Abstract: OBJECTIVE: The aim of this study was to compare the effect of glimepiride and pioglitazone on endothelial function in patients with type 2 diabetes already on metformin. METHODS: Twenty-eight patients with type 2 diabetes already on metformin, without known cardiovascular disease, were randomized in 2 groups; glimepiride (4 mg od) was added in group A (n=14) and pioglitazone (30 mg od) in group B (n=14) for 6 months. Flow-mediated dilation (FMD) in the brachial artery was assessed in all patients, at baseline and at follow-up. RESULTS: The 2 groups did not differ in age (mean+/-S.D., 63.6+/-7.3 years vs 62.8+/-7.2 years respectively), or any measured variable at baseline. Fasting glucose and glycated haemoglobin improved similarly in both groups. There were significant differences between the 2 groups in the absolute changes observed at follow-up in waist circumference, +1.86+/-3.11 cm vs -1.86+/-1.88 cm in groups A and B respectively; fasting insulin levels, +14.79+/-12.56 pmol/L vs -25.84+/-28.09 pmol/L; homeostasis model assessment (HOMA), +0.66+/-1.01 vs -1.83+/-1.38; HDL cholesterol levels, -0.07+/-0.22 mmol/L vs +0.14+/-0.20 mmol/L and FMD, +0.14+/-1.09% vs +2.02+/-2.05% (p<0.05 for all). The only independent predictor factor of the FMD improvement was treatment-induced changes in HOMA (R(2): 0.488, slope: -0.782, [95% CI: -1.128, -0.436], p=0.0001). CONCLUSIONS: In patients with type 2 diabetes already on metformin, addition of pioglitazone as compared to glimepiride, improved endothelial function despite similar glycemic control. The improvement in endothelial function was mainly due to a reduction in insulin resistance.
Abstract: The arrhythmogenic effects of endothelin-1 (ET-1) are mediated via ETA-receptors, but the role of ETB-receptors is unclear. We examined the pathophysiologic role of ETB-receptors on ventricular tachyarrhythmias (VT/VF) during myocardial infarction (MI). MI was induced by coronary ligation in two animal groups, namely in wild-type (n = 63) and in ETB-receptor-deficient (n = 61) rats. Using a telemetry recorder, VT/VF episodes were evaluated during phase I (the 1st hour) and phase II (2-24 h) post-MI, with and without prior beta-blockade. Action potential duration at 90% repolarization (APD90) was measured from monophasic epicardial recordings and indices of sympathetic activation were assessed using fast-Fourier analysis of heart rate variability. Serum epinephrine and norepinephrine were measured with radioimmunoassay. MI size was similar in the two groups. There was a marked temporal variation in VT/VF duration; during phase I, it was higher (p = 0.0087) in ETB-deficient (1,519 +/- 421 s) than in wild-type (190 +/- 34 s) rats, but tended (p = 0.086) to be lower in ETB-deficient (4.2 +/- 2.0 s) than in wild-type (27.7 +/- 8.0 s) rats during phase II. Overall, the severity of VT/VF was greater in ETB-deficient rats, evidenced by higher (p = 0.0058) mortality (72.0% vs. 32.1%). There was a temporal variation in heart rate and in the ratio of low- to high-frequency spectra, being higher (<0.001) during phase I, but lower (p < 0.05) during phase II in ETB-deficient rats. Likewise, 1 h post-MI, serum epinephrine (p = 0.025) and norepinephrine (p < 0.0001) were higher in ETB-deficient (4.20 +/- 0.54, 14.24 +/- 1.39 ng/ml) than in wild-type (2.30 +/- 0.59, 5.26 +/- 0.67 ng/ml) rats, respectively. After beta-blockade, VT/VF episodes and mortality were similar in the two groups. The ETB-receptor decreases sympathetic activation and arrhythmogenesis during the early phase of MI, but these effects diminish during evolving MI.
Abstract: The effects of dual (ETA and ETB) endothelin receptor blockade on ventricular arrhythmogenesis during acute myocardial infarction are not well defined. We randomly allocated Wistar rats to bosentan (100 mg/kg daily, n=24), a dual endothelin receptor antagonist, or vehicle (n=23). After 7 days of treatment, myocardial infarction was induced by permanent coronary ligation. Ventricular tachyarrhythmias were evaluated for 24 h following ligation, using a miniature telemetry electrocardiogram recorder. Action potential duration was measured from monophasic epicardial recordings and sympathetic activation was assessed by heart rate variability and catecholamine serum level measurements. Compared to controls (1012+/-185 s), bosentan (59+/-24 s) markedly decreased (P<0.00001) the total duration of ventricular tachyarrhythmias during the delayed (1-24 h) phase post-ligation, with a modest effect during the early (0-1 h) phase (132+/-38 s, versus 43+/-18 s, respectively, P=0.053). Treatment did not affect infarct size or total mortality. Action potential duration at 90% repolarization prolonged in controls (from 93.1+/-4.7 ms to 117.6+/-6.9 ms), displaying increased temporal dispersion (from 4.14+/-0.45 ms to 10.42+/-2.51 ms, both P<0.001), but was preserved in treated animals. Bosentan decreased norepinephrine, but increased epinephrine levels 24 h post-ligation. Low frequency spectra of heart rate variability, an index of net sympathetic tone, were lower in bosentan-treated rats. Dual endothelin-1 receptor blockade decreases ventricular tachyarrhythmias during myocardial infarction without reperfusion, by preventing repolarization inhomogeneity. Diverse treatment effects on sympathetic activation may ameliorate the antiarrhythmic action.
Abstract: OBJECTIVE: Growth hormone and insulin-like growth factor-1 participate in post-myocardial infarction healing, but their relative importance is unclear. We compared the treatment effects of these agents on left ventricular remodelling. DESIGN: Wistar rats were randomised into a single dose of either growth hormone (0.5microg, n=29), or insulin-like growth factor-1 (0.5microg, n=27), delivered by direct intramyocardial punctures, and were compared with controls (n=30). Five minutes after treatment, myocardial infarction was generated by permanent ligation of the left coronary artery. Twenty-four hours post-ligation, serum levels of catecholamines were measured using radioimmunoassay and infarct size as well as infarct expansion index were calculated. The expression of genes related to extracellular matrix and angiogenesis was measured using polymerase chain reaction. RESULTS: Infarct expansion index was lower in growth hormone-treated rats (0.28+/-0.03, p=0.007) and in insulin-like growth factor-1-treated rats (0.35+/-0.03, p=0.044) compared to controls (0.51+/-0.06). Infarct size was significantly (p=0.0076) lower in growth hormone-treated rats (32.2+/-2.0%) and marginally (p=0.094) lower in insulin-like growth factor-1-treated rats (36.2+/-2.3%) compared to controls (42.0+/-2.7%). Survival rates were comparable in the three groups. Epinephrine was lower in the growth hormone group (2.8+/-0.2microg/l) compared to either controls (5.0+/-0.6microg/l, p=0.007), or to insulin-like growth factor-1-treated rats (6.3+/-0.6microg/l, p=0.0001). Collagen I and III expression in the infarct zone was higher in the growth hormone group compared to either the insulin-like growth factor-1 group or to controls. CONCLUSIONS: Both growth hormone and insulin-like-growth factor-1 decrease early infarct expansion, but growth hormone results in more favourable extracellular matrix remodelling and sympathetic activation.
Abstract: INTRODUCTION: The benefit of implantable cardioverter defibrillator (ICD) therapy in patients with haemodynamically stable ventricular tachycardia (VT) is not well documented. METHODS: In this single-centre observational study, we examined the medical records of 53 patients (48 men, mean age 66 +/- 1 years) treated with an ICD. The patients were classified into four groups with comparable clinical and electrophysiological characteristics, as follows: patients presenting with (a) stable VT, (b) unstable VT, (c) cardiac arrest, and (d) non-sustained VT and induced sustained VT or ventricular fibrillation (VF) on electrophysiological study. Kaplan-Meier event-free survival curves were constructed and the incidence of appropriate device therapy was compared among the four groups. RESULTS: All patients had structural heart disease with a mean ejection fraction of 32.5 +/- 1.3%. During a mean follow-up period of 35.5 +/- 2.7 months, event-free survival was similar in the four groups. However, appropriate device therapy occurred in 9 (81.8%) patients with stable VT, in 6 (44.4%) patients with unstable VT, in 2 (33.3%) patients with cardiac arrest and in 6 (33.3%) patients with non-sustained VT and induced sustained VT/VF. Compared to the total patient cohort, appropriate therapy was significantly (p = 0.024) more common in patients presenting with stable monomorphic VT. In 2 (22.2%) of these patients, the tachycardia rate was faster than the presenting VT. CONCLUSIONS: High recurrence rates are observed in patients with structural heart disease and stable VT, with a considerable proportion being faster than the presenting VT. ICD therapy is beneficial and should be offered in these patients.
Abstract: A two-peaked circadian variation in acute myocardial infarction has been demonstrated, with a morning peak attributed to physiological changes produced by nocturnal sleep. To investigate the causes of the secondary peak, we compared meal habits and circadian variation in patients with acute myocardial infarction who were accustomed to afternoon naps (group A) to those who were not (group B). One hundred and fifty two patients formed group A and 65 group B. The main meal was lunch in group A (77%) and dinner in group B (74%). Both groups displayed a significant circadian variation, (group A: x2=51.3, group B: x2=60.4, both p < 0.0001), but the secondary peak occurred earlier (2pm-4pm) in group A, than in group B (6pm-8pm). We conclude that ingestion of the main daily meal, followed by a period of physical inactivity, with or without sleep, is a trigger for acute myocardial infarction.
