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)

Vasodilators used in chronic congestive heart failure are not optimal in that nitrates are predominant venodilators, prazosin is associated with tolerance development, and hydralazine produces chronic toxicity. Therefore, we studied the acute hemodynamic effects of a single dose of minoxidil in 18 patients with chronic left ventricular failure caused by ischemic or primary cardiomyopathy. Peak effects were observed 5 hours after single oral doses of minoxidil, averaging 15.3 +/- 1.4 mg (SEM). Heart rate rose slightly, from 85.4 +/- 2.9 to 90.9 +/- 3.2 beats/min, after minoxidil (p less than 0.02) and mean arterial pressure fell slightly, from 88.0 +/- 2.3 to 84.9 +/- 2.5 mm Hg (p less than 0.05). Cardiac index increased from 2.34 +/- 0.l4 to 2.95 +/- 0.29 l/min/m2 after minoxidil (p less than 0.02) and systemic vascular resistance fell from 19.6 +/- 1.5 to 15.0 +/- 1.3 units (p less than 0.01). Minoxidil did not affect right atrial, pulmonary arterial and pulmonary wedge pressures. Hemodynamic effects of minoxidil persisted for at least 8 hours after a single dose. Minoxidil appears to be an effective arterial dilating agent in patients with heart failure and resembles hydralazine in its actions. Because of its potency, prolonged duration of action and relatively low toxicity, minoxidil may be a useful vasodilator for heart failure. However, its long-term effect must be further evaluated.
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PMID:Effects of minoxidil on hemodynamics in patients with congestive heart failure. 700 52

The effect of 2.5 mg prazosin orally was monitored for one hour by cardiac catheterisation in 11 patients with cardiac insufficiency as a result of primary cardiomyopathy. Mean pressures of the pulmonary capillary bed and pulmonary artery decreased on average by 9 mm Hg, of the right atrium by 2.5 mm Hg and systemically by 8 mm Hg. Judging by the increase of cardiac index patients were divided into a group of 7 "responders", all showing congestive cardiomyopathy, and a group of 4 "nonresponders" with various cardiomyopathies. During prazosin treatment cardiac index increased by 23% and pulmonary arteriole resistance decreased by 4% and pulmonary arteriole resistance increased by 41%. It is concluded that not all forms of left ventricular failure respond favourably to prazosin. Divergent effects of prazosin may possibly be caused by unequal effects on pre- and after-load of both ventricles and on variable behaviour of lung arteriole resistance.
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PMID:[Variable acute effects of prazosin on left ventricular failure (author's transl)]. 743 46

The variability of the heart rate is a sign of the activation of the autonomic nervous system. This parameter was studied in 21 control subjects and 72 patients with chronic cardiac failure (20 stage II, 37 stage III and 15 stage IV of the NYHA) due to ischaemic heart disease in 48 cases and idiopathic in 24 cases. Spectral and non-spectral analysis of the variability of the heart rate recorded during 24 hour Holter monitoring was performed with the Marquette Electronics 8000 software. Plasma noradrenaline was measured in whole blood by HPLC. The left ventricular ejection fraction was measured by echocardiography. There was a superior to 40% decrease in non-spectral and over 50% decrease in spectral parameters in patients with cardiac failure. This was more pronounced when the cardiac failure was in an advanced stage. The decrease in sinus rhythm variability was proportional to the functional class (SDANN stage II: 96 +/- 34 ms; stage III: 63 +/- 34 ms; stage IV: 54 +/- 33 ms). Moreover, the non-spectral parameters were correlated to the ejection fraction and plasma noradrenaline levels (p < 0.01). In addition, with the same NYHA stage, plasma noradrenaline concentration, ejection fraction and heart rate, the SDNN and the pNN50 were over 50% lower in idiopathic cardiomyopathy than in ischaemic cardiomyopathy. In conclusion, the variability of the heart rate is reduced in chronic cardiac failure in relation with the severity and aetiology of the underlying disease.
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PMID:[Heart rate variability in chronic cardiac failure insufficiency. Effect of severity and etiology]. 764 35

We conclude that Lyme disease is not a common cause of idiopathic heart failure in the Midwestern United States and that false-positive Lyme disease serologic results are not rare among patients with severe heart failure. Patients with significant cardiac disease who are found to be EIA seropositive should have confirmatory Western blots performed before consideration of treatment. Based on our findings, we cannot recommend either the routine serologic screening of patients with idiopathic cardiomyopathy or aggressive (e.g., parenteral) antibiotic treatment of seropositive patients unless the specific clinical history suggests antecedent Lyme disease.
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PMID:A prospective study of the seroprevalence of Borrelia burgdorferi infection in patients with severe heart failure. 779 18

