with improved quality of life.
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PMID:PD treatment for severe congestive heart failure. 872 98

To determine the prognosis and risk factors for ischemic heart disease in chronic uremia, a cohort of 432 dialysis patients were followed prospectively from start of dialysis therapy until death or renal transplantation. Baseline demographic, clinical and echocardiographic data were obtained. After the initiation of dialysis laboratory data were collected at monthly intervals, and clinical and echocardiographic data at yearly intervals. Twenty-two percent of patients (N = 95) had either a history of angina pectoris or myocardial infarction on starting dialysis therapy. Median time to onset of heart failure was 24 months in those with ischemic heart disease on initiation of dialysis, compared to 55 months in those without (P < 0.0001). This effect was independent of age, diabetes and underlying cardiomyopathy. Median survival was 44 months in those with ischemic disease compared to 56 months in those without (P = 0.0001). This adverse impact was independent of age and diabetes mellitus but, when cardiac failure was added to the Cox's model, ischemic heart disease was no longer an independent predictor of survival. De novo ischemic heart disease, not evident on starting dialysis therapy, occurred in 41 (9%) patients. When compared to patients who never developed ischemic disease (N = 296; 69%), significant and independent predictors of de novo disease were older age (P = 0.0007), diabetes mellitus (P = 0.0001), high blood pressure during follow up on dialysis (P = 0.02) and hypoalbuminemia (P = 0.03), whereas anemia was not an independent predictor. LV mass index was 174 +/- 7 g/m2 in those who developed de novo ischemic disease compared to 155 +/- 3 g/m2 (P < 0.001) in those who did not. Concentric LV hypertrophy, LV dilation and systolic dysfunction were independent risk factors for de novo ischemic heart disease. We conclude that ischemic heart disease occurs frequently in dialysis patients, that its adverse impact is mediated through the development of heart failure, and that the most important, potentially reversible risk factors are hypertension, hypoalbuminemia, and underlying cardiomyopathy.
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PMID:Outcome and risk factors of ischemic heart disease in chronic uremia. 873 Nov 10

Plasma viscosity (PV) was examined in healthy (n = 122) and sick (n = 58) dogs. The mean value of PV in healthy adult dogs is 1.22 mPas. PV is remarkably increased in case of illness. In dogs with chronic heart failure the mean value was 1.46 mPas. Patients suffering from uraemia or pyometra revealed mean values of 1.90 mPas and 1.96 mPas respectively. An elevation of the PV is correlated with an increase of the "acute-phase-proteins". The examination of PV is useful for a better assessment of microcirculation. The PV is a parameter, which is important in diagnostics as well as in follow-up during special therapeutical procedures.
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PMID:[Plasma viscosity in the dog]. 899 4

Cardiomyopathy in chronic uremia results from pressure and volume overload. The former causes concentric left ventricular [LV] hypertrophy, results from hypertension and aortic stenosis, and is also associated with diabetes mellitus and anemia. Volume overload causes LV dilatation, results from arteriovenous shunting, salt and water overload, and anemia, and is also associated with ischemic heart disease, hypertension, and hypoalbuminemia. Decreased major arterial compliance and an early return of arterial wave reflections are also associated with the extent of LV hypertrophy. Cardiomyopathy predisposes to diastolic and systolic dysfunction. The latter results from myocyte death, and predisposing factors include ischemic heart disease and the uremic environment. Ischemic heart disease may be atherosclerotic or nonatherosclerotic in origin. Multiple factors contribute to the vascular pathology of chronic uremia, including injury to the vessel wall, dyslipidemia, prothrombotic factors, increased oxidant stress, and hyperhomocysteinemia. Ischemic risk factors include hypertension, LV hypertrophy, hypoalbuminemia, and perhaps hyperparathyroidism. The clinical consequences of cardiomyopathy include heart failure, ischemic heart disease, dialysis hypotension, and arrhythmias. The adverse impact of ischemic heart disease is probably mediated through the development of cardiac failure.
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PMID:Cardiac disease in chronic uremia: pathogenesis. 923 25