Notes: 1874-1754 (Electronic) xD;1874-1754 (Linking) xD;Comparative Study xD;Letter
Abstract: Clenbuterol, a compound classified as a beta2-adrenoceptor (AR) agonist, has been employed in combination with left ventricular assist devices (LVADs) to treat patients with severe heart failure. Previous studies have shown that chronic administration of clenbuterol affects cardiac excitation-contraction coupling. However, the acute effects of clenbuterol and the signaling pathway involved remain undefined. We investigated the acute effects of clenbuterol on isolated ventricular myocyte sarcomere shortening, Ca2+ transients, and L-type Ca2+ current and compared these effects to two other clinically used beta2-AR agonists: fenoterol and salbutamol. Clenbuterol (30 microM) produced a negative inotropic response, whereas fenoterol showed a positive inotropic response. Salbutamol had no significant effects. Clenbuterol reduced Ca2+ transient amplitude and L-type Ca2+ current. Selective beta1-AR blockade did not affect the action of clenbuterol on sarcomere shortening but significantly reduced contractility in the presence of fenoterol and salbutamol (P < 0.05). Incubation with 2 microg/ml pertussis toxin significantly reduced the negative inotropic effects of 30 microM clenbuterol. In addition, overexpression of inhibitory G protein (Gi) by adenoviral transfection induced a stronger clenbuterol-mediated negative inotropic effect, suggesting the involvement of the Gi protein. We conclude that clenbuterol does not increase and, at high concentrations, significantly depresses contractility of isolated ventricular myocytes, an effect not seen with fenoterol or salbutamol. In its negative inotropism, clenbuterol predominantly acts through Gi, and the consequent downstream signaling pathways activation may explain the beneficial effects observed during chronic administration of clenbuterol in patients treated with LVADs.
Abstract: OBJECTIVE: We investigated the relation between the endothelin system and atrial fibrillation. BACKGROUND: Endothelin has been implicated in the pathophysiology of atrial fibrillation, but the exact role of A- and B-receptors is unknown. METHODS: We obtained right atrial biopsies from patients in sinus rhythm and preserved left ventricular function, undergoing off-pump coronary artery bypass grafting. The expression of endothelin, A- and B-receptors was measured using real time reverse-transcribed polymerase chain reaction. RESULTS: We studied 52 patients (45 male, mean age 66+/-1 years, mean ejection fraction 52+/-1%). During a 5-day post-operative period, persistent atrial fibrillation occurred in 15 patients (28.8%). Endothelin mRNA expression was comparable in patients who subsequently developed atrial fibrillation and in those maintaining sinus rhythm. However, the former group displayed down-regulation of endothelin A- (by approximately 60%, p=0.0059) and of B-receptors (by approximately 40%, p=0.0084). The decreased endothelin A-receptor expression could predict atrial fibrillation occurrence (Wilks lambda=0.86, F=6.16, p=0.017). CONCLUSION: Decreased endothelin A- and B-receptor expression is associated with atrial fibrillation after bypass surgery.
Abstract: GH (growth hormone) administration during acute MI (myocardial infarction) ameliorates subsequent LV (left ventricular) dysfunction. In the present study, we examined the effects of such treatment on arrhythmogenesis. A total of 53 Wistar rats (218+/-17 g) were randomized into two groups receiving two intraperitoneal injections of either GH (2 international units/kg of body weight; n=26) or normal saline (n=27), given at 24 h and 30 min respectively, prior to MI, which was generated by left coronary artery ligation. A single-lead ECG was recorded for 24 h post-MI, using an implanted telemetry system. Episodes of VT (ventricular tachyarrhythmia) and VF (ventricular fibrillation) during the first hour (phase I) and the hours following (phase II) MI were analysed. Monophasic action potential was recorded from the lateral LV epicardium at baseline and 24 h post-MI, and APD90 (action duration at 90% of repolarization) was measured. Infarct size was calculated 24 h post-MI. Infarct size and phase I VT+VF did not differ significantly between groups, but phase II hourly duration of VT+VF episodes was 82.8+/-116.6 s/h in the control group and 18.3+/-41.2 s/h in the GH group (P=0.0027), resulting in a lower arrhythmic (P=0.016) and total (P=0.0018) mortality in GH-treated animals. Compared with baseline, APD90 was prolonged significantly 24 h post-MI in the control group, displaying an increased beat-to-beat variation, but remained unchanged in the GH group. We conclude that GH decreases phase II VTs during MI in the rat. This finding may have implications in cardiac repair strategies.
Abstract: OBJECTIVE: Cardiac ascites remains a rare entity with unique clinical and pathogenetic features that are not adequately recognized by clinicians. The purpose of this study was to contribute towards elucidating the nature of cardiac ascites. MATERIAL AND METHODS: We describe a series of 26 ascitic fluid samples from eight patients with cardiac ascites that were referred and further evaluated for the etiology and nature of their ascites. RESULTS: In all samples ascitic fluid was an exudate with an increased serum-ascitic fluid albumin gradient, a pattern unique in ascites. Other causes of ascites were excluded, often through a protracted differential diagnostic procedure. CONCLUSIONS: The unique pattern of cardiac ascites should allow for rapid diagnosis and characterization: The clinical implications of furosemide use in its response and biochemical properties warrant further description.
Abstract: The effects of dronedarone, a non-iodinated derivative of amiodarone, on ventricular tachycardia and ventricular fibrillation post-myocardial infarction are not well established. Fifty-five Wistar rats were randomly allocated to a 2-week oral treatment with either vehicle (n=18), amiodarone (30 mg/kg, n=20), or dronedarone (30 mg/kg, n=17). After acute coronary artery ligation, a single-lead electrocardiogram was continuously recorded for 24 h and episodes of ventricular tachycardia/fibrillation as well as mortality rates were analysed. Monophasic action potential recordings were obtained from the left ventricular epicardium at baseline and 24 h post-myocardial infarction. Thyroid hormones and catecholamines were measured using radioimmunoassay. Thyroid function was similar in the 3 groups. Compared to controls, amiodarone and dronedarone equally decreased the number of ventricular tachycardia/fibrillation episodes by approximately 75%. Both agents prevented the increase in monophasic action potential duration and in beat-to-beat variation. Norepinephrine levels were lower only after amiodarone treatment. Despite the observed antiarrhythmic effect, total mortality did not differ between groups (38.8% in controls, 30.0% in the amiodarone group and 58.8% in the dronedarone group), because of excess bradyarrhythmic mortality in both drug groups that reached significance in the dronedarone group. Dronedarone and amiodarone display similar antiarrhythmic efficacy post-myocardial infarction, partly by preventing repolarization inhomogeneity. However, dronedarone increases bradyarrhythmic mortality possibly secondary to its negative inotropic effects.
Notes: 0014-2999 (Print) xD;0014-2999 (Linking) xD;Comparative Study xD;Journal Article
Abstract: INTRODUCTION: Pulmonary hypertension portends an adverse outcome. Animal models have improved current understanding of the complex pathophysiology of the disease, but may be technically demanding. Moreover, plexiform vascular lesions are rarely observed, limiting the extrapolation to human pathophysiology. The aim of the present study was first, to assess the feasibility of closed-chest pressure recordings, and mainly, to further characterise a new model of endothelin receptor-B deficient rats. METHODS: Jugular venous catheterisation was assessed in 15 Wistar rats. Pressure recordings via a left lateral thoracotomy and histological findings were compared in three rat groups (age 20 +/- 1 weeks, weight 200-250 g): (a) wild type (n = 10, group A); (b) wild type after monocrotaline injection (n=10, group B); and (c) endothelin receptor-B deficient rats (n = 10, group C) after monocrotaline injection. RESULTS: Pressure recordings via the jugular approach were feasible in only 3 (20%) rats. Compared to group A, there was a trend (H = 4.6, p = 0.0962) towards increased mortality in groups B and C, due to respiratory arrest during intubation attempts. Pulmonary artery systolic pressure in group C was 24.7 +/- 1.3 mmHg, higher than in group B (21.5 +/- 1.2, p = 0.036) or group A (11.8 +/- 0.5, p < 0.0001). Adverse pulmonary vascular remodelling was more prominent in group C than in group B. CONCLUSIONS: Endothelin receptor-B deficient rats constitute a useful model of pulmonary artery hypertension after monocrotaline injection. The ease of pressure recordings via a left lateral thoracotomy may aid in the more widespread use of this model.
Abstract: OBJECTIVE: Although nitroglycerin- and isoproterenol-augmented tilt tests are of equal value in the diagnosis of neurocardiogenic syncope in adults, no data exist in children. We compared the sensitivity and specificity of the 2 tests in a pediatric population. PATIENTS AND METHODS: We studied 85 patients (33 boys; mean age: 11.6 +/- 2.9 years). Of them, 56 had a diagnostic history of neurocardiogenic syncope, whereas 29 served as controls. After a negative passive phase, they were randomly assigned to either intravenous isoproterenol or sublingual nitroglycerin, and tilt was continued for 20 minutes. RESULTS: Sensitivity was 0.78 for the isoproterenol test and 0.79 for the nitroglycerin test, but specificity was significantly higher for isoproterenol test compared with nitroglycerin test. In patients with a positive test, the duration of the recovery period was significantly longer after nitroglycerin (8.4 +/- 2.7 minutes) than after isoproterenol (5.1 +/- 1.6 minutes). CONCLUSIONS: Nitroglycerin- and isoproterenol-augmented tilt tests are associated with equal sensitivity in the diagnosis of neurocardiogenic syncope in children and adolescents. However, nitroglycerin results in more false-positive tests and produces more prolonged vasovagal symptoms. Our data do not support the routine use of nitroglycerin in the evaluation of syncope in this age group.
Abstract: AIMS: This study investigated whether chronic and acute amiodarone treatment has differential effects on ventricular arrhythmogenesis during acute myocardial infarction in rats. METHODS AND RESULTS: Forty-six rats were randomly allocated into vehicle, chronic oral amiodarone (30 mg/kg daily for 2 weeks), or acute amiodarone (a single dose, 100 mg/kg). Five additional rats were sham-operated. Myocardial infarction was generated by left coronary artery ligation 2 weeks after chronic treatment. Amiodarone was administered acutely 5 min post-ligation. The electrocardiogram was recorded for 24 h, using an implanted telemetry transmitter. Episodes of ventricular tachyarrhythmias and mortality rates were analysed. Serum catecholamines and infarct size were measured 24 h post-ligation. No differences were found in infarct size. Compared with controls (22.7 +/- 10.9), there was a similar reduction in the number of tachyarrhythmia episodes after either chronic (2.6 +/- 1.6, P = 0.0011) or acute (3.6 +/- 1.7, P = 0.031) amiodarone administration. Norepinephrine levels were lower only after chronic treatment. Mortality in both amiodarone treatment arms was exclusively due to bradyarrhythmia secondary to cardiac failure, whereas mortality in controls was mainly attributed to tachyarrhythmic death. CONCLUSIONS: A rapid antiarrhythmic effect was observed after acute amiodarone administration in the rat. Norepinephrine levels decreased after chronic treatment and may be associated with bradyarrhythmic mortality.
