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

Chronic cardiac insufficiency can be produced by a variety of causes which may be partly determined by means of macroscopic, histological and electron microscopic investigations. By using quantitative histochemical methods, changes of substances in the myocardium can be observed indicating myocardial insufficiency and giving an explanation of its cause. Hypertrophied hearts without insufficiency show cardiac muscle fibres having increased in width, volume and dry weight up to a maximum value which will not be exceeded even in further progressing cardiac hypertrophy. The biochemically determined amount of collagen increases significantly with the growing weight of the myocardium. Both the myocardial amount of DNA and the amount of myoglobin, correlated with the width of the fibres, have also increased. The heart muscle nuclei showed a polyploidization which is also correlated with the weight of the myocardium. In insufficient hearts suffering from myocardial hypertrophy, the increase of the total DNA content is significantly decreased as compared to non-insufficient hearts. The mean ploidy level is increased in case of lower weights of the myocardium and decreased in higher weights in comparison to non-insufficient hearts of the same weight. In insufficient hearts a more significantly increased amount of the connective tissue cells is observed than in the case of cardiac hypertrophy alone. In contrast to this, the increase of the heart muscle cells is significantly reduced. A lack of contractile proteins, decreased DNA synthesis, increased fibrozation and, in particular, the reduced number of cardiac muscle cells must be considered as essential factors for cardiac insufficiency.
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PMID:Histochemically determinable changes in cardiac insufficiency and their functional significance. 294 64

Of 20 patients who presented to our hospital with the histologically confirmed diagnosis of SLE, nine met the criteria of presence of both a rapidly progressive disease state and contraindications for conventional therapy required for admission to our plasma exchange programme. Five patients improved; two patients progressed to end-stage renal failure; two patients died as a result of complications of advanced SLE. Severe lupus erythematosus (SLE) is usually treated with a combination of steroids and cytotoxic drugs. Even when treated with high dose therapy some patients develop life-threatening complications, such as renal failure, heart failure and respiratory insufficiency. Moreover, both treatment with high dose of corticosteroids and long lasting cytotoxic therapy may produce troublesome side-effects, including severe infections, gastroduodenal ulcers, bone marrow depressions and lymphomas (1, 2). One of the manifestation of SLE is the presence of antibodies against ds-DNA and ss-DNA. These antibodies can either react with DNA bound to te basement membrane and induce an inflammatory reaction (3), or can form circulating immune complexes which deposit in tissues and may impair the function of lymphocytes or macrophages in the RES (4, 5). The presence of anti-DNA-antibodies appears to be secondary to enhanced B-cell activity along with a depression of suppressor T-cells function proteins mediating the inflammatory process, such as fibrinogen, may deposit in membranes already compromised by the disease. Even though the pathogenic mechanisms operating in SLE are not completely understood, it can be expected, from a theoretical point of view, that the extracorporeal removal of any immunopathogens could improve the disease state.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma exchange in systemic lupus erythematosus. 664 35

Fatal cytomegalovirus (CMV) myocarditis occurred in a 2 year old boy with acute lymphoblastic leukemia (ALL) in remission. The patient showed mild hepatic dysfunction and a rapid progress of pancytopenia after complete remission had been achieved. At the fifth week of complete remission, he presented signs of heart failure such as tachycardia, S4 gallop on auscultation and decreased ejection fraction on echocardiography. However, no significant electrocardiographic changes were recognized. In addition to the cardiac dysfunction, the patient presented a marked tachypnea and dyspnea associated with hypoxemia. These were dramatically improved by methylprednisolone pulse therapy (30 mg/kg per day, for 3 days) and CMV high titer immunoglobulin (400 mg/kg per day, for 3 days). On the sixth day after signs of respiratory failure were improved, the patient suddenly presented a paroxysmal atrial tachycardia followed by a fatal ventricular fibrillation. Although we could detect neither a specific IgM antibody, a significant increase of IgG antibody, nor CMV genome by DNA hybridization techniques during the course of the illness, microscopic examination of necropsy specimens of the heart showed a marked disruption and disintegration of muscle bands associated with cytomegalic inclusion bodies. Polymerase chain reaction (PCR) yielded a 305 bp amplification product in the heart and lung tissues, supporting the view that myocarditis was caused by CMV.
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PMID:Fatal cytomegalovirus myocarditis in a seronegative ALL patient. 779 59

