Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to evaluate the effects of rapid digitalization on LV volumes, ejection fraction, and asynergy, 21 patients without heart failure were studied with a combination of hemodynamic and angiographic techniques before and after administration of intravenous ouabain (0.007 mg./Kg.). Seven patients had no CAD and served as normal (control) subjects (Group I), while 14 patients had extensive coronary disease (Group II). All pre-ouabain parameters were within the normal limits in Group I. After ouabain infusion, all indices of LV contractility: dP/dt, VCF, and ejection fraction rose significantly in the normal group, while LV filling pressure and end-diastolic volume remained unchanged. The baseline hemodynamic and volumetric values for Group II patients corresponded closely to their normal (Group I) counterparts, and exhibited similar changes after ouabain administration. Eight patients in Group II also had regional disorders of LV contractility, delineated by 23 abnormal hemiaxes of shortening. After ouabain, 15 out of 23 asynergic segments (65 per cent) improved, seven remained unchanged, and one worsened. It is therefore concluded that rapid digitalization not only enhances LV performance in normal subjects and in patients with CAD, but can also markedly reduce the extent of LV asynergy.
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PMID:Effects of rapid digitalization on total and regional myocardial performance in patients with coronary artery disease. 68 6

1. We studied the effects of chronic calcium antagonist (calcium entry blocker, CEB; nifedipine, verapamil, diltiazem) treatment on beta-adrenoceptor density (assessed by (-)-[125I]-iodocyanopindolol [ICYP] binding) and subtype distribution in right atria from 65 patients without apparent heart failure undergoing elective coronary artery bypass grafting (CAD-patients) and from 13 patients with moderate heart failure (NYHA class III to class III-IV) undergoing mitral valve replacement (MVD-patients). 2. In CAD-patients atrial beta-adrenoceptor density was 79.3 +/- 7.9 fmol ICYP bound mg-1 protein (n = 18), the beta 1:beta 2-adrenoceptor ratio 69:31%. Chronic CEB-treatment did not affect either atrial beta-adrenoceptor density or beta 1:beta 2-adrenoceptor ratio. 3. In contrast, in CAD-patients chronically treated with beta 1-adrenoceptor antagonists (atenolol, bisoprolol, metoprolol) and CEB, atrial beta-adrenoceptor density was significantly increased (108.6 +/- 10.5 fmol ICYP bound mg-1 protein, n = 21); this increase was due to a selective increase in beta 1-adrenoceptors. 4. In MVD-patients atrial beta-adrenoceptor density (55.5 +/- 8.7 fmol ICYP bound mg-1 protein, n = 7) was significantly lower (P less than 0.05) than in CAD-patients; beta 1:beta 2-adrenoceptor ratio, however, was not changed (67:33%). Chronic CEB-treatment of MVD-patients did not prevent the decrease in atrial beta-adrenoceptors. 5. We conclude that chronic CEB-treatment does not affect human right atrial beta-adrenoceptor density, either in patients without apparent heart failure or in patients with moderate heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lack of effect of chronic calcium antagonist treatment on beta 1- and beta 2-adrenoceptors in right atria from patients with or without heart failure. 131 61

