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

Missing the moment for application of ventricular assist devices (VAD) may be one of the major causes of multiple organ failure in patients who are to be weaned from cardiopulmonary bypass (CPB) with the aid of VAD. To determine the optimal timing for application of VAD in such patients, we examined the effect of a CPB assist on cardiac functional recovery from severe global ischemia using an experimental canine system. In the present study we created myocardial ischemia by clamping the aorta for 20 minutes (Group I; N = 7) or 45 minutes (Group II; N = 11) under normothermic CPB. The reliability of the method in creating severe cardiac failure was confirmed by testing the levels of adenosine triphosphate (ATP), creatine phosphate (CP), and lactate. After reperfusion of the myocardium, the heart was assisted by a totally vented CPB. The left ventricular end-systolic pressure-volume relationship (Emax), which is a load-independent index of contractility, was obtained every 15 minutes for up to 120 minutes of reperfusion. The Emax revealed that the function of the damaged heart recovers exponentially with time after reperfusion. From curves of the functional recovery of the heart, CPB support appeared to be beneficial for the first 60 minutes after reperfusion, and aided in the recovery of cardiac function in hearts damaged by global myocardial ischemia. However, CPB assist thereafter may not be effective in further improving cardiac function. We therefore concluded that the decision to use VAD should be determined by cardiac function by 60 minutes of reperfusion to avoid prolonging CPB time.
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PMID:Optimal timing for application of ventricular assist devices in patients who cannot be weaned from cardiopulmonary bypass. An experimental study. 319 47

Prolonged circulatory support for cardiac failure has been increasingly successful in adults but has had very limited use in children. From January 1982 to December 1985, 13 children with postoperative cardiac failure refractory to conventional therapy were treated with extracorporeal membrane oxygenation. Ages ranged from 9 days to 17.6 years (mean = 3.8 years); weights ranged from 2.8 to 50 kg (mean = 13.8 kg). Seven patients had obstructive lesions of the right ventricle, such as pulmonary stenosis and tetralogy; the other patients had tricuspid atresia, truncus arteriosus, complete transposition, total anomalous pulmonary venous connection, pericardial tamponade, and a drug reaction after heart transplantation. One patient (nonsurvivor), who could not be separated from cardiopulmonary bypass, required extracorporeal membrane oxygenation in the operating room. In the remaining 12, the interval between operation and the start of extracorporeal membrane oxygenation ranged from 9 to 50 hours (mean = 22.2 hours). Four patients were cannulated through the groin and nine through the chest. Peak flows ranged from 1.05 to 2.74 L/min/m2 (mean 1.92 L/min/m2). Duration of oxygenator support ranged from 12 hours to 9 days (mean = 3.4 days). Seven patients required reexploration for bleeding. Renal insufficiency developed in five patients, four of whom underwent hemodialysis or ultrafiltration during extracorporeal membrane oxygenation. Two patients had evidence of clots in the oxygenator circuit. Seven patients were weaned from extracorporeal membrane oxygenation. Failure to wean from the oxygenator was related to neurologic sequelae of prolonged hypotension before institution of oxygenation in three patients. Mediastinitis developed in three of the seven patients who were weaned. One of these three died in the hospital 74 days after being weaned from the oxygenator. There has been one late death 6 months after oxygenator support was withdrawn. At most recent examination, five children were well, with normal cardiac function 7 months to 4.3 years postoperatively (mean = 32 months). This series suggests that profound cardiac insufficiency in children after cardiac operations can be successfully managed with extracorporeal membrane oxygenation with excellent functional recovery, although major complications are common in this critically ill group of patients.
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PMID:Extracorporeal membrane oxygenation for postoperative cardiac support in children. 379 29

