Evidence of compensatory preload adjustment on early filling phase in patients with stable angina pectoris and good left ventricular systolic function.
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Adult↗
Biomedical subjects
O Visioli
Publications and source records attributed to O Visioli.
Tumor necrosis factor soluble receptors in patients with various degrees of congestive heart failure.
BACKGROUND: Tumor necrosis factor alpha (TNF-alpha) increases in patients with severe congestive heart failure (CHF) and cachexia. Two naturally occurring modulators of TNF-alpha activity have been identified in human serum. These two soluble proteins are the extracellular domains of the TNF receptors (sTNF-RI and sTNF-RII, respectively). The determination of circulating sTNF-Rs could provide us with some additional information about the activation of this cytokine in CHF. METHODS AND RESULTS: This study was undertaken to examine the concentration of sTNF-Rs and of bioactive and antigenic TNF-alpha in 37 consecutive patients with various degrees of CHF compared with that of 26 age-matched healthy subjects. Antigenic TNF-alpha increased (from 14.3 +/- 7.08 to 33.5 +/- 13.1 pg/mL, P < .001) in preterminal patients with severe CHF (New York Heart Association [NYHA] class IV). In these patients, sTNF-Rs were also increased (sTNF-RI from 1.17 +/- 0.43 to 4.43 +/- 2.14 ng/mL and sTNF-RII from 2.2 +/- 0.44 to 7.55 +/- 2.28 ng/mL, P < .001). When measured by cytolytic bioassay, TNF-alpha was undetectable (< 100 pg/mL). Addition of 625 pg/mL recombinant human TNF-alpha (rhTNF-alpha), corresponding in the bioassay to 60% of the lethal dose, to the serum of healthy subjects resulted in a significant increase of the expected cytotoxicity (from 625 to 1290 +/- 411 pg/mL, P < .001). Addition of the same dose of rhTNF-alpha to the serum of patients with mild to moderate CHF (NYHA classes II and III) increased the cytotoxicity from 625 to 877 +/- 132 pg/mL, P < .001. In 4 patients with severe CHF (class IV), the expected cytotoxicity was completely inhibited, whereas it was reduced from 625 to 263 +/- 198 pg/mL, P < .001, in the remaining 8 patients. Ten patients died within 1 month of entry into the study. They had the highest level of sTNF-RII (8.18 +/- 1.92 ng/mL). sTNF-RII was a more powerful independent indicator of mortality than TNF-alpha, sTNF-RI, NYHA class, norepinephrine, and atrial natriuretic peptide. CONCLUSIONS: Measurement of sTNF-Rs, in addition to antigenic and bioactive TNF-alpha, is essential for evaluation of the activation of this cytokine in CHF. Both sTNF-Rs increase in preterminal patients with severe CHF and might inhibit the in vitro cytotoxicity of TNF-alpha. Antigenic TNF-alpha also increases in severe CHF. The increased levels of sTNF-RII independently correlate with poor short-term prognosis.
Adult↗
Left ventricular false aneurysm: an unusually prolonged natural history.
A case of left ventricular false aneurysm of postinfarctual etiology with an unusually prolonged natural history (12 years survival) is reported. A first diagnosis of this rare cardiac complication was made in 1982 on the basis of hemodynamic and echocardiographic results. At that time the patient rejected surgical therapy. Eleven years later the patient came back to our attention after resuscitation from a sudden cardiac death. Hemodynamic and echocardiographic (transesophageal) tests showed a remarkable impairment of left ventricular function and an abnormal enlargement (10 x 8 cm) of a pseudoaneurysmatic cavity full of thrombi. The patient died suddenly in April 1994. We emphasize the unusual, prolonged survival of our patient suffering from an unresected left ventricular false aneurysm of postinfarctual etiology.
Aged↗
[Chronic thromboembolic pulmonary hypertension: a surgical syndrome?].
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Chronic Disease↗
[Contemporary medicine: between possibility and motivation].
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Clinical Medicine↗
Echocardiography during infusion of dobutamine for identification of reversibly dysfunction in patients with chronic coronary artery disease.
