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

Premature cardiovascular disease is the leading cause of morbidity and mortality in patients with end-stage renal failure. Natriuretic peptides, specifically brain natriuretic peptide, are released from the heart in response to chamber distension and thus increased in the presence of volume expansion and cardiac overload. Their physiological role is to cause vasodilatation and promote natriuresis to maintain volume homeostasis. Increasingly serum levels of brain natriuretic peptide are used to both diagnose and manage cardiovascular disorders. Furthermore, augmenting the beneficial hemodynamic actions of brain natriuretic peptide may have a therapeutic role in decompensated heart failure. However, the diagnostic role of serum brain natriuretic peptide levels in patients with advanced renal dysfunction remains to be defined. These patients have a high prevalence of left ventricular disorders, specifically left ventricular hypertrophy, which may reduce the diagnostic utility of brain natriuretic peptide. In addition, ventricular stretch may be determined by intravascular volume status rather than by cardiac dysfunction. Nonetheless, as the prognosis of patients with end-stage renal failure and co-existing heart failure is so poor, the availability of a further marker of cardiac ''distress'' may in the future become a useful diagnostic tool and in due course may become a primary goal for titration and tailoring of therapy.
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PMID:Diagnostic, prognostic, and therapeutic implications of brain natriuretic peptide in dialysis and nondialysis-dependent chronic renal failure. 1724 21

The mitochondrial phospholipid cardiolipin is required for optimal mitochondrial respiration. In this study, cardiolipin molecular species and cytochrome oxidase (COx) activity were studied in interfibrillar (IF) and subsarcolemmal (SSL) cardiac mitochondria from Spontaneously Hypertensive Heart Failure (SHHF) and Sprague-Dawley (SD) rats throughout their natural life span. Fisher Brown Norway (FBN) and young aortic-constricted SHHF rats were also studied to investigate cardiolipin alterations in aging versus pathology. Additionally, cardiolipin was analyzed in human hearts explanted from patients with dilated cardiomyopathy. A loss of tetralinoleoyl cardiolipin (L(4)CL), the predominant species in the healthy mammalian heart, occurred during the natural or accelerated development of heart failure in SHHF rats and humans. L(4)CL decreases correlated with reduced COx activity (no decrease in protein levels) in SHHF cardiac mitochondria, but with no change in citrate synthase (a matrix enzyme) activity. The fraction of cardiac cardiolipin containing L(4)CL became much lower with age in SHHF than in SD or FBN mitochondria. In summary, a progressive loss of cardiac L(4)CL, possibly attributable to decreased remodeling, occurs in response to chronic cardiac overload, but not aging alone, in both IF and SSL mitochondria. This may contribute to mitochondrial respiratory dysfunction during the pathogenesis of heart failure.
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PMID:Loss of cardiac tetralinoleoyl cardiolipin in human and experimental heart failure. 1742 48

Urocortin 1 (Ucn1) may be involved in the pathophysiology of heart failure (HF), but the impact of Ucn1 administration on progression of the disease is unknown. The aim of this study was to investigate the effects of Ucn1 in sheep from the onset of cardiac overload and during the subsequent development of HF. Eight sheep underwent two 4-day periods of HF induction by rapid left ventricular pacing (225 beats/min) in conjunction with continuous infusions of Ucn1 (0.1 microg.kg(-1).h(-1) iv) and a vehicle control (0.9% saline). Compared with control, Ucn1 attenuated the pacing-induced decline in cardiac output (2.43 +/- 0.46 vs. 3.70 +/- 0.89 l/min on day 4, P < 0.01) and increases in left atrial pressure (24.9 +/- 1.0 vs. 11.9 +/- 1.1 mmHg, P < 0.001) and peripheral resistance (38.7 +/- 9.4 vs. 25.2 +/- 6.1 mmHg.l(-1).min, P < 0.001). Ucn1 wholly prevented increases in plasma renin activity (4.02 +/- 1.17 vs. 0.87 +/- 0.1 nmol.l(-1).h(-1), P < 0.001), aldosterone (1,313 +/- 324 vs. 413 +/- 174 pmol/l, P < 0.001), endothelin-1 (3.8 +/- 0.5 vs. 2.0 +/- 0.1 pmol/l, P < 0.001), and vasopressin (10.8 +/- 4.1 vs. 1.8 +/- 0.2 pmol/l, P < 0.05) during pacing alone and blunted the progressive increases in plasma epinephrine (2,132 +/- 697 vs. 1,250 +/- 264 pmol/l, P < 0.05), norepinephrine (3.61 +/- 0.73 vs. 2.07 +/- 0.52 nmol/l, P < 0.05), and atrial (P < 0.05) and brain (P < 0.01) natriuretic peptide levels. Ucn1 administration also maintained urine sodium excretion (0.75 +/- 0.34 vs. 1.59 +/- 0.50 mmol/h on day 4, P < 0.05) and suppressed pacing-induced declines in creatinine clearance (P < 0.05). These findings indicate that Ucn1 treatment from the onset of cardiac overload has the ability to repress the ensuing hemodynamic and renal deterioration and concomitant adverse neurohumoral activation, thereby delaying the development of overt HF. These data strongly support a use for Ucn1 as a therapeutic option early in the course of the disease.
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PMID:Urocortin 1 administration from onset of rapid left ventricular pacing represses progression to overt heart failure. 1752 50

