[Congestive heart failure. A systemic or a multiregional syndrome?].
Explore the source record for details and available documents.
Heart↗
Biomedical subjects
O Visioli
Publications and source records attributed to O Visioli.
[The accuracy of echocardiography during the infusion of low-dose dobutamine in identifying vital myocardium in patients with obstructive coronary disease and chronic left ventricular dysfunction].
The identification of viable myocardium has important therapeutic implications in patients with coronary artery disease (CAD) and chronic left ventricular dysfunction. To assess the accuracy of transthoracic echocardiography (TTE) during dobutamine infusion for identification of viable myocardium, we have analyzed 14 patients affected by CAD and chronic abnormalities of left ventricular wall motion (RWM), present at rest, referred for coronary artery bypass grafting (CABG): 8 of 14 patients had a history of myocardial infarction with evidence of Q waves at the surface ECG. All patients had a clinical stable CAD. RWM response to dobutamine (5 mcg/kg/min and 10 mcg/kg/min) was evaluated using TTE and compared to RWM changes after CABG analyzed by intraoperative epicardial echocardiography (EE). RWM was analyzed qualitatively by dividing the left ventricle into 16 segments and a score index was assigned to each region (0: normal; 1: hypokinetic; 2: akinetic; 3: dyskinetic). Of 125 akinetic segments present at rest before CABG, 93 showed functional improvement after CABG at intraoperative EE. The RWM response to dobutamine infusion predicted intraoperative improvement after CABG in 85 of 93 segments (sensitivity: 91.3%) and identified 25 of the 32 segments which did not exhibit intraoperative improvement (specificity: 78.1%). The TTE performed 15 days after CABG showed no worsening or further improvement in RWM when compared with intraoperative EE study. Summed segment scores in 14 patients showed significantly improvement from 17.9 +/- 7, medium values at rest, to 5.1 +/- 4 after dobutamine infusion (p less than 0.001) and 5 +/- 7 after CABG (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Treatment of refractory heart failure.
Explore the source record for details and available documents.
Acute Disease↗
Oxygen free radicals and myocardial damage: protective role of thiol-containing agents.
It has been suggested that the sudden presence of oxygen during reperfusion after a period of ischemia may be toxic for the myocardial cell. The oxygen molecule is capable of producing reactions in the cell, forming highly reactive free radicals, and inducing lipid peroxidation of membranes, altering their integrity and increasing their fluidity and permeability. The ischemic and reperfused cardiac cell is the prime candidate for this reaction sequence and may explain the molecular mechanism underlying the pathologic events related to membrane dysfunction and calcium homeostasis. However, the myocardium has a series of defense mechanisms including the enzymes superoxide dismutase (SOD), catalase, and glutathione peroxidase plus other endogenous antioxidants such as vitamin E, ascorbic acid, and cysteine to protect the cell against the cytotoxic oxygen metabolites. The prerequisite for oxygen free radical involvement in ischemia and reperfusion damage is that ischemia alters the defense mechanisms against oxygen toxicity. It is known that ischemia may impair mitochondrial SOD and, with reperfusion, oxidative stress may occur as shown by tissue accumulation and release of oxidized glutathione. This tripeptide molecule in the cofactor of glutathione peroxidase, the enzyme that removes hydrogen and lipid peroxides. Its formation and subsequent release is a reliable index of oxidative damage. In our study, we investigated the effects of N-acetylcysteine on oxidative damage in the isolated rabbit heart. N-acetylcysteine increases, in a dose-dependent manner (from 10(-7) to 10(-5) M), the myocardial glutathione content and provides an important degree of protection against ischemia and reperfusion. Oxidative stress does not occur, mitochondrial function is maintained, enzyme release is reduced, and contractile recovery is increased. Similarly, we administered N-acetylcysteine in the pulmonary artery of coronary artery disease patients undergoing coronary bypass grafting (150 mg/kg in 1 hour followed by 150 mg/kg in 4 hours). The degree of oxidative stress on reperfusion was reduced and recovery of cardiac function improved. In this article, we review the cardioprotective role of thiol-containing agents.