OBJECTIVES: The aim of this study was to test whether the contractile response of akinetic myocardium to low dose dobutamine is useful for detecting myocardial viability in patients with coronary artery disease and persistent left ventricular dysfunction. BACKGROUND: In some patients with chronic coronary artery disease, persistent abnormalities of left ventricular wall motion can be reversed by successful coronary artery bypass surgery. Thus, identification of potentially reversible dysfunction has important therapeutic and prognostic implications. Echocardiography during infusion of low dose dobutamine can detect viable myocardium in patients after thrombolytic therapy. However, there is no detailed information on the use of this method in patients with chronic left ventricular dysfunction without reperfusion. METHODS: We studied 33 selected patients with angiographically proved coronary artery disease and persistent left ventricular dysfunction. The effect of dobutamine infusion (5 micrograms/kg body weight per min, followed by 10 micrograms/kg per min) on left ventricular wall motion was evaluated by transthoracic echocardiography before coronary artery bypass grafting and compared with that obtained immediately after the operation (evaluated by intraoperative epicardial echocardiography) and both 2 weeks and 3 months later. Left ventricular wall motion was analyzed qualitatively by dividing the left ventricle into 16 segments, and a score was assigned to each region. RESULTS: Before coronary artery bypass surgery, 314 segments were akinetic. Of these, 183 became normokinetic immediately after revascularization, and 15 became hypokinetic. Dobutamine infusion was able to predict improvement in 178 of the 205 segments that recovered function after revascularization (sensitivity 86.8%) and to identify 89 of the 109 segments that did not recover postoperatively (specificity 81.6%). Mean (+/- SD) segment scores were 2.24 +/- 0.35 at baseline, 1.49 +/- 0.34 (p < 0.001) after dobutamine infusion, 1.51 +/- 0.38 (p < 0.001) immediately after and 1.51 +/- 0.38 (p < 0.001) 2 weeks after coronary artery bypass and 1.55 +/- 0.37 (p < 0.001) at 3-month follow-up. CONCLUSIONS: Echocardiography during infusion of low dose dobutamine is a safe and accurate method for identifying reversible dysfunctioning myocardium and predicts early reversibility of wall motion after surgical revascularization in selected patients with coronary artery disease with chronic left ventricular dysfunction.
Coronary Artery Bypass↗
How do calcium antagonists differ in clinical practice?
The majority of calcium antagonists used clinically belong to three distinct chemical classes: the phenylalkylamines, the dihydropyridines, and the benzothiazepines. In recent years their mode of action has been unravelled, their limitations recognized, and their efficacy and use in the management of patients with a broad spectrum of cardiovascular and other disorders defined. It is clear, however, that these drugs are not all alike, providing an explanation for their differing effects. The final therapeutic effect in humans depends on the mechanisms of action at the molecular level, the tissue selectivity, and the hemodynamic changes of each agent. All these aspects are examined in detail in this article. Concepts that are highlighted are as follows: (a) Molecular biology has allowed recognition of the polypeptide components of the alpha 1 subunit of the L-type Ca2+ channel and the finding of peptide segments covalently labelled by all three classes of drugs. (b) The location of these segments within the peptides is different: Binding sites for dihydropyridines are located externally, whereas those for verapamil and diltiazem are located internally, in the cytosolic part of the membrane. (c) Dihydropyridine binding is voltage dependent. This explains the selectivity of this class of drugs for vascular smooth muscle, which is more depolarized than cardiac muscle. (d) Phenylalkylamines and benzothiazepines reach their receptors at the internal surface of the sarcolemma through the channel lumen. Their binding is facilitated by the repetitive depolarization of atrioventricular and cardiac tissue, a phenomenon described as use dependence. This explains why these drugs are not highly selective, but equipotent for the myocardium, the atrioventricular conducting tissue, and the vasculature. (e) Dihydropyridines act through selective vasodilatation and may increase heart rate and contractility via a reflex mechanism. On the contrary, phenylalkylamines and diltiazem act through a combination of effects, including reduction of afterload, heart rate, and contractility. When taken together, all these differences distinguish the preferential clinical utilization of one of these compounds for a given cardiovascular pathology.