We describe six patients with an uncommon variant of infantile hemangioma that we have termed reticular, occurring in the extremity, which were associated with intractable ulceration, anogenito-urinary-sacral anomalies, and sometimes cardiac overload. The extreme end of the spectrum is exemplified by a male neonate who presented with a stained, enlarged, pulsatile lower extremity, and cardiac failure. He also had hepatic hemangiomas and ambiguous genitalia. Progressive soft tissue necrosis and bony destruction necessitated amputation. The histopathologic features differed from those of typical infantile hemangioma: infiltrative (not lobular) and involving fascia, muscle, and bone. The mid-spectrum is illustrated by five females with reticular infantile hemangioma of the lower limb, buttock, and perineum. Four of these infants had a ventral-caudal anomaly, including omphalocele, recto-vaginal fistula, solitary/duplex kidney, imperforate anus, and tethered cord; one infant also had hepatic hemangiomas. Deep ulcerations healed following corticosteroid therapy; one patient required skin graft for closure of a thigh wound. The minor end of the spectrum is exemplified a patchy lesion in the distal limb. The reticular variant of infantile hemangioma can be confused with other vascular anomalies in the limb, such as capillary malformation, cutis marmorata telangiectasia congenita, diffuse arteriovenous malformation (Parkes Weber syndrome) and capillary-lymphatico-venous malformation (Klippel-Trenaunay syndrome). The macular network-like appearance of the tumor and coexisting ventral-caudal structural anomalies is analogous to the association of posterior fossa brain malformations, hemangiomas, arterial anomalies, coarctation of the aorta and cardiac defects, and eye abnormalities association in the craniofacial region.
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PMID:Reticular infantile hemangioma of the limb can be associated with ventral-caudal anomalies, refractory ulceration, and cardiac overload. 1784 55

Surgical management of heart failure patients receiving hemodialysis (HD) is a challenge to surgeons and reports are limited. Five patients receiving HD underwent a mitral annuloplasty with or without restoration of the left ventricle because of class III or IV heart failure due to mitral regurgitation and poor ventricular functions. Of those, three fully recovered to NYHA class I after the cardiac procedure, however, two patients remained symptomatic and required an adjunctive procedure. For that, we converted the arteriovenous dialysis shunt to an inter-arterial bypass by dividing the venous side of the shunt and anastomosing it to the proximal radial artery (RA), followed by ligation of the RA between the two anastomoses so that the RA was bypassed by the cephalic vein. Following this procedure, left ventricular end-diastolic pressure and volume were reduced, and heart failure symptoms diminished. This simple procedure was able to reduce the cardiac overload, while keeping the vascular access intact and may be a relevant adjunct to surgical reverse remodeling in end-stage heart failure patients receiving HD.
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PMID:Novel adjunct to surgery for end-stage cardiomyopathy receiving hemodialysis. 1805 53

Indirect observations are compatible with cardiac vitamin C deficiency as one contributory factor to oxidative stress in heart failure, but data on ventricular vitamin C content are lacking. Here, we used the well established model of aortic-banded rats at the stage of compensated hypertrophy (6 weeks after banding) and at the transition to cardiac failure (22 weeks after banding) to analyze vitamin C, vitamin E, protein carbonyls and malondialdehyde tissue content together with the respective plasma concentrations. Furthermore, we investigated the expression of the vitamin C transporters SVCT1 and SVCT2 in the left ventricle (LV). Aortic-banded rats, independently from their age, had higher malondialdehyde and protein carbonyl levels in plasma and LV tissue compared to sham-operated animals indicating increased oxidative stress. Plasma vitamin C remained unaffected from cardiac overload, while LV vitamin C was elevated in both stages of hypertrophy together with an increased expression of the vitamin C transporter SVCT2 suggesting increased vitamin C uptake. The levels of antioxidants and lipid peroxides were similar 6 and 22 weeks after aortic banding. Therefore, the accumulation of vitamin C in compensated hypertrophy and in decompensated failure excludes cardiac vitamin C deficiency as a primary factor to oxidative stress in this model.
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PMID:Enhanced myocardial vitamin C accumulation in left ventricular hypertrophy in rats is not attenuated with transition to heart failure. 1828 1