Animals↗
Stunning: damaging or protective to the myocardium?
There are several potential outcomes of myocardial ischemia. When ischemia is severe and prolonged, irreversible damage occurs and there is no recovery of contractile function. Interventions aimed at reducing mechanical activity and oxygen demand, either before ischemia or during reperfusion, have been shown to delay the onset of ischemic damage and to improve recovery on reperfusion. When myocardial ischemia is less severe but still prolonged, myocytes may remain viable but exhibit depressed contractile function. Under these conditions, reperfusion restores complete contractile performance. This type of ischemia, leading to a reversible, chronic left ventricular dysfunction, has been termed hibernating myocardium. Depression of mechanical activity is, actually, a protective mechanism whereby the hibernating cells reduce their oxygen demands in the setting of reduced oxygen supply. A third possible outcome after a short period of myocardial ischemia is a transient postischemic ventricular dysfunction, a situation termed stunned myocardium. As in the case of hibernating myocardium, the depressed contractile function occurring during stunning could be a protective mechanism, allowing the reperfused cells to gradually recover their metabolism and function.
Animals↗
The occurrence of oxidative stress during reperfusion in experimental animals and men.
Reperfusion is the prerequisite for the ischemic myocardium to recover its metabolic and mechanical function. However, reperfusion after a prolonged period of ischemia in the experimental animal may exacerbate, or at least accelerate, the occurrence of ischemic injury, whilst in humans at the least it is not beneficial. This entity has been called reperfusion damage, since much of the damage is believed to be caused by events occurring at the moment of reperfusion rather than by changes occurring during ischemia. The existence of reperfusion damage, however, has been questioned, and evidence in favour of the concept is sparse. At the moment the molecular events occurring at the time of reperfusion are not completely understood, and the relative importance of several proposed deleterious mechanisms is not yet established. One of the most fashionable ideas for the cause of reperfusion damage is that the function of cell membrane is modified by oxygen radicals generated at the moment of reperfusion. Evidence in favour of and against this hypothesis is described in detail in the present article.
Animals↗
The effect of propionyl-L-carnitine on the ischemic and reperfused intact myocardium and on their derived mitochondria.
To assess whether propionyl-L-carnitine protects rabbit heart against the deterioration caused by ischemia and reperfusion, isolated hearts were infused with a medium containing it in different concentrations. During control, normoxic perfusion, and 60 minutes of low-flow ischemia (37 degrees C) followed by 30 minutes of reperfusion, diastolic, and developed pressures were monitored; coronary effluent was collected and assayed for lactate and creatine phosphokinase (CPK); mitochondria were harvested and assayed for oxidative phosphorylation and calcium content; and tissues for concentration of adenosine triphosphate (ATP) and creatine phosphate. Propionyl-L-carnitine reduced the ischemic deterioration of mitochondrial function and the depletion of tissue stores of ATP. On reperfusion, hearts treated with it recovered better than the untreated hearts with respect to left ventricular performance, replenishment of ATP and CP stores, and mitochondrial function. The reperfusion-induced mitochondrial calcium overload and release of CPK were also reduced. The effect of propionyl-L-carnitine was dose dependent. At 10(-8) M it failed to modify ischemic and reperfusion damage but protected well at 10(-7) M. No further protection was obtained at 10(-6) M. Propionyl-L-carnitine thus protects the myocardium against some of the deleterious effects of ischemia and reperfusion. In particular it protects mitochondrial function, perhaps partly by preventing mitochondrial calcium overload. Because this protection occurs in the absence of a negative inotropic effect during normoxia or of a coronary dilatatory effect during ischemia, it cannot be attributed to an energy-sparing effect or to the improvement of oxygen delivery.
