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)

Patients with severe hypertension with retinoscopic bilateral papilloedema only are not classically regarded as having malignant hypertension (MHT). We have encountered 23 such patients between 1965-1993, whilst over a similar period we have seen 315 patients who fulfilled the conventional criteria for MHT with bilateral retinal haemorrhages, exudates with or without papilloedema. We hypothesised that patients with "lone" papilloedema and severe hypertension were suffering from a disease which was identical in aetiology and outcome to conventional MHT. There were no significant differences in age, mean blood pressure, proteinuria or renal function at presentation, ethnic composition, smoking status and followup blood pressure control between the papilloedema group and those presenting with conventional MHT. Clinical features at presentation in the papilloedema only group included strokes in 4, visual disturbance in 2, headaches in 3 and heart failure in 1 patient. Many patients however had no complications at presentation. After a mean followup of 59.8 months, of the "lone" papilloedema group, 7 patients (30.4%) were still alive, 1 patient was on renal dialysis therapy, 13 were dead (56.5%) and 2 (8.7%) were lost to followup. The commonest causes of death were stroke in 4 patients, renal failure in 4 and heart disease in 2. This was a similar pattern of mortality to those patients with "conventional" MHT. Lifetable analyses showed a median survival of 35.9 months for the papilloedema group which was significantly worse than the 108.7 months for the conventional MHT group (Lee-Desu statistic 4.04, p = 0.045). We suggest that patients with high blood pressure and lone bilateral papilloedema may comprise a hitherto unrecognised subgroup of patients with MHT. Once intracerebral pathology has been excluded, these patients need to be treated as aggressively as those with MHT.
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PMID:Severe hypertension with lone bilateral papilloedema: a variant of malignant hypertension. 874

ACE inhibitors effectively reduce systemic vascular resistance in patients with hypertension, heart failure or chronic renal disease. This antihypertensive efficacy probably accounts for an important part of their long term renoprotective effects in patients with diabetic and non-diabetic renal disease. The renal mechanisms underlying the renal adverse effects of ACE inhibitors--intrarenal efferent vasodilation with a consequent fall in filtration pressure--are held to be involved in their renoprotective effects as well. The fall in filtration pressure presumably contributes to the antiproteinuric effect as well as to long term renoprotection. The former is suggested by the positive correlation between the fall in filtration fraction and the reduction in proteinuria found during ACE inhibition. The latter is suggested by the correlation between the (slight) reduction in glomerular filtration rate at onset of therapy and a more favourable course of renal function in the long term. Such a fall in filtration rate at the onset of ACE inhibitor treatment is reversible after withdrawal, and can be considered the trade-off for long term renal protection in patients with diabetic and nondiabetic chronic renal disease. In conditions in which glomerular filtration is critically dependent on angiotensin II-mediated efferent vascular tone (such as a post-stenotic kidney, or patients with heart failure and severe depletion of circulating volume), ACE inhibition can induce acute renal failure, which is reversible after withdrawal of the drug. Systemic and renal haemodynamic effects of ACE inhibition, both beneficial and adverse, are potentiated by sodium depletion. Consequently, sodium repletion contributes to the restoration of renal function in patients with ACE inhibitor-induced acute renal failure. Our the other hand, co-treatment with diuretics and sodium restriction can improve therapeutic efficacy in patients in whom the therapeutic response of blood pressure or proteinuria is insufficient. Patients at the greatest risk for renal adverse effects (those with heart failure, diabetes mellitus and/or chronic renal failure) also can expect the greatest benefit. Therefore, ACE inhibitors should not be withheld in these patients, but dosages should be carefully titrated, with monitoring of renal function and serum potassium levels.
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PMID:ACE inhibitors and the kidney. A risk-benefit assessment. 887 74