Abstract: Atrial fibrillation (AF) is the most common arrhythmia encountered in clinical practice representing a major health hazard. Owing to relative inefficacy and side effects of classic antiarrhythmic drugs, current interest has shifted to treatments that target AF substrate. Accumulating evidence suggests that there is a link between oxidative processes and AF. In atrial myocardium during AF, there is substantial oxidative damage that may contribute to atrial remodeling. Several pathophysiological changes that possibly associated with increased oxidative stress in AF have been proposed. These include changes in gene transcriptional profiles and mitochondrial DNA, increased activity of enzymes such as NAD(P)H oxidase and xanthine oxidase, inflammatory processes, activation of the renin-angiotensin system and others. Moreover, oxidative stress is involved in the pathophysiology of several predisposing factors and cardiovascular disorders that correspondingly associated with AF. Preliminary studies using dietary antioxidants such as vitamin C have shown promising results. More evidence has been obtained from studies examining agents with pleiotropic effects, including antioxidant, such as inhibitors of the renin-angiotensin system, statins, corticosteroids and carvedilol. Further investigations are needed in order to elucidate the impact of oxidative stress on atrial remodeling. The clarification of these processes in the setting of AF may lead to the development of novel therapeutic strategies.
Abstract: Asynchronous depolarization and contraction sequence, secondary to intraventricular conduction defects or to permanent right ventricular apical pacing, is associated with adverse effects that may be clinically evident in the failing heart. Experimental and clinical studies have suggested that asynchronous ventricular contraction deteriorates left ventricular performance and induces unfavourable left ventricular remodelling. Although such contraction does not appear to affect resting coronary artery blood flow, it increases endomyocardial pressure during diastole and decreases regional myocardial perfusion in the interventricular septum. The magnitude of these effects may correlate with the duration of the asynchrony. Despite these detrimental effects, there is no evidence that ventricular asynchrony reduces collateral myocardial blood flow, myocardial oxygen consumption or cardiac efficiency, neither in patients with normal coronary arteries, nor in patients with coronary artery disease. Furthermore, in patients with acute ischaemic syndromes, ventricular asynchrony exerts a neutral effect on the ischaemic myocardium. Cardiac resynchronization therapy improves left ventricular systolic and diastolic function without an increase in myocardial oxygen consumption or energy cost. This therapy may decrease the inhomogeneity in regional oxidative metabolism, myocardial perfusion and cardiac efficiency. Further experimental and clinical studies are needed on this area.
Abstract: Partial right-sided pericardial defect is an extremely rare congenital anomaly and is often associated with other congenital abnormalities. We describe a unique case of congenital aortic valve disease associated with right-sided pericardial defect. The clinical implications are discussed and a review of the literature is presented.
Abstract: We describe herein the case of a 49-year-old female patient with pulmonary sarcoidosis (stage II) with cardiac manifestation. This consisted of systolic dysfunction without dilatation of the left ventricle and severe mitral insufficiency, possibly due to thinning of the posteromedial left ventricular free wall, based on our echocardiographic observations.
Abstract: OBJECTIVE: Ventricular remodeling is a common corollary of myocardial infarction. We hypothesized that this process may be attenuated by growth hormone, administered as a single high-dose, selectively in the infarct zone, early postmyocardial infarction. DESIGN: In 35 pigs (29+/-4 kg), myocardial infarction was generated by inflation of an over-the-wire angioplasty balloon in the circumflex artery for 60 min and 5 further pigs were sham-operated. Ten minutes after reperfusion, the pigs were randomized (2:1) to either growth hormone (1 IU/kg) (n=23) or normal saline (n=12), delivered via the balloon catheter. All survivors were treated with captopril and were sacrificed 4 weeks after myocardial infarction. RESULTS: Compared to controls, growth hormone-treated animals displayed lower heart weight (4.1+/-0.5 g/kg body weight, versus 3.4+/-0.4 g/kg, respectively, p=0.003) and dimensions (left ventricular short axis diameter 46+/-7 mm versus 37+/-6 mm, p=0.01; right ventricular short axis diameter 38+/-7 mm versus 30+/-5 mm p=0.001). Growth hormone increased wall thickness in the infarct (6.0+/-1.8 in controls versus 9.9+/-3.7 in treated animals, p=0.004) and non-infarct zones (10.6+/-1.8 in controls versus 15.5+/-3.8 in treated animals, p=0.0006) and produced higher (p<0.05) microvascular density in both zones. CONCLUSION: Intracoronary administration of growth hormone attenuates left and right ventricular remodeling by inducing hypertrophy and by enhancing angiogenesis.
Abstract: OBJECTIVE: To assess the effectiveness and safety of pharmacological conversion of persistent atrial fibrillation (AF) with a combined propafenone plus ibutilide regimen. METHODS AND RESULTS: 100 consecutive patients (66 men, mean (SD) age 65 (10) years) with persistent AF (mean (SD) duration 99 (92) days) admitted for elective pharmacological cardioversion were randomly assigned to treatment with either intravenous ibutilide (1 mg plus an additional 1 mg, if required; n = 51) or oral propafenone (600 mg) plus intravenous ibutilide at the same dose (n = 49). Success rates were 41.1% (21 of 51 patients) for ibutilide alone and 71.4% (35 of 49 patients) for propafenone plus ibutilide (p = 0.0044). However, cardioversion occurred earlier in the ibutilide alone group (55 (20) minutes) compared with the combination group (81 (32) minutes, p = 0.0019). A comparable increase in the QTc interval was observed in both groups but one case of sustained torsade de pointes, requiring electrical cardioversion, was observed in the propafenone plus ibutilide group. No other complications were noted during the hospitalisation period. CONCLUSION: Concurrent administration of propafenone plus ibutilide for pharmacological cardioversion of persistent AF is safe and more effective than ibutilide alone.
Abstract: We report a case of successful radiofrequency catheter ablation in a patient with dilated cardiomyopathy, who presented with multiple, haemodynamically poorly tolerated episodes of monomorphic ventricular tachycardia, resistant to antiarrhythmic drug treatment. The ablation procedure consisted of focal ablation of three mapped left ventricular sites, using pace and activation mapping. Additional linear ablation lesions were created across these sites. After the procedure, the patient remained free of tachycardia episodes and seven days post-ablation he underwent implantation of a cardioverter-defibrillator. During a twelve-month follow-up period, the patient has remained free of monomorphic ventricular tachycardia episodes. Radiofrequency catheter ablation is feasible in electrical storm, using conventional mapping techniques, even in haemodynamically unstable tachycardias.
Abstract: We report a case of transient complete atrioventricular block in a 38-year-old man, after intake of a mixture of herbs, intended to aid cigarette smoking cessation. Since all other causes of conduction disturbances were excluded, a side-effect of the herbal remedy was identified as the most likely diagnosis. Given that most patients are unaware of the potential risks of the intake of various herbs, we would urge that their usage be regulated.
Abstract: BACKGROUND: Intrapericardial drug delivery is a promising new technique, but the pharmacologic properties of various agents delivered via this route are not known. Furthermore, the long-term safety of intrapericardial catheters has not been previously examined. METHODS: Using a pericardial access device, a catheter connected to a drug-delivery system was implanted in five pigs. Plasma levels and electrocardiographic measurements were obtained after intravenous and intrapericardial administration of digoxin and procainamide. Histological examination was performed after the device had been implanted for a total of 6 months. RESULTS: The QTc interval did not change significantly after digoxin or procainamide intravenous administration. QTc decreased by 47+/-23 ms (p=0.046) 8 h after digoxin intrapericardial administration and increased by 128+/-60 ms (p=0.002) 1 h after procainamide intrapericardial administration. The QRS duration did not change significantly after intravenous administration of either agent, but it increased by 17+/-9 ms (p=0.004) 1 h and by 15+/-4 ms (p=0.01) 8 h after procainamide intrapericardial administration. After intravenous procainamide the RR interval decreased, but it did not change significantly after intrapericardial administration of either agent. Histology showed moderate inflammatory infiltration and fibrosis adjacent to the catheter. CONCLUSIONS: Intrapericardial delivery of digitalis and procainamide produces unique electrophysiological properties. In contrast to satisfactory success of the implantation technique, long-term dwell of the catheter in the pericardium induces moderate, albeit probably clinically significant, fibrosis.
Abstract: OBJECTIVE: Endothelin-1 (ET-1) production increases during acute myocardial infarction (MI) and may contribute to the genesis of ventricular tachycardia (VT) and ventricular fibrillation (VF). However, the antiarrhythmic effects of ET-1 receptor blockade, examined shortly after MI, have been debated. In the present study, we examined the effects of such treatment on VT/VF during the first 24 h post-MI. METHODS: Thirty-five Wistar rats (223+/-22 g) were randomly allocated to either the ET-1 receptor-A (ETA) antagonist BQ-123 (0.4 mg/kg, BQ-123 group, n=17), or normal saline (control group, n=18) and were subjected to coronary artery ligation. A single-lead electrocardiogram was continuously recorded for 24 h post-MI, using an implanted telemetry system, and episodes of VT/VF were analyzed. Monophasic action potential (MAP) recordings were obtained from the left (LV) and right (RV) ventricular epicardium at baseline, 5 min after treatment and 24 h post-MI. RESULTS: There were 15.94+/-19.35 episodes/h/rat of VT/VF in the control group and 1.66+/-2.22 in the BQ-123 group (p=0.010), resulting in a lower (p=0.030) arrhythmic mortality in treated animals. The mean episode duration was 7.40+/-7.16 s for the control group and 2.30+/-1.37 s for the BQ-123 group (p=0.011). The maximum decrease in VT/VF was observed during the 1st, 5th and 6th hours post-MI. In the control group, LV MAP duration increased 24 h post-MI, displaying an increased beat-to-beat variation, but remained unchanged in the BQ-123 group. CONCLUSION: Acute ETA blockade reduces the incidence of VT/V F during the first 24-h post-MI in the rat, through a decrease in the dispersion of repolarization.
