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

The safety and efficacy of intravenous quinidine were evaluated in a patient population with a high prevalence of left ventricular dysfunction and intraventricular conduction delays. Quinidine gluconate (mean dose 9.1 +/- 1.6 mg/kg) was administered during electrophysiologic study to 100 patients with ventricular or supraventricular tachyarrhythmias. Clinical heart failure was present in 68 percent of the patients. Left ventricular end-diastolic pressure, cardiac index, and left ventricular ejection fraction were abnormal in 62, 48, and 70 percent, respectively. Major intraventricular conduction delays (QRS of 120 msec or more) were present in 27 percent, and the H-V interval was prolonged (over 55 msec) in 28 percent. Despite the prevalence of these abnormalities, quinidine was discontinued because of hypotension in only 10 patients. Saline solution was infused to maintain preload in 37 percent, and hypotension responded promptly to saline solution infusion or discontinuation of quinidine infusion in all subjects. Hypotension was not more common in patients with more severe left ventricular dysfunction. QRS duration, H-V interval, QTc, and right ventricular effective refractory period increased significantly (p less than 0.001) after quinidine administration. Heart block or QRS widening of 50 percent or more did not occur. Quinidine prevented arrhythmia induction in 26 percent of patients who received full doses. Ventricular tachycardia cycle length increased in all 41 patients in whom identical forms were induced before and after quinidine (287 +/- 71 msec versus 361 +/- 93 msec, p less than 0.001). Intravenous quinidine may be administered safely to patients with intraventricular conduction delays and moderate heart failure. When antiarrhythmic efficacy is assessed by electrophysiologic study, quinidine compares favorably with other antiarrhythmic agents.
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PMID:Safety and efficacy of intravenous quinidine. 685 83

Isolated congenital complete heart block has a heterogenous aetiology. In approximately one-third of the patients in the present material the mothers had symptoms or signs of connective tissue disease. The mortality is highest in the neonatal period, much lower during childhood and adolescence and increases slowly later in life. There are elderly patients who are completely asymptomatic but patients are also encountered with signs and symptoms of more or less severe myocardial damage. Stokes-Adams attacks may occur at any age. About 10% of patients below 15 years of age in this material and about 25% of those above 15 years (mean age 30 years) were paced. In the neonatal period the predominant indication for pacing was heart failure. It is difficult to make a prognosis in the individual patient. Apart from already known risk factors, a fixed or decreasing low ventricular rate neonatally and a prolonged QT time seem to be bad prognostic signs.
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PMID:Review article. Congenital complete heart block. 701 Aug 97

Patients with mitochondrial disease may present to the Intensive Care Unit (ICU) with a variety of neurological and general medical disorders. Eleven patients were admitted to a neurological ICU between 1970 and 1992 because of respiratory insufficiency, status epilepticus and/or metabolic encephalopathy associated with mitochondrial disease. Respiratory impairment occurred in eight patients and was associated with nocturnal hypoventilation due to respiratory muscle weakness, aspiration due to bulbar weakness and abnormalities of central control leading to a reduced CO2 drive, irregular respiratory patterns and sleep apnoea. Seven patients received continuous respiratory support during the acute illness; three were subsequently weaned to domiciliary ventilation, and four died. Five patients had stroke-like episodes, which in two were recurrent. Four patients developed tonic-clonic grand mal epilepsy associated with myoclonic fits (2 patients), absences (2), focal fits (1) and status epilepticus (2). Encephalopathy was associated with recurrent lactic acidosis (2 patients), cardiac failure (2), hyponatraemia (2), renal abnormalities (3) and complete heart block (1). Although rare, mitochondrial disease should be considered in any patient with unexplained respiratory failure, intractable epilepsy, lactic acidosis or recurrent stroke.
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PMID:Management of mitochondrial disease on an intensive care unit. 776 70

In a 4 1/2 year period fetal, echocardiographic studies were performed on 1600 fetuses. In 55 with arrhythmia, 44 had supraventricular ectopic beats, resolved in all, and none had heart disease. Sustained arrhythmias occurred in 11 fetuses. Atrial flutter was present in 3 all with heart disease (Ebstein disease, right atrial tumour and WPW diagnosed after birth). Another 3 fetuses had supraventricular tachycardia (SVT), all with a normal heart. In the bradycardia group, 2 had complete heart block (CHB) associated with AVSD; 2 sinus bradycardia and one had non conducted atrial ectopic beats. Digoxin was the first choice drug for tachyarrhythmia therapy; association with Verapamil, Flecainide, Quinidine and Procainamide was used in 4 of the 6. One fetus with CHB received Orciprenaline with no results. Atrial flutter resolved or improved; in SVT 2 fetuses converted to sinus rhythm and one died in utero. All fetuses with CHB died in cardiac failure. Mortality was 27% (3 cases) in utero and global 36%. In our experience most fetal arrhythmias (90%) were transitory ectopic beats or non lasting bradycardia in normal heart and did not trigger other kinds of arrhythmias. In sustained arrhythmias, heart failure and heart disease had a negative effect on prognosis.
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PMID:[Fetal arrhythmia. A case load of 4 years and a half]. 777 Dec 7

