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

A case of arrhythmogenic right ventricular dysplasia in a 27 year-old woman is presented, the first one published in Mexico. Palpitations and episodes of syncope were the most important symptoms. Ventricular premature beats and bigeminy without evidence of cardiomegaly or heart failure were disclosed on physical examination. Electrocardiograms revealed frequent, multifocal ventricular extrasystoles with complete left bundle branch block morphology suggesting a right ventricular origin. Dilatation, hypokinesia and decreased ejection fraction were found by both, bidimensional, echocardiography and radionuclear grammography. Right heart catheterization revealed normal pressures and confirmed the hypokinesia, dilatation and decreased ejection fraction; furthermore, irregularities in the endocardial contour of the right ventricle produced a "cauliflower-like" image. Lidocaine suppressed the episodes of ventricular tachycardia, but prevention of recurrences was only obtained with the administration of amiodarone. A review of the literature regarding the diagnosis of this disease is discussed; in addition to the clinical, anatomic and functional aspects above mentioned, an electrophysiological study may be indicated to confirm the right ventricular origin of the arrhythmias with re-entry mechanism.
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PMID:[Arrhythmogenic dysplasia of the right ventricle. First case reported in the Republic of Mexico]. 622 23

Cardiac receptors include both mechanically and chemically sensitive receptors located in atria and in ventricles. Atrial receptors innervated by myelinated vagal afferent fibers reflexly regulate heart rate and intravascular volume. On the other hand, stimulation of ventricular receptors can cause either reflex bradycardia and hypotension or, alternatively, excitation of the cardiovascular system. The former response is mediated by vagal afferents, whereas the latter is mediated by sympathetic (spinal) afferents. Under normal circumstances, cardiac receptors sense changes in wall motion or diastolic pressure and perhaps provide a fine tuning of the cardiovascular system. However, under certain pathological conditions such as coronary ischemia, which cause release of substances such as bradykinin and prostaglandins, there is an exaggerated response of the ventricular receptors. Because these receptors cause a reflex depression of the cardiovascular system and, in particular, induce renal vasodilation, they may protect the heart and kidney by lessening myocardial oxygen requirements and by increasing renal blood flow. In the situation of heart failure both atrial and ventricular receptors are reset and therefore provide for an exaggerated neurohumoral discharge. Finally, patients with aortic stenosis may demonstrate a paradoxical vasodilation and syncope during exercise when there likely is excessive stimulation of left ventricular receptors by the high transmural pressure.
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PMID:Cardiac receptors: their function in health and disease. 638 3

The angiotensin converting enzyme inhibitor captopril improves the altered hemodynamics in many patients with chronic heart failure, but the first dose may precipitate hypotension. Ten patients with chronic heart failure were studied, nine with high plasma concentrations of renin and one with a low concentration. Frequent measurements of plasma concentrations of angiotensin II, renin, and catecholamines were made over 60 minutes after a small dose (6.25 mg) of captopril and related to concurrently measured hemodynamic variables. Captopril caused a decrease in systemic and pulmonary artery pressure and an increase in cardiac index, and these changes coincided with reductions in the plasma concentrations of angiotensin II and increases in plasma concentrations of renin. The hemodynamic changes were accompanied by reductions in the plasma concentrations of norepinephrine but transient increases in plasma concentrations of epinephrine in patients in whom vasomotor syncope developed. The patient with a low plasma renin concentration showed little hemodynamic response to the drug. It is concluded that vasomotor syncope occurs quite frequently in patients with severe chronic heart failure after captopril in a small dose and is associated with a selective increase in epinephrine secretion from the adrenal medulla.
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PMID:Angiotensin II levels, hemodynamics, and sympathoadrenal function after low-dose captopril in heart failure. 638 25

This study analyses the results of cardiac pacing in 241 children operated between 1965 and March 1982 in 9 french cardiac centres. The ages at primary implantation were: less than 5 years, 32.8 p. 100, 6 to 10 years, 33.6 p. 100 and 11 to 16.5 years, 33.6 p. 100. Atrioventricular block was congenital in 40.7 p. 100 of cases (98 children) and postoperative in 56.4 p. 100 (136 children) with 67 cases, after repair of isolated ventricular septal defect and 18 after repair of an endocardial cushion defect. The symptoms preceding pacing were syncope (67 cases), bradycardia (92 cases) and cardiac failure (33 cases). The electrocardiographic indications were third degree block in 66.8 p. 100 of cases. The pulse generators were usually implanted in the abdominal wall (71.8 p. 100). The power sources in service (August 1982) were lithium (74 p. 100) and isotopic batteries (26 p. 100). Myocardial electrodes were used in 93.4 p. 100 of cases; 82.2 p. 100 were made by Medtronic. Early problems included: infection (10 cases), displacement of endocavitary electrodes (3 cases), elevated thresholds (2 cases). The late problems encountered were due to fracture of the pacing electrodes (19 cases) and elevated thresholds (50 cases). Two hundred and seven children are alive and well. A total of 341 pulse generators were implanted, 90 p. 100 being VVI mode. In August 1982, 56.6 p. 100 were programmable or multiprogrammable. Despite the technical problems involved, the myocardial approach is still used with good results, especially in young children and babies. The endocavitary approach is an alternative after 5 years of age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cardiac stimulation in children. A multicenter study of 241 patients]. 644 May 1