Abstract: Left ventricular (LV) remodeling after myocardial infarction (MI) may lead to congestive heart failure, disability and death. It consists of expansion of the infarct zone and dilatation of the non-infarcted myocardium, causing shape distortion and ventricular enlargement. Experimental studies have shown that treatment with growth hormone (GH) stimulates cardiac repair, resulting in increased infarct zone collagen scar formation and possibly enhanced proteinosynthesis. These actions may ameliorate the process of LV remodeling. We hypothesize that these beneficial effects may be more prominent, if GH is delivered selectively in the infarct area, during the early phase of acute MI. Experimental and clinical studies are necessary to validate this hypothesis.
Abstract: Inflammation has been recently implicated in the pathophysiology of atrial fibrillation (AF). The aim of this study was to examine the variation of inflammatory indexes during the first week after successful electrical cardioversion of persistent AF. Successive measurements of white blood cell (WBC) count, C-reactive protein (CRP) and fibrinogen levels were performed in 30 cardioverted patients. At the end of the 7-day follow-up period, AF had recurred in 30% of patients. A significant variance was found in serial measurements of fibrinogen levels in the two groups (non-relapse and relapse, p = 0.005). Fibrinogen levels increased significantly in patients who relapsed into AF, but remained stable in patients who remained in sinus rhythm. In the latter patients, CRP values tended to decrease post-cardioversion, but WBC count was significantly lower (p < 0.001) on the 7th day (6083 +/- 1335), compared with baseline values (6648 +/- 1395). The variation of inflammatory indices post-cardioversion might have prognostic implications with regard to sinus rhythm maintenance.
Notes: 1368-5031 (Print) xD;1368-5031 (Linking) xD;Comparative Study xD;Journal Article
Abstract: BACKGROUND: Inflammation and oxidative stress have been recently implicated in the pathophysiology of atrial fibrillation (AF). The aim of this study was to examine the potential benefit of vitamin C on the early recurrence rates and on inflammatory indices after successful cardioversion of persistent AF, as well as to investigate the time course of changes in these indices post-cardioversion. METHODS: We prospectively studied 44 consecutive patients after successful electrical cardioversion of persistent AF. All patients received standard treatment and were randomised in one to one fashion to either oral vitamin C administration or no additional therapy. We followed-up the patients for 7 days performing successive measurements of white blood cell (WBC) count, C-reactive protein (CRP), fibrinogen, and ferritin levels. RESULTS: One week after successful cardioversion, AF recurred in 4.5% of patients in the vitamin C group and in 36.3% of patients in the control group (p=0.024). Compared to baseline values, inflammatory indices decreased after cardioversion in patients receiving vitamin C but did not change significantly in the control group. A significant variance was found in the serial measurements of WBC counts (F=5.86, p=0.001) and of fibrinogen levels (F=4.10, p=0.0084) in the two groups. In the vitamin C group CRP levels were lower on the seventh day (p<0.05). CRP and fibrinogen levels were higher in patients who relapsed into AF compared to patients who maintained sinus rhythm (F=2.77, p=0.044 and F=3.51, p=0.017, respectively). CONCLUSIONS: These findings suggest that vitamin C reduces the early recurrence rates after cardioversion of persistent AF and attenuates the associated low-level inflammation. These effects indicate that therapeutic approaches targeting at inflammation and oxidative stress may exert favourable effects on atrial electrical remodeling.
Abstract: Atrial fibrillation (AF) is the most common arrhythmia encountered in clinical practice while it has a significant impact on morbidity and mortality. The errors and pitfalls in the management of AF patients are not uncommon. These include errors in detection and management of the underlying conditions that promote and perpetuate the arrhythmia, in the selection and monitoring of antithrombotic treatment, in the selection of appropriate strategy for arrhythmia management (rate or rhythm control), in the cardioversion procedure, in the prevention of recurrence after cardioversion, in the acute or chronic control of heart rate, and in the monitoring of drug toxicities. The heterogeneity of the disease along with the diversity of current treatment options mainly account for these problems. Nevertheless, deep knowledge of the evidence-based therapeutic approaches, as well as the development of individualized therapeutic strategies, can substantially improve the effective management of such patients.
Abstract: We evaluated the extent of agreement among three algorithms used for the localization of accessory pathways in patients with overt preexcitation. By the use of one algorithm, three independent couples of observers localized the accessory pathway in 95 consecutive patients showing overt preexcitation in the 12-lead surface electrocardiogram. We defined the following regions: Left atrioventricular ring (LAVR), Right atrioventricular ring (RAVR), Left lateral/left anterolateral (LL/LAL), Left posterior/left posterolateral (LP/LPL), Left posteroseptal (LPS), Right midseptal (RMS), Right posteroseptal (RPS), Right posterior/right posterolateral (RP/RPL), Right lateral/right anterolateral (RL/RAL), and Right anterior/right anteroseptal (RA/RAS). The extent of agreement in each region was evaluated and compared with the expected one, as calculated from the reported. The extent of agreement was as expected: (1) high in the regions LAVR, RAVR, LL/LPS and (2) limited in the regions LPS, RPS, and (3) clearly lower than expected in the regions LP/LPL, RA/RAS, RMS, RL/RAL. In cases with total or partial disagreement, the number of electrocardiograms with duration of QRS complex smaller than 120 ms was greater than in cases with total agreement (30/46 vs 22/50, P < 0.05). The observed agreement among algorithms is clearly lower than the expected one. Minimal preexcitation, limited number of patients, and arbitrarily defined regions were possibly the reasons for some unexpected results.
Abstract: Gallstone ileus is an unusual cause of colonic obstruction. The formation of a fistula between the gall bladder and the bowel wall may allow a gallstone to enter the intestinal tract. Plain abdominal films, abdominal ultrasound and abdominal computed tomography aid in the diagnosis. Although surgery is the treatment of choice in cases of colonic gallstone ileus, colonoscopic removal of the impacted stone should be attempted. We describe the case of an 85-year-old man who presented with symptoms and signs of large bowel obstruction. Diagnostic evaluation revealed a large gallstone impacted in the sigmoid colon, which is a rather unusual impaction site. Despite our efforts we could not extract the stone endoscopically, mainly due to its large size. Yet, despite its large size, the stone was spontaneously evacuated a few hours later.
Abstract: Three cases of local thrombolysis in the treatment of acute lower limb ischemia complicating the utilization of the Duett sealing device are presented. Routine usage of several vascular closure devices after cardiac catheterization and percutaneous coronary intervention (PCI) has been adopted in our institution during the last 3 years (September 1999 to April 2003). The Duett closure device has been used in 420 patients (post-coronary angiography, 359; post-PCI, 61). Three patients (0.7%) demonstrated acute leg ischemia used by inadvertent intravascular administration of the sealing material related to this device. All three were treated successfully by catheter-directed local thromolysis (tissue plasminogen activator 5 mg bolus followed initially by 1 mg/hr and consequently by 0.5-1.0 mg/hr depending upon the development of significant hematoma and lasting for 24 hr). In conclusion, interventional treatment using local thrombolysis should be the first-line treatment in acute lower limb ischemia complicating the utilization of the Duett sealing device.
Abstract: Inadvertent implantation of a pacemaker lead in the left ventricle is an uncommon complication. We report a case of a permanent pacemaker lead inadvertently placed through the left subclavian artery, across the aortic valve into the left ventricle. A chest X-ray one month after the procedure showed an unusual course of the lead and a 12-lead ECG and a transthoracic echocardiogram confirmed the diagnosis. The patient refused surgical removal and remained on full anticoagulation. No clinical events were recorded during a 3-year follow-up. In such cases we propose life-long full anticoagulation as an alternative to surgical lead extraction.
Abstract: Selective endothelin receptor-A antagonists are a promising new treatment in patients with heart failure and/or pulmonary hypertension. Animal studies have suggested that these agents may have additional cardiac electrophysiologic actions, however, no data exist in man. We examined the effects of acute endothelin receptor-A blockade on the sinus node, the atrioventricular node and on the ventricular myocardium, in patients with single-vessel coronary artery disease and preserved left ventricular function. The selective endothelin receptor-A antagonist BQ-123 was administered by the intracoronary route, in order to achieve maximum local cardiac effects. After endothelin receptor-A blockade, QT interval increased from 373 +/- 30 msec (mean +/- SD) to 395 +/- 20 msec (p < 0.01) and QTc interval increased from 394 +/- 36 msec to 421 +/- 28 msec (p < 0.01). QT-dispersion, calculated from 12-lead ECG, decreased from 40 +/- 18 msec to 24 +/- 8 msec (p < 0.01) and QTc-dispersion decreased from 44 +/- 20 msec to 26 +/- 9 msec (p < 0.05). These changes were evident only after infusion in the left, but not in the right coronary artery. No effect was found on the sinus node, the atrioventricular node, or the ventricular effective refractory periods. We conclude that selective endothelin receptor A blockade lengthens ventricular repolarization and decreases its inhomogeneity. Further studies are needed to evaluate possible antiarrhythmic actions of this class of agent.
Abstract: Swimming in cold water during the winter season is an extreme sport, with fans all over the world. However, its effects on health have been debated. This article examines the hypothesis that the effects of winter swimming may depend on previous exposure to cold stimuli. Immersion in cold water in unaccustomed persons may lead to detrimental consequences, while, in regular winter swimmers, adaptive physiologic mechanisms increase tolerance to cold. Furthermore, these mechanisms may prevent the occurrence of a wide variety of diseases. Prospective studies and epidemiological data are needed to test this hypothesis.
Abstract: An 82-year old man was admitted with acute pulmonary edema. Myocardial ischemia and electrolyte abnormalities were excluded and he responded promptly to frusemide, nitrates and morphine. On admission, the duration of the QRS interval was markedly abnormal at 240 ms with a nonspecific intraventricular conduction defect pattern, of left bundle branch block type. This finding was not present three weeks prior to his admission, and was felt to be the result of drug interaction between propafenone and antineoplastic agents, as evidenced by resolution of the clinical and electrocardiographic picture after discontinuation of these agents.