Adenosine Triphosphate↗
Different effects of captopril and other angiotensin converting enzyme inhibitors on cardiovascular preparations.
The effects of captopril and of other angiotensin-converting enzyme inhibitors (zofenopril, fosenopril and enalaprilic acid) were tested on the isolated rabbit heart and aorta. Captopril elicited an erratic negative inotropic effect and a reduction in basal coronary perfusion pressure (10(-5)-10(-4) M). The increase of coronary perfusion pressure induced by vasopressin, methoxamine, angiotensin II and Bay K 8644 was partially antagonized by captopril (10(-7)-10(-4) M) in a non-specific manner. These actions were not modified by saralasin or indomethacin and by ex vivo pretreatment with captopril itself. On the aortic strips, the contraction plateau induced by KCl and angiotensin II was partially inhibited (10(-6)-10(-4) M), while no effect was observed on those induced by noradrenaline, serotonin and PGF2 alpha. The Ca2+ concentration-response curve appeared shifted to the right in a non-competitive manner. The other angiotensin-converting enzyme inhibitors showed no effect up to 10(-4) M on isolated heart or aorta. Results obtained with captopril were consistent with vasorelaxant activity independent of the tissue renin-angiotensin system. Modulatory activity on the intracellular calcium movement may be involved.
Angiotensin-Converting Enzyme Inhibitors↗
Calcium channel blockers and ischaemic heart disease: theoretical expectations and clinical experience.
There are several reasons for using calcium antagonists to protect ischaemic and reperfused myocytes and to treat coronary artery disease (CAD) patients. At the molecular level, calcium antagonists induce: coronary dilatation and improvement of the supply of oxygen and substrate to the area at risk; energy sparing secondary to dilatation of the peripheral vasculature and, at least in the case of phenylalkylamines and benzothiazepines, a reduction in contractility and heart rate; attenuation of reperfusion-induced arrhythmias; inhibition of platelet aggregation (only at high concentration); reduction of loss of adenosine precursor; reduction of the release of lysosomal enzymes; a direct protective effect on the sarcolemma (for the phenylalkylamines); a protective effect of the mitochondria and specific reduction of mitochondrial calcium transport (for benzothiazepines and some phenylalkylamines; attenuation of the ischaemia-reperfusion-induced displacement of endogenous noradrenaline (for the phenylalkylamines). Evidence of a protective role has been obtained in a variety of experiments provided the calcium antagonists were introduced prior to ischaemia. It is believed that this protective effect is an indirect consequence of the ability to modulate the function of the calcium channels and the energy-sparing effect is of major importance. Conversely, protection has not been obtained when calcium antagonists are added after ischaemia or during reperfusion. Thus is not surprising that when administered after the signs of human myocardial infarction, calcium antagonists do not reduce infarct size or avoid subsequent complications or decrease mortality. Diltiazem and verapamil, however, are two recent exceptions to this general tendency.
Calcium Channel Blockers↗
Reversal of left ventricular hypertrophy following recombinant human erythropoietin treatment of anaemic dialysed uraemic patients.
To clarify the role of chronic anaemia in the pathogenesis of the left ventricular hypertrophy (LVH) of chronic uraemia, nine normotensive dialysed patients were studied before and 3 and 6 months after start of intravenous treatment with recombinant human erythropoietin (rHuEpo). M-Mode echocardiographic estimations of left ventricular mass indices (LVMi) and plasma noradrenaline determinations were made at 3 and 6 months, and total blood volume (TBV) only at 6 months. Resting haemoglobin values were 5.9 +/- 1.3 (SD) g/dl, increased within 3 months to 10.2 +/- 1.2 (P less than 0.001), then remained unchanged. Baseline LVMi was 115 +/- 18 g/m2 body surface area (b.s.a.) and decreased significantly (P less than 0.0025) over the entire period to a final value of 78 +/- 13 g, which did not differ from the average value for 19 healthy controls. Resting plasma noradrenaline was 1.45 +/- 0.44 pmol/ml and did not change significantly, although values were reduced at the 3rd month, when decreased heart rates and slightly and non-significantly increased blood pressures were recorded. TBV did not vary because the increased erythrocyte mass was compensated for by parallel decreases in plasma volume. These data demonstrate the existence of a cause-effect relationship between uraemic anaemia and LVH, although the precise mechanism remains unknown. Amelioration of anaemia with rHuEpo, by allowing recovery from the attendant LVH, might improve long-term cardiovascular prognosis in some dialysed uraemic patients.