The monitoring and predictive value of the electroencephalography (EEG) and neurological signs was evaluated in 125 patients who had sustained critical brain ischaemia during circulatory arrest of primary cardiovascular aetiology. Cranial nerve areflexia with mydriasis or extension of the upper limb in response to cutaneous stimulation reliably indicated brain death and appearance of the flexion reflex or of intermittent spikes and sharp waves in the EEG predicted an unfavourable outcome; but other EEG configurations and nuerological signs per se were inaccurate variables to assess the outcome. By contrast, the recovery course and rate were accurately assessed by the time for appearance of cerebral functions; the caloric vestibular reflex, decorticate posturing, stereotypic reactivity, intermittent and continuous electrocortical activity were regained within ultimate time limits of 900, 540, 455, 450, and 1020 min, respectively, corresponding to the longest delay compatible with recovery of function at all, and within critical time limits of 165, 180, 180, 200, and 630 min, respectively, corresponding to the longest delay compatible with recovery of consciousness. Moreover, intermittent electrocortical activity, consciousness, speech and ability to cope with personal necessities were regained within supercritical time limits of 3, 47, 156, and 336 h, respectively, corresponding to the longest delay compatible with complete restoration of post-awakening faculties within 1 year of resuscitation. Prognosis was currently ascertained during the period of unconsciousness as cephalic reactivities, and electrocortical activities were regained in an exponential relationship to time. Bradycardia or asystole prior to resuscitation and metabolic acidosis, hypotensive heart failure, recurrent circulatory arrest and pneumonia thereafter influenced the cerebral recovery adversely.
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PMID:Natural history of global and critical brain ischaemia. Part III: cerebral prognostic signs after cardiopulmonary resuscitation. Cerebral recovery course and rate during the first year after global and critical ischaemia monitored and predicted by EEG and neurological signs. 725 54

Thirty-one age-matched, conscious, virgin, male Sprague-Dawley rats and spontaneously hypertensive rats (SHRs) were individually injected with a single subcutaneous dose of 85 mg/kg dl-isoproterenol to determine the degree and time course of drug-induced cardiac failure and functional recovery. At 24 hr and 1 week postisoproterenol, rats were anesthetized and prepared for the recording of cardiac output and arterial pressure. Calculated cardiac index was used to determine normal cardiac function. Following that measurement, a 2-min, 15.3 ml/min infusion of Tyrode's solution was performed via a right jugular vein cannula. Volume-loaded peak-cardiac outputs and peak stroke volumes were also used as indices of cardiac function. Twenty-four hours after the injection of isoproterenol to he normotensive Sprague-Dawley rats, cardic failure was evident only during the stress of volume loading. Normal cardiac index was unaffected, but peak cardiac output and peak stroke volume were depressed. By 1 week after isoproterenol, the volume loaded measures of cardiac function had returned to normal. Interestingly, by 1 week postisoproterenol, total peripheral resistance was reduced. This reduced vascular resistance may have aided myocardial repair. At 24 hr postisoproterenol, the volume loaded peak cardiac outputs and peak stroke volumes in the SHRs were reduced to the same degree as in the Sprague-Dawley rats. Here, also, no change in normal cardiac index occurred. In the SHRs, however, total peripheral resistances were elevated at both 24 hr and 1 week. These increases in resistance appeared to impair the myocardial healing process, as both normal cardiac index and volume-loaded peak cardiac output and peak stroke volume were depressed at 1 week postisoproterenol. In normotensive and hypertensive rats, different vascular responses to isoproterenol or its initial cardiac effects may determine the duration and eventual degree of cardiac failure.
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PMID:Isoproterenol-induced cardiac failure in the spontaneously hypertensive rat. 732 63

At least theoretically, ACE-inhibitors may influence each of the factors involved in the regulation of salt and water metabolism. Angiotensin II exerts an antidiuretic and antinatriuretic action on the kidney through influences on the glomerular filtration coefficient, glomerular filtration rate, mesangial tone, filtration fraction, proximal and distal tubule. Angiotensin II and renin also regulate the input of water and salt through an unequivocal dipsogenic effect. In congestive heart failure angiotensin II participates in the preservation of the glomerular filtration rate through its vasoconstrictor properties on the systemic vessels (maintenance of the perfusion and filtration pressure) as well as on the efferent arteriole (maintenance of the filtration pressure). ACE-inhibition weakens or abolishes these influences. However, two favorable mechanisms may also come into action: rise of cardiac output and improvement in renal blood flow; widening of the filtration surface and increment of the filtration coefficient. The efficacy of these factors depends on renal function, age, functional recovery of the heart, treatment with diuretics, duration of treatment with ACE-inhibitors, duration of action of the ACe-inhibitor used, blockade of the facilitating action on the adrenergic vasoconstriction, formation of vasodilating prostaglandins, reduced degradation of kinins. All these effects may account for the variable and often contradictory clinical results, in particular as concerns the relationship between ACE-inhibition and use of diuretics in congestive heart failure. This also explains the variability of efficacy (from the development of pulmonary edema and requirement of diuretics to diuretic withdrawal and clinical improvement) of the ACE-inhibitors as monotherapy in mild to moderate heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[ACE-inhibitors and water metabolism in heart failure]. 763 56

