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

The effect of intravenous digoxin (0.01 mg/kg) on ventricular function, coronary arterial haemodynamics and myocardial oxygen uptake was studied in 12 patients with essential hypertension but no heart failure, significant left ventricular hypertrophy and normal coronary arteriogram. There was a definite, velocity-related increase in the inotropic function of the left ventricle, by 19.4%, 50 min after digoxin injection, while ventricular pumping function decreased by between 6.5 and 11.2%. Coronary blood flow through the left ventricle decreased by 8.8%. On the other hand, coronary vascular resistance and coronary arteriovenous oxygen difference increased by 11 and 5.9%, respectively. Oxygen uptake remained essentially unchanged (-2.1%). These results indicate that the increase in inotropism caused by intravenous digoxin in essential hypertension without heart failure produces not only no therapeutically useful improvement in left ventricular pumping function: there is also a coronary constrictor and ischaemia-inducing effect on the coronary arterial system.
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PMID:[The hypertensive heart. VI. Ventricular function and coronary artery haemodynamics as influnced by digitalis glycosides (author's transl)]. 69

A 2-day-old female infant was presented with severe cyanosis without cardiac failure. The ECG revealed a normal axis and left ventricular hypertrophy. Chest X-ray examination showed a slightly but uncharacteristically enlarged heart. Cardiac catheterization and angiography showed isolated right ventricular hypoplasia with atrial septal defect. A large right to left shunt at atrial level produced marked systemic arterial desaturation. Up to the age of now nine months the patient remained in good health without cardiac failure. The clinical findings and surgical treatment of this rare malformation are discussed. Differential diagnosis with clinically similar malformations such as tricuspid atresia type 1 B or pulmonary atresia type 1 (with intact ventricular septum) is impossible without angiography.
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PMID:[Isolated right ventricular hypoplasia]. 73 6

Thirty cases of CIV in the first year of life are presented. Association with prematurity and other malformations anticipate cardiac failure. Left ventricular hypertrophy is more frequent in conal defects. Repolarization disturbances were found in 73% of the cases in left precordial derivation with significative relief after surgical repair (banding). Conduction disturbances after surgical closure of ventricular septal defect was found in 15% of the cases. Surgical treatment during the first year was needed in 86% of patients. Only one case had good evolution without surgery. After four months of life total correction of septal defect as prefered. In patients with previous pulmonary artery banding, correction must be made one or two years later.
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PMID:[Ventricular septal defect in the first year of life (author's transl)]. 87 13

The heart was screened for amyloid deposits in an unselected post-mortem series of 244 patients over 60 who had been admitted to a geriatric department. Cardiac amyloidosis was found in 121 cases (49-6 per cent) but was limited to minor atrial involvement in 55 (22-5 per cent). The prevalence and severity of cardiac amyloidosis were significantly related to age and sex, females having the higher prevalence (56 per cent compared with 37 1/2 per cent). Cardiac amyloidosis was also significantly correlated with the occurrence of atrial fibrillation and of cardiac failure during the period of admission to hospital. Cardiac amyloidosis showed no significant correlations with other factors studied which included ECG evidence of left ventricular hypertrophy, ischaemia and bundle branch block, pathological evidence of cardiac enlargement or ischaemia, diagnosis of malignant disease, generalized wasting and the occurrence of digitalis toxicity.
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PMID:The clinical significance of senile cardiac amyloidosis: a prospective clinico-pathological study. 91 53

Striking variability has been observed in the presenting features in infancy of patients subsequently shown to have tetralogy of Fallot. Some patients presented with severe cyanosis in the neonatal period while others had a systolic murmur and cyanosis only on crying. In these latter patients cyanosis became present at rest over the subsequent months. Yet others presented with episodic attacks of unconsciousness, and a final group presented with dyspnoea and heart failure, accompanying a left-to-right shunt. Angiography demonstrates corresponding variations in the anatomy of the ventricular outflow tracts. In the severely cyanosed patients, the conus septum was deviated so as to obstruct the pulmonary outflow tract, and was best visualized in the lateral projection. In the patients with increasing cyanosis or episodic attacks of unconsciousness, the conus septum again obstructed the pulmonary infundibulum, but was obliquely orientated, not being seen clearly on either lateral or frontal projections. The episodic attacks were considered to be related to infundibular spasm, as previously shown to occur in Fallot's tetralogy. In contrast, increasing cyanosis was believed to be related to hypertrophy of infundibular musculature. In the patients with an initial left-to-right shunt, the arteries were orientated side-by-side so that the conus septum was observed in the frontal projection. Again, subsequent cyanosis was related to ventricular hypertrophy producing outflow tract obstruction. These findings are interpreted in the setting of a recent study, indicating that Fallot's tetralogy is produced by rotation of the embryonic conus together with sinistro-anterior deviation of the conus septum.
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PMID:Variations in clinical presentation of Fallot's tetralogy in infancy. Angiographic and pathogenetic implications. 119 55