We report the case of a 28-year old asthmatic female patient, who developed an acute heart failure beginning with diarrhea, fever, and dyspnea 5 weeks after delivery. After improvement of all vital functions and dismissal from hospital care unit a marked blood hypereosinophilia, left ventricular congestive heart failure, pericardium effusion and fever up to 40 degrees C followed. Endomycardial, bone marrow and skeletal muscle biopsies and the pericardial fluid showed a marked eosinophilic infiltration or polymyositis, respectively, which could be treated successfully with steroids and azathioprin. During steroid medication cytomegalovirus-associated myocarditis developed and was diagnosed by in situ hybridization. CMV hyperimmunoglobulin treatment (Cytotect, Biotest) was started (2 ml/kg bw on day 1 and 3, and 1 ml/kg on days 5, 7 and 9), which led to the eradication of the residual infiltrate and CMV-DNA in the myocardium. After discontinuation of all medication, eosinophilia and asthma recurred so that immunosuppressive treatment was continued.
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PMID:[Eosinophilic endomyocarditis post partum or pregnancy-related cardiomyopathy]. 792 30

Post-mortem findings in a girl aged 2 years and 4 months who had been infected with Hantaan virus are reported. The child fell ill with acute renal failure in her 8th month of life and had to be subjected to chronic dialysis. There was a progressive cardiac insufficiency. Specific IgG and IgM antibodies to Hantaan virus were demonstrated by serology from the 18th month of life. Autopsy revealed endomyocardial fibrosis and cardiomegaly. Hantaan RNA could be demonstrated in formalin-fixed, paraffin-embedded specimens of lung, liver and spleen tissue by means of RT-PCR followed by DNA sequencing. A possible association between the Hantaan virus infection and the pathological findings in the heart are discussed.
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PMID:[Pathological-anatomical findings after serologic and molecular biologic evidence of Hantaan virus infection]. 794 24

Proliferating cell nuclear antigen (PCNA) is a late growth-regulated gene that is expressed at the G1-S boundary of the cell cycle and is required for DNA synthesis and cell proliferation. Since quantitative results suggest that myocyte hyperplasia occurs in the decompensated human heart, we postulated that induction of the PCNA gene may be present in the failing heart in humans. PCNA protein was detected in myocardial samples obtained from the left and right ventricles of patients with congestive heart failure. Endomyocardial biopsies collected from donor subjects were used as control tissue. The percentage of positively stained myocyte nuclei in the ventricles was established by using PCNA monoclonal antibody and the immunoperoxidase technique. The localization of PCNA in myocytes was confirmed by alpha-sarcomeric actin antibody staining. PCNA labeling was present in left ventricular myocytes of 29 of the 32 hearts examined. In the right ventricle, 24 of the 29 samples showed positive staining. In a subset of 25 patients, the percentage of PCNA-labeled myocyte nuclei was measured and found to constitute 49 +/- 22% of left ventricular myocytes. A similar analysis for the right ventricle, conducted in 21 patients, showed that 49 +/- 19% of the myocyte nuclei exhibited PCNA protein. In addition, mitotic figures in myocytes were documented. A quantitative analysis of this cellular process revealed that 11 myocyte nuclei per 1 million cells exhibited mitotic images in chronic heart failure. Immediately after myocardial infarction, two cells per million showed mitotic division, and this phenomenon was restricted to the region adjacent to the necrotic tissue. No PCNA labeling or nuclear mitotic images were detected in the ventricular myocardium of control subjects. Thus, the observation that diffuse PCNA labeling and myocyte mitotic division are present in hearts with end-stage failure strongly suggests that adult ventricular myocytes are not terminally differentiated cells and that myocyte cellular hyperplasia may constitute a growth reserve mechanism of the diseased heart.
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PMID:End-stage cardiac failure in humans is coupled with the induction of proliferating cell nuclear antigen and nuclear mitotic division in ventricular myocytes. 795 43

The heterocyclic aromatic amine 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) is a potent hepatocarcinogen in cynomolgus and rhesus monkeys. The finding of high cardiac IQ-DNA adduct levels prompted a histopathological study of perfusion-fixed hearts from 10 tumor-bearing monkeys chronically dosed with IQ at 10 mg/kg or 20 mg/kg 5 days per week for 48-80 months. Two monkeys dosed only with the vehicle for IQ, hydroxypropylcellulose, served as controls. All the monkeys had normal heart weights, and no abnormalities were observed upon gross inspection of the hearts. Microscopically, focal myocardial lesions were observed in 8 of 10 monkeys dosed with IQ. Light microscopic abnormalities included myocyte necrosis with or without chronic inflammatory infiltrates, interstitial fibrosis with myocyte hypertrophy or atrophy, and vasculitis. Electron microscopic findings included disruption of the mitochondrial architecture (i.e., mitochondrial swelling and clearing of matrix densities), myofibrillar loss, disorganization of the normal alignment of sarcomeres, and occasional myocytes showing nuclear hypertrophy or peripheral clumping of the nuclear chromatin. There was some correlation between the cumulative dose of IQ and the extent of the myocardial abnormalities. These findings suggest that chronic exposure to IQ can lead to myocardial damage in monkeys. Although focal and not associated with clinical evidence of heart failure, these abnormalities may represent the initial stages of IQ-induced toxic cardiomyopathy.
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PMID:Cardiac damage induced by 2-amino-3-methyl-imidazo[4,5-f]quinoline in nonhuman primates. 803 33