In 18 patients with acute myocardial infarction admitted to the Cardiological Care Department within 6 hours after the onset of chest pain, before administration of drugs and then in the 2nd, 3rd, 5th and 7th day, the levels of glucose, pyruvate, lactate in venous blood, the lactate/pyruvate ratio (L/P) and pH, actual hydrocarbons, PCO2 and PO2 in capillary arterialized were determined. Depending on the clinical status at admission the patients were classified into 2 groups: I--without complications (I class according to Killip-Kimbal; n = 10), and II--with complications (II-IV class of cardiac failure according to Killip-Kimbal and/or complex ventricular arrhythmias e.i. III-V class according to Lown and heart block of Mobitz--type II and III degree; n = 8). None of the patients had diabetes, chronic respiratory tract diseases, renal failure and liver cirrhosis. The control group consisted of 11 healthy persons. On the first day of myocardial infarction, the significant increase of blood glucose, lactate, pyruvate, as well as significant decrease of blood pH, HCO3- and PO2, and non significant increase of L/P ratio were observed in both groups as compared to the control group. Also there were non significant difference of the glucose, lactate, pyruvate L/P ratio and pH, PCO2 and HCO3- values between the I and II group on the first day of the acute myocardial infarction, with exception of the PO2, which was significantly lower in the group II. In the following days an increase of PO2 was observed. Since this effect coincided with a decrease of lactate concentration (significant only in the group II) it could be concluded, that the observed decrease of the lactate concentration resulted from the higher supply of oxygen. The obtained results have shown, that increase of glycaemia values and decrease of PO2 values may be considered as biochemical markers for hemodynamic complications of acute myocardial infarction.
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PMID:[Lactate metabolism in acute myocardial infarction]. 780 May 82

Between January 1, 1985 and June 30, 1992, 37 patients (25 women and 12 men, aged 13-65 years) who had undergone a radiation treatment to the anterior chest and mediastinum, were admitted to our Institution for cardiac evaluation, which included left and right heart catheterisation in all, but 3 patients. Seventeen had signs or symptoms of ischaemic heart disease, in 8 a pericardial disease was suspected, 5 had a complete heart block, 4 were in congestive heart failure caused by valvular dysfunction, and 3 had a dilated, hypokinetic left ventricle. Diagnostic criteria in these patients were as follows. Stenoses of the coronary ostia were always considered to be caused by radiation damage, in the absence of coronary risk factors. Obstructions of other coronary segments were taken to be of X-ray origin only when accompanied by damage to other cardiac structures. Pericardial lesions were always reckoned to be of X-ray origin in the absence of other recognisable causes. The same held true for aortic stenosis or insufficiency of any degree and for mitral insufficiency > or = 3+. Cases of complete heart block were diagnosed according to Slama's criteria. A restrictive cardiomyopathy was recognised only in patients operated on for pericardiectomy, in whom clinical or haemodynamic signs of "constriction" persisted after the operation, or extensive subendocardial fibrosis was found at biopsy. According to the above-mentioned criteria, it was established that radiation therapy was the cause of the cardiac problems in 19 cases: 4 with ischaemic symptoms, 8 with pericardial disease, 4 with complete atrioventricular block, and 3 with valvular disease and congestive heart failure. Coronary ostial lesions were found in all patients with angina, and in 8 of the 14 patients without angina (in 1 the coronary arteries were not investigated), and were critical in 4. Eleven patients were operated on. A myocardial revascularisation was performed in 7 cases, a pericardiectomy in 6, a valve replacement or repair was done in 4. A combined procedure was performed in 4 instances. A pacemaker was implanted in 3 cases, 2 patients had a pericardial drainage, and 3 patients continued their medical treatment. Of the 11 operated patients, 1 died at surgery, in refractory cardiac failure, from what was suspected to be a restrictive disease (normal preoperative left ventricular volume and ejection fraction, extensive myocardial fibrosis at autopsy).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Cardiopathy due to therapeutic irradiation of the thorax. The diagnostic criteria]. 833 5