1. A comparison was made on the protective effects of the following: ME3221, a competitive angiotensin AT1 receptor antagonist; losartan, in which a major active metabolite is a non-competitive angiotensin AT1 receptor antagonist; and enalapril, an angiotensin-converting enzyme inhibitor, using the salt-loaded stroke-prone spontaneously hypertensive rats (SHRSP). 2. SHRSP received orally ME3221 (3 and 10 mg/kg per day), losartan (10 mg/kg per day) and enalapril (10 mg/kg per day) from the 6th to the 20th week of age. All the control rats showed rapid elevation of systolic blood pressure (SBP), accompanied by hypertensive complications, and died by 15 weeks of age. 3. ME3221, losartan and enalapril suppressed the elevation of SBP in the salt-loaded SHRSP to a comparable degree. ME3221 and losartan increased the survival rate to > 90%, and diminished hypertensive complications such as cerebral apoplexy (stroke), renal injury (increased proteinuria, and total N-acetyl-beta-D-glucosaminidase activity) and heart failure (cardiac hypertrophy and pleural effusion). 4. Competitive (ME3221) and non-competitive (losartan) angiotensin AT1 receptor antagonists showed comparable efficacy against the complications and mortality of the salt-loaded SHRSP; both were more potent than enalapril in the protective effect.
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PMID:Protective effects of ME3221 on hypertensive complications and lifespan in salt-loaded stroke-prone spontaneously hypertensive rats. 893 13

1. The protective effect of ME3221, a surmountable AT1 antagonist, on the hypertension and its concomitant complications in aged (32 week old) stroke-prone spontaneously hypertensive rats (SHRSP) was studied following long-term (32 weeks) oral administration, and compared with those of losartan (metabolite EXP3174 is an insurmountable AT1 antagonist) and enalapril. 2. During the treatment period, ME3221, at a dose of 10 mg/kg per day steadily reduced the systolic blood pressure, and no tolerance was developed to the fall in blood pressure. The reference drugs showed similar activity, but the antihypertensive effect of ME3221 was more potent. 3. In the control group, rats began to die from 52 weeks of age and all rats had died by 64 weeks of age. In contrast, no rats treated with ME3221, losartan or enalapril died before 64 weeks of age. 4. ME3221, losartan and enalapril suppressed the hypertensive complications observed in control SHRSP, that is, cerebral apoplexy (stroke and cerebral oedema), renal injury (increased proteinuria, total N-acetyl-beta-D-glucosaminidase activity and ascites) and heart failure (cardiac hypertrophy and pleural effusion). 5. These results indicate that ME3221 has a stable anti-hypertensive effect, prevents hypertensive complications and prolongs survival in aged SHRSP equally as well as losartan and enalapril.
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PMID:Effect of chronic treatment with ME3221 on blood pressure and mortality in aged stroke-prone spontaneously hypertensive rats. 907 29

Amyloid cardiomyopathy may exist when echocardiography does not suggest infiltration. Clinicians should be alert for the presence of a monoclonal protein, nephrotic range proteinuria, or peripheral neuropathy in a patient with heart failure.
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PMID:Endomyocardial biopsy-proven light chain amyloidosis (AL) without echocardiographic features of infiltrative cardiomyopathy. 920 31

Racial and ethnic minority populations are growing segments of our society. The prevalence of hypertension in these populations differs across groups, and control rates are not as good as in the general population. Clinicians should be aware of these management challenges, taking social and cultural factors into account. Guidelines are provided for management of children and women with hypertension. In older persons, diuretics are preferred and long-acting dihydropyridine calcium antagonists may be considered. Specific therapy for patients with LVH, coronary artery disease, and heart failure are outlined. Patients with renal insufficiency with greater than 1 g/d of proteinuria should be treated to a therapy blood pressure goal of 125/75 mm Hg; those with less proteinuria should be treated to a blood pressure goal of 130/85 mm Hg. ACE inhibitors have additional renoprotective effects over other antihypertensive agents. Patients with diabetes should be treated to a therapy blood pressure goal of below 130/85 mm Hg. Hypertension may coexist with various other conditions and may be induced by various pressor agents.
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PMID:The sixth report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure. 1187 36