Abstract: Atrial fibrillation (AF) represents the most common arrhythmia encountered in clinical practice. The pathophysiology of AF is complex, but in most cases it may be caused by multiple random re-entering wavelets. As generally known, the development of AF leads to electrophysiological and cellular changes in the atria that tend to sustain AF, a process known as electrical remodeling. In addition, it has been proposed that electrical remodeling contributes to the high incidence of early recurrence of AF after cardioversion. The principal characteristics of this process are the shortening of the refractory period with increased dispersion, the loss of rate adaptation, and the reduction of atrial conductivity. On the molecular level, calcium accumulation in myocytes seems to trigger electrophysiological changes leading to reduction in the intensity of L-type calcium current. Currently, the role of inflammation and oxidative stress on electrical remodeling is under investigation. C-reactive protein (CRP), a major inflammatory marker, has been found to be increased in both persistent and paroxysmal AF. Additionally, CRP may have prognostic significance regarding successful cardioversion of AF, and may predict recurrences of arrhythmia. On the other hand, it has been demonstrated that increased oxidative damage occurs in the atria of AF patients and may contribute to electrical remodeling. Interestingly, a prodromal antioxidant intervention study showed beneficial effects from vitamin C on incidence of postoperative AF. The role of inflammation and oxidative stress in AF deserves further study, since amelioration of atrial electrical remodeling by conventional antiarrhythmics has been proved ineffective.
Abstract: OBJECTIVE: To examine the effects of baseline left ventricular function on the haemodynamic and catecholamine responses to ventricular tachycardia. DESIGN: Experimental cohort study. SETTING: Cardiac catheterisation laboratory in tertiary referral centre. SUBJECTS: 24 patients (19 male, 5 female; mean (SD) age, 59 (10) years) without coronary artery disease, divided into two groups with normal or impaired left ventricular function: group A, ejection fraction > 65% (n = 10); group B, ejection fraction < 45% (n = 14). Other medical and demographic factors were similar in the two groups. INTERVENTIONS: Ventricular tachycardia was simulated with rapid pacing at 150 beats/min for 10 minutes. MAIN OUTCOME MEASURES: Arterial blood pressure; venous plasma catecholamine concentrations. RESULTS: During rapid pacing, blood pressure was lower in group B (with impaired left ventricular function) than in group A: systolic blood pressure, 102 (11) v 115 (9) mm Hg (p = 0.005); mean blood pressure, 79 (6) v 85 (6) mm Hg (p = 0.02). The ejection fraction correlated with the lowest systolic blood pressure (r = 0.64, p = 0.0006). Although the rise in adrenaline was comparable between the two groups, the rise in noradrenaline was more pronounced (p < 0.05) in patients in group B. CONCLUSION: At low rates and in selected patients, the underlying state of left ventricular function affects haemodynamic tolerance of ventricular tachycardia. Patients with impaired left ventricular function have a lower blood pressure during ventricular tachycardia, despite an exaggerated noradrenaline release.
Abstract: BACKGROUND: Controversy exists regarding inhibition of ischemic preconditioning in hyperlipidemic animals. In this study, we tested the hypothesis that hyperlipidemia inhibits the normal reduction of myocardial ischemia on repeated balloon inflations (BIs) during angioplasty. METHODS: We studied 33 patients undergoing coronary angioplasty. All underwent a minimum of three BIs. Patients were grouped according to the following plasma cholesterol levels: 13 patients had total cholesterol levels < 200 mg/dL (the normal cholesterol group); and 20 patients had total cholesterol levels > or = 200 mg/dL (the elevated cholesterol group). Surface ST-segment elevations were recorded at the end of each BI. RESULTS: In the normal cholesterol group, the mean (+/- SD) ST-segment elevation decreased from 0.21 +/- 0.15 mV during the first BI to 0.11 +/- 0.11 mV during the third BI (p < 0.05). In the elevated cholesterol group, the respective decrease was from 0.18 +/- 0.16 to 0.14 +/- 0.15 mV (p = not significant) [between-group comparisons: F = 3.97; p = 0.02]. The decrease in ST-segment elevation was correlated with the total cholesterol levels (r = -0.48; p = 0.005), the low-density lipoprotein (LDL) cholesterol levels (r = -0.50; p = 0.003), and the high-density lipoprotein/LDL levels (r = 0.44; p = 0.01). CONCLUSION: Hyperlipidemia prevents the normal reduction of myocardial ischemia on repeated BIs during angioplasty. This leads to the clinical implication that reduction of cholesterol plasma levels, apart from its other known benefits, could also have a beneficial effect on cardioprotection.
Abstract: PURPOSE: We compared the safety and efficacy of three closure devices (Angioseal, Vasoseal and Duett) used to close arterial puncture sites in patients who underwent coronary percutaneous procedures. METHODS: A prospective randomized, single-center trial was carried out of consecutive patients who underwent coronary angiography [705 patients: Angioseal (243),Vasoseal (228) and Duett (234)] or angioplasty [146 patients:Angioseal (47), Vasoseal (52) and Duett (47)]. RESULTS: In the angiography patients the device deployment rates were similar, with the Angioseal been significantly slower in achieving hemostasis (p = 0.0001) but resulting in earlier ambulation (p = 0.0001). In the coronary angioplasty patients the deployment rates were similar to those for angiography: time to hemostasis was longer for the Angioseal (p = 0.003), while ambulation times were not different, although prolonged compared with angiography (p = 0.0001). The three devices had similar major complication rates. The Vasoseal had a higher major complication rate after angioplasty than after angiography (p = 0.004). The incidence rate of peripheral embolization was lower when the Angioseal was utilized. Severe complications were mainly seen in patients who received abciximab. CONCLUSIONS: The three closure devices had high rates of successful deployment and were relatively safe. The Angioseal resulted in earlier ambulation after angiography. Utilization of closure devices after abciximab administration possibly increased the complications.
Abstract: It is known that myocardial ischaemia increases platelet aggregatory response to various agonists, ex vivo. We investigated the platelet aggregatory response to platelet activating factor (PAF), ex vivo, in patients with non-ST elevation acute coronary syndromes and determined the specificity and sensitivity of this response. Thirty-two consecutive patients with non-ST elevation acute coronary syndromes and 20 healthy volunteers were studied. Platelet aggregation in platelet-rich plasma was studied on the day of admission. The maximal aggregation achieved within 2 min after the addition of PAF (100 nM) was expressed as a percentage of 100% light transmission. PAF EC50 values were defined as the concentration that induces 50% of maximal aggregation. The PAF EC50 values of the non-ST elevation acute coronary syndromes patients were significantly lower compared to those of the controls (p < 0.0001). The maximal percentage of aggregation was also significantly higher (p < 0.0005). Ninety-one per cent of the patients were correctly classified using PAF EC50 values (specificity 90.0% and sensitivity 91.2%); the corresponding results using the maximal percentage of aggregation were 80% (specificity 70.0% and sensitivity 87.5%). The estimated values used as thresholds were 22.47 nM and 17.97 for the PAF EC50 and the maximal percentage of aggregation, respectively. The results of the present study suggest that platelet hyperaggregability to PAF, ex vivo, in non-ST elevation acute coronary syndromes is characterised by a high specificity and sensitivity, and thus it may represent a mechanism contributing to the pathophysiology of acute coronary syndromes.
Abstract: STUDY OBJECTIVES: Pacing-induced asynchrony may deteriorate left ventricular function; however, limited data exists in humans. The aim of our study was to compare left ventricular hemodynamics during short-term atrioventricular sequential pacing from the right ventricular apex and from the outflow tract of the right ventricle. DESIGN: Three 5-min pacing intervals were applied in a random order, at a rate of 15 beats/min above the resting sinus rate. Atrioventricular sequential pacing from the two sites was compared with atrial pacing. During each pacing mode, left ventricular pressure was recorded, and cardiac output was calculated using Doppler echocardiography. SETTING: Cardiac catheterization laboratory. PATIENTS: Twenty patients (18 male, mean age 62 +/- 11 years) without structural heart disease were studied. RESULTS: During atrial pacing, maximum negative first derivative of pressure (dp/dt) was 1,535 +/- 228 mm Hg/s; during pacing from the apex it decreased to 1,221 +/- 294 mm Hg/s (p = 0.0001), but was not significantly different during pacing from the outflow tract (1,431 +/- 435 mm Hg/s, p > 0.05). Isovolumic relaxation time constant (tau) during atrial pacing was 39.7 +/- 11.9 ms; during pacing from the apex, it increased to 47.9 +/- 14.0 (p = 0.001), but was not significantly different during pacing from the outflow tract (42.5 +/- 11.2, p > 0.05). Peak systolic pressure decreased significantly during atrioventricular sequential pacing from either site; however, it did not differ between the two sites. No differences in end-diastolic pressure, maximum positive dp/dt, or cardiac output could be demonstrated. CONCLUSION: In patients with no structural heart disease, short-term right ventricular outflow tract pacing is associated with more favorable diastolic function, compared to right ventricular apical pacing.
Notes: 0012-3692 (Print) xD;0012-3692 (Linking) xD;Comparative Study xD;Journal Article
Abstract: BACKGROUND: Myocardial ischemia and reperfusion are associated with increased production of endothelin (ET)-1. METHODS AND RESULTS: We examined the effects of BQ-123, a selective ET(A) receptor antagonist, in 80 patients. All patients were randomly allocated to an intracoronary infusion of saline or BQ-123 (6 micromol/L over 20 minutes). The reference group consisted of 20 patients undergoing coronary angiography. BQ-123 produced a 10% (P:<0.005) increase in distal coronary artery diameter. The main study group consisted of 30 patients undergoing coronary angioplasty. All patients underwent a minimum of 3 balloon inflations (BIs). Surface and intracoronary electrocardiographic ST-segment shift as well as pain score were recorded at the end of each BI. BQ-123 or saline was given by intracoronary infusion between the second and the third BI in random allocation. In the saline group, intracoronary ST-elevation decreased from 1.26+/-0.55 mV during the first BI to 0.77+/-0.56 mV during the third BI (P:<0.05) and the surface ST elevation decreased from 0.20+/-0.15 to 0.10+/-0.07 mV (P:<0.05). In the BQ-123 group, the respective values were 1.22+/-0.48 mV and 1.13+/-0.62 mV (intracoronary) and 0.17+/-0.18 and 0.17+/-0.21 mV (surface) (both P:=NS). The decrease in pain score was significantly higher in the saline group (F:=5.97, P:=0.004). In 30 patients (collateral circulation group), the angioplasty protocol was repeated with the use of a pressure guide wire. BQ-123 produced a significant (F:=3.30, P:=0.04) decrease in coronary wedge pressure. CONCLUSIONS: Acute ET(A) receptor antagonism prevents the normal reduction of myocardial ischemia on repeated BIs during angioplasty. This may be explained by a "steal" effect through coronary collaterals.