Several aspects of giant cell myocarditis remain controversial, including the natural history of the disease and the nature of the giant cells. We have observed three patients who had long survival with chronic active giant cell myocarditis. The first patient was a 59-yr-old female who had a 10-yr history of complete heart block which was found at autopsy to have been caused by giant cell myocarditis. The second patient is a 36-yr-old female who received a heart transplant 5 yr after a biopsy proven episode of active myocarditis, and examination of the explanted heart revealed giant cell myocarditis. The third patient was a 41-yr-old male who received a heart transplant 2 yr after developing progressive heart failure, and the explanted heart had giant cell myocarditis. On immunohistochemical study of the three hearts, the giant cells stained with the macrophage markers lysozyme and KP-1 (CD-68). Staining of the same cells with desmin and actin was focally positive in a punctate pattern, correlating with the ultrastructural presence of myofibrils within giant cell phagolysosomes. The associated lymphocytic infiltrate stained primarily for the T-cell markers CD-3, CD-45RO, and CD-43 whereas only a few of the lymphocytes stained with the B-cell marker CD-20. The long histories of cardiac dysfunction in the three patients show that giant cell myocarditis may have a protracted course. The morphologic studies show that the giant cells are of histiocytic origin but can contain phagocytosed components of myocytes, observations that may account for the controversy surrounding the nature of the giant cells in giant cell myocarditis.
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PMID:Long survival with giant cell myocarditis. 841 83

A patient with end stage heart failure underwent permanent implantation of a Novacor left ventricular assist system. Progressive right ventricular dysfunction developed during the first two postoperative weeks. Temporary and subsequently permanent atrioventricular pacing to correct first degree heart block improved the performance of the device, with sustained resolution of his right ventricular failure.
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PMID:Permanent pacing in a patient with a left ventricular assist system. 866 50

Hypertrophic cardiomyopathy is characterized by abnormalities of the myocardium, and the activation and conduction tissues, that may have separate manifestations, but often occur together in complex clinical pictures. The subaortic gradient, although not always present, is the most classical manifestation of the disease, with its typical dynamic behavior, changing with preload, afterload and contractility. In most cases it is due to systolic motion of the mitral valve against the septum in systole, but in a few it is caused by midventricular "constriction". Alteration of diastolic ventricular function is important, and probably the main cause of heart failure, that is usually accompanied by normal systolic function. Mitral insufficiency is common in the obstructive forms, due to the abnormal mitral valve motion, but in some cases it may be due to structural abnormalities of the valve. There may be systolic constriction, or nonatherosclerotic occlusion of the intramyocardial coronary arteries, causing myocardial infarction and ventricular aneurysms, that may lead to systolic dysfunction. The electrocardiogram is rarely normal. Hypertrophy patterns, deeply inverted T waves, deep Q waves, QRS slurring suggestive of WPW syndrome without true preexcitation are the most common manifestations. Rhythm disturbances are common and include sinus node dysfunction, superconductor atrioventricular node or heart block. Atrial fibrillation is frequent and may have catastrophic consequences, including systemic embolism. Non-sustained ventricular arrhythmias are often present, but its predictive value for sudden death is unclear. Monomorphic ventricular tachycardia is infrequent, and programmed stimulation is more likely to precipitate polymorphic ventricular tachycardia of difficult clinical interpretation. Sudden death may be due to multiple mechanisms, and it is difficult to predict and prevent.
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PMID:[Hemodynamic and electrophysiologic changes in hypertrophic cardiomyopathy]. 868 13

Adenosine versus Verapamil and other Antiarrhythmic Drugs: Paroxysmal supraventricular tachycardia is the most common sustained arrhythmia during pregnancy. Verapamil has been the most commonly used agent for the treatment of PSVT with a narrow QRS complex. Potential side effects of verapamil including systemic hypotension, acute heart failure, bradyarrhythmia and heart block may occur in pregnant women; after placental transfer bradycardia, heart block, depression of contractility and hypotension may be induced in the fetus. We report on the case of a 22-year old pregnant woman with hypotension and tachycardia, who was admitted for suspected haemorhagic shock. Indeed, she suffered from paroxysmal supraventricular tachycardia, which was successfully terminated by intravenous adenosine. Because of its known rapid onset, high effectivity, low incidence and brevity of side effects in the mother and comparative safety in the fetus, adenosine seems to be the drug of choice for treating PSVT during pregnancy.
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PMID:[Paroxysmal supraventricular tachycardia in pregnancy. Value of adenosine and other anti-arrhythmia agents]. 876 89


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