Revascularization after prolonged complete limb ischemia may result in severe damage to skeletal muscle and systemic alterations (postischemic syndrome). Our previous experimental studies have shown that this injury can be reduced substantially by treating the jeopardized extremity by controlling the conditions of reperfusion and composition of the initial reperfusate. In the present study this concept of controlled limb reperfusion was applied in patients with prolonged severe limb ischemia. Controlled limb reperfusion was used in 14 patients after prolonged complete uni- or bilateral ischemia. The ischemic interval ranged from 5 to 21 h. Two patients were in cardiogenic shock, 11 had associated cardiac disease, and seven coexistent peripheral vascular disease. After systemic heparinization, standard thromboembolectomy was done using a Fogarty catheter. Cannulas were placed into the iliac, profunda, and superficial femoral arteries and were connected to a reperfusion set. Oxygenated blood was drawn from the iliac artery and mixed with an asanguineous solution (ratio 6:1). This controlled reperfusate was delivered into the profunda and superficial femoral arteries using a single rollerpump. The system allows control of the composition of the reperfusate (calcium, pH, osmolarity, glucose, substrate, pO2, free radical scavengers) and the conditions of reperfusion (pressure, flow, temperature). After 30 min of controlled limb reperfusion, the cannulas were removed and normal blood reperfusion started. All 12 patients who were stable hemodynamically before the operation survived the revascularization. Eleven patients, including one with acute aortic occlusion for several hours, were discharged with functional recovery of their extremities. Despite the severe ischemic insult, controlled limb reperfusion avoided amputation and profound systemic complications. Two patients who were in cardiogenic shock preoperatively died from progressive cardiac failure. We conclude that controlled arterioarterial limb reperfusion may reduce the local manifestations of the postischemic syndrome after prolonged periods of ischemia, may salvage limbs thought previously to be damaged irreversibly by prolonged ischemia, and can be done easily in the operating room.
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PMID:New surgical treatment for severe limb ischemia. 800 66

Modern therapeutic options in ischemic coronary disease such as thrombolysis, coronary angioplasty, new emerging strategies in treating heart failure and secondary prevention have resulted in decreasing cardiac mortality over the last ten years. In the era of interventional cardiology a new focus of clinical interest is the process of transition from loss of contractile function to definitive necrosis of severely ischemic myocardium. The decision for bypass surgery or angioplasty in patients with compromised contractile function should be based on evidence of viable myocardium with some or full potential for functional recovery; otherwise prognostic benefit may be questionable or dubious. The clinical substrate of non-contractile, but viable myocardial tissue may be present in patient presenting with both stable and unstable angina, in cases of acute or chronic myocardial infarction and in the setting of congestive heart failure resulting from ischemic cardiomyopathy. Various diagnostic methods are theoretically useful to assess residual myocardial viability both in hibernating myocardium (contractile down-regulation) and post-ischemic stunned (reperfused) myocardial tissue. Myocardial viability is confirmed both in presence of systolic wall motion or systolic wall thickening as evidenced from (contrast or radionuclide) left ventricular angiograms or echograms. Moreover, myocardial tissue perfusion by thallium-201 or other radioactive perfusion agents as documented by uptake of tracer is considered clear evidence of viability; however, lack of uptake of perfusion agents may not always exclude viable myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Myocardial vitality: clinical correlates and diagnostic concepts]. 815 Apr 10