Binding Sites↗
Left ventricular dysfunction due to stunning and hibernation in patients.
Left ventricular dysfunction is in most cases the consequence of myocardial ischemia. It may occur transiently during an attack of angina and usually it is reversible. It may persist over hours or even days in patients after an episode of ischemia followed by reperfusion, leading to the so-called condition of stunning. In patients with persistent limitation of coronary flow, left ventricular dysfunction may be present over months and years, or indefinitely in subjects with fibrosis, scar formation, and remodeling after myocardial infarction. However, chronic left ventricular dysfunction does not mean permanent or irreversible cell damage. Hypoperfused myocytes can remain viable but akinetic. This type of dysfunction has been called hibernating myocardium. The dysfunction due to hibernation can be partially or completely restored to normal by reperfusion. It is, therefore, important to clinically recognize a hibernating myocardium. In the present article we evaluate stunning and hibernation with respect to clinical decision making and, when possible, we refer to our ongoing clinical experience.
Humans↗
Do inotropic drugs always induce a positive lusitropic effect? A comparison between k-strophanthidin and dobutamine in patients with coronary artery disease.
The interaction between systolic and diastolic effects of inotropic drugs is an important subject which has not yet been fully clarified in the cardiological literature. The effects of the inotropic drugs k-strophanthidin and dobutamine on left ventricular (LV) relaxation and early filling phase were compared in patients with coronary artery disease (CAD) and preserved systolic function. Twenty-two patients were randomly divided into two groups; group I was infused with 0.0035 mg.kg-1 of k-strophanthidin for 10 min and group II with dobutamine at a rate of 10 micrograms.kg-1.min-1 for 10 min. Both groups underwent simultaneous haemodynamic and echo 2D-Doppler evaluations at controlled heart rate. K-strophanthidin improved contractility indexes (peak of LV systolic pressure P < 0.001, max dP/dt + P < 0.05 and dP/dt P < 0.01) and worsened T constant and LV lowest diastolic pressure, (LVLDP) (P < 0.001 and P < 0.05 respectively) without changing early transmitral filling parameters. Dobutamine induced a significant increase in contractility in group II but at the same time significantly improved LV relaxation variables (max dP/dt - P < 0.01 and T constant P < 0.001). In addition, dobutamine reduced LVLDP (P < 0.05) and significantly increased LV early filling parameters. These results show that an acute administration of either k-strophanthidin or dobutamine enhances contractility, whereas these drugs have the opposite effect on the early diastolic phase.
Age Factors↗
Carotid sinus hypersensitivity and syndrome in patients with chronic atrial fibrillation.
Carotid sinus hypersensitivity (CSH) has been studied in subjects in sinus rhythm, but it has never been studied in patients with chronic atrial fibrillation (AF). After a finding of CSH in a patient with chronic AF and syncope, we studied the effects of carotid sinus stimulation in a group of patients with AF. Ten patients with chronic AF and normal ventricular rates who complained of dizziness or loss of consciousness underwent right and left carotid sinus massage (CSM) during ECG monitoring. A control group of ten patients with AF but without neurological symptoms was likewise investigated. CSH was present in eight symptomatic patients (5 patients presented right CSH, 1 left and 2 bilateral CSH), but only in three of the control patients. The mean duration of asystole induced by right CSM was 5.94 +/- 2.10 seconds; the mean asystolic interval induced by left CSM lasted 8.58 +/- 1.42 seconds. Six patients in the symptomatic group had a recurrence of spontaneous symptomatology during CSM, so that a diagnosis of carotid sinus syndrome was established. All symptomatic patients (8 patients with CSH, 2 patients with ventricular standstills but without CSH) received a permanent ventricular pacemaker. Following pacing, all patients, except for one with a significant drop of systolic blood pressure during CSM, became completely asymptomatic. In elder patients with chronic AF, CSH can induce prolonged ventricular asystole, which may be responsible for neurological symptoms such as dizziness, presyncope, or syncope, as observed in patients in sinus rhythm with carotid sinus syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
[Stable angina: long-term results].