We review recent publications involving molecular biology and heart failure. There was some further evolution in our knowledge of the basis for the simplest of molecular genetic diseases--single gene disorders. This year, hypertrophic cardiomyopathy had further genes identified as causative mutations; was shown to have the same genetic defects in spontaneous and familial cases; and demonstrated phenotypic alteration by environmental factors. Several rare cardiomyopathies were linked to the dystrophin gene, previously identified as the mutated gene responsible for forms of muscular dystrophy. Molecular methods were applied to linking viral infection to dilated cardiomyopathy by hunting for viral genomes in heart muscle, and for seeking mutations in mitochondrial DNA. Molecular treatment of restenosis after angioplasty showed promise through the application of gene transfer to vascular tissue by oligonucleotides as well as adenovirus-mediated gene transfer. The ethical aspects of diagnosing and treating human disease using genetic information, which receive frequent discussion in print, are also reviewed.
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PMID:The molecular and cellular biology of heart failure. 804 84

Polymorphism in the angiotensin-converting enzyme (ACE) gene has been shown to correlate with circulating ACE concentrations, and also to be an independent risk factor for the development of myocardial infarction, particularly in men thought to be at low risk by standard criteria. We determined the genotypes of individuals with end-stage heart failure due to either ischaemic dilated cardiomyopathy (102) or idiopathic dilated cardiomyopathy (112) and compared these to organ donors with normally functioning hearts (79). Genotypes were determined by the polymerase chain reaction with oligonucleotide primers flanking the polymorphic region in intron 16 of the ACE gene to amplify template DNA isolated from patients. Compared with the DD frequency in the control population, the frequency of the ACE DD genotype was 48% higher in individuals with idiopathic dilated cardiomyopathy (p = 0.008) and 63% higher in subjects with ischaemic cardiomyopathy (p = 0.008), suggesting that an ACE gene variant may contribute to the pathogenesis of both types of cardiomyopathy.
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PMID:Angiotensin-converting enzyme DD genotype in patients with ischaemic or idiopathic dilated cardiomyopathy. 810 4

To determine whether cardiac failure produced by chronic coronary artery stenosis was associated with the activation of myocyte cellular hyperplasia in the myocardium, the changes in number and size of left ventricular myocytes were measured in rats 3 months after surgery. The hypertrophied left ventricle was found to possess 44%, 32%, 49%, and 48% fewer mononucleated, binucleated, trinucleated, and tetranucleated myocytes, respectively. In contrast, the hypertrophied right ventricle contained 1.49 x 10(6) more myocytes as a result of a 2.1-fold, 1.4-fold, and 1.4-fold increase in mononucleated, binucleated, and tetranucleated myocytes. Myocyte cell volume was seen to increase 49% and 21% in left and right ventricular myocytes, respectively. The process of myocyte cellular hyperplasia in the right ventricular myocardium was accompanied by capillary proliferation, and these events were responsible for the parallel addition of newly formed cells and capillaries within the wall and mural thickening. Moreover, the in-series insertion of new myocytes contributed to right ventricular dilatation after coronary artery stenosis. In view of the fact that extensive myocardial damage and cell loss may have masked the phenomenon of myocyte cellular hyperplasia in the left ventricle, the presence of DNA synthesis in myocyte nuclei was evaluated at 3 days, 1 week, 2 weeks, 1 month, and 3 months after coronary artery stenosis. Bromodeoxyuridine (BrdU) labeling markedly increased in myocyte nuclei of both ventricles, reaching its peak at 1 and 2 weeks. BrdU labeling of nonmyocyte nuclei also increased but mostly at 2 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocyte cellular hyperplasia and myocyte cellular hypertrophy contribute to chronic ventricular remodeling in coronary artery narrowing-induced cardiomyopathy in rats. 811 47


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