We studied the effect of a volume load induced by a 45 degrees Trendelenburg position on atrial natriuretic peptide (ANP) secretion in awake and anaesthetized patients with coronary artery disease undergoing aortocoronary bypass surgery. ANP was measured in different parts of the circulation before and after induction of high dose fentanyl anaesthesia at fixed times prior to and after extracorporeal circulation. METHOD. In eight patients with coronary artery disease (NYHA classification II-III), who received neither diuretic nor positive inotropic therapy, ANP was measured in the various parts of the circulation: in a peripheral vein, a radial artery, in the pulmonary artery and in the coronary sinus. The measurements were made in the supine and 45 degrees Trendelenburg position. Measurements of mean arterial pressure (MAP), central venous pressure (RAP), pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), cardiac index (CI) and heart rate (HR) were taken simultaneously. The measurements were taken in the awake patient, during steady-state high-dose fentanyl anaesthesia with 50% O2 in N2O and after extracorporeal circulation. RESULTS. Compared to measurements in a control group, ANP levels were significantly higher in all parts of the circulation in patients with coronary artery disease, although clinical symptoms of heart failure were absent. After extracorporeal circulation, significantly higher levels of ANP were found at all measurement sites; however the concentration gradient of ANP between coronary sinus and arterial or venous blood was reduced. In awake and anaesthetized patients a change in body position, causing a significant increase in filling pressures, did not produce an increase in ANP levels at all measurement sites. The induction of high-dose fentanyl anaesthesia did not have an influence on plasmatic ANP levels. CONCLUSION. The results of this study lead to the following conclusions: 1. ANP levels in patients with CAD are increased, even if clinical heart failure symptoms are absent. 2. ANP is secreted in the coronary vessels. Following dilution in the atrial blood, it is metabolized to inactive compounds in the periphery. 3. Basic ANP levels are not changed by high-dose fentanyl anaesthesia. Marked increases of the filling pressures do not correlate with atrial ANP levels either before or after induction of anaesthesia. 4. After extracorporeal circulation ANP levels are significantly increased in all parts of the circulation. The concentration gradient between coronary sinus blood, on the one hand, and arterial and venous blood on the other hand is reduced. This phenomenon is probably caused by an alteration in the metabolism of ANP during hypothermic extracorporeal circulation.
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PMID:[The concentration of atrial natriuretic peptides (ANP). ANP in different sections of the circulation during atrial volume load with and without anesthesia]. 148 72

The beta-blocker carvedilol has been shown to induce vasodilation in patients with coronary artery disease. In a double-blind, randomized, placebo-controlled cross-over study, we looked for the acute vasodilating effect after i.v. administration in patients with heart failure. In 10 patients with coronary artery disease and six patients with dilated cardiomyopathy, all with an ejection fraction lower than 40%, the rate-pressure-product during supine ergometry and Swan-Ganz-catheterization rose to a significantly smaller extent after 5 mg carvedilol i.v. compared to placebo. This was mainly due to a lower heart rate at rest and during exercise, while blood pressure was not changed compared to placebo. Calculated total peripheral resistance during exercise after carvedilol was higher--significantly so in the CAD-group--than after placebo. These results show that in patients with heart failure, an acute vasodilating effect of i.v. carvedilol is not detectable.
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PMID:[Acute hemodynamic effects of the vasodilator beta blocker carvedilol in heart failure]. 197

Cardiac transplantation for the treatment of end-stage congestive heart failure has been shown to be of benefit regardless of the etiology. With few exceptions, the evaluation of patients with end-stage heart failure is the same, regardless of the etiology. In those with cardiomyopathy not as a result of CAD, special attention must be given to exclude secondary causes of cardiomyopathy such as amyloidosis, hemochromatosis, and sarcoidosis, as well as generalized systemic illnesses that may also involve the heart, either secondary or hereditary, because special consideration must be given to these patients on a case-by-case basis to determine that there is no general systemic involvement of the illness that would preclude satisfactory rehabilitation after transplantation. Before cardiac transplantation becomes widely available, there must be a greater number of donor hearts, the lack of which now severely limits the number of transplants performed in comparison with the estimated need.66 Additionally, more effective and specific immunosuppressive agents must be identified in order to reduce the incidence of rejection, infection, and accelerated atherosclerosis that now limits the longevity of transplant recipients. Furthermore, the ideal immunosuppressive agent should be associated with fewer side effects than those currently available. The emotional and economic burdens placed on the patient, the family, and society must be balanced against the benefits generated by the procedure. Despite these limitations, cardiac transplantation continues to offer hope for the terminally ill patient, which must be tempered by an understanding of the real limitations of transplantation.
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PMID:Patient selection and results of cardiac transplantation in patients with cardiomyopathy. 304 84