We report on 345 patients who underwent percutaneous transluminal coronary angioplasty (PTCA) for stable angina in a 5-year period, with an average follow-up of 34 months (range 12-72). The primary success rate was 94.5%. The late mortality and incidence of myocardial infarction were 1.5% and 2.1% respectively. The rate of recurrence of angina was 34.5% and required PTCA (28.5%) and/or coronary artery bypass grafting (7%). At the end of follow-up 79.5% of patients were free from angina and a further 10% had improved. Our data confirm the importance of PTCA in stable angina.
Adult↗
Acute and chronic effects of the dihydropyridine calcium antagonist nisoldipine on the resting and exercise hemodynamics, neurohumoral parameters, and functional capacity of patients with chronic heart failure.
The acute and chronic effects of the dihydropyridine calcium antagonist nisoldipine were studied in patients with chronic heart failure (LV EF < .35; peak VO2 < 25 ml/kg/min) caused by idiopathic or postinfarction cardiomyopathy. The study group initially consisted of 16 patients; two patients were excluded from the acute study due to side effects of the drug and two more patients were excluded during the chronic part of the study because of excessive tachycardia or worsening heart failure, respectively; therefore, the final study group consisted of 12 patients. Each patient was evaluated at rest, in the supine and sitting positions, and during maximal bicycle exercise, before and after acute and chronic (2-3 months) oral nisoldipine therapy (20 mg bid). Plasma levels of renin activity, aldosterone, norepinephrine, and epinephrine were measured before and 1 hour after nisoldipine in 10 patients. Concomitant therapy with digitalis and diuretics was kept constant throughout the study. At rest, in the supine position, nisoldipine (20 mg orally) induced an acute increase of cardiac index from 2.87 +/- 0.52 to 3.93 +/- 1.52 l/min/m2, with a reduction of mean arterial pressure from 97 +/- 7 to 85 +/- 9 mmHg and systemic vascular resistance from 1417 +/- 201 to 968 +/- 257 dynes sec/sec cm5 without significant changes of right atrial and pulmonary pressures. Hemodynamic effects peaked 1 hour after its administration and persisted for 6 hours. Similar changes were observed in the resting sitting position.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Effectiveness of intravenous rTPA in the treatment of massive pulmonary embolism and right heart thromboembolism.
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Aged↗
Parapharyngeal space lesions syncope-syndrome. A newly proposed reflexogenic cardiovascular syndrome.
An intense vaso-vagal reaction characterizes those reflex cardiovascular syncopes in which the glossopharyngeal nerve constitutes the main afferent nerve pathway. In these syndromes, afferent fibres of the glossopharyngeal nerve project from the baroreceptorial area to the medullary cardiac and vasomotor centres, from which efferent fibres descend into the vagus. The most common reflex cardiovascular syndromes linked to the IX nerve are carotid sinus syndrome (CSS) and glossopharyngeal neuralgia-asystole syndrome (GNS). Eleven male patients (mean age 65.4 years) with recurrent and severe vaso-vagal attacks are described. The episodes were characterized by asthenia and general malaise, pallor, sudation, unrecordable or very low (40-60 mmHg) arterial blood pressure, mental disorientation and/or syncope. The admission diagnosis in these patients was CSS, but the clinical picture was quite different from classic CSS: triggering factors were not present, vasovagal episodes were longer, syncopes were more frequent and severe and VVI pacing was ineffective. Further investigation, including computerized tomography, showed in all patients a malignant or benign pathological growth occupying and compressing the parapharyngeal space. The authors think that the symptoms exhibited by their patients may be attributed to parapharyngeal space involvement. The pathogenetic mechanism of syncope in these cases could be similar to that occurring in GNS except for the absence of neuralgia itself. Surgical carotid sinus denervation or A-V sequential DDD pacing were ineffective in completely controlling symptoms. Intracranial section of the IX nerve appears to be the most effective mechanism for controlling the syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Cardioprotection by nisoldipine: role of timing of administration.