For purposes of evaluating the clinical features in the prehospital phase of acute myocardial infarction, 22 patients presenting prehospital syncope and patients presenting in-hospital re-attack were chiefly studied. Cardiac or ventricular standstill, acute mechanical failure, ventricular fibrillation, serious block, bradycardia-hypotension syndrome, cardiogenic shock, cardiac failure and cardiac rupture may be cited as the complications likely to occur in the early phase of the onset of acute myocardial infarction. Among these complications, cardiac or ventricular standstill results from overactivity of the vagus nerve, and acute mechanical failure is a result of drastically decreased cardiac output due to extensive infarction. There is no report of either complication, and both may be considered to be the fatal complications occurring almost simultaneously with the onset of acute myocardial infarction. The time intervals from the onset of symptoms to hospital admission were perspectively analyzed on 72 patients transported by the MCCU and 139 by ordinary ambulance. The interval from the onset of symptoms to medical help and that from the examination by personal physician to the call for ambulance were the greatest of all time factors, while the interval for emergency transport of the patient was short. There was no significant difference in the interval to hospital admission between the patients transported by the MCCU and those by ordinary ambulance. However, the in-transit death rate was 1/72 patients transported by the MCCU and 8/139 by ordinary ambulance: in other words, this death rate tended to be high in the latter. Twenty-two normal volunteers were studied for changes in heart rate, blood pressure and double product with the speed of transport. The transport at a low speed caused less changes in these parameters than that at a high speed.
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PMID:The clinical feature of pre-hospital phase of acute myocardial infarction--the advantages and limitations of the MCCU. 647 50

The safety and efficacy of intravenous quinidine gluconate, using intermittent boluses of 80 mg/cc every 5 minutes to a total dose of 800 mg, was evaluated in 61 patients referred for electrophysiologic studies (EPS). Patients were referred because of out-of-hospital cardiac arrest (12), symptomatic ventricular tachycardia (VT) (24), asymptomatic VT (18), syncope of unknown origin (6), and supraventricular arrhythmias (1). Clinical heart failure was present in 74% of patients, with a mean ejection fraction of 45 +/- 3 for all patients. Quinidine prevented VT induction in 78% of patients at a mean dose of 9.6 mg/kg and facilitated VT induction in 7% of patients. Quinidine failed to decrease mean arterial pressure in 14 patients, and in the remaining 47 patients arterial pressure decreased by 16%. Six patients had hemodynamically significant hypotension. Two patients had hypotension severe enough to require saline administration, while four had hypotension not needing fluid replacement. Sixteen percent of patients experienced other side effects. Quinidine can be administered safely by intermittent infusion and is effective in preventing programmed stimulation induction of VT. Carefully monitored, intravenous intermittent bolus administration of quinidine should be utilized more frequently in EPS, since significant adverse side effects are infrequent.
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PMID:Intravenous quinidine by intermittent bolus for electrophysiologic studies in patients with ventricular tachycardia. 650 39

Retrospective analysis was performed to assess the natural history in relation to clinical and haemodynamic features in 37 patients in whom hypertrophic cardiomyopathy had been diagnosed in childhood. At diagnosis they were aged 1 to 14 years (mean 9 years). Eighteen presented with chest pain and either dyspnoea or symptoms of impaired consciousness or both; 19 were asymptomatic and were referred for evaluation of abnormalities detected during physical examination. During a mean follow up of nine years, 18 patients died, a cumulative annual medical mortality of 4.8%. Five patients experienced severe dyspnoea or chest pain: two of these had progressive dyspnoea and died in cardiac failure, and three died after myectomy. The 19 survivors were compared with the 11 sudden deaths. Eleven of the survivors and five of the sudden deaths were asymptomatic. Of 18 clinical, electrocardiographic, and haemodynamic features only syncope and electrocardiographic evidence of right ventricular hypertrophy were associated with sudden death. In children with hypertrophic cardiomyopathy sudden death was common and was not well predicted by clinical, electrocardiographic, or haemodynamic findings. Hypertrophic cardiomyopathy indicates a poor prognosis even if symptoms are absent or mild.
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PMID:Hypertrophic cardiomyopathy: an important cause of sudden death. 654 94