Abstract: We report a case of a prominent aneurysm of the right coronary artery secondary to atherosclerotic coronary artery disease. The aneurysm was complicated by recurrent myocardial infarction despite optimal medical treatment. It was successfully treated with coronary artery stenting, using a novel device, consisting two stents with a layer of expandable graft material placed between them. Follow-up angiography 6 months after the procedure showed a sustained excellent result.
Abstract: This article reviews the current knowledge on the effects of pacing on coronary hemodynamics. In particular, the possible effects of heart rate, atrioventricular delay, ventricular depolarization sequence, and ventricular pacing site on the coronary circulation are examined.
Abstract: Experimental animal data have indicated that the site of ventricular tachycardia origin and, hence, the degree of asynchronous contraction, may influence the hemodynamic tolerance during sustained ventricular tachycardia. However, data in man are scarce. We studied patients with preserved left ventricular function and absence of significant coronary artery disease. Ventricular tachycardia was simulated with rapid pacing (at 120 and 150 beats/min), performed randomly, from the right ventricular apex or the right ventricular outflow tract. Following pacing from one site, it was repeated from the alternate site. Compared to outflow tract pacing, QRS duration was significantly longer during rapid pacing from the apex. Left ventricular pressure was recorded using a micromanometer-tipped catheter. During sinus rhythm, peak systolic pressure was 142 +/- 14 mmHg; at 120 beats/min, it decreased to 109 +/- 12 mmHg during pacing from the apex and to 127 +/- 21 mmHg during pacing from the outflow tract (P = 0.008). This difference diminished at 150 beats/min (101 +/- 16 mmHg vs 112 +/- 16 mmHg, respectively, P = 0.21). During sinus rhythm end-diastolic pressure was 13 +/- 1 mmHg, which did not change significantly during pacing at 120 beats/min. During pacing at 150 beats/min, end-diastolic pressure increased to 21 +/- 3 mmHg during pacing from the apex and to 16 +/- 2 mmHg during pacing from the outflow tract (P = 0.005). Changes in first derivative of pressure and in isovolumic relaxation time constant were comparable during pacing from the two sites. Thus, it seems that tachycardias originating from the right ventricular outflow tract result in more favorable left ventricular hemodynamics, compared to those from the right ventricular apex.
Abstract: OBJECTIVE: To test the hypothesis that coronary flow reserve could increase in the angiographically normal contralateral artery after successful coronary angioplasty of an ipsilateral coronary artery. DESIGN: Coronary flow reserve was estimated using a Doppler flow guide wire, by giving intracoronary adenosine in the contralateral artery, before and 15 minutes after the end of angioplasty. SETTING: Tertiary referral centre. PATIENTS: 31 patients, mean (SD) age 56 (11) years, with stable angina and single vessel disease, undergoing angioplasty of the right coronary or the left anterior descending artery. RESULTS: In the contralateral artery baseline average peak velocity was 21 (9) cm/s before angioplasty and decreased to 12 (6) cm/s after (p < 0.005), while hyperaemic average peak velocity was 47 (19) cm/s before and decreased to 34 (15) cm/s after (p < 0.005). However, coronary flow reserve in the contralateral artery was 2.4 (0.7) before angioplasty and increased to 2.9 (0.6) after (p < 0.05). The contralateral coronary flow reserve after angioplasty increased by 0.8 (0.4) in 11 patients with visible collaterals before angioplasty and by 0.3 (0.6) in the remaining patients without visible collaterals (p < 0.05). Blood pressure and heart rate were unchanged after the procedure. CONCLUSIONS: Coronary flow reserve in an angiographically normal contralateral artery increases after successful coronary angioplasty of the ipsilateral artery in patients with spontaneously visible collateral vessels before the procedure.
Abstract: Previous studies have indicated that ventricular asynchrony may significantly affect resting coronary blood flow velocity. Our study argues against this hypothesis, as comparable left anterior descending blood flow velocities were found during three pacing modalities, associated with varying degrees of asynchrony: (a) atrial pacing, (b) atrioventricular (AV) sequential pacing from the right ventricular apex and (c) AV sequential pacing from the proximal right ventricular septum.
Notes: 0167-5273 (Print) xD;0167-5273 (Linking) xD;Comparative Study xD;Journal Article
Abstract: The effect of beta-adrenergic blockade on coronary collateral blood flow has not been clarified. We examined the acute effects of beta-adrenergic blockade on coronary collateral blood flow. Fifteen patients (Part A) with stable angina were studied while undergoing coronary angioplasty. According to the protocol, all patients underwent a minimum of three balloon inflations. Collateral flow velocity was determined during balloon inflations using the Doppler flow guidewire positioned distally to the lesion. The two tested balloon inflations, the second and third, were maintained for the same length of time. Between the second and third balloon inflations, 1 mg of propranolol was administered IC into the treated artery. Ten controls were studied following saline infusion. In 10 other patients (Part B), the effect of 1 mg IC propranolol on the coronary artery area distal to the lesion was studied, and five patients served as controls. In the treated group, in Part A blood pressure remained stable during the balloon inflations tested. Heart rate decreased from 79 +/- 11 to 73 +/- 12 beats/min (P < .05), velocity time integral from 9.6 +/- 8.2 to 6.6 +/- 4.1 cm (P < .05), and ST elevation from 1.3 +/- .9 to .9 +/- 1.0 mV (P < .05) between the second and third balloon inflations. In the controls the variables examined did not change during the balloon inflations tested. In Part B, neither propranolol nor normal saline had any significant effect on coronary artery lumen area. Thus, IC administration of beta-adrenergic blockade decreases coronary collateral blood flow, and this potentially worsens the ischemic zone. However, beta-adrenergic blockade ameliorates myocardial ischemia during coronary angioplasty.
Abstract: Altered sequence of ventricular activation sequence results in marked derangements in mechanical events. In the present study, we investigated the comparative effects of atrial and AV sequential pacing on collateral blood flow during angioplasty. Twenty-eight patients with stable angina and left anterior descending artery disease undergoing balloon angioplasty were studied. Collateral flow was determined during balloon inflation from the distal flow velocity of the ipsilateral artery (17 patients) or from the increase of the maximal diastolic blood flow velocity (Vc) of the contralateral artery (11 patients). Flow measurements were made using the Doppler flow guidewire. The relative resistance in the collateral vascular bed (RR) also was estimated in the latter group of patients. After the first balloon inflation, two similar consecutive balloon inflations were done under atrial and AV sequential pacing, at a rate of 15 beats/min higher than the sinus rate, in the absence of vasoactive medication. One minute after the initiation of pacing, the second and third balloon inflations were begun and the pacing continued until the balloon inflations were completed. In the ipsilateral group, average peak velocity was 84.6 +/- 24.2 mm/2 during atrial pacing and 82.7 +/- 29.7 mm/s during AV sequential pacing (P = NS). In the contralateral group, Vc was 18% +/- 12% during atrial pacing and 17% +/- 14% during AV sequential pacing, and the RR was 4.5 +/- 4.7 and 4.9 +/- 6.4, respectively (both P = NS). The coronary wedge/mean blood pressure was similar during the two tested balloon inflations. Short-term AV sequential pacing at rest does not adversely affect collateral blood flow and resistance in patients with left anterior descending artery disease.
Notes: 0147-8389 (Print) xD;0147-8389 (Linking) xD;Comparative Study xD;Journal Article
Abstract: This study examined the effects of different atrioventricular (AV) intervals, during AV sequential pacing, on hemodynamics and coronary blood flow in individuals with normal hearts. Left anterior descending artery blood flow velocity was measured, using intracoronary Doppler, in 17 normal individuals. Five pacing tests were applied in random order for 5 min, at 15 beats/min above the sinus rate. Four tests using AV sequential pacing with AV intervals of 175, 150, 100, and 50 ms, and one using atrial pacing were applied. Mean flow velocity was 21 +/- 9 cm/s, 20 +/- 9 cm/s, 17 +/- 7 cm/s, 17 +/- 7 cm/s, and 22 +/- 10 cm/s, respectively (F = 8.87, p = .00001). The hemodynamic effects of these 5 pacing tests were assessed in 8 different normal subjects. Isovolumic relaxation time constant and left ventricular systolic pressure decreased, whereas right atrial pressure increased during AV sequential pacing with short AV intervals. Thus, during short-term AV sequential pacing at rest, coronary blood flow in a normal left anterior descending artery decreases with short AV intervals.
Abstract: To evaluate the safety and long-term efficacy of internal transcatheter cardioversion, forty patients with chronic, lone atrial fibrillation were studied. The patients were randomised to internal transcatheter cardioversion or to conventional external cardioversion. In cases where the procedure was unsuccessful, cross-over to the alternate method was performed. Oral anticoagulation therapy was started three weeks prior to the procedure and was maintained for another three weeks following successful cardioversion. Sinus rhythm was restored in 16/18 patients (88%) in the internal cardioversion group, versus 9/22 patients (40%) in the external cardioversion group (p < 0.01). In addition, 8/13 (61%) patients who were crossed-over to internal cardioversion were successfully cardioverted to sinus rhythm. In contrast, both patients who were crossed-over to external cardioversion remained in atrial fibrillation. During a mean follow-up period of 23 months, 13 (39.3%) patients maintained sinus rhythm. Using the intention to treat principle, the recurrence rate was not statistically different between the two methods. It is concluded that internal cardioversion is more effective in acutely restoring sinus rhythm compared to external cardioversion. However, both methods have similar long-term recurrence rates.