Nisoldipine was administered at 10(-9) M, a dose lacking negative inotropism, to isolated and perfused rabbit hearts submitted to 60 min ischaemia (1 ml.min-1) followed by 30 min reperfusion. The drug was delivered either 30 min before ischaemia, at the onset and after 30 min of ischaemia and during reperfusion only. Cardiac protection was evaluated in terms of recovery of left ventricular pressure during reperfusion, release of creatine phosphokinase (CPK), mitochondrial function, tissue content of adenosine triphosphate (ATP) and creatine phosphate (CP), calcium homeostasis and the occurrence of oxidative stress, established measuring content and release of reduced and oxidized glutathione. The cytoprotective action of nisoldipine occurs in the absence of negative inotropism and is closely related to the time of administration. Optimal myocardial preservation is achieved when nisoldipine is given before or at the onset of ischaemia. Prophylactic administration of nisoldipine improved the recovery of the developed pressure from 15.9 +/- 1.0 (SE) mmHg to 47.8 +/- 1.9 mmHg, P < 0.01 and reduced the release of CPK from 830 +/- 29 to 229 +/- 27 mU.min-1 g-1 wet wt, P < 0.01. The accumulation of tissue and mitochondrial calcium was reduced from 58 +/- 11 and 49 +/- 9 to 14 +/- 6 and 10 +/- 4 mmol.kg-1 dry wt respectively, P < 0.01. This resulted in a significant (P < 0.01) preservation of all indices of mitochondrial function, allowing a higher recovery of ATP and CP after reperfusion (from 4.1 +/- 0.7 and 10.0 +/- 0.6 to 16.1 +/- 1.0 and 29.9 +/- 0.2 mumol.g-1 dry wt respectively, P < 0.001). Reperfusion-induced myocardial accumulation and release of oxidized glutathione were reduced from 0.493 +/- 0.07 nmol.mg-1 protein and 0.768 +/- 0.063 nmol.min-1 g-1 wet wt to 0.225 +/- 0.07 and 0.157 +/- 0.038 respectively, P < 0.01. Similar data were obtained when nisoldipine was given at the time of ischaemia, while administration 30 min after the onset of ischaemia showed only a trend towards protection. Nisoldipine lost its protective effect when given on reperfusion. A multifactorial analysis of the data suggest that the cardioprotective effect of nisoldipine is related to the maintenance of membrane integrity, possibly since nisoldipine is highly lipophilic.
Adenosine Triphosphate↗
Myocardial damage during ischaemia and reperfusion.
Reperfusion, without doubt, is the most effective way to treat the ischaemic myocardium. Late reperfusion may, however, cause further damage. We attempted to identify the nature and time-course of metabolic changes occurring during ischaemia followed by reperfusion either in isolated and perfused rabbit hearts or in coronary artery disease (CAD) patients undergoing intracoronary thrombolysis or aortocoronary bypass grafting. In isolated hearts, reperfusion after prolonged ischaemia causes exacerbation of cell damage, leading to a breakdown of the permeability barrier of ions as well as of larger molecules, such as creatine phosphokinase. As consequence, reperfusion results in a large increase in intracellular calcium, leading to mitochondrial calcium overload with subsequent damage to the mitochondrial structure and loss of the ability to produce adenosine triphosphate (ATP). The ultimate mediator of the membrane damage is not known. It has been suggested that myocardial production of oxygen free radicals above the neutralizing capacity of the myocytes is an important cause of reperfusion damage. There is evidence that prolonged ischaemia reduces the naturally occurring defence mechanisms of the heart against oxygen free radicals, particularly mitochondrial manganese superoxide dismutase, and the intracellular pool of reduced glutathione. Consequently, reperfusion results in severe oxidative damage, as evidenced by tissue accumulation and release of oxidized glutathione. An oxygen free radical-mediated impairment of mechanical function also occurs during reperfusion of the human heart. During surgical reperfusion of CAD patients, we observed a prolonged and sustained release of oxidized glutathione; the degree of oxidative stress can inversely correlated with recovery of mechanical and haemodynamic function.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
[Stress and ischemic heart disease].