Biochemical analyses from endomyocardial biopsies indicate that cardiac energy metabolism is altered in patients with end-stage cardiac failure. Myocardial energy production is predominantly based on fatty acid oxidation. Carnitine, a naturally occurring compound, plays an essential role in fatty acid oxidation by carrying long-chain fatty acids into the mitochondrial matrix where they undergo beta-oxidation. In experimental animals, myocardial carnitine deficiency may cause cardiomyopathies which are reversible with carnitine substitution. Rare human diseases, as systemic carnitine deficiency, are associated with impaired cardiac function. We therefore investigated carnitine metabolism in patients with cardiac failure. Plasma and myocardial carnitine levels were measured in 55 patients undergoing cardiac transplantation because of end-stage cardiac failure based on dilated cardiomyopathy (DC, n = 30) or coronary artery disease (CAD, n = 22). Elevated plasma carnitine levels (controls: 49 +/- 12 microM; DC: 82 +/- 38 microM; p less than 0.001, CAD: 86.9 +/- 21.6 microM; p less than 0.05) were found in both patient groups (Fig. 1). Plasma carnitine did not correlate with creatinine (Fig. 2). Compared to controls, myocardial carnitine levels were significantly reduced: DC: 5.9 +/- 1.45 nmol/mg NCP; CAD: 5.84 +/- 1.84 nmol/mg NCP; controls: 15.6 +/- 5.4 nmol/mg NCP (Fig. 3). No correlation between myocardial and plasma levels was found (Fig. 5).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Carnitine metabolism--changes in the end stage of dilated cardiomyopathy and ischemic heart muscle disease]. 332 28

A prospective study was conducted in 267 patients with angiographically defined coronary artery disease without documented ventricular tachycardia to determine the prognostic significance of repetitive ventricular response (RVR) after programmed electrical stimulation (PES). The patients were classified inducible if RVR with 3 or more echo beats (RVR greater than or equal to 3) could be induced. 89 patients without previous myocardial infarction (MI), 61 survivors of MI occurring between 6 weeks and 3 months before and 117 patients who had survived longer than 3 months after MI were studied. A standardized stimulation protocol with single (S1S2) and double (S1S2S3) extrastimuli during ventricular drive at a cycle length of 600, 500 and 430 ms with a current strength below 5 mA at the right ventricular apex was employed. Ventricular responses with 3 to 5 echo beats (RVR3-5) and with 6 and more echo beats (RVR greater than or equal to 6) were distinguished. In 68 (25%) patients RVR3-5 and in 38 (14%) patients RVR greater than or equal to 6 was observed; in 11 patients with RVR greater than or equal to 6 sustained VT was initiated which was monomorphic in 5 of them. The occurrence of RVR greater than or equal to 6 was related to the time interval to prior MI and most frequently found within 3 months of MI. A higher incidence of RVR greater than or equal to 6 was observed in more advanced CAD, although the angiographic findings were unable to predict the results of PES. During a mean follow up of 20 months 11 patients died, 8 suddenly, 3 in cardiac failure. Those who died had more extensive CAD, RVR greater than or equal to 3 was found in 4 of them and nonsustained VT in one. The sensitivity of RVR greater than or equal to 3 as a predictor of sudden death (SD) was 36% and the specifity 60%. The predictive value of inducibility of RVR greater than or equal to 3 as indicator of SD was 4% and the predictive value of noninducibility was 98%. It is concluded that in patients with chronic CAD without spontaneous VT, RVR with 3 more echo beats does not identify a predisposition to die suddenly.
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PMID:Prognostic significance of repetitive ventricular response in chronic coronary artery disease. 404 6