Analysis of 109 well documented cases of permanent total atrial paralysis reported in the literature illustrated the features of this arrhythmia which is a well defined entity consisting of suppression of all electrical and mechanical activity of both atria lasting for more than 6 months. Standard electrocardiogram reveals junctional bradycardia of about 40 bpm without any visible P waves and narrow supraventricular QRS complexes in 80% of cases. This diagnosis can only be confirmed by meticulous bipolar endocavitary recordings exploring all atrial walls without recording an auriculogram and by right intra-atrial and coronary sinus stimulation which proves to be ineffective. This disease has a male predominance in two-thirds of cases and a familial nature in 18% of cases. Seventy one per cent of affected subjects are under the age of 50 years. In 33% of cases, it is associated with Emery-Dreifuss muscular dystrophy, in which it constitutes a specific sign allowing this dystrophy to be differentiated from all other forms, especially facio-scapulo-humeral myopathy, and in 30% of cases, it is associated with a degenerative disease such as diabetes, amyloidosis or primary cardiomyopathy. Idiopathic dilatation of the right atrium is revealed in 15% of cases. The arrhythmia is responsible for syncope or faintness in 31% of cases, cerebral vascular accidents in 21% of cases and heart failure in 35% of cases. Cardiac activation is dependent on a junctional escape rhythm. The mechanism of the lesion responsible is atrial fibrosis which may extend to the sinoatrial node. The treatment of choice consists of implantation of a VVI or VVIR mode cardiac pacemaker in combination with anticoagulant therapy.
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PMID:[Total permanent auricular paralysis. Review of the literature apropos of 109 cases]. 779 52

The case of a 12 year old schoolgirl with heart failure due to varicella myocarditis is reported. Heart failure and cardiogenic shock were evident 21 days after the appearance of the rash, and cardiac transplantation was performed two weeks later. Myocarditis is a serious complication of varicella zoster infection and heart failure may be fulminant. Endomyocardial biopsy changes consistent with myocarditis were documented six days after the start of heart failure. The histological changes, however, developed into those of idiopathic dilated cardiomyopathy (with anisonucleosis and fibre width variation) over a seven day period. This case provides further evidence for the link between viral myocarditis and idiopathic cardiomyopathy and underlines the value of immediate endomyocardial biopsy in heart failure of recent onset. Cardiac transplantation led to a rapid and full recovery.
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PMID:Varicella zoster myocarditis progressing to cardiomyopathy and cardiac transplantation. 803 8

Chylothorax associated with right-sided congestive heart failure was diagnosed in 5 cats. One cat had restrictive pericardial disease, with mild pericardial effusion, and a heart-base chemodectoma. Two other cats had congestive cardiac disease (tetralogy of Fallot and tricuspid regurgitation in 1 cat, and endocardial cushion defect and tricuspid dysplasia in the other), and 2 cats had idiopathic cardiomyopathy. All cats had jugular venous distention, and echocardiographic evaluation helped define the nature of the cardiac disease in these cats. Subtotal pericardiectomy resulted in resolution of the chylothorax in the cat with the heart-base tumor, whereas medical management of the right-sided heart failure temporarily decreased pleural effusion in the cat with tetralogy of Fallot and in the 2 cats with cardiomyopathy.
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PMID:Chylothorax associated with right-sided heart failure in five cats. 812 26