The role of mental stress in ischemic heart disease is two-fold: as a risk factor of coronary artery disease and as a trigger of acute ischemic attacks in patients with established coronary atherosclerosis. The role of stress as a risk factor is still controversial. Data regarding the relationship between occupational factors and development of coronary atherosclerosis have not been confirmed. A type personality, above all when anger and hostility traits are present, seems to be a predisposing factor for the development of coronary artery disease. These data however, were not confirmed in study groups including patients with a higher prevalence of other, more important, risk factors. Stress can have an important role as a trigger of acute ischemic attacks. This is indirectly shown by the circadian distribution of the main manifestations of ischemic heart disease (sudden death, myocardial infarct, ST segment depression). In fact, their incidence is significantly higher in the morning hours, after awakening, when mental stress is higher. In the laboratory setting, mental stress can induce myocardial ischemia in a variable percentage of patients (0 to 80%). Prevalence of mental stress-induced myocardial ischemia varies depending on the stressor used, the patients group and, above all, the diagnostic tool. Ischemic episodes induced by mental stress, in fact, are generally silent and less severe and extensive than those elicited by exercise stress testing. It is therefore often necessary to use methods, such as myocardial scintigraphy, with higher sensitivity for the detection of myocardial ischemia in comparison with ECG. Patients with mental stress-induced myocardial ischemia tend to present higher scores on measures of aggressivity, anger and hostility. These psychological features are related to a hightened cardiovascular reactivity with a brisk and greater increase in heart rate and blood pressure after exposure to stress. It would be therefore useful to identify patients with such a behaviour by psychological assessment and/or analysis of sympatho-vagal balance by analysis of heart rate variability. The mechanism by which mental stress can induce myocardial ischemia is represented by an increase in myocardial oxygen demand, through the increased heart rate and blood pressure, probably associated with an increase in coronary vascular resistance. This last phenomenon is likely caused by small coronary vessel constriction mediated by alpha-adrenergic activation and by a reduced EDRF release by the damaged endothelium.
Acute Disease↗
[Congestive heart failure: from cardiac muscle to skeletal muscle].
It is well established that in patients with chronic heart failure, exercise capacity and clinical symptoms such as fatigue or dyspnea correlate poorly with the extent of left ventricular dysfunction. The increase in cardiac output caused by vasodilators, cannot be translated immediately into increased exercise capacity and peak oxygen consumption in patients with chronic heart failure. These observations have prompted the hypothesis that in chronic heart failure intrinsic abnormalities of skeletal muscle emerge that prevent acute improvement in peak VO2 and blood lactate accumulation. Studies using nuclear magnetic resonance demonstrate abnormal skeletal muscle metabolism during exercise, even in the absence of reduced flow or under ischaemic conditions. Histological examination of skeletal muscle reveals a variable extent of atrophy, increased interstitial cellularity and increase in type IIb fibres. Ultrastructural analysis shows abnormalities indicative of depressed oxidative capacity. Biochemical analysis of skeletal muscle biopsies demonstrates reduced activity of enzymes involved in aerobic metabolism and free fatty acid accumulation. These data indicate morphological, biochemical and metabolic alterations of skeletal muscle that should contribute significantly to the reduced muscle strength and rapid fatigue in patients with chronic heart failure. It has also been speculated that a generalized myopathy may occur in a subset of patients with dilated cardiomyopathy. These findings have clinical implications. Prolonged immobilization of patients with chronic heart failure was often suggested, is not practised anymore. Physical training in chronic heart failure has been shown to improve skeletal muscle function, exercise capacity and clinical symptoms in small controlled trials. Pharmacological treatment might be targeted for skeletal muscle disorders in patients with heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
Chronic Disease↗