Abstract: The Multicenter Automatic Defibrillator Implantation Trial (MADIT) showed improved survival with defibrillator therapy but was restricted to coronary artery disease patients with nonsustained ventricular tachycardia (NSVT) and inducible nonsupressible VT. The outcome of patients without inducible VT or inducible but suppressed VT still remains unclear. We performed risk stratification at electrophysiologic (EP) study in 111 consecutive unselected patients with nonsustained VT and coronary artery disease and randomized them to drug or device therapy. Follow-up on selected therapy was 1-71 (mean 27 +/- 20) months. Of 111 patients, 39 patients (35%) had inducible sustained VT at baseline EP study and were stratified to a "higher" risk group (group 1) for sudden death. In 9 of these patients (group 1A), sustained VT was suppressed with class IA antiarrhythmic drugs; in the remaining 30 patients (group 1B) sustained VT was not suppressed with class IA antiarrhythmic drugs. The other 72 of 111 patients (65%) had no inducible sustained VT at EP study and were stratified to a "lower"-risk group (group 2) for sudden death. Mean LVEF in group 1 was 30 +/- 10% versus 37 +/- 9% in group 2 (p = 0.001). Selected therapy in group 1 was an implantable cardioverter defibrillator (16 patients) or guided drug therapy (electrophysiologically guided class I antiarrhythmic drugs = 7 patients; Holter-guided class III antiarrhythmic drugs = 16 patients). In group 2, empiric drug therapy included beta blockers in 29 patients or Holter-guided class III antiarrhythmic drugs in 17 patients, with no antiarrhythmic drug therapy being administered in 26 patients. Mean LVEF tended to be lower in patients receiving class III antiarrhythmic drug therapy (34 +/- 12%) than in patients receiving beta blockers (40 +/- 10%, p = 0.06). Three-year total survival was comparable in group 1 (70%) and in group 2 (81%), but sudden cardiac death mortality tended to be lower in group 1 versus group 2 (0 vs 9%, p = 0.09). Patients receiving class III antiarrhythmic therapy had significantly higher 3-year all cause (40%, p = 0.04) and sudden death (25%, p = 0.06) mortality than patients receiving beta blockers (17% and 8% respectively) or no antiarrhythmic drug therapy (4% and 0%, respectively). The following conclusions can be drawn from this analysis: (1) Electrophysiologically guided drug therapy and implantable defibrillators can minimize the risk of sudden cardiac death in patients with coronary artery disease and inducible sustained VT stratified to higher risk of sudden death. A comparable outcome with respect to sudden death prevention in drug-suppressed or drug-refractory patients suggests limited prognostic benefit of class IA drug testing. (2) Lower-risk patients with severely depressed LVEF and minimal or no symptoms do not have a favorable outcome with respect to sudden and all-cause mortality on Holter-guided class III drug therapy. However, asymptomatic patients with mildly depressed left ventricular function have low sudden death event rates on beta blocker or no antiarrhythmic drug therapy.
Abstract: Several factors may influence hemodynamic tolerance of a ventricular tachycardia (VT) episode but, to date, only VT rate has been used as a major detection criterion in selecting implantable cardioverter-defibrillator therapy algorithms. We examined hemodynamic changes during VT in humans and a possible correlation between left and right ventricular hemodynamic indexes. Right ventricular hemodynamic indexes could reflect systemic hemodynamics but previous studies have been inconclusive. Patients with coronary artery disease and a history of recurrent, sustained VT were studied. Aortic pressure and right and left ventricular pressures were simultaneously recorded with 2 dual micromanometer-tipped high-fidelity pressure catheters during sinus rhythm and during induced sustained monomorphic VT. Beat-to-beat analysis was performed using custom-made software. Nine patients (7 men, mean age 60 +/- 8 years, mean ejection fraction 24 +/- 8%) with 11 VT episodes (mean cycle length 283 +/- 48 ms) were studied. During VT, left and right ventricular systolic pressures showed a mean decrease of 57% and 26%, respectively, with weak correlation (r = 0.67, p = 0.06) between both values. There was also an increase in mean left and right ventricular end-diastolic pressures of 26% and 74%, respectively, and no correlation was seen (r = -0.2, p = 0.6). A significant correlation was found between changes in left and right ventricular maximal positive dP/dt (55% and 28% decrease, respectively (r = 0.69, p = 0.03) and between changes in left and right ventricular maximal negative dP/dt (64% vs 39% decrease, r = 0.71, p = 0.02). Most ventricular time parameters in both ventricles differed significantly during VT compared with sinus rhythm; however, only the decrease in right ventricular time to end-diastolic pressure correlated with the decrease in left ventricular systolic pressure, at the 10th VT beat (r = 0.8, p = 0.01). We conclude that left and right ventricles are hemodynamically unequally affected during rapid VT. Although right ventricular pressures cannot be reliably used to assess changes in the hemodynamic status of the left ventricle, additional parameters, such as dP/dt or changes in ventricular time intervals, should be further evaluated for inclusion in implantable cardioverter-defibrillator algorithms.
Abstract: Experimental animal data have indicated that altered left ventricular depolarization sequence as a result of right ventricular pacing may diminish coronary blood flow in the distribution of the left anterior descending coronary artery. To further investigate this, we compared the effects of atrial, ventricular, and atrioventricular (AV) sequential pacing on coronary flow reserve. Twenty-seven patients (24 male, mean age 55 +/- 7 years) with normal left anterior descending coronary arteries were studied. Coronary flow reserve was calculated as the ratio of mean flow velocity at maximal coronary vasodilatation to mean flow velocity at baseline. The study consisted of two parts. In the first part, AV sequential pacing was compared to atrial pacing at the same rate; coronary flow reserve did not differ significantly between the two pacing modes (14 patients, 4.85 +/- 1.88 vs 5.47 +/- 1.55, respectively, P > 0.05). In the second part, all three pacing modalities were compared; coronary flow reserve was significantly higher during ventricular compared to AV sequential pacing, but not significantly different compared to atrial pacing (3.69 +/- 1.42 vs 2.90 +/- 0.86 vs 3.11 +/- 0.89, respectively, P < 0.05). This difference was secondary to a significant decrease in mean baseline velocity during ventricular pacing, while mean velocity during hyperemia was comparable between the three pacing modes. It is concluded that AV sequential pacing does not appear to exert a significant effect on coronary flow reserve. Ventricular pacing, however, may lower resting coronary blood velocity in some patients, without affecting maximal coronary blood velocity, resulting in a higher coronary flow reserve.
Notes: 0147-8389 (Print) xD;0147-8389 (Linking) xD;Comparative Study xD;Journal Article
Abstract: We undertook a prospective randomized clinical trial evaluating efficacy and safety of internal atrial defibrillation in patients with drug-refractory atrial fibrillation (AF). Consecutive patients with paroxysmal or chronic AF were randomly tested with 3 internal atrial defibrillation lead configurations and biphasic shocks. Patients with implanted cardiac pacemakers were tested with the right atrium (RA) and left pulmonary artery or coronary sinus (CS) configuration. Shocks were initially delivered without anesthesia to assess patient tolerance. The need for backup ventricular defibrillation and pacing support was evaluated. Eighteen patients with (n = 15) or without (n = 3) structural heart disease, mean left ventricular ejection fraction 36 +/- 14%, and mean left atrial diameter 4.5 +/- 0.6 cm were studied. The mean defibrillation threshold in the best randomized lead configuration was 9.9 +/- 7.7 J. Mean defibrillation threshold for the right ventricle (RV) and superior vena cava configuration was 13.3 +/- 5 J, which was significantly lower than the RA and axilla configuration (20.1 +/- 7.4 J, p < 0.04) but not the RV to RA configuration (16.5 +/- 11 J, p > 0.2). The mean defibrillation threshold using the RA-left pulmonary artery/CS configuration was 8.9 +/- 9 J (p > 0.2 vs RV-superior vena cava). There was a bimodal distribution of defibrillation thresholds. Low atrial defibrillation thresholds correlated with absence of heart disease, higher ejection fraction, and smaller left ventricular end-diastolic diameter. Shocks were hemodynamically well tolerated, but 2 of 18 patients (11%) had nonsustained ventricular tachycardia after shock delivery. Six of 18 patients (33%) had postshock bradyarrhythmias. Fourteen of 16 patients perceived shocks > or = 3 J as intolerable.(ABSTRACT TRUNCATED AT 250 WORDS) [corrected]
Abstract: There is controversy over the effects of beta-blockade on the left ventricular systolic response of the heart of the elderly to stress. In this study we compared the effects of acute beta-blockade in normal older and younger adult left ventricles during exercise. The study population consisted of 17 healthy elderly people, 67 +/- 3 years old, while 18 young normal subjects, 31 +/- 4 years old, served as controls. A symptom-limited exercise treadmill test was performed before and 15 minutes after intravenous administration of 0.12 mg propranolol/kg. M-mode echocardiographic studies were performed before and immediately after each test. Intravenous propranolol at rest decreased heart rate by 14 +/- 7 beats/min in the elderly and by 7.5 +/- 8 beats/min in the young (p = 0.02), decreased the double product by 2500 +/- 1200 mmHg/min and 1830 +/- 970 mmHg/min (p = 0.05), respectively; changed the left ventricular end-systolic dimension by +0.21 +/- 0.36 cm and +0.03 +/- 0.24 cm (p = 0.09), respectively; and changed the end-diastolic dimension by +0.22 +/- 0.46 cm in the elderly and by -0.02 +/- 0.32 cm in the young (p = 0.08). The change in fractional shortening was -1.22 +/- 4.17% in the elderly and -0.78 +/- 4.05% in the young (p > 0.05), and the decrease in the systolic blood pressure/end-systolic dimension ratio was 5.9 +/- 7 mmHg/cm and 4.3 +/- 3.8 mmHg/cm, respectively (p > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Notes: 0920-3206 (Print) xD;0920-3206 (Linking) xD;Comparative Study xD;Journal Article