Hypertrophic cardiomyopathy is a heterogeneous disease with autosomal dominant Mendelian inheritance. In 1989, the 1st locus for hypertrophic cardiomyopathy was mapped to cardiac myosin genes located on chromosome 14q1. Soon, several mutations that cosegregated with inheritance of the disease were identified in the beta-myosin heavy chain gene, or MHY7. More than 30 missense mutations and 1 deletion mutation in the beta-myosin heavy chain gene have since been described. Recently, expression of both the mutant beta-myosin heavy chain mRNA and the mutant protein has been shown in the cardiac and skeletal muscles of individuals with hypertrophic cardiomyopathy. Characterization of the clinical features of beta-myosin heavy chain mutations has shown that certain mutations, such as Arg403Gln and Arg719Trp mutations, are associated with high rate of sudden cardiac death. In addition to the beta-myosin heavy chain gene, 3 new loci for hypertrophic cardiomyopathy have recently been described, but the candidate genes have not yet been identified. Dilated cardiomyopathy can be inherited as an autosomal dominant, autosomal recessive, and X-linked disease. The familial form of dilated cardiomyopathy comprises approximately 20% of the cases of idiopathic cardiomyopathy. Echocardiographic abnormalities such as left ventricular enlargement are present in 10% of asymptomatic relatives. No gene for familial dilated cardiomyopathy has been identified, but linkage studies using polymorphic, short-tandem repeat markers are ongoing. Dilated cardiomyopathy is a common manifestation of Duchenne/Becker muscular dystrophy. Heart failure is a common cause of death in the affected individuals. The gene responsible for this disease is the dystrophin gene located on X chromosome. There have been reports in these patients of several dystrophin-gene deletion mutations, which result in a decrease in the expression of the dystrophin protein in the cardiac and skeletal tissues. X-linked cardiomyopathy, in which the disease is restricted to the heart, has also been linked to the dystrophin gene. Myotonic dystrophy is an autosomal dominant disease that commonly involves the myocardium and the conduction tissue, resulting in conduction defects and heart failure. Sudden cardiac death is the most common cause of mortality in patients with myotonic dystrophy. Recently, the myotonin protein kinase gene located on chromosome 19 was identified as the gene responsible for this disease. Expansion of the number of trinucleotide repeats in the myotonin protein kinase gene results in myotonic dystrophy. Mutations in mitochondrial DNA have been associated with hypertrophic and dilated cardiomyopathy. The inheritance of mitochondrial cardiomyopathy is maternal and the disease is associated with certain systemic disorders.
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PMID:Molecular basis of hypertrophic and dilated cardiomyopathy. 818 May 12

This report describes the first long-term (505-day) application of the vented electric (VE) HeartMate left ventricular assist device (LVAD) (Thermo Cardiosystems, Inc). The device consists of an abdominally placed, battery-powered titanium blood pump that, in contrast to earlier pneumatically powered systems, allows patients untethered freedom of movement. The batteries last 5 to 8 hours and can be changed on a rotating basis indefinitely. The patient, a 33-year-old man (90 kg, blood type O) with idiopathic cardiomyopathy, experienced end-organ heart failure (New York Heart Association [NYHA] class IV) while he was awaiting heart transplantation. When his hemodynamic criteria met those outlined in the protocol, we implanted the VE-LVAD as a bridge to transplantation. The patient was supported by the device for more than 16 months. His cardiac status returned to NYHA class I, and he was eventually allowed to take day trips outside the hospital as he awaited transplantation. The VE-LVAD enabled the patient to participate in activities such as eating in restaurants, going to movies, and practicing basketball shots. Unfortunately, the patient died suddenly due to a neurological thromboembolic event that occurred on day 503 of VE-LVAD support. The VE-LVAD improved native left ventricular function by chronic unloading, and ventricular remodeling resulted in a more normal configuration anatomically, physiologically, and ultimately, histologically and pathologically.
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PMID:First use of an untethered, vented electric left ventricular assist device for long-term support. 820 7

In patients with alcoholic cardiomyopathy there is evidence that mild heart failure is reversible if patients abstain from alcohol, but there is no consensus whether the disease is progressive once structural myocardial dilation has evolved. The aim of the present study was to compare the long-term course of congestive heart failure due to alcoholic and idiopathic dilated cardiomyopathy. Of 75 patients with overt congestive heart failure, 23 had alcoholic cardiomyopathy and were compared to 52 patients with idiopathic cardiomyopathy. The mean age was 48 +/- 12 years. Despite medical therapy, heart failure class New York Heart Association III-IV was present in 52% of patients with alcoholic and 47% of patients with idiopathic cardiomyopathy (not significant). Their mean left ventricular ejection fraction was 30 +/- 12% vs 28 +/- 12% and left ventricular end-diastolic volumes were 264 +/- 125 ml and 254 +/- 100 ml respectively (not significant). Overall survival at 1, 5 and 10 years was 100%, 81% and 81% for the group with alcoholic dilated cardiomyopathy and 89%, 48% and 30% for the group with idiopathic cardiomyopathy, respectively (P = 0.041), and the difference was even greater for transplant-free survival P = 0.005). Clinical and invasive signs of left and right heart failure as well as left ventricular dimensions were predictive of a fatal outcome; however, symptom duration and left ventricular volumes were only predictive in patients with idiopathic cardiomyopathy, suggesting that in the two patient groups different mechanisms may lead to death. Mortality in patients with severe congestive heart failure and left ventricular dilatation due to alcoholic cardiomyopathy is significantly lower than that in patients with idiopathic cardiomyopathy and similar degrees of heart failure. Thus, despite structural changes inherent in marked left ventricular dilatation, disease progression in alcoholic dilated cardiomyopathy is different from that in idiopathic cardiomyopathy and thus may have implications for the choice of therapy.
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PMID:Differences of disease progression in congestive heart failure due to alcoholic as compared to idiopathic dilated cardiomyopathy. 873 67


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