Adult↗
Protective effects of calcium antagonists against ischaemia and reperfusion damage.
The most positive results in this area have been those of the second Danish Study Group on Verapamil in Myocardial Infarction (1990) which assessed the benefit of treatment with verapamil from the second week after myocardial infarction. Verapamil produced a significant reduction in both mortality and reinfarction rates. Consequently, it may be concluded that treatment with calcium antagonists, such as verapamil and diltiazem, should not be used in the acute phase of myocardial infarction, but rather as prophylaxis to prevent reinfarction by protecting against myocardial ischaemia. The lack of reported cardioprotective efficacy with calcium antagonists, which contrasts with experimental predictions, can be explained by the inappropriate timing of administration and the use of dihydropyridine, which can be detrimental in myocardial infarction. These is little or no evidence to show that calcium antagonists are cardioprotective in patients with myocardial infarction or unstable angina. Thus, the randomised trials studying acute myocardial infarction reveal no overall effect of treatment on mortality in the short or long term. The prototype calcium antagonists differ in their effects on the reinfarction rate in these patients. With verapamil there is a small tendency for a reduction in reinfarction, with nifedipine a clear worsening, and with diltiazem a reduction almost reaching statistical significance. The general lack of protective efficacy is presumably a result of the drugs being administered too late after the onset of ischaemia.
Calcium↗
[Is lipid peroxidation responsible for the damage caused by postischemic reperfusion?].
Peroxidation of membrane phospholipid polyunsaturated fatty acids is considered a major mechanism of the damage occurring during post-ischemic reperfusion. The evidences in support for this mechanism of damage are based on tissue malondialdehyde (MDA) quantitation by the thiobarbituric acid test (TBA-test). In an attempt to verify this topic we have subjected isolated and Langendorff perfused rabbit hearts to a period of 60 min of severe ischemia plus 30 min of reperfusion. At appropriate time points MDA was determined in the tissue by means of TBA-test and directly by reversed phase, high pressure, liquid chromatography (HPLC). We have found no correlation between the 2 compared assays. During reperfusion, there was the formation of non-lipid related, MDA like, TBA-reactive substance which leads to overestimation of the extent of lipid peroxidation. On the contrary, by direct HPLC quantitation, there was a decrease of tissue MDA during ischemia and during the early phases of reperfusion. Our results demonstrate that TBA-test is not a reliable index of lipid peroxidation in organ systems and that MDA accumulation does not precede the evidence of the functional alterations occurring on reperfusion of the previously ischemic myocardium. These results are of relevance in the understanding of the exact mechanism of reperfusion damage as, in the same experimental model, oxy radicals have been shown to be generated and antioxidants are protective.
Animals↗
[Hemodynamic and clinical effects and treatment tolerance with low-dose iv amrinone in patients with refractory heart failure: a multicenter study. The Group for Research on Amrinone in the Treatment of Refractory Heart Failure].