The course of a Wilson-Mikity-syndrome in biovular twins born 19 weeks prematurely is reported. The disease started in the second week of life, reached its peak in the ninth week and it was complicated by a bronchopneumonia as well as a spastic bronchitis resulting in cardiac failure in both infants. On infant suffered spontaneous fracture of the ribs. Both patients were stationary for 26 weeks and 31 weeks respectively. A routine-examination at the age of 1 year revealed still distinct lung abnormalities, but nevertheless showing a tendency of improvement. Signs of right ventricular hypertrophy were found in the ECG of both children but more distinctly in the girl. The neurological development of the infants were found to be normal.
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PMID:[Wilson-Mikity-syndrome in twins (author's transl)]. 125 Jun 32

One of the earliest structural changes in the heart adapting to hypertension is left ventricular hypertrophy, which can now be exactly measured by echocardiography. Left ventricular hypertrophy increases the incidence of coronary artery disease, heart failure, and sudden death severalfold, independent of the blood pressure levels. Left ventricular hypertrophy requires specific antihypertensive therapy that controls both high blood pressure and increased left ventricular mass. Preliminary data from clinical studies indicate that regression of left ventricular hypertrophy leads to a better cardiovascular prognosis. Sympatholytic substances, angiotensin-converting enzyme (ACE) inhibitors, and calcium antagonists are antihypertensive agents that effected adequate reductions in blood pressure as well as regression of left ventricular hypertrophy.
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PMID:Hypertensive heart disease--significance of left ventricular hypertrophy. 128 90

The past decade has seen a shift in the strategy for hypertension treatment from stepped therapy--a highly structured monolithic series of steps--to recommendations for a more individualized selection of treatment. Severe hypertension is a clear indicator to bypass traditional steps. Demographic factors, such as age, gender, and race, are often cited, but have proved to be less helpful. Concomitant medical conditions and problems are very common and are more often the crucial determinants in the selection of antihypertensive therapy. Coronary artery disease, diabetes mellitus, heart failure, azotemia, asthma, and chronic obstructive pulmonary artery disease, anxiety, and depression are all common, and each has implications for the selection of antihypertensive therapy. Blood pressure reduction is a surrogate for reduction of cardiovascular risk, and therefore, consideration of concomitant medical problems has extended to left ventricular hypertrophy, obesity, mild hyperlipidemia, and insulin resistance, as additional risk factors in hypertension. Consideration of all these factors makes it possible to individualize antihypertensive therapy in most patients today.
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PMID:Treatment of hypertension: the place of angiotensin-converting enzyme inhibitors in the nineties. 128 28

Sudden cardiac death accounts for at least 50% of the mortality of patients with heart failure. Available clinical evidence suggests that lethal ventricular arrhythmias are responsible for the vast majority of cases of sudden death in heart failure. However, despite extensive clinical investigation over the last decade, there has been relatively little experimental study of the mechanisms underlying the development of lethal ventricular arrhythmias in heart failure. In addition to the original process leading to myocardium alterations, the role of other arrhythmogenic mechanisms such as ventricular overload and neuro endocrine activation remains to be elucidated. In ventricular hypertrophy both reentry and triggered activity may induce arrhythmias. Some studies on experimental models of heart failure did not provide consistent results concerning electrophysiological modifications and their relations with arrhythmias. Few studies in man in vivo are in favor of prolongation as well as increased dispersion of repolarisation in patients undergoing heart transplantation for idiopathic dilated cardio-myopathy. Further studies will need to be undertaken to clarify mechanisms underlying arrhythmias in heart failure.
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PMID:Approaches to experimental arrhythmias in heart failure. 129 18

Left ventricular hypertrophy is a major risk factor associated with the appearance of adverse cardiovascular events. A distortion in myocardial structure, mediated by an abnormal accumulation of fibrillar collagen within the adventitia of intramyocardial coronary arteries and neighbouring interstitial spaces, alters the electrical and mechanical behaviour of the myocardium. The mechanisms responsible for the regulation of cardiac myocyte growth and collagen accumulation are therefore of considerable interest. Herein we review results of in vivo studies conducted in the authors' laboratory that addressed these issues in various experimental models. The findings indicate that in arterial hypertension myocardial hypertrophy is related to ventricular systolic pressure work. Myocardial fibrosis, on the other hand, is not related to haemodynamic workload, but rather the presence of mineralocorticoid excess relative to sodium intake and excretion. Accordingly, fibrosis can appear in both the hypertensive left and non-hypertensive right ventricles. Pharmacological probes, administered in variable doses, were used to further test and support this hypothesis. In both primary and secondary hyperaldosteronism, it was possible to prevent the pathological structural remodelling of the myocardium with an aldosterone receptor antagonist, while in unilateral renal ischaemia ACE inhibition was similarly cardioprotective. Other studies demonstrated that it was feasible to regress the fibrous tissue response and normalise diastolic stiffness. This concept of cardioreparation suggests that heart failure due to this type of structural remodelling may be reversible.
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PMID:Regulatory mechanisms of myocardial hypertrophy and fibrosis: results of in vivo studies. 130 Dec 54


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