A critical review of the data available in the literature today permits a better understanding of the multiple actions of atrial natriuretic peptide (ANP) on the cardiovascular system. Moreover, the results of chronobiological studies suggest a role for this peptide in the determination of the circadian rhythm of blood pressure (BP). ANP can affect BP by several mechanisms, including modification of renal function and vascular tone, counteraction of the renin-angiotensin-aldosterone system, and action on brain regulatory sites. A series of interrelated events may follow from very small changes in the plasma levels of ANP. The endpoints are blood volume and BP reduction, but they are rapidly offset (mainly by reactive sympathetic activation) as soon as blood volume or pressure is threatened. The circadian rhythms of BP and ANP are antiphasic under normal conditions and in essential hypertension. The loss in the nocturnal decrease of BP is accompanied by a comparable loss in the nocturnal surge of ANP in hypertensive renal failure and hypotensive heart failure. In the latter condition, BP and ANP variabilities correlate significantly both before and after therapy-induced functional recovery, independently of the mean BP levels. Autonomic function modulates the secretion of ANP, which seems more apt to determine only transient changes in BP levels, as suggested by the short half-life of the peptide and the buffering role of its clearance receptors. There is now sufficient evidence that ANP contributes to short-term control over BP and electrolyte balance, in contrast and in opposition to the renin-angiotensin-aldosterone system, which is involved primarily in long-term BP control. By interfering with other well-established neurohormonal factors, ANP appears to be an additional modulator of the circadian rhythm of BP.
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PMID:Atrial natriuretic peptide and circadian blood pressure regulation: clues from a chronobiological approach. 839 98

The two primary goals of mechanical circulatory support are to provide adequate perfusion of the vital organs and to decrease cardiac work. The support of the myocardium is in an effort to cause a reversal of cardiac damage. The recovery process apparently takes place in two stages. Initially, there is a rapid functional recovery of cells in marginally ischemia areas. Then there is a slower process of hypertrophy of normal and recovering myofibers. The process involves the reversal of interstitial and of intercellular myocardial edema in areas of viable myocardium while halting the extension of necrosis into reversibly ischemic areas. It appears that this process is extended from 3 to 5 days, and functional recovery can occur for up to 2 weeks. After a 2-week period, there appears to be little functional recovery of myocardial cells. In autopsy series of nonsurvivors, it appears that most of the patients had suffered from biventricular failure. Biventricular failure appears to be one of the more common complications of the support patient. Right ventricular failure will be attempted to be supported by right ventricular assist devices. The right ventricular assist device, unfortunately, adds a level of complication to the recovery process for the bridge-to-transplant or cardiomyopathy patient. The patients who are involved in support fall into three categories: (1) the bridge-to-transplant patient, (2) the patient recovering from postcardiotomy, and (3) the patient who recovers from an acute myocardial insult. It appears that after 2 weeks the recovery period for all of these groups demonstrates no further functional recovery. The bridge-to-transplant patients usually need to be supported until the transplant occurs. The postcardiotomy patient and the acute myocardial failure patient are the most disappointing support group, since they have a higher morbidity and mortality, and a lower chance of recovery. Salvage rates appear to be in approximately the 25% range in the acute insult category.
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PMID:Cardiac assist devices. 879 47

Tumour necrosis factor-alpha (TNF-alpha) is an autocrine contributor to myocardial dysfunction and cardiomyocyte death in ischaemia-reperfusion injury (I/R), sepsis, chronic heart failure and cardiac allograft rejection. Cardiac resident macrophages, infiltrating leucocytes, and cardiomyocytes themselves produce TNF-alpha. Although adenosine reduces macrophage TNF-alpha production and protects myocardium against I/R, it remains unknown whether I/R induces an increase in cardiac TNF-alpha in a crystalloid-perfused model (in the absence of blood), and, whether adenosine decreases cardiac TNF-alpha and protects function after I/R. To study this, isolated rat hearts were crystalloid-perfused using the Langendorff method and subjected to I/R, with or without adenosine pretreatment. Post-ischaemic cardiac TNF-alpha (enzyme-linked immunosorbent assay and bioassay) and function were determined (Langendorff). I/R increased cardiac TNF-alpha and impaired myocardial function. Adenosine decreased cardiac TNF-alpha and improved post-ischaemic functional recovery. This study demonstrates that: first, I/R induces an increase in cardiac tissue TNF-alpha in a crystalloid-perfused model: second, adenosine decreases cardiac TNF-alpha and improves post-ischaemic myocardial function; third, decreased cardiac TNF-alpha may represent a mechanism by which adenosine protects myocardium; and fourth, adenosine-induced suppression of cardiac TNF-alpha may provide an anti-inflammatory link to preconditioning and have implications for cardiac allograft preservation.
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PMID:Adenosine decreases post-ischaemic cardiac TNF-alpha production: anti-inflammatory implications for preconditioning and transplantation. 949 88


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