We report the results of a multicenter study performed on 70 patients with severe congestive heart failure of different etiology (ischemic, idiopathic, alcoholic, valvular and secondary to antiblastic drugs) to evaluate the clinical and hemodynamic effects and tolerability of low dose amrinone iv (0.75 mg bolus followed by a continuous 48-hour infusion at the dose of 5-10 mcg/kg/min). Forty-one patients underwent invasive hemodynamic monitoring with right heart Swan-Ganz catheterization. Heart rate (HR), systolic (SBP) and diastolic blood pressure (DBP), mean arterial pressure (MAP), cardiac index (CI), stroke volume index (SVI), stroke work index (SWI), right atrial pressure (RAP), pulmonary wedge pressure (PWP), mean arterial pulmonary pressure (PAP), systemic vascular resistance (SVR), pulmonary vascular resistance (PVR) and total pulmonary resistance (TPR) were evaluated before and after 1, 4, 6, 24 and 48 hours of amrinone infusion and 2 and 4 hours after amrinone withdrawal. Clinical parameters (dyspnea, orthopnea, pulmonary congestion) were quantitated using a score; diuresis was assessed hourly; hematochemical parameters were evaluated before and 48 hours after amrinone infusion. HR and MAP were not significantly changed; CI, SVI and SWI presented, respectively, a significant 31.6, 55.1 and 72% increment, which peaked 48 hours after amrinone infusion. Concomitantly RAP, PAP, PWP, SVR, PVR and TPR were significantly reduced to 36.6, 22, 23.6, 9.4, 39.2 and 37.7% of the basal values, respectively. Two and 4 hours after amrinone withdrawal, hemodynamic changes similar to those observed acutely, were still present. Diuresis increased from 58.25 ml/hr to 113.18 ml/hr after 24 hours (+95%) and to 88.9 ml/hr (+53%) after 48 hours.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[The prognosis of the patient with heart failure: an analysis of the most significant clinical and instrumental parameters].
Despite the progress of the medical and surgical therapy of cardiac failure, the prognosis of this syndrome remains severe. We studied in a group of cardiac failure patients (n = 203; 18-74 years old) admitted in our division from 1982 to 1987 the most significant clinical and instrumental parameters of prognostic importance. The clinical parameters considered were: age, sex, heart rate, blood pressure, NYHA class, presence of mitral insufficiency, episodes of acute heart failure. The instrumental parameters were: presence of complete left bundle branch block (LBBB), atrial fibrillation, episodes of ventricular tachycardia, cardiothoracic index (C/T), end-diastolic and end-systolic diameters, ejection fraction (EF). Statistical analysis was performed in order to correlate single parameters with mortality. The total survival at 5 years was 50%, being higher in patients with coronary artery disease than in patients with primary dilated cardiomyopathy. The parameters worsening the prognosis were: mitral insufficiency, III-IV NYHA class, occurrence of repeated episodes of acute heart failure in the last year, complete LBBB, C/T greater than 0.55 and EF less than 20%. In conclusion, considering instrumental parameters high risk patients are detected with a precision of 80%.
Adolescent↗
[New findings on cardiac metabolism in ischemic cardiopathy].
This article review the biological and clinical importance of 2 potential outcomes of myocardial ischemia: the stunned and the hibernated myocardium. As for the stunned myocardium it is considered the possibility that either or oxygen free radicals, energy deficient or calcium overload are involved. As for the hibernated myocardium an hypothesis linked to the effects of intracellular acidosis and residual coronary flow on the metabolism of the myocyte is proposed.
Animals↗
[Malignant ventricular arrhythmias: nonpharmacological therapies].
In these last few years the indications for non pharmacological options in the therapy of malignant ventricular arrhythmias have been extended. Some of these approaches (antiarrhythmic surgery, cardiac transplant, automatic implantable cardioverter defibrillator) have an exact clinical collocation, some others are still experimental. Our personal experience and the recent literature have been analysed to explain the state of the art of these therapies. We undoubtedly think that these options are a valid alternative to drugs in non responder patients. The choice needs an accurate evaluation. The clinical picture, not only arrhythmic, and the specific aim of each procedure should be carefully considered.
Adolescent↗
[Radiography of a congress and significance of a society].
Explore the source record for details and available documents.
Cardiology↗
[From the viewpoint of fathers. From paternalism to paternity in service, organizational and pedagogical relations].
Explore the source record for details and available documents.
Family↗