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

Nine patients with cardiac failure which was refractory to medical treatment, and which was caused by chronic malfunction of the posterior papillary muscle, as a result of a myocardial infarction, were studied by cardiac catheterisation and coronary arteriography. The mean pulmonary capillary pressure was 31+/-16 mm of mercury with a nu wave at 51+/-27 mm of mercury. The end diastolic volume was increased (141+/-68 ml/m2) and the ejection fraction lowered (0.40+/-0.13). The left ventricle had overall hypokinesia in 5 patients and akinesia of the inferior wall, representing 21+/-24% of the end diastolic perimeter, in 3 others. All these patients had significant lesions of two or three of the main coronary trunks. At operation lengthening of the posterior papillary muscle and/or the cordae was found. All patients had a replacement mitral valve of the Starr-Edwards type, associated with an aorto-coronary bypass of the anterior descending artery. The operative mortality was zero. At a mean follow-up period of 21 months, there had been no late death, and all the patients were improved.
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PMID:[Surgical treatment by valve replacement and aorto-coronary bypass in mitral valve insufficiency caused by chronic dysfunction of the posterior papillary muscle]. 10 89

In eleven patients with chronic heart failure forearm blood flow (FBF) was measured by plethysmography with a mercury-in-silastic strain gauge and splanchnic blood flow (SBF) with indocyanine green (ICG) infusion clearance at rest during right heart catheterization. The measurements were repeated during 8 min supine exercise on a bicycle ergometer, SBF during exercise being calculated from the changes of the brachial artery to hepatic vein oxygen differences and the ICG values at rest. Close correlations were found between cardiac output and FBF, and cardiac output and SBF at rest. During exercise forearm and splanchnic vascular resistances were both closely correlated with the brachial to pulmonary artery oxygen difference. It is concluded that in patients with heart failure vasoconstriction occurs during exercise in resting limbs and visceral organs, both closely related to the circulatory strain.
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PMID:Forearm and splanchnic blood flow at rest and during exercise in relation to the systemic arteriovenous oxygen difference in cardiac patients. 33 63

Congestive heart failure is associated with a reduction in limb venous volume at an effective venous pressure of 30 mm Hg (VV[30]). Further, an attenuated arteriolar dilation in response to a metabolic stimulus has been demonstrated. It was the purpose of this study to determine to what extent the chronic elevation in venous pressure seen in heart failure might explain these abnormalities of the limb circulation. Ten normal human volunteers were subjected to venous congestion of one arm for three hours at 70 mm Hg. A mercury-in-rubber strain gauge plethysmograph was used to measure forearm VV [30] and forearm blood flow at rest after release of five minutes of arterial occlusion (the reactive hyperemia response). Congestion reduced VV [30] 22%, resting forearm blood flow 49% and peak reactive hyperemia blood flow 25%. Thus, chronic venous congestion per se may significantly reduce limb venous volume as well as resting and reactive hyperemia blood flow.
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PMID:The effects of short-term venous congestion on forearm venous volume and reactive hyperemia blood flow in human subjects. 63 98

Muscle fatigue is a prominent symptom in patients with chronic heart failure (CHF). To determine whether it results from an intrinsic abnormality of vasodilating capacity of the vasculature in exercising muscle, we studied local forearm blood flow (FBF) during exercise in 13 patients with severe CHF and in eight normal untrained subjects of similar age. Intermittent forearm static exercise was performed by squeezing a hand dynamometer for 5 seconds, three times per minute, for 5 minutes at 15%, 30%, and 45% of maximum voluntary contraction. FBF was measured by mercury-in-rubber strain gauge venous plethysmography at baseline before exercise and during the last 3 minutes of each exercise state. Exercise was repeated after 24 hours of intravenous administration of milrinone in the patients with CHF. FBF increased with forearm exercise in a reproducible manner during 24 hours in the normal subjects: rest, 2.54 +/- 0.23 (0 hours), 2.90 +/- 0.23, (24 hours); 15%, 7.25 +/- 0.92, 5.85 +/- 0.56; 30%, 9.20 +/- 1.08, 10.05 +/- 0.85; 45%, 14.62 +/- 1.64, 13.85 +/- 1.09 ml/100 ml/min; p = NS, 0 versus 24 hours. In patients with CHF, FBF was reduced at baseline compared with normal subjects (1.70 +/- 0.15 ml/100 ml/min, p less than 0.05), but no significant differences from normal subjects were observed during exercise (15%, 5.04 +/- 0.65; 30%, 7.64 +/- 0.99; 45%, 12.56 +/- 1.20 ml/100 ml/min). Peak exercise blood flow was correlated negatively with central venous pressure (r = -0.65, p less than 0.05) and positively with right ventricular ejection fraction (r = 0.59, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Muscle blood flow during forearm exercise in patients with severe heart failure. 237 94