The clinical data and presenting signs of 17 cases of atrial myxoma (14 left atrial, 3 right atrial myxomas) were analysed. The aim of the study was to assess changes in the presenting features since the introduction of non-invasive methods of cardiovascular investigation. Two groups of patients were identified according to whether the tumour has been diagnosed before (Group A) or after (Group B) the advent of echocardiography. The diagnosis of cardiac tumour, especially myxoma, has become easier with echocardiography and radio-isotope techniques. The presentation of myxoma, recognised earlier, has changed; the features of advanced valvular disease with resistant heart failure are no longer seen. Variable, atypical clinical signs are now encountered (syncope, pyrexia of uknknown origin, transient ischaemic attacks). The average delay between the first sign and diagnosis was 30 +/- 32 months in Group A, compared to 4,6 +/- 6,5 months in Group B (p < 0, 005). Of the 7 patients in Group B, three had normal cardiac auscultation, and normal ECG, and four had normal ESRs. The diagnosis of myxoma should be considered at the least doubt and an echocardiographic examination, preferably with 2-dimensional echo should be requested. It not only allows positive diagnosis but also orientates the patient to surgery without further investigation.
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PMID:[Atrial myxoma. Changes in clinical and paraclinical data. Apropos of 17 cases]. 677 89

The long-term outcome of myocardial infarction (MI) with bundle branch block (BBB) was studied retrospectively by a direct questionnaire and a registry enquiry in order to define the prognostic significance of data obtained during hospitalisation and to discuss the possible indications of permanent pacing in these patients. Out of 2 720 acute MI hospitalised between October 1969 and April 1977, 231 and BBB (unknown before infarction): 58 right, 53 left and 120 bilateral BBB. 113 patients survived the acute phase of MI and 111 patients were followed up for 72 +/- 24 months: 80 patients died, and 30 survive - a global survival rate of only 13% at 6 years. The post-admission mortality rate was not related to the type of BBB or the site of infarction. It was significantly higher in patients with previous myocardial infarction and in a sub group of patients without advanced AV block in the acute phase who had severe cardiac failure (Classes III and IV, Killip). The hospital mortality was higher in patients with advanced AV block in the acute stage (62,5% compared to 45,9%) in patients without advanced AV block, p < 0,025. On the other hand, the post-admission mortality was not significantly different in these two sub groups (77,8% compared to 69,8% : NS). Stokes-Adams syncope was rarely authentified in the post-admission course of the patients. An increased risk of secondary sudden death directly related to a conduction defect has not been proved. The indications for permanent pacing therefore remain uncertain. They should not be widened further than the indications for permanent pacing in chronic degenerative block.
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PMID:[Long-term course of patients with myocardial infarction and bundle branch block]. 677 24

The prognosis of congestive cardiomyopathy was studied in 132 consecutive patients (110 male, 22 female, average age 45 +/- 11 years) in whom a thorough clinical evaluation had excluded a secondary cause. The patients presented with left ventricular failure, a history of systemic embolism, syncope or radiological cardiomegaly. Right (100 p. 100) and left (81 p. 100) heart catheterisation was performed and left ventricular endiastolic volumes (202 +/- 77 ml/m2) and ejection fractions (31 +/- 12 p. 100) calculated from angiography in the 30 degrees right anterior oblique projection. Regional abnormalities of contraction were observed in 32 patients. The average follow up period was 40,4 +/- 23,8 months. At the end of the study 48 patients (37 p. 100) had died and 2 had been lost to follow up. Survival rates were calculated by actuarial methods. Age, sex, the period they had been symptomatic, alcoholic intoxication and the degree of cardiac dilatation were not significant prognostic factors. Patients in Class IV NYHA had the worst prognosis: 63 p. 100 2 year mortality. Atrioventricular conduction defects were observed in 56 patients and were associated with a significantly increased mortality rate (43 p. 100 compared with 23 p. 100, p < 0.001). Atrial fibrillation (32 patients) was a better prognostic factor than the persistence of sinus rhythm; 2 year mortality 11,1 p. 100 compared to 37,6 p. 100 (p < 0.001). Increased left ventricular end diastolic pressures greater than 20 mmHg were related with a mortality of 51,5 p. 100. Also, the patients with a ejection fraction of 30 p. 100 and a 2 year mortality rate of 44 p. 100 compared to 17,5 p. 100 when the ejection fraction was greater than 30 p. 100 (p < 0,001). In conclusion : 1. Regional abnormalities of left ventricular contraction are not rare in primary cardiomyopathy. 2. The prognosis is directly related to the degree of cardiac failure and the extent of left ventricular dysfunction.
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PMID:[Prognosis of primary non-obstructive cardiomyopathies]. 677 38


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