All consecutive cases of chronic renal failure (CRF) seen over a twelve-month period (January-December 1992) were evaluated. Those that fulfilled strict diagnostic criteria for hypertension induced CRF (HICRF) were further studied to determine peculiarities of its clinico-pathological features that may render this possibly preventable condition readily identifiable. Twenty one (23.1%) of the 91 cases of CRF satisfied these criteria. There was a male preponderance (M.F.4.3:1). Nocturia was a prominent symptom predating other symptoms of CRF in all. Throbbing frontal headache necessitating significant consumption of analgesic was found in 13(61.9%). Hypertension had been diagnosed in the patients for periods ranging from 2-15 years and compliance to therapy was adjudged poor. Ten smoked cigarette in significant quantities. Hypertension occurred in 8 of the families of the patients. Hypertension was severe in all, with evidence of accelerated phase in 19(90.5%). A majority (71.4%) presented with severe uraemia (serum creatinine > or = 100 umol/l). Target organ damage, evident in cardiomegaly with heart failure occurred in 15, while ultrasonographic features of bilateral shrunken kidneys was seen in all. Blood pressure control was largely inadequate with a combination of 3 drugs. Mortality rate was 51% in the first year. Renal histopathological findings of glomerular sclerosis, malignant arteriolar changes with absence of glomerular cellular proliferation were observed in renal biopsies and 6 autopsy tissues. It is concluded that HICRF is a major cause of mortality; renal failure is often advanced at presentation, and blood pressure is usually in the accelerated phase. Significant cigarette smoking, severe headache necessitating consumption of significant quantity of analgesics, and a family history of hypertension are striking features.
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PMID:Hypertension induced chronic renal failure: clinical features, management and prognosis. 971 16

Angiotensin converting enzyme (ACE) inhibitors are useful in the treatment of hypertension and heart failure. However, acute renal failure (ARF) may occur in patients who are taking these drugs in situations associated with decreased glomerular filtration pressure, such as dehydration caused by acute diarrhea or diuretic therapy. Sixty-four patients who were admitted to the intensive care unit for ARF associated with ACE inhibitor therapy were followed for more than 5 years. In this historical retrospective study, we documented that 45 patients were treated for hypertension (group I) and 19 were treated for heart failure (group II). Their mean age was 71.2+/-11.6 years. Patients with ARF presented with overt dehydration in 91% and 84% of the cases in groups I and II, respectively. Hypovolemia was caused by diuretics or gastrointestinal fluid loss. Bilateral artery-renal stenosis or stenosis in a solitary kidney was documented in 22% and 10% of patients in groups I and II, respectively. The probability of survival was 91% and 49% at 1 year and 64% and 18% at 5 years, for groups I and II, respectively. Acute renal failure required hemodialysis in seven patients, but none of them became dialysis dependent. In the subgroup of patients with preexisting chronic renal failure, all the patients except for one who belonged to group II died within 2 years. In both groups, after resolution of ARF, plasma creatinine concentration returned to baseline level and the course of renal function was not significantly worsened. In conclusion, ARF associated with ACE inhibitors is likely to occur in many patients without renal artery stenosis after unexpected dehydration, especially in older patients with congestive heart failure. In both groups of patients, in the absence of preexisting chronic uremia, recovery of renal function occurred without sequelae, even after an episode of acute tubular necrosis requiring dialysis.
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PMID:Long-term follow-up of acute renal failure caused by angiotensin converting enzyme inhibitors. 1056 Jul 94