The purpose of this study was to determine if arterial baroreflex control of sympathetic nerve traffic is impaired in heart failure. We recorded renal nerve activity during changes in arterial pressure while simultaneously recording from aortic baroreceptor afferent fibers in 10 dogs with heart failure induced by rapid ventricular pacing and in 10 sham animals. Sensitivity of the aortic baroreceptors (percent change in nerve activity per millimeters mercury change in mean arterial pressure) was reduced in the heart failure group (heart failure, 2.3 +/- 0.3; sham, 3.6 +/- 0.4, p = 0.02). Despite the reduced sensitivity of aortic baroreceptors in heart failure, there was no difference in the baroreflex gain of renal nerve activity (heart failure, -5.5 +/- 1.4; sham, -5.8 +/- 1.3, p = NS). These values tended to decrease in both groups after vagotomy. The relation between baroreceptor input and renal sympathetic output, or central baroreflex gain (percent change in renal nerve activity divided by percent change in aortic nerve activity) was similar in both groups before vagotomy (heart failure, -2.4 +/- 0.6; sham, -2.3 +/- 0.5, p = NS). Vagotomy reduced central gain in the sham group (-0.9 +/- 0.1, p = 0.03) but not in the heart failure group (-1.7 +/- 0.5, p = NS), suggesting that the contribution of vagal afferents in the baroreflex arc is reduced in heart failure. Baroreflex control of R-R interval was attenuated in heart failure when assessed by blood pressure elevation but not reduction, indicating abnormal parasympathetic but preserved cardiac sympathetic mechanisms in heart failure. Thus, dogs with heart failure exhibit reduced sensitivity of aortic baroreceptors but preserved baroreflex control of renal nerve activity. Reduced baroreceptor sensitivity with preservation of baroreflex control of sympathetic nerve activity may contribute to the sympathoexcitatory state known to exist in heart failure.
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PMID:Baroreflex control of renal sympathetic nerve activity is preserved in heart failure despite reduced arterial baroreceptor sensitivity. 258 88

Arterial baroreflex control of the heart and peripheral circulation is markedly impaired in humans and animals with congestive heart failure. After reversal of heart failure in animal models, arterial baroreflex control of heart rate remains impaired for up to 8 months. Cardiac transplantation restores normal ventricular function and completely reverses heart failure, but does it normalize arterial baroreflex control of heart rate in humans? We studied baroreflex sensitivity in 11 patients with severe heart failure, six normal control patients, and 23 patients at 2 weeks to 4 years after orthotopic cardiac transplantation. Baroreflex sensitivity was assessed with intravenous bolus injections of phenylephrine and is expressed as change in RR or PP interval (msec) per millimeters of mercury rise in systolic arterial pressure. Atrial rate of both donor (denervated) and recipient (innervated) atria were measured in the transplant group. Baroreflex sensitivity in patients with severe heart failure was 2.0 +/- 0.3 msec/mm Hg, but in patients after cardiac transplantation, it was 13.0 +/- 0.9 msec/mm Hg (p less than 0.001). The responses in the transplant group were similar to those observed in normal controls (10 +/- 1.2 msec/mm Hg, p = NS). Our data indicate that patients with severe congestive heart failure have marked abnormalities of baroreflex control, which are reversed as early as 2 weeks after cardiac transplantation. In view of this rapid reversal, we consider it unlikely that abnormal baroreflex sensitivity seen in heart failure is due to structural alterations in the baroreceptors. We speculate that neurohumoral rather than structural abnormalities account for depressed baroreflex sensitivity in heart failure.
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PMID:Arterial baroreflex abnormalities in heart failure. Reversal after orthotopic cardiac transplantation. 266 Oct 55

Altogether 107 patients with transmural myocardial infarction were investigated by determination over time the volumetric blood flow rate in the forearm using a plethysmograph with mercury-rubber gages and A-V oxyhemoglobin difference. With relation to a degree of expression of acute heart failure all the patients were divided into 4 groups. Considerable volumetric peripheral blood flow rate changes were noted in the acute phase of transmural myocardial infarction. A degree of a decrease in the rate well correlated with expression of clinical signs of heart failure. Indices of A-V oxyhemoglobin difference also showed correlation with expression of acute heart failure growing with its increase. The combined determination of these indices, probably reflecting 2 tendencies (blood flow decrease and centralization), is of certain prognostic value.
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PMID:[Peripheral circulatory changes in patients in the acute period of transmural myocardial infarct]. 361 42