Abstract: The purpose of this randomized controlled study was to assess the haemodynamic effects, safety and tolerability in acute myocardial infarction (AMI) of one month of oral captopril, one month of oral isosorbide mononitrate and 24 h of intravenous magnesium. It was carried out in four United Kingdom and six Polish hospitals in consecutive phases: oral captopril vs oral mononitrate vs placebo were compared among 400 patients in a 'three-way' study; and then oral captopril vs placebo and oral mononitrate vs placebo were compared among 474 patients in '2 x 2' and '2 x 2 x 2' factorial studies (with 208 patients in the latter study also randomized between intravenous magnesium and open control). The factorial studies differed from the three-way study in that one group of patients was allocated both oral captopril and oral mononitrate, a higher maintenance dose of captopril was used (following the same initial dose), and once daily controlled-release mononitrate was used. In the three-way study, the mean of the lowest systolic blood pressures recorded during the first 4 h after randomization were (mmHg +/- standard error): 104 +/- 2 captopril vs 105 +/- 1 mononitrate vs 112 +/- 2 placebo (P < 0.001 for captopril or for mononitrate vs placebo), and in the factorial studies were 105 +/- 1 captopril vs 110 +/- 1 placebo (P < 0.01) and 106 +/- 1 mononitrate vs 108 +/- 1 placebo (NS). There was an excess of hypotension recorded among patients allocated active treatment (captopril > mononitrate > placebo) and there was a small, but significant, excess of cardiogenic shock with captopril compared with control in the factorial study. However, in these studies, neither captopril nor mononitrate were associated with any overall increase in the incidence of hypotension considered severe enough to lead to treatment being stopped. No other serious complications were observed, and compliance with study tablets at hospital discharge was not significantly different between the active and placebo groups. Patients allocated magnesium in the 2 x 2 x 2 factorial study had a slightly lower mean systolic blood pressure just after the initial 15 min bolus injection (126 +/- 2 magnesium vs 134 +/- 3 control; P < 0.05) but there were no significant differences during the subsequent 24 h maintenance infusion period. Apart from some facial flushing, magnesium did not appear to be associated with any complications.(ABSTRACT TRUNCATED AT 400 WORDS)
Notes: 0195-668X (Print) xD;0195-668X (Linking) xD;Clinical Trial xD;Comparative Study xD;Journal Article xD;Multicenter Study xD;Randomized Controlled Trial xD;Research Support, Non-U.S. Gov't
Abstract: Despite substantial progress in the management of ischemic heart disease and congestive heart failure, long-term mortality rates as a result of sudden cardiac death in such patients remain significant. Risk stratification that uses a combination of several predictors of clinical outcome has improved our ability to identify persons at high risk for future arrhythmic events. beta-Blockers and amiodarone are effective in primary prevention of sudden death in selected populations. In view of the impressive reduction in sudden death rates by implantable cardioverter defibrillators (ICDs) in patients with a history of cardiac arrest, prophylactic implantation may also be beneficial. The best way to treat these patients is not known. Three ongoing controlled clinical trials have been designed for drugs, ICDs, or both and will provide answers about whether prophylactic antiarrhythmic intervention with ICDs improves survival and whether device therapy is superior to pharmacologic treatment. Brief reports on these clinical trials are discussed in this review.
Abstract: OBJECTIVE--To assess the effects of oral vasodilator treatment on ventricular arrhythmias in acute myocardial infarction. SETTING--Coronary care units at the John Radcliffe Hospital, Oxford, and the Royal Infirmary, Edinburgh. PATIENTS--100 patients with suspected acute myocardial infarction entered the study at a mean of 13 hours from symptom onset. DESIGN OF INTERVENTION--Double blind randomisation to 4 weeks treatment with captopril (12.5 mg three times a day after a 6.25 mg test dose (n = 32)) or isosorbide mononitrate (20 mg three times a day (n = 31)) or placebo control (n = 37). OUTCOME MEASURES--Ventricular arrhythmic events assessed by 48 hours of Holter monitoring starting at the time of randomisation. RESULTS--The number of ventricular extrasystoles/hour for captopril, mononitrate, and placebo was respectively (median and range) 6 (0-162), 4 (0-38), and 10 (0-932) (2p < 0.02 mononitrate v placebo). The number of episodes of multiple extrasystoles/hour was 0.2 (0-22), 0.3 (0-4), and 0.5 (0-19); (2p < 0.02 mononitrate v placebo). Episodes of ventricular tachycardia showed a non-significant decrease in the captopril and mononitrate groups (mean (SEM) 3.2 (0.8), 2.4 (0.7), and 4.7 (1.3) for the 48 hour period). The incidence of idioventricular rhythm was also reduced in both active treatment groups (28%, 19%, and 46% (2p < 0.05 mononitrate v placebo)). CONCLUSIONS--Oral mononitrate (and perhaps also captopril) seems to reduce the incidence of ventricular arrhythmias in the early phase of acute myocardial infarction. The effects on life-threatening arrhythmias, such as ventricular fibrillation, and on death can only be assessed in a much larger trial.
Abstract: We report a case of a 72-year-old lady with rheumatic heart disease and chronic, long-lasting atrial fibrillation, who reverted spontaneously to sinus rhythm. Doppler study showed evidence of mechanical contraction of the right but not of the left atrium. This may be a sign of marked histologic changes in the atria and may require the insertion of a permanent pacemaker, because of subsequent development of sinus bradycardia.
Abstract: This investigation was undertaken to evaluate the effects of short-term atrial vs atrio-ventricular pacing on myocardial ischaemia. The study was in two parts. In part one, 12 coronary artery disease patients were studied to investigate the effects of the two pacing modes on angina pectoris, coronary sinus O2 saturation and lactate. The two pacing modes were each applied for 5 min at 25 beats.min-1 more than the maximum heart rate of the exercise test. Coronary sinus O2 saturation and lactate were estimated before and after pacing. In part two, 13 patients with left anterior descending coronary artery disease were studied to investigate the effects of the two pacing modes on coronary flow reserve, using a Doppler catheter in the above mentioned branch after the administration of 10 mg intracoronary papaverine. The pacing rate was 15 beats.min-1 greater than the resting heart rate. Coronary sinus lactate and O2 saturation changes were the same and angina pectoris developed at about the same time from the beginning of pacing under both modes. Coronary flow reserve was 2.1 +/- 0.7 during atrial pacing and 2.1 +/- 1.1 during atrio-ventricular pacing (ns). It is concluded that short-term atrial and atrio-ventricular pacing have the same effects on myocardial ischaemia in coronary artery disease patients.
Abstract: OBJECTIVE--To assess the influence of vasodilator treatment started early after myocardial infarction on left ventricular size and function. SETTING--Coronary care unit, Royal Infirmary, Edinburgh. PATIENTS--105 patients with acute myocardial infarction (systolic blood pressure > 90 mm Hg) were randomised within 24 hours of the start of pain. Unlike previous studies 88% of the patients received thrombolysis. METHODS--Double blind randomised placebo controlled study with either 12.5 mg of captopril three times daily or 20 mg of isosorbide mononitrate three times daily for 28 days. MAIN OUTCOME MEASURES--Clinical outcome and left ventricular size and function assessed by echocardiography, radionuclide ventriculography, and magnetic resonance imaging. RESULTS--There was no difference in left ventricular size or function in either treatment group as measured one week after the end of the trial. Even the placebo group tended to decrease left ventricular diameter over the four week study period (one week: 5.0 (0.1) v, five weeks: 4.8 (0.1) cm, NS). Four patients had an adverse clinical outcome in the placebo group whereas no adverse outcome was seen in the captopril group. CONCLUSIONS--Vasodilator treatment may be of limited value or of no benefit for most infarct patients, particularly those treated with thrombolytic agents. Captopril, however, may benefit patients at high risk.
Abstract: The records of 100 patients with permanent atrial pacemakers implanted over a 7-year period were reviewed to assess the role and results of this mode of pacing. Indications for pacing were sick sinus syndrome in 91, carotid sinus hypersensitivity in 3, and use of an antitachycardia device in 6 patients. The mean follow-up period was 32.9 months. Symptomatic relief was good. Lead dislodgment occurred in 11 patients (usually in the first week). Threshold rises not amenable to reprogramming occurred in three patients and loss of sensing occurred in seven patients but only one required intervention. Overall, 21 patients required reoperation. The type of lead did not influence the need for reoperation that appeared to be related to the experience of the operator. Complete atrioventricular block occurred in three patients, two of whom had carotid sinus hypersensitivity and one had sick sinus syndrome. Chronic atrial fibrillation occurred in five patients, none of whom required revision of the pacemaker system. Atrial pacing is a satisfactory pacing mode in patients with sick sinus syndrome. Provided satisfactory atrioventricular conduction has been shown by incremental atrial pacing to at least 120 beats/min and carotid hypersensitivity is absent, progression to complete atrioventricular block is uncommon. Greater implanting skills are required for good results.
Abstract: We studied the clinical and angiographic outcome of patients with prior coronary arterial bypass grafting who underwent percutaneous transluminal coronary angioplasty at the Royal Infirmary of Edinburgh. Over a 4 year period, 47 patients with prior bypass surgery underwent angioplasty of 23 stenotic graft sites and 37 stenotic sites of native vessels. The procedure was performed a mean of 31.3 months after surgery for recurrence of symptoms refractory to maximal medical treatment. Satisfactory angiographic results were achieved in 42 patients (58 stenotic grafts or native vessels). At a median follow up period of 18 months, 20 patients were symptomatically improved, but 22 patients experienced recurrence of symptoms a mean of 4.7 months after angioplasty, despite a good initial angiographic result. Overall, 4 patients had a repeat bypass grafting and 9 patients had a repeat angioplasty. Angioplasty can be used as an alternative to a repeat operation in patients with prior bypass grafting who experience recurrence of symptoms. Initial success rates are high and complication rates low. Restenosis or development of new lesions in the native circulation, and/or in the grafts, remain significant problems. Patients with a long asymptomatic interval (greater than 6 months) between the bypass operation and recurrence of symptoms are more likely to have better long-term results after successful angioplasty, perhaps because of slower progression of atherosclerotic heart disease.