This paper studies the problem of identification of suitable biological variables for optimal effectiveness of a CAD. To identify suitable error signals, a closed loop simulation and analysis of the assisted circulation was carried out. Results show that the combination of heart rate and left atrial pressure is very effective as an input error signal for either series or parallel assisted circulation when simulated heart failure is severe (greater than 50% decrease in left ventricular elastance). During simulated exercise (50% reduction in peripheral resistance) such a combination is even more effective. In addition, simulation results show that aortic pressure and cardiac output are not suitable control variables for CAD.
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PMID:Control system for circulatory assist devices: determination of suitable control variables. 716 28

We evaluated 198 consecutive survivors of acute myocardial infarction and performed selective coronary angiography in 117 of 131 (89 percent) patients who were deemed candidates for angiography by clinical criteria. Overall, left main CAD (greater than or equal to 70 percent stenosis) was found in ten patients (8.5 percent), three vessel CAD in 41 patients (35 percent), two vessel CAD in 37 patients (31.5 percent), single vessel disease in 27 patients (23 percent) and zero vessel disease in two patients (2 percent). Factors suggesting multivessel disease included older age, history of prior myocardial infarction, and post-infarction convalescence complicated by angina pectoris. Factors not discriminating between single and multivessel disease were sex, infarct extent (transmural vs non-transmural), (3) infarct location (anterior vs inferior), and post-infarction convalescence complicated by late arrhythmia or heart failure. This study demonstrates that multivessel coronary artery disease is common in survivors of myocardial infarction and is suggested by the occurrence of post-infarction angina and by the history of an antecedent myocardial infarction. Coronary angiography can be performed safely within 30 days after myocardial infarction in patients with an uncomplicated convalescence and with mild risk in those with a complicated convalescence.
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PMID:Coronary angiography soon after myocardial infarction. 735 Nov 48

The effects of anaesthesia for major abdominal vascular surgery on coronary flow regulation and mechanisms of myocardial ischaemia were studied in 56 patients with CAD, using a randomized, partly double-blinded protocol. After induction with fentanyl (3 micrograms.kg-1) and thiopentone (2-4 mg.kg-1) and tracheal intubation, principal anaesthetics were nitrous oxide/oxygen (60/40) with isoflurane (n = 20), halothane (n = 19) or fentanyl (15-20 micrograms.kg-1) (n = 17). Conventional invasive techniques and coronary venous retrograde thermodilution were used to assess systemic and coronary haemodynamics. Coronary vascular resistance was estimated from myocardial oxygen extraction. Myocardial ischaemia was diagnosed by 12-lead ECG and/or anterior wall motion abnormalities by cardiokymography and/or myocardial lactate production. When adjustment of anaesthetic dose was insufficient for haemodynamic control, i.v. phenylephrine and nitroglycerine were administered to treat hypotension and hypertension or cardiac failure respectively. Measurements were performed at four specific intervals; awake, before surgery and 10 and 30 min after abdominal incision. Comparable changes of systemic haemodynamics and myocardial oxygen consumption were observed in the three groups. Coronary vasodilation was evidenced in isoflurane patients only and was linearly dose-dependent (P < 0.001). Partial Least Squares Projections to Latent Structures modelling with cross validation confirmed this dose-dependency and ruled out a clinically measurable influence by intervention drugs or simultaneous systemic haemodynamic abnormalities. The incidence of myocardial ischaemia during anaesthesia and surgery was comparable in the three groups (35, 37 and 24%, respectively) and there was an association with systemic haemodynamic aberrations in 19 of the 27 ischaemic episodes. In contrast to ischaemic halothane and fentanyl patients, isoflurane patients with ischaemia had significantly lower myocardial oxygen extraction (P = 0.008 and P = 0.001, respectively), indicating that the oxygen extraction reserve was not utilized in a normal way during ischaemia.
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PMID:Anaesthesia for abdominal vascular surgery in patients with coronary artery disease (CAD), Part I: Isoflurane produces dose-dependent coronary vasodilation. 788 99


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