A 46-year-old man was admitted to our clinic because of acute heart failure. Six years before admission he was pointed out cardiomegary and hematuria. One year later, he was diagnosed as having jugular foramen syndrome. On admission, he had a fever and dyspnea. Pansystolic blowing murmur was audible at the apex. The chest ratio on his chest X-ray was 52.5%. An electrocardiogram showed left ventricular hypertrophy. An echocardiogram showed marked dilatation and severe dysfunction of left ventricle. Radionuclide scanning with technetium 99 m pyrophosphate identified inflammatory change in the apex. Myocardial biopsy showed fibrotic degeneration and IgG deposits in myocardium. Blood examination showed anemia, lymphopenia. positive anti-nuclear antibody (1000 times, shaggy pattern), positive anti ds-DNA antibody and hypocomplementemia. Furthermore, proteinuria was pointed out. Renal biopsy showed focal segmental glomerulonephritis with active necrotizing lesion (type III nephritis). Lupus myocarditis and nephritis was diagnosed. After prednisolone (80 mg/day) was administered. left ventricular function and hypocomplementemia improved. The ACE inhibitor was also used for proteinuria. In spite of a little amount of blood transfusion, he showed hepatic hemosiderosis. We suspect that the cause of hemosiderosis was related chronic inflammation of active lupus. It was treated with Erythropoietin.
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PMID:[A case of lupus myocarditis and nephritis with transient foramen jugular syndrome]. 939 74

We reviewed clinical presentation, investigations, therapy, prognosis and outcome of 232 patients with primary (AL) cardiac amyloidosis. There were 142 men and 90 women. Median age at presentation was 59 years (range 29-85). AL heart disease was unusual both in patients under the age of 40 (3.0%) and in non-Caucasians (6.5%). Fatigue and weakness were the commonest presenting symptoms. Hallmark features of periorbital ecchymoses and macroglossia were present in 12.5% and 27.2%, respectively. AL cardiac amyloidosis was unusual in isolation (3.9%), and most frequently patients had features of multiorgan dysfunction; heavy proteinuria and features of malabsorption predominating in this respect. Heart involvement represents the worst prognostic indicator, with a median survival from diagnosis of 1.08 years, falling to 0.75 years with the onset of heart failure. Current therapeutic procedures appear to prolong survival, with left ventricular wall thickness, mass and ejection fraction on echocardiography and late potentials on signal averaged electrocardiography of use in prognostic stratification. Cardiac involvement from AL amyloidosis is rapidly fatal. It should be suspected in all patients with heart failure who have wall thickening on echo, normal chamber sizes, low EKG voltages and evidence suggesting a multisystem disease.
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PMID:The clinical features of immunoglobulin light-chain (AL) amyloidosis with heart involvement. 957 96

A 29-year-old nulliparous woman had development of hypertension, proteinuria, and congestive heart failure during the third trimester of her pregnancy. Her symptoms and cardiovascular changes were consistent with congestive heart failure and severe preeclampsia. The underlying pathophysiology was believed to be caused by the high-output state of pregnancy and by the increased peripheral vascular resistance of preeclampsia. The patient underwent an elective cesarean section, but her cardiovascular symptoms did not resolve. Soon after delivery, the patient was found to have an arteriovenous fistula of the right renal artery that caused the high-output cardiac state. Embolization and surgical removal of the arteriovenous fistula resulted in complete resolution of the patient's high-output heart failure. All previously reported cases of renal arteriovenous fistulas and malformations that have occurred during pregnancy are reviewed.
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PMID:High-output heart failure due to a renal arteriovenous fistula in a pregnant woman with suspected preeclampsia. 973 27

Angiotensin II, the principal effector of the renin-angiotensin cascade, stimulates a variety of physiological responses that support blood pressure and renal function. Abnormal generation of angiotensin II also contributes to the pathogenesis of hypertension, arterial diseases, cardiac hypertrophy, heart failure and proteinuric progressive renal diseases. It is well recognized that angiotensin-converting enzyme inhibitors effectively limit the progression of diabetic and non-diabetic proteinuric renal diseases towards end-stage renal disease, a capacity not necessarily shared by other blood pressure lowering agents. Whether angiotensin II type 1 receptor antagonists have the same renoprotective effect as angiotensin-converting enzyme inhibitors in progressive renal diseases remains ill defined. Angiotensin II type 1 receptor antagonists as antiproteinuric agents have been used originally in animal models of renal disease progression. Results have shown that angiotensin II type 1 receptor blockers are as effective as angiotensin-converting enzyme inhibitors in normalizing proteinuria in models of renal disease. Studies in humans are very few, but those that have been undertaken report consistent antiproteinuric effects of angiotensin II type 1 receptor antagonists that are similar to those with angiotensin-converting enzyme inhibitors. Long-term studies, however, are required to examine whether the antiproteinuric effects of angiotensin II type 1 receptor antagonists can be translated into renoprotection.
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PMID:Angiotensin II receptor antagonists and treatment of hypertension and renal disease. 981 6


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