Atherosclerotic renovascular disease (ARVD) continues to challenge the clinician as we enter the third millenium. ARVD frequently complicates patients with other vascular pathological states, and it is an increasingly common cause of end-stage renal failure. Although renovascular interventional procedures are now widely available and are of benefit to some patients with ARVD, a large proportion still progress to dialysis. Recent epidemiological investigations have emphasized the relationship between ARVD and other vascular diseases, and these are notable in patients with coronary artery disease and/or cardiac failure. Increased awareness of the possible coexistence of ARVD in patients with these latter conditions may allow earlier diagnosis and a minimization of complications (eg, angiotensin-converting enzyme inhibitor-related uremia or flash pulmonary edema). Contemporary studies also highlight the importance of intrarenal vascular and parenchymal injury in the cause of chronic renal failure in many patients with ARVD. Severe renal structural damage often coexists with proximal renal arterial narrowing, and this can explain the variability of renal functional outcomes known to accompany revascularization procedures. More appropriate selection of those patients likely to benefit from renovascular revascularization is now required. Large-scale trials that will identify the optimal approach to improving renal functional and survival outcomes in this high-risk group of patients are now long overdue.
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PMID:New insights into the epidemiologic and clinical manifestations of atherosclerotic renovascular disease. 1073 76

Cardiovascular disease is the principal cause of morbidity and mortality in dialysis patients. The principal alterations responsible are left ventricular hypertrophy and arterial disease characterized by an enlargement and hypertrophy of arteries and the high prevalence of atheromatous plaques. Left ventricular hypertrophy is the consequence of combined effects of chronic hemodynamic overload and nonhemodynamic biochemical and neurohumoral factors characteristic of uremia. The hemodynamic overload is due to flow and pressure overload. The flow overload is tightly related to hyperkinetic circulation caused by anemia, arteriovenous fistula, or overhydration and is characterized by an enlargement of the left ventricular cavity. The pressure overload in these patients is more tightly related to abnormal geometry and function of large conduit arteries, principally the stiffening of arterial tree. The flow overload is also in large part responsible for remodeling of arterial tree, and as the heart and vessels are a coupled interactive physiological system, cardiac and vascular alterations occur in parallel, being induced to a great extent by the same hemodynamic abnormalities. The principal clinical consequences of left ventricular hypertrophy and arterial alterations are heart failure, ischemic heart disease, and peripheral artery disease. Cardiovascular alterations are only partly reversible, and efforts should be directed toward early prevention.
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PMID:Pathophysiology of cardiovascular disease in hemodialysis patients. 1093 11

Morbidity and mortality of heartfailure are decreasing because of improved medical treatment. The recompensation balance can however be very fragile, which is illustrated by three patients. A woman aged 73 and a man aged 62, both known with heart failure, became seriously ill after diarrhoea; examination revealed uraemia, hyperpotassaemia and raised digitalis levels. A man aged 72, also with heart failure and diarrhoea, developed sensory disorders in both feet. He, also, was found to suffer from renal insufficiency. All patients used an angiotensin converting enzyme inhibitor or an angiotensin-II-antagonist and an aldosterone receptor blocker as well. During the (innocent) intercurrent disease by which their intravascular volume diminished they developed a severe renal insufficiency which needed clinical, intensive treatment. After haemodialysis, all three recovered well. Renal function plays an essential role in the fragile treatment balance that exists in recompensated cardiac patients. The medication that is beneficial for the cardiac functioning may at the same time compromise the renal perfusion. Good monitoring and good instructions about what to do in case of intercurrent diseases are of vital importance in these patients.
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PMID:[Acute renal insufficiency due to vomiting or diarrhea: the Achilles heel of medical support for heart failure]. 1102 Aug 33

Microcirculation of the bulbar conjunctiva and nailbed was studied in 120 patients with chronic renal failure (CRF) and its complications. Peritoneal, pleural and pericardial circulation was investigated in 15 dogs with experimental chronic uremia. It was found that the degree and frequency of microcirculatory disorders in chronic uremia correlate with the stage of CRF and diseases causing CRF. The presence of cardiac insufficiency aggravated CRF. Clinical, morphological, light and electron microscopic examinations of microcirculation in CRF revealed alterations in all the regions of microcirculation. Additional data on etiopathogenesis of cardiovascular disorders in CRF were obtained basing on the changes in peritoneal, pleural and pericardial microvessels in the experimental model of chronic uremia.
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PMID:[Microcirculation bed in chronic uremia]. 1118 91


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