Volume overload frequently caused in dogs by chronic degenerative valvular disease (CDVD), eventually leads to cardiac failure. Experimental and clinical evidences demonstrate that increased interleukin-1beta serum level in patients with heart insufficiency correlates with the severity of failure irrespective of its etiology. Very little is known about the IL-1beta expression in failing vs. non-failing myocardium. IL-1beta transcript level was determined in the CDVD dogs (n=17) and control animals (n=9) without cardiac insufficiency by real-time PCR. IL-1beta transcript level in failing hearts was higher than in the control. In both groups the highest IL-1beta level was detected in the left ventricles. Although IL-1beta is a major pro-inflammatory cytokine most of the CDVD dogs displayed no inflammatory infiltrates into the myocardium. Massive fibrosis was observed in the control group, unlike the failing hearts, in which cardiomyocyte hypertrophy and atrophy dominated. The alternative IL-1beta transcript identified here (IL-1betasv1) was significantly elevated in the failing myocardium compared with the control group. Increased IL-1beta expression seems to be associated with mechanical heart overload. Its endogenous origin, and certain histopathological findings attributed to IL-1beta indicate its importance in cardiac hypertrophy and failure. The lack of some typical IL-1beta actions, i.e. inflammatory, pyrogenic and fibrotic, may suggest a different role of this cytokine in myocardium. It appears that the canine IL-1beta gene can be transcribed in two ways in heart tissue, with the IL-1betasv1 form present mainly in failing hearts.
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PMID:Increased expression of interleukin-1beta and its novel splice variant in canine hearts with volume overload. 1900 21

Circulatory distress can occur in the long term after the formation of a traumatic arteriovenous fistula (AVF), but cardiac failure rarely occurs in a patient with an AVF in the lower extremity. The present patient underwent surgery to treat a traumatic popliteal AVF 9 years after sustaining the injury. Although the patient was asymptomatic with regard to cardiac circulation, cardiomegaly was noted and it resolved promptly after the surgical treatment. Cardiac insufficiency should be borne in mind even when a patient is asymptomatic because young patients have a high tolerance for cardiac overload.
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PMID:Recovery of cardiomegaly after treatment of traumatic popliteal arteriovenous fistula. 1907 19

Heart failure is a common clinical syndrome occurring as a result of cardiac overload, injury, and a complex interplay among genetic, neurohormonal, inflammatory, and biochemical factors. Occurrence of arrhythmias in heart failure is largely a consequence of disease-induced electrical remodeling of cardiac myocytes, a phenomenon consisting of alterations of ion channels and the ion-transport function that predispose patients to develop lethal arrhythmias. In most cases, the mechanism is the rapid onset of a ventricular tachyarrhythmia progressing to ventricular fibrillation and hemodynamic compromise. This paper highlights some of the important changes in ion channel expression and function that underlie electrical remodeling of the failing heart. Particular attention will be focused on the presence, features, and pharmacologic modulation of f channels expressed in ventricular cardiac myocytes.
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PMID:Electrophysiologic changes in heart failure: focus on pacemaker channels. 1923 71

The increasing number of patients with progressive or exacerbated heart failure that is refractory to medical treatment necessitates the development of innovative cardiac assist devices. The aim of this study was to investigate whether a new percutaneously inserted system, which allows continuous aortic flow augmentation (CAFA), could be shown to be clinically effective with neurohormonal benefit in patients admitted with decompensated heart failure. Patients with exacerbations of chronic heart failure were recruited for the study. A percutaneous circulation assist device (Cancion system) promoting CAFA was implanted for up to 4 days in each patient. Clinical improvement was evaluated by measuring the clinical status according to the New York Heart Association (NYHA) classification and biochemical parameters including troponin and B-type natriuretic peptide (BNP) as markers of cardiac necrosis and cardiac overload; these parameters were measured before, during, and after CAFA treatment. The decrease in BNP was determined after implantation, reaching, on average, a maximum decrease of 57% at 72 h (P = 0.04). The neurohumoral response remained significant (P < 0.05) up to 120 h after implantation, with a decrease in BNP levels of 37%, on average, compared to baseline values. Troponin I did not show any significant change during mechanical assistance (P > 0.2). All patients had improved clinical status according to the NYHA classification, and the improvement lasted for more than 1 week. Percutaneous heart-assist devices promoting CAFA offer clinical improvement and a neurohumoral response, with a significant BNP reduction in severe exacerbation of chronic heart failure that is refractory to medical treatment.
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PMID:Neurohumoral response and clinical effectiveness of continuous aortic flow augmentation in patients with decompensated heart failure. 1989 90


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