To characterize any digitalis-induced differences in intestinal blood flow autoregulation, we studied the circulatory responses of the rat intestine in control (n = 7) and chronically digitalized (n = 7) animals. Data were generated from denervated isoperfused small intestinal preparations. Arterial pressure, venous pressure, and oxygen consumption were continuously monitored. Determinations of intestinal blood flow allowed calculation of mesenteric vascular resistance and oxygen consumption. Animals underwent stepwise reductions in arterial pressure and acute venous hypertension (10 to 15 mm Hg). There were no differences in baseline hemodynamic or metabolic parameters in control (C) or digitalized (D) animals. Blood flow and oxygen consumption were autoregulated in both C and D rats until perfusion pressure decreased below 50 mm Hg. The response to acute venous hypertension was different. In D rats, venous hypertension resulted in increased vascular resistance (millimeters of mercury per milliliter per minute per 100 gm) [0.89 +/- 0.05 to 0.97 +/- 0.07; p less than 0.05], whereas C rats demonstrated no change [0.92 +/- 0.08 to 0.95 +/- 0.09]. The decrease in oxygen consumption in D rats (-14%) was slightly but significantly greater than that observed in C rats (-9%). Digitalized rats demonstrated a heightened myogenic response to acute venous hypertension with deleterious effects on vascular resistance and oxygen consumption. This reaction was intrinsic to the mesenteric circulation and not mediated by sympathetic nerves or central reflexes. Nonocclusive mesenteric ischemia in digitalized patients may reflect a similar abnormal response to the acute increases in portal pressure accompanying cardiac failure.
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PMID:Chronic digitalis administration alters mesenteric vascular reactivity. 382 Apr 9

Diuretics are the mainstay of drug therapy in the treatment of many cardiovascular disorders. However, perusal of knowledge of their haemodynamic activities in heart failure and hypertension reveals major gaps. In left ventricular failure complicating acute myocardial infarction, intravenous frusemide reduces the elevated left heart filling pressure with little change in systemic blood pressure, heart rate or cardiac output, and restores the ability of the left heart to handle an acute increase in filling volume. But there is little knowledge of the haemodynamic effects of other intravenous diuretics, oral diuretics or diuretics other than those acting on the loop of Henle in this emergency clinical situation. Even less information is available on the haemodynamic effects of diuretics in patients in chronic heart failure. In patients with valvular heart disease, parenteral mercury and oral thiazides reduce right heart and pulmonary vascular pressures with variable (dose-dependent?) changes in cardiac output. Information on the effect of loop diuretics, the comparative effects of intravenous versus oral routes of administration and dose-response correlations are all lacking. In hypertension, the dose-blood pressure lowering response relationship of orally administered diuretics is relatively flat. The majority of information relates to oral thiazides; there is little reliable information on the anti-hypertensive efficacy of the loop diuretics. The acute and chronic effects of the majority of commonly used diuretics on cardiac and peripheral vascular functions is unexplained. More is known of their potentially adverse metabolic effects than of their possible circulatory benefits in hypertensive patients. Many unwanted side-effects of these drugs have been described; their potential importance is related directly to the disease state and doses in which they are used. In acute heart failure, their potential danger is probably minimal. In the treatment of chronic heart failure their most sinister potential is in the excessive secretion of potassium and magnesium. In hypertensive patients their long-term administration in high-doses may lead to undesirable metabolic effects that tend to offset their blood pressure lowering activity. Despite their drawbacks, diuretics continue to provide the natural first-line treatment of choice of these common cardiovascular syndromes. But more information on their mechanisms of vascular activities and the differences in non-diuretic activity between different compounds is urgently required.
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PMID:Diuretics in cardiovascular therapy. Perusing the past, practising in the present, preparing for the future. 389 Mar 92

Physical, neurological and psychological examinations as well as laboratory tests were performed in the group of 147 workers, engaged in the production of chlorine, acetic aldehyde and soda lye, exposed to metallic mercury vapours and in the control group (n = 49). In the evaluation of laboratory tests, morphology of peripheral blood, liver function tests and lipid balance were analysed in the first part of the work. Electroencephalography, electrocardiography and chest X-ray were also performed as auxiliary examinations. There was a certain percentage of cases with symptoms of organic damage of the brain mostly in the form of cerebellar syndrome. Psychological organic tests proved to be of little value in the evaluation of effects of exposure to mercury. The results suggest that occupational exposure to metallic mercury vapours can enhance the risk of hypertension and myocardial failure. Harmful effect of occupational exposure to metallic mercury vapour on the respiratory and haemopoietic systems as well as on the liver and lipid balance was not observed.
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PMID:[Examination of health effects after exposure to metallic mercury vapors in workers engaged in production of chlorine and acetic aldehyde. I. Evaluation of